Prevalence of intimate partner violence against women in Republic of Benin

The present study was conducted to estimate the prevalence of intimate partner violence against women (IPVAW) of reproductive age in Benin and to assess the factors related to the experience of IPVAW and attitude towards wife beating among women. The study also assessed whether a family history of violence is a risk factor for experiencing IPVAW. The study used the Benin Demographic and Health Survey 2017-18 data for analyses. A national representative sample of 4488 ever married women was selected to respond to a domestic violence and abuse questionnaire. Cross-tabulation and multivariate logistic regression analyses were performed. The prevalence of IPVAW experience in Benin was as follows: emotional violence, 35.4%; physical violence, 18.4%; and sexual violence, 8.2%. Older age, rural residence, the practice of Vodoun religion, living in a household headed by a male member, family history of domestic violence, and attitudes towards wife beating were significantly associated with the prevalence of IPVAW. Thirty-two percent of women supported wife beating. Women residing in urban areas, having higher educational qualification, higher socioeconomic status, and no family history of domestic violence were less likely to support wife beating. Policymakers should place emphasis on evidence-based prevention programs, gender equality, women empowerment, and policy priority for curbing IPVAW

The modulation of hypoxia-inducible factor-1α/plasminogen activator inhibitor-1 axis in human gingival fibroblasts stimulated with cyclosporine A

Background/PurposeThe prominent side effect of the immunosuppressive drug cyclosporine A (CsA) is gingival overgrowth. Hypoxia-inducible factor (HIF)-1α regulates a wide variety of profibrogenic genes, which are closely associated with tissue fibrosis. The aim of this study was to compare HIF-1α expression in normal gingival tissues and CsA-induced gingival overgrowth specimens and further explore the potential mechanisms that may lead to induction of HIF-1α expression.MethodsFifteen CsA-induced gingival overgrowth specimens and five normal gingival tissues were examined by immunohistochemistry. Western blot was used to investigate the effects of CsA on the expression of HIF-1α in cultured human gingival fibroblasts. The effects of CsA on plasminogen activator inhibitor (PAI)-1 expression were evaluated in environmental hypoxia.ResultsHIF-1α staining in gingival tissue was stronger in CsA-induced gingival overgrowth group than normal gingival group (p < 0.05). The expression of HIF-1α was significantly higher in CsA-induced gingival overgrowth specimens with higher levels of inflammatory infiltrates (p = 0.041). CsA was found to upregulate HIF-1α protein in a dose-dependent manner (p < 0.05). Hypoxia increased CsA-induced PAI-1 protein expression than normoxic conditions (p < 0.05).ConclusionThese results suggest that HIF-1α expression is significantly upregulated in CsA-induced gingival overgrowth specimens. The activation of HIF-1α may promote fibrogenesis by an increase of PAI-1 expression and a subsequent elevation of extracellular matrix production in gingival tissues

The SPEAR Instrument and On-Orbit Performance

The SPEAR (or 'FIMS') instrumentation has been used to conduct the first large-scale spectral mapping of diffuse cosmic far ultraviolet (FUV, 900-1750 AA) emission, including important diagnostics of interstellar hot (10^4 K - 10^6 K) and photoionized plasmas, H_2, and dust scattered starlight. The instrumentation's performance has allowed for the unprecedented detection of astrophysical diffuse far UV emission lines. A spectral resolution of 550 and an imaging resolution of 5' is achieved on-orbit in the Short (900 - 1175 AA) and Long (1335 - 1750 AA) bandpass channels within their respective 7.4 deg x 4.3' and 4.0 deg x 4.6' fields of view. We describe the SPEAR imaging spectrographs, their performance, and the nature and handling of their data

Effect of proton pump inhibitors on sympathetic hyperinnervation in infarcted rats: Role of magnesium.

The long-term use of proton pump inhibitors (PPIs) has been shown to increase the risk of cardiovascular mortality, however the molecular mechanisms are unknown. Superoxide has been implicated in the regulation of nerve growth factor (NGF), a mediator of sympathetic innervation. The purpose of this study was to determine whether PPIs increase ventricular arrhythmias through magnesium-mediated superoxide production in infarcted rats. Male Wistar rats were randomly assigned to receive vehicle, omeprazole, omeprazole + magnesium sulfate, or famotidine treatment for 4 weeks starting 24 hours after the induction of myocardial infarction by ligating the coronary artery. Increased myocardial superoxide and nitrotyrosine levels were noted post-infarction, in addition to a significant upregulation of NGF expression on mRNA and protein levels. Sympathetic hyperinnervation after infarction was confirmed by measuring myocardial norepinephrine and immunofluorescent analysis. Compared with the vehicle, omeprazole-treated infarcted rats had significantly reduced myocardial magnesium content, increased oxidant production, and increased sympathetic innervation, which in turn increased ventricular arrhythmias. These effects were prevented by the coadministration of magnesium sulfate. In an in vivo study, an omeprazole-induced increase in NGF was associated with a superoxide pathway, which was further confirmed by an ex vivo study showing the attenuation of NGF levels after coadministration of the superoxide scavenger Tiron. Magnesium sulfate did not further attenuate NGF levels compared with omeprazole + Tiron. Our results indicate that the long-term administration of PPIs was associated with reduced tissue magnesium content and increased myocardial superoxide production, which exacerbated ventricular arrhythmias after infarction. Magnesium may be a potential target for PPI-related arrhythmias after infarction

