Positive interactions among Corynebacterium glutamicum and keystone bacteria producing SCFAs benefited T2D mice to rebuild gut eubiosis.

Accumulating evidences strongly support the correlations between the compositions of gut microbiome and therapeutic effects on Type 2 diabetes (T2D). Notably, gut microbes such as Akkermansia muciniphila are found able to regulate microecological balance and alleviate dysmetabolism of mice bearing T2D. In order to search out similarly functional bacteria, bacteriophage MS2 with a good specificity to bacteria carrying fertility (F) factor were used to treat T2D mice. Based on multi-omics analysis of microbiome and global metabolism of mice, we observed that gavage of bacteriophage MS2 and metformin led to a significant increase in the abundance of Corynebacterium glutamicum and A. muciniphila, respectively. Consequently, the gut microbiota were remodeled, leading to variations in metabolites and a substantial increase in short-chain fatty acids (SCFAs). In which, the amount of acetate, propionate, and butyrate presented negative correlations to that of proinflammatory cytokines, which was beneficial to repairing the intestinal barriers and improving their functions. Moreover, main short fatty acid (SCFA) producers exhibited positive interactions, further facilitating the restoration of gut eubiosis. These findings revealed that C. glutamicum and its metabolites may be potential dietary supplements for the treatment of T2D. Moreover, our research contributes to a novel understanding of the underlying mechanism by which functional foods exert their anti-diabetic effects.

GLUT10 is a novel immune regulator involved in lung cancer immune cell infiltration and predicts worse survival when transcriptionally downregulated.

Background: Glucose transporter 10 (GLUT10) is encoded by the SLC2A10 gene. Our recent investigations have shown that GLUT10 is not only involved in glucose metabolism but also involved in the body's immune response to cancer cells. However, the role of GLUT10 in tumor prognosis and in tumor immunity has not been reported. Methods: We knocked down SLC2A10 and performed transcriptome sequencing to analyse the biological function of GLUT10 and found that GLUT10 may be involved in immune signaling. Then, we studied the expression level of SLC2A10 in cancers by the Oncomine database and Tumor Immune Estimation Resource (TIMER) site. We also evaluated the prognostic potential of SLC2A10 in different cancers using the Kaplan‒Meier plotter database and PrognoScan online software. The correlations between SLC2A10 expression and immune infiltrates were analysed by TIMER. In addition, correlations between SLC2A10 expression and gene marker sets of immune infiltrates were analysed by TIMER and Gene Expression Profiling Interactive Analysis (GEPIA). Immunofluorescence staining of cyclooxygenase-2 (COX-2) and GLUT10 in lung cancer tissue and adjacent tissue was performed to confirm our findings from the database research. Results: Knocking down SLC2A10 widely activated immune and inflammatory signaling. SLC2A10 was abnormally expressed in several tumors. The expression level of SLC2A10 was closely correlated with cancer prognosis. Low SLC2A10 expression was related to poorer prognosis and increased malignancy of lung cancer. Lung cancer patients with low expression of SLC2A10 have a much shorter median survival time than patients with high expression of SLC2A10. SLC2A10 expression is closely related to the infiltration of different types of immune cells, particularly macrophages. Both database research and lung cancer sample research revealed that GLUT10 might modulate immune cell infiltration via the COX-2 pathway. Conclusions: By transcriptome experiments, database studies, and human sample studies, we found that GLUT10 is a new immune signaling molecule involved in tumor immunity, especially in the immune cell infiltration of lung adenocarcinoma (LUAD). GLUT10 may modulate the immune cell infiltration of LUAD via the COX-2 pathway.

Optoelectronic Memristive Synapse Behavior for the Architecture of Cu2ZnSnS4@BiOBr Embedded in Poly(methyl methacrylate).

The great potential of artificial optoelectronic devices that are capable of mimicking biosynapse functions in brain-like neuromorphic computing applications has aroused extensive interest, and the architecture design is decisive yet challenging. Herein, a new architecture of p-type Cu2ZnSnS4@BiOBr nanosheets embedded in poly(methyl methacrylate) (PMMA) films (CZTS@BOB-PMMA) is presented acting as a switching layer, which not only shows the bipolar resistive switching features (SET/RESET voltages, ∼ -0.93/+1.35 V; retention, >104 s) and electrical- and near-infrared light-induced synapse plasticity but also demonstrates electrical-driven excitatory postsynaptic current, spiking-time-dependent plasticity, paired pulse facilitation, long-term plasticity, long- and short-term memory, and "learning-forgetting-learning" behaviors. The approach is a rewarding attempt to broaden the research of optoelectric controllable memristive devices for building neuromorphic architectures mimicking human brain functionalities.

