Cartographie des mesures de soutien à la santé mentale des étudiant.es et des employé.es de l’UQAC

Cartographie des mesures de soutien à la santé mentale des étudiant.es et des employé.es de l’UQA

Santé mentale et population universitaire : un laboratoire-vivant au service de la communauté : rapport de recherche

Cette étude a trois objectifs : 1) Identifier les principaux enjeux de santé des étudiant·es et des employé·es de l’UQAC en contexte pandémique, 2) Répertorier l’ensemble des mesures de soutien à la santé mises à la disposition des étudiant·es et des employé·es de l’UQAC, et 3) Identifier de nouvelles solutions à mettre en place afin de pallier les manques et de soutenir les étudiant·es et les employé·es de l’UQAC

Doping controls and the ?Mature Minor? elite athlete: towards clarification?

status: publishe

Differential effect of angiotensin II and blood pressure on hippocampal inflammation in mice

Abstract Background Angiotensin II (Ang II), a peptide hormone involved in the development of hypertension, causes systemic and cerebral inflammation, affecting brain regions important for blood pressure control. The cause-and-effect relationship between hypertension and inflammation is two-way, but the role of blood pressure in the induction of cerebral inflammation is less clear. The vulnerability of specific brain regions, particularly those important for memory, is also of interest. Methods We used molecular biology approaches, immunohistochemistry, and electron microscopy to examine the interdependence between the hypertensive and pro-inflammatory effects of Ang II. We examined the effect of blood pressure by administering a subpressive (200 ng/kg/min) or a pressive Ang II dose (1000 or 1900 ng/kg/min) with and without hydralazine (150 mg/L) for 1 week and used phenylephrine to increase blood pressure independently of the renin-angiotensin system. Results Ang II increased ionized calcium-binding adaptor molecule 1 (Iba-1) levels (marker of microgliosis) in the whole brain and in the hippocampus in a dose-dependent manner. Pressive Ang II induced specific changes in microglial morphology, indicating differences in functional phenotype. An increase in hippocampal glial fibrillary acidic protein (GFAP) was seen in mice receiving pressive Ang II, while no induction of cerebral gliosis was observed after 7 days of subpressive Ang II infusion. Although phenylephrine led to increased astrogliosis, it did not affect Iba-1 expression. Pressive Ang II stimulated TNF-α production in the hippocampus, and daily treatment with hydralazine prevented this increase. Hydralazine also reduced GFAP and Iba-1 levels. With longer perfusion (14 days), subpressive Ang II led to some but not all the inflammatory changes detected with the pressive doses, mainly an increase in CD68 and Iba-1 but not of GFAP or TNF-α. Conclusions Blood pressure and Ang II differentially contribute to hippocampal inflammation in mice. Control of blood pressure and Ang II levels should prevent or reduce brain inflammation and therefore brain dysfunctions associated with hypertension

Portrait de la santé mentale des communautés universitaires.

Ces douze infographies ont été élaborées dans le cadre d’un projet ayant pour titre « Santé mentale et accessibilité en milieu universitaire : la diversité constitue-t-elle une barrière ? ». Jumelant synthèse des écrits et données de recherche, elles visent à effectuer le portrait de la santé mentale des étudiant.es et des employé.es qui s’identifient à l’un ou plusieurs des six groupes désignés suivants : Femmes, minorités visibles, personnes en situation de handicap, personnes autochtones, personnes de la diversité sexuelle et de genre, et personnes de l’international

Additional file 2: of Differential effect of angiotensin II and blood pressure on hippocampal inflammation in mice

Figure S1.. Effect of extended perfusion of subpressive Ang II on cerebral inflammation. Iba-1 (A) and GFAP (B) were examined by Western blotting in cerebral homogenates after 2 weeks systemic perfusion of Ang II 200 ng/kg/min or 0.9% saline (CTL). Densitometry values of Iba-1 and GFAP were normalized to actin, and the results are expressed relative to the control group. Representative immunoblots are shown (two-tailed Student’s t test, n = 3). CD68 mRNA (C) and GFAP mRNA (D) gene expression were analyzed by qRT-PCR in microdissected hippocampi after 2 weeks systemic perfusion of Ang II 200 ng/kg/min or 0.9% saline (CTL). In each experiment, a treated-to-control ratio was calculated (**p < 0.01, Ang II 200 versus control, by two-tailed Student’s t test, n = 7). ELISA analysis of TNF-α in plasma (E) and in whole brain homogenates (F) after 2 weeks perfusion of Ang II 200 ng/kg/min or 0.9% saline (CTL). A treated-to-control ratio was calculated (two-tailed Student’s t test, n = 6–8). (TIFF 1442 kb

Additional file 1: of Differential effect of angiotensin II and blood pressure on hippocampal inflammation in mice

Supplementary Methods. (DOCX 59 kb