Genomic characterization and outbreak investigations of methicillin-resistant Staphylococcus aureus in a county-level hospital in China.

Methicillin-resistant Staphylococcus aureus (MRSA) is a common pathogen contributing to healthcare-associated infections, which can result in multiple sites infections. The epidemiological characteristics of MRSA exhibit variability among distinct regions and healthcare facilities. The aim of this study was to investigate the molecular epidemiology and nosocomial outbreak characteristics of MRSA in a county-level hospital in China. A total of 130 non-repetitive MRSA strains were collected from December 2020 to November 2021. Whole-genome sequencing (WGS) was performed to identify antimicrobial resistance and virulence factors. Phylogenetic analysis was conducted to ascertain genetic diversity and phylogenetic relationships. Independent transmission scenarios were determined by the phylogeny derived from single nucleotide polymorphisms (SNPs) within the core genome. All the MRSA isolates were collected from the intensive care unit (30.00%, 39/130), the department of otorhinolaryngology (10.00%, 13/130) and the department of burn unit (9.23%, 12/130). The clinical samples mainly included phlegm (53.85%, 70/130), purulent fluid (24.62%, 32/130), and secretions (8.46%, 11/130). The resistance rates to erythromycin, clindamycin and ciprofloxacin were 75.38, 40.00, and 39.23%, respectively. All the isolates belonged to 11 clonal complexes (CCs), with the major prevalent types were CC5, CC59, and CC398, accounting for 30.00% (39/130), 29.23% (38/130), and 16.92% (22/130), respectively. Twenty sequence types (STs) were identified, and ST59 (25.38%, 33/130) was the dominant lineage, followed by ST5 (23.84%, 31/130) and ST398 (16.92%, 22/130). Three different SCCmec types were investigated, most of isolates were type IV (33.85%, 44/130), followed by type II (27.69%, 36/130) and type III (0.77%, 1/130). The common clonal structures included CC5-ST5-t2460-SCCmec IIa, CC59-ST59-t437-SCCmec IV and CC398-ST398-t034-SCCmec (-), with rates of 16.92% (22/130), 14.62% (19/130), and 13.84% (18/130), respectively. Only 12 panton-valentine leucocidin (PVL) positive strains were identified. Two independent clonal outbreaks were detected, one consisting of 22 PVL-negative strains belongs to CC5-ST5-t2460-SCCmec IIa and the other consisting of 8 PVL-negative strains belongs to CC5-ST5-t311-SCCmec IIa. Overall, our study indicated that the CC5 lineage emerged as the predominant epidemic clone of MRSA, responsible for nosocomial outbreaks and transmission within a county-level hospital in China, highlighting the necessity to strengthen infection control measures for MRSA in such healthcare facilities.

The role of JAK/STAT signaling pathway in cerebral ischemia-reperfusion injury and the therapeutic effect of traditional Chinese medicine: A narrative review.

Cerebral ischemia is a cerebrovascular disease with symptoms caused by insufficient blood or oxygen supply to the brain. When blood supplied is restored after cerebral ischemia, secondary brain injury may occur, which is called cerebral ischemia-reperfusion injury (CIRI). In this process, the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway plays an important role. It mediates neuroinflammation and participates in the regulation of physiological activities, such as cell proliferation, differentiation, and apoptosis. After CIRI, M1 microglia is activated and recruited by the damaged tissue. The inflammatory factors are produced by M1 microglia through the JAK/STAT pathway, eventually leading to cell apoptosis. Meanwhile, the JAK2/STAT3 signaling pathway and the expression of lipocalin-2 and caspase-3 could increase. In the pathway, phosphorylated JAK2 and phosphorylated STAT3 function of 2 ways. They not only promote the proliferation of neurons, but also affect the differentiation direction of neural stem cells by further acting on the Notch signaling pathway. Recently, traditional Chinese medicine (TCM) is a key player in CIRI, through JAK2, STAT3, STAT1 and their phosphorylation. Therefore, the review focuses on the JAK/STAT signaling pathway and its relationship with CIRI as well as the influence of the TCM on this pathway. It is aimed at providing the basis for future clinical research on the molecular mechanism of TCM in the treatment of CIRI.

