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2.
Int J Prev Med ; 11: 97, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-33042494

RESUMEN

The world is combating a common and invisible enemy severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), a highly transmissible virus responsible for serious respiratory illness coronavirus disease-2019 (COVID-19). As with all respiratory viruses, public health measures are focused on contact tracing, isolation, and treatment of affected individuals, who have respiratory symptoms. However, it is spreading efficiently, and it can be explained from its stealth transmission from presymptomatic and asymptomatic individuals. Droplet and contact precautions are followed universally. Healthcare workers are at higher risk of acquiring infection and they are additionally required to follow airborne and eye protection. Recent studies indicate viral particles can be isolated from many body fluids including feces, saliva, semen, and tears, suggesting transmission could be possibly occurring through some of these routes as well. We have done an evidence-based review of all potential modes of transmission and discussed preventive measures to stop the spread. There is an urgent need for educating the healthcare professionals, governments, and public regarding other potential modes of transmission. Strict preventive measures need to be used to stop the spread.

3.
Am J Ther ; 27(4): e400-e402, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32366740

RESUMEN

Ibuprofen is an over-the-counter medication that is used widely for the treatment of pain and fever during COVID-19 pandemic. A concern was raised regarding the safety of ibuprofen use because of its role in increasing ACE2 levels within the Renin-Angiotensin-Aldosterone system. ACE2 is the coreceptor for the entry of SARS-CoV-2 into cells, and so, a potential increased risk of contracting COVID-19 disease and/or worsening of COVID-19 infection was feared with ibuprofen use. However, available data from limited studies show administration of recombinant ACE2 improves lung damage caused by respiratory viruses, suggesting ibuprofen use may be beneficial in COVID-19 disease. At this time, there is no supporting evidence to discourage the use of ibuprofen.


Asunto(s)
Antiinflamatorios no Esteroideos/efectos adversos , Infecciones por Coronavirus/complicaciones , Ibuprofeno/efectos adversos , Neumonía Viral/complicaciones , Enzima Convertidora de Angiotensina 2 , Inhibidores de la Enzima Convertidora de Angiotensina/uso terapéutico , Animales , Antiinflamatorios no Esteroideos/uso terapéutico , Betacoronavirus , COVID-19 , Infecciones por Coronavirus/tratamiento farmacológico , Medicina Basada en la Evidencia , Humanos , Ibuprofeno/uso terapéutico , Pulmón/efectos de los fármacos , Pandemias , Peptidil-Dipeptidasa A/biosíntesis , Neumonía Viral/tratamiento farmacológico , Receptores Virales/efectos de los fármacos , Sistema Renina-Angiotensina/efectos de los fármacos , SARS-CoV-2
4.
Mol Genet Metab ; 110(3): 319-28, 2013 Nov.
Artículo en Inglés | MEDLINE | ID: mdl-23856419

RESUMEN

Mucopolysaccharidosis VII (MPS VII) is due to the deficient activity of ß-glucuronidase (GUSB) and results in the accumulation of glycosaminoglycans (GAGs) in lysosomes and multisystemic disease with cardiovascular manifestations. The goal here was to determine the pathogenesis of mitral valve (MV) disease in MPS VII dogs. Untreated MPS VII dogs had a marked reduction in the histochemical signal for structurally-intact collagen in the MV at 6 months of age, when mitral regurgitation had developed. Electron microscopy demonstrated that collagen fibrils were of normal diameter, but failed to align into large parallel arrays. mRNA analysis demonstrated a modest reduction in the expression of genes that encode collagen or collagen-associated proteins such as the proteoglycan decorin which helps collagen fibrils assemble, and a marked increase for genes that encode proteases such as cathepsins. Indeed, enzyme activity for cathepsin B (CtsB) was 19-fold normal. MPS VII dogs that received neonatal intravenous injection of a gamma retroviral vector had an improved signal for structurally-intact collagen, and reduced CtsB activity relative to that seen in untreated MPS VII dogs. We conclude that MR in untreated MPS VII dogs was likely due to abnormalities in MV collagen structure. This could be due to upregulation of enzymes that degrade collagen or collagen-associated proteins, to the accumulation of GAGs that compete with proteoglycans such as decorin for binding to collagen, or to other causes. Further delineation of the etiology of abnormal collagen structure may lead to treatments that improve biomechanical properties of the MV and other tissues.


Asunto(s)
Enfermedades de las Válvulas Cardíacas/etiología , Válvula Mitral/patología , Mucopolisacaridosis VII/complicaciones , Animales , Cuerdas Tendinosas/metabolismo , Colágeno/metabolismo , Perros , Matriz Extracelular/genética , Matriz Extracelular/metabolismo , Femenino , Glicosaminoglicanos/metabolismo , Enfermedades de las Válvulas Cardíacas/metabolismo , Masculino , Válvula Mitral/metabolismo , Mucopolisacaridosis VII/metabolismo , Péptido Hidrolasas/genética , Péptido Hidrolasas/metabolismo , Transducción de Señal
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