Preventive and therapeutic effect of N-Acetyl-L-cysteine on infection-associated preterm labor in mice

Objective: To study the preventive and therapeutic effect of N-Acetyl-L-cysteine on infection-associated preterm labor in mice. Methods: A total of 66 C57BL/6 inbred strain pregnant mice were selected and randomly divided into groups A, B and C, with 22 cases in each group. Group A, B and C were regarded as model group, prevention group and treatment group, respectively. The model of infection-associated preterm labor was built by intraperitoneal injection of Escherichia coli. Ten mice of each group were taken and observed the preterm birth rates and live birth rates, respectively. Three mice of each group were killed at 3 h, 6 h, 12 h and 24 h after building the model. Their uterus tissues were collected and the expressions of the AP-1 and MCP-1 in those tissues were assayed with immunohistochemical method and the expressions of NF- kappa Bp65 and TNF- protein in the placenta tissues of those mice were also detected with immunohistochemical method. Results: The pretem: birth rates of mice in groups B and C were significantly lower than that in group A, while their live birth rates were distinctly higher than that in group A (P<0.05); the expressions of the AP-1 and MCP-1 in the uterus tissues and NF- kappa Bp65 and TNF- protein in the placenta tissues of mice in groups B and C were evidently lower than those in group A (P<0.05); the comparison of the expressions of the NF- kappa Bp65 and TNF- between group B and C showed no statistical differences (P>0.05). Conclusions: N-Acetyl-L-cysteine can lower the incidence rate of infection-associated preterm labor by prohibiting the activation of the protein AP-1/MCP-1 and decreasing the expression of NF- kappa Bp65 and TNF- in the pregnant tissues of premature mice to reduce the inflammatory reactions.

Infection-associated Hemophagocytic Syndrome in Critically Ill Patients with COVID-19

Infection-associated hemophagocytic syndrome(IAHS),a severe complication of various infections,is potentially fatal.This study aims to determine whether IAHS occurs in critically ill patients with coronavirus disease 2019(COVID-19).We conducted a retrospective observational study on 268 critically ill patients with COVID-19 between February 1st,2020 and February 26th,2020.Demographics,clinical characteristics,laboratory results,information on concurrent treatments and outcomes were collected.A diagnosis of secondary hemophagocytic lymphohistiocytosis(sHLH)was made when the patients had an HScore greater than 169.Histopathological examinations were performed to confirm the presence of hemophagocytosis.Of 268 critically ill patients with confirmed SARS-CoV-2 infection,17(6.3%)patients had an HScore greater than 169.All the 17 patients with sHLH died.The interval from the onset of symptom of COVID-19 to the time of a diagnosis of sHLH made was 19 days and the interval from the diagnosis of sHLH to death was 4 days.Ten(59%)patients were infected with only SARS-CoV-2.Hemophagocytosis in the spleen and the liver,as well as lymphocyte infiltration in the liver on histopathological examinations,was found in 3 sHLH autopsy patients.Mortality in sHLH patients with COVID-19 is high.And SARS-CoV-2 is a potential trigger for sHLH.Prompt recognition of IAHS in critically ill patients with COVID-19 could be beneficial for improving clinical outcomes.

Hierarchical and selective roles of galectins in hepatocarcinogenesis, liver fibrosis and inflammation of hepatocellular carcinoma

Hepatocellular carcinoma(HCC)represents a global health problem.Infections with hepatitis B or C virus,non-alcoholic steatohepatitis disease,alcohol abuse,or dietary exposure to aflatoxin are the major risk factors to the development of this tumor.Regardless of the carcinogenic insult,HCC usually develops in a context of cirrhosis due to chronic inflammation and advanced fibrosis.Galectins are a family of evolutionarily-conserved proteins defined by at least one carbohydrate recognition domain with affinity forβ-galactosides and conserved sequence motifs.Here,we summarize the current literature implicating galectins in the pathogenesis of HCC.Expression of"proto-type"galectin-1,"chimera-type"galectin-3 and"tandem repeat-type"galectin-4 is up-regulated in HCC cells compared to their normal counterparts.On the other hand,the"tandemrepeat-type"lectins galectin-8 and galectin-9 are downregulated in tumor hepatocytes.The abnormal expression of these galectins correlates with tumor growth,HCC cell migration and invasion,tumor aggressiveness,metastasis,postoperative recurrence and poor prognosis.Moreover,these galectins have important roles in other pathological conditions of the liver,where chronic inflammation and/or fibrosis take place.Galectin-based therapies have been proposed to attenuate liver pathologies.Further functional studies are required to delineate the precise molecular mechanisms through which galectins contribute to HCC.