PurposePoor quality of sleep and excessive daytime sleepiness affect cognitive ability and have a negative impact on the academic performance of medical students. This study aims to determine the prevalence of excessive daytime sleepiness, sleep quality and psychological distress as well as assess their association with low academic performance in this population.Participants and methodsA cross-sectional study was conducted among 457 medical students from the Faculty of Medicine and Pharmacy of Rabat, Morocco, who completed the Pittsburgh Sleep Quality Index (PSQI) questionnaire and the Epworth Sleepiness Scale to determine the quality of sleep and excessive daytime sleepiness, respectively. Sociodemographic variables and psychological distress (Kessler Psychological Distress Scale) were also measured. Multivariate linear regression was performed in order to evaluate the link between low academic performance and sleep quality after adjusting for other covariates.ResultsAmong the included students, the median age was 20 (19; 21) years; 70.7% of the participants were females. Almost one-third of the students (36.6%) had excessive daytime sleepiness and this was more frequently observed in female students (43% vs 20.1%, <0.001). Furthermore, 58.2% of the students were poor sleepers (PSQI ≥5), while 86.4% of them had psychological distress. The bivariate analysis showed that psychological distress was associated with decreased risk of low performance (ß=0.04; 95% CI=0.005–0.07; P=0.024). Being a poor sleeper was statistically associated with poor academic performance (ß= −0.07; 95% CI=−0.14 to −0.002; P=0.04) in the multivariate analysis. In our study, daytime sleepiness was not statistically associated with academic performance.ConclusionA poor sleep quality determined by PSQI ≥5 was related to poor academic achievement at the end of the study year in medical students.

The synchronous combination of a blood test plus LSE improves the accuracy of the non-invasive diagnosis of liver fibrosis and, consequently, markedly decreases the biopsy requirement in the diagnostic algorithm, notably to <10% in cirrhosis diagnosis.

Exposure of the ileum to nutrients markedly inhibits several upper gastrointestinal functions. Hormonal peptides of the ileal wall, i.e. peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and neurotensin (NT), are thought to play a role in this negative feedback mechanism. The present study was conducted to comparatively assess the secretion of PYY, GLP-1, and NT upon luminal infusion of a variety of individual luminal factors in the isolated vascularly perfused rat ileum preparation. PYY, GLP-1, and NT were measured in the portal effluent with specific RIAs. Glucose (250 mM) induced a pronounced release of the three peptides, whereas a physiological concentration of 5 mM did not induce peptide secretion. Peptone (5%, wt/vol) evoked a sustained release of PYY, GLP-1, and NT. Only NT secretion was increased upon luminal administration of 100 mM sodium oleate.Short chain fatty acids (20 mM) evoked an early and transient release of the three peptides. In contrast, taurocholate (20 mM) induced a sustained release of PYY, GLP-1, and NT, but the threshold concentration for peptide release was lower for NT than for PYY or GLP-1. Cellulose or pectin (0.5%, wt/vol) did not modify peptide secretion. In conclusion, glucose and peptone are potent stimulants of PYY, GLP-1, and NT release. Only NT is released upon oleic acid stimulation. Finally, taurocholate is a potent stimulant of the release of the three peptides. Overall, PYY, GLP-1, and NT may participate cooperatively in the ileal brake. As relatively high concentrations of the various stimulants were required to elicit peptide release, it seems likely that this mechanism operates in cases of maldigestion or malabsorption. (Endocrinology 139: 3780 -3786, 1998) U NABSORBED nutrients reaching the ileum influence the functions of the upper gut to increase the efficiency of digestion and absorption. For example, unabsorbed fat or protein in the ileum delays the passage of material through the small intestine. As a delay in small bowel transit increases the contact time between luminal contents and absorptive epithelium, this mechanism may serve to increase the absorption of a meal. This negative feedback mechanism referred to as the ileal brake presumably involves hormonal intermediates. As the ileal mucosa contains several distinct populations of endocrine cells, many studies focused on the effects of the products of these cells on gastrointestinal functions. Neurotensin (NT), the major product of the so-called N cells, and peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), which are cosynthesized in the so-called L cells, have been implicated in these feedback mechanisms.Circulating levels of NT, PYY, and GLP-1 rapidly increase in response to oral ingestion of a mixed meal, thus suggesting that their release is triggered in part by hormonal and/or neural signals originating from the upper small intestine. As NT, PYY, and GLP-1 are contained in open-type cells, nutrients making contact with the ileal mucosa are also capable of eliciting peptide secretion. In...