Effects of normoxic and hypoxic exercise training on the bactericidal capacity and subsequent apoptosis of neutrophils in sedentary men.

Phagocytosis and oxidative burst are essential mechanisms of innate immunity by which neutrophils eliminate invading pathogens. Afterwards, phagocytic neutrophils are dissipated by facilitating apoptosis to control inflammation. This study investigates how exercise training with or without hypoxic exposure affects the bactericidal activity and subsequent apoptosis of neutrophils following strenuous exercise. A total of 60 healthy, sedentary men were randomly divided into four groups (n = 15 in each group), who were exposed to 21% O2 [normoxic control (NC)] or 15% O2 [hypoxic control (HC)] at rest or were trained at 50% of peak work rate at 21% O2 [normoxic training (NT)] or 15% O2 [hypoxic training (HT)] for 30 min/day, 5 days/week for 4 weeks. Before the intervention, acute strenuous exercise (SE) enhanced the phagocytosis of Escherichia coli (E. coli) by neutrophils and the release of neutrophil oxidant products in response to E. coli, accompanied by increases in the expression of adhesion molecules (CD62L, CD11b, and CD11a), an opsonic receptor (FcγIIIBR), and complement receptors (C1qRp and CD5aR) on neutrophils. Subsequently, the SE facilitated caspase-3 activation and phosphatidylserine exposure in E. coli-stimulated neutrophils. Furthermore, 4 weeks of HT promoted the expressions of adhesion molecules and opsonic/complement receptors on neutrophils, and it also augmented the bactericidal and apoptotic activities of neutrophils at rest or after SE. However, NT, HC, and NC did not influence these neutrophil-related immune responses to strenuous exercise. Therefore, we conclude that the HT regimen effectively promotes the bactericidal capacity of neutrophils, and facilitates their subsequent apoptosis both at rest and following SE.

Inhibition of PKC-Induced COX-2 and IL-8 Expression in Human Breast Cancer Cells by Glucosamine.

Breast cancer is a common cancer leading to many deaths among females. Cyclooxygenase-2 (COX-2) and interleukin-8 (IL-8) are two highly expressed inflammatory mediators to be induced by the protein kinase C (PKC) signaling via various inflammatory stimuli and both contribute significantly to cancer metastasis/progression. Glucosamine has been shown to act as an anti-inflammation molecule. The aim of this study was to clarify the role and acting mechanism of glucosamine during the PKC-regulation of COX-2/IL-8 expression and the associated impact on breast cancer. In MCF-7 breast cancer cells, glucosamine effectively suppresses the PKC induction of COX-2 and IL-8 promoter activity, mRNA and protein levels, as well as the production of prostaglandin E(2) (PGE(2)) and IL-8. Glucosamine is able to promote COX-2 protein degradation in a calpain-dependent manner and IL-8 protein degradation in calpain-dependent and proteasome-dependent manners. The MAPK and NF-κB pathways are involved in PKC-induced COX-2 expression, but only the NF-κB pathway is involved in PKC-induced IL-8 expression. Glucosamine attenuates PKC-mediated IκBα phosphorylation, nuclear NF-κB translocation, and NF-κB reporter activation. Both PGE(2) and IL-8 promote cell proliferation and IL-8 induces cell migration; thus, glucosamine appears to suppress PKC-induced cell proliferation and migration. Furthermore, glucosamine significantly inhibits the growth of breast cancer xenografts and this is accompanied by a reduction in COX-2 and IL-8 expression. In conclusion, glucosamine seems to attenuate the inflammatory response in vitro and in vivo and this occurs, at least in part by targeting to the NF-κB signaling pathway, resulting in an inhibition of breast cancer cell growth.

From indirect to direct contacts on Facebook: A big-data approach to the making of triadic network closure.

The rise of the Big Data paradigm has made it more feasible to track how personal networks evolve on social media, where auto-generated contact records and fine-grained temporal data sequences help capture how and when interpersonal ties and contacts change their roles. Using a sample of matched survey data and social media records, we investigated the mechanisms by which indirect contacts ("degree-2 alters") transform into direct contacts ("degree-1 alters") from a Facebook user's (ego's) point of view. To highlight the temporal sequences, we assigned different roles to the same alters depending on how each of them is connected with ego at different periods of time. Multilevel event history analyses pinpoint several online actions and network features of ego, degree-1 alters, and degree-2 alters, as the key factors that contribute to the transformation from indirect contacts into direct contacts.

L"essor du paradigme du Big Data a rendu plus réalisable le suivi de l"évolution des réseaux personnels sur les médias sociaux, où les enregistrements de contacts générés automatiquement et les séquences de données temporelles à grain fin permettent de saisir comment et quand les liens interpersonnels et les contacts changent de rôle. À l"aide d"un échantillon de données d"enquête et d"enregistrements de médias sociaux appariés, nous avons étudié les mécanismes par lesquels les contacts indirects ("altérations de degré 2″) se transforment en contacts directs ("altérations de degré 1″) du point de vue d"un utilisateur de Facebook (ego). Pour mettre en évidence les séquences temporelles, nous avons attribué des rôles différents aux mêmes alters en fonction de la façon dont chacun d"entre eux est connecté avec ego à différentes périodes de temps. Les analyses multiniveaux de l"historique des événements mettent en évidence plusieurs actions en ligne et caractéristiques du réseau d"ego, des alters de degré 1 et des alters de degré 2, comme étant les facteurs clés qui contribuent à la transformation des contacts indirects en contacts directs.