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[DCTN4] as a modifier of [chronic Pseudomonas aeruginosa infection] in [cystic fibrosis] [Pseudomonas aeruginosa (Pa) infection] in [cystic fibrosis] ([CF]) patients is associated with worse long-term [pulmonary disease] and shorter survival, and [chronic Pa infection] ([CPA]) is associated with reduced lung function, [faster rate of lung decline], increased rates of [exacerbations] and shorter survival. By using [exome sequencing] and extreme phenotype design, it was recently shown that [isoforms] of [dynactin 4] ([DCTN4]) may influence [Pa infection] in [CF], leading to worse [respiratory disease]. The purpose of this [study] was to investigate the role of [DCTN4] missense [variants] on [Pa infection] incidence, age at first [Pa infection] and [chronic Pa infection] incidence in a [cohort] of adult [CF] patients from a single [centre]. [Polymerase chain reaction] and [direct sequencing] were used to screen [DNA samples] for [DCTN4] [variants]. A total of 121 adult [CF] patients from the [Cochin Hospital CF centre] have been included, all of them carrying two [CFTR] defects: 103 developed at least 1 [pulmonary infection] with [Pa], and 68 patients of them had [CPA]. [DCTN4] [variants] were identified in 24% (29/121) [CF] patients with [Pa infection] and in only 17% (3/18) [CF] patients with no [Pa infection]. Of the patients with [CPA], 29% (20/68) had [DCTN4] missense [variants] vs 23% (8/35) in patients without [CPA]. Interestingly, [p.Tyr263Cys] tend to be more frequently observed in [CF] patients with [CPA] than in patients without [CPA] (4/68 vs 0/35), and [DCTN4] missense [variants] tend to be more frequent in male [CF] patients with [CPA] bearing two [class II mutations] than in male [CF] patients without [CPA] bearing two [class II mutations] (P = 0.06). Our observations reinforce that [DCTN4] missense [variants], especially [p.Tyr263Cys], may be involved in the [pathogenesis] of [CPA] in male [CF].	[DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [chronic Pseudomonas aeruginosa infection]{Disorders} is Infection Pseudomonas aeruginosa [cystic fibrosis]{Disorders} is Cystic Fibrosis [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [Pseudomonas aeruginosa (Pa) infection]{Disorders} is Infection Pseudomonas aeruginosa [chronic Pseudomonas aeruginosa infection]{Disorders} is Infection Pseudomonas aeruginosa [cystic fibrosis]{Disorders} is Cystic Fibrosis [CF]{Disorders} is Cystic Fibrosis [cystic fibrosis]{Disorders} is Cystic Fibrosis [pulmonary disease]{Disorders} is Pulmonary disease [chronic Pa infection]{Disorders} is Infection Pseudomonas aeruginosa [CPA]{Disorders} is Infection Pseudomonas aeruginosa [faster rate of lung decline]{Disorders} is LUNG FUNCTION, ACCELERATED RATE OF DECLINE IN, SMOKING-RELATED [exacerbations]{Disorders} is Exacerbation [exome sequencing]{Procedures} is Exome Sequencing [isoforms]{Chemicals & Drugs} is Isoforms [dynactin 4]{Chemicals & Drugs} is DCTN4 protein, human [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [Pa infection]{Disorders} is Infection Pseudomonas aeruginosa [CF]{Disorders} is Cystic Fibrosis [respiratory disease]{Disorders} is Respiratory disease [study]{Procedures} is Study [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [variants]{Chemicals & Drugs} is Isoforms [Pa infection]{Disorders} is Infection Pseudomonas aeruginosa [Pa infection]{Disorders} is Infection Pseudomonas aeruginosa [chronic Pa infection]{Disorders} is Infection Pseudomonas aeruginosa [cohort]{Living Beings} is Cohort [CF]{Disorders} is Cystic Fibrosis [centre]{Organizations} is Health centre [Polymerase chain reaction]{Procedures} is Polymerase Chain Reaction [direct sequencing]{Procedures} is Direct Sequencing [DNA samples]{Anatomy} is DNA - Deoxyribonucleic acid sample [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [variants]{Chemicals & Drugs} is Isoforms [CF]{Disorders} is Cystic Fibrosis [Cochin Hospital CF centre]{Organizations} is Hospital [CFTR]{Genes & Molecular Sequences} is CFTR [pulmonary infection]{Disorders} is Pulmonary infection [Pa]{Living Beings} is Bacillus aeruginosus [CPA]{Disorders} is Infection Pseudomonas aeruginosa [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [variants]{Chemicals & Drugs} is Isoforms [CF]{Disorders} is Cystic Fibrosis [Pa infection]{Disorders} is Infection Pseudomonas aeruginosa [CF]{Disorders} is Cystic Fibrosis [Pa infection]{Disorders} is Infection Pseudomonas aeruginosa [CPA]{Disorders} is Infection Pseudomonas aeruginosa [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [variants]{Chemicals & Drugs} is Isoforms [CPA]{Disorders} is Infection Pseudomonas aeruginosa [p.Tyr263Cys]{Chemicals & Drugs} is Isoforms [CF]{Disorders} is Cystic Fibrosis [CPA]{Disorders} is Infection Pseudomonas aeruginosa [CPA]{Disorders} is Infection Pseudomonas aeruginosa [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [variants]{Chemicals & Drugs} is Isoforms [CF]{Disorders} is Cystic Fibrosis [CPA]{Disorders} is Infection Pseudomonas aeruginosa [class II mutations]{Physiology} is Mutations [CF]{Disorders} is Cystic Fibrosis [CPA]{Disorders} is Infection Pseudomonas aeruginosa [class II mutations]{Physiology} is Mutations [DCTN4]{Chemicals & Drugs} is DCTN4 protein, human [variants]{Chemicals & Drugs} is Isoforms [p.Tyr263Cys]{Chemicals & Drugs} is Isoforms [pathogenesis]{Disorders} is Pathogenesis [CPA]{Disorders} is Infection Pseudomonas aeruginosa [CF]{Disorders} is Cystic Fibrosis
Prevascularized [silicon] membranes for the enhancement of transport to [implanted medical devices] Recent advances in [drug delivery] and sensing devices for [in situ] [applications] are limited by the diffusion -limiting [foreign body response] of fibrous encapsulation. In this study, we fabricated prevascularized synthetic device ports to help mitigate this limitation. Membranes with rectilinear arrays of [square] pores with widths ranging from 40 to 200 μm were created using materials (50 μm thick double-sided [polished silicon]) and processes (photolithography and directed reactive ion etching) common in the manufacturing of microfabricated sensors. [Vascular endothelial cells] responded to membrane geometry by either forming [vascular tubes] that [extended] through the pore or completely filling membrane pores after 4 days in culture. Although tube formation began to predominate [overgrowth] around 75 μm and continued to increase at even larger pore sizes, tubes formed at these large pore sizes were not completely [round] and had relatively thin [walls]. Thus, the optimum range of pore size for prevascularization of these membranes was estimated to be 75-100 μm. This [study] lays the foundation for creating a prevascularized port that can be used to reduce fibrous encapsulation and thus enhance diffusion to [implanted medical devices] and sensors. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1602-1609, 2016.	[silicon]{Chemicals & Drugs} is Silicones [implanted medical devices]{Disorders} is Implanted Medical Device [silicon]{Chemicals & Drugs} is Silicones [drug delivery]{Devices} is Drug Delivery [in situ]{Concepts & Ideas} is In Situ [applications]{Procedures} is Application [implanted medical devices]{Disorders} is Implanted Medical Device [foreign body response]{Disorders} is Host Tissue Response To Foreign Body [square]{Concepts & Ideas} is Square [polished silicon]{Chemicals & Drugs} is Silicones [Vascular endothelial cells]{Anatomy} is Vascular Endothelial Cells [vascular tubes]{Anatomy} is Vascular structure [extended]{Concepts & Ideas} is Extended [overgrowth]{Disorders} is Overgrowth [round]{Concepts & Ideas} is Round [walls]{Concepts & Ideas} is Wall structure [study]{Procedures} is Study [implanted medical devices]{Disorders} is Implanted Medical Device
[Seated] maximum [flexion]: An alternative to [standing] maximum [flexion] for determining presence of [flexion] - relaxation? The [flexion] - relaxation phenomenon (FRP) in [standing] is a specific and sensitive [diagnostic tool] for [low back pain]. [Seated flexion] as an alternative could be beneficial for certain [populations], yet the behavior of the [trunk extensors] during [seated] maximum [flexion] compared to [standing] [flexion] remains unclear. Compare FRP occurrences and [spine] [angles] between [seated] and [standing] [flexion] postures in three levels of the [erector spinae muscles]. Thirty-one [participants] free of [back pain] performed [seated] and [standing] maximum [trunk] [flexion]. Electromyographical signals were recorded from the [bilateral lumbar (L3)], [lower-thoracic (T9)], and [upper-thoracic (T4)] [erector spinae] and assessed for the occurrence of FRP. [Spine angles] corresponding to FRP onset and cessation were determined, and FRP occurrences and [angles] were compared between posture and [muscle]. FRP occurrence was similar in [standing] and [seated] maximum [flexion] across all [muscles], with the [lumbar muscles] showing the greatest consistency. [Standing] FRP onset and cessation angles were consistently greater than the corresponding [seated] FRP angles. Considering the similar number of FRP occurrences, [seated] maximum [flexion] may constitute an objective criterion for [low back pain] [diagnosis]. Future work should seek to confirm the utility of this test in [individuals] with [low back pain].	[Seated]{Disorders} is Seated [flexion]{Physiology} is Flexion [standing]{Concepts & Ideas} is Standing [flexion]{Physiology} is Flexion [flexion]{Physiology} is Flexion [Seated]{Disorders} is Seated [flexion]{Physiology} is Flexion [flexion]{Physiology} is Flexion [standing]{Concepts & Ideas} is Standing [standing]{Concepts & Ideas} is Standing [flexion]{Physiology} is Flexion [diagnostic tool]{Procedures} is Diagnostic Method [flexion]{Physiology} is Flexion [low back pain]{Disorders} is Low back pain [Seated flexion]{Physiology} is Flexion [populations]{Living Beings} is Population [trunk extensors]{Anatomy} is Muscle tissue (body structure) [seated]{Disorders} is Seated [flexion]{Physiology} is Flexion [standing]{Concepts & Ideas} is Standing [flexion]{Physiology} is Flexion [spine]{Anatomy} is Dorsal spine [angles]{Concepts & Ideas} is Angle [seated]{Disorders} is Seated [standing]{Concepts & Ideas} is Standing [flexion]{Physiology} is Flexion [erector spinae muscles]{Anatomy} is Erector spinae muscle [participants]{Living Beings} is Participant [back pain]{Disorders} is Pain back [seated]{Disorders} is Seated [standing]{Concepts & Ideas} is Standing [trunk]{Anatomy} is TRUNK [flexion]{Physiology} is Flexion [bilateral lumbar (L3)]{Anatomy} is Third lumbar vertebra [lower-thoracic (T9)]{Anatomy} is Ninth thoracic vertebra [upper-thoracic (T4)]{Anatomy} is T4 part of thoracic duct [erector spinae]{Anatomy} is Erector spinae muscle [Spine angles]{Concepts & Ideas} is Angle [angles]{Concepts & Ideas} is Angle [muscle]{Anatomy} is Muscle tissue (body structure) [standing]{Concepts & Ideas} is Standing [seated]{Disorders} is Seated [flexion]{Physiology} is Flexion [muscles]{Anatomy} is Muscle tissue (body structure) [lumbar muscles]{Anatomy} is Muscle tissue (body structure) [Standing]{Concepts & Ideas} is Standing [seated]{Disorders} is Seated [seated]{Disorders} is Seated [flexion]{Physiology} is Flexion [low back pain]{Disorders} is Low back pain [diagnosis]{Disorders} is Diagnosis [individuals]{Living Beings} is Persons [low back pain]{Disorders} is Low back pain
The Relationship Between Distance and [Post-operative] Visit Attendance Following Medical [Male Circumcision] in [Nyanza Province], [Kenya] To date, there is no [research] on voluntary medical [male circumcision] ([VMMC]) [catchment areas] or the relationship between distance to a [VMMC] [facility] and attendance at a [post-operative] [follow-up visit]. We [analyzed] data from a randomly selected [subset] of [males] [self-seeking circumcision] at one of 16 participating [facilities] in [Nyanza Province], [Kenya] between 2008 and 2010. Among 1437 [participants], 46.7 % attended [follow-up]. The [median] distance from [residence] to utilized [facility] was 2.98 km (IQR 1.31-5.38). Nearly all [participants] (98.8 %) lived within 5 km from a [facility], however, 26.3 % visited a [facility] more than 5 km away. Stratified results demonstrated that among those utilizing fixed [facilities], greater distance was associated with higher odds of [follow-up] non-attendance (OR 5.01-10km vs. 0-1km = 1.71, 95 % CI 1.08, 2.70, p = 0.02; OR >10km vs. 0-1 km = 2.80, 95 % CI 1.26, 6.21, p = 0.01), adjusting for age and district of [residence]. We found 5 km marked the threshold distance beyond which [follow-up] attendance significantly dropped. These results demonstrate distance is an important predictor of attending [follow-up], and this relationship appears to be modified by [facility] type.	[Post-operative]{Disorders} is Post operative (finding) [Male Circumcision]{Procedures} is Male Circumcision [Nyanza Province]{Geographic Areas} is Province [Kenya]{Geographic Areas} is Kenya [research]{Procedures} is Research [Post-operative]{Disorders} is Post operative (finding) [male circumcision]{Procedures} is Male Circumcision [VMMC]{Procedures} is Male Circumcision [catchment areas]{Geographic Areas} is Catchment Area [Male Circumcision]{Procedures} is Male Circumcision [Nyanza Province]{Geographic Areas} is Province [Kenya]{Geographic Areas} is Kenya [VMMC]{Procedures} is Male Circumcision [facility]{Organizations} is Health Facility [post-operative]{Disorders} is Post operative (finding) [follow-up visit]{Procedures} is Follow-up visit [analyzed]{Procedures} is Analyzed [subset]{Concepts & Ideas} is Subset [males]{Living Beings} is Human, Male [self-seeking circumcision]{Procedures} is Male Circumcision [facilities]{Organizations} is Health Facility [Nyanza Province]{Geographic Areas} is Province [Kenya]{Geographic Areas} is Kenya [participants]{Living Beings} is Participant [follow-up]{Procedures} is Follow-up [median]{Concepts & Ideas} is Median [residence]{Concepts & Ideas} is Residence [facility]{Organizations} is Health Facility [participants]{Living Beings} is Participant [facility]{Organizations} is Health Facility [facility]{Organizations} is Health Facility [facilities]{Organizations} is Health Facility [follow-up]{Procedures} is Follow-up [residence]{Concepts & Ideas} is Residence [follow-up]{Procedures} is Follow-up [follow-up]{Procedures} is Follow-up [facility]{Organizations} is Health Facility
Promoting lifestyle behaviour change and [well-being] in hospital patients: a [pilot study] of an evidence-based psychological [intervention] Lifestyle risk behaviours show an inverse social gradient, clustering in [vulnerable groups]. We designed and piloted an [intervention] to address barriers to lifestyle behaviour change among hospital patients. We designed our [intervention] using effective components of behaviour change [interventions] informed by [psychological theory]. Delivered by a [health psychologist] based at the Royal Free London NHS Foundation Trust, the 4-week [intervention] included detailed [baseline assessment], personalized [goal setting], psychological skills development, [motivation support] and [referral to] [community services]. Primary outcomes were feasibility and patient acceptability. We also evaluated changes to health and [well-being]. From 1 July 2013 to 31 September 2014, 686 patients were referred, 338 (49.3%) attended a first appointment and 172 (25.1%) completed [follow-up]. Furthermore, 72.1% of attenders were female with the median age 55 years and poor self-reported baseline health. After 4 weeks, [self-efficacy], health and well-being scores [significantly improved]: 63% of lifestyle goals and 89% of health management [goals] were fully [achieved]; 58% of [referrals to] [community] lifestyle behaviour change services and 79% of referrals to other [services] (e.g. [Citizen's Advice Bureau]) were accepted; 99% were [satisfied] / very satisfied with the [service]. Our [hospital-based intervention] was feasible, acceptable and showed [preliminary health and well-being gains].	[well-being]{Disorders} is Mental well-being [pilot study]{Procedures} is Pilot Study [intervention]{Procedures} is Interventional [well-being]{Disorders} is Mental well-being [vulnerable groups]{Living Beings} is Population Groups [pilot study]{Procedures} is Pilot Study [intervention]{Procedures} is Interventional [intervention]{Procedures} is Interventional [intervention]{Procedures} is Interventional [interventions]{Procedures} is Interventional [psychological theory]{Concepts & Ideas} is Psychological Theory [health psychologist]{Living Beings} is Health psychologist [intervention]{Procedures} is Interventional [baseline assessment]{Procedures} is Baseline behavioral assessment [goal setting]{Procedures} is Goal setting [motivation support]{Procedures} is Emotional support [referral to]{Procedures} is Referral to [community services]{Organizations} is Community Services [well-being]{Disorders} is Mental well-being [follow-up]{Procedures} is Follow-up [self-efficacy]{Physiology} is Self-Efficacy [significantly improved]{Disorders} is Improved [goals]{Concepts & Ideas} is Goals [achieved]{Disorders} is Goal achieved [referrals to]{Procedures} is Referral to [community]{Organizations} is Community Services [services]{Procedures} is Health Services [Citizen's Advice Bureau]{Living Beings} is Organizational [satisfied]{Concepts & Ideas} is Satisfied [service]{Procedures} is Health Services [hospital-based intervention]{Procedures} is Interventional [preliminary health and well-being gains]{Disorders} is Finding (finding)
Combining electrostatic powder with an [insecticide]: effect on stored - product [beetles] and on the [commodity] The opportunity to reduce the amount of [pirimiphos-methyl] applied to [grain] by formulating it in an electrostatic powder was investigated. The [insecticidal] efficacy of [pirimiphos-methyl] in [EC formulation] or formulated using electrostatic powder (EP) as an inert carrier was investigated against [Sitophilus oryzae] (L.), [Oryzaephilus surinamensis] (L.), [Rhyzopertha dominica] (F.) and [Tribolium confusum Jacquelin du Val]. Furthermore, the adhesive properties of EP to [rice], [corn] and [wheat], together with the effect on bulk density and [bread] - and [pasta] - making properties, were investigated. The results showed that [pirimiphos-methyl] formulated with EP provided better efficacy against [adults] when compared with [EC formulation] for [O. surinamensis] and [T. confusum], but there was no difference for [R. dominica]. Progeny production was consistently lower in [grain] [treated with] the EP formulation than in [grain] [treated with] the [EC]. Tests showed that EP adhered to the [kernels] for longer on hard [wheat] than on [maize] or [rice]. In most [commodities], EP did not alter the bulk density. Finally, the addition of EP did not affect [flour] - and [bread] - making properties, nor the [pasta] -making properties. The results of the present study suggest that an EP could be used to reduce the amount of [pirimiphos-methyl] applied to [grain] for effective pest control, with no detrimental effects on [grain] quality. © 2016 Society of Chemical Industry.	[insecticide]{Chemicals & Drugs} is Insecticide [beetles]{Living Beings} is Beetles [commodity]{Objects} is Uncooked Foods [insecticide]{Chemicals & Drugs} is Insecticide [pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl [grain]{Objects} is Cereal Grain [beetles]{Living Beings} is Beetles [commodity]{Objects} is Uncooked Foods [insecticidal]{Chemicals & Drugs} is Insecticide [pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl [EC formulation]{Chemicals & Drugs} is Insecticide [Sitophilus oryzae]{Living Beings} is Sitophilus oryzae [Oryzaephilus surinamensis]{Living Beings} is Oryzaephilus surinamensis [Rhyzopertha dominica]{Living Beings} is Rhyzopertha dominica [Tribolium confusum Jacquelin du Val]{Living Beings} is Tribolium confusum [rice]{Objects} is Rice [corn]{Objects} is Corn [wheat]{Objects} is Wheat [bread]{Objects} is Bread [pasta]{Objects} is Pasta [pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl [adults]{Living Beings} is Adult insect [EC formulation]{Chemicals & Drugs} is Insecticide [O. surinamensis]{Living Beings} is Oryzaephilus surinamensis [T. confusum]{Living Beings} is Tribolium confusum [R. dominica]{Living Beings} is Rhyzopertha dominica [grain]{Objects} is Cereal Grain [treated with]{Procedures} is Treated with [grain]{Objects} is Cereal Grain [treated with]{Procedures} is Treated with [EC]{Chemicals & Drugs} is Insecticide [kernels]{Objects} is Food or Food Substance [wheat]{Objects} is Wheat [maize]{Objects} is Corn [rice]{Objects} is Rice [commodities]{Objects} is Uncooked Foods [flour]{Objects} is Flour [bread]{Objects} is Bread [pasta]{Objects} is Pasta [pirimiphos-methyl]{Chemicals & Drugs} is Pirimiphosmethyl [grain]{Objects} is Cereal Grain [grain]{Objects} is Cereal Grain
[Radiofrequency ablation] of [posteroseptal accessory pathways] associated with [coronary sinus diverticula] [Posteroseptal accessory pathways] may be associated with a [coronary sinus (CS) diverticulum]. Our purpose was to describe the clinical characteristics, mapping and [ablation of these pathways]. This was a [retrospective study] of all patients who underwent [ablation] of [posteroseptal accessory pathways] in a [single centre]. Patients with a [diverticulum of the CS] or one of its tributaries were included in group I, while the other patients formed group II. Clinical presentation, [ablation procedure] and outcome were compared between the two groups. A total of 51 patients were included, 16 in group I and 35 in group II. There were no significant differences in age or sex distribution. [Atrial fibrillation] ([AF]) and previous unsuccessful [ablation] were more common in group I. A [negative] [delta wave] in lead II was the [ECG] [finding] with best sensitivity and specificity for the presence of a [diverticulum]. A [pathway] potential was common at the successful [site] in group I, and the interval between local ventricular electrogram and [delta wave] onset was shorter (19.5 ± 8 vs 33.1 ± 7.6 ms, p < 0.001). There was a trend toward lower procedural success rate and higher recurrence rate in group I, although this was not significant. [CS diverticula] should be suspected in patients with manifest [posteroseptal accessory pathways] who have a previous failed [ablation], documented [AF] or typical [electrocardiographic signs]. A discrete potential is frequently seen at the successful site, but the local ventricular electrogram is not as early as in other [accessory pathways].	[Radiofrequency ablation]{Procedures} is Radiofrequency ablation [posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway [coronary sinus diverticula]{Disorders} is Coronary sinus diverticulum [Radiofrequency ablation]{Procedures} is Radiofrequency ablation [Posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway [posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway [coronary sinus (CS) diverticulum]{Disorders} is Coronary sinus diverticulum [coronary sinus diverticula]{Disorders} is Coronary sinus diverticulum [ablation of these pathways]{Procedures} is ABLATION, ACCESSORY PATHWAYS [retrospective study]{Procedures} is Retrospective Study [ablation]{Procedures} is Ablation [posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway [single centre]{Concepts & Ideas} is Centre [diverticulum of the CS]{Disorders} is Coronary sinus diverticulum [ablation procedure]{Procedures} is Ablation [Atrial fibrillation]{Disorders} is Fibrillation atrial [AF]{Disorders} is Fibrillation atrial [ablation]{Procedures} is Ablation [negative]{Disorders} is Negative for [delta wave]{Disorders} is Delta Wave [ECG]{Procedures} is Electrocardiography NOS (procedure) [finding]{Disorders} is Finding (finding) [diverticulum]{Disorders} is Diverticulum [pathway]{Anatomy} is Posteroseptal accessory pathway [site]{Concepts & Ideas} is Sites [delta wave]{Disorders} is Delta Wave [CS diverticula]{Disorders} is Coronary sinus diverticulum [posteroseptal accessory pathways]{Anatomy} is Posteroseptal accessory pathway [ablation]{Procedures} is Ablation [AF]{Disorders} is Fibrillation atrial [electrocardiographic signs]{Disorders} is Electrocardiographic Finding [accessory pathways]{Anatomy} is Accessory pathway
