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排序方式: 共有3466条查询结果,搜索用时 62 毫秒
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Araujo VP Aguiar-Oliveira MH Oliveira JL Rocha HM Oliveira CR Rodrigues TM Nunes MA Britto IM Ximenes R Barreto-Filho JA Meneguz-Moreno RA Pereira RM Valença EH Oliveira-Neto LA Vicente TA Blackford A Salvatori R 《European journal of endocrinology / European Federation of Endocrine Societies》2012,166(6):977-982
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Adolfo Pisanu Isabella Reccia Giulia Porceddu Alessandro Uccheddu 《Journal of gastrointestinal surgery》2013,17(11):2029-2030
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Friedrich M. Wurst Hans-Jürgen Rumpf Gregory E. Skipper John P. Allen Isabella Kunz Petra Beschoner Natasha Thon 《General hospital psychiatry》2013
Objective
Surveys assessing alcohol use among physicians have most commonly employed the Alcohol Use Disorders Identification Test (AUDIT) or the AUDIT-C, the most common short version of the AUDIT. As with other screeners, prevalence estimation is dependent on the accuracy of the test as well as choice of the cutoff value. The aim of the current study is to derive more precise prevalence estimates of alcohol problems in physicians by correcting for false-positive and false-negative results.Method
In the context of a survey, the AUDIT was sent out via email or standard postal service to all 2484 physicians in Salzburg, Austria. A total of 456 physicians participated. A published correction formula was used to estimate the real prevalence of alcohol use problems.Results
Applying a cutoff of 5 points for the AUDIT-C, 15.7% of female and 37.7% of male physicians screened positive. Use of a correction based on general population data and the sensitivity and specificity of the AUDIT-C resulted in much lower prevalence rates: 4.0% for female and 9.5% for male physicians. Using the full AUDIT, 19.6% of the female physicians and 48% of the male physicians were screened positive. Using the correction, the estimated prevalence rates for females and males were 6.3% and 15.5%, respectively.Conclusions
Our findings demonstrate that uncorrected screening results may markedly overestimate the prevalence of physicians drinking problems. 相似文献58.
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Miryam Carecchio MD Monia Magliozzi BSc Massimiliano Copetti PhD Alessandro Ferraris MD PhD Laura Bernardini PhD Monica Bonetti BSc Giovanni Defazio MD Mark J. Edwards PhD Isabella Torrente BSc Fabio Pellegrini MSc Cristoforo Comi MD PhD Kailash P. Bhatia MD FRCP Enza Maria Valente MD PhD 《Movement disorders》2013,28(6):787-794
Mutations or exon deletions of the epsilon‐sarcoglycan (SGCE) gene cause myoclonus‐dystonia (M‐D), but a subset of M‐D patients are mutation‐negative and the sensitivity and specificity of current genetic testing criteria are unknown. We screened 46 newly enrolled M‐D patients for SGCE mutations and deletions; moreover, 24 subjects previously testing negative for SGCE mutations underwent gene dosage analysis. In our combined cohorts, we calculated sensitivity, specificity, positive and negative predictive values, and area under the curve of 2 published sets of M‐D diagnostic criteria. A stepwise logistic regression was used to assess which patients' characteristics best discriminated mutation carriers and to calculate a new mutation predictive score (“new score”), which we validated in previously published cohorts. Nine of 46 (19.5%) patients of the new cohort carried SCGE mutations, including 5 novel point mutations and 1 whole‐gene deletion; in the old cohort, 1 patient with a complex phenotype carried a 5.9‐Mb deletion encompassing SGCE. Current diagnostic criteria had a poor ability to discriminate SGCE‐positive from SGCE‐negative patients in our cohort; conversely, age of onset, especially if associated with psychiatric features (as included in the new score), showed the best discriminatory power to individuate SGCE mutation carriers, both in our cohort and in the validation cohort. Our results suggest that young age at onset of motor symptoms, especially in association with psychiatric disturbance, are strongly predictive for SGCE positivity. We suggest performing gene dosage analysis by multiple ligation‐dependent probe amplification (MLPA) to individuate large SGCE deletions that can be responsible for complex phenotypes. © 2013 Movement Disorder Society 相似文献