Both PKA and Epac pathways mediate N-acetylcysteine-induced Connexin43 preservation in rats with myocardial infarction.

Cardiac remodeling was shown to be associated with reduced gap junction expression after myocardial infarction. A reduction in gap junctional proteins between myocytes may trigger ventricular arrhythmia. Therefore, we investigated whether N-acetylcysteine exerted antiarrhythmic effect by preserving connexin43 expression in postinfarcted rats, focusing on cAMP downstream molecules such as protein kinase A (PKA) and exchange protein directly activated by cAMP (Epac). Male Wistar rats after ligating coronary artery were randomized to either vehicle, or N-acetylcysteine for 4 weeks starting 24 hours after operation. Infarct size was similar between two groups. Compared with vehicle, cAMP levels were increased by N-acetylcysteine treatment after infarction. Myocardial connexin43 expression was significantly decreased in vehicle-treated infarcted rats compared with sham operated rats. Attenuated connexin43 expression and function were blunted after administering N-acetylcysteine, assessed by immunofluorescent analysis, dye coupling, Western blotting, and real-time quantitative RT-PCR of connexin43. Arrhythmic scores during programmed stimulation in the N-acetylcysteine-treated rats were significantly lower than those treated with vehicle. In an ex vivo study, enhanced connexin43 levels afforded by N-acetylcysteine were partially blocked by either H-89 (a PKA inhibitor) or brefeldin A (an Epac-signaling inhibitor) and completely blocked when H-89 and brefeldin A were given in combination. Addition of either the PKA specific activator N6Bz or Epac specific activator 8-CPT did not have additional increased connexin43 levels compared with rats treated with lithium chloride alone. These findings suggest that N-acetylcysteine protects ventricular arrhythmias by attenuating reduced connexin43 expression and function via both PKA- and Epac-dependent pathways, which converge through the inactivation of glycogen synthase kinase-3β

cAMP-regulated PKA and Epac augment NAC-induced Cx43 levels in Experiment 2.

<p>In a rat isolated heart model, effect of PKA and Epac was assessed on gap junctional communication and Western blot using antibody against Cx43 and GSK-3β. Significantly decreased Cx43 amount, P1/P0 ratio, and gap junctional communication are noted in the groups treated with SQ-22536, H-89 and brefeldin A compared with NAC alone. Compared with vehicle (Veh), NAC administration showed significantly decreased p-GSK-3β, which can be partially reversed after adding either H-89 or brefeldin A. SQ-22536 significantly reduced augmentation of NAC-induced Cx43 levels to a much greater extent than either H-89 or brefeldin A alone. Relative abundance was obtained by normalizing the density of Cx43 protein against that of β-actin. Each point is an average of 3 separate experiments (n = 10 per group). LY, Lucifer yellow; P0, nonphosphorylated Cx43; P1, phosphorylated Cx43; RD, rhodamine-conjugated dextran. *p<0.05 compared with groups treated with vehicle, NAC+SQ-22536, NAC+H-89, NAC+brefeldin A, and NAC+H-89+brefeldin A; †p<0.05 compared with groups treated with vehicle, NAC+SQ-22536, and NAC+H-89+brefeldin A.</p

Western blot analysis of Cx43 and GSK-3β.

<p>Ventricular remodeling after MI was associated with marked decreased amount of phosphorylated Cx43 (P1). Significantly increased Cx43 amount and P1/P0 ratio had taken place in the NAC-treated group compared with vehicle (Veh). However, a significantly decreased p-GSK-3β is noted in the NAC-treated group compared with vehicle. Relative abundance was obtained by normalizing the density of Cx43 protein against that of β-actin. Densitometric quantification of phosphorylation levels was expressed as the ratio of the density of phosphorylated band over total GSK-3β. Each point is an average of 3 separate experiments. P0, nonphosphorylated Cx43; P1, phosphorylated Cx43. *p<0.05 compared with sham and NAC-treated group; †p<0.05 compared with sham.</p