Association of [RBP4] levels with increased [arterial stiffness] in adolescents with [family history of type 2 diabetes] The aim of this [study] was to explore the impact of [family history of type 2 diabetes] ([FH2D]) on [arterial stiffness] in young [people] and its relationship to [adipocytokines]. This [case-control study] included 52 adolescents (male / female 28/24) with [FH2D] ([FH2D+]) and 40 adolescents (male / female 21/19) without [FH2D] ([FH2D-]). Anthropometric measurements, including height, weight, [waist circumference] ([WC]), and [blood pressure], were obtained. [Blood samples] were collected, [fasting plasma glucose] ([FPG]), [serum lipids], [Retinol Binding Protein 4] ([RBP4]), [C reactive protein] ([CRP]), [adiponectin] and [visfatin] were examined. Brachial-ankle pulse wave velocity (baPWV) was used to evaluate [arterial stiffness]. Visceral fat area (VFA) was measured by [computerized tomography]. Compared with [FH2D-] [group], [FH2D+] [group] had a significantly higher oral glucose tolerance test (OGTT) 2-hour insulin, [RBP4] and baPWV levels, a lower [adiponectin] and glucose infusing rate (GIR) (P<0.05). BaPWV was positively correlated with age, [systolic blood pressure] ([SBP]), [diastolic blood pressure] ([DBP]), 2-hour (OGTT) insulin, [RBP4], and VFA, and negatively correlated with GIR in [FH2D+] [group]. After multivariate analysis, age, [SBP], [RBP4] and VFA maintained an independent association with baPWV in [FH2D+] [group] (P<0.05), while only age, [SBP], and VFA were independent predictors of baPWV in [FH2D-] [group] (P<0.05). These [findings] led to the conclusion that [RBP4] level was associated with increased [arterial stiffness] in young [subjects] with [family history of type 2 diabetes].	[RBP4]{Chemicals & Drugs} is RBP4 protein, human [arterial stiffness]{Physiology} is Arterial Stiffness [family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2 [RBP4]{Chemicals & Drugs} is RBP4 protein, human [study]{Procedures} is Study [arterial stiffness]{Physiology} is Arterial Stiffness [family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2 [family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2 [FH2D]{Disorders} is Family history of diabetes mellitus type 2 [arterial stiffness]{Physiology} is Arterial Stiffness [people]{Living Beings} is People [adipocytokines]{Chemicals & Drugs} is Adipocytokine [case-control study]{Procedures} is Case-control study [FH2D]{Disorders} is Family history of diabetes mellitus type 2 [FH2D+]{Disorders} is Family history of diabetes mellitus type 2 [FH2D]{Disorders} is Family history of diabetes mellitus type 2 [FH2D-]{Disorders} is NEGATIVE [waist circumference]{Physiology} is Waist Circumference [WC]{Physiology} is Waist Circumference [blood pressure]{Physiology} is Blood pressure [Blood samples]{Anatomy} is Blood sample [fasting plasma glucose]{Procedures} is Plasma fasting glucose level [FPG]{Procedures} is Plasma fasting glucose level [serum lipids]{Procedures} is Serum lipids [Retinol Binding Protein 4]{Chemicals & Drugs} is RBP4 protein, human [RBP4]{Chemicals & Drugs} is RBP4 protein, human [C reactive protein]{Procedures} is C Reactive Protein [CRP]{Procedures} is C Reactive Protein [adiponectin]{Procedures} is Adiponectin [visfatin]{Chemicals & Drugs} is NAMPT Protein [arterial stiffness]{Physiology} is Arterial Stiffness [computerized tomography]{Procedures} is Computerized tomography [FH2D-]{Disorders} is NEGATIVE [group]{Living Beings} is Population Group [FH2D+]{Disorders} is Family history of diabetes mellitus type 2 [group]{Living Beings} is Population Group [RBP4]{Chemicals & Drugs} is RBP4 protein, human [adiponectin]{Procedures} is Adiponectin [systolic blood pressure]{Physiology} is Systolic Blood Pressure [SBP]{Physiology} is Systolic Blood Pressure [diastolic blood pressure]{Physiology} is Diastolic Blood Pressure [DBP]{Physiology} is Diastolic Blood Pressure [RBP4]{Chemicals & Drugs} is RBP4 protein, human [FH2D+]{Disorders} is Family history of diabetes mellitus type 2 [group]{Living Beings} is Population Group [SBP]{Physiology} is Systolic Blood Pressure [RBP4]{Chemicals & Drugs} is RBP4 protein, human [FH2D+]{Disorders} is Family history of diabetes mellitus type 2 [group]{Living Beings} is Population Group [SBP]{Physiology} is Systolic Blood Pressure [FH2D-]{Disorders} is NEGATIVE [group]{Living Beings} is Population Group [findings]{Disorders} is Finding (finding) [RBP4]{Chemicals & Drugs} is RBP4 protein, human [arterial stiffness]{Physiology} is Arterial Stiffness [subjects]{Living Beings} is Research Subjects [family history of type 2 diabetes]{Disorders} is Family history of diabetes mellitus type 2
The effect of [total hip arthroplasty] on [sagittal] [spinal] - [pelvic-leg] alignment and [low back pain] in patients with severe [hip osteoarthritis] [Sagittal] [spinopelvic] [malalignment] has been reported in [spinal disorders] such as [low back pain] ([LBP]), and restoration of normal alignment is targeted when [treating] these [disorders]. [Abnormal] [sagittal] [spinal] - [pelvic-leg] alignment has been reported in patients with severe [hip osteoarthritis] ([OA]), who have a high prevalence of associated [LBP]. This [prospective longitudinal study] aimed to investigate changes in [sagittal] [spinal] - [pelvic-leg] alignment after [total hip arthroplasty] ([THA]) in patients with severe [hip OA], and whether these changes contribute to [LBP] [relief]. Patients undergoing primary [THA] due to severe unilateral [hip OA] were recruited. [Physical examination] and [X-ray films] were taken to rule out any [spinal disorder]. [Sagittal] alignment of [pelvis], [hip], and [spine] was analyzed on lateral radiographs taken before (baseline) and 1 year after ([follow-up]) [THA]. [Functional instruments] were completed by patients including: [visual analog scale] ([VAS]) for [LBP], [Roland-Morris Disability Questionnaire] ([RMDQ]), and [Harris Hip Score] ([HHS]). Comparisons were carried out at baseline and [follow-up], and between patients with and without [LBP]. The recruited 69 patients showed significantly reduced hip flexion and improved [global spinal balance] at [follow-up] compared with baseline. [LBP] was reported by 39 patients (56.5 %) before surgery; at [follow-up], 17 reported complete resolution, while 22 reported significant [relief]. Significant decreases in [VAS] and [RMDQ] scores in [lumbar spine] and increase in [hip] [HHS] were observed. [THA] in patients with severe [hip OA] could help correct abnormal [sagittal] [spinal] - [pelvic-leg] alignment and relieve [comorbid] [LBP]. Improvements in hip flexion and global [spinal] [balance] might be involved in the mechanism of [LBP] [relief].	[total hip arthroplasty]{Procedures} is Prosthetic total arthroplasty of the hip [sagittal]{Anatomy} is Sagittal [spinal]{Concepts & Ideas} is Spinal [pelvic-leg]{Anatomy} is Body part [low back pain]{Disorders} is Low back pain [hip osteoarthritis]{Disorders} is Hip Osteoarthritis [Sagittal]{Anatomy} is Sagittal [spinopelvic]{Anatomy} is Body part [total hip arthroplasty]{Procedures} is Prosthetic total arthroplasty of the hip [malalignment]{Disorders} is Bone Malalignment [sagittal]{Anatomy} is Sagittal [spinal]{Concepts & Ideas} is Spinal [spinal disorders]{Disorders} is Spinal Cord Disorders [pelvic-leg]{Anatomy} is Body part [low back pain]{Disorders} is Low back pain [low back pain]{Disorders} is Low back pain [LBP]{Disorders} is Low back pain [hip osteoarthritis]{Disorders} is Hip Osteoarthritis [treating]{Procedures} is TREAT [disorders]{Disorders} is Spinal Cord Disorders [Abnormal]{Disorders} is Abnormal [sagittal]{Anatomy} is Sagittal [spinal]{Concepts & Ideas} is Spinal [pelvic-leg]{Anatomy} is Body part [hip osteoarthritis]{Disorders} is Hip Osteoarthritis [OA]{Disorders} is Hip Osteoarthritis [LBP]{Disorders} is Low back pain [prospective longitudinal study]{Procedures} is Study, Prospective [sagittal]{Anatomy} is Sagittal [spinal]{Concepts & Ideas} is Spinal [pelvic-leg]{Anatomy} is Body part [total hip arthroplasty]{Procedures} is Prosthetic total arthroplasty of the hip [THA]{Procedures} is Prosthetic total arthroplasty of the hip [hip OA]{Disorders} is Hip Osteoarthritis [LBP]{Disorders} is Low back pain [relief]{Disorders} is Relief [THA]{Procedures} is Prosthetic total arthroplasty of the hip [hip OA]{Disorders} is Hip Osteoarthritis [Physical examination]{Procedures} is Physical Examination [X-ray films]{Devices} is X-Ray Films [spinal disorder]{Disorders} is Spinal Cord Disorders [Sagittal]{Anatomy} is Sagittal [pelvis]{Anatomy} is PELVIS [hip]{Anatomy} is HIP [spine]{Anatomy} is Dorsal spine [follow-up]{Procedures} is Follow-up [THA]{Procedures} is Prosthetic total arthroplasty of the hip [Functional instruments]{Devices} is Instruments [visual analog scale]{Procedures} is Visual Analog Scale [VAS]{Procedures} is Visual Analog Scale [LBP]{Disorders} is Low back pain [Roland-Morris Disability Questionnaire]{Concepts & Ideas} is Roland Morris Disability Questionnaire [RMDQ]{Concepts & Ideas} is Roland Morris Disability Questionnaire [Harris Hip Score]{Disorders} is Harris hip score [HHS]{Disorders} is Harris hip score [follow-up]{Procedures} is Follow-up [LBP]{Disorders} is Low back pain [global spinal balance]{Disorders} is Finding (finding) [follow-up]{Procedures} is Follow-up [LBP]{Disorders} is Low back pain [follow-up]{Procedures} is Follow-up [relief]{Disorders} is Relief [VAS]{Physiology} is Visual analogue scale score [RMDQ]{Concepts & Ideas} is Roland Morris Disability Questionnaire [lumbar spine]{Anatomy} is Lumbar Spine [hip]{Anatomy} is HIP [HHS]{Disorders} is Harris hip score [THA]{Procedures} is Prosthetic total arthroplasty of the hip [hip OA]{Disorders} is Hip Osteoarthritis [sagittal]{Anatomy} is Sagittal [spinal]{Concepts & Ideas} is Spinal [pelvic-leg]{Anatomy} is Body part [comorbid]{Disorders} is Comorbid conditions [LBP]{Disorders} is Low back pain [spinal]{Concepts & Ideas} is Spinal [balance]{Physiology} is Balance [LBP]{Disorders} is Low back pain [relief]{Disorders} is Relief
Impact of totally [laparoscopic] combined management of [colorectal cancer] with synchronous [hepatic metastases] on severity of complications: a propensity-score -based analysis Thanks to widespread diffusion of [minimally invasive approach] in the setting of both [colorectal] and [hepatic surgeries], the interest in combined resections for [colorectal cancer] and synchronous [liver metastases] ([SCLM]) by [totally laparoscopic approach] ([TLA]) has increased. Aim of this study was to compare outcome of combined resections for [SCLM] performed by [TLA] or by open approach, in a propensity-score-based study. All 25 patients undergoing combined [TLA] for [SCLM] at [San Raffaele Hospital] in Milano were compared in a [case-matched analysis] with 25 out of 91 patients undergoing [totally open approach] ([TOA group]). [Groups] were matched with 1:2 ratio using propensity scores based on covariates representing disease severity. Main endpoints were postoperative morbidity and long-term outcome. The [Modified Accordion Severity Grading System] was used to quantify complications. The groups resulted comparable in terms of patients and disease characteristics. The [TLA group], as compared to the [TOA group], had lower [blood loss] (350 vs 600 mL), shorter postoperative stay (9 vs 12 days), lower [postoperative morbidity index] (0.14 vs 0.20) and severity score for complicated patients (0.60 vs 0.85). [Colonic anastomosis] [leakage] had the highest fractional complication burden in both [groups]. In spite of comparable long-term overall survival, the [[TLA] group] had better [recurrence-free survival]. [TLA] for combined resections is feasible, and its indications can be widened to encompass a larger population of patients, provided its benefits in terms of reduced overall risk and severity of complications, rapid [functional recovery] and favorable long-term outcomes.	[laparoscopic]{Procedures} is Laparoscopic [colorectal cancer]{Disorders} is COLORECTAL CANCER [hepatic metastases]{Disorders} is Hepatic metastases [laparoscopic]{Procedures} is Laparoscopic [minimally invasive approach]{Procedures} is Minimally Invasive Surgery [colorectal cancer]{Disorders} is COLORECTAL CANCER [colorectal]{Procedures} is Colorectal surgery [hepatic metastases]{Disorders} is Hepatic metastases [hepatic surgeries]{Procedures} is Hepatic operation [colorectal cancer]{Disorders} is COLORECTAL CANCER [liver metastases]{Disorders} is Hepatic metastases [SCLM]{Disorders} is Hepatic metastases [totally laparoscopic approach]{Procedures} is Laparoscopic [TLA]{Procedures} is Laparoscopic [SCLM]{Disorders} is Hepatic metastases [TLA]{Procedures} is Laparoscopic [TLA]{Procedures} is Laparoscopic [SCLM]{Disorders} is Hepatic metastases [San Raffaele Hospital]{Organizations} is Hospital [case-matched analysis]{Procedures} is Matched Case-Control Study [totally open approach]{Procedures} is Open Surgery [TOA group]{Living Beings} is Population Group [Groups]{Living Beings} is Population Group [Modified Accordion Severity Grading System]{Procedures} is Grading system used [TLA group]{Living Beings} is Population Group [TOA group]{Living Beings} is Population Group [blood loss]{Disorders} is SURG BLOOD LOSS [postoperative morbidity index]{Concepts & Ideas} is Morbidity index [Colonic anastomosis]{Procedures} is Colonic anastomosis [leakage]{Disorders} is Extravasation (morphologic abnormality) [groups]{Living Beings} is Population Group [TLA]{Procedures} is Laparoscopic [TLA group]{Living Beings} is Population Group [recurrence-free survival]{Disorders} is Recurrence free survival [TLA]{Procedures} is Laparoscopic [functional recovery]{Disorders} is Function Recovery
Application of an Analytical Solution as a [Screening] [Tool] for Sea Water Intrusion Sea water intrusion into aquifers is [problematic] in many [coastal areas]. The physics and chemistry of this issue are complex, and sea water intrusion remains challenging to quantify. Simple [assessment tools] like [analytical models] offer advantages of rapid application, but their applicability to field situations is unclear. This [study] examines the reliability of a popular sharp-interface analytical approach for estimating the extent of sea water in a homogeneous [coastal] aquifer subjected to pumping and regional flow effects and under steady-state conditions. The [analytical model] is tested against observations from [Canada], the [United States], and [Australia] to assess its utility as an initial [approximation] of sea water extent for the purposes of rapid [groundwater] management [decision making]. The occurrence of sea water intrusion resulting in increased [salinity] at pumping wells was correctly predicted in approximately 60% of cases. Application of a correction to account for [dispersion] did not markedly [improve] the results. Failure of the [analytical model] to provide correct predictions can be attributed to mismatches between its simplifying assumptions and more complex field settings. The best results occurred where the toe of the [salt water] [wedge] is expected to be the closest to the [coast] under predevelopment conditions. Predictions were the poorest for aquifers where the [salt water] [wedge] was expected to extend further [inland] under predevelopment conditions and was therefore more dispersive prior to pumping. Sharp-interface solutions remain useful [tools] to [screen] for the vulnerability of [coastal] aquifers to sea water intrusion, although the significant sources of uncertainty identified in this [study] require careful consideration to avoid misinterpreting sharp-interface results.	[Screening]{Procedures} is Screenings [Tool]{Concepts & Ideas} is Method (attribute) [problematic]{Disorders} is Problem [Screening]{Procedures} is Screenings [Tool]{Concepts & Ideas} is Method (attribute) [coastal areas]{Concepts & Ideas} is Coastal environment [assessment tools]{Concepts & Ideas} is Intellectual Product [analytical models]{Concepts & Ideas} is Theoretical Models [study]{Procedures} is Study [coastal]{Concepts & Ideas} is Coastal environment [analytical model]{Concepts & Ideas} is Theoretical Models [Canada]{Geographic Areas} is Canada [United States]{Geographic Areas} is United States [Australia]{Geographic Areas} is Australia [approximation]{Procedures} is Approximation - action [groundwater]{Concepts & Ideas} is Groundwater [decision making]{Physiology} is Decision making [salinity]{Phenomena} is Salinity [dispersion]{Concepts & Ideas} is Dispersion [improve]{Disorders} is Improved [analytical model]{Concepts & Ideas} is Theoretical Models [salt water]{Chemicals & Drugs} is Salt water [wedge]{Concepts & Ideas} is Wedge [coast]{Geographic Areas} is Area [salt water]{Chemicals & Drugs} is Salt water [wedge]{Concepts & Ideas} is Wedge [inland]{Geographic Areas} is Inland water [tools]{Concepts & Ideas} is Method (attribute) [screen]{Procedures} is Screenings [coastal]{Concepts & Ideas} is Coastal environment [study]{Procedures} is Study
The Role of [TRAF4] and [B3GAT1] [Gene Expression] in the [Food Hypersensitivity] and [Insect Venom Allergy] in [Mastocytosis] [Mastocytosis] is an uncommon [disease] classified as a [myeloproliferative neoplasm], however, its [symptoms] are broad and place patients at crossroads between [dermatology], [hematology] and allergology. Patients with [mastocytosis] often suffer from [symptoms] resulting from the activation and release of mediators from the [mast cells], such as generalized [itching], [redness], [headache], [abdominal cramps], [diarrhea], [bone pain] or [arthritis], [hypotension] and [shock]. The possible severe, fatal or near fatal reactions caused by [food hypersensitivity] are reasons for the research focused on [marker] identification. The aim of the [study] was to analyse the [gene expression] differences in [mastocytosis] patients with and without [food] and [drug hypersensitivity] and [insect venom allergy] ([IVA]). A total of 57 [Caucasian] patients with [mastocytosis] were studied (median age 41.8; range 18-77 years; 15 (26.3 %) males and 42 (73.7 %) females). [Quantitative RT-PCRs] of 11 [genes] plus [ribosomal 18S RNA] were run. [Symptoms] of [food hypersensitivity] were found in 12 patients (21 %), including 3 patients (13 %) with [cutaneous mastocytosis] ([CM]), and 9 (28 %) with [indolent systemic mastocytosis] ([ISM]). [IVA] was confirmed in 13 patients (22.8 %) including 6 patients (10.5 %) with [CM], and 7 patients (12.3 %) with [ISM]. [Drug hypersensitivity] was [diagnosed] in 10 patients (17.5 %). Significant differences in the [gene expression] were found for [TRAF4] (p = 0.008) in the comparison of the [mastocytosis] patients with and without concomitant [food hypersensitivity]. Furthermore significant differences were found in [gene expression] for [B3GAT1] (p = 0.003) in patients with [IVA] compared to patients without [insect sting] [anaphylaxis] in the medical history. The [expression] of studied [genes] did not differ according to the presence of [drug hypersensitivity]. The [TRAF4] [expression] was higher in [mastocytosis] patients with [food hypersensitivity] in their [medical history], the [B3GAT1] [expression] was lower in [mastocytosis] patients with [IVA] in history.	[TRAF4]{Genes & Molecular Sequences} is TRAF4 [B3GAT1]{Genes & Molecular Sequences} is B3GAT1 [Gene Expression]{Physiology} is Gene Expression [Food Hypersensitivity]{Disorders} is Food Hypersensitivity [Insect Venom Allergy]{Disorders} is Allergy disorder [Mastocytosis]{Disorders} is Mastocytosis [Mastocytosis]{Disorders} is Mastocytosis [TRAF4]{Genes & Molecular Sequences} is TRAF4 [B3GAT1]{Genes & Molecular Sequences} is B3GAT1 [disease]{Disorders} is Disease [Gene Expression]{Physiology} is Gene Expression [Food Hypersensitivity]{Disorders} is Food Hypersensitivity [myeloproliferative neoplasm]{Disorders} is Myeloproliferative neoplasms [Insect Venom Allergy]{Disorders} is Allergy disorder [symptoms]{Disorders} is Symptoms [Mastocytosis]{Disorders} is Mastocytosis [dermatology]{Occupations} is Dermatology [hematology]{Occupations} is Hematology [mastocytosis]{Disorders} is Mastocytosis [symptoms]{Disorders} is Symptoms [mast cells]{Anatomy} is Mast Cells [itching]{Disorders} is Itching [redness]{Disorders} is Skin red [headache]{Disorders} is Headache [abdominal cramps]{Disorders} is Abdominal Cramps [diarrhea]{Disorders} is D - Diarrhea [bone pain]{Disorders} is Pain bone [arthritis]{Disorders} is Arthritis [hypotension]{Disorders} is Vascular Hypotension [shock]{Disorders} is Shock [food hypersensitivity]{Disorders} is Food Hypersensitivity [marker]{Physiology} is Marker [study]{Procedures} is Study [gene expression]{Physiology} is Gene Expression [mastocytosis]{Disorders} is Mastocytosis [food]{Disorders} is Food Hypersensitivity [drug hypersensitivity]{Disorders} is Drug hypersensitivity [insect venom allergy]{Disorders} is Allergy disorder [IVA]{Disorders} is Allergy disorder [Caucasian]{Living Beings} is Caucasian (ethnic group) [mastocytosis]{Disorders} is Mastocytosis [Quantitative RT-PCRs]{Procedures} is Quantitative Real-Time PCRs [genes]{Genes & Molecular Sequences} is Genes [ribosomal 18S RNA]{Chemicals & Drugs} is RIBOSOMAL RNA 18S [Symptoms]{Disorders} is Symptoms [food hypersensitivity]{Disorders} is Food Hypersensitivity [cutaneous mastocytosis]{Disorders} is Cutaneous mastocytosis [CM]{Disorders} is Cutaneous mastocytosis [indolent systemic mastocytosis]{Disorders} is Indolent systemic mastocytosis [ISM]{Disorders} is Indolent systemic mastocytosis [IVA]{Disorders} is Allergy disorder [CM]{Disorders} is Cutaneous mastocytosis [ISM]{Disorders} is Indolent systemic mastocytosis [Drug hypersensitivity]{Disorders} is Drug hypersensitivity [diagnosed]{Disorders} is Diagnosed [gene expression]{Physiology} is Gene Expression [TRAF4]{Genes & Molecular Sequences} is TRAF4 [mastocytosis]{Disorders} is Mastocytosis [food hypersensitivity]{Disorders} is Food Hypersensitivity [gene expression]{Physiology} is Gene Expression [B3GAT1]{Genes & Molecular Sequences} is B3GAT1 [IVA]{Disorders} is Allergy disorder [insect sting]{Disorders} is Insect Sting [anaphylaxis]{Disorders} is Obsolete anaphylaxis [expression]{Physiology} is Gene Expression [genes]{Genes & Molecular Sequences} is Genes [drug hypersensitivity]{Disorders} is Drug hypersensitivity [TRAF4]{Genes & Molecular Sequences} is TRAF4 [expression]{Physiology} is Gene Expression [mastocytosis]{Disorders} is Mastocytosis [food hypersensitivity]{Disorders} is Food Hypersensitivity [medical history]{Disorders} is Medical History [B3GAT1]{Genes & Molecular Sequences} is B3GAT1 [expression]{Physiology} is Gene Expression [mastocytosis]{Disorders} is Mastocytosis [IVA]{Disorders} is Allergy disorder
