OBJECTIVE: To assess the predictors and outcomes of acute kidney injury (AKI) among patients with coronavirus disease 2019 (COVID-19). OBJECTIVE: This retrospective observational study was conducted among patients with a confirmed diagnosis of COVID-19 admitted to Hankou Hospital between January, 5 and March 8, 2020. We evaluated the association of AKI with the demographic and biochemical parameters and clinical outcomes of the patients using univariate regression analysis. OBJECTIVE: Atotal of 287 COVID-19 patients, including 55 with AKI and 232 without AKI, were included in the analysis. Compared with the patients without AKI, the patients with AKI were older, predominantly male, and were more likely to have hypoxia and pre-existing hypertension and cerebrovascular diseases. The patients with AKI also had higher levels of white blood cells, D-dimer, aspartate aminotransferase, total bilirubin, creatine kinase, lactate dehydrogenase, procalcitonin, C-reactive protein, a higher prevalence of hyperkalemia, lower lymphocyte counts, and higher chest computed tomographic scores. The incidence of stage 1 AKI was 14.3% and that of stage 2 or 3 AKI was 4.9%. The patients with AKI had much higher mortality rate than those without AKI. OBJECTIVE AKI is an important complication of COVID-19. An older age, a male gender, multiple pre- existing comorbidities, lymphopenia, increased infection indicators, elevated D-dimer, and impaired heart and liver functions are all potential risk factors ofAKI. COVID- 19 patients with AKI that progresses into stages 2 or 3 AKI have a high mortality rate. Prevention of AKI and monitoring kidney function is critical in the care of COVID-19 patients.
Acute Kidney Injury/epidemiology* ; Aged ; COVID-19 ; China/epidemiology* ; Humans ; Male ; Retrospective Studies ; SARS-CoV-2

[ ABSTRACT] Myosin light chain kinase ( MLCK) activates the regulatory light chain of myosin II, and the phos-phorylated myosin light chain leads to actomyosin contractile activity, as well as the cell contraction and increasing intercel-lular gap, which finally results in endothelial barrier dysfunction.MLCK-dependent hyperpermeability occurs in response to multiple cell signaling molecules and signaling pathways, including Ca2+, Src, PKC, NO, cGMP and mitogen activated protein kinases ( MAPK) .In this review, different mechanisms of endothelial hyperpermeability mediated by MLCK are discussed.

Objective To investigate lipopolysaccharide (LPS)-induced changes of cytoskeletal filamentous actin in primary isolated pulmonary microvascular endothelial cells (PMVECs) from wild-type and RAGE knock-out mouse. Methods The lungs of wild-type and RAGE knock-out mice were digested with collagenase type I to obtain endothelial cells purified by anti-CD31-coupled magnetic beads. The PMVEC identified by factor VIII labeling were stimulated with LPS at different concentrations and the changes of filamentous actin were observed by confocal microscopy. Results The cultured primary cells showed typical endothelial cell phenotype as examined with factor VIII labeling. LPS stimulation caused rearrangement of the cytoskeletal filament F-actin in wild-type mouse PMVECs with stress fiber formation, but such changes were not obvious in RAGE knock-out mouse PMVECs. Conclusion Mouse PMVECs of a high purity can be obtained by immune magnetic beads. RAGE is involved in LPS-induced destruction of mouse PMVEC cytoskeletons.

Objective To investigate lipopolysaccharide (LPS)-induced changes of cytoskeletal filamentous actin in primary isolated pulmonary microvascular endothelial cells (PMVECs) from wild-type and RAGE knock-out mouse. Methods The lungs of wild-type and RAGE knock-out mice were digested with collagenase type I to obtain endothelial cells purified by anti-CD31-coupled magnetic beads. The PMVEC identified by factor VIII labeling were stimulated with LPS at different concentrations and the changes of filamentous actin were observed by confocal microscopy. Results The cultured primary cells showed typical endothelial cell phenotype as examined with factor VIII labeling. LPS stimulation caused rearrangement of the cytoskeletal filament F-actin in wild-type mouse PMVECs with stress fiber formation, but such changes were not obvious in RAGE knock-out mouse PMVECs. Conclusion Mouse PMVECs of a high purity can be obtained by immune magnetic beads. RAGE is involved in LPS-induced destruction of mouse PMVEC cytoskeletons.

