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The Canadian population is aging. With aging, biological and social changes occur increasing the risk of developing chronic conditions and functional loss leading to frailty. Older adults living with frailty are more vulnerable to minor stressors, take longer to recover from illness, and have difficulty participating in daily activities. The Canadian Frailty Network’s (CFN) mis-sion is to improve the lives of older adults living with frailty. In September 2019, CFN launched the Activity & Exercise, Vaccination, Optimization of medications, Interaction & Socialization, and Diet & Nutrition (AVOID) Frailty public health campaign to promote assessing and reducing risk fac-tors leading to the development of frailty. As part of the cam-paign, CFN held an Enabling Healthy Aging Symposium with 36 stakeholders from across Canada. Stakeholders identified individual and community-level opportunities and challenges for the enablement of healthy aging and frailty mitigation, as part of a focused consultative process. Stakeholders ranked the three most important challenges and opportunities at the individual and community levels for implementing AVOID Frailty recommendations. Concrete actions, further research areas, policy changes, and existing resources/programs to enhance the AVOID Frailty campaign were identified. The results will help inform future priorities and behaviour change strategies for healthy aging in Canada.

Thirteen new derivatives of picolinic acid (4–7) were designed and synthesized from the starting parent molecule, picolinic acid. The new compounds were characterized by ATR-FTIR, 1HNMR, and CHNS analysis. A molecular docking study was performed to evaluate the binding affinity of the synthesized compounds toward EGFR kinase domain that indicated occupation of the critical site of EGFR kinase pocket and excellent positioning of the compounds in the pocket. The cytotoxic activity of the compounds against two human cancer cell lines (A549 and MCF-7), the non-tumorigenic MCF10A cell line, and white blood cells (WBC) was evaluated using the MTT assay. Compound 5 showed anticancer activity against A549 lung cancer cells (IC50 = 99.93 µM) but not against MCF-7 breast cancer cells or normal cells. Compound 5 mediated cytotoxicity in A549 lung cancer cells by inducing apoptotic cell death, as suggested by fragmented nuclei after DAPI staining, and agarose gel electrophoresis. Moreover, compound 5 triggered the activation of caspases 3, 4 and 9. However, compound 5 treatment did not affect the release of cytochrome c from the mitochondria to the cytosol, as compared to the vehicle-treated control cells. Nevertheless, compound 5-treated cells reported greater release of smac/DIABLO to the cytosol. In the same context, both compound 5 and thapsigargin (specific inhibitor of sarco/endoplasmic reticulum Ca2+-ATPase (SERCA)) enhanced eIF2 phosphorylation, reflecting the activation of the atypical ER stress pathway and the potential applicability of compound 5 in lung cancer treatment.

The new triazole compounds derived from the parent flufenamic acid (FLU) were synthesized by a conventional method. The molecular-docking study of the synthesized compounds(s) against EGFR kinase revealed that such compounds occupied the critical site of EGFR kinase pocket with good positioning. Compound 8 exhibited cytotoxic activity against MCF-7 breast cancer cells (GI50 0.78 µM), and not against A549 lung cancer cells or normal cells, and this toxic effect was due to induction of the intrinsic apoptotic pathway. Moreover compound 8 showed an inhibitory effect against EGFR kinase. Novel compounds were synthesized and confirmed by spectroscopic analysis, including AT-IR, 1HNMRS and CHNS. Compound 8 apoptosis induction was evident by fragmented nuclei after DAPI staining and smeared DNA by agarose gel electrophoresis. Additionally, treating MCF-7 cells with compound 8 resulted in an increment in the level of caspase 9 mRNA level, and its activation. Moreover, compound 8-treated MCF-7 cells showed enhanced cytochrome-c release from the mitochondria to cytosol indicating an induction for the intrinsic apoptotic pathway. Finally, compound 8 showed comparable EGFR kinase inhibitory activity (3.4 µM) to erlotinib (1.22 µM), which was matched by the molecular docking studies that showed that the target compounds may be considered as potential inhibitors of EGFR kinase.

New derivatives (4A-4D) were designed and synthesized from, picolinic acid (PA). The newly synthesized compounds were confirmed by ATR-FTIR, 1HNMRS, 13CNMR and CHNS analysis. The molecular docking methodology of (4A-4D) against EGFR kinase revealed that certain compounds occupied the vital site of EGFR kinase pocket and with a good fit. By employing the MTT assay, it was found that. compound 4C has anti-tumor activity against MCF-7 breast cancer cell line (GI50 = 86.8 µg/mL), but not against the A549 lung cancer cell line or normal cells (MCF10A and WBC). Compound 4C caused MCF-7 cell death by apoptosis as visualized by fragmented nuclei and smeared genomic DNA. Furthermore, compound 4C increased caspase 9 mRNA levels and caused its activation. Additionally, compound 4C-treated MCF-7 cells showed enhanced cytochrome -c- release from a mitochondria to the cytosol, reflecting the initiation of the intrinsic apoptotic pathway. Finally, compound 4C exhibited EGFR kinase inhibitory activity (7.15 µM) which was supported by the molecular docking studies that showed compound 4C might be considered as a potential inhibitor of EGFR kinase.

