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The higher T2D risk among ethnic minority populations compared with Dutch did not decrease after adjustment for last snack or length of sleep. Conclusions Although prevalence of circadian disruptors was higher among ethnic minority populations and some disruptors were associated with T2D, disruptors did not account for ethnic differences in T2D risk.Background Steroidogenesis decline is reported to be one of the mechanisms associated with obesity-induced male factor subfertility/infertility. Objectives We explored the possible preventive/therapeutic effects of orlistat (a medication prescribed for weight loss) on obesity-induced steroidogenesis and spermatogenesis decline. Materials and methods Twenty-four adult male Sprague Dawley rats weighing 250-300 g were randomized into four groups (n = 6/group), namely; normal control, high-fat diet, high-fat diet plus orlistat preventive group and high-fat diet plus orlistat treatment group. Orlistat (10 mg/kg/b.w./d suspended in distilled water) was either concurrently administered with high-fat diet for 12 weeks (high-fat diet plus orlistat preventive group) or administered from week 7-12 post- high-fat diet feeding (high-fat diet plus orlistat treatment group). Thereafter, serum, testes and epididymis were collected for analyses. Results Obesity increased serum leptin and decreased adiponectin levels, decrease and associated genes in high-fat diet-induced obese male rats, with the preventive group (high-fat diet plus orlistat preventive group) having better results relative to the treatment group (high-fat diet plus orlistat treatment group). Discussion and conclusion Orlistat attenuated impaired spermatogenesis and steroidogenesis decline by up-regulating steroidogenic genes. This may not be unconnected to its significant effect in lowering serum leptin levels, since the hormone is known to dampen fertility potential. Therefore, orlistat may improve fertility potential in overweight/obese men.In localized tumours, basement membrane (BM) prevents invasive outgrowth of tumour cells into surrounding tissues. When carcinomas become invasive, cancer cells either degrade the BM or reprogram the stromal fibroblasts to breach the BM barrier and lead invasion of cancer cells into surrounding tissues in a process called fibroblast-led invasion. However, tumour-derived factors orchestrating fibroblast-led invasion remains poorly understood. Here we show that although early-stage primary colorectal adenocarcinoma (SW480) cells are themselves unable to invade MatrigelTM matrix, they secrete exosomes that reprogram normal fibroblasts to acquire de novo capacity to invade matrix and lead invasion of SW480 cells. Strikingly, cancer cells follow the leading fibroblasts as collective epithelial-clusters, thereby circumventing the need for epithelial to mesenchymal transition, a key event associated with invasion. Moreover, acquisition of pro-invasive phenotype by fibroblasts treated with SW480-derived exosomes relied on exosome-mediated MAPK pathway activation. Mass spectrometry-based protein profiling revealed that cancer exosomes upregulated CRL1541 proteins implicated in focal adhesion (ITGA2/A6/AV, ITGB1/B4/B5, EGFR, CRK), regulators of actin cytoskeleton (RAC1,ARF1, ARPC3, CYFIP1,NCKAP1, ICAM1, ERM complex) and signalling pathways (MAPK, Rap1, RAC1, Ras) important in pro-invasive remodelling of the extracellular matrix. Blocking tumour exosome-mediated signalling to stromal fibroblasts could therefore represent an attractive therapeutic strategy in restraining tumours by perturbing stroma-driven invasive outgrowth. This article is protected by copyright. DFOM All rights reserved.This editorial shows how the principles of demand‐capacity modelling lead to the conclusion that COVID‐19 disease will require the UK NHS to run its serves at a far higher working capacity (in terms of hospital, intensive care and social care beds, operating theatres and staff) than it has been used to. The analysis leads to key questions that should form the basis for rational planning in a post‐COVID NHS.Within the present study, we investigate the lasting effect of laboratory peer group interactions on the end of year attainment of Biosciences and Chemistry students. By asking students to identify who they primarily work with within the laboratory environment and evaluating the interactions through cluster analysis, we identified two main categories of laboratory peer groups the first long-lived well-established pairings of two students, 'swans', who work together for all or the majority of the laboratory sessions; and the second dynamic fluid groups, 'dolphins', of between three and nine students who work with each other interchangeably. Statistical analysis is presented, which demonstrates that individuals within each laboratory peer group were likely to achieve a similar average mark at the end of the first year of study on the course. We identified the driving factors for the formation of these groups as friendship and perceived work ethic. There is a preference for high-achieving students to work with other high-achieving students and lower-achieving to group around a shared social background. Targeted interventions, in which pairings were selected by the tutor at the onset of the study, altered the ratio from long-lived pairs to more dynamic groups and increased students' willingness to work with others outside of their group but did not change the drivers of group formation or resulting pattern of achievement. We conclude with recommendations around group working within the laboratory environment.Background/purpose Although ursodeoxycholic acid (UDCA) is a first-line treatment for primary biliary cholangitis (PBC), 20%-30% of patients with PBC exhibit an incomplete response to UDCA. Recently, the UDCA Response Score was proposed for predicting response to UDCA using pretreatment parameters in patients with PBC. We aimed to validate the UDCA Response Score in Japanese patients with PBC. Methods Registry data of Japanese patients (n = 873) were collected. Patients with data on all clinical parameters required for calculating the UDCA Response Score were selected. The endpoint was UDCA response, defined as alkaline phosphatase less then 1.67 times the upper limit of the normal value after 12 months of UDCA treatment. Results All parameters were available in 804 patients (male/female = 120/684, age 58.9 [interquartile range 51.1-66.9] years). Bezafibrate was commenced within 12 months of UDCA in 78 patients (9.7%) because of the lack of an early response. We found that the endpoint was not reached in these 78 patients, and the area under the receiver operating characteristic curve (AUROC) of the score was 0.
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