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1.
Eur Rev Med Pharmacol Sci ; 24(8): 4597-4606, 2020 04.
Artículo en Inglés | MEDLINE | ID: mdl-32374000

RESUMEN

The last two decades have witnessed two large-scale pandemics caused by coronaviruses, including severe acute respiratory syndrome (SARS) and the Middle East respiratory syndrome (MERS). At the end of 2019, another novel coronavirus, designated as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), hit Wuhan, a city in the center of China, and subsequently spread rapidly to the whole world. Latest reports revealed that more than 800 thousand people in over 200 countries are involved in the epidemic disease by SARS-CoV-2. Due to the high mortality rate and the lack of optimum therapeutics, it is crucial to understand the biological characteristics of the virus and its possible pathogenesis to respond to the SARS-CoV-2. Rapid diagnostics and effective therapeutics are also important interventions for the management of infection control. However, the rapid evolution of SARS-CoV-2 exerted tremendous challenges on its diagnostics and therapeutics. Therefore, there is an urgent need to summarize the existing research results to guide decision-making on the prioritization of resources for research and development. In this review, we focus on our current understanding of epidemiology, pathogenesis, diagnostics and therapeutics of coronavirus disease 2019 (COVID-19).


Asunto(s)
Betacoronavirus/patogenicidad , Infecciones por Coronavirus , Pandemias , Neumonía Viral , Enzima Convertidora de Angiotensina 2 , COVID-19 , Infecciones por Coronavirus/diagnóstico , Infecciones por Coronavirus/epidemiología , Infecciones por Coronavirus/patología , Infecciones por Coronavirus/terapia , Humanos , Peptidil-Dipeptidasa A/química , Neumonía Viral/diagnóstico , Neumonía Viral/epidemiología , Neumonía Viral/patología , Neumonía Viral/terapia , Juego de Reactivos para Diagnóstico , SARS-CoV-2
2.
Iran J Vet Res ; 18(4): 282-286, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-29387103

RESUMEN

The microanatomy of the intestinal epithelium in the Chinese soft-shelled turtle (CST) was studied by light and transmission electron microscopy (TEM). The small intestinal epithelium (SIE) was single layered or pseudostratified. The enterocytes contained mitochondria or mitochondria and lipid droplets. The enterocytes were arranged tightly in the apical parts of epithelium and connected by desmosomes and interdigitations. The large intestinal epithelium (LIE) was pseudostratified and the enterocytes did not contain lipid droplets. Enterocytes were arranged compactly in the apical part, forming spaces in the middle and basal parts of epithelium. Numerous mucous cells were scattered in the epithelium and there were intraepithelial lymphocytes (IELs) with their pseudopodia extended into the intestinal lumen. This study provides detailed features of intestinal epithelium in the Pelodiscus sinensis that could be related to function. In addition, these findings are discussed in relation to other vertebrates.

3.
Neuroscience ; 184: 54-63, 2011 Jun 16.
Artículo en Inglés | MEDLINE | ID: mdl-21463664

RESUMEN

Previous data demonstrate that traumatic brain injury (TBI) activates autophagy, and increases microtubule-associated protein 1 light chain 3 (LC3) immunostaining mainly in neurons. However, the role of autophagy in traumatic brain damage remains elusive. The aim of the present study was to investigate the autophagic mechanisms participating in traumatic brain injury. The autophagy inhibitors 3-methyladenine (3-MA) and bafliomycin A1 (BFA) were administered with a single i.c.v. injection before TBI. We first examined the protein levels of Beclin-1 and LC3 II, which have been found to promote autophagy previously. Immunoblotting analysis showed that 3-MA pretreatment reduced post-TBI Beclin-1 and LC3-II levels, and maintained p62/SQSTM1 (p62) levels. In addition, double immunolabeling showed that the increased punctate LC3-II dots colocalizing with Propidium Iodide (PI)-stained nuclei at 24 h after injury, were partially inhibited by 3-MA pretreatment. Furthermore, inhibition of autophagy could reduce TBI-induced cell injury assessed with i.p. injection of PI and lesion volume, and attenuate behavioral outcome evaluated by motor test and Morris water maze. The neuroprotective effects were associated with an inhibition on TBI-induced up-regulation of LC3, Beclin-1, cathepsin B, caspase-3 and the Beclin-1/Bcl-2 ratio. Taken together, these data imply that the autophagy pathway is involved in the pathophysiologic responses after TBI, and inhibition of this pathway may help attenuate traumatic damage and functional outcome deficits.


Asunto(s)
Autofagia/fisiología , Lesiones Encefálicas/fisiopatología , Muerte Celular/fisiología , Aprendizaje por Laberinto/fisiología , Animales , Proteínas Reguladoras de la Apoptosis/metabolismo , Beclina-1 , Encéfalo/metabolismo , Encéfalo/patología , Encéfalo/fisiopatología , Lesiones Encefálicas/metabolismo , Lesiones Encefálicas/patología , Masculino , Ratones , Proteínas Asociadas a Microtúbulos/metabolismo , Neuronas/metabolismo , Neuronas/fisiología
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