Objective To explore the effects of leukoaraiosis on cognitive function in elderly patients after acute cerebral infarction.Methods From May 2010 to August 2011,a total of 147 elderly patients with acute cerebral infarction were enrolled,including 96 patients with leukoaraiosis and 51 patients without leukoaraiosis.The Montreal Cognitive Assessment (MOCA) and the correlative factors of cognitive function were assessed in all patients.Results There was no statistical difference in general information between patients with and without leukoaraiosis.There were significant differences in the MoCA scores between patients with and without leukoaraiosis (x2 =19.15,P＜0.01),as well as between the vital and non-vital positions of cerebral infarction (x2=21.41,P＜0.01).The Logistic regression analysis showed that the vital position of infarction and leukoaraiosis were related to the cognitive impairment (OR=12.27,6.60,both P＜0.01),while the area of infarction and the type of cerebral infarction in Oxford County Community Stroke Project (OCSP) had no effects on cognitive impairment.Pearson correlation analysis showed that there was a positive relationship between the degree of white matter lesions and the decline in cognitive function (r=-0.87,P＜0.01).Conclusions The position of acute cerebral infarction and leukoaraiosis are independent risk factors for cognitive function after acute cerebral infarction,and the former plays a more important role than does the latter.

OBJECTIVETo investigate the role of Fas pathway in H(2)O(2)-induced apoptosis of L02 human hepatocytes and the effect of schisandrin B on Fas pathway.

METHODSReal-time quantitative PCR was used to detect the expressions of FAS, fas associated death domain protein (FADD) and caspase-8 mRNA in L02 cells exposed to H(2)O(2). Flow cytometry was employed to assess the cell apoptosis. ELISA, Western blotting and spectrophotometric assay were performed to determine the expressions of FAS protein, FADD protein and caspase-8 activity.

RESULTSWithin the dose range of 5-15 mol/L, schisandrin B dose-dependently inhibited FAS and FADD expressions and caspase-8 activation.

CONCLUSIONSchisandrin B can partially inhibit H(2)O(2)-induced L02 cell apoptosis possibly by affecting the FAS-FADD-caspase-8 pathway.

Apoptosis ; drug effects ; Caspase 8 ; metabolism ; Cell Line ; Cyclooctanes ; pharmacology ; Fas-Associated Death Domain Protein ; metabolism ; Flow Cytometry ; Hepatocytes ; drug effects ; metabolism ; Humans ; Hydrogen Peroxide ; adverse effects ; Lignans ; pharmacology ; Polycyclic Compounds ; pharmacology ; Signal Transduction ; fas Receptor ; metabolism

The effects of advanced glycation end products(AGE)on phosphorylation of ezrin/radixin/ moesin(ERM)protein in human umbilical vein endothelial ceils were detected by immunofluorescence cytochemistry and its mechanism was explored.AGE stimulated the phosphorylation of ERM protein in dose-and time-dependent manners(all P<0.05),which was involved in AGE receptor,Rho kinase,and p38 mitogen-activated protein kinase pathways.

In recent years, researchers have made some breakthroughs on human embryonic stem cells, in particular, on reprogramming differentiated cell (such as human skin fibroblast) into human embryonic stem cell. Induced pluripotent stem cells could be generated from human skin fibroblasts by inducting into four transcription factors known as OCT3/4, SOX2, C-MYC and KLF4. This approach enables better understanding the pathogenesis of diseases from the perspective of genetic component and promising in the treatment of related diseases. This article introduces the latest advancement of those researches.

Objective To gain a higher quality of pathophysiology experiment teaching of students studying abroad.Methods To improve greatly in knowing the characteristics of students studying abroad,preparation before class, teaching method and effect judgement.Results We have a conspicuous improvement in the quality and effect of pathophysiology experiment teaching. Conclusions To gain a higher quality of pathophysiology experiment teaching of students studying abroad,we should improve greatly in knowing the characteristics of students studying abroad,preparation before class,teaching method and effect judgement.

Objective To study the role of P38 mitogen-activated protein kinase(P38 MAPK) activation in high level glucose-induced microvascular hyperpermeability.Methods Rats were induced to diabetis by intraperitoneal injection of streptozotocin(STZ).The rats were divided into 5 groups,including normal,diabetes,control,MKK6b(A) and MKK6b(E) groups.The permeability coefficient to albumin(Pa) was measured in venules of in vivo mesenterium using a fluorescence ratio technique;Morphological changes of microvascular endothelial cell were monitored by observing fluorescence of F-actin stained with rhodamine-phalloidin.Results The permeability of diabetic rats was obviously increased.The activation of P38 MAPK by MKK6b(E) could increase microvascular permeability in normal rats,and the inhibition of P38 MAPK by MKK6b(A) could inhibit hyperpermeability of diabetic rats.Conclusion The activation of P38 MAPK induced by hyperglycemia may play a role in diabetic microvascular hyperpermeability.