Efficacy of Antidepressant Drugs for the Treatment of Covid-19

In adult populations (18-65), does the administration of antidepressants, compared to not administering antidepressants, reduce the severity of the Covid-19 infection? Current treatment protocols for Covid-19 virus are still new and needing improvement. Discovering a new pharmacologic approach has been on the forefront of medical research since the beginning of the pandemic. The purpose of this paper is analyzing the efficacy of antidepressant drugs for reducing morbidity and mortality associated with Covid-19 virus. A literature search was conducted using Cinahl, Google Scholar, and UMaine Nursing Reference Center. The search words included covid, covid-19, pandemic, coronavirus, antidepressants, and SSRI. The inclusion criteria were all adults, male and female aged 18-65. The exclusion criteria included all viruses other than Covid-19, patients under 18, and patients over 65. Our search included 10 articles. Studies found that the administration of antidepressants has the potential to decrease the severity of the Covid-19 infection and improve outcomes. Specific antidepressants including fluoxetine and fluvoxamine were shown to decrease mortality in patients with Covid. Other studies suggest venlafaxine, mirtazapine, paroxetine, and escitalopram limited the need for intubation in those with serious covid infections. Promising research has emerged in the past few years suggesting there may be a link between antidepressant use and decreased symptoms of Covid-19. Some even suggest the use of certain antidepressants can decrease the risk of contracting the virus. Because Covid-19 is a relatively new disease, more research is needed to truly determine the applications antidepressants could have on patients who have contracted the virus

Gay guys using gay language: Friendship, shared values and the intent-context-effect matrix

This article draws on in-depth interviews with 35 openly gay male undergraduates from four universities in England to develop an understanding of the changing nature of language related to homosexuality. In addition to finding a diminution in the prevalence of homophobic language, we demonstrate that participants maintain complex and nuanced understandings of phrases that do not use homophobic pejoratives, such as ‘that’s so gay’. The majority of participants rejected the notion that these phrases are inherently homophobic, instead arguing that the intent with which they are said and the context in which they are used are vital in understanding their meaning and effect. We conceptualize an intent-context-effect matrix to understand the interdependency of these variables. Highlighting the situated nature of this matrix, we also demonstrate the importance of the existence of shared norms between those saying and hearing the phrase when interpreting such language

Enterococcus faecalis Gelatinase Mediates Intestinal Permeability via Protease-Activated Receptor 2

Microbial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a dysbiotic enteric microbiota can lead to disease. This mechanism was investigated using the colitogenic, protease-secreting enteric microbe Enterococcus faecalis . Caco-2 and T-84 epithelial cell monolayers and the mouse colonic epithelium were exposed to concentrated conditioned media (CCM) from E. faecalis V583 and E. faecalis lacking the gelatinase gene ( gelE ). The flux of fluorescein isothiocyanate (FITC)-labeled dextran across monolayers or the mouse epithelium following exposure to CCM from parental or mutant E. faecalis strains indicated paracellular permeability. A protease-activated receptor 2 (PAR2) antagonist and PAR2-deficient (PAR2 −/− ) mice were used to investigate the role of this receptor in E. faecalis -induced permeability. Gelatinase (GelE) purified from E. faecalis V583 was used to confirm the ability of this protease to induce epithelial cell permeability and activate PAR2. The protease-mediated permeability of colonic epithelia from wild-type (WT) and PAR2 −/− mice by fecal supernatants from ulcerative colitis patients was assessed. Secreted E. faecalis proteins induced permeability in epithelial cell monolayers, which was reduced in the absence of gelE or by blocking PAR2 activity. Secreted E. faecalis proteins induced permeability in the colonic epithelia of WT mice that was absent in tissues from PAR2 −/− mice. Purified GelE confirmed the ability of this protease to induce epithelial cell permeability via PAR2 activation. Fecal supernatants from ulcerative colitis patients induced permeability in the colonic epithelia of WT mice that was reduced in tissues from PAR2 −/− mice. Our investigations demonstrate that GelE from E. faecalis can regulate enteric epithelial permeability via PAR2

Accumulative Extremism: The Post-war Tradition of Anglo-American Neo-Nazi and Anti-Semitic Networks of Support

This essay explores the development of a transnational, Anglo-American neo-Nazi culture from the end of the Second World War to the present day. It stresses that it was the unique friendship between Colin Jordan and George Lincoln Rockwell that fuelled this tradition of cooperation, and plots how their World Union of National Socialists developed a mutual understanding between British and American activists in the 1960s. This survey of an emergent, post-war ‘tradition’ of Anglo-American interaction also highlights how Holocaust denial brought together British and American activists, and the from the 1980s onwards, we see a more complex series of interchanges emerge, including Blood & Honour and Combat 18. The chapter concludes by examining how this ‘tradition’ is now reproduced by a variety of websites

Enterococcus faecalis Gelatinase Mediates Intestinal Permeability via Protease-Activated Receptor 2

Microbial protease-mediated disruption of the intestinal epithelium is a potential mechanism whereby a dysbiotic enteric microbiota can lead to disease. This mechanism was investigated using the colitogenic, protease-secreting enteric microbe Enterococcus faecalis. Caco-2 and T-84 epithelial cell monolayers and the mouse colonic epithelium were exposed to concentrated conditioned media (CCM) from E. faecalis V583 and E. faecalis lacking the gelatinase gene (gelE). The flux of fluorescein isothiocyanate (FITC)-labeled dextran across monolayers or the mouse epithelium following exposure to CCM from parental or mutant E. faecalis strains indicated paracellular permeability. A protease-activated receptor 2 (PAR2) antagonist and PAR2-deficient (PAR2(−/−)) mice were used to investigate the role of this receptor in E. faecalis-induced permeability. Gelatinase (GelE) purified from E. faecalis V583 was used to confirm the ability of this protease to induce epithelial cell permeability and activate PAR2. The protease-mediated permeability of colonic epithelia from wild-type (WT) and PAR2(−/−) mice by fecal supernatants from ulcerative colitis patients was assessed. Secreted E. faecalis proteins induced permeability in epithelial cell monolayers, which was reduced in the absence of gelE or by blocking PAR2 activity. Secreted E. faecalis proteins induced permeability in the colonic epithelia of WT mice that was absent in tissues from PAR2(−/−) mice. Purified GelE confirmed the ability of this protease to induce epithelial cell permeability via PAR2 activation. Fecal supernatants from ulcerative colitis patients induced permeability in the colonic epithelia of WT mice that was reduced in tissues from PAR2(−/−) mice. Our investigations demonstrate that GelE from E. faecalis can regulate enteric epithelial permeability via PAR2