[Generalized Weakness] in a [Transplant] Patient: A [Case Presentation] [Generalized weakness] in [transplant] patients is a major complaint in tertiary [rehabilitation hospitals]. The [diagnosis] and [management] of [generalized weakness] in this [population] pose challenges for [physicians]. We present the case of a [transplant] patient with [generalized weakness] who was eventually [diagnosed] with [calciphylaxis] using a [multidisciplinary diagnostic approach] of [electrodiagnostics], [vascular] [study], and [skin biopsy]. [Calciphylaxis] is a rare [cutaneous disorder] that mimics other [collagen vascular diseases] in its presentation and fulminant course. [Physiatrists] should be cognizant of [calciphylaxis], as it signals a [poor prognosis] if not correctly diagnosed and treated in a timely manner, with high incidence of [sepsis], [wound pain], and [disability]. V.	[Generalized Weakness]{Disorders} is Weakness generalized [Transplant]{Disorders} is Transplant [Case Presentation]{Concepts & Ideas} is CASE ONLY [Generalized weakness]{Disorders} is Weakness generalized [transplant]{Disorders} is Transplant [Transplant]{Disorders} is Transplant [Case Presentation]{Concepts & Ideas} is CASE ONLY [rehabilitation hospitals]{Organizations} is Rehabilitation hospital [diagnosis]{Disorders} is Diagnosis [management]{Procedures} is Symptom management [generalized weakness]{Disorders} is Weakness generalized [population]{Living Beings} is Population [physicians]{Living Beings} is Physicians [transplant]{Disorders} is Transplant [generalized weakness]{Disorders} is Weakness generalized [diagnosed]{Disorders} is Diagnosis [calciphylaxis]{Disorders} is Calciphylaxis [multidisciplinary diagnostic approach]{Procedures} is Multidisciplinary assessment [electrodiagnostics]{Procedures} is Electrodiagnoses [vascular]{Anatomy} is Vascular structure [study]{Procedures} is TESTS DIAG [skin biopsy]{Procedures} is Skin Biopsy [Calciphylaxis]{Disorders} is Calciphylaxis [cutaneous disorder]{Disorders} is Cutaneous Disorder [collagen vascular diseases]{Disorders} is Collagen-vascular disease [Physiatrists]{Living Beings} is Physiatrists [calciphylaxis]{Disorders} is Calciphylaxis [poor prognosis]{Disorders} is Poor prognosis [sepsis]{Disorders} is Sepsis (disorder) [wound pain]{Disorders} is Wound pain [disability]{Disorders} is Disability
Use of ecoacoustics to determine biodiversity [patterns] across [ecological] gradients The variety of [local] [animal] sounds characterizes a [landscape]. We used ecoacoustics to noninvasively assess the [species] richness of various [biotopes] typical of an ecofriendly forest plantation with diverse [ecological] gradients and both nonnative and indigenous [vegetation]. The reference [area] was an [adjacent] large [World Heritage Site protected area] ([PA]). All [sites] were in a [global biodiversity hotspot]. Our results showed how taxa segregated into various [biotopes]. We identified 65 singing [species], including [birds], [frogs], [crickets], and [katydids]. Large, natural, protected [grassland sites] in the [PA] had the highest mean acoustic diversity (14.1 [species] / [site]). [Areas] covered in [nonnative timber] or [grass] [species] were devoid of [acoustic species]. [Sites] grazed by native and domestic [megaherbivores] were fairly rich (5.1) in [acoustic species] but none were unique to this [habitat type], where acoustic diversity was greater than in intensively managed [grassland] [sites] (0.04). Natural vegetation patches inside the plantation mosaic supported high mean acoustic diversity (indigenous forests 7.6, [grasslands] 8.0, wetlands 9.1), which increased as [plant] heterogeneity and [patch size] increased. Indigenous forest patches within the plantation mosaic contained a highly characteristic [acoustic species] assemblage, emphasizing their complementary contribution to [local] biodiversity. Overall, acoustic signals determined spatial biodiversity [patterns] and can be a useful tool for guiding conservation.	[patterns]{Concepts & Ideas} is Patterns [ecological]{Concepts & Ideas} is Ecological environment [local]{Concepts & Ideas} is Local (qualifier value) [animal]{Living Beings} is Animal [patterns]{Concepts & Ideas} is Patterns [landscape]{Concepts & Ideas} is Landscapes [ecological]{Concepts & Ideas} is Ecological environment [species]{Concepts & Ideas} is Species [biotopes]{Geographic Areas} is Area [ecological]{Concepts & Ideas} is Ecological environment [vegetation]{Living Beings} is Chlorobionta Bremer, 1985 [area]{Geographic Areas} is Area [adjacent]{Concepts & Ideas} is Adjacent [World Heritage Site protected area]{Geographic Areas} is Area [PA]{Geographic Areas} is Area [sites]{Concepts & Ideas} is Sites [global biodiversity hotspot]{Geographic Areas} is Area [biotopes]{Geographic Areas} is Area [species]{Concepts & Ideas} is Species [birds]{Living Beings} is Birds [frogs]{Living Beings} is Frogs [crickets]{Living Beings} is Crickets [katydids]{Living Beings} is Eucaryotae [grassland sites]{Concepts & Ideas} is Grassland [PA]{Geographic Areas} is Area [species]{Concepts & Ideas} is Species [site]{Concepts & Ideas} is Sites [Areas]{Concepts & Ideas} is Area [nonnative timber]{Living Beings} is Chlorobionta Bremer, 1985 [grass]{Living Beings} is Grass [species]{Concepts & Ideas} is Species [acoustic species]{Concepts & Ideas} is Species [Sites]{Concepts & Ideas} is Sites [megaherbivores]{Living Beings} is Herbivores [acoustic species]{Concepts & Ideas} is Species [habitat type]{Concepts & Ideas} is Habitats [grassland]{Concepts & Ideas} is Grassland [sites]{Concepts & Ideas} is Sites [grasslands]{Concepts & Ideas} is Grassland [plant]{Living Beings} is Chlorobionta Bremer, 1985 [patch size]{Concepts & Ideas} is Size of patch [acoustic species]{Concepts & Ideas} is Species [local]{Concepts & Ideas} is Local (qualifier value) [patterns]{Concepts & Ideas} is Patterns
Relationship between [XspI] [Site Polymorphisms] of [LDL-R Gene] and [Serum IL-2] and [IL-10] in Patients with [Hypercholesterolemia] Relationship has been identified in [sporadic reports] between polymorphisms and [hypercholesterolemia]. However, the relationship between inflammatory [cytokines] and polymorphism of [low-density lipoprotein receptor (LDL-R) gene] in [hypercholesterolemia] is unclear. This [study] aimed to explore the relationship and significance between polymorphisms of [LDL-R gene] and [serum Interleukin-2] ([IL-2]), [IL-10] in patients with [hypercholesterolemia]. [PCR-RFLP] and [direct DNA sequencing assay] were [employed] to determine polymorphism of [LDL-R gene] in 900 patients with [hypercholesterolemia] and 400 healthy cases. [ELISA] was applied to assay serum concentration of [IL-2] and [IL-10]. Blood lipid [indexes] were tested in all cases. Compared with the healthy controls, level of [IL-2] increased significantly, while [IL-10] decreased significantly (P < 0.05). [Correlation analysis] showed that [IL-2] was positively correlated with [total cholesterol] ([TC]), [LDL-c], and genotype (r = 0.542, 0.410, 0.598, P < 0.05) and [negatively] correlated with [HDL-c] (r = -0.352, P < 0.05). [Negative] relationship also was found between [TC], [LDL-c], genotype, and [IL-10] (r = -0.452, -0.390, -0.613, P < 0.05), and [positive] correlation between [HDL-c] and [IL-10] (r = 0.398, P < 0.05). Multiple linear regression showed that genotypes and [TC] were independent factors affecting the [levels of [IL-2]] and [IL-10] (P < 0.05). [IL-2] and [IL-10] were related to gene polymorphisms of [LDL-R], which might be involved in the development and progress of [hypercholesterolemia].	[XspI]{Chemicals & Drugs} is Endodeoxyribonuclease XspI [Site Polymorphisms]{Disorders} is Restriction Site Polymorphism [LDL-R Gene]{Genes & Molecular Sequences} is LDLR Gene [Serum IL-2]{Chemicals & Drugs} is IL 002 [IL-10]{Chemicals & Drugs} is IL 010 [Hypercholesterolemia]{Disorders} is Hypercholesterolemias [XspI]{Chemicals & Drugs} is Endodeoxyribonuclease XspI [Site Polymorphisms]{Disorders} is Restriction Site Polymorphism [sporadic reports]{Disorders} is Finding (finding) [LDL-R Gene]{Genes & Molecular Sequences} is LDLR Gene [Serum IL-2]{Chemicals & Drugs} is IL 002 [IL-10]{Chemicals & Drugs} is IL 010 [hypercholesterolemia]{Disorders} is Hypercholesterolemias [Hypercholesterolemia]{Disorders} is Hypercholesterolemias [cytokines]{Chemicals & Drugs} is Cytokine [low-density lipoprotein receptor (LDL-R) gene]{Genes & Molecular Sequences} is LDLR Gene [hypercholesterolemia]{Disorders} is Hypercholesterolemias [study]{Procedures} is Study [LDL-R gene]{Genes & Molecular Sequences} is LDLR Gene [serum Interleukin-2]{Chemicals & Drugs} is IL 002 [IL-2]{Chemicals & Drugs} is IL 002 [IL-10]{Chemicals & Drugs} is IL 010 [hypercholesterolemia]{Disorders} is Hypercholesterolemias [PCR-RFLP]{Procedures} is RFLP analysis [direct DNA sequencing assay]{Procedures} is DNA Sequencing [employed]{Disorders} is Employed [LDL-R gene]{Genes & Molecular Sequences} is LDLR Gene [hypercholesterolemia]{Disorders} is Hypercholesterolemias [ELISA]{Procedures} is ELISA [IL-2]{Chemicals & Drugs} is IL 002 [IL-10]{Chemicals & Drugs} is IL 010 [indexes]{Concepts & Ideas} is Indexes [IL-2]{Chemicals & Drugs} is IL 002 [IL-10]{Chemicals & Drugs} is IL 010 [Correlation analysis]{Procedures} is Correlation Study [IL-2]{Chemicals & Drugs} is IL 002 [total cholesterol]{Chemicals & Drugs} is Total cholesterol [TC]{Chemicals & Drugs} is Total cholesterol [LDL-c]{Chemicals & Drugs} is LDL Cholesterol [negatively]{Disorders} is Finding (finding) [HDL-c]{Chemicals & Drugs} is HDL Cholesterol [Negative]{Disorders} is Negative for [TC]{Chemicals & Drugs} is Total cholesterol [LDL-c]{Chemicals & Drugs} is LDL Cholesterol [IL-10]{Chemicals & Drugs} is IL 010 [positive]{Disorders} is Positive for [HDL-c]{Chemicals & Drugs} is HDL Cholesterol [IL-10]{Chemicals & Drugs} is IL 010 [TC]{Chemicals & Drugs} is Total cholesterol [levels of IL-2]{Procedures} is Laboratory procedure (procedure) [IL-2]{Chemicals & Drugs} is IL 002 [IL-10]{Procedures} is Laboratory procedure (procedure) [IL-2]{Chemicals & Drugs} is IL 002 [IL-10]{Chemicals & Drugs} is IL 010 [LDL-R]{Genes & Molecular Sequences} is LDLR Gene [hypercholesterolemia]{Disorders} is Hypercholesterolemias
Low [serum] [vitamin D] is associated with higher [cortical] porosity in [elderly] [men] [Bone loss] at [peripheral] [sites] in the [elderly] is mainly [cortical] and involves increased [cortical] porosity. However, an association between [bone loss] at these [sites] and [25-hydroxyvitamin D] has not been reported. To investigate the association between [serum] [levels of 25-hydroxyvitamin D], [bone microstructure] and [areal bone mineral density] ([BMD]) in [elderly] [men]. A [population] -based [cohort] of 444 [elderly] [men] (mean ± SD age 80.2 ± 3.5 years) was investigated. [Bone microstructure] was measured by [high-resolution peripheral quantitative computed tomography], [areal BMD] by [dual-energy X-ray absorptiometry] and [serum] [25-hydroxyvitamin D] and [parathyroid hormone levels] by [immunoassay]. Mean [cortical] porosity at the [distal tibia] was 14.7% higher (12.5 ± 4.3% vs. 10.9 ± 4.1%, P < 0.05) whilst [cortical] [volumetric BMD], [area], [trabecular bone] volume fraction and [femoral neck] [areal BMD] were lower in [men] in the lowest quartile of [vitamin D levels] compared to the highest. In [men] with [vitamin D deficiency] (<25 nmol L(-1)) or insufficiency (25-49 nmol L(-1), in combination with an elevated [serum] [level of parathyroid hormone] (>6.8 pmol L(-1))), [cortical] porosity was 17.2% higher than in [vitamin D] - sufficient [men] (P < 0.01). A linear regression [model] including age, weight, height, daily calcium intake, physical activity, smoking [vitamin D] [supplementation] and [parathyroid hormone] showed that [25-hydroxyvitamin D] independently predicted [cortical] porosity (standardized β = -0.110, R(2) = 1.1%, P = 0.024), [area] (β = 0.123, R(2) = 1.4%, P = 0.007) and [cortical] [volumetric BMD] (β = 0.125, R(2) = 1.4%, P = 0.007) of the [tibia] as well as [areal BMD] of the [femoral neck] (β = 0.102, R(2) = 0.9%, P = 0.04). [Serum] [vitamin D] is associated with [cortical] porosity, [area] and [density], indicating that [bone] [fragility] as a result of low [vitamin D] could be due to changes in [cortical] [bone microstructure] and [geometry].	[serum]{Anatomy} is Serum [vitamin D]{Chemicals & Drugs} is Vitamin D product [cortical]{Anatomy} is Cortex of bone [elderly]{Living Beings} is ELDERLY [men]{Living Beings} is Men [Bone loss]{Disorders} is Bone Loss [serum]{Anatomy} is Serum [vitamin D]{Chemicals & Drugs} is Vitamin D product [peripheral]{Concepts & Ideas} is Peripheral [sites]{Anatomy} is Site [elderly]{Living Beings} is ELDERLY [cortical]{Anatomy} is Cortex of bone [cortical]{Anatomy} is Cortex of bone [elderly]{Living Beings} is ELDERLY [men]{Living Beings} is Men [cortical]{Anatomy} is Cortex of bone [bone loss]{Disorders} is Bone Loss [sites]{Anatomy} is Site [25-hydroxyvitamin D]{Chemicals & Drugs} is 25-hydroxyvitamin D [serum]{Anatomy} is Serum [levels of 25-hydroxyvitamin D]{Procedures} is 25-Hydroxyvitamin D [bone microstructure]{Anatomy} is Bone structure [areal bone mineral density]{Physiology} is Bone Mineral Density [BMD]{Physiology} is Bone Mineral Density [elderly]{Living Beings} is ELDERLY [men]{Living Beings} is Men [population]{Living Beings} is Population [cohort]{Living Beings} is Cohort [elderly]{Living Beings} is ELDERLY [men]{Living Beings} is Men [Bone microstructure]{Anatomy} is Bone structure [high-resolution peripheral quantitative computed tomography]{Procedures} is Computed Tomography [areal BMD]{Physiology} is Bone Mineral Density [dual-energy X-ray absorptiometry]{Procedures} is Dual-Energy X-Ray Absorptiometry [serum]{Anatomy} is Serum [25-hydroxyvitamin D]{Procedures} is 25-Hydroxyvitamin D [parathyroid hormone levels]{Procedures} is Parathyroid hormone [immunoassay]{Procedures} is Immunoassay [cortical]{Anatomy} is Cortex of bone [distal tibia]{Anatomy} is Distal tibia [cortical]{Anatomy} is Cortex of bone [volumetric BMD]{Physiology} is Bone Mineral Density [area]{Concepts & Ideas} is Area [trabecular bone]{Anatomy} is Trabecular bone [femoral neck]{Anatomy} is Femoral neck [areal BMD]{Physiology} is Bone Mineral Density [men]{Living Beings} is Men [vitamin D levels]{Procedures} is Vitamin D [men]{Living Beings} is Men [vitamin D deficiency]{Disorders} is Vitamin D Deficiency [serum]{Anatomy} is Serum [level of parathyroid hormone]{Procedures} is Parathyroid hormone [cortical]{Anatomy} is Cortex of bone [vitamin D]{Chemicals & Drugs} is Vitamin D product [men]{Living Beings} is Men [model]{Concepts & Ideas} is Model [vitamin D]{Chemicals & Drugs} is Vitamin D product [supplementation]{Chemicals & Drugs} is Vitamin supplementation [parathyroid hormone]{Chemicals & Drugs} is Hormone, Parathyroid [25-hydroxyvitamin D]{Chemicals & Drugs} is 25-hydroxyvitamin D [cortical]{Anatomy} is Cortex of bone [area]{Concepts & Ideas} is Area [cortical]{Anatomy} is Cortex of bone [volumetric BMD]{Physiology} is Bone Mineral Density [tibia]{Anatomy} is TIBIA [areal BMD]{Physiology} is Bone Mineral Density [femoral neck]{Anatomy} is Femoral neck [Serum]{Anatomy} is Serum [vitamin D]{Chemicals & Drugs} is Vitamin D product [cortical]{Anatomy} is Cortex of bone [area]{Concepts & Ideas} is Area [density]{Physiology} is Bone Mineral Density [bone]{Anatomy} is Bone structure [fragility]{Disorders} is Fragility [vitamin D]{Chemicals & Drugs} is Vitamin D product [cortical]{Anatomy} is Cortex of bone [bone microstructure]{Anatomy} is Bone structure [geometry]{Concepts & Ideas} is Structural
Rapid Fabrication of a [Cell] - [Seeded] [Collagen] [Gel] -Based [Tubular Construct] that Withstands [Arterial Pressure]: Rapid Fabrication of a [Gel] -Based Media Equivalent Based on plastically compressed [cell] - [seeded] [collagen] [gels], we fabricated a small-diameter [tubular construct] that withstands [arterial pressure] without prolonged [culture] in vitro. Specifically, to mimic the [microstructure] of [vascular media], the [cell] - [seeded] [collagen] [gel] was uniaxially stretched prior to plastic compression to align [collagen fibers] and hence [cells] in the [gel]. The resulting [gel] [sheet] was then wrapped around a custom-made multi-layered braided tube to form aligned [tubular constructs] whereas the [gel] [sheet] prepared similarly but without uniaxial stretching formed control [constructs]. With the braided tube, fluid in the [gel] [construct] was further removed by [vacuum suction] aiming to consolidate the concentric layers of the [construct]. The [construct] was finally treated with [transglutaminase]. Both [SEM] and [histology] confirmed the absence of gaps in the wall of the [construct]. Particularly, [cells] in the wall of the aligned [tubular construct] were circumferentially aligned. The [enzyme] -mediated crosslinking increased burst pressure of both the [constructs] significantly; the extent of the increase of burst pressure for the aligned [tubular construct] was greater than that for the control counterpart. Increasing crosslinking left the compliance of the aligned [tubular construct] unchanged but reduced that of the control [construct]. [Cells] remained viable in [transglutaminase] -treated plastically compressed [gels] after 6 days in culture. This [study] demonstrated that by combining stretch-induced [fiber] alignment, plastic compression, and [enzyme] -mediated crosslinking, a [cell] - [seeded] [collagen] [gel] -based [tubular construct] with potential to be used as [vascular media] can be made within 3 days.	[Cell]{Anatomy} is Cell Type [Seeded]{Procedures} is Scaffold Seeding [Collagen]{Chemicals & Drugs} is Collagen [Gel]{Chemicals & Drugs} is Drug gel [Tubular Construct]{Devices} is Tube, device [Arterial Pressure]{Physiology} is Arterial pulse pressure [Gel]{Chemicals & Drugs} is Drug gel [Cell]{Anatomy} is Cell Type [Seeded]{Procedures} is Scaffold Seeding [cell]{Anatomy} is Cell Type [Collagen]{Chemicals & Drugs} is Collagen [seeded]{Procedures} is Scaffold Seeding [Gel]{Chemicals & Drugs} is Drug gel [collagen]{Chemicals & Drugs} is Collagen [gels]{Chemicals & Drugs} is Drug gel [Tubular Construct]{Devices} is Tube, device [Arterial Pressure]{Physiology} is Arterial pulse pressure [tubular construct]{Devices} is Tube, device [arterial pressure]{Physiology} is Arterial pulse pressure [Gel]{Chemicals & Drugs} is Drug gel [culture]{Procedures} is Culture - general [microstructure]{Concepts & Ideas} is Structure [vascular media]{Anatomy} is Vascular Media [cell]{Anatomy} is Cell Type [seeded]{Procedures} is Scaffold Seeding [collagen]{Chemicals & Drugs} is Collagen [gel]{Chemicals & Drugs} is Drug gel [collagen fibers]{Anatomy} is Collagen fiber [cells]{Anatomy} is Cell Type [gel]{Chemicals & Drugs} is Drug gel [gel]{Chemicals & Drugs} is Drug gel [sheet]{Chemicals & Drugs} is Biocompatible Materials (Chemical/Ingredient) [tubular constructs]{Devices} is Tube, device [gel]{Chemicals & Drugs} is Drug gel [sheet]{Chemicals & Drugs} is Biocompatible Materials (Chemical/Ingredient) [constructs]{Devices} is Tube, device [gel]{Chemicals & Drugs} is Drug gel [construct]{Devices} is Tube, device [vacuum suction]{Devices} is Suction regulator [construct]{Devices} is Tube, device [construct]{Devices} is Tube, device [transglutaminase]{Chemicals & Drugs} is Transglutaminase [SEM]{Procedures} is Scanning Electron Microscopies [histology]{Procedures} is Histology [construct]{Devices} is Tube, device [cells]{Anatomy} is Cell Type [tubular construct]{Devices} is Tube, device [enzyme]{Chemicals & Drugs} is Enzyme [constructs]{Devices} is Tube, device [tubular construct]{Devices} is Tube, device [tubular construct]{Devices} is Tube, device [construct]{Devices} is Tube, device [Cells]{Anatomy} is Cell Type [transglutaminase]{Chemicals & Drugs} is Transglutaminase [gels]{Chemicals & Drugs} is Drug gel [study]{Procedures} is Study [fiber]{Anatomy} is Collagen fiber [enzyme]{Chemicals & Drugs} is Enzyme [cell]{Anatomy} is Cell Type [seeded]{Procedures} is Scaffold Seeding [collagen]{Chemicals & Drugs} is Collagen [gel]{Chemicals & Drugs} is Drug gel [tubular construct]{Devices} is Tube, device [vascular media]{Anatomy} is Vascular Media
[Expression] and [Purification] of [E2 Glycoprotein] from [Insect] [Cells] ([Sf9]) for Use in [Serology] [Chikungunya virus] ([CHIKV]) is a [mosquito] - [borne] [arbovirus] which poses a major threat to global [public health]. Definitive [CHIKV] [diagnosis] is crucial, especially in distinguishing the [disease] from [dengue virus], which co-circulates in endemic [areas] and shares the same [mosquito vectors]. [Laboratory diagnosis] is mainly based on serological or molecular approaches. The [E2 glycoprotein] is a good candidate for [serological diagnosis] since it is the [immunodominant antigen] during the course of [infection], and reacts with seropositive [CHIKV] [sera]. In this chapter, we describe the generation of stable [clone] [Sf9] ([Spodoptera frugiperda]) [cells] [expressing] [secreted], [soluble], and native recombinant [CHIKV] [E2 glycoprotein]. We use direct [plasmid] [expression] in [insect] [cells], rather than the traditional technique of generating recombinant baculovirus. This [recombinant protein] is useful for [serological diagnosis] of [CHIKV] [infection].	[Expression]{Physiology} is Protein expression [Purification]{Procedures} is Protein Purification [E2 Glycoprotein]{Chemicals & Drugs} is Glycoprotein [Insect]{Living Beings} is Insect [Cells]{Anatomy} is Cells set [Sf9]{Anatomy} is Sf9 Cell [Serology]{Procedures} is Serology [Expression]{Physiology} is Protein expression [Chikungunya virus]{Living Beings} is Chikungunya Virus [Purification]{Procedures} is Protein Purification [CHIKV]{Living Beings} is Chikungunya Virus [mosquito]{Living Beings} is Mosquito [E2 Glycoprotein]{Chemicals & Drugs} is Glycoprotein [borne]{Disorders} is Does carry [arbovirus]{Living Beings} is Arboviruses [Insect]{Living Beings} is Insect [Cells]{Anatomy} is Cells set [Sf9]{Anatomy} is Sf9 Cell [Serology]{Procedures} is Serology [public health]{Procedures} is Public health service [CHIKV]{Living Beings} is Chikungunya Virus [diagnosis]{Disorders} is Diagnosis [disease]{Disorders} is Disease [dengue virus]{Living Beings} is Dengue Virus [areas]{Concepts & Ideas} is Area [mosquito vectors]{Living Beings} is Mosquito Vectors [Laboratory diagnosis]{Procedures} is Laboratory Diagnosis [E2 glycoprotein]{Chemicals & Drugs} is Glycoprotein [serological diagnosis]{Procedures} is Serology [immunodominant antigen]{Chemicals & Drugs} is Immunodominant Antigens [infection]{Disorders} is Infections [CHIKV]{Living Beings} is Chikungunya Virus [sera]{Anatomy} is Sera [clone]{Anatomy} is Clone Cell [Sf9]{Anatomy} is Sf9 Cell [Spodoptera frugiperda]{Living Beings} is Spodoptera frugiperdas [cells]{Anatomy} is Clone Cell [expressing]{Physiology} is Protein expression [secreted]{Physiology} is Secreted [soluble]{Anatomy} is Soluble [CHIKV]{Living Beings} is Chikungunya Virus [E2 glycoprotein]{Chemicals & Drugs} is Glycoprotein [plasmid]{Chemicals & Drugs} is Plasmid [expression]{Procedures} is Expression [insect]{Living Beings} is Insect [cells]{Anatomy} is Cells set [recombinant protein]{Chemicals & Drugs} is Recombinant protein [serological diagnosis]{Procedures} is Serology [CHIKV]{Living Beings} is Chikungunya Virus [infection]{Disorders} is Infections
