Objective: To examine the regulatory effect of ginsenoside Rg1 (G-Rg1) on endoplasmic reticulum stress and its effect on hepatocellular apoptosis in carbon tetrachloride (CCl₄)-induced acute liver failure (ALF). Methods: Forty healthy, adult male C57/BL mice were randomly divided into normal saline control (NS) group, G-Rg1 blank control (G-Rg1) group, CCl₄ model (CCl₄) group, and G-Rg1 preventive treatment (CCl₄+G-Rg1) group, and an ALF mouse model was established by CCl₄ induction. Blood and liver specimens were collected from all mice upon sacrifice at 12 hours post-intraperitoneal injection. Serum alanine aminotransferase (ALT), serum aspartate aminotransferase (AST) and total bilirubin (TBil) levels were determined using commercial test kits. The mRNA expression of glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) was measured using real-time PCR. The protein expression of GRP78, CHOP, caspase12, and caspase3 were measured by Western blot. Histological changes in the liver were assessed by hematoxylin-eosin staining, and the expression of GRP78 and caspase3 was detected by immunohistochemistry. Hepatocyte apoptosis was determined using terminal transferase dUTP nick end labeling. Quantitative data were analyzed using one-way ANOVA, and subsequent pairwise comparisons were performed using the LSD-t method. Results: Serum ALT, AST, and TBil levels in the CCl₄+G-Rg1 group were significantly reduced compared with those in the CCl₄ group (ALT: 691.30 ± 108.06 U/L vs 980.66 ± 110.29 U/L, F = 365.07, P < 0.05; AST: 195.40 ± 15.41 U/L vs 319.44 ± 89.32 U/L, F = 115.64, P < 0.05; TBil: 1.09 ± 0.11 mg/dl vs 1.56 ± 0.12 mg/dl, F = 211.29, P < 0.05). The relative mRNA expression of GRP78 and CHOP was significantly lower in the CCl₄ + G-Rg1 group than in the CCl₄ group (P < 0.05). The relative protein expression of caspase3, GRP78, caspase12, and CHOP was significantly reduced to different extents in the CCl₄+G-Rg1 group compared with those in the CCl4 group (P < 0.05). The CCl₄ + G-Rg1 group showed reduced liver tissue degeneration and necrosis compared with the CCl₄ group. Furthermore, the CCl₄+G-Rg1 group showed significantly fewer brown granules in the liver than the CCl4 group (P < 0.05), indicating that G-Rg1 preventive treatment reduced CCl₄-induced hepatocyte apoptosis. Conclusion G-Rg1 prophylaxis can inhibit inflammation and reduce hepatocyte necrosis and apoptosis during CCl₄-induced ALF. Its mechanism may involve the suppression of endoplasmic reticulum stress-related signaling molecules to alleviate hepatocyte endoplasmic reticulum stress and apoptosis. The results of this study suggest that G-Rg1 may inhibit liver inflammation and hepatocyte apoptosis through multiple targets to protect liver function.

Objective To investigate the prevalence and clinical characteristics of heterogeneous vancomycin-intermediate Staphylococcus aureus (hVISA) in the First Affiliated Hospital of Chongqing Medical University. Methods Clinical isolates of S. aureus were collected from the hospital during the period from 2012 to 2015 and were tested for susceptibility to vancomycin using agar dilution method. The results were interpreted according to CLSI 2016 breakpoints. VISA and hVISA strains were screened out by population analysis profile-area under the curve (PAP-AUC). E-test was carried out to determine the MIC of VISA. The clinical data of the patients infected with S. aureus were reviewed retrospectively. Results A total of 105 patients were included in this analysis. And 105 strains of S. aureus were isolated from these patients, including methicillin-resistant S. aureus (MRSA) strains (58.1％, 61/105). PAP-AUC identified 19 (18.1％) hVISA strains and 10 (9.5％) VISA strains. Overall, 52 of the 105 patients were nosocomial infections and 53 community infections. The prevalence of MRSA was 69.2％ (36/52) in nosocomial infections, higher than that in community infections (47.2％, 25/53) (P＜0.05). The prevalence of hVISA in community infections (20.8％, 11/53) did not show significant difference from that in nosocomial infections (15.4％, 8/52) (P＞0.05). The clinical outcome (P＞0.05) and length of hospital stay (P＞0.05) did not show significant difference between hVISA and non-hVISA infections, or between VISA and non-VISA infections. Conclusions The prevalence of hVISA is high in this hospital, which does not show difference between S. aureus nosocomial infection and community infection, or between MRSA and MSSA. The length of hospital stay of hVISA infection is not significantly longer than that of nonhVISA infection. The clinical outcome of hVISA infection does not show difference from that of non-hVISA infection. Larger sample size is required to better understand the prevalence and clinical features of hVISA.

Objective To investigate the epidemiological and etiological characteristics of gram-negative bacilli (GNB) isolated from patients with intra-abdominal infection (IAI). Methods The patients with abdominal infection were identified retrospectively during the period from 2011 to 2015. The clinical and microbiological data were analyzed by WHONET 5.6 and SPSS 20.0. Results A total of 478 cases of IAI [hospital-acquired (HA) 290 cases, community-acquired (CA) 188 cases] were included in this analysis. CA-IAI patients at low risk were associated with significantly better outcome, and lower acute physiology and chronic health evaluation (APACHE) Ⅱ score and sequential organ failure assessment (SOFA) score than the CA-IAI and HA-IAI patients at high risk. The most common gram-negative bacillus isolated from intra-abdominal infections was E. coli and K. pneumoniae. The prevalence of ESBLs-producing E. coli and K. pneumoniae isolates was 75.8％ and 35.8％, respectively. The E. coli isolates remained highly susceptible to amikacin, piperacillin-tazobactam, and carbapenems during the 5-year period, while the K. pneumoniae isolates showed poorer susceptibility to ampicillin-sulbactam. Conclusions The prevalence of ESBLs-producing GNB is increasing in the patients with IAI. Such isolates were resistant to commonly used antimicrobial agents, but generally susceptible to carbapenems. It is important to strengthen the monitoring of antimicrobial resistance in IAIs, and choose antimicrobial therapy rationally based on the results of antimicrobial susceptibility test.