Background According to the 2015 report of the Joint United Nations Program on Human Immunodeficiency Virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS), the prevalence rates of HIV infection among men who have sex with men (MSM) varied from 6 to 37% depending on the country, far exceeding the national prevalence rates. The present study on HIV infection among men who have sex with men in sub-Saharan Africa was conducted to describe the different sampling methods used to identify this target population and compare the prevalence rates of HIV infection among MSM to that of men in the general population. Methods The selection of studies to be included was carried out in the principal electronic databases. The 2009 Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) directives were used throughout the entire process. Bias evaluation was performed using the Mixed Methods Appraisal Tool. For each country, HIV prevalence values in both groups were calculated. A prevalence ratio was also calculated to compare the prevalence rates of the two groups. Results Seventeen articles were selected. Most of the studies (82.35%) used the Respondent-Driven Sampling method. The average prevalence rate was 17.81% (range: 3.7–33.46) for MSM and 6.15% (range: 0.5–19.7) for men in the general population. Overall, the human HIV prevalence rate was 4.94 times higher among MSM than among men in the general population (95%CI: 2.91–8.37). The western and central regions of Africa, as well as low-prevalence countries (prevalence Conclusion MSM are at higher risk of HIV infection than men in the general population. The prevalence ratios are particularly elevated in West and Central Africa as well as in low-prevalence countries. Close monitoring of the situation, research and preventive measures are essential to control the epidemic amongst MSM.

Du sport sans artifice au sport bionique... Amélioration ou condamnation ? Le sport est aujourd'hui visité par les techniques d'amélioration des capacités humaines. Celles-ci permettent d'accroître ou de restaurer efficacement les capacités de l'être humain. Des innovations spectaculaires sont enregistrées dans des secteurs comme les nanotechnologies, les biotechnologies, les sciences cognitives, l'informatique, etc. Leur introduction dans le domaine du sport, du haut niveau à la pratique de masse ou de loisir, chez les athlètes valides ou handicapés, perturbe souvent les certitudes et suscite prises de position, interrogations et inquiétudes. D'un côté amélioration dans l'accompagnement des sportifs d'excellence ou libération des sportifs handicapés, de l'autre condamnation de la culture sportive séculaire et aliénation progressive des sportifs ? Relativisme des normes et des valeurs du sport face aux avancées technologiques ? Progrès ou régression dans la quête humaniste ? Autant de questions qui méritent d'être abordées et traitées. D'ailleurs, à ce jour, existe-t-il des instances régulatrices suffisamment armées pour appréhender ces problèmes ? La 31ème Université Sportive d'Été a été accueillie à Montpellier, dans un lieu prestigieux et de circonstance : Pierresvives, au sein de la « Cité des savoirs et du Sport pour tous », du 4 au 6 septembre 2013, avec le soutien du Montpellier Université Club. Organisée par l'UNCU et l'UJSF, elle s'est attelée à la tâche en donnant la parole à une quinzaine de personnalités issues de la recherche universitaire, fondamentale ou appliquée, des sciences de l'homme et de la société, du journalisme, des sciences et des techniques de l'ingénieur, du sport et de l'éducation, faisant face à un public des plus motivés.

Photo 1 – L’accueil de l’USE. De gauche à droite Christian Bénézis, Colette Andrusyszyn et Thierry Buffalon. Photo 2 – Séance d’ouverture. De gauche à droite : Daniel Bonzoms, Colette Andrusyszyn et Jean-Paul Callède. Photo 3 – Le Professeur Michel Audran. Photo 4 – Le Professeur Bernard Andrieu. Photo 5 – Table ronde. De gauche à droite : Sylvain Paillette, Anne Marcellini, Christian Montaignac, Olivier Coste et Jean-Paul Callède. Photo 6 – Un public très attentif. « J’ai rendez-vous av...

Additional file 3. Data collection guide.

Aberrant activation of caspase-6 (C6) in the absence of other hallmarks of apoptosis has been demonstrated in cells and tissues from patients with Huntington disease (HD) and animal models. C6 activity correlates with disease progression in patients with HD and the cleavage of mutant huntingtin (mHTT) protein is thought to strongly contribute to disease pathogenesis. Here we show that the mHTT1-586 fragment generated by C6 cleavage interacts with the zymogen form of the enzyme, stabilizing a conformation that contains an active site and is prone to full activation. This shift toward enhanced activity can be prevented by a small-molecule inhibitor that blocks the interaction between C6 and mHTT1-586. Molecular docking studies suggest that the inhibitor binds an allosteric site in the C6 zymogen. The interaction of mHTT1-586 with C6 may therefore promote a self-reinforcing, feedforward cycle of C6 zymogen activation and mHTT cleavage driving HD pathogenesis.