Acute [risk factors] for [suicide attempts] and [death]: [prospective findings] from the STEP - [BD] [study] [Suicide] is unfortunately common in [psychiatric] [practice], but difficult to predict. The present [study] sought to assess which clinical [symptoms] increase in the months before [suicidal behavior] in a sample of [psychiatric] outpatients with [bipolar disorder]. Data from the Systematic Treatment Enhancement Program for [Bipolar Disorder] (STEP - [BD]) [trial] were used. A total of 103 [participants] who [attempted suicide] or died by [suicide] during the [trial] were included; a 15% random sample of the remaining [participants] (n = 427) was used as a comparison sample. Linear mixed models in the six months before [suicidal behavior] were conducted for each of five proposed acute [risk factors] for [suicidal behavior]. [Participants] were assessed using the [Clinical Monitoring Form] ([CMF]) at each [visit] for the following potential acute [risk factors] for [suicidal behavior]: [suicidal ideation], [loss of interest], [anxiety], [psychomotor agitation], and high-risk behavior. Each of the five [symptoms] was elevated overall in [individuals] who engaged in [suicidal behavior] (p < 0.05). The severity of both [suicidal ideation] and [loss of interest] significantly increased in the months before [suicidal behavior] (p < 0.001). [Anxiety] demonstrated comparable effect [sizes] across [multiple models]. [Psychomotor agitation] and high-risk behavior were not significantly elevated before [suicidal behavior]. [Suicidal ideation], [loss of interest] and, to a lesser [extent], [anxiety] may represent acute [suicide] [risk factors] up to four months before [suicidal behavior] in outpatients with [bipolar disorder]. Further [investigation] of these potential acute [risk factors] in [prospective analyses] is warranted.	[risk factors]{Disorders} is Risk Factors [suicide attempts]{Disorders} is Suicide Attempt [death]{Disorders} is Death (finding) [prospective findings]{Procedures} is Study, Prospective [BD]{Disorders} is Psychoses, Bipolar Affective [study]{Procedures} is Study [Suicide]{Disorders} is Suicides [risk factors]{Disorders} is Risk Factors [suicide attempts]{Disorders} is Suicide Attempt [psychiatric]{Occupations} is Psychiatric [death]{Disorders} is Death (finding) [practice]{Physiology} is Practice Experience [prospective findings]{Procedures} is Study, Prospective [BD]{Disorders} is Psychoses, Bipolar Affective [study]{Procedures} is Study [study]{Procedures} is Study [symptoms]{Disorders} is Symptoms [suicidal behavior]{Disorders} is Suicidal behavior [psychiatric]{Occupations} is Psychiatric [bipolar disorder]{Disorders} is Psychoses, Bipolar Affective [Bipolar Disorder]{Disorders} is Psychoses, Bipolar Affective [BD]{Disorders} is Psychoses, Bipolar Affective [trial]{Procedures} is Trial [participants]{Living Beings} is Participant [attempted suicide]{Disorders} is Suicide Attempt [suicide]{Disorders} is Suicides [trial]{Procedures} is Trial [participants]{Living Beings} is Participant [suicidal behavior]{Disorders} is Suicidal behavior [risk factors]{Disorders} is Risk Factors [suicidal behavior]{Disorders} is Suicidal behavior [Participants]{Living Beings} is Participant [Clinical Monitoring Form]{Procedures} is Clinical Trials, Monitoring [CMF]{Procedures} is Clinical Trials, Monitoring [visit]{Procedures} is Visit [risk factors]{Disorders} is Risk Factors [suicidal behavior]{Disorders} is Suicidal behavior [suicidal ideation]{Disorders} is Suicidal Ideation [loss of interest]{Disorders} is Loss of interest [anxiety]{Disorders} is ANXIETY [psychomotor agitation]{Disorders} is Psychomotor agitation [symptoms]{Disorders} is Symptoms [individuals]{Living Beings} is Individual (person) [suicidal behavior]{Disorders} is Suicidal behavior [suicidal ideation]{Disorders} is Suicidal Ideation [loss of interest]{Disorders} is Loss of interest [suicidal behavior]{Disorders} is Suicidal behavior [Anxiety]{Disorders} is ANXIETY [sizes]{Concepts & Ideas} is Size [multiple models]{Concepts & Ideas} is Models [Psychomotor agitation]{Disorders} is Psychomotor agitation [suicidal behavior]{Disorders} is Suicidal behavior [Suicidal ideation]{Disorders} is Suicidal Ideation [loss of interest]{Disorders} is Loss of interest [extent]{Concepts & Ideas} is Extent [anxiety]{Disorders} is ANXIETY [suicide]{Disorders} is Suicides [risk factors]{Disorders} is Risk Factors [suicidal behavior]{Disorders} is Suicidal behavior [bipolar disorder]{Disorders} is Psychoses, Bipolar Affective [investigation]{Procedures} is Evaluation Procedure [risk factors]{Disorders} is Risk Factors [prospective analyses]{Procedures} is Study, Prospective
Measurement of Outcomes of Upper Limb Reconstructive Surgery for [Tetraplegia] Reconstructive arm/hand surgery for [tetraplegia] is performed to [improve] [arm/hand function] and therefore personal well-being for [individuals] who accept such [elective surgeries]. However, changes at an impairment level do not always translate into functional or quality of life changes. Therefore, multiple outcome tools should be used that incorporate sufficient responsiveness to [detect] changes in [arm/hand function], activity and participation, and quality of life of the [individuals] involved. This narrative review aims to [assist] [clinicians] to choose the most appropriate tools to assess the need for reconstructive surgery and to [evaluate] its outcomes. Our specific [objectives] are (1) to describe aspects to consider when choosing a measure and (2) to describe the measures advised by an international therapist consensus group established in 2007. All advised measures are appraised in terms of the underlying [construct], [administration], and clinical relevance to [arm/hand reconstructions]. Essentially there are currently no criterion standard measures to [evaluate] the consequences of reconstructive arm/hand surgery. However, with judicious use of available measures it is possible to ensure the [questions asked] or tasks completed are relevant to the [surgical reconstruction] (s) undertaken. Further work in this field is required. This would be best met by immediate collaboration between 2 outcome's tool developers and by analysis of pre - and postoperative data already held in various international sites, which would allow further [evaluation] of the measures already in use, or components thereof.	[Tetraplegia]{Disorders} is Tetraplegia [tetraplegia]{Disorders} is Tetraplegia [improve]{Disorders} is Improved [Tetraplegia]{Disorders} is Tetraplegia [arm/hand function]{Physiology} is Hand functions [individuals]{Living Beings} is Individual (person) [elective surgeries]{Procedures} is Elective surgery [detect]{Disorders} is Detected [arm/hand function]{Physiology} is Hand functions [individuals]{Living Beings} is Individual (person) [assist]{Procedures} is Assisting [clinicians]{Living Beings} is Clinician [evaluate]{Procedures} is Evaluate [objectives]{Concepts & Ideas} is Objective [construct]{Concepts & Ideas} is Construct [administration]{Procedures} is Administration [arm/hand reconstructions]{Procedures} is Hand reconstruction [evaluate]{Procedures} is Evaluate [questions asked]{Disorders} is Asks questions [surgical reconstruction]{Procedures} is Surgical reconstruction [evaluation]{Procedures} is Evaluate
Factors preventing [kneeling] in a group of pre-educated patients post [total knee arthroplasty] [Difficulties in kneeling], one of the [poorest scoring functional outcomes] post [total knee arthroplasty] ([TKA]),have been attributed to a lack of patient education. This is the first study to investigate specific factors affecting a patient's [perceived] ability to kneel post [TKA], following exposure to a preoperative [kneeling] education session. A [cross-sectional study] was conducted following [TKA] with patients who had been educated about [kneeling] prior to the [operation]. Patients completed [kneeling] [questionnaires] at 6 (n = 115) and 12 (n = 82) months post [TKA]. In addition to the 12-month [kneeling] [questionnaire], patients also completed the [Oxford knee score] ([OKS]) survey. Seventy-two percent of patients [perceived] they could [kneel] at 12 months post [TKA]. Overall, [pain] and [discomfort] were the most common factors deterring patients from [kneeling]. [Perceived] [kneeling] ability was the poorest scored outcome on the [OKS] with patients reporting mild to moderate [difficulty] with this task. [Kneeling] scores were strongly correlated with overall [knee function scores] (R = 0.70), strongly correlated with [pain scores] (R = 0.45) and weakly correlated with [knee stability scores] (R = 0.29). When asked about other factors preventing [kneeling] other than [pain] or [discomfor] t, 75 % had reasons [unrelated] to the [knee] or [TKA]. The most common reason was 'problems with the other [knee] ' (n = 19). Patients in this study were provided with education regarding their [kneeling] ability post [TKA], yet still experienced limitations in [perceived] [kneeling] ability post operatively. Contrary to previous research, our study suggests that factors other than patient education [affect] a patient's [perceived] [kneeling] ability post [TKA].	[kneeling]{Physiology} is Kneeling function [total knee arthroplasty]{Procedures} is Total Knee Arthroplasty [Difficulties in kneeling]{Disorders} is Difficulty kneeling [kneeling]{Physiology} is Kneeling function [poorest scoring functional outcomes]{Disorders} is Investigation Finding [total knee arthroplasty]{Procedures} is Total Knee Arthroplasty [total knee arthroplasty]{Procedures} is Total Knee Arthroplasty [TKA]{Procedures} is Total Knee Arthroplasty [perceived]{Physiology} is Perceived [TKA]{Procedures} is Total Knee Arthroplasty [kneeling]{Physiology} is Kneeling function [cross-sectional study]{Procedures} is Cross-Sectional Study [TKA]{Procedures} is Total Knee Arthroplasty [kneeling]{Physiology} is Kneeling function [operation]{Procedures} is Operation [kneeling]{Physiology} is Kneeling function [questionnaires]{Concepts & Ideas} is Questionnaire [TKA]{Procedures} is Total Knee Arthroplasty [kneeling]{Physiology} is Kneeling function [questionnaire]{Concepts & Ideas} is Questionnaire [Oxford knee score]{Physiology} is Oxford knee score [OKS]{Physiology} is Oxford knee score [perceived]{Physiology} is Perceived [kneel]{Physiology} is Kneeling function [TKA]{Procedures} is Total Knee Arthroplasty [pain]{Disorders} is Pain finding [discomfort]{Disorders} is Actual Discomfort [kneeling]{Physiology} is Kneeling function [Perceived]{Physiology} is Perceived [kneeling]{Physiology} is Kneeling function [OKS]{Physiology} is Oxford knee score [difficulty]{Disorders} is Difficulty kneeling [Kneeling]{Physiology} is Kneeling function [knee function scores]{Disorders} is Investigation Finding [pain scores]{Disorders} is Pain score [knee stability scores]{Disorders} is Investigation Finding [kneeling]{Physiology} is Kneeling function [pain]{Disorders} is Pain finding [discomfor]{Disorders} is Actual Discomfort [unrelated]{Disorders} is Unrelated [knee]{Anatomy} is Bone structure of knee [TKA]{Procedures} is Total Knee Arthroplasty [knee]{Anatomy} is Bone structure of knee [kneeling]{Physiology} is Kneeling function [TKA]{Procedures} is Total Knee Arthroplasty [perceived]{Physiology} is Perceived [kneeling]{Physiology} is Kneeling function [affect]{Procedures} is Assessment of affect [perceived]{Physiology} is Perceived [kneeling]{Physiology} is Kneeling function [TKA]{Procedures} is Total Knee Arthroplasty
[Improved] diagnostic yield of [neuromuscular disorders] applying clinical [exome sequencing] in patients arising from a consanguineous [population] [Neuromuscular diseases] ([NMDs]) include a broad range of [disorders] affecting [muscles], [nerves] and [neuromuscular junctions]. Their overlapping phenotypes and heterogeneous genetic nature have created challenges in [diagnosis] which calls for the implementation of [massive parallel sequencing] as a candidate strategy to increase the diagnostic yield. In this [study], total of 45 patients, mostly offspring of consanguineous marriages were examined using [whole exome sequencing]. Data analysis was performed to identify the most probable [pathogenic] [rare variants] in known [NMD] [genes] which led to identification of causal variants for 33 out of 45 patients (73.3%) in the following known [genes]: [CAPN3], [Col6A1], [Col6A3], [DMD], [DYSF], [FHL1], [GJB1], [ISPD], [LAMA2], [LMNA], [PLEC1], [RYR1], [SGCA], [SGCB], [SYNE1], [TNNT1] and 22 novel [pathogenic] [variants] were [detected]. Today, the advantage of [whole exome sequencing] in [clinical diagnostic] strategies of [heterogeneous disorders] is clear. In this [cohort], a diagnostic yield of 73.3% was achieved which is quite high compared to the overall reported diagnostic yield of 25% to 50%. This could be explained by the consanguineous background of these patients and is another strong advantage of offering clinical [exome sequencing] in diagnostic [laboratories], especially in [populations] with high rate of [consanguinity].	[Improved]{Disorders} is Improved [neuromuscular disorders]{Disorders} is Neuromuscular disorders [exome sequencing]{Procedures} is Exome Sequencing [population]{Living Beings} is Population [Improved]{Disorders} is Improved [Neuromuscular diseases]{Disorders} is Neuromuscular disorders [NMDs]{Disorders} is Neuromuscular disorders [neuromuscular disorders]{Disorders} is Neuromuscular disorders [disorders]{Disorders} is Disorders [exome sequencing]{Procedures} is Exome Sequencing [muscles]{Anatomy} is Muscle [nerves]{Anatomy} is Nervus [neuromuscular junctions]{Anatomy} is Neuromuscular Junctions [population]{Living Beings} is Population [diagnosis]{Disorders} is Diagnosis [massive parallel sequencing]{Procedures} is Massively Parallel Sequencing [study]{Procedures} is Study [whole exome sequencing]{Procedures} is Exome Sequencing [pathogenic]{Disorders} is Pathogenic [rare variants]{Genes & Molecular Sequences} is Gene Variant [NMD]{Disorders} is Neuromuscular disorders [genes]{Genes & Molecular Sequences} is Genes [genes]{Genes & Molecular Sequences} is Genes [CAPN3]{Genes & Molecular Sequences} is CAPN3 [Col6A1]{Genes & Molecular Sequences} is COL6A1 [Col6A3]{Genes & Molecular Sequences} is COL6A3 [DMD]{Genes & Molecular Sequences} is DMD [DYSF]{Genes & Molecular Sequences} is DYSF [FHL1]{Genes & Molecular Sequences} is FHL1 gene [GJB1]{Genes & Molecular Sequences} is GJB1 [ISPD]{Genes & Molecular Sequences} is IspD [LAMA2]{Genes & Molecular Sequences} is LAMA2 [LMNA]{Genes & Molecular Sequences} is LMNA [PLEC1]{Genes & Molecular Sequences} is PLEC [RYR1]{Genes & Molecular Sequences} is RYR1 [SGCA]{Genes & Molecular Sequences} is SGCA [SGCB]{Genes & Molecular Sequences} is SGCB [SYNE1]{Genes & Molecular Sequences} is SYNE1 [TNNT1]{Genes & Molecular Sequences} is TNNT1 [pathogenic]{Disorders} is Pathogenic [variants]{Genes & Molecular Sequences} is Gene Variant [detected]{Disorders} is Detected [whole exome sequencing]{Procedures} is Exome Sequencing [clinical diagnostic]{Procedures} is Clinical diagnosis [heterogeneous disorders]{Disorders} is Heterogeneous disorder [cohort]{Living Beings} is Cohort [exome sequencing]{Procedures} is Exome Sequencing [laboratories]{Organizations} is Laboratories [populations]{Living Beings} is Population [consanguinity]{Disorders} is Consanguinities
Laser -facilitated [epicutaneous] [immunotherapy] to [IgE-mediated allergy] [Allergen specific immunotherapy] has been shown to be the only effective [treatment] for long-lasting clinical benefit to [IgE-mediated allergic diseases], but a fewer than 5% of patients choose the [treatment] because of inconvenience and a [high risk of] [anaphylaxis]. Recently, [epicutaneous allergen-specific immunotherapy] ([EPIT]) has proven effective, yet with limitations owing to [strong skin reactions]. We demonstrate here safer and faster [EPIT], named [μEPIT], by delivering [powdered allergen] and [adjuvants] into many [micropores] in the [epidermis]. We fabricated a microarray [patch] fractionally coated with a [powder mixture of ovalbumin] ([OVA]) model [allergen], [CpG], and [1,25-dihydroxyvitamin D3] ([VD3]). Topical application of the [patch] onto [laser-microperforated] [skin] resulted in a high level of [epidermal] delivery while greatly minimizing [allergen] [leakage] into [circulation system] as compared to current [subcutaneous immunotherapy] ([SCIT]). Moreover, only three times of [μEPIT] over two weeks could sufficiently inhibit [allergen-specific IgE] responses in [mice] suffering [OVA] -induced [airway hyperresponsivness] ([AHR]), which was unattainable by eight times of [SCIT] over three weeks. Mechanistically, [μEPIT] preferably enhanced [IgG2a] [production] suggesting [TH1-biased] [immune responses] and induced a high level of [T-regulatory] ([Treg]) [cells] against repeated [allergen sensitization]. The [immune tolerance] was confirmed by marked [reduction] in [airway wall] [thickness] as well as [eosinophil] and [neutrophil infiltration] into the [respiratory airway]. The [μEPIT] represents a novel and painless technology to [treat] [IgE-mediated allergic diseases] with little [local skin reaction] and a minimal risk of [anaphylaxis].	[epicutaneous]{Procedures} is ADMIN CUTANEOUS [immunotherapy]{Procedures} is Immunotherapy [IgE-mediated allergy]{Disorders} is Atopic IgE-mediated allergic disorder [Allergen specific immunotherapy]{Procedures} is Allergen immunotherapy [epicutaneous]{Procedures} is ADMIN CUTANEOUS [immunotherapy]{Procedures} is Immunotherapy [IgE-mediated allergy]{Disorders} is Atopic IgE-mediated allergic disorder [treatment]{Procedures} is Treatments [IgE-mediated allergic diseases]{Disorders} is Atopic IgE-mediated allergic disorder [treatment]{Procedures} is Treatments [high risk of]{Disorders} is High risk of [anaphylaxis]{Disorders} is Obsolete anaphylaxis [epicutaneous allergen-specific immunotherapy]{Procedures} is Allergen immunotherapy [EPIT]{Procedures} is Allergen immunotherapy [strong skin reactions]{Physiology} is Reaction skin [EPIT]{Procedures} is Allergen immunotherapy [μEPIT]{Procedures} is Allergen immunotherapy [powdered allergen]{Chemicals & Drugs} is ALLERGEN [adjuvants]{Chemicals & Drugs} is ADJUVANTS IMMUNOL [micropores]{Anatomy} is Pore [epidermis]{Anatomy} is Epidermis structure [patch]{Devices} is Skin patch [powder mixture of ovalbumin]{Chemicals & Drugs} is Ovalbumin [OVA]{Chemicals & Drugs} is Ovalbumin [allergen]{Chemicals & Drugs} is ALLERGEN [CpG]{Chemicals & Drugs} is CpG [1,25-dihydroxyvitamin D3]{Chemicals & Drugs} is 1,25-Dihydroxyvitamin D3 [VD3]{Chemicals & Drugs} is 1,25-Dihydroxyvitamin D3 [patch]{Devices} is Skin patch [laser-microperforated]{Disorders} is Microperforation [skin]{Anatomy} is Skin of body [epidermal]{Anatomy} is Epidermis structure [allergen]{Chemicals & Drugs} is ALLERGEN [leakage]{Disorders} is Leakage [circulation system]{Anatomy} is Circulatory system [subcutaneous immunotherapy]{Procedures} is Subcutaneous immunotherapy [SCIT]{Procedures} is Subcutaneous immunotherapy [μEPIT]{Procedures} is Allergen immunotherapy [allergen-specific IgE]{Chemicals & Drugs} is Allergen specific IgE [mice]{Living Beings} is Laboratory Mice [OVA]{Chemicals & Drugs} is Ovalbumin [airway hyperresponsivness]{Disorders} is Airway Hyper Responsiveness [AHR]{Disorders} is Airway Hyper Responsiveness [SCIT]{Procedures} is Subcutaneous immunotherapy [μEPIT]{Procedures} is Allergen immunotherapy [IgG2a]{Chemicals & Drugs} is IgG2A [production]{Phenomena} is Antibody Production [TH1-biased]{Anatomy} is Th1 cell [immune responses]{Physiology} is Immune Response [T-regulatory]{Anatomy} is Regulatory T-Cells [Treg]{Anatomy} is Regulatory T-Cells [cells]{Anatomy} is Cells set [allergen sensitization]{Disorders} is Food allergen sensitization [immune tolerance]{Disorders} is Immune Tolerance [reduction]{Procedures} is Reduction [airway wall]{Anatomy} is Airway [thickness]{Disorders} is Increased thickness [eosinophil]{Anatomy} is Eosinophil [neutrophil infiltration]{Physiology} is Neutrophil Infiltration [respiratory airway]{Anatomy} is Respiratory Tract [μEPIT]{Procedures} is Allergen immunotherapy [treat]{Procedures} is Treatments [IgE-mediated allergic diseases]{Disorders} is Atopic IgE-mediated allergic disorder [local skin reaction]{Physiology} is Reaction skin [anaphylaxis]{Disorders} is Obsolete anaphylaxis
Predicting real - [world] functional milestones in [schizophrenia] [Schizophrenia] is a [severe disorder] that often causes impairments in major areas of functioning, and most patients do not achieve expected real - [world] functional milestones. The aim of this [study] was to identify which variables of demography, [illness] activity, and [functional capacity] predict patients ' ability to attain real - [world] functional milestones. [Participants] were 235 outpatients, 149 [men] and 86 [women], [diagnosed] with [schizophrenia] [spectrum disorder]. Our results showed that younger patients managed to achieve a higher level of functioning in [educational level], marital status, and [social contacts]. Patients ' [functional capacity] was primarily associated with [educational level] and housing situation. We also found that [women] needed less support regarding housing and obtained a higher level of marital status as compared with [men]. Our [findings] demonstrate the importance of considering current [symptoms], especially [negative] [symptoms], and [remission] stability over time, together with age, duration of illness, gender, [educational level], and current [functional capacity], when predicting patients ' future real - [world] functioning. We also conclude that there is an advantage in exploring [symptoms] divided into [positive], [negative], and general domains considering their probable impact on functional achievements.	[world]{Living Beings} is World [schizophrenia]{Disorders} is Schizophrenia [Schizophrenia]{Disorders} is Schizophrenia [world]{Living Beings} is World [severe disorder]{Disorders} is Severe disorder [schizophrenia]{Disorders} is Schizophrenia [world]{Living Beings} is World [study]{Procedures} is Study [illness]{Disorders} is Illness [functional capacity]{Disorders} is Functional capacity [world]{Living Beings} is World [Participants]{Living Beings} is Participant [men]{Living Beings} is Men [women]{Living Beings} is Women [diagnosed]{Disorders} is Diagnosed [schizophrenia]{Disorders} is Schizophrenia [spectrum disorder]{Disorders} is Mental disorder (disorder) [educational level]{Disorders} is Educational Level [social contacts]{Disorders} is Finding (finding) [functional capacity]{Disorders} is Functional capacity [educational level]{Disorders} is Educational Level [women]{Living Beings} is Women [men]{Living Beings} is Men [findings]{Disorders} is Finding (finding) [symptoms]{Disorders} is Symptoms [negative]{Disorders} is Negative for [symptoms]{Disorders} is Symptoms [remission]{Disorders} is Remission [educational level]{Disorders} is Educational Level [functional capacity]{Disorders} is Functional capacity [world]{Living Beings} is World [symptoms]{Disorders} is Symptoms [positive]{Disorders} is Positive for [negative]{Disorders} is Negative for
