Background Effect of race/ethnicity on the risk of diabetes associated with sleep duration has not been systematically investigated. This study assessed whether blacks reporting short (≤ 5 hours) or long (≥ 9 hours) sleep durations were at greater risk for diabetes than their white counterparts. In addition, this study also examined whether the influence of race/ethnicity on associations between abnormal sleep durations and the presence of diabetes were independent of individuals’ sociodemographic and medical characteristics. Methods A total of 29,818 Americans (age range: 18–85 years) enrolled in the 2005 National Health Interview Survey (NHIS), cross-sectional household interview survey, provided complete data for this analysis. Results Of the sample, 85% self-ascribed their ethnicity as white and 15% as black. The average age was 47.4; 56% were female. Results of univariate regression analysis adjusted for medical comorbidities showed that black and white participants who reported short sleep duration (≤ 5 hours) were more likely to have diabetes than individuals who reported sleeping 6 to 8 hours [OR = 1.66; OR = 1.87, respectively]. Similarly, black and white participants reporting long sleep duration (≥ 9 hours) had a greater likelihood to report diabetes compared with those with sleeping 6 to 8 hours [OR = 1.68; OR = 2.33, respectively]. Significant interactions of short and long sleep with black and white race were observed. Compared with white participants, greater diabetes risk was associated with being black short or long sleepers. Conclusion The present findings suggest that American the black short and long sleepers may be at greater risk for diabetes, independently of their sociodemographic profile or the presence of co-morbid medical conditions, which have previously been shown to influence habitual sleep durations. Among black individuals at risk for diabetes, healthcare providers should stress the need for adequate sleep.

To date, the role of pancreatic hormones in pancreatic islet growth and differentiation is poorly understood. To address this issue, we examined mice with a disruption in the gene encoding prohormone convertase 2 (PC2). These mice are unable to process proglucagon, prosomatostatin, and other neuroendocrine precursors into mature hormones. Initiation of insulin (IN) expression during development was delayed in PC2 mutant mice. Cells containing IN were first detected in knockout embryos on d 15 of development, 5 d later than in wild-type littermates. However, the IN(+) cells of d 15 PC2 mutant mice coexpressed glucagon, as did the first appearing beta-cells of controls. In addition, lack of PC2 perturbed the pattern of expression of transcription factors presumed to be involved in the determination of the mature alpha-cell phenotype. Thus, in contrast to controls, alpha-cells of mutant mice had protracted expression of Nkx 6.1 and Pdx-1, but did not express Brn-4. Islets of adult mutant mice also contained cells coexpressing insulin and somatostatin, an immature cell type found only in islets of the wild-type strain during development. In addition to the effects on islet cell differentiation, the absence of PC2 activity resulted in a 3-fold increase in the rate of proliferation of proglucagon cells during the perinatal period. This increase contributed to the development of alpha-cell hyperplasia during postnatal life. Furthermore, the total beta-cell volume was increased 2-fold in adult mutants compared with controls. This increase was due to islet neogenesis, as the number of islets per section was significantly higher in knockout mice compared with wild-type mice, whereas both strains had similar rates of IN cell proliferation. These results indicate that hormones processed by PC2 affected processes that regulate islet cell differentiation and maturation in embryos and adults.

Nipple discharge is the third most common breast complaint after breast pain and breast mass. It is most often a benign process. Up to 50% women in their reproductive years can express one or more drops of fluid from the breast. Nipple discharge can be of several types, including milky, multicolored and sticky, purulent, clear and watery, yellow or serous, pink or serosanguinous, bloody or sanguinous. The characteristics of the nipple discharge help in the early diagnosis and management of breast disease. The most common cause of pathologic nipple discharge is a benign papilloma followed by ductal ectasia, and the least likely is carcinoma. Most nipple discharges are the result of a clinically insignificant benign process; therefore, less invasive, nonsurgical diagnostic modalities have been explored to reduce the need for surgical intervention. The evaluation and diagnosis of nipple discharge is important for the early detection of carcinoma, when present; and, in the case of benign disease, it is necessary to stop the incommodious discharge.

Background: Patients with overactive bladder (OAB) are under-diagnosed in the primary care setting. Primary care physicians (PCP) approach to the patient and appropriate patient disclosure may contribute to under-diagnosis.

We have investigated the mitogenic effect of three mutant forms of human insulin on insulin-producing f3 cells of the developing pancreas. We examined transgenic embryonic and adult mice expressing (i) Insulin is a peptide hormone that plays a crucial role in the control of blood glucose. It contains two separate polypeptide chains, the A chain containing 21 amino acid residues and the B chain containing 30 residues, which are linked to each other by a pair of disulfide bonds (1). Insulin is synthesized by ,3 cells of the pancreatic islets in the form of a precursor called preproinsulin (1), which is processed into proinsulin in the rough endoplasmic reticulum and transported via a regulated secretory pathway to storage granules, where it is cleaved to yield insulin and a 31-residue fragment called the C peptide. A small amount of proinsulin (0.5-2%) escapes from this route and is released through a constitutive, unregulated pathway (1-4). The expression of insulin solely by ,B cells has been controversial (5, 6). However, since we previously documented the expression of a chimeric gene containing the insulin I promoter in neurons of transgenic mice (7), the possibility was raised that, in addition to ,3 cells, insulin may be expressed by other cell types but at concentrations that are below the level of detection of the immunohistochemical techniques. To test this possibility, we initiated an analysis of transgenic mice overexpressing a human insulin analog. The transgene codes for the expression of a proinsulin molecule in which the amino acid histidine in position 10 of the B chain was replaced by aspartic acid. The substitution at B10 produced an aberrant intracellular sorting of the mutant hormone ([AspBlO]-proinsulin) resulting in secretion of up to 15% of the humanThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact. 6239[AspBlO]proinsulin via an unregulated pathway (8). However, processing of mouse and human proinsulin within secretory granules in the islets of transgenic mice was not impaired, and the residual mouse and most of the human proinsulin were converted to insulin and secreted normally (1). Surprisingly, this mutant form of insulin has a 4-to 5-fold higher biological activity than normal insulin (9, 10). The appearance of the vaginal plug was considered to be day 0.5 of gestation. Pregnant females were killed by cervical dislocation, the embryos were dissected, the trunk was processed for Southern blotting analysis, and the head and abdomen were fixed in 4% paraformaldehyde buffered to pH 7.4 with 0.1 M sodium phosphate buffered saline (PBS) for 1 hr. Embryos were examined daily from embryonic day (E) 7.5, corresponding to four or five pairs of somites (15) to E17.5. Adult mice were perfused through the heart with fixative solution; the pancreas was removed and post-fixed for 1 hr in