Rush University Medical Center

About: Rush University Medical Center is a healthcare organization based out in Chicago, Illinois, United States. It is known for research contribution in the topics: Population & Medicine. The organization has 13915 authors who have published 29027 publications receiving 1379216 citations. The organization is also known as: Rush Presbyterian St. Luke's Medical Center.

Case-control study of endogenous steroid hormones and endometrial cancer.

Abstract: Background: It has been suggested that identified risk factors for endometrial cancer operate through a single etiologic pathway, i.e., exposure to relatively high levels of unopposed estrogen (estrogen in the absence of progestins). Only a few studies, however, have addressed this issue directly. Purpose: We assessed the risk of developing endometrial cancer among both premenopausal and postmenopausal women in relation to the circulating levels of steroid hormones and sex hormone-binding globulin (SHBG). The independent effect of hormones was assessed after adjustment for other known risk factors. Methods: The data used in the analysis are from a case-control study conducted in five geographic regions in the United States. Incident cases were newly diagnosed during the period from June 1,1987, through May 15,1990. The case patients, aged 20-74 years, were matched to control subjects by age, race, and geographic region. The community control subjects were obtained by random-digit-dialing procedures (for subjects 20-64 years old) and from files of the Health Care Financing Administration (for subjects ^65 years old). Additional control subjects who were having a hysterectomy performed for benign conditions were obtained from the participating centers. Women reporting use of exogenous estrogens or oral contraceptives within 6 months of interview were excluded, resulting in 68 case patients and 107 control subjects among premenopausal women and 208 case patients and 209 control subjects among postmenopausal women. The hormone analyses were performed on blood samples obtained from case patients or from hysterectomy control subjects before surgery. The odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by use of an unconditional logistic regression analysis after we controlled for matching variables and potential confounders. All P values were two-sided. Results: High circulating levels of androstenedione were associated with 3.6-fold and 2.8-fold increased risks among premenopausal and postmenopausal women, respectively, after adjustment for other factors (P for trend = .01 and <.001, respectively). Risks related to other hormone fractions varied by menopausal status. Among postmenopausal women, a reduced risk was associated with high SHBG levels and persisted after adjustment was made for obesity and other factors (OR = 0.51; 95% CI = 0.27-0.95). High estrone levels were associated with increased risk (OR = 3.8; 95% CI = 2.2-6.6), although adjustment for other risk factors (particularly body mass index) diminished the effect (OR = 2.2; 95% CI = 1.2-4.4). Albumin-bound estradiol (E2), a marker of the bioavailable fraction, also remained an important risk factor after adjustment was made for other factors (OR = 2.0; 95% CI = 1.0-3.9). In contrast, high concentrations of total, free, and albumin-bound E2 were unrelated to increased risk in premenopausal women. In both premenopausal and postmenopausal groups, risks associated with obesity and fat distribution were not affected by adjustment for hormones. Conclusion: High endogenous levels of unopposed estrogen are related to increased risk of endometrial cancer, but their independence from other risk factors is inconsistent with being a common underlying biologic pathway through which all risk factors for endometrial cancer operate. Implications: Further research should focus on alternative endocrinologic mechanisms for risk associated with obesity and body fat distribution and for the biologic relevance of the increased risk associated with androstenedione in both premenopausal and postmenopausal disease. [J Natl Cancer Inst 1996; 88:1127-35]

Race and Financial Strain are Independent Correlates of Sleep in Midlife Women: The SWAN Sleep Study