[LDLR], [ApoB] and [ApoE genes] polymorphisms and classical [risk factors] in [premature coronary artery disease] [Lipoproteins] play a central role in the development of [atherosclerotic disease]. So, with their ability to affect [lipid levels], the [LDLR], [ApoB] and [ApoE] polymorphisms could be one of the factors influencing development of [atherosclerosis]. This hypothesis has been [tested] in different populations with conflicting results. The purpose of the present study was to investigate the association between the [LDLR], [ApoB] and [ApoE genes] polymorphisms with [premature CAD] ([PCAD]) in [Egyptians]. One hundred thirty-five patients of [PCAD] and one hundred thirty-two ages and sex matched control subjects were included in the study. [LDLR] and [ApoB genes] polymorphisms were [analyzed] by [polymerase chain reaction] ([PCR]). The [ApoE] genotypes were identified by [multiplex amplification refractory mutation system] ([multi-AMRS]). We found that [LDLR A(+)A(+)] genotype, [ApoB X(+)] [allele] and [ApoE E4] [allele] increased the risk of [PCAD] by 1.8, 2.1 and 12.1 respectively. The present study proved that smoking, [metabolic syndrome], [ApoB X(+)X(+)] genotype and [ApoE E4] [allele] were independent [risk factors] for the development of [PCAD]. This is the first study investigate the association between [low density lipoprotein receptor], [apolipoprotein B] and [apolipoprotein E genes] polymorphisms with [PCAD] and [lipid levels] in [Egyptians] and we concluded that the [LDLR A(+)A(+)] genotype, [ApoB X(+)] [allele] and [ApoE E4] [allele] may be associated with an increased risk for development of [PCAD] by elevated [levels of total cholesterol (TC)] and [low density lipoprotein] ([LDLc]). The coexistence of [CAD] [risk factors] with [LDLR A(+)A(+)] genotype, [ApoB X(+)] [allele] and [ApoE E4] [allele] may increase the risk of the development of [PCAD] in [Egyptian] patients.	[LDLR]{Genes & Molecular Sequences} is LDLR Gene [ApoB]{Genes & Molecular Sequences} is APOB [ApoE genes]{Genes & Molecular Sequences} is APOE gene [risk factors]{Disorders} is Risk Factors [premature coronary artery disease]{Disorders} is Premature coronary artery disease [LDLR]{Genes & Molecular Sequences} is LDLR Gene [Lipoproteins]{Chemicals & Drugs} is Lipoproteins [ApoB]{Genes & Molecular Sequences} is APOB [ApoE genes]{Genes & Molecular Sequences} is APOE gene [risk factors]{Disorders} is Risk Factors [atherosclerotic disease]{Disorders} is Atherosclerotic cardiovascular disease [premature coronary artery disease]{Disorders} is Premature coronary artery disease [lipid levels]{Phenomena} is Lipid level [LDLR]{Genes & Molecular Sequences} is LDLR Gene [ApoB]{Genes & Molecular Sequences} is APOB [ApoE]{Genes & Molecular Sequences} is APOE gene [atherosclerosis]{Disorders} is Atherosclerotic cardiovascular disease [tested]{Concepts & Ideas} is Tests [LDLR]{Genes & Molecular Sequences} is LDLR Gene [ApoB]{Genes & Molecular Sequences} is APOB [ApoE genes]{Genes & Molecular Sequences} is APOE gene [premature CAD]{Disorders} is Premature coronary artery disease [PCAD]{Disorders} is Premature coronary artery disease [Egyptians]{Living Beings} is Egyptians [PCAD]{Disorders} is Premature coronary artery disease [LDLR]{Genes & Molecular Sequences} is LDLR Gene [ApoB genes]{Genes & Molecular Sequences} is APOB [analyzed]{Procedures} is Analyzed [polymerase chain reaction]{Procedures} is Polymerase Chain Reaction [PCR]{Procedures} is Polymerase Chain Reaction [ApoE]{Genes & Molecular Sequences} is APOE gene [multiplex amplification refractory mutation system]{Procedures} is Analysis using amplification refractory mutation system PCR [multi-AMRS]{Procedures} is Analysis using amplification refractory mutation system PCR [LDLR A(+)A(+)]{Genes & Molecular Sequences} is LDLR Gene [ApoB X(+)]{Genes & Molecular Sequences} is APOB [allele]{Genes & Molecular Sequences} is Allele [ApoE E4]{Genes & Molecular Sequences} is APOE gene [allele]{Genes & Molecular Sequences} is Allele [PCAD]{Disorders} is Premature coronary artery disease [metabolic syndrome]{Disorders} is Metabolic syndrome [ApoB X(+)X(+)]{Genes & Molecular Sequences} is APOB [ApoE E4]{Genes & Molecular Sequences} is APOE gene [allele]{Genes & Molecular Sequences} is Allele [risk factors]{Disorders} is Risk Factors [PCAD]{Disorders} is Premature coronary artery disease [low density lipoprotein receptor]{Genes & Molecular Sequences} is LDLR Gene [apolipoprotein B]{Genes & Molecular Sequences} is APOB [apolipoprotein E genes]{Genes & Molecular Sequences} is APOE gene [PCAD]{Disorders} is Premature coronary artery disease [lipid levels]{Phenomena} is Lipid level [Egyptians]{Living Beings} is Egyptians [LDLR A(+)A(+)]{Genes & Molecular Sequences} is LDLR Gene [ApoB X(+)]{Genes & Molecular Sequences} is APOB [allele]{Genes & Molecular Sequences} is Allele [ApoE E4]{Genes & Molecular Sequences} is APOE gene [allele]{Genes & Molecular Sequences} is Allele [PCAD]{Disorders} is Premature coronary artery disease [levels of total cholesterol (TC)]{Procedures} is Cholesterol level [low density lipoprotein]{Procedures} is Low density lipoprotein measurement [LDLc]{Procedures} is Low density lipoprotein measurement [CAD]{Disorders} is Premature coronary artery disease [risk factors]{Disorders} is Risk Factors [LDLR A(+)A(+)]{Genes & Molecular Sequences} is LDLR Gene [ApoB X(+)]{Genes & Molecular Sequences} is APOB [allele]{Genes & Molecular Sequences} is Allele [ApoE E4]{Genes & Molecular Sequences} is APOE gene [allele]{Genes & Molecular Sequences} is Allele [PCAD]{Disorders} is Premature coronary artery disease [Egyptian]{Living Beings} is Egyptians
[Mandibular] [kinesiographic pattern] of [women] with chronic [TMD] after [management] with [educational] and [self-care therapies]: A [double-blind], [randomized clinical trial] [Limited mandibular movements] are one of the most important [signs] of [temporomandibular disorders] ([TMDs]) and may cause functional difficulties. The purpose of this [double-blind], [randomized clinical trial] was to [evaluate] the effect of [treatment] with only [educational] or [education] associated with [self-care therapies] on the [pattern] of [mandibular] [movements] of [women] with [chronic painful] [TMDs]. Forty-two [women] were selected and randomly divided into 3 groups, control group (CG, n=13), education group (EG, n=16), and education and self-care group (ESG, n=13), according to the sequence of [treatment] they received. A [kinesiograph device] recorded [mandibular] [movements] during maximum [mouth] [opening] and [mastication] at baseline (T0) and at 30-day (T1) and 60-day (T2) [follow-up]. [Kinesiographic data] were statistically analyzed using 1-way ANOVA, followed by the Bonferroni test for multiple comparisons of means (α=.05). The ESG group demonstrated an improvement in the [maximum vertical opening] ([MVO] = 5.1 ±3.4 mm; P=.012) and [anteroposterior mandibular movement] ([MAM]) during maximum [opening] (7.4 ±9.5; P=.019), significantly higher than that of the EG ([MVO] =1.8 ±3.5 mm; [MAM] =0.8 ±5.0 mm) and the CG ([MVO] =0.9 ±3.8 mm; [MAM] =0.8 ±4.4 mm) after 30 days of [follow-up]. Moreover, at T1, [vertical] [mandibular] [movement] during [mastication] was significantly higher in the ESG group (17.4 ±1.7 mm) than in the EG group (15.0 ±2.8, P=.027). [No significant] differences were [found] between the [women] who received [treatment] with [educational] and [self-care therapies] for 60 days and the [women] who received this [treatment] for 30 days. In the short-term, [education] and [self-care treatment] [positively] influenced the [mandibular] [movement] [pattern] of [women] with [chronic painful] [TMDs].	[Mandibular]{Anatomy} is Mandibular [kinesiographic pattern]{Concepts & Ideas} is Intellectual Product [women]{Living Beings} is Women [TMD]{Disorders} is TMJ DIS [management]{Procedures} is DIS MANAGEMENT [educational]{Concepts & Ideas} is Education [self-care therapies]{Procedures} is Self-care practice (regime/therapy) [double-blind]{Procedures} is Double-Blinded [randomized clinical trial]{Procedures} is Randomized clinical trial [Mandibular]{Anatomy} is Mandibular [Limited mandibular movements]{Disorders} is Limited mandibular mobility [kinesiographic pattern]{Concepts & Ideas} is Intellectual Product [women]{Living Beings} is Women [TMD]{Disorders} is TMJ DIS [signs]{Disorders} is SIGNS SYMPTOMS [management]{Procedures} is DIS MANAGEMENT [temporomandibular disorders]{Disorders} is TMJ DIS [educational]{Concepts & Ideas} is Education [TMDs]{Disorders} is TMJ DIS [self-care therapies]{Procedures} is Self-care practice (regime/therapy) [double-blind]{Procedures} is Double-Blinded [randomized clinical trial]{Procedures} is Randomized clinical trial [double-blind]{Procedures} is Double-Blinded [randomized clinical trial]{Procedures} is Randomized clinical trial [evaluate]{Procedures} is Evaluate [treatment]{Procedures} is Treatments [educational]{Concepts & Ideas} is Education [education]{Concepts & Ideas} is Education [self-care therapies]{Procedures} is Self-care practice (regime/therapy) [pattern]{Concepts & Ideas} is Intellectual Product [mandibular]{Anatomy} is Mandibular [movements]{Physiology} is Movements [women]{Living Beings} is Women [chronic painful]{Disorders} is Chronic Pain [TMDs]{Disorders} is TMJ DIS [women]{Living Beings} is Women [treatment]{Procedures} is Treatments [kinesiograph device]{Devices} is Device [mandibular]{Anatomy} is Mandibular [movements]{Physiology} is Movements [mouth]{Anatomy} is Cavity of mouth [opening]{Physiology} is Movements [mastication]{Physiology} is Mastication (function) [follow-up]{Procedures} is Follow-up [Kinesiographic data]{Concepts & Ideas} is Clinical Data [maximum vertical opening]{Physiology} is Movements [MVO]{Physiology} is Movements [anteroposterior mandibular movement]{Physiology} is Movements [MAM]{Physiology} is Movements [opening]{Physiology} is Movements [MVO]{Physiology} is Movements [MAM]{Physiology} is Movements [MVO]{Physiology} is Movements [MAM]{Physiology} is Movements [follow-up]{Procedures} is Follow-up [vertical]{Concepts & Ideas} is Vertical [mandibular]{Anatomy} is Mandibular [movement]{Physiology} is Movements [mastication]{Physiology} is Mastication (function) [No significant]{Disorders} is Not significant [found]{Disorders} is Found [women]{Living Beings} is Women [treatment]{Procedures} is Treatments [educational]{Concepts & Ideas} is Education [self-care therapies]{Procedures} is Self-care practice (regime/therapy) [women]{Living Beings} is Women [treatment]{Procedures} is Treatments [education]{Concepts & Ideas} is Education [self-care treatment]{Procedures} is Self-care practice (regime/therapy) [positively]{Disorders} is Positive for [mandibular]{Anatomy} is Mandibular [movement]{Physiology} is Movements [pattern]{Concepts & Ideas} is Intellectual Product [women]{Living Beings} is Women [chronic painful]{Disorders} is Chronic Pain [TMDs]{Disorders} is TMJ DIS
[MiR-211] is [epigenetically regulated] by [DNMT1] mediated [methylation] and inhibits [EMT] of [melanoma cells] by [targeting] [RAB22A] [MiR-211] has strong inhibitive effects on [melanoma] [cell growth], [invasion] and [metastasis]. However, how it is [downregulated] and whether other [genes] are involved its [downstream] [regulation] in [melanoma] are not clear. In this study, we firstly verified the [expression] of [miR-211] in [melanoma cell lines] and observed that its [downregulation] is associated with increased [DNMT1] [expression]. By performing [qRT-PCR] and [MSP analysis], we confirmed that [DNMT1] is [negatively] correlated with [miR-211] [expression] and can [modulate] [DNA methylation] in the [promoter region] of [miR-211]. By performing [bioinformatics analysis], we found that [RAB22A] is a possible target of [miR-211], which has two broadly [conversed] [binding sites] with [miR-211] in the [3'UTR]. Following dual [luciferase] [assay], [qRT-PCR] and [western blot analysis] confirmed the direct [binding] between [miR-211] and [RAB22A] and the [suppressive effect] of [miR-211] on [RAB22A] [expression]. [Knockdown] of [RAB22A] increased epithelial properties and impaired mesenchymal properties of the [melanoma cells], suggesting that [miR-211] [modulates] [epithelial mesenchymal transition] ([EMT]) of [melanoma cells] via [downregulating] [RAB22A]. In summary, the present study firstly demonstrated that [DNMT1] mediated [promoter] [methylation] is a mechanism of [miRNA] [suppression] in [melanoma] and revealed a new [tumor suppressor] role of the [miR-211] by [targeting] [RAB22A] in [melanoma]. The [DNMT1] / [miR-211] / [RAB22A] axis provides a novel insight into the [pathogenesis] of [melanoma], particularly in the [EMT process].	[MiR-211]{Genes & Molecular Sequences} is MIR211 [epigenetically regulated]{Physiology} is Regulation of gene expression, epigenetic [DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene [methylation]{Physiology} is Methylations [EMT]{Physiology} is EMT [melanoma cells]{Anatomy} is Melanoma Cell [targeting]{Procedures} is Gene Targeting [RAB22A]{Genes & Molecular Sequences} is RAB22A [MiR-211]{Genes & Molecular Sequences} is MIR211 [epigenetically regulated]{Physiology} is Regulation of gene expression, epigenetic [DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene [melanoma]{Disorders} is Melanoma [cell growth]{Physiology} is Cell Growth [methylation]{Physiology} is Methylations [invasion]{Disorders} is Cell Invasion [metastasis]{Disorders} is Metastasis [EMT]{Physiology} is EMT [melanoma cells]{Anatomy} is Melanoma Cell [targeting]{Procedures} is Gene Targeting [downregulated]{Physiology} is Downregulation [RAB22A]{Genes & Molecular Sequences} is RAB22A [genes]{Genes & Molecular Sequences} is Genes [downstream]{Concepts & Ideas} is Downstream [regulation]{Physiology} is Downregulation [melanoma]{Disorders} is Melanoma [expression]{Physiology} is Expression [miR-211]{Genes & Molecular Sequences} is MIR211 [melanoma cell lines]{Anatomy} is Melanoma Cell [downregulation]{Physiology} is Downregulation [DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene [expression]{Physiology} is Expression [qRT-PCR]{Procedures} is QRT-PCR [MSP analysis]{Procedures} is Microspectrophotometries [DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene [negatively]{Disorders} is NEGATIVE [miR-211]{Genes & Molecular Sequences} is MIR211 [expression]{Physiology} is Expression [modulate]{Concepts & Ideas} is Modulate [DNA methylation]{Physiology} is DNA methylation [promoter region]{Chemicals & Drugs} is Promoter Region [miR-211]{Genes & Molecular Sequences} is MIR211 [bioinformatics analysis]{Occupations} is Bioinformatics [RAB22A]{Genes & Molecular Sequences} is RAB22A [miR-211]{Genes & Molecular Sequences} is MIR211 [conversed]{Genes & Molecular Sequences} is CONSERVED SEQ [binding sites]{Chemicals & Drugs} is Binding Sites [miR-211]{Genes & Molecular Sequences} is MIR211 [3'UTR]{Genes & Molecular Sequences} is 3'UTR [luciferase]{Chemicals & Drugs} is Luciferase [assay]{Procedures} is BIOL ASSAY [qRT-PCR]{Procedures} is QRT-PCR [western blot analysis]{Procedures} is Blot, Western [binding]{Physiology} is Binding [miR-211]{Genes & Molecular Sequences} is MIR211 [RAB22A]{Genes & Molecular Sequences} is RAB22A [suppressive effect]{Physiology} is SUPPRESSION GENET [miR-211]{Genes & Molecular Sequences} is MIR211 [RAB22A]{Genes & Molecular Sequences} is RAB22A [expression]{Physiology} is Expression [Knockdown]{Procedures} is Gene Knockdown [RAB22A]{Genes & Molecular Sequences} is RAB22A [melanoma cells]{Anatomy} is Melanoma Cell [miR-211]{Genes & Molecular Sequences} is MIR211 [modulates]{Concepts & Ideas} is Modulate [epithelial mesenchymal transition]{Physiology} is EMT [EMT]{Physiology} is EMT [melanoma cells]{Anatomy} is Melanoma Cell [downregulating]{Physiology} is Downregulation [RAB22A]{Genes & Molecular Sequences} is RAB22A [DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene [promoter]{Chemicals & Drugs} is Promoter Region [methylation]{Physiology} is Methylations [miRNA]{Chemicals & Drugs} is MiRNA [suppression]{Physiology} is SUPPRESSION GENET [melanoma]{Disorders} is Melanoma [tumor suppressor]{Genes & Molecular Sequences} is Tumor Suppressor [miR-211]{Genes & Molecular Sequences} is MIR211 [targeting]{Procedures} is Gene Targeting [RAB22A]{Genes & Molecular Sequences} is RAB22A [melanoma]{Disorders} is Melanoma [DNMT1]{Genes & Molecular Sequences} is DNMT1 Gene [miR-211]{Genes & Molecular Sequences} is MIR211 [RAB22A]{Genes & Molecular Sequences} is RAB22A [pathogenesis]{Disorders} is Pathogenesis [melanoma]{Disorders} is Melanoma [EMT process]{Physiology} is EMT
[Body mass index] and [suicide] methods [Overweight] and [obesity] is associated with lower rates of [suicide]. However, little is known about the association with different [suicide] methods. We studied the association between groups of [body mass index] and [suicide] methods. We identified all [medicolegal] [autopsy] cases with a [cause of death] due to external causes in [Sweden] during 1999-2013 (N = 39,368) and included 11,715 [suicides] and 13,316 accidents or homicides as controls. We applied multinomial [regression models] adjusted for age, sex, year and season of [death]. [Obesity] was associated with [suicidal] [intoxication], OR 1.15 (95% confidence interval (CI) 1.02, 1.30) and [negatively] associated with all other [suicide] methods studied. [Underweight] showed a [negative] association with [suicidal] [drowning] and there was an indication towards a [negative] association with [hanging] in [men] OR 0.81 (95% CI 0.65, 1.01). We conclude that [body mass index] ([BMI]) is associated with the choice of [suicide] method. This may be of importance in a [public health perspective], e.g. potential for [prevention] of [intoxications]. In the practice of [forensic medicine], the [physician's] level of [suspicion] may rise if the apparent [suicidal] method is less common for the individual characteristics of the [deceased], such as [BMI].	[Body mass index]{Physiology} is Body Mass Index [suicide]{Disorders} is Suicides [Overweight]{Disorders} is Overweight [Body mass index]{Physiology} is Body Mass Index [obesity]{Disorders} is Obesity (disorder) [suicide]{Disorders} is Suicides [suicide]{Disorders} is Suicides [suicide]{Disorders} is Suicides [body mass index]{Physiology} is Body Mass Index [suicide]{Disorders} is Suicides [medicolegal]{Concepts & Ideas} is Medicolegal aspects [autopsy]{Procedures} is Autopsy [cause of death]{Disorders} is Cause of Death [Sweden]{Geographic Areas} is Sweden [suicides]{Disorders} is Suicides [regression models]{Concepts & Ideas} is REGRESSION ANAL [death]{Disorders} is Death (finding) [Obesity]{Disorders} is Obesity (disorder) [suicidal]{Disorders} is Suicidal [intoxication]{Disorders} is Intoxication [negatively]{Disorders} is Negative for [suicide]{Disorders} is Suicides [Underweight]{Disorders} is Underweight [negative]{Disorders} is Negative for [suicidal]{Disorders} is Suicidal [drowning]{Disorders} is Drowning [negative]{Disorders} is Negative for [hanging]{Disorders} is Hanging [men]{Living Beings} is Men [body mass index]{Physiology} is Body Mass Index [BMI]{Physiology} is Body Mass Index [suicide]{Disorders} is Suicides [public health perspective]{Procedures} is Public health service [prevention]{Procedures} is Suicide prevention [intoxications]{Disorders} is Intoxication [forensic medicine]{Occupations} is Forensic Medicine [physician's]{Living Beings} is Physician [suspicion]{Physiology} is Suspicion [suicidal]{Disorders} is Suicidal [deceased]{Physiology} is Deceased [BMI]{Physiology} is Body Mass Index
[Cognitive impairment] in [HIV] and [HCV] [co-infected] patients: a systematic [review] and [meta-analysis] [Cognitive impairment] has been well documented in [human immunodeficiency virus] ([HIV]) and [hepatitis C virus] ([HCV]) [mono-infections]. However, in the context of [HIV] / [HCV] [co-infection] the research is more limited. The aim of this systematic [review] was to describe the characteristics of [cognitive impairment] in [HIV] / [HCV] [co-infection] and to [examine] the differences in [cognitive performance] between [HIV] / [HCV] and [HIV] and [HCV] [mono-infected] patients. Of the 437 records initially [screened], 24 papers met the inclusion criteria and were included in the systematic [review]. Four [studies] were included in the [meta-analysis]. Most [studies] indicated that [HIV] / [HCV] [co-infected] patients had a higher level of [cognitive impairment] than [HIV] [mono-infected] patients. [Meta-analysis] also indicated that [HIV] [mono-infected] patients had a significantly lower global deficit score than [co-infected] patients. The results also indicated that [co-infected] patients were more likely to be [impaired] in information processing speed than [HIV] [mono-infected] patients. These [findings] can be challenged by biasing factors such as the small number of included [studies], heterogeneity of the samples and a large diversity of methodological procedures. Future research with consistent and comprehensive [neuropsychological batteries] and covering a greater diversity of [risk factors] is needed, in order to clarify the effects of both [viruses] on [cognitive function] and the mechanisms that underlie these effects. Because [cognitive impairments] may pose significant [challenges] to [medication adherence], quality of life and overall functioning, such knowledge may have important implications to the [planning] and [implementation] of effective interventions aimed at optimising the [clinical management] of these [infections].	[Cognitive impairment]{Disorders} is Cognitive impairment [HIV]{Living Beings} is HIV [HCV]{Living Beings} is HCV [co-infected]{Disorders} is Co-infections [review]{Concepts & Ideas} is Review [meta-analysis]{Procedures} is Meta-analysis [Cognitive impairment]{Disorders} is Cognitive impairment [HIV]{Living Beings} is HIV [HCV]{Living Beings} is HCV [co-infected]{Disorders} is Co-infections [human immunodeficiency virus]{Living Beings} is HIV [review]{Concepts & Ideas} is Review [HIV]{Living Beings} is HIV [meta-analysis]{Procedures} is Meta-analysis [hepatitis C virus]{Living Beings} is HCV [HCV]{Living Beings} is HCV [mono-infections]{Disorders} is Infections [HIV]{Living Beings} is HIV [HCV]{Living Beings} is HCV [co-infection]{Disorders} is Co-infections [review]{Concepts & Ideas} is Review [cognitive impairment]{Disorders} is Cognitive impairment [HIV]{Living Beings} is HIV [HCV]{Living Beings} is HCV [co-infection]{Disorders} is Co-infections [examine]{Disorders} is Examined [cognitive performance]{Physiology} is Cognitive functions [HIV]{Living Beings} is HIV [HCV]{Living Beings} is HCV [HIV]{Living Beings} is HIV [HCV]{Living Beings} is HCV [mono-infected]{Disorders} is Infections [screened]{Procedures} is Screenings [review]{Concepts & Ideas} is Review [studies]{Procedures} is Study [meta-analysis]{Procedures} is Meta-analysis [studies]{Procedures} is Study [HIV]{Living Beings} is HIV [HCV]{Living Beings} is HCV [co-infected]{Disorders} is Co-infections [cognitive impairment]{Disorders} is Cognitive impairment [HIV]{Living Beings} is HIV [mono-infected]{Disorders} is Infections [Meta-analysis]{Procedures} is Meta-analysis [HIV]{Living Beings} is HIV [mono-infected]{Disorders} is Infections [co-infected]{Disorders} is Co-infections [co-infected]{Disorders} is Co-infections [impaired]{Disorders} is Cognitive impairment [HIV]{Living Beings} is HIV [mono-infected]{Disorders} is Infections [findings]{Disorders} is Finding (finding) [studies]{Procedures} is Study [neuropsychological batteries]{Concepts & Ideas} is Neuropsychological battery [risk factors]{Disorders} is Risk Factors [viruses]{Living Beings} is Virus [cognitive function]{Physiology} is Cognitive functions [cognitive impairments]{Disorders} is Cognitive impairment [challenges]{Procedures} is Challenge [medication adherence]{Disorders} is Medication adherence [planning]{Procedures} is Health Planning [implementation]{Procedures} is Health Plan Implementation [clinical management]{Procedures} is Clinical Management [infections]{Disorders} is Infections
Usefulness of [Embolization] for [Iatrogenic] [Dural Arteriovenous Fistula] Associated with Recurrent [Chronic Subdural Hematoma]: A [Case Report] and [Literature Review] Refractory [chronic subdural hematomas] due to [iatrogenic] [dural arteriovenous fistulas] ([dAVFs]) are difficult to treat. We report our experience and propose a guideline on basis of a [literature review] for the usefulness of [embolization] of [middle meningeal artery] ([MMA]) for the [treatment] of the same. We report a case with [right hemiparesis] and [aphasia] 1 month after a [fall] from a bicycle. [Computed tomography scan] of the [head] showed [left] [chronic subdural hematoma], which was evacuated by burr-hole drainage. The postoperative course was complicated by [reaccumulation] within short period of time. On [superselective digital subtraction angiography] of [MMA], [iatrogenic] [dAVF] was found on [left side]. We [embolized] successfully it using [n-butyl cyanoacrylate] after a third [irrigation]. No [reaccumulation] found in the postoperative period or at last [follow-up]. We propose [treatment protocol] based on our experience and [literature review]. Refractory [chronic subdural hematoma] with [reaccumulation] within a short interval should be subjected to [digital subtraction angiography] of the [MMA]. [Embolization] of [ipsilateral] [MMA] is safe, effective, and a useful option for the [treatment] of [iatrogenic] [dAVF] and resolution of [hematoma].	[Embolization]{Procedures} is Embolization [Iatrogenic]{Disorders} is Iatrogenesis [Dural Arteriovenous Fistula]{Disorders} is Dural arteriovenous fistula [Chronic Subdural Hematoma]{Disorders} is Chronic subdural hematoma [Case Report]{Concepts & Ideas} is Case report [Literature Review]{Concepts & Ideas} is Review Literature [chronic subdural hematomas]{Disorders} is Chronic subdural hematoma [Embolization]{Procedures} is Embolization [Iatrogenic]{Disorders} is Iatrogenesis [Dural Arteriovenous Fistula]{Disorders} is Dural arteriovenous fistula [iatrogenic]{Disorders} is Iatrogenesis [dural arteriovenous fistulas]{Disorders} is Dural arteriovenous fistula [dAVFs]{Disorders} is Dural arteriovenous fistula [Chronic Subdural Hematoma]{Disorders} is Chronic subdural hematoma [Case Report]{Concepts & Ideas} is Case report [Literature Review]{Concepts & Ideas} is Review Literature [literature review]{Concepts & Ideas} is Review Literature [embolization]{Procedures} is Embolization [middle meningeal artery]{Anatomy} is Structure of middle meningeal artery [MMA]{Anatomy} is Structure of middle meningeal artery [treatment]{Procedures} is Treatments [right hemiparesis]{Disorders} is Right hemiparesis [aphasia]{Disorders} is Aphasia [fall]{Disorders} is Fall [Computed tomography scan]{Procedures} is Computed tomography scan - [head]{Anatomy} is Heads [left]{Concepts & Ideas} is Left sided [chronic subdural hematoma]{Disorders} is Chronic subdural hematoma [reaccumulation]{Disorders} is Accumulation [superselective digital subtraction angiography]{Procedures} is Digital Subtraction Angiography [MMA]{Anatomy} is Structure of middle meningeal artery [iatrogenic]{Disorders} is Iatrogenesis [dAVF]{Disorders} is Dural arteriovenous fistula [left side]{Concepts & Ideas} is Left side [embolized]{Procedures} is Embolization [n-butyl cyanoacrylate]{Chemicals & Drugs} is N-butyl-cyanoacrylate [irrigation]{Procedures} is Therapeutic Irrigation [reaccumulation]{Disorders} is Accumulation [follow-up]{Procedures} is Follow-up [treatment protocol]{Procedures} is Treatment Protocol [literature review]{Concepts & Ideas} is Review Literature [chronic subdural hematoma]{Disorders} is Chronic subdural hematoma [reaccumulation]{Disorders} is Accumulation [digital subtraction angiography]{Procedures} is Digital Subtraction Angiography [MMA]{Anatomy} is Structure of middle meningeal artery [Embolization]{Procedures} is Embolization [ipsilateral]{Concepts & Ideas} is Ipsilateral [MMA]{Anatomy} is Structure of middle meningeal artery [treatment]{Procedures} is Treatments [iatrogenic]{Disorders} is Iatrogenesis [dAVF]{Disorders} is Dural arteriovenous fistula [hematoma]{Disorders} is Hematoma subdural
