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Several epidemiological studies have investigated the association between sugar intake, the levels of systolic blood pressure (SBP) and diastolic blood pressure (DBP) and the risk of hypertension, but findings have been inconsistent. We carried out a systematic review and meta-analysis of observational studies to examine the associations between sugar intake, hypertension risk, and BP levels. Articles published up to February 2, 2021 were sourced through PubMed, EMBASE and Web of Science. Pooled relative risks (RRs) and 95% confidence intervals (CIs) were estimated using a fixed- or random-effects model. Restricted cubic splines were used to evaluate dose-response associations. Overall, 35 studies were included in the present meta-analysis (23 for hypertension and 12 for BP). Sugar-sweetened beverages (SSBs) and artificially sweetened beverages (ASBs) were positively associated with hypertension risk: 1.26 (95% CI, 1.15–1.37) and 1.10 (1.07–1.13) per 250-g/day increment, respectively. For SBP, only SSBs were significant with a pooled β value of 0.24 mmHg (95% CI, 0.12–0.36) per 250 g increase. Fructose, sucrose, and added sugar, however, were shown to be associated with elevated DBP with 0.83 mmHg (0.07–1.59), 1.10 mmHg (0.12–2.08), and 5.15 mmHg (0.09–10.21), respectively. Current evidence supports the harmful effects of sugar intake for hypertension and BP level, especially SSBs, ASBs, and total sugar intake. [ABSTRACT FROM AUTHOR]

Purpose: Mitochondrial metabolism is essential for energy production and the survival of brain cells, particularly in astrocytes. Cuproptosis is a newly identified form of programmed cell death that occurs due to the disruption of mitochondrial metabolism caused by excessive copper toxicity. However, the relationship between cuproptosis-related genes (CRGs) in the tumor microenvironment (TME) and the prognosis of gliomas remains unclear. Patients and Methods: In this study, we utilized 32,293 cells obtained from three in-house single-cell RNA sequencing (scRNA-seq) datasets, along with 6,148 cells acquired from the Chinese Glioma Genome Atlas (CGGA) involving 14 glioma patients, to identify and validate the TME of gliomas. Results: Based on an analysis of 32,293 single cells, we investigated intra-tumor heterogeneity, intercellular communication, and astrocyte differentiation trajectories in gliomas. Our findings revealed that the TGFβ signaling pathway exhibited a higher relative strength in astrocyte subpopulations. Additionally, we identified a novel three-gene signature (CDKN2A, SOX2, and MPC1) was identified for prognostic prediction. Furthermore, glioma patients with a high-risk score demonstrated poorer overall survival (OS) compared to those with a low-risk score in both training and testing datasets (Ptraining set < 0.001; Ptest set = 0.037). Conclusion: Our study revealed the prognostic value of the CRGs in astrocytes exhibiting tumor immunosuppressive characteristics in glioma. We established a novel three-gene prognostic model that offers new insights into the prognosis and treatment strategies for gliomas. [ABSTRACT FROM AUTHOR]

Aims: To investigate the association of methylation risk score (MRS) and its interactions with environmental factors with type 2 diabetes mellitus (T2DM) risk. Methods: We conducted a nested case–control study with 241 onset cases and 241 matched controls. Conditional logistic regression models were employed to identify risk CpG sites. Simple and weighted MRSs were constructed based on the methylation levels of ATP‐binding cassette G1 gene, fat mass and obesity associated gene, potassium voltage‐gated channel member 1 gene, and thioredoxin‐interacting protein gene previously associated with T2DM to estimate the association of MRS with T2DM risk. Stratified analyses were used to investigate interactions between MRS and environmental factors. Results: A total of 10 CpG loci were identified from the aforementioned genes to calculate MRS. After controlling for potential confounding factors, taking tertile 1 as reference, the odds ratios (ORs) and 95% confidence intervals (CIs) for T2DM of tertile 3 was 2.39 (1.36–4.20) for simple MRS and 2.59 (1.45–4.63) for weighted MRS. With per SD score increment in MRS, the OR (95% CI) was 1.66 (1.29–2.14) and 1.60 (1.24–2.08) for simple and weighted MRSs, respectively. J‐curved associations were observed between both simple and weighted MRSs and T2DM risks. Additionally, multiplication interactions for smoking and hypertension with simple MRS on the risk of T2DM were found, similarly for smoking and obesity with weighted MRS on the risk of T2DM (all Pinteraction <.05). Conclusion: Elevated simple and weighted MRSs were associated with increased risk of T2DM. Environmental risk factors may influence the association between MRS and T2DM. [ABSTRACT FROM AUTHOR]