Abstract: MOUNTING EVIDENCE SUGGESTS THAT SLEEP DIFFERS SIGNIFICANTLY ACROSS RACIAL AND ETHNIC GROUPS IN WAYS THAT MAY BE IMPORTANT TO health and functioning.1–5 Most consistent among these effects is a marked decrease in laboratory-assessed slow wave sleep and a concomitant increase in stages 1 and 2 of NREM sleep in African Americans compared to Caucasians.3–7 Other dimensions of sleep shown to differ between African Americans and Caucasians include sleep duration, continuity and subjective sleep quality, although these relationships are not as strong and consistent as those observed for sleep architecture.8 Far fewer studies have compared sleep across other racial and ethnic groups. Hale and Do9 evaluated data from 32,749 respondents to the 1990 health promotion supplement of the National Health Interview Survey (NHIS) and found that, compared to Caucasians, the prevalence of short sleepers (< 6 hours/night) was higher among all racial and ethnic minorities surveyed including African Americans, Hispanics and non-Hispanic “others.” As measured by one night of in-home polysomnography (PSG) collected in the population-based Sleep Heart Health Study (SHHS), Redline and colleagues reported that American Indians and African Americans had lighter sleep than Caucasians, Hispanics, or Asian Americans.10 Despite growing evidence that sleep differs by race and/or ethnic minority status, few studies have evaluated possible causes or correlates of these differences. It has been suggested that socioeconomic status (SES), which is closely tied to race and ethnic minority status in many countries, including the United States, may play an important role in the relationship between minority racial/ethnic status and disturbed sleep.5,6,11 Indeed, a number of studies have reported significant associations among subjective sleep complaints and various indices of SES including lower education, occupational status and income, although these studies did not evaluate the influence of race on the SES-sleep relationship.12–17 Three recent studies reported that both race/ethnicity and traditional measures of SES, income, and education, were significant correlates of behavioral or PSG-assessed indices of sleep.2,6,18 For instance, Mezick and colleagues evaluated the independent effects of race and SES on sleep in a cohort of midlife men and women who were self-identified as either non-Hispanic Caucasian or African American. Lower SES, as measured by a composite score of income and education, was associated with greater PSG-assessed wakefulness after sleep onset, after adjusting for other confounding variables, including race. Sleep quality, duration, and architecture were unrelated to SES in the Mezick et al., study. These studies provide some support for the hypothesis that certain dimensions of sleep may be related to traditional markers of SES, independent of race. The extent to which other dimensions of SES affect, or are affected by, sleep have received less empirical attention. We have hypothesized that financial strain, which is a key chronic stressor associated with lower SES, may be a sensitive marker of the SES-sleep relationship.11 We reported that financial strain, operationalized as difficulties with paying for basics like food and housing, was a significant correlate of increased subjective sleep quality complaints in a sample of 462 midlife women, one-third of whom were African American.11 In multivariate models, financial strain attenuated the relationship between income and sleep quality, which is consistent with the hypothesis that stress pathways are important to the SES-sleep relationship. Stress pathways by which financial strain might interfere with sleep include increased worries and negative affect, as well as endocrine and autonomic dysregulation.19–24 More recently, we demonstrated that chronic and ongoing financial strain was associated with significant decreases in PSG-assessed sleep efficiency in a large sample of community-dwelling elders, after adjusting for a host of variables known to impact sleep in late life.25 Although these studies suggest that financial strain may be an important correlate of sleep, the extent to which financial strain plays a role in the SES-sleep or race-sleep relationship has not been evaluated. The present study evaluated relationships among race and markers of SES in relation to sleep in a multiracial sample of midlife women enrolled in the SWAN Sleep Study, which was designed to characterize sleep during the menopausal transition. Sleep during the menopausal transition provides an opportune model for evaluating the influence of race and SES on sleep because subjective sleep complaints and some sleep disorders are much more frequent in perimenopausal and menopausal women.26–30 Moreover, sleep disturbances that arise during the menopausal transition may be a marker for the development of later chronic health conditions and declines in general health and functioning occurring in the postmenopausal years. SWAN Sleep Study participants included African American, Caucasian, and Chinese women. Measures of sleep were subjective sleep quality, as measured by the validated Pittsburgh Sleep Quality Index (PSQI),31 and indices of sleep duration, continuity, and architecture including NREM electroencephalographic (EEG) power, as measured by multinight in-home PSG. We hypothesized that African American race would be associated with worse sleep, compared to Caucasian and Chinese participants. We further hypothesized that markers of SES, as measured by educational attainment and financial strain, would affect the race-sleep relationship. Specifically, we hypothesized that lower educational attainment and financial strain would attenuate observed relationships among race and sleep after adjusting for other factors that might confound relationships among race, SES, and sleep in midlife women.

