Changes in student physical health behaviour: an opportunity to turn the concept of a Healthy University into a reality.

AIMS:: Previous studies have reported a high prevalence of unhealthy behaviours in the student population, which the Healthy University concept is now seeking to address, by taking a settings approach to health promotion. This study investigated how far students are already seeking to make changes to improve their health behaviour while in a university setting, to help inform the development of Healthy Universities. METHODS:: Data on student health behaviour change, health indicators and demographics were gathered from 550 students attending two London universities, via an online questionnaire released through the student union email system at one university and through iPads at a student centre at the other. RESULTS:: In total, 84% of respondents reported making changes to try to become healthier while at university, primarily for proactive health reasons rather than reacting to a perceived health or weight issue. Universities and student unions were reported as influencing behaviour change by only five students. Compared with previous studies, a higher proportion of respondents were pursuing healthier lifestyles, including only 11% reporting they smoked. There were some statistically significant demographic differences as regards alcohol consumption, physical activity, the types of food students were seeking to avoid and the reasons for this. CONCLUSION:: The findings provide a novel perspective on student health behaviour and suggest that the traditional stereotype of a hedonistic student lifestyle freed from family constraints may need to be reassessed. Universities and student unions appear to have a significant opportunity to build on a more health conscious cohort of students, employing targeted approaches where appropriate, to encourage positive health behaviour change and make the Healthy Universities concept a reality, with important public health implications.

Systematic review: psychosocial factors associated with pain in inflammatory bowel disease.

BACKGROUND: Pain is a frequently reported symptom of inflammatory bowel disease (IBD) experienced by patients in active disease and remission. Psychological factors play a significant role in pain, but have not been systematically reviewed in IBD. AIM: To review psychosocial factors associated with pain in adults diagnosed with IBD. METHODS: Electronic (PsycInfo, MEDLINE, EMBASE, Cochrane Library, CINAHL, Web of Science), and hand-searching were conducted February-May 2017. Two authors carried out screening and data extraction. RESULTS: Fifteen studies including 5539 IBD patients were identified. Emotional, cognitive-behavioural and personality factors were associated with IBD-pain. Depression and anxiety were the most commonly explored constructs, followed by perceived stress and pain catastrophising, all of which were positively associated with greater pain. Greater abdominal pain was associated with a concurrent mood disorder over fivefold (OR 5.76, 95% CI 1.39, 23.89). Coping strategies and pain fear avoidance correlated with pain levels. Perceived social support (r = .26) and internal locus of control (r = .33) correlated with less pain. Patients reporting pain in IBD remission more frequently had an existing diagnosis of a mood disorder, a chronic pain disorder and irritable bowel syndrome. Six studies controlled for disease activity, of which 4 found that psychosocial factors significantly predicted pain. The majority of studies (n = 10) were of high quality. CONCLUSION: Psychosocial factors appear to play a significant role in IBD-pain. Further research is required to explore psychosocial constructs in relation to IBD-pain, with use of validated pain measures, large sample sizes and clearer characterisation of disease activity.

Methadone withdrawal when starting an antiretroviral regimen including nevirapine.

Antiretrovirals from three drug classes, nucleoside analogs, nonnucleoside analogs, and protease inhibitors, can be combined to achieve viral suppression. The nonnucleoside analog nevirapine is an inducer of cytochrome P450 3A4 liver metabolism and has interactions with protease inhibitors and oral contraceptives. Methadone has two roles in human immunodeficiency viral infection: pain management and treatment of opioid abuse. A drug-drug interaction may result in decreased methadone blood levels when administered with nevirapine. A patient experienced methadone withdrawal symptoms when combining these agents.

Microtubule polarity in the peripheral processes of trigeminal ganglion cells: relevance for the retrograde transport of herpes simplex virus.

The directional movement of many cellular organelles in neurons is dependent on polarized microtubules and direction-specific motor molecules. Microtubules are also thought to mediate the retrograde transport of herpes simplex virus (HSV) in sensory neurons. To define the cellular machinery responsible for retrograde axonal transport of HSV, we have investigated the polarity of microtubules in the peripheral axons of trigeminal ganglion neurons. The long ciliary nerves of rabbits were prepared for a standard "hook assay" of microtubule polarity. Axons in cross-sectioned nerves contained microtubules with almost uniform orientation. The fast-growing, plus ends of these axonal microtubules are located distal to the cell body and the slow-growing, minus ends are directed centrally. To determine the role played by microtubules in the retrograde transport of HSV in these axons, we injected the retrobulbar space of mice with the microtubule-inhibiting drugs colchicine, vinblastine, or nocodazole or with the microfilament inhibitor cytochalasin D and 1 d later inoculated the cornea with HSV. We found that colchicine, vinblastine, or nocodazole reduced by 52-87% the amount of virus recovered from the ganglion 3 d postinoculation, compared to vehicle-treated animals. In contrast, cytochalasin D or beta-lumicolchicine did not significantly reduce the amount of HSV recovered from the ganglion. We conclude that the retrograde axonal transport of HSV from axon endings in the cornea to the trigeminal ganglion cell bodies requires intact microtubules and occurs in a plus-to-minus direction on the microtubules. Our data are consistent with the hypothesis that the retrograde axonal transport of HSV is mediated by a minus end-directed motor molecule, for example, cytoplasmic dynein.

Ultrastructural immunocytochemical localization of herpes simplex virus (type 1) in trigeminal ganglion neurons.

Four days after corneal inoculation of mice with herpes simplex (type 1) virus (HSV), infected trigeminal ganglion cells with and without calcitonin gene-related peptide (CGRP) antigenicity were examined by electron microscopy in sections treated with colloidal gold labeled antibodies. Cells that contain CGRP were identified by the dense gold labeling of small vesicles about 100 nm in diameter. Adjacent thin sections were stained using an indirect colloidal gold immunocytochemical technique to reveal HSV-1 antigens. In CGRP-positive neurons, HSV antigens were located over both nuclear and cytoplasmic compartments. HSV label was found over cytoplasmic vesicles that were significantly larger than those labeled with anti-CGRP antisera; the HSV-containing vesicles ranged in profile diameter from less than 170 to greater than 400 nm. There was no overlap in the distribution of the two labels. Thus, for this time period, the organelles involved in transport of the endogenous neuropeptide and HSV appear to remain discrete. Furthermore, there was no significant difference in the distribution of HSV in CGRP-reactive and CGRP-negative trigeminal ganglion cells. Thus, there is no indication of a preferential distribution or limited replication of HSV in CGRP-positive neurons.

Lipid synthesis in stringent Escherichia coli: an artifact in acetate labeling of phospholipids during a shiftdown in growth rate.

The use of (14C)acetate to label the phospholipids of stringent Escherichia coli, after a decrease in agitation, leads to artifacts resulting from a decrease in the specific activity of the acetyl coenzyme A pool.