Atherosclerosis (AS) in diabetic patients is often associated with low stability, which might be largely attributed to unfavorable macrophage polarization and increased inflammatory response induced by hyperglycaemia. Ginsenoside Rg3 is one of the main active principles of Panax Ginseng, which has been reported to be a natural ligand of peroxisome proliferator-activated receptor-gamma (PPARγ), a key nuclear transcriptional factor involved in inflammation and macrophage differentiation. However, it remains unclear if Rg3 could exert protective effects on plaque stability in diabetes. In this study, we investigated the role of ginsenoside 20(S)-Rg3 in macrophage polarization and AS plaque stability using advanced glycation end products-treated macrophages and diabetic AS mice models. In vitro, advanced glycation end products (AGEs) treatment promoted the expression of proinflammatory molecules and M1 surface markers, whereas 20(S)-Rg3 could reverse the M1 polarization to the M2 phenotype. In vivo, the administration of 20(S)-Rg3 promoted AS lesion stability and reduced the plaque burden, accompanied by increased M2 macrophages and reduced M1 macrophages. In addition, PPARγ antagonist GW9662 co-administration mostly blocked these effects, suggesting the important role of PPARγ pathways in mediating 20(S)-Rg3 effects in macrophage polarization and atherosclerosis progression. Together, these results demonstrated an immunomodulatory role of ginsenoside 20(S)-Rg3 in promoting macrophages to a profile of the M2 type through PPARγ-dependent mechanisms, and indicated a potential role of 20(S)-Rg3 in the prevention and treatment of diabetic atherosclerosis.

Background Red blood cell distribution width (RDW) and N‐terminal pro brain natriuretic peptide (NT‐proBNP) may predict the prognosis of heart failure (HF). However, the impact of combined RDW and NT‐proBNP levels as a prognostic marker of HF remains unclear and the significance of this combination at various time‐points has not been sufficiently studied. Hypothesis RDW can predict prognosis in HF at various time‐points and combination with NT‐proBNP improves the prognostic value. Methods Patients admitted to HF care unit of Fuwai Hospital CAMS&PUMC (Beijing, China) with a diagnosis of HF from November 2008 to November 2018 were analyzed retrospectively. Results In total, 3231 patients with available RDW data at admission were evaluated (median age 58 years, 71.9% males, 39.7% coronary heart disease, 68.6% New York Heart Association [NYHA] III or IV). Median RDW and NT‐proBNP at admission were 13.4% (interquartile range [IQR]: 12.7%–14.5%), and 1723.00 pg/ml (IQR: 754.00–4006.25 pg/ml), respectively. During 2.9‐year median follow‐up, all‐cause death occurred in 1075 (33.27%) patients. Kaplan–Meier survival curve and Cox proportional‐hazard models, showed patients in the top quarter RDW had a 32.0% increased mortality compared to the bottom quarter (hazard ratio: 4.39, 95% confidence interval: 3.59–5.38; p <.001). The top quarter RDW retained independent prognostic value across HF with reduced ejection fraction [HFrEF], HF with mid‐range ejection fraction [HFmrEF], and HF with preserved ejection fraction [HFpEF] subgroups. Patients were subsequently divided into four groups by median RDW and NT‐proBNP. Comparison of Kaplan–Meier survival curves for various groups showed good risk stratification ( p < .001). Conclusions RDW is an independent predictor of mortality among patients with HF in the short‐, medium‐, and long‐term. Combination of RDW and NT‐proBNP improves the prognostic value. This is true across all clinical subtypes of heart failure (HFrEF, HFmrEF, HFpEF), and among most subgroups of patients with various comorbidities (infection, diabetes, hypertension).

Background Group A rotavirus (RVA), despite being a leading cause of gastroenteritis in infants and young children, is less studied in Shanxi Province, China. The current study was conducted to determine the prevalence and genetic characterization of RVA in hospitalized children younger than 10 years of age with the diagnosis of acute gastroenteritis in Shanxi Province, China. Methods A hospital-based active surveillance of rotavirus gastroenteritis was conducted at Children’s Hospital of Shanxi from Jan 1, 2015, through Dec 31, 2019. Rotavirus was detected in stool samples by real-time quantitative reverse transcription PCR (qRT-PCR). G- and P-genotypes were determined by reverse transcription PCR (RT-PCR) and nucleotide sequencing. Results A total of 961 children younger than 10 years of age was enrolled over the study period, of whom 183 (19.0%) were positive for RVA. The highest RVA-infection frequency (23.7%) was found among children aged 12–23 months, and the seasonal peak was in December. G9P[8] was most prevalent (76.0%), followed by G3P[8] (7.1%), G2P[4] (3.3%), G1P[8] (0.5%) and G9P[4] (0.5%). Conclusions These results report for the first time that RVA was one of the main causes of severe infectious gastroenteritis in children, and a high proportion of G9P[8] strains circulating in most areas of Shanxi Province. While the protective efficacy of the rotavirus vaccines has been demonstrated against G9P[8] strains, our results highlight that the dominant strains have not been effectively controlled in China.

A hospital-based surveillance of shigellosis was conducted in Taiyuan from 2005 to 2015. A total of 2655 stool cultures were collected from patients with diarrhea, 115 were identified as S. flexneri and 107 were S. sonnei. The highest infection rates were found among children under 5 years of age (34.2 %), and during the summer (61.0 %). ​Six serotypes were identified among S. flexneriisolates:1a, 2a, 2b, Xv, X and Y. Serotype 2a and Xv were the dominant serotypes in two periods, 2012-2015 and 2005-2008, respectively. High shigellosis rates over the past decade highlight shigellosis is still a major public health problem in Taiyuan.

Background N6-methyladenosine (m6A) RNA regulation was recently reported to be important in carcinogenesis and cancer development. However, the characteristics of m6A modification and its correlations with clinical features, genome instability, tumor microenvironments (TMEs), and immunotherapy responses in hepatocellular carcinoma (HCC) have not been fully explored. Methods We systematically analyzed the m6A regulator-based expression patterns of 486 patients with HCC from The Cancer Genome Atlas and Gene Expression Omnibus databases, and correlated these patterns with clinical outcomes, somatic mutations, TME cell infiltration, and immunotherapy responses. The m6A score was developed by principal component analysis to evaluate m6A modifications in individual patients. Results M6A regulators were dysregulated in HCC samples, among which 18 m6A regulators were identified as risk factors for prognosis. Three m6A regulator-based expression patterns, namely m6A clusters, were determined among HCC patients by m6A regulators with different m6A scores, somatic mutation counts, and specific TME features. Additionally, three distinct m6A regulator-associated gene-based expression patterns were also identified based on prognosis-associated genes that were differentially expressed among the three m6A clusters, showing similar properties as the m6A regulator-based expression patterns. Higher m6A scores were correlated with older age, advanced stages, lower overall survival, higher somatic mutation counts, elevated PD-L1 expression levels, and poorer responses to immune checkpoint inhibitors. The m6A score was validated as an independent and valuable prognostic factor for HCC. Conclusion M6A modification is correlated with genome instability and TME in HCC. Evaluating m6A regulator-based expression patterns and the m6A score of individual tumors may help identify candidate biomarkers for prognosis prediction and immunotherapeutic strategy selection.