Incidence of [crown fracture] and [risk factors] in the [primary dentition]: a [prospective longitudinal study] Few studies have assessed the incidence and [risk factors] to [crown fractures] in preschool children. The aim of this study was to estimate the incidence of [crown fracture] in the [primary dentition] over a 1-year [follow-up] period, identify [risk factors], and test the hypothesis that children with previous [crown fracture] are more prone to experience further cases of [crown fracture] independently of other [risk factors]. This study was developed in two phases: [cross-sectional] and [prospective longitudinal study]. The [cross-sectional study] was carried out 261 preschool children. The [prospective longitudinal study] was carried out 194 children allocated to two groups: [exposed group] (children with prior exposure to [crown fracture]) and [non] - [exposed group] (children without prior exposure). On both occasions, children were examined for the [diagnosis] of [crown fracture] and evaluation of [lip] coverage and [overjet]. The parents were interviewed with regard to the socioeconomic indicators. New cases of [crown fracture] were identified based on the comparison of the two examinations. Data analysis involved [Pearson's chi-square test], [McNemar's test], and [Poisson regression] with robust variance. Among the 261 children who participated in the [cross-sectional study], 194 were re-examined (65 in the [exposed group] and 129 in the [non] - [exposed group]). The overall incidence of [crown fracture] was 55.7% (n = 108). The difference in percentage of [increased risk of] [crown fracture] in exposed and [non] - [exposed groups] was 13.4%. A greater incidence of [crown fracture] was found in the exposed group (64.6%; P < 0,001). The children exposed (RR: 1.30; 95% CI: 1.01-1.67) had a [greater risk of] developing new cases of [crown fracture] in comparison with the [non] - [exposed group]. The incidence of [crown fracture] was high and children with previous [crown fracture] had a [greater risk of] suffering new cases of [crown fracture] during the 1-year [follow-up] period.	[crown fracture]{Disorders} is Tooth crown fracture [risk factors]{Disorders} is Risk Factors [primary dentition]{Anatomy} is Primary dentition [prospective longitudinal study]{Procedures} is Longitudinal Study [crown fracture]{Disorders} is Tooth crown fracture [risk factors]{Disorders} is Risk Factors [risk factors]{Disorders} is Risk Factors [primary dentition]{Anatomy} is Primary dentition [crown fractures]{Disorders} is Tooth crown fracture [prospective longitudinal study]{Procedures} is Longitudinal Study [crown fracture]{Disorders} is Tooth crown fracture [primary dentition]{Anatomy} is Primary dentition [follow-up]{Procedures} is Follow-up [risk factors]{Disorders} is Risk Factors [crown fracture]{Disorders} is Tooth crown fracture [crown fracture]{Disorders} is Tooth crown fracture [risk factors]{Disorders} is Risk Factors [cross-sectional]{Procedures} is Cross-Sectional Study [prospective longitudinal study]{Procedures} is Longitudinal Study [cross-sectional study]{Procedures} is Cross-Sectional Study [prospective longitudinal study]{Procedures} is Longitudinal Study [exposed group]{Living Beings} is Exposed Group [crown fracture]{Disorders} is Tooth crown fracture [non]{Disorders} is NEGATIVE [exposed group]{Living Beings} is Exposed Group [diagnosis]{Disorders} is Diagnosis [crown fracture]{Disorders} is Tooth crown fracture [lip]{Anatomy} is LIP [overjet]{Disorders} is Overjet [crown fracture]{Disorders} is Tooth crown fracture [Pearson's chi-square test]{Concepts & Ideas} is Hypothesis Test [McNemar's test]{Concepts & Ideas} is Hypothesis Test [Poisson regression]{Concepts & Ideas} is REGRESSION ANAL [cross-sectional study]{Procedures} is Cross-Sectional Study [exposed group]{Living Beings} is Exposed Group [non]{Disorders} is NEGATIVE [exposed group]{Living Beings} is Exposed Group [crown fracture]{Disorders} is Tooth crown fracture [increased risk of]{Disorders} is High risk of [crown fracture]{Disorders} is Tooth crown fracture [non]{Disorders} is NEGATIVE [exposed groups]{Living Beings} is Exposed Group [crown fracture]{Disorders} is Tooth crown fracture [greater risk of]{Disorders} is High risk of [crown fracture]{Disorders} is Tooth crown fracture [non]{Disorders} is NEGATIVE [exposed group]{Living Beings} is Exposed Group [crown fracture]{Disorders} is Tooth crown fracture [crown fracture]{Disorders} is Tooth crown fracture [greater risk of]{Disorders} is High risk of [crown fracture]{Disorders} is Tooth crown fracture [follow-up]{Procedures} is Follow-up
An Efficient and Reliable [Statistical Method] for Estimating Functional [Connectivity] in Large Scale [Brain] [Networks] Using Partial Correlation Currently, [network-oriented] [analysis] of [fMRI] data has become an important tool for understanding [brain] [organization] and [brain] [networks]. Among the range of [network] modeling methods, partial correlation has shown great promises in accurately [detecting] true [brain] [network] [connections]. However, the application of partial correlation in investigating [brain] [connectivity], especially in large-scale [brain] [networks], has been limited so far due to the technical challenges in its estimation. In this paper, we propose an efficient and reliable [statistical method] for estimating partial correlation in large-scale [brain] [network] [modeling]. Our [method] derives partial correlation based on the precision matrix estimated via [Constrained L1-minimization Approach] ([CLIME]), which is a recently developed [statistical method] that is more efficient and demonstrates better performance than the existing [methods]. To help select an appropriate tuning parameter for sparsity control in the [network] estimation, we propose a new [Dens-based selection method] that provides a more informative and flexible [tool] to allow the users to select the tuning parameter based on the desired sparsity level. Another appealing feature of the [Dens-based method] is that it is much faster than the existing [methods], which provides an important advantage in [neuroimaging applications]. [Simulation studies] show that the [Dens-based method] demonstrates comparable or better performance with respect to the existing [methods] in [network] estimation. We applied the proposed partial correlation [method] to investigate [resting state functional connectivity using rs-fMRI data] from the Philadelphia Neurodevelopmental Cohort (PNC) study. Our results show that partial correlation [analysis] removed considerable between-module [marginal connections] identified by full [correlation analysis], suggesting these [connections] were likely caused by global effects or common [connection] to other [nodes]. Based on partial correlation, we find that the most significant direct [connections] are between homologous [brain] [locations] in the [left] and [right hemisphere]. When comparing partial correlation derived under different sparse tuning parameters, an important finding is that the sparse regularization has more shrinkage effects on [negative] functional [connections] than on [positive] [connections], which supports previous findings that many of the [negative] [brain] [connections] are due to [non-neurophysiological effects]. An [R package "DensParcorr"] can be downloaded from [CRAN] for implementing the proposed [statistical methods].	[Statistical Method]{Procedures} is Statistical Method [Connectivity]{Concepts & Ideas} is Connection [Brain]{Anatomy} is Brains [Networks]{Physiology} is Nerve network [network-oriented]{Physiology} is Nerve network [Statistical Method]{Procedures} is Statistical Method [analysis]{Procedures} is Analyzed [fMRI]{Procedures} is FMRI [Connectivity]{Concepts & Ideas} is Connection [brain]{Anatomy} is Brains [Brain]{Anatomy} is Brains [organization]{Physiology} is Organization [Networks]{Physiology} is Nerve network [brain]{Anatomy} is Brains [networks]{Physiology} is Nerve network [network]{Physiology} is Nerve network [detecting]{Disorders} is Detected [brain]{Anatomy} is Brains [network]{Physiology} is Nerve network [connections]{Concepts & Ideas} is Connection [brain]{Anatomy} is Brains [connectivity]{Concepts & Ideas} is Connection [brain]{Anatomy} is Brains [networks]{Physiology} is Nerve network [statistical method]{Procedures} is Statistical Method [brain]{Anatomy} is Brains [network]{Physiology} is Nerve network [modeling]{Procedures} is Modeling [method]{Concepts & Ideas} is Methods [Constrained L1-minimization Approach]{Procedures} is Statistical Method [CLIME]{Procedures} is Statistical Method [statistical method]{Procedures} is Statistical Method [methods]{Concepts & Ideas} is Methods [network]{Physiology} is Nerve network [Dens-based selection method]{Procedures} is Statistical Method [tool]{Concepts & Ideas} is Software Tool [Dens-based method]{Procedures} is Statistical Method [methods]{Concepts & Ideas} is Methods [neuroimaging applications]{Procedures} is Neuroimaging [Simulation studies]{Procedures} is Simulation [Dens-based method]{Procedures} is Statistical Method [methods]{Concepts & Ideas} is Methods [network]{Physiology} is Nerve network [method]{Concepts & Ideas} is Methods [resting state functional connectivity using rs-fMRI data]{Procedures} is Resting State Functional Connectivity MRI [analysis]{Procedures} is Analyzed [marginal connections]{Concepts & Ideas} is Connection [correlation analysis]{Procedures} is Correlation Study [connections]{Concepts & Ideas} is Connection [connection]{Concepts & Ideas} is Connection [nodes]{Anatomy} is Node [connections]{Concepts & Ideas} is Connection [brain]{Anatomy} is Brains [locations]{Anatomy} is Location [left]{Anatomy} is Left Brain Hemisphere [right hemisphere]{Anatomy} is Right Brain Hemisphere [negative]{Disorders} is Negative for [connections]{Concepts & Ideas} is Connection [positive]{Disorders} is Positive for [connections]{Concepts & Ideas} is Connection [negative]{Disorders} is Negative for [brain]{Anatomy} is Brains [connections]{Concepts & Ideas} is Connection [non-neurophysiological effects]{Physiology} is Unknown Physiological Effect [R package "DensParcorr"]{Concepts & Ideas} is Software Tool [CRAN]{Concepts & Ideas} is Intellectual Product [statistical methods]{Procedures} is Statistical Method
[Metabolite] Profiling of [Italian] [Tomato] Landraces with Different [Fruit] Types Increased interest toward traditional [tomato] varieties is fueled by the need to rescue desirable organoleptic traits and to [improve] the quality of fresh and processed [tomatoes] in the [market]. In addition, the phenotypic and genetic variation preserved in [tomato] landraces represents a means to understand the genetic basis of traits related to health and organoleptic aspects and improve them in modern varieties. To establish a framework for this approach, we [studied] the content of several [metabolites] in a panel of [Italian] [tomato] landraces categorized into three broad [fruit] type classes (flattened / ribbed, [pear] / [oxheart], [round] / elongate). Three modern hybrids, corresponding to the three [fruit] [shape] [typologies], were included as reference. [Red ripe fruits] were [morphologically] characterized and biochemically analyzed for their content in [glycoalkaloids], [phenols], [amino acids], and [Amadori products]. The [round] / elongate types showed a higher content in [glycoalkaloids], whereas flattened types had higher levels of [phenolic compounds]. Flattened [tomatoes] were also rich in total [amino acids] and in particular in [glutamic acid]. Multivariate analysis of [amino acid content] clearly separated the three classes of [fruit] types. Making allowance of the very low number of genotypes, phenotype-marker relationships were [analyzed] after retrieving [single nucleotide polymorphisms] ([SNPs]) among the landraces available in the [literature]. Sixty-six [markers] were significantly associated with the [studied] traits. The positions of several of these [SNPs] showed correspondence with already described genomic regions and [QTLs] supporting the reliability of the association. Overall the data indicated that significant changes in quality -related [metabolites] occur depending on the genetic background in traditional [tomato] [germplasm], frequently according to specific [fruit] [shape] categories. Such a variability is suitable to harness association mapping for metabolic quality traits using this [germplasm] as an experimental population, paving the way for investigating their genetic / molecular basis, and facilitating [breeding] for quality-related [compounds] in [tomato] [fruits].	[Metabolite]{Chemicals & Drugs} is Metabolite [Italian]{Geographic Areas} is Italy [Tomato]{Objects} is Tomato [Fruit]{Objects} is Fruit [Metabolite]{Chemicals & Drugs} is Metabolite [Italian]{Geographic Areas} is Italy [Tomato]{Objects} is Tomato [tomato]{Objects} is Tomato [Fruit]{Objects} is Fruit [improve]{Disorders} is Improved [tomatoes]{Objects} is Tomato [market]{Geographic Areas} is Market [tomato]{Objects} is Tomato [studied]{Procedures} is Study [metabolites]{Chemicals & Drugs} is Metabolite [Italian]{Geographic Areas} is Italy [tomato]{Objects} is Tomato [fruit]{Objects} is Fruit [pear]{Objects} is Pear [oxheart]{Objects} is Fruit [round]{Concepts & Ideas} is Round [fruit]{Objects} is Fruit [shape]{Concepts & Ideas} is SHAPE [typologies]{Concepts & Ideas} is General Typologies [Red ripe fruits]{Objects} is Fruit [morphologically]{Concepts & Ideas} is Morphological [glycoalkaloids]{Chemicals & Drugs} is Alkaloids [phenols]{Chemicals & Drugs} is Phenols [amino acids]{Chemicals & Drugs} is Amino Acids [Amadori products]{Chemicals & Drugs} is Organic Chemical [round]{Concepts & Ideas} is Round [glycoalkaloids]{Chemicals & Drugs} is Alkaloids [phenolic compounds]{Chemicals & Drugs} is Phenols [tomatoes]{Objects} is Tomato [amino acids]{Chemicals & Drugs} is Amino Acids [glutamic acid]{Chemicals & Drugs} is Glutamic acid [amino acid content]{Procedures} is Amino acid level [fruit]{Objects} is Fruit [analyzed]{Procedures} is Analyzed [single nucleotide polymorphisms]{Genes & Molecular Sequences} is Single Nucleotide Polymorphisms [SNPs]{Genes & Molecular Sequences} is Single Nucleotide Polymorphisms [literature]{Concepts & Ideas} is Literature [markers]{Genes & Molecular Sequences} is DNA Markers [studied]{Procedures} is Study [SNPs]{Genes & Molecular Sequences} is Single Nucleotide Polymorphisms [QTLs]{Genes & Molecular Sequences} is QTL [metabolites]{Chemicals & Drugs} is Metabolite [tomato]{Objects} is Tomato [germplasm]{Anatomy} is Germ plasm [fruit]{Objects} is Fruit [shape]{Concepts & Ideas} is SHAPE [germplasm]{Anatomy} is Germ plasm [breeding]{Physiology} is Breeding [compounds]{Chemicals & Drugs} is Compound [tomato]{Objects} is Tomato [fruits]{Objects} is Fruit
[Cross-reactivity] features of [deoxynivalenol] ([DON])-targeted [immunoaffinity] columns aiming to achieve simultaneous [analysis] of [DON] and major [conjugates] in [cereal] samples [Immunoafﬁnity] columns (IACs) are a well-established tool in the determination of regulated [mycotoxins] in [food] and [feed commodities]. However, they also have the potential to become attractive pre-concentration and clean-up materials for the determination of masked (also called modified) [mycotoxins], which have been recognised as important contributors to the [toxicological] hazard deriving from fungal spoilage of [goods]. However, the information available in the literature concerning the [cross-reactivity] of [DON] - IACs against the major [conjugates] ([DON-3-G], [15-AcDON] and [3-AcDON]) is incomplete and often contradictory. We have carried out a detailed characterisation of the [cross-reactivity] of the four main IACs brands against [DON] and its [conjugates] as well as an assessment of the competition among the [analytes]. Only one IAC enabled the simultaneous [analysis] of all relevant [DON] forms while two missed [15-AcDON] and the fourth one missed [DON-3-G] and [3-AcDON]. In the case of the multivalent IAC, the [analytes] modified at the C-3 position compete for the [antibody binding] with preference for [3-AcDON] (less spatially hindered) while [DON-3-G] has the more-hindered access to the [active sites]. Taking into consideration the levels of [DON] [conjugates] existing in real samples, the [cross-reactivity] of one [DON] - IAC allows a quantitative analysis of all of these [analytes]. Important but rather neglected aspects such as the continuous supply of IACs with identical characteristics, and of columns which are strictly blank, are also addressed in this paper.	[Cross-reactivity]{Physiology} is Cross Reactivity [deoxynivalenol]{Chemicals & Drugs} is Deoxynivalenol [DON]{Chemicals & Drugs} is Deoxynivalenol [immunoaffinity]{Procedures} is Immunoaffinity Chromatography [analysis]{Procedures} is Analysis of substances [DON]{Chemicals & Drugs} is Deoxynivalenol [conjugates]{Chemicals & Drugs} is Derivatives [cereal]{Objects} is Cereal [Immunoafﬁnity]{Procedures} is Immunoaffinity Chromatography [Cross-reactivity]{Physiology} is Cross Reactivity [deoxynivalenol]{Chemicals & Drugs} is Deoxynivalenol [DON]{Chemicals & Drugs} is Deoxynivalenol [immunoaffinity]{Procedures} is Immunoaffinity Chromatography [mycotoxins]{Chemicals & Drugs} is Mycotoxins [food]{Objects} is Food [analysis]{Procedures} is Analysis of substances [feed commodities]{Objects} is Food [DON]{Chemicals & Drugs} is Deoxynivalenol [conjugates]{Chemicals & Drugs} is Derivatives [cereal]{Objects} is Cereal [mycotoxins]{Chemicals & Drugs} is Mycotoxins [toxicological]{Phenomena} is Toxicological Concept [goods]{Objects} is Food [cross-reactivity]{Physiology} is Cross Reactivity [DON]{Chemicals & Drugs} is Deoxynivalenol [conjugates]{Chemicals & Drugs} is Derivatives [DON-3-G]{Chemicals & Drugs} is DON-3-Glc [15-AcDON]{Chemicals & Drugs} is Deoxynivalenol [3-AcDON]{Chemicals & Drugs} is Deoxynivalenol [cross-reactivity]{Physiology} is Cross Reactivity [DON]{Chemicals & Drugs} is Deoxynivalenol [conjugates]{Chemicals & Drugs} is Derivatives [analytes]{Chemicals & Drugs} is Deoxynivalenol [analysis]{Procedures} is Analysis of substances [DON]{Chemicals & Drugs} is Deoxynivalenol [15-AcDON]{Chemicals & Drugs} is Deoxynivalenol [DON-3-G]{Chemicals & Drugs} is DON-3-Glc [3-AcDON]{Chemicals & Drugs} is Deoxynivalenol [analytes]{Chemicals & Drugs} is Deoxynivalenol [antibody binding]{Chemicals & Drugs} is Antibody binding site [3-AcDON]{Chemicals & Drugs} is Deoxynivalenol [DON-3-G]{Chemicals & Drugs} is DON-3-Glc [active sites]{Chemicals & Drugs} is Antibody binding site [DON]{Chemicals & Drugs} is Deoxynivalenol [conjugates]{Chemicals & Drugs} is Derivatives [cross-reactivity]{Physiology} is Cross Reactivity [DON]{Chemicals & Drugs} is Deoxynivalenol [analytes]{Chemicals & Drugs} is Deoxynivalenol
Improving Early Identification and Ongoing Care of Children With [Autism Spectrum Disorder] Poor adherence to recommended [screening] for [autism spectrum disorder] ([ASD]) and [pediatricians] ' [lack of confidence] in providing care for children with [ASD] reflect quality gaps in [primary care]. This [study] aimed to increase the proportion of toddlers screened for [ASD] and [improve] [physicians] ' [self-efficacy] in providing care to children with [ASD]. Twenty-six Utah [primary care practices] participated in a 3 to 6 month [learning collaborative] ([LC]) to [improve] [identification] and ongoing care of children with [ASD]. Monthly chart audits assessed whether an [ASD] [screening tool] was administered at 18- and 24- month [visits]. [Physicians] completed pre-LC and post-LC [surveys] to assess changes in [self-efficacy] in providing care and changes in [perceived] barriers to implementation of [screening] and caring for children with [ASD]. Before the [LC], 15% of 18- and 24- month [visits] had [documented] [ASD] [screening], compared with 91% during the last month of the [LC] (P < .001). This rate of [ASD] [screening] was sustained 4 years after the [LC] by most practices. Compared with [survey] responses before the [LC], [physicians] reported significant improvement in their ability to care for children with [ASD] and decreases in their [perceived] barriers to [screening] and caring for children with [ASD]. The [LC] was effective in increasing and sustaining recommended [ASD] [screening] of toddlers and improving [physicians] ' perceived [self-efficacy] in caring for children with [ASD]. Improving [primary care] [screening], skills, and knowledge may [improve] the timing of [diagnosis], initiation of [treatment], [quality of care], and outcomes for children with [ASD].	[Autism Spectrum Disorder]{Disorders} is Autism or autism spectrum disorder [screening]{Procedures} is Screening Generic [autism spectrum disorder]{Disorders} is Autism or autism spectrum disorder [Autism Spectrum Disorder]{Disorders} is Autism or autism spectrum disorder [ASD]{Disorders} is Autism or autism spectrum disorder [pediatricians]{Living Beings} is Pediatricians [lack of confidence]{Disorders} is Lacks confidence [ASD]{Disorders} is Autism or autism spectrum disorder [primary care]{Procedures} is Primary Care [study]{Procedures} is Study [ASD]{Disorders} is Autism or autism spectrum disorder [improve]{Disorders} is Improved [physicians]{Living Beings} is Physicians [self-efficacy]{Physiology} is Self-Efficacy [ASD]{Disorders} is Autism or autism spectrum disorder [primary care practices]{Procedures} is Primary Care [learning collaborative]{Organizations} is Entity - organization [LC]{Organizations} is Entity - organization [improve]{Disorders} is Improved [identification]{Physiology} is Identification [ASD]{Disorders} is Autism or autism spectrum disorder [ASD]{Disorders} is Autism or autism spectrum disorder [screening tool]{Procedures} is Screening Generic [visits]{Procedures} is Visit [Physicians]{Living Beings} is Physicians [surveys]{Concepts & Ideas} is Surveys [self-efficacy]{Physiology} is Self-Efficacy [perceived]{Physiology} is Perceived [screening]{Procedures} is Screening Generic [ASD]{Disorders} is Autism or autism spectrum disorder [LC]{Organizations} is Entity - organization [visits]{Procedures} is Visit [documented]{Procedures} is Documented [ASD]{Disorders} is Autism or autism spectrum disorder [screening]{Procedures} is Screening Generic [LC]{Organizations} is Entity - organization [ASD]{Disorders} is Autism or autism spectrum disorder [screening]{Procedures} is Screening Generic [LC]{Organizations} is Entity - organization [survey]{Procedures} is Health Survey [LC]{Organizations} is Entity - organization [physicians]{Living Beings} is Physicians [ASD]{Disorders} is Autism or autism spectrum disorder [perceived]{Physiology} is Perceived [screening]{Procedures} is Screening Generic [ASD]{Disorders} is Autism or autism spectrum disorder [LC]{Organizations} is Entity - organization [ASD]{Disorders} is Autism or autism spectrum disorder [screening]{Procedures} is Screening Generic [physicians]{Living Beings} is Physicians [self-efficacy]{Physiology} is Self-Efficacy [ASD]{Disorders} is Autism or autism spectrum disorder [primary care]{Procedures} is Primary Care [screening]{Procedures} is Screening Generic [improve]{Disorders} is Improved [diagnosis]{Procedures} is DIAGNOSIS [treatment]{Procedures} is Treatments [quality of care]{Procedures} is Quality of Care [ASD]{Disorders} is Autism or autism spectrum disorder