Epilepsy is a chronic brain disease that places a heavy burden on society and patients themselves. The correlation between epilepsy and gut microbiota is becoming increasingly important. The gut microbiota may influence the development of epilepsy through immune-inflammatory responses, neurotransmitters, and short-chain fatty acids. Ketogenic diet is a traditional non-drug treatment method for epilepsy, which can effectively improve the intestinal microenvironment to control the occurrence of epilepsy. Fecal microbiota transplantation and probiotic intervention have also been research hotspots in epilepsy treatment in recent years. This article summarizes relevant research, and systematically reviews relevant etiological basis and pathogenesis, providing new clues for future clinical treatment research on epilepsy.

Objective:To investigate the mechanisms of interleukin-17A (IL-17A) regulating the expressions of IL-1β and IL-23 in mouse keratinocytes (KCs).Methods:Primary KCs were isolated from the skin of 400 newborn male and female wild type C57BL/6 mice and cultured in 24-well plates with Roswell Park Memorial Institute 1640 medium containing fetal bovine serum in the volume fraction of 10% for the following experiments. (1) The cells were divided into phosphate buffer solution (PBS) control group and IL-17A stimulation group according to the random number table (the same grouping method below), which were cultured with 10 μL PBS or 10 μL IL-17A in the mass concentration of 100 ng/mL for 6 hours, respectively. The expression levels of IL-1β and IL-23 mRNA in cells were detected by real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-PCR), with 3 samples in each group. (2) The cells were divided into dimethyl sulfoxide (DMSO) control group, IL-17A+ DMSO group, IL-17A+ nuclear factor κB (NF-κB) inhibitor group, IL-17A+ signal transduction and activator of transcription 3 (STAT3) inhibitor group, IL-17A+ extracellular signal-regulated kinase 1 (ERK1) inhibitor group, IL-17A+ ERK2 inhibitor group, and IL-17A+ c-Jun N-terminal kinase (JNK) inhibitor group. The reagents were added to cells in corresponding groups respectively and cultured for 6 hours. The volume of each reagent was 10 μL, the mass concentration of IL-17A was 100 ng/mL, and the molarity concentrations of NF-κB, STAT3, ERK1, ERK2, JNK signal pathway inhibitors PDTC, S3I-201, SCH772984, SCH772984, SP600125 were 5 μmol/L, 100 μmol/L, 4 nmol/L, 1 nmol/L, and 10 μmol/L, respectively. The expression levels of IL-1β mRNA and IL-23 mRNA in cells were detected by real-time fluorescence quantitative RT-PCR, with 3 samples in each group. (3) The cells were grouped and treated the same as those in experiment (1). The levels of NF-κB phosphorylation, STAT3 phosphorylation, ERK phosphorylation, and JNK phosphorylation were detected by Western blotting, with 3 samples in each group. Data were statistically analyzed with two-tailed Student t test, one-way analysis of variance, t test, and Bonferroni correction. Results:(1) After culture of 6 hours, compared with those in PBS control group, the expression levels of IL-1β and IL-23 mRNA in cells in IL-17A stimulation group were significantly increased ( t=13.46, 6.72, P<0.01). (2) After culture of 6 hours, the expression levels of IL-1β and IL-23 mRNA in cells in DMSO control group, IL-17A+ DMSO group, IL-17A+ NF-κB inhibitor group, IL-17A+ STAT3 inhibitor group, IL-17A+ ERK1 inhibitor group, IL-17A+ ERK2 inhibitor group, and IL-17A+ JNK inhibitor group were 1.00±0.11, 4.01±0.32, 0.32±0.06, 1.76±0.43, 3.62±0.24, 3.80±0.43, 4.26±0.74 and 1.03±0.29, 4.08±0.34, 4.76±0.38, 4.70±0.21, 1.06±0.42, 0.92±0.21, 0.39±0.05, respectively. Compared with those in DMSO control group, the expression levels of IL-1β and IL-23 mRNA in cells in IL-17A+ DMSO group were significantly increased ( t=9.24, 12.60, P<0.01). Compared with that in IL-17A+ DMSO group, the expression level of IL-1β mRNA was significantly decreased in cells in IL-17A+ NF-κB inhibitor group and IL-17A+ STAT3 inhibitor group ( t=11.34, 6.91, P<0.01). Compared with that in IL-17A+ DMSO group, the expression level of IL-23 mRNA was significantly decreased in cells in IL-17A+ ERK1 inhibitor group, IL-17A+ ERK2 inhibitor group, and IL-17A+ JNK inhibitor group ( t=12.44, 13.03, 15.21, P<0.01). (3) After culture of 6 hours, compared with those in PBS control group, the levels of NF-κB phosphorylation, STAT3 phosphorylation, ERK phosphorylation, and JNK phosphorylation in cells in IL-17A stimulation group were significantly increased. Conclusions:IL-17A promotes the transcription of IL-1β in mouse KCs through the phosphorylation of NF-κB and STAT3 pathways and IL-23 through the phosphorylation of ERK and JNK pathways.