Coffeyhammond3155

Transgelin is a protein reported to be a marker of several cancers. However, previous studies have shown both up- and down-regulation of transgelin in tumors when compared with non-tumor tissues and the mechanisms whereby transgelin may affect the development of cancer remain largely unknown. Transgelin is especially abundant in smooth muscle cells and is associated with actin stress fibers. These contractile structures participate in cell motility, adhesion, and the maintenance of cell morphology. Here, the role of transgelin in breast cancer is focused on. Initially, the effects of transgelin on cell migration of the breast cancer cell lines, BT 549 and PMC 42, is studied. Interestingly, transgelin silencing increased the migration of PMC 42 cells, but decreased the migration of BT 549 cells. To clarify these contradictory results, the changes in protein abundances after transgelin silencing in these two cell lines are analyzed using quantitative proteomics. The results confirmed the role of transgelin in the migration of BT 549 cells and suggest the involvement of transgelin in apoptosis and small molecule biochemistry in PMC 42 cells. The context-dependent function of transgelin reflects the different molecular backgrounds of these cell lines, which differ in karyotypes, mutation statuses, and proteome profiles. © 2020 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.BACKGROUND To assess the growth outcomes at 18 months corrected age in very low birth weight (VLBW) infants compared to standardized norms, and in VLBW infants with and without bronchopulmonary dysplasia (BPD) or fetal growth restriction (FGR). METHODS In all, 1149 VLBW infants completed anthropometrics at 18 months corrected age. To derive weight, height, and body mass index (BMI) percentiles and z-scores at 18 months, we used the SAS macro from the Centers for Disease Control and Prevention (CDC). z-scores for a child's sex and age are based on the World Health Organization's growth charts for children less then 24 months of age. RESULTS Female and male VLBW infants had higher body-mass-index (BMI)-for-age z-scores compared to normative data (0.82 and 1.77 respectively). No significant difference was found in BMI-for-age z-scores in BPD and non-BPD (1.76 vs. 2.3; p = 0.4), nor in FGR and non-FGR (1.24 vs. 2.16; p = 0.2). CONCLUSIONS At 18 months corrected age, VLBW infants, including those with BPD or FGR, had BMI-for-age z-scores higher than reference standards. No significant difference was seen comparing BMI-for-age z-scores in the BPD/non-BPD and FGR/non-FGR groups.Overlap syndrome (OVS) is the concurrence of chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA), and is associated with poor outcomes. Caspase inhibitor in vivo We hypothesized that physiological changes in COPD may affect the pathogenesis of OSA in important ways. We therefore sought to measure the anatomical and nonanatomical OSA traits in individuals with OVS and compare to those with OSA alone. Patients with established OVS were recruited, along with age, gender, and BMI matched OSA only controls. Smoking and relevant comorbidities or medications were excluded. Subjects underwent baseline polysomnography followed by an overnight physiological research study to measure the OSA traits (Veupnea , Varousal , Vpassive , Vactive , and loop gain). Fifteen subjects with OVS and 15 matched controls with OSA alone were studied (overall 66 ± 8 years, 20% women, BMI 31 ± 4 kg/m2 , apnea-hypopnea index 49 ± 36/hr). Mixed-modeling was used to incorporate each measurement (range 52-270 measures/trait), and account for age, gender, and BMI. There were no significant differences in the traits between OVS and OSA subjects, although OVS subjects potentially tolerated a lower ventilation before arousal (i.e., harder to wake; p = .06). Worsened lung function was significantly associated with worsened upper airway response and more unstable breathing (p  less then  .05 for all). Consistent differences in key OSA traits were not observed between OVS and OSA alone. However, worse lung function does appear to exert an influence on several OSA traits. These findings indicate that a diagnosis of OVS should not generally influence the approach to OSA, but that lung function might be considered if utilizing OSA trait-specific treatment. © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.OBJECTIVE This study aimed to provide updated lifetime prevalence estimates of eating disorders, specifically bulimia nervosa (BN) and binge eating disorder (BED) and investigate changes over time in lifetime prevalence by age. METHOD Two thousand nine hundred seventy-seven participants from South Australia were interviewed in the Health Omnibus Survey. DSM-5 criteria were used for current and broad (in accord with the International Statistical Classification of Diseases and Related Health Problems-11 [ICD-11]) criteria for lifetime prevalence of BED. RESULTS This study found that the lifetime prevalence of BN was 1.21% (95% CI [0.87, 1.67]) and 2.59% (95% CI [2.07, 3.22]) for males and females, respectively, and that lifetime prevalence for BED-broad was 0.74% (95% CI [0.49, 1.11]) and 1.85% (95% CI [1.42, 2.40]) for males and females, respectively, which is higher than reported in previous research. Current prevalence (past 3 months) of BN was 0.40% (95% CI [0.23, 0.70]) and 0.81% (95% CI [0.54, 1.20]) for males and females, respectively, and current prevalence for BED was found to be 0.03 (95% CI [0.01, 0.04]) and 0.20% (95% CI [0.09, 0.44]) for males and females, respectively. CONCLUSIONS The current study confirmed the moderate community prevalence of BN and BED. BED was found to be less prevalent than BN in the present study, and a significant lifetime prevalence by age effect was found for both. Lifetime prevalence by age indicated that past increases in prevalence may be waning in this century and that overall BN and BED are not increasing in Australia. © 2020 John Wiley & Sons, Ltd and Eating Disorders Association.