Describing Self-Care [Self-Efficacy]: [Definition], Measurement, Outcomes, and Implications The [pragmatic utility method] of concept [analysis] was used to explore the usefulness of the concept self-care [self-efficacy]. Empirical studies across disciplines published between 1996 and 2015 were used as data. A data matrix was developed. Analytical questions and [responses] were derived from the data to understand patterns, develop new [knowledge] and achieve synthesis. Usefulness of the concept is contingent on how it is defined and measured. Self-care [self-efficacy] is associated with performance of self-care activities and [positive] health outcomes in diverse [populations]. [Research] can guide development of targeted [interventions] to increase patients ' self-care [self-efficacy], thus reducing costs, and [assisting] [people] to achieve optimal health.	[Self-Efficacy]{Physiology} is Self-Efficacy [Definition]{Concepts & Ideas} is Definition [pragmatic utility method]{Procedures} is Pragmatic Clinical Trial [Self-Efficacy]{Physiology} is Self-Efficacy [Definition]{Concepts & Ideas} is Definition [analysis]{Procedures} is Analyzed [self-efficacy]{Physiology} is Self-Efficacy [responses]{Concepts & Ideas} is Response [knowledge]{Concepts & Ideas} is Knowledge [self-efficacy]{Physiology} is Self-Efficacy [positive]{Disorders} is Positive for [populations]{Living Beings} is Population [Research]{Procedures} is Research [interventions]{Procedures} is Nursing interventions [self-efficacy]{Physiology} is Self-Efficacy [assisting]{Procedures} is Assisting - action [people]{Living Beings} is People
Dynamics of [intestinal] [metabolites] and morphology in response to [necrotic enteritis] [challenge] in [broiler chickens] Despite the relatively small contribution to metabolizable energy that [volatile fatty acids] ([VFAs]) provide in [chickens], these [organic acids] have been [reported] to play beneficial roles in the [gastrointestinal tract] ([GIT]) of [birds], for example, [inhibition of the growth] of some pathogenic [bacteria]. However, information regarding the dynamics of these [metabolites] in the [GIT] of [chickens] is still scarce, especially under [disease conditions] such as [necrotic enteritis] ([NE]). Here, we investigated the dynamics of [VFAs] and [lactic acid], and [intestinal] morphology in response to [NE] predisposing factors, that is, excessive [dietary] fishmeal and [Eimeria] [inoculation], and [causative agent] [Clostridium perfringens] producing [NetB toxin]. The [experiment] was [designed] in a 2 × 2 × 2 factorial [arrangement] of [treatments] with or without: fishmeal feeding, [Eimeria] [inoculation] and [C. perfringens] [challenge]. The results showed that these factors significantly influenced [composition] and concentration of [VFAs] and [lactic acids], pH and histomorphometry in one way or another. These changes may be important for the onset of [NE] or only the synergetic responses to micro environmental [stress]. [Eimeria] appeared to be more important than fishmeal in predisposing [birds] to [NE], thus the application of [Eimeria] in [NE] [challenge] provides more consistent success in inducing the [disease]. The metabolic responses to various [adverse] factors such as excessive [dietary] fishmeal and [Eimeria] [infection] are complex. Thus, intensive [efforts] are required to better [understand] [NE] so as to achieve the [control of the disease] in the absence of [antibiotics].	[intestinal]{Anatomy} is Intestinal [metabolites]{Chemicals & Drugs} is Metabolite [necrotic enteritis]{Disorders} is Necrotic enteritis [challenge]{Procedures} is Challenge [broiler chickens]{Living Beings} is Broiler Chicken [intestinal]{Anatomy} is Intestinal [metabolites]{Chemicals & Drugs} is Metabolite [necrotic enteritis]{Disorders} is Necrotic enteritis [volatile fatty acids]{Chemicals & Drugs} is Volatile Fatty Acids [challenge]{Procedures} is Challenge [VFAs]{Chemicals & Drugs} is Volatile Fatty Acids [broiler chickens]{Living Beings} is Broiler Chicken [chickens]{Living Beings} is Broiler Chicken [organic acids]{Chemicals & Drugs} is Organic acid [reported]{Procedures} is Reporting [gastrointestinal tract]{Anatomy} is Gastrointestinal Tract [GIT]{Anatomy} is Gastrointestinal Tract [birds]{Living Beings} is Birds [inhibition of the growth]{Physiology} is Inhibition of growth [bacteria]{Living Beings} is BACTERIA [metabolites]{Chemicals & Drugs} is Metabolite [GIT]{Anatomy} is Gastrointestinal Tract [chickens]{Living Beings} is Broiler Chicken [disease conditions]{Disorders} is Disease condition finding [necrotic enteritis]{Disorders} is Necrotic enteritis [NE]{Disorders} is Necrotic enteritis [VFAs]{Chemicals & Drugs} is Volatile Fatty Acids [lactic acid]{Chemicals & Drugs} is Lactic Acid [intestinal]{Anatomy} is Intestinal [NE]{Disorders} is Necrotic enteritis [dietary]{Objects} is Dietary [Eimeria]{Living Beings} is Eimerias [inoculation]{Procedures} is Inoculate [causative agent]{Disorders} is Causative agent [Clostridium perfringens]{Living Beings} is Clostridium perfringens [NetB toxin]{Chemicals & Drugs} is NetB toxin, Clostridium perfringes [experiment]{Procedures} is Animal Experiment [designed]{Procedures} is EXPER DESIGN [arrangement]{Procedures} is Arrangement of care [treatments]{Procedures} is Treatments [Eimeria]{Living Beings} is Eimerias [inoculation]{Procedures} is Inoculate [C. perfringens]{Living Beings} is Clostridium perfringens [challenge]{Procedures} is Challenge [composition]{Physiology} is Composition [VFAs]{Chemicals & Drugs} is Volatile Fatty Acids [lactic acids]{Chemicals & Drugs} is Lactic Acid [NE]{Disorders} is Necrotic enteritis [stress]{Disorders} is State of stress [Eimeria]{Living Beings} is Eimerias [birds]{Living Beings} is Birds [NE]{Disorders} is Necrotic enteritis [Eimeria]{Living Beings} is Eimerias [NE]{Disorders} is Necrotic enteritis [challenge]{Procedures} is Challenge [disease]{Disorders} is Disease [adverse]{Disorders} is Adverse effects [dietary]{Objects} is Dietary [Eimeria]{Living Beings} is Eimerias [infection]{Disorders} is Infections [efforts]{Physiology} is Effort [understand]{Physiology} is Understanding [NE]{Disorders} is Necrotic enteritis [control of the disease]{Procedures} is Infectious disease prevention / control [antibiotics]{Chemicals & Drugs} is Antibiotics
[Ehlers-Danlos syndrome] The [Ehlers-Danlos syndromes] ([EDSs]) were originally [described] by [Ehlers] in [Denmark] and [Danlos] in [Paris] in 1898 and 1908, respectively. They had both published individual [case studies] in which the common factor was [laxity of ligaments] leading to [joint hypermobility] and [hyperextensibility of the skin]. The choice of the [name] of this [eponymous disease] had been made by [Dr Parkes Weber], an eminent [London] [physician] in the 1930s, who had a penchant for [eponymous diseases], having had no less than seven attributed to himself, at least in part. Unfortunately, this was before the age of a [computerised literature] search, and [Parkes Weber] had inadvertently overlooked the very first [description] of [EDS] which had been made by [Tchernabogov], a [Russian] [dermatologist], whose [description] was published in 1891 and remains one of the best [descriptions] of [EDS] in the [literature].	[Ehlers-Danlos syndrome]{Disorders} is Ehlers-danlos syndrome [Ehlers-Danlos syndrome]{Disorders} is Ehlers-danlos syndrome [Ehlers-Danlos syndromes]{Disorders} is Ehlers-danlos syndrome [EDSs]{Disorders} is Ehlers-danlos syndrome [described]{Concepts & Ideas} is DESCR [Ehlers]{Living Beings} is Homo sapiens (organism) [Denmark]{Geographic Areas} is Denmark [Danlos]{Living Beings} is Homo sapiens (organism) [Paris]{Geographic Areas} is Paris, France [case studies]{Concepts & Ideas} is Case Studies [laxity of ligaments]{Disorders} is Laxity of ligaments [joint hypermobility]{Disorders} is Joint Hypermobility [hyperextensibility of the skin]{Disorders} is Hyperextensibility of the skin [name]{Concepts & Ideas} is Names [eponymous disease]{Concepts & Ideas} is Intellectual Product [Dr Parkes Weber]{Living Beings} is Homo sapiens (organism) [London]{Geographic Areas} is London [physician]{Living Beings} is Physician [eponymous diseases]{Concepts & Ideas} is Intellectual Product [computerised literature]{Concepts & Ideas} is Literature [Parkes Weber]{Living Beings} is Homo sapiens (organism) [description]{Concepts & Ideas} is DESCR [EDS]{Disorders} is Ehlers-danlos syndrome [Tchernabogov]{Living Beings} is Homo sapiens (organism) [Russian]{Living Beings} is Russian [dermatologist]{Living Beings} is Dermatologist [description]{Concepts & Ideas} is DESCR [descriptions]{Concepts & Ideas} is DESCR [EDS]{Disorders} is Ehlers-danlos syndrome [literature]{Concepts & Ideas} is Literature
[Assessment] of [laparoscopic stomach preserving surgery] with [sentinel basin dissection] versus standard [gastrectomy] with [lymphadenectomy] in [early gastric cancer] -A [multicenter randomized phase III clinical trial (SENORITA trial) protocol] Along with the marked increase in [early gastric cancer] ([EGC]) in the [Eastern countries], there has been an effort to adopt the [sentinel node] concept in [EGC] to preserve [gastric function] and reduce the occurrence of [postoperative complications]. Based on promising results from a [previous quality control study], this [prospective multicenter randomized controlled phase III clinical trial] aims to elucidate the [oncologic] [safety] of [laparoscopic stomach-preserving surgery] with [sentinel basin dissection] ([SBD]) compared to a standard [laparoscopic] [gastrectomy]. This trial is an investigator-initiated, open-label, [multicenter randomized controlled phase III trial] with a [non-inferiority design]. Patients diagnosed with a [single lesion] of clinical stage T1N0M0 [gastric adenocarcinoma], with a diameter of 3 cm or less are eligible for the present study. A total of 580 patients (290 per group) will be [randomized] to either [laparoscopic stomach-preserving surgery] with [SBD] or [standard surgery]. The primary end-point is 3-year disease-free survival (DFS) and the secondary endpoints include postoperative morbidity and mortality, quality of life, 5-year DFS, and overall survival. [Qualified investigators] who completed the prior quality control study are exclusively allowed to participate in this [phase III clinical trial]. The proposed trial is expected to verify whether [laparoscopic stomach-preserving surgery] with [SBD] achieves similar [oncologic outcomes] and improved quality of life compared to a [standard gastrectomy] in [EGC] patients. This study was registered at the NIH ClinicalTrial.gov database (NCT01804998) on March 4th, 2013.	[Assessment]{Procedures} is Assessment - action [laparoscopic stomach preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach [sentinel basin dissection]{Procedures} is Node Dissection, Lymph [gastrectomy]{Procedures} is Gastrectomy [lymphadenectomy]{Procedures} is Lymphadenectomy [early gastric cancer]{Disorders} is Early Gastric Cancer [multicenter randomized phase III clinical trial (SENORITA trial) protocol]{Procedures} is Phase III Clinical Trial [Assessment]{Procedures} is Assessment - action [laparoscopic stomach preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach [early gastric cancer]{Disorders} is Early Gastric Cancer [EGC]{Disorders} is Early Gastric Cancer [sentinel basin dissection]{Procedures} is Node Dissection, Lymph [Eastern countries]{Geographic Areas} is Area [gastrectomy]{Procedures} is Gastrectomy [lymphadenectomy]{Procedures} is Lymphadenectomy [sentinel node]{Anatomy} is Sentinel Node [early gastric cancer]{Disorders} is Early Gastric Cancer [EGC]{Disorders} is Early Gastric Cancer [multicenter randomized phase III clinical trial (SENORITA trial) protocol]{Procedures} is Phase III Clinical Trial [gastric function]{Physiology} is Gastric function [postoperative complications]{Disorders} is Postoperative Complications [previous quality control study]{Procedures} is Historical Control Study [prospective multicenter randomized controlled phase III clinical trial]{Procedures} is Phase III Clinical Trial [oncologic]{Occupations} is Oncologic (qualifier value) [safety]{Procedures} is SAFETY [laparoscopic stomach-preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach [sentinel basin dissection]{Procedures} is Node Dissection, Lymph [SBD]{Procedures} is Node Dissection, Lymph [laparoscopic]{Concepts & Ideas} is Laparoscopic [gastrectomy]{Procedures} is Gastrectomy [multicenter randomized controlled phase III trial]{Procedures} is Phase III Clinical Trial [non-inferiority design]{Procedures} is EXPER DESIGN [single lesion]{Disorders} is Single lesion [gastric adenocarcinoma]{Disorders} is Gastric adenocarcinoma [randomized]{Disorders} is RANDOMIZED [laparoscopic stomach-preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach [SBD]{Procedures} is Node Dissection, Lymph [standard surgery]{Procedures} is Gastrectomy [Qualified investigators]{Living Beings} is CLIN INVESTIGATORS [phase III clinical trial]{Procedures} is Phase III Clinical Trial [laparoscopic stomach-preserving surgery]{Procedures} is Laparoscopic Procedures on the Stomach [SBD]{Procedures} is Node Dissection, Lymph [oncologic outcomes]{Disorders} is Disease Outcome [standard gastrectomy]{Procedures} is Gastrectomy [EGC]{Disorders} is Early Gastric Cancer
Association of [Metabolites] with [Obesity] and [Type 2 Diabetes] Based on [FTO] Genotype The [single nucleotide polymorphism] [rs9939609 of the gene FTO], which encodes fat mass and [obesity] -associated [protein], is strongly associated with [obesity] and [type 2 diabetes] ([T2D]) in multiple [populations]; however, the underlying mechanism of this association is unclear. The present [study] aimed to investigate [FTO] genotype -dependent [metabolic] changes in [obesity] and [T2D]. To elucidate metabolic dysregulation associated with [disease risk] genotype, [genomic] and [metabolomic datasets] were recruited from 2,577 [participants] of the [Korean Association REsource (KARE) cohort], including 40 homozygous [carriers] of the [FTO] risk [allele (AA)], 570 heterozygous [carriers] (AT), and 1,967 [participants] carrying no risk [allele (TT)]. A total of 134 [serum] [metabolites] were quantified using a targeted [metabolomics] approach. Through comparison of various [statistical methods], seven [metabolites] were identified that are significantly altered in [obesity] and [T2D] based on the [FTO] risk [allele] (adjusted p < 0.05). These identified [metabolites] are relevant to [phosphatidylcholine] metabolic pathway, and previously reported to be [metabolic markers] of [obesity] and [T2D]. In conclusion, using [metabolomics] with the information from [genome-wide association studies] revealed significantly altered [metabolites] depending on the [FTO] genotype in complex disorders. This [study] may contribute to a better understanding of the biological mechanisms linking [obesity] and [T2D].	[Metabolites]{Chemicals & Drugs} is Metabolite [Obesity]{Disorders} is Obesity (disorder) [Type 2 Diabetes]{Disorders} is Type 2 Diabetes [FTO]{Genes & Molecular Sequences} is FTO [single nucleotide polymorphism]{Genes & Molecular Sequences} is Single nucleotide polymorphism [Metabolites]{Chemicals & Drugs} is Metabolite [Obesity]{Disorders} is Obesity (disorder) [rs9939609 of the gene FTO]{Genes & Molecular Sequences} is FTO [Type 2 Diabetes]{Disorders} is Type 2 Diabetes [FTO]{Genes & Molecular Sequences} is FTO [obesity]{Disorders} is Obesity (disorder) [protein]{Chemicals & Drugs} is Protein [obesity]{Disorders} is Obesity (disorder) [type 2 diabetes]{Disorders} is Type 2 Diabetes [T2D]{Disorders} is Type 2 Diabetes [populations]{Living Beings} is Population [study]{Procedures} is Study [FTO]{Genes & Molecular Sequences} is FTO [metabolic]{Physiology} is Metabolic process [obesity]{Disorders} is Obesity (disorder) [T2D]{Disorders} is Type 2 Diabetes [disease risk]{Physiology} is Disease Susceptibility (Disease/Finding) [genomic]{Concepts & Ideas} is Data Set [metabolomic datasets]{Concepts & Ideas} is Data Set [participants]{Living Beings} is Participant [Korean Association REsource (KARE) cohort]{Living Beings} is Cohort [carriers]{Disorders} is GENET CARRIERS [FTO]{Genes & Molecular Sequences} is FTO [allele (AA)]{Genes & Molecular Sequences} is Allele [carriers]{Disorders} is GENET CARRIERS [participants]{Living Beings} is Participant [allele (TT)]{Genes & Molecular Sequences} is Allele [serum]{Anatomy} is Serum [metabolites]{Chemicals & Drugs} is Metabolite [metabolomics]{Occupations} is Metabolomics [statistical methods]{Procedures} is Statistical Method [metabolites]{Chemicals & Drugs} is Metabolite [obesity]{Disorders} is Obesity (disorder) [T2D]{Disorders} is Type 2 Diabetes [FTO]{Genes & Molecular Sequences} is FTO [allele]{Genes & Molecular Sequences} is Allele [metabolites]{Chemicals & Drugs} is Metabolite [phosphatidylcholine]{Chemicals & Drugs} is Phosphatidylcholine [metabolic markers]{Chemicals & Drugs} is Metabolic Marker [obesity]{Disorders} is Obesity (disorder) [T2D]{Disorders} is Type 2 Diabetes [metabolomics]{Occupations} is Metabolomics [genome-wide association studies]{Procedures} is Genome-Wide Association Studies [metabolites]{Chemicals & Drugs} is Metabolite [FTO]{Genes & Molecular Sequences} is FTO [study]{Procedures} is Study [obesity]{Disorders} is Obesity (disorder) [T2D]{Disorders} is Type 2 Diabetes
[Anthology] of Venezuelan [psychiatry] Reception of [Psychiatry] in [Venezuela] since the 19th Century to the late 20th Century merits a historical approach. The following work proposes to [research] some of the very origins of Venezuelan [psychiatry] and its possible influence on contemporary [mental health practice]. Through documental research, the early works of [local authors] from the 19th Century through 20th Century finals: [Carlos Arvelo], [Lisandro Alvarado], [Francisco Herrera Luque], [Jose Luis Vethencourt] and [Jose Solanes], are subjected to study. This journey illustrates a descriptive panoramic view which allows to better comprenhend the current state of our [psychiatry]. In a brief introduction the most important events are described, since the arrival of [Pinel's] ideas, followed by the early research paperworks published and the beginnings of the academic teachings of this specialty in [Venezuela] and displaying the main contemporary research groups [thorough the country].	[Anthology]{Concepts & Ideas} is Collections (publication) [psychiatry]{Occupations} is Psychiatry [Anthology]{Concepts & Ideas} is Collections (publication) [Psychiatry]{Occupations} is Psychiatry [psychiatry]{Occupations} is Psychiatry [Venezuela]{Geographic Areas} is Venezuela [research]{Procedures} is Research [psychiatry]{Occupations} is Psychiatry [mental health practice]{Procedures} is Health Care [local authors]{Living Beings} is Authors [Carlos Arvelo]{Living Beings} is Homo sapiens (organism) [Lisandro Alvarado]{Living Beings} is Homo sapiens (organism) [Francisco Herrera Luque]{Living Beings} is Homo sapiens (organism) [Jose Luis Vethencourt]{Living Beings} is Homo sapiens (organism) [Jose Solanes]{Living Beings} is Homo sapiens (organism) [psychiatry]{Occupations} is Psychiatry [Pinel's]{Living Beings} is Homo sapiens (organism) [Venezuela]{Geographic Areas} is Venezuela [thorough the country]{Geographic Areas} is Venezuela
How variation [between] [individuals] affects [species] coexistence Although the effects of variation [between] [individuals] within [species] are traditionally ignored in [studies] of [species] coexistence, the magnitude of intraspecific variation in nature is forcing [ecologists] to reconsider. Compelling intuitive arguments suggest that [individual] variation may provide a previously unrecognised [route] to diversity maintenance by blurring [species] - level competitive differences or substituting for [species] - level niche differences. These arguments, which are [motivating] a large [body] of empirical work, have rarely been evaluated with quantitative theory. Here we incorporate intraspecific variation into a common [model] of competition and identify three pathways by which this variation affects coexistence: (1) changes in competitive [dynamics] because of nonlinear averaging, (2) changes in [species] ' mean interaction strengths because of variation in underlying traits (also via nonlinear averaging) and (3) effects on stochastic demography. As a consequence of the first two mechanisms, we [find] that intraspecific variation in competitive ability increases the dominance of superior [competitors], and intraspecific niche variation reduces [species] - level niche differentiation, both of which make coexistence more difficult. In addition, [individual] variation can exacerbate the effects of demographic stochasticity, and this further destabilises coexistence. Our work provides a [theoretical foundation] for emerging empirical [interests] in the effects of intraspecific variation on [species] diversity.	[between]{Concepts & Ideas} is Between [individuals]{Living Beings} is Individual (person) [species]{Concepts & Ideas} is Species [between]{Concepts & Ideas} is Between [individuals]{Living Beings} is Individual (person) [between]{Concepts & Ideas} is Between [species]{Concepts & Ideas} is Species [individuals]{Living Beings} is Individual (person) [species]{Concepts & Ideas} is Species [studies]{Procedures} is Study [species]{Concepts & Ideas} is Species [ecologists]{Living Beings} is Ecologist [individual]{Living Beings} is Individual (person) [route]{Concepts & Ideas} is Route [species]{Concepts & Ideas} is Species [species]{Concepts & Ideas} is Species [motivating]{Physiology} is Motivation finding [body]{Concepts & Ideas} is Structural [model]{Concepts & Ideas} is Model [dynamics]{Concepts & Ideas} is Nonlinear Dynamics [species]{Concepts & Ideas} is Species [find]{Disorders} is Finding (finding) [competitors]{Living Beings} is Group (social concept) [species]{Concepts & Ideas} is Species [individual]{Living Beings} is Individual (person) [theoretical foundation]{Procedures} is Theoretical Study [interests]{Physiology} is Interest [species]{Concepts & Ideas} is Species