[The effect of resistin on nuclear factor-kB and tumor necrosis factor-a expression in hepatic steatosis].

OBJECTIVE: To investigate the potential regulatory role played by the hormone resistin in lipid metabolism and expression of nuclear factor (NF)-kB and tumor necrosis factor (TNF)-a during hepatic steatosis. METHODS: A non-alcoholic fatty liver disease (NAFLD) cell model was established by treating the normal human hepatic cell line, L02, with palmitic acid. Four research groups of L02 cells were generated: C group (control, no palmitic acid treatment), P group (NAFLD model, treated with 20 microg/ml palmitic acid), CR group (C group treated with 50 microg/L recombinant human resistin), and PR group (P group treated with 50 microg/L recombinant human resistin). All treatments were carried out for 72 hours. Oil red O staining was used to detect the intracellular changes in lipid drops. Biochemical assays were used to measure triglycerides (TGs), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transpeptidase (GGT) levels in culture medium. The mRNA and protein expression levels of insulin receptor substrate (IRS)-2, NF-kB, and TNF-a were determined by reverse transcription-polymerase chain reaction and Western blot analysis, respectively. RESULTS: The TG, ALT, AST, and GGT levels were higher in the P, CR, and PR groups than in the C group. The NF-kB mRNA level was also higher in the P, CR, and PR groups (Student's t = 17.64, 22.03, 26.06 respectively) than in the C group, as was the TNFa mRNA level ( t = 5.67, 5.38, 11.64), but the IRS-2 mRNA level was lower ( t = 8.19, 9.23, 20.93) (all, P less than 0.05). In addition, no significant difference in these mRNA levels were found between the P group and the CR group (NF-kB: t = 1.75, TNFa: t = 0.58, IRS-2: t = 2.14; all, P more than 0.05). The detected protein levels of NF-kB, TNFa, and IRS-2 were consistent with the mRNA levels. CONCLUSION: Resistin can promote steatosis in LO2 cells through the NF-kB signaling pathway, thereby contributing to the NAFLD pathogenic process.

Efficient Fractionation of Graphene Oxide Based on Reversible Adsorption of Polymer and Size-Dependent Sodium Ion Storage.

Graphene oxide (GO) is not only a unique class of two-dimensional (2D) materials but also an important precursor for scalable preparation of graphene. The efficient size fractionation of GO is of great importance to the fundamental and applied studies of chemically modified graphene, but remains a great challenge. Herein, we report an efficient and scalable fractionation method of GO employing reversible adsorption/desorption of temperature-responsive poly( N-isopropylacrylamide) on GO to amplify its mass difference and significantly improve the fractionation efficiency. Furthermore, size-dependent sodium ion storage of the resulting fractionated reduced GO (RGO) is revealed for the first time with high sodium storage performance achieved for the smallest RGO because of its largest d-spacing and most defect sites. This work provides valuable insights into the size fractionation and size-dependent electrochemical performance of graphene, which can be potentially extended to other 2D materials.

[Effects of resistin on hepatic fibrosis: possible mechanisms in non-alcoholic fatty liver disease in in vitro and in vivo].

To investigate the effects and possible mechanisms of resistin on hepatic fibrosis in non-alcoholic fatty liver disease, this review used an in vivo model utilizing Wistar rats with a high fat diet. Recombinant resistin was selected to play role in hepatic stellate cells in the HSC-T6 cell line. We observed the degrees of hepatic fibrosis, measured the levels of Liver fibrosis spectrum and detected expression levels of resistin mRNA and protein in liver tissue as well as the expression levels of TGFß-1 and TNF-α mRNA in HSC-T6. The results showed that expression of resistin in rat liver tissue and the degree of hepatic fibrosis increased over time with a high fat diet. Along with the increased concentration of resistin and levels of fibrosis index, TGFß-1and TNF-α also increased in HSC-T6 cells. Compared with the control group, significant differences were found between each group, suggesting resistin by proinflammatory cytokine TNF-α and TGF-ß1 induced the occurrence and development of NAFLD in hepatic fibrosis.