Peripheral Lymphocyte Count and Viral Clearance in COVID-19.

The objective of the study was to investigate whether the peripheral lymphocyte count was independently negative association with viral clearance time of SARS-CoV-2 in Chinese patients with COVID-19. Total 202 patients were chosen for the last data analysis. The patients' mean age was 41.39±12.47 years. Male was accounted for 48.51% and female was 51.49% respectively. The average viral clearance time was 19.40±9.03 days. Adjusted linear regression result showed peripheral lymphocyte count was associated with viral clearance time negatively after adjusting confounders (ß, -2.79; 95% CI, -5.21 to -0.36). The trend of peripheral lymphocyte count treated as a categorical variable in linear regression was also consistent with the result when peripheral lymphocyte count was treated as a continuous variable. There was a negative association between peripheral lymphocyte count and viral clearance time of SARS-CoV-2 in Chinese patients with COVID-19. Key Words: Peripheral lymphocyte count, Viral clearance, COVID-19.

Perioperative Fluoroquinolone Treatment Deteriorates Prognosis Following Coronary Artery Bypass Grafting.

Background: Former studies have revealed that fluoroquinolone (FQ) can induce aortic expansion and rupture. While FQ is widely used in perioperative anti-infection therapy, its impact on graft patency and patient survival is unknown. Methods: Coronary artery bypass grafting (CABG) data were extracted from the MIMIC-III database. Chi-square tests, Fisher's exact tests, t-tests, or ANOVAs were used to compare baseline data between groups determined by FQ therapy status, depending on the data type. Propensity score matching was used to establish a balanced cohort. Cox regression was used to investigate the impact of FQ on CABG patient survival, whereas paired t-tests were used to analyze secondary results. Results: Of the 5030 patients who underwent CABG, 937 (18.6%) received oral or intravenous FQ therapy. Using propensity score matching, these 819 patients were successfully matched with 819 controls in a 1:1 ratio. Cox regression showed that FQ significantly decreased survival among CABG patients (HR: 1.62, 95% CI: 1.21−2.15, p = 0.001). Furthermore, FQ usage was associated with longer hospitalization (<0.0001), ICU duration (<0.0001), ventilation period (<0.0001), and duration of vasopressor administration (<0.0001). Conclusions: Perioperative FQ therapy was associated with worse prognosis and a more difficult recovery among patients with CABG.

An updating meta-analysis of the GSTM1, GSTT1, and GSTP1 polymorphisms and prostate cancer: a HuGE review.

It has been postulated that individuals with GSTM1, GSTT1 deficiency and, GSTP1 (105Ile/Val transition) have increased susceptibility to carcinogens and are more likely to develop prostate cancer. In recent years, GST status has been extensively studied as a prostate cancer risk factor; however, the results are inconsistent. To re-examine this controversy, we have undertaken an updating meta-analysis of 29 studies with GSTM1 genotyping (4,564 prostate cancer cases and 5,464 controls), 22 studies with GSTT1 genotyping (3,837 cases and 4,552 controls), and 24 studies with GSTP1 genotyping (5,301 cases and 5,621 controls). The random effects odds ratio was 1.33 [95% confidence interval (95% CI): 1.15, 1.55; I(2) = 68.9%, P for heterogeneity = 0.00] for the GSTM1 null versus present genotype and 1.05 (95% CI: 0.86, 1.27; I(2) = 68.2%, P for heterogeneity = 0.00) for the GSTT1 null versus present genotype, and 1.06 (95% CI: 0.91, 1.24; I(2) = 71.5%, P for heterogeneity = 0.00) for the GSTP1-Val versus GSTP1-Ile allele. For GSTM1 polymorphism, similar results reached in Caucasians and Asians, with exception for Africans. No association between GSTT1 or GSTP1 polymorphisms and prostate cancer risk was detected in different racial. In conclusion, the major finding of our study suggested that GSTM1 polymorphism conferred an increasing risk of prostate cancer on a wide population basis, however, no relationship was found between GSTT1 and GSTP1 status and the risk of prostate cancer.