Mosques in Japan responding to COVID-19 pandemic: Infection prevention and support provision

Religious activities tend to be conducted in enclosed, crowded, and close-contact settings, which have a high potential of transmitting the coronavirus disease, 2019 (COVID-19); therefore, religious communities are expected to take appropriate infection prevention measures. Meanwhile, during past disasters, religious communities have provided various types of support to affected people; hence, their role in disaster risk reduction has received much attention. In this study, we aimed to identify the infection prevention measures and support provision implemented by mosques—Islamic institutions managed and operated mainly by foreign Muslims living in Japan—during the one year from January 2020. We collected information from newspaper articles (18 articles on 19 mosques) and interviews with representatives of three mosques. We found that various infection control measures were implemented in mosques—refraining from mass prayers and closing buildings from an early stage (around February 2020); canceling large-scale events during the month of Ramadan; moving some activities online; and ensuring indoor ventilation and safe physical distance even when continuing face-to-face prayer activities. We also found that various types of support were provided by mosques—donating masks to the local government; listening to problems of people affected by COVID-19 regardless of their nationality; providing financial support to them; translating and disseminating information to foreign Muslims; and providing religious meals for them. This study provides actual examples of infection prevention measures taken by mosques in a Muslim-minority society and suggests that mosques appropriately responded to the needs of religious minorities during disasters, including COVID-19

744-3 Inhibition of Nitric Oxide Synthesis does not Increase Cardiac Contractile Response but Reduces Coronary Blood Flow Response to β-Adrenergic Stimulation in Normal Dogs

Although the induction of nitric oxide (NO) synthesis has been implicated as a cause of cytokine-induced depression of cardiac β-adrenergic responsiveness. whether the NO system constitutively present in the normal myocardium plays a role in its physiologic response to β-adrenergic stimulation in vivoremains controversial. Accordingly, we examined the effects of low and high doses of NW-nitro-L-arginine methyl ester (L-NAME)(10 and 100 μg/kg/min for 10 min), an NO synthase inhibitor, administered into left circumflex coronary artery (LCX) on responses of peak left ventricular (LV) dP/dt, regional wall thickening in LCX region and LCX blood flow to graded intracoronary (IC) doses of isoproterenol (ISO:0.002 to 0.016 μg/kg/min) in 7 anesthetized dogs. IC L-NAME was associated with dose-related reductions in IC acetylcholine-induced coronary vasodilation. Effects of L-NAME on ISO-induced changes are shown:baselineISO:0.0020.0040.008.0016Peak LV dP/dt (mmHg/sec) (n=7)control2029±1362586±1922820±2003309±2554120±419*low L-NAME2171±1492566±1762894±2063214±2233707±250*high L-NAME2114±1662326±1932560±1523014±1403354±171*Wall thickening (%) (n=2)control22±725±629±533±735±9low L-NAME25±1125±1528±1931±1836±21high L-NAME28±1725±1525±1531±1934±15LCX blood flow (ml/min)(n=7)control33±648±752±661±870±9*low L-NAME36±741±844±947±852±9*high L-NAME33±736±838±740±748±8*mean ± SEM*p<0.05Thus, inhibition of NO synthesis by L-NAME did not change baseline contractility nor did it increase its response to ISO. It also did not alter baseline blood flow, but reduced significantly its response to ISO. These data strongly suggest that the NO system in the normal myocardium does not modulate contractility, but NO formation in the vasculature contributes to the β-adrenergic coronary vasodilation

Myocardial ischemia and reperfusion: The role of oxygen radicals in tissue injury

Thrombolytic therapy has gained widespread acceplance as a means of treating coronary artery thrombosis in patients with acute myocardial infarction. Although experimental data have demonstrated that timely reperfusion limits the extent of infarction caused by regional ischemia, there is growing evidence that reperfusion is associated with an inflammatory response to ischemia that exacerbates the tissue injury. Ischemic myocardium releases archidonate and complement-derived chemotactic factors, e.g., leukotriene B 4 and C 5a , which attract and activate neutrophils. Reperfusion of ischemic myocardium accelerates the influx of neutrophils, which release reactive oxygen products, such as superoxide anion and hydrogen peroxide, resulting in the formation of a hydroxyl radical and hypochlorous acid. The latter two species may damage viable endothelial cells and myocytes via the peroxidation of lipids and oxidation of protein sulfhydryl groups, leading to perturbations of membrane permeability and enzyme function. Neutrophil depletion by antiserum and inhibition of neutrophil function by drugs, e.g., ibuprofen, prostaglandins (prostacyclin and PGE 1 ), or a monoclonal antibody, to the adherence-promoting glycoprotein Mo-1 receptor, have been shown to limit the extent of canine myocardial injury due to coronary artery occlusion/reperfusion. Recent studies have challenged the hypothesis that xanthine-oxidase-derived oxygen radicals are a cause of reperfusion injury. Treatment with allopurinol or oxypurinol may exert beneficial effects on ischemic myocardium that are unrelated to the inhibition of xanthine oxidase. Furthermore, the human heart may lack xanthine oxidase activity. Further basic research is needed, therefore, to clarify the importance of xanthine oxidase in the pathophysiology of reperfusion injury. Current data are highly suggestive of a deleterious role of the neutrophil in organ reperfusion and justify consideration of the clinical investigation of neutrophil inhibitors in patients receiving thrombolytic agents during the evolution of an acute myocardial infarction.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44595/1/10557_2004_Article_BF00133206.pd