Genome-wide association study of recurrent early-onset major depressive disorder.

Abstract: A genome-wide association study was carried out in 1020 case subjects with recurrent early-onset major depressive disorder (MDD) (onset before age 31) and 1636 control subjects screened to exclude lifetime MDD. Subjects were genotyped with the Affymetrix 6.0 platform. After extensive quality control procedures, 671 424 autosomal single nucleotide polymorphisms (SNPs) and 25 068 X chromosome SNPs with minor allele frequency greater than 1% were available for analysis. An additional 1 892 186 HapMap II SNPs were analyzed based on imputed genotypic data. Single-SNP logistic regression trend tests were computed, with correction for ancestry-informative principal component scores. No genome-wide significant evidence for association was observed, assuming that nominal P<5 × 10−8 approximates a 5% genome-wide significance threshold. The strongest evidence for association was observed on chromosome 18q22.1 (rs17077540, P=1.83 × 10−7) in a region that has produced some evidence for linkage to bipolar-I or -II disorder in several studies, within an mRNA detected in human brain tissue (BC053410) and approximately 75 kb upstream of DSEL. Comparing these results with those of a meta-analysis of three MDD GWAS data sets reported in a companion article, we note that among the strongest signals observed in the GenRED sample, the meta-analysis provided the greatest support (although not at a genome-wide significant level) for association of MDD to SNPs within SP4, a brain-specific transcription factor. Larger samples will be required to confirm the hypothesis of association between MDD (and particularly the recurrent early-onset subtype) and common SNPs.

The biomechanical evaluation of four fixation techniques for proximal biceps tenodesis.

Abstract: Purpose: The purpose of this study was to compare the cyclic displacement and ultimate failure strength of 4 proximal biceps tendon tenodesis fixation methods: the open subpectoral bone tunnel (SBT) biceps tenodesis, the arthroscopic suture anchor (SA) tenodesis, the open subpectoral interference screw (SIS) fixation technique, and the arthroscopic interference screw (AIS) technique. Type of Study: Biomechanical experimental control. Methods: Twenty fresh-frozen cadaver shoulders were dissected free of soft tissues, leaving the proximal humerus and the proximal biceps tendon as a free graft. Specimens were randomized to 1 of 4 groups with 5 total specimens in each group. A proximal biceps tenodesis was performed according to the techniques listed above. The specimens were mounted for an axial pull of the biceps tendon on a servohydraulic materials testing system with a 100-N load cycled at 1 Hz for 5,000 cycles, followed by an axial load to failure test. Cyclic displacement, ultimate load to failure, and site of failure were recorded for each specimen. Results: The mean cyclic displacement recorded for each experimental group was as follows: SBT group, 9.39 2.82 mm; AIS group, 5.26 2.60 mm; SIS group, 1.53 0.60 mm; and SA group, 3.87 2.11 mm. The mean ultimate failure loads after 5,000 cycles were as follows: SBT group, 242.4 51.33 N; AIS group, 237.6 27.58 N; SIS group, 252.4 68.63 N; and SA group, 164.8 37.47 N. Each specimen failed at the tenodesis site. Conclusions: The SBT group showed statistically significant greater displacement than the other tenodesis methods. There were no statistically significant differences in ultimate failure strength between any of the biceps tenodesis methods tested. Clinical Relevance: The data serve as a guide to the surgeon performing a proximal biceps tenodesis in choosing a fixation method. Key Words: Biceps tenodesis—Interference screw—Subpectoral.