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Ira Bernstein

Publications and source records attributed to Ira Bernstein.

3 recordsLinked to original sources

The Montgomery Asberg and the Hamilton ratings of depression: a comparison of measures.

The 17-item Hamilton Rating Scale for Depression (HRSD(17)) and the Montgomery Asberg Depression Rating Scale (MADRS) are two widely used clinician-rated symptom scales. A 6-item version of the HRSD (HRSD(6)) was created by Bech to address the psychometric limitations of the HRSD(17). The psychometric properties of these measures were compared using classical test theory (CTT) and item response theory (IRT) methods. IRT methods were used to equate total scores on any two scales. Data from two distinctly different outpatient studies of nonpsychotic major depression: a 12-month study of highly treatment-resistant patients (n=233) and an 8-week acute phase drug treatment trial (n=985) were used for robustness of results. MADRS and HRSD(6) items generally contributed more to the measurement of depression than HRSD(17) items as shown by higher item-total correlations and higher IRT slope parameters. The MADRS and HRSD(6) were unifactorial while the HRSD(17) contained 2 factors. The MADRS showed about twice the precision in estimating depression as either the HRSD(17) or HRSD(6) for average severity of depression. An HRSD(17) of 7 corresponded to an 8 or 9 on the MADRS and 4 on the HRSD(6). The MADRS would be superior to the HRSD(17) in the conduct of clinical trials.

Adolescent↗

Fetal body composition.

PURPOSE OF REVIEW: The purpose of this review is to highlight recent developments in the evaluation of fetal growth, focusing on the determination of fetal body composition. The ultimate goal of this area of investigation is to improve predictions of perinatal morbidity and mortality beyond that achieved employing estimated fetal weight as the primary discriminator of the risk associated with abnormal fetal growth. RECENT FINDINGS: Several validated techniques have emerged which appear capable of quantifying fetal lean body mass and fat mass. Preliminary investigations suggest that these body composition parameters do distinguish, with a higher degree of precision than estimates of fetal weight alone, clinical influences that contribute to abnormal fetal growth. Studies linking estimates of fetal body composition to improved prediction of perinatal morbidity and mortality are currently limited. SUMMARY: Quantitative estimates of fetal body composition can currently be achieved with recently developed and validated ultrasound tools. Their utility for the improved prediction of perinatal morbidity and mortality has not yet been rigorously examined.

Adult↗

Correlation between serum estradiol in the follicular phase of the ovarian cycle and decay acceleration factor (DAF) expression on red blood cells and coxsackiervirus B-3 induced hemagglutination in young cycling women.

Decay accelerating factor (DAF) is a widely distributed glycoprotein which aids in the inactivation of complement. DAF is also a cellular receptor for certain group B coxsackieviruses (CVB) and is responsible for the viral hemagglutinating activity for human red blood cells (RBC). Healthy, young female volunteers donated blood on days 11 and 22 of the ovarian cycle. Samples were categorized into luteal and follicular phases based on serum progesterone level (P4 either < 2.0 ng/mL, follicular; P4 > or = 2.0 ng/mL, luteal) and analyzed by flow cytomtery for DAF expression on RBC and CD21 + B lymphocytes. Cycling females showed significant variation in CVB-induced hemagglutination and % RBC or CD19 + cells which were DAF +. There was a strong correlation between serum estradiol levels and % RBC expressing DAF (P < 0.01) in the follicular, but not in the luteal ovarian phase. Infection of white blood cells with green-fluorescent protein CVB (GFP-CVB) showed a correlation between infectivity of CD19+ cells and DAF expression. This indicates that women may show differential susceptibility to CVB infection in the luteal and follicular phases of the ovarian cycle.

Antigens, CD19↗