Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether infectious diseases might have contributed to the present-day decline of northern fur seals (Callorhinus ursinus), preweaned pups (n=2,735), subadult males (n=98), and adults (n=179) were examined postmortem from 1986 to 2006 on St. Paul Island, Alaska. Gross necropsy findings and histologic lesions were used to determine causes of death. Five general categories of mortality were identified for pups: emaciation (1,454 pups, 53%), trauma (497 pups, 18%), perinatal mortality (516 pups, 19%), infectious diseases (82 pups, 3%), and miscellaneous causes (186 pups, 7%). A condition of unknown etiology characterized by multifocal necrotizing myopathy and cardiomyopathy was found in 92 pups. Thirty-three congenital anomalies were identified in 49 pups, including a rare multicentric ganglioneuroblastoma. General linear models were used to examine change in pup mortality and condition (i.e., pup mass) over time. The prevalence of perinatal mortality appeared to increase during the study and relative to past reports. Trauma and infectious conditions appeared to decrease slightly from 1986 to 2006. Although relatively stable during this investigation, emaciation was greater than that reported for past studies. Emaciated pups weighed less than expected during 1988, 1996, and 2004 and more than expected during 1987, 1989, 1990, and 1994 (P</=0.003). Average annual weights for all other categories of mortality did not change significantly from 1986 to 2006. Fatal conditions for subadult males included hyperthermia, blunt trauma, entanglement, and bite wounds; nonfatal conditions included seizures, orange discoloration of the blubber, neoplasia, and parasitism. Causes of mortality for most adults included bite wounds with cellulitis and secondary infections, pulmonary edema, dystocia, blunt trauma, and neoplasia. We found no evidence to implicate infectious diseases as a cause in the recent decline of northern fur seals.
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PMID:Causes of mortality in northern fur seals (Callorhinus ursinus), St. Paul Island, Pribilof Islands, Alaska, 1986-2006. 2068 38

The high mortality of specific groups from COVID-19 highlights the importance of host-viral interactions and the potential benefits from enhancing host defenses. SARS-CoV-2 requires angiotensin converting enzyme (ACE)2 as a receptor for cell entry and infection. While both ACE inhibitors and spironolactone can upregulate tissue ACE2, there are important points of discrimination between these approaches. The virus requires proteolytic processing of its spike protein by transmembrane protease receptor serine type 2 (TMPRSS2) to enable binding to cellular ACE2. Since TMPRSS2 contains an androgen promoter, it may be downregulated by the antiandrogenic actions of spironolactone. Furin and plasmin also process the spike protein. They are inhibited by protease nexin 1 or serine E2 (PN1) that is upregulated by angiotensin II but downregulated by aldosterone. Therefore, spironolactone should selectively downregulate furin and plasmin. Furin also promotes pulmonary edema while plasmin promotes hemovascular dysfunction. Thus, a downregulation of furin and plasmin by PN1 could be a further benefit of MRAs beyond their well established organ protection. We review the evidence that spironolactone may be the preferred RASSi to increase PN1 and decrease TMPRSS2, furin and plasmin activities and thereby to reduce viral cell binding, entry, infectivity and bad outcomes. This hypothesis requires direct investigation.
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PMID:Is spironolactone the preferred renin-angiotensin-aldosterone inhibitor for protection against COVID-19? 3327 89