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Hepatitis C virus genotype 3 (HCV G3) infection is the second most prevalent hepatitis C genotype globally, with higher rates of disease progression and mortality compared with other genotypes. After the advent of direct-acting antiviral drugs (DAAs), the efficacy of antiviral therapy for hepatitis C patients has been greatly improved, but the therapy for G3 type is less effective than that for other genotypes, so it is considered to be one of the most difficult subtypes to treat. This article reviews the available treatment options for HCV G3 patients and their sustained virological response rates to provide clinical reference.
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Objective To understand the distribution and antimicrobial resistance of pathogenic bacteria isolated from patients in the department of infectious diseases in Xiangya Hospital.Methods The distribution and antimicrobial susceptibility testing results of pathogenic bacteria isolated from patients in this department in 2011 -2015 were analyzed retrospectively.Results A total of 560 strains were isolated during 5 years,of which gram-posi-tive bacteria and gram-negative bacteria accounted for 44.1 % (n =247)and 55.9%(n =313)respectively.69.8%(81/116)of coagulase-negative staphylococcus and 24.3%(9/37)of Staphylococcus aureus were methicillin-resistant (MRCNS,MRSA)respectively.Enterococcus was highly susceptible to vancomycin,linezolid,and phosphonomy-cin (>81 %).Enterobacteriaceae remained highly susceptible to carbapenems (88.9%-100.0%),and was suscep-tible to amikacin,cefoperazone/sulbactam,and piperacillin/tazobactam (>84%).Acinetobacter baumannii was the major isolated multidrug-resistant organism (MDRO),isolation rate of imipenem-resistant Acinetobacter baumannii increased from 50.0% in 2011 to 77.8% in 2015,its resistance rate to imipenem was 64.9%.Conclusion The majority of clinically isolated pathogenic bacteria from this department is gram-negative bacilli,and detection rate of MDROs showed an upward trend;antimicrobial agents should be chosen according to distribution and antimicrobial resistance of pathogenic bacteria.
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Objective To detect the protective role of high mobility group box-1 protein (HMGB1 )antibody in concanavalin A(ConA)-induced liver injury in mice.Methods The healthy male Balb/c mice were grouped into con-trol group (saline injection),model group(ConA injection)and experimental group(ConA+HMGB1 antibody injec-tion).After 6 hours of injection,mice blood was collected for detecting alanine transaminase (ALT)and HMGB1 , liver tissue was used to do HE stain,Tunel,and immunofluorescence detection.Results Pathological inflammation in experimental group was slighter than model group.The levels of ALT and HMGB1 in mice serum were (52.00± 8.34)U/L and (7.54 ±0.53)ng/mL in control group,(5 551 .50 ±1 445.74)U/L and (18.06 ±1 .65 )ng/mL in model group,(1 977.40±654.89)U/L and (10.77±0.71)ng/mL in experimental group,respectively;the expres-sion levels of HMGB1 mRNA and HMGB1 (relative value)in liver tissue were 1 .886±0.253 and 0.086±0.028 in control group,4.718±0.341 and 0.268±0.043 in model group,3.005 ±0.331 and 0.116±0.008 in experimental group,respectively;the expression levels of ALT and HMGB1 in serum,as well as HMGB1 mRNA and HMGB1 in liver tissue of experimental group were all lower than model group(all P <0.001).Apoptosis and HMGB1 migra-tion in the liver cell (normalized)were 1 ±0 and 1 ±0 in control group,4.67 ±0.33 and 4.50 ±0.22 in model group,2.67±0.21 and 2.33 ±0.21 in experimental group,respectively;apoptosis and HMGB1 migration in liver tissue of experimental group were both lower than model group(both P <0.001).Conclusion HMGB1 antibody can improve the pathological injury of liver tissue,and protect mice liver against the injury induced by ConA.
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The aim of this study was to investigate the effect of Paris saponin I (PS I) on human gastric carcinoma cell growth and apoptosis and to explore the potential mechanisms. The proliferation of SGC7901 cells was monitored by the MTT cell viability assay, while the nuclear morphology of apoptotic cells was assessed by Hoechst 33258 staining. Flow cytometry was performed to analyze the cell cycle progression of propidium iodide (PI)-stained SGC7901 cells and the apoptotic rate of annexin V/PI-stained cells. Western blotting was used to examine the expression of several cell cycle proteins, including cyclin B1 and Cdk1, and the apoptosis-regulated proteins Bcl-2, Bax, cytochrome c, procaspase-9, and procaspase-3. The MTT assay demonstrated that PS I could induce significant dose- and time-dependent inhibition of SGC7901 cell proliferation. Marked morphological changes, including condensation of chromatin, nuclear fragmentation and apoptotic bodies were clearly shown on Hoechst 33258 staining. PSI treatment also resulted in the disruption of the cell cycle at G(2)/M and the induction of apoptosis. Following PSI treatment, the cell cycle-related proteins cyclin B1 and Cdk1 were down-regulated. Expression of the pro-apoptotic protein Bax was increased, while anti-apoptotic protein Bcl-2 decreased. PSI treatment resulted in elevated cytoplasmic cytochrome c and activation of the apoptotic proteases caspase-9 and caspase-3. These data indicate that PS acts as an inhibitor of proli I feration in SGC7901 cells by inducing cell cycle arrest and mitochondria-dependent apoptosis. PSI is a potential therapeutic agent against human gastric carcinoma.