PD-1 inhibition can partly mitigate TNBS-induced colitis and restore the enteric microbiota by enriching the abundance of SCFA-producing bacteria.

There is increasing evidence that dietary intake of sugars may be a risk factor for prostate cancer (PCa) and elevate the concentration of serum prostate-specific antigen (PSA). However, there is limited evidence of the correlation between total dietary intake of sugars and serum PSA concentrations for adult American males. Herein, we evaluated the association between total dietary intake of sugars and serum PSA concentrations in men without a malignant tumor diagnosis in the United States (US) National Health and Nutrition Examination Survey (NHANES) database.

. Glesatinib concentration In this secondary data analysis, a total of 6,403 men aged ≥40 years and without malignant tumor history were included from 2003 to 2010. The independent variable of this study was the total dietary intake of sugars, and the dependent variable was serum PSA concentrations. Covariates included dietary, comorbidity, physical examination, and demographic data.

The average age of participants included in this study was 58.1 years (±13.6). After adjusting for the dietary, comorbidity, physical examination, and demographic data, we observed that a dietary intake increase of one gram of total dietary intake of sugars was associated with an increase of serum PSA concentrations by 0.003 ng/mL (after log2 transformed, 95% CI 0.001 to 0.005) with a

value for trend less than 0.05. Sensitivity analysis using the generalized additive model (GAM) supported the linear association between total dietary intake of sugars and serum PSA concentrations.

The total dietary intake of sugars is independently and positively associated with serum PSA concentrations in adult American males who are without a personal history of malignant tumors.

The total dietary intake of sugars is independently and positively associated with serum PSA concentrations in adult American males who are without a personal history of malignant tumors.

The publications of application and development of shock wave therapy showed consistent growth. The aim of this study was to investigate the global status and trends in the shock wave therapy field.

Publications about shock wave therapy from 1990 to 2019 were collected from the Web of Science database. The data were studied and indexed by using bibliometric methodology. For a visualized study, VOSviewer software was used to conduct bibliographic coupling analysis, coauthorship analysis, cocitation analysis, and co-occurrence analysis and to analyze the publication trends in shock wave therapy.

A total of 3,274 articles were included. The number of publications was increasing per year globally. The USA made the largest contributions to the global research with the most citations (the highest

-index). The Journal of Urology had the highest publication number. The University of California System was the most contributive institution. Studies could be divided into seven clusters urology, hepatology, cardiology, orthopedics, mechanism research of shock wave therapy, andrology, and principle of shock wave therapy. Orthopedics, andrology, and mechanism research of shock wave therapy could be the next hot topics in this field.

Base on the trends, shock wave therapy is the theme of a globally active research field which keeps developing and extends from bench to bedside.

Base on the trends, shock wave therapy is the theme of a globally active research field which keeps developing and extends from bench to bedside.Diabetes-related macrovascular and microvascular complications lead to poor prognosis. Insulin receptor substrate p53 (IRSp53) is known to act as a substrate for the insulin receptor tyrosine kinase, but its role in endothelial dysfunction remains unclear. Human umbilical vein endothelial cells (HUVECs) treated with D-glucose at different concentrations and a streptozocin-induced rat diabetes mellitus (DM) model were used to investigate the effects of hyperglycemia on the expression levels of IRSp53 and galectin-3 (gal-3) and the inflammatory state and mobility of HUVECs. Thereafter, IRSp53-overexpressing HUVECs and IRSp53-knockdown HUVECs were established using IRSp53-overexpressing lentivirus or IRSp53-siRNA to explore the role of IRSp53 in the HUVEC inflammatory state and HUVEC mobility. D-glucose at high concentration (HG) and hyperglycemia were found to induce downregulation of IRSp53 and upregulation of gal-3 in vitro and in vivo. Treatment with HG resulted in activation of NF-κB in HUVECs and impaired HUVEC mobility. Insulin restored HG-induced changes in the expression levels of IRSp53 and gal-3 in HUVECs and protected the cells from NF-κB activation and impaired mobility. Overexpression of IRSp53 inhibited the activation of NF-κB in HUVECs and strengthened HUVEC migration. Knockdown of IRSp53 facilitated the activation of NF-κB in HUVECs and decreased HUVEC migration. However, neither overexpression nor knockdown of IRSp53 altered the effects of insulin on HG-induced detrimental changes in HUVECs. HG and hyperglycemia resulted in downregulation of IRSp53 in vitro and in vivo. IRSp53 is concluded to inhibit the activation of NF-κB in HUVECs and to strengthen HUVEC migration.Natural killer T (NKT) cells are a key component of innate immunity. Importantly, a growing body of evidence indicates that NKT cells play an integral role in various acute and chronic liver injuries. NKT cells participate in the progression of an injury through the secretion of cytokines, which promote neutrophil infiltration and enhance Fas ligand (FasL) and granzyme-mediated NKT cytotoxic activity. Therefore, examining the role of NKT cells in hepatic disease is critical for a comprehensive understanding of disease pathogenesis and may provide insight into novel approaches for treatment. For more than a century, mouse models that imitate the physiopathological conditions of human disease have served as a critical tool in biological and medical basic research, including studies of liver disease. Here, we review the role of NKT cells in various mouse models of hepatitis.