[Intracellular Metabolism] of α,β-Unsaturated Carbonyl Compounds, [Acrolein], [Crotonaldehyde] and [Methyl Vinyl Ketone], Active Toxicants in [Cigarette Smoke]: Participation of [Glutathione] [Conjugation] Ability and [Aldehyde-Ketone Sensitive Reductase Activity] The major toxicants in [cigarette smoke], [α,β-unsaturated aldehydes], such as [acrolein] ([ACR]) and [crotonaldehyde] ([CA]), and [α,β-unsaturated ketone], [methyl vinyl ketone] ([MVK]), are known to form Michael-type adducts with [glutathione] ([GSH]) and consequently cause [intracellular] [GSH] depletion, which is involved in [cigarette smoke] - induced [cytotoxicity]. We have previously clarified that exposure to [cigarette smoke extract] ([CSE]) of a [mouse] [melanoma cell] [culture medium] causes rapid reduction of [intracellular] [GSH] levels, and that the [GSH] - [MVK] adduct can be [detected] by [LC/MS analysis] while the [GSH] - [CA] adduct is hardly [detected]. In the present [study], to clarify why the [GSH] - [CA] adduct is difficult to [detect] in the [cell] [medium], we conducted detailed investigation of the [structures] of the reaction products of [ACR], [CA], [MVK] and [CSE] in the [GSH] solution or the [cell] [culture medium]. The [mass spectra] indicated that in the presence of the [cells], the [GSH] - [CA] and [GSH] - [ACR] adducts were almost not [detected] while their [corresponding alcohols] were [detected]. On the other hand, both the [GSH] - [MVK] adducts and their reduced products were [detected]. In the absence of the [cells], the reaction of [GSH] with all α,β-unsaturated carbonyls produced only their corresponding adducts. These results show that the [GSH] adducts of [α,β-unsaturated aldehydes], [CA] and [ACR], are quickly reduced by certain [intracellular] [carbonyl reductase(s)] and excreted from the [cells], unlike the [GSH] adduct of [α,β-unsaturated ketone], [MVK]. Such a difference in reactivity to the [carbonyl reductase] might be related to differences in the [cytotoxicity] of [α,β-unsaturated aldehydes] and [ketones].	[Intracellular Metabolism]{Physiology} is Cellular metabolism [Acrolein]{Chemicals & Drugs} is Acrolein [Crotonaldehyde]{Chemicals & Drugs} is Crotonaldehyde [Methyl Vinyl Ketone]{Chemicals & Drugs} is Methyl vinyl ketone [Cigarette Smoke]{Chemicals & Drugs} is Cigarette smoke [Glutathione]{Chemicals & Drugs} is Glutathione [Conjugation]{Physiology} is Molecular function [Aldehyde-Ketone Sensitive Reductase Activity]{Physiology} is Aldehyde reductase 1 [Intracellular Metabolism]{Physiology} is Cellular metabolism [cigarette smoke]{Chemicals & Drugs} is Cigarette smoke [α,β-unsaturated aldehydes]{Chemicals & Drugs} is Aldehydes [Acrolein]{Chemicals & Drugs} is Acrolein [Crotonaldehyde]{Chemicals & Drugs} is Crotonaldehyde [acrolein]{Chemicals & Drugs} is Acrolein [ACR]{Chemicals & Drugs} is Acrolein [Methyl Vinyl Ketone]{Chemicals & Drugs} is Methyl vinyl ketone [crotonaldehyde]{Chemicals & Drugs} is Crotonaldehyde [CA]{Chemicals & Drugs} is Crotonaldehyde [α,β-unsaturated ketone]{Chemicals & Drugs} is Ketone [Cigarette Smoke]{Chemicals & Drugs} is Cigarette smoke [methyl vinyl ketone]{Chemicals & Drugs} is Methyl vinyl ketone [MVK]{Chemicals & Drugs} is Methyl vinyl ketone [Glutathione]{Chemicals & Drugs} is Glutathione [Conjugation]{Physiology} is Molecular function [Aldehyde-Ketone Sensitive Reductase Activity]{Physiology} is Aldehyde reductase 1 [glutathione]{Chemicals & Drugs} is Glutathione [GSH]{Chemicals & Drugs} is Glutathione [intracellular]{Concepts & Ideas} is Intracellular [GSH]{Chemicals & Drugs} is Glutathione [cigarette smoke]{Chemicals & Drugs} is Cigarette smoke [cytotoxicity]{Disorders} is Cytotoxicity [cigarette smoke extract]{Chemicals & Drugs} is Cigarette smoke [CSE]{Chemicals & Drugs} is Cigarette smoke [mouse]{Living Beings} is Laboratory Mouse [melanoma cell]{Anatomy} is Melanoma Cell [culture medium]{Chemicals & Drugs} is Culture medium [intracellular]{Concepts & Ideas} is Intracellular [GSH]{Chemicals & Drugs} is Glutathione [GSH]{Chemicals & Drugs} is Glutathione [MVK]{Chemicals & Drugs} is Methyl vinyl ketone [detected]{Disorders} is Detected [LC/MS analysis]{Procedures} is LC/MS [GSH]{Chemicals & Drugs} is Glutathione [CA]{Chemicals & Drugs} is Crotonaldehyde [detected]{Disorders} is Detected [study]{Procedures} is Study [GSH]{Chemicals & Drugs} is Glutathione [CA]{Chemicals & Drugs} is Crotonaldehyde [detect]{Disorders} is Detected [cell]{Anatomy} is Melanoma Cell [medium]{Chemicals & Drugs} is Culture medium [structures]{Concepts & Ideas} is 3D Molecular Structures [ACR]{Chemicals & Drugs} is Acrolein [CA]{Chemicals & Drugs} is Crotonaldehyde [MVK]{Chemicals & Drugs} is Methyl vinyl ketone [CSE]{Chemicals & Drugs} is Cigarette smoke [GSH]{Chemicals & Drugs} is Glutathione [cell]{Anatomy} is Melanoma Cell [culture medium]{Chemicals & Drugs} is Culture medium [mass spectra]{Procedures} is Mass Spectrum [cells]{Anatomy} is Melanoma Cell [GSH]{Chemicals & Drugs} is Glutathione [CA]{Chemicals & Drugs} is Crotonaldehyde [GSH]{Chemicals & Drugs} is Glutathione [ACR]{Chemicals & Drugs} is Acrolein [detected]{Disorders} is Detected [corresponding alcohols]{Chemicals & Drugs} is Alcohols [detected]{Disorders} is Detected [GSH]{Chemicals & Drugs} is Glutathione [MVK]{Chemicals & Drugs} is Methyl vinyl ketone [detected]{Disorders} is Detected [cells]{Anatomy} is Melanoma Cell [GSH]{Chemicals & Drugs} is Glutathione [GSH]{Chemicals & Drugs} is Glutathione [α,β-unsaturated aldehydes]{Chemicals & Drugs} is Aldehydes [CA]{Chemicals & Drugs} is Crotonaldehyde [ACR]{Chemicals & Drugs} is Acrolein [intracellular]{Concepts & Ideas} is Intracellular [carbonyl reductase(s)]{Chemicals & Drugs} is Carbonyl reductase (NADPH) [cells]{Anatomy} is Melanoma Cell [GSH]{Chemicals & Drugs} is Glutathione [α,β-unsaturated ketone]{Chemicals & Drugs} is Ketone [MVK]{Chemicals & Drugs} is Methyl vinyl ketone [carbonyl reductase]{Physiology} is Aldehyde reductase 1 [cytotoxicity]{Disorders} is Cytotoxicity [α,β-unsaturated aldehydes]{Chemicals & Drugs} is Aldehydes [ketones]{Chemicals & Drugs} is Ketone
[Strategies] for [Assaying] [Lysosomal Membrane] [Permeabilization] [Late endosomal] [organelles] have an acidic pH and contain [hydrolytic enzymes] to degrade cargo delivered either from the [extracellular] [environment] by [endocytosis] or from within the [cell] itself by [autophagy]. In the event of [lysosomal membrane] [permeabilization] ([LMP]), the contents of [late endosomes] and [lysosomes] can be released into the [cytosol] and then initiate [apoptosis]. Compounds that can trigger [LMP] are therefore candidates for the induction of [apoptosis], in particular in [anticancer therapy]. Alternatively, [drug-delivery systems], such as nanoparticles, can have side effects that can include [LMP], which has [toxic consequences] for the [cells]. To determine when, to what extent, and with what consequences [LMP] occurs is therefore of paramount importance for the [evaluation] of new potentially [LMP] - inducing compounds. In this introduction, we provide an overview of some [basic assays] for assessing [LMP], such as staining with [lysosomotropic dyes] and measurement of [cysteine] [cathepsin] [activity], and discuss additional [strategies] for the [detection] of the release of endogenous [lysosomal] molecules or preloaded exogenous [tracers] into the [cytosol].	[Strategies]{Procedures} is Intervention Strategies [Assaying]{Procedures} is Assay technique [Lysosomal Membrane]{Anatomy} is Lysosomal membrane [Permeabilization]{Physiology} is Cell Function [Strategies]{Procedures} is Intervention Strategies [Late endosomal]{Anatomy} is Late Endosome [Assaying]{Procedures} is Assay technique [organelles]{Anatomy} is Organelles [Lysosomal Membrane]{Anatomy} is Lysosomal membrane [Permeabilization]{Physiology} is Cell Function [hydrolytic enzymes]{Chemicals & Drugs} is Hydrolase [extracellular]{Anatomy} is Extracellular [environment]{Concepts & Ideas} is Environment [endocytosis]{Physiology} is Endocytosis [cell]{Anatomy} is Cell Type [autophagy]{Physiology} is Autophagy [lysosomal membrane]{Anatomy} is Lysosomal membrane [permeabilization]{Physiology} is Cell Function [LMP]{Physiology} is Cell Function [late endosomes]{Anatomy} is Late Endosome [lysosomes]{Anatomy} is Lysosomes [cytosol]{Anatomy} is Cytosols [apoptosis]{Physiology} is Apoptosis [LMP]{Physiology} is Cell Function [apoptosis]{Physiology} is Apoptosis [anticancer therapy]{Procedures} is Anticancer therapy [drug-delivery systems]{Devices} is Drug Delivery Systems [LMP]{Physiology} is Cell Function [toxic consequences]{Disorders} is Toxic effect [cells]{Anatomy} is Cell Type [LMP]{Physiology} is Cell Function [evaluation]{Procedures} is Evaluations [LMP]{Physiology} is Cell Function [basic assays]{Procedures} is Assay technique [LMP]{Physiology} is Cell Function [lysosomotropic dyes]{Chemicals & Drugs} is Dyes [cysteine]{Chemicals & Drugs} is Cysteine [cathepsin]{Chemicals & Drugs} is Cathepsin [activity]{Physiology} is Enzyme activity [strategies]{Procedures} is Intervention Strategies [detection]{Procedures} is Detection [lysosomal]{Anatomy} is Lysosomes [tracers]{Chemicals & Drugs} is Tracer [cytosol]{Anatomy} is Cytosols
Stimulation of [cell proliferation] by [glutathione monoethyl ester] in [aged bone marrow stromal cells] is associated with the assistance of [TERT] [gene expression] and [telomerase activity] The [proliferation] and [differentiation] potential of [aged bone marrow stromal cells] ([BMSCs]) are significantly reduced. In order to [improve] the performance of the aged [BMSCs], these [cells] were treated with 2 mM [glutathione monoethyl ester] ([GSH-MEE]) for 24 h. [Proliferation] rate, [telomerase activity], [telomere] length, and [differentiation] to [cholinergic neuron-like cells] ([CNLCs]) were observed to increase. Though, the expression level of [telomerase reverse transcriptase gene] increased, but [CTC1] and [TEN1 genes] from [Ctc1-Stn1-Ten1 complex] encoding [proteins] with [regulatory function] significantly decreased. [Trypan blue exclusion assay] was used to analyze the [proliferation] and, while [telomere] length, its several related [gene expressions], and [telomerase activity] were measured using the [real time reverse transcription-polymerase chain reaction] and [polymerase chain reaction] [enzyme-linked immunosorbent assay techniques], respectively. [CNLCs] [differentiation] potential was evaluated by estimating the percentage of [choline acetyltransferase] [immunereactive cells] .The results suggested that [GSH-MEE] could [improve] aged [rat] [BMSC] properties and would be of potential benefit for enhancing the performance of [aged people's] [BMSCs].	[cell proliferation]{Physiology} is Cell proliferation [glutathione monoethyl ester]{Chemicals & Drugs} is Glutathione monoethyl ester [aged bone marrow stromal cells]{Anatomy} is Bone Marrow Stromal Cells [TERT]{Genes & Molecular Sequences} is TERT Gene [gene expression]{Physiology} is Gene Expression [telomerase activity]{Physiology} is Telomerase activity [proliferation]{Physiology} is Cell proliferation [cell proliferation]{Physiology} is Cell proliferation [differentiation]{Physiology} is Cell Differentiation [glutathione monoethyl ester]{Chemicals & Drugs} is Glutathione monoethyl ester [aged bone marrow stromal cells]{Anatomy} is Bone Marrow Stromal Cells [aged bone marrow stromal cells]{Anatomy} is Bone Marrow Stromal Cells [BMSCs]{Anatomy} is Bone Marrow Stromal Cells [improve]{Disorders} is Improved [TERT]{Genes & Molecular Sequences} is TERT Gene [gene expression]{Physiology} is Gene Expression [telomerase activity]{Physiology} is Telomerase activity [BMSCs]{Anatomy} is Bone Marrow Stromal Cells [cells]{Anatomy} is Cells set [glutathione monoethyl ester]{Chemicals & Drugs} is Glutathione monoethyl ester [GSH-MEE]{Chemicals & Drugs} is Glutathione monoethyl ester [Proliferation]{Physiology} is Cell proliferation [telomerase activity]{Physiology} is Telomerase activity [telomere]{Anatomy} is Telomere [differentiation]{Physiology} is Cell Differentiation [cholinergic neuron-like cells]{Anatomy} is Cholinergic Neuron [CNLCs]{Anatomy} is Cholinergic Neuron [telomerase reverse transcriptase gene]{Genes & Molecular Sequences} is TERT Gene [CTC1]{Genes & Molecular Sequences} is CTC1 [TEN1 genes]{Genes & Molecular Sequences} is TEN1 gene [Ctc1-Stn1-Ten1 complex]{Anatomy} is Cell component [proteins]{Chemicals & Drugs} is Proteins [regulatory function]{Physiology} is Gene Action Regulation [Trypan blue exclusion assay]{Procedures} is BIOL ASSAY [proliferation]{Physiology} is Cell proliferation [telomere]{Anatomy} is Telomere [gene expressions]{Physiology} is Gene Expression [telomerase activity]{Physiology} is Telomerase activity [real time reverse transcription-polymerase chain reaction]{Procedures} is Reverse Transcription Polymerase Chain Reaction [polymerase chain reaction]{Procedures} is Polymerase Chain Reaction [enzyme-linked immunosorbent assay techniques]{Procedures} is Enzyme-linked immunosorbent assay [CNLCs]{Anatomy} is Cholinergic Neuron [differentiation]{Physiology} is Cell Differentiation [choline acetyltransferase]{Genes & Molecular Sequences} is CHOLINE ACETYLTRANSFERASE [immunereactive cells]{Anatomy} is Cells set [GSH-MEE]{Chemicals & Drugs} is Glutathione monoethyl ester [improve]{Disorders} is Improved [rat]{Living Beings} is Rat (organism) [BMSC]{Anatomy} is Bone Marrow Stromal Cells [aged people's]{Living Beings} is People [BMSCs]{Anatomy} is Bone Marrow Stromal Cells
[Wild food plants] and [fungi] used in the [mycophilous] [Tibetan] community of [Zhagana] ([Tewo County], [Gansu], [China]) The aim of the [study] was to investigate [knowledge] and use of [wild food plants] and [fungi] in a highland [valley] in the [Gannan Tibetan Autonomous Region] on the north-eastern edges of the [Tibetan Plateau]. Field research was carried out in four neighbouring [villages] in a [mountain] [valley] of the [Diebu (Tewo) county], surrounded by spruce forests. The [study] consisted of 30 interviews with single informants, or [group interviews] (altogether 63 informants). Apart from collecting voucher specimens, we also identified [fungi] using [DNA barcoding]. We recorded the use of 54 [species] of [vascular plants]. We also recorded the use of 22 [mushroom taxa], which made up the largest category of [wild foods]. [Fruits] formed the largest category of [food plants], with 21 [species], larger than the [wild greens] category, which consisted of 20 [species] [eaten] after boiling or frying and 7 as raw [snacks]. We also recorded the alimentary use of 10 [species] of [edible flowers] and 3 [species] with underground [edible organs]. On average, 20.8 [edible taxa] were listed per interview (median - 21). The most listed category of [wild foods] was [green vegetables] (mean - 7.5 [species], median - 8 [species]), but [fruits] and [mushrooms] were listed nearly as frequently (mean - 6.3, median - 6 and mean - 5.8, - median 6 respectively). Other category lists were very short, e.g., [flowers] (mean - 1.3, median - 1) and underground [edible parts] (mean - 0.7, median - 1). [Wild vegetables] are usually boiled and/or fried and served as side-dishes, or their [green parts] are [eaten] as [snacks] during [mountain] treks (e.g., [peeled rhubarb shoots]). [Wild fruits] are mainly collected by children and [eaten] raw, they are not stored for further use. The most widely used [wild staple foods] are [Potetilla anserina] [roots], an important [ceremonial food] served on such occasions as New Year or at funerals. They are boiled and served with [sugar] and [butter]. The most important famine [plants] remembered by [people] are the [aerial bulbils] of [Persicaria vivipara]. [Flowers] are used as children's [snacks] - their [nectar] is sucked. The number of [wild taxa] [eaten] in the studied [valley] is similar to that of other [Tibetan areas]. The structure of [wild food plant] taxa is also very typical for Tibetan speaking [areas] (e.g., the use of [rhubarb shoots], [Potentilla anserina], [Persicaria vivipara]). The studied community show a high level of [mycophilia].	[Wild food plants]{Objects} is Food Plants [fungi]{Living Beings} is Fungi [mycophilous]{Objects} is Mushroom - dietary [Tibetan]{Geographic Areas} is Tibet [Zhagana]{Geographic Areas} is Area [Tewo County]{Geographic Areas} is Area [Gansu]{Geographic Areas} is Area [China]{Geographic Areas} is China [Wild food plants]{Objects} is Food Plants [study]{Procedures} is Study [fungi]{Living Beings} is Fungi [mycophilous]{Objects} is Mushroom - dietary [knowledge]{Concepts & Ideas} is Knowledge [Tibetan]{Geographic Areas} is Tibet [wild food plants]{Objects} is Food Plants [Zhagana]{Geographic Areas} is Area [Tewo County]{Geographic Areas} is Area [fungi]{Living Beings} is Fungi [Gansu]{Geographic Areas} is Area [China]{Geographic Areas} is China [valley]{Concepts & Ideas} is Valley [Gannan Tibetan Autonomous Region]{Geographic Areas} is Area [Tibetan Plateau]{Geographic Areas} is Tibet [villages]{Geographic Areas} is Village [mountain]{Geographic Areas} is Mountain [valley]{Concepts & Ideas} is Valley [Diebu (Tewo) county]{Geographic Areas} is Area [study]{Procedures} is Study [group interviews]{Procedures} is Group Interviews [fungi]{Living Beings} is Fungi [DNA barcoding]{Procedures} is Taxonomic DNA Barcoding [species]{Concepts & Ideas} is Species [vascular plants]{Living Beings} is Vascular plants [mushroom taxa]{Objects} is Mushroom - dietary [wild foods]{Objects} is Foods [Fruits]{Objects} is Fruits [food plants]{Objects} is Food Plants [species]{Concepts & Ideas} is Species [wild greens]{Living Beings} is Wild plant [species]{Concepts & Ideas} is Species [eaten]{Physiology} is Eat [snacks]{Objects} is Snacks [species]{Concepts & Ideas} is Species [edible flowers]{Living Beings} is Flowers [species]{Concepts & Ideas} is Species [edible organs]{Objects} is Food Plants [edible taxa]{Objects} is Food Plants [wild foods]{Objects} is Foods [green vegetables]{Objects} is Green Vegetable [species]{Concepts & Ideas} is Species [species]{Concepts & Ideas} is Species [fruits]{Objects} is Fruits [mushrooms]{Objects} is Mushroom - dietary [flowers]{Living Beings} is Flowers [edible parts]{Objects} is Food Plants [Wild vegetables]{Objects} is Vegetables [green parts]{Living Beings} is Green plants [eaten]{Physiology} is Eat [snacks]{Objects} is Snacks [mountain]{Geographic Areas} is Mountain [peeled rhubarb shoots]{Living Beings} is Shoot [Wild fruits]{Objects} is Fruits [eaten]{Physiology} is Eat [wild staple foods]{Objects} is Foods [Potetilla anserina]{Living Beings} is Potentilla anserina [roots]{Living Beings} is Plant Roots [ceremonial food]{Objects} is Foods [sugar]{Chemicals & Drugs} is SUGAR [butter]{Objects} is Butter [plants]{Living Beings} is Green plants [people]{Living Beings} is People [aerial bulbils]{Living Beings} is Green plants [Persicaria vivipara]{Living Beings} is Persicaria vivipara [Flowers]{Living Beings} is Flowers [snacks]{Objects} is Snacks [nectar]{Chemicals & Drugs} is Nectars [wild taxa]{Living Beings} is Wild plant [eaten]{Physiology} is Eat [valley]{Concepts & Ideas} is Valley [Tibetan areas]{Geographic Areas} is Tibet [wild food plant]{Objects} is Food Plants [areas]{Geographic Areas} is Area [rhubarb shoots]{Living Beings} is Shoot [Potentilla anserina]{Living Beings} is Potentilla anserina [Persicaria vivipara]{Living Beings} is Persicaria vivipara [mycophilia]{Objects} is Mushroom - dietary
Comparison of [Head] [Elevation Protocols] Following [Femoral Artery Sheath] [Removal] After [Coronary Angiography] To compare 2 standard [protocols] for [head] [elevation] following removal of a [femoral artery sheath] after [coronary angiography] and their effects on [bleeding] [complications] and reported levels of [back pain]. One [protocol] involved flat [supine] [bed rest]; the other allowed progressive [head] [elevation]. A prospective [comparative study] of 80 adult patients undergoing [coronary angiography] via the [femoral] [approach]. The [Numeric Rating Scale] was used as the measure of reported [pain]. No [bleeding] [complications] occurred in either group. Both groups had very low mean [pain scores]. Repeated- measures [analysis] demonstrated that the experience of [pain] differed significantly over time by [location] (F5,70 = 3.864, P = .004), with a notable decrease in [pain scores] more than 1 hour after [sheath] [removal] at the [location] that used the progressive [head] [elevation protocol]. Patients ' satisfaction scores after discharge did not differ significantly between the 2 groups. Patients with a [history] of chronic [back pain] had consistently higher [pain scores], but those [pain scores] did not differ significantly by [location] (or [protocol]). It appears that using a progressive [head] - [elevation protocol] within the first 3 hours after diagnostic [angiography] is not associated with an increased risk of [bleeding] [complications] at the [access site] and warrants further exploration in the mitigation of [back pain] associated with prolonged [supine] [bed rest].	[Head]{Anatomy} is Heads [Elevation Protocols]{Procedures} is Elevation [Femoral Artery Sheath]{Anatomy} is Femoral Artery [Removal]{Procedures} is Removal - action [Coronary Angiography]{Procedures} is Coronary angiography [Head]{Anatomy} is Heads [Elevation Protocols]{Procedures} is Elevation [protocols]{Procedures} is CLIN PROTOCOLS [head]{Anatomy} is Heads [elevation]{Procedures} is Elevation [Femoral Artery Sheath]{Anatomy} is Femoral Artery [Removal]{Procedures} is Removal - action [femoral artery sheath]{Anatomy} is Femoral Artery [Coronary Angiography]{Procedures} is Coronary angiography [coronary angiography]{Procedures} is Coronary angiography [bleeding]{Disorders} is Bleeding [complications]{Disorders} is Complication [back pain]{Disorders} is Pain back [protocol]{Procedures} is CLIN PROTOCOLS [supine]{Concepts & Ideas} is Supine [bed rest]{Procedures} is Bed rest [head]{Anatomy} is Heads [elevation]{Procedures} is Elevation [comparative study]{Procedures} is Comparative study research [coronary angiography]{Procedures} is Coronary angiography [femoral]{Anatomy} is Femoral [approach]{Concepts & Ideas} is Approach [Numeric Rating Scale]{Concepts & Ideas} is Numeric Rating Scale [pain]{Disorders} is Pain finding [bleeding]{Disorders} is Bleeding [complications]{Disorders} is Complication [pain scores]{Disorders} is Pain score [analysis]{Procedures} is Analyzed [pain]{Disorders} is Pain finding [location]{Anatomy} is Location [pain scores]{Disorders} is Pain score [sheath]{Anatomy} is Femoral Artery [removal]{Procedures} is Removal - action [location]{Anatomy} is Location [head]{Anatomy} is Heads [elevation protocol]{Procedures} is Elevation [history]{Disorders} is Medical History [back pain]{Disorders} is Pain back [pain scores]{Disorders} is Pain score [pain scores]{Disorders} is Pain score [location]{Anatomy} is Location [protocol]{Procedures} is CLIN PROTOCOLS [head]{Anatomy} is Heads [elevation protocol]{Procedures} is Elevation [angiography]{Procedures} is Angiography [bleeding]{Disorders} is Bleeding [complications]{Disorders} is Complication [access site]{Concepts & Ideas} is Site of access [back pain]{Disorders} is Pain back [supine]{Concepts & Ideas} is Supine [bed rest]{Procedures} is Bed rest

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Dataset Card for MedMentions

MedMentions is a new manually annotated resource for the recognition of biomedical concepts. What distinguishes MedMentions from other annotated biomedical corpora is its size (over 4,000 abstracts and over 350,000 linked mentions), as well as the size of the concept ontology (over 3 million concepts from UMLS 2017) and its broad coverage of biomedical disciplines.

Corpus: The MedMentions corpus consists of 4,392 papers (Titles and Abstracts) randomly selected from among papers released on PubMed in 2016, that were in the biomedical field, published in the English language, and had both a Title and an Abstract.

Annotators: We recruited a team of professional annotators with rich experience in biomedical content curation to exhaustively annotate all UMLS® (2017AA full version) entity mentions in these papers.

Annotation quality: We did not collect stringent IAA (Inter-annotator agreement) data. To gain insight on the annotation quality of MedMentions, we randomly selected eight papers from the annotated corpus, containing a total of 469 concepts. Two biologists ('Reviewer') who did not participate in the annotation task then each reviewed four papers. The agreement between Reviewers and Annotators, an estimate of the Precision of the annotations, was 97.3%.

Citation Information

@misc{mohan2019medmentions,
      title={MedMentions: A Large Biomedical Corpus Annotated with UMLS Concepts},
      author={Sunil Mohan and Donghui Li},
      year={2019},
      eprint={1902.09476},
      archivePrefix={arXiv},
      primaryClass={cs.CL}
}