Background: Proliferation, metabolism, tumor occurrence and development in gliomas are greatly influenced by RNA modifications. However, no research has integrated the four RNA methylation regulators of m6A, m1A, m5C and m7G in gliomas to analyze their relationship with glioma prognosis and intratumoral heterogeneity. Methods: Based on three in‐house single‐cell RNA‐sequencing (scRNA‐seq) data, the glioma heterogeneity and characteristics of m6A/m1A/m5C/m7G‐related regulators were elucidated. Based on publicly available bulk RNA‐sequencing (RNA‐seq) data, a risk‐score system for predicting the overall survival (OS) for gliomas was established by three machine learning methods and multivariate Cox regression analysis, and validated in an independent cohort. Results: Seven cell types were identified in gliomas by three scRNA‐seq data, and 22 m6A/m1A/m5C/m7G‐related regulators among the marker genes of different cell subtypes were discovered. Three m6A/m1A/m5C/m7G‐related regulators were selected to construct prognostic risk‐score model, including EIFA, NSUN6 and TET1. The high‐risk patients showed higher immune checkpoint expression, higher tumor microenvironment scores, as well as higher tumor mutation burden and poorer prognosis compared with low‐risk patients. Additionally, the area under the curve values of the risk score and nomogram were 0.833 and 0.922 for 3 year survival and 0.759 and 0.885 for 5 year survival for gliomas. EIF3A was significantly highly expressed in glioma tissues in our in‐house RNA‐sequencing data (p < 0.05). Conclusion: These findings may contribute to further understanding of the role of m6A/m1A/m5C/m7G‐related regulators in gliomas, and provide novel and reliable biomarkers for gliomas prognosis and treatment. [ABSTRACT FROM AUTHOR]

Background: This study used a bidirectional 2-sample Mendelian randomization study to investigate the potential causal links between mtDNA copy number and cardiometabolic disease (obesity, hypertension, hyperlipidaemia, type 2 diabetes [T2DM], coronary artery disease [CAD], stroke, ischemic stroke, and heart failure). Methods: Genetic associations with mtDNA copy number were obtained from a genome-wide association study (GWAS) summary statistics from the UK biobank (n = 395,718) and cardio-metabolic disease were from largest available GWAS summary statistics. Inverse variance weighting (IVW) was conducted, with weighted median, MR-Egger, and MR-PRESSO as sensitivity analyses. We repeated this in the opposite direction using instruments for cardio-metabolic disease. Results: Genetically predicted mtDNA copy number was not associated with risk of obesity (P = 0.148), hypertension (P = 0.515), dyslipidemia (P = 0.684), T2DM (P = 0.631), CAD (P = 0.199), stroke (P = 0.314), ischemic stroke (P = 0.633), and heart failure (P = 0.708). Regarding the reverse directions, we only found that genetically predicted dyslipidemia was associated with decreased levels of mtDNA copy number in the IVW analysis (β= − 0.060, 95% CI − 0.044 to − 0.076; P = 2.416e−14) and there was suggestive of evidence for a potential causal association between CAD and mtDNA copy number (β= − 0.021, 95% CI − 0.003 to − 0.039; P = 0.025). Sensitivity and replication analyses showed the stable findings. Conclusions: Findings of this Mendelian randomization study did not support a causal effect of mtDNA copy number in the development of cardiometabolic disease, but found dyslipidemia and CAD can lead to reduced mtDNA copy number. These findings have implications for mtDNA copy number as a biomarker of dyslipidemia and CAD in clinical practice. [ABSTRACT FROM AUTHOR]

Background: It's still controversial whether Helicobacter pylori (H. pylori) eradication can reverse atrophic gastritis (AG) and intestinal metaplasia (IM). Therefore, we performed a meta‐analysis to estimate the effect of H. pylori eradication on AG and IM. Methods: We searched the PubMed, Web of Science and EMBASE datasets through April 2023 for epidemiological studies, which provided mean glandular atrophy (GA) or IM score before and after H. pylori eradication, or provided ORs, RRs or HRs and 95% CIs for the association of AG or IM with H. pylori eradication. Weighted mean difference (WMD) and pooled ORs and 95%CIs were used to estimate the effect of H. pylori eradication on AG and IM. Results: Twenty articles with a total of 5242 participants were included in this meta‐analysis. H. pylori eradication significantly decreased GA score in the antrum (WMD −0.36; 95% CI: −0.52, −0.19, p < 0.01), GA score in the corpus (WMD −0.35; 95% CI: −0.52, −0.19, p < 0.01), IM score in the antrum (WMD −0.16; 95% CI: −0.26, −0.07, p < 0.01) and IM score in the corpus (WMD −0.20; 95% CI: −0.37, −0.04, p = 0.01). H. pylori eradication significantly improved AG (pooled OR 2.96; 95% CI: 1.70, 5.14, p < 0.01) and IM (pooled OR 2.41; 95% CI: 1.24, 4.70, p < 0.01). The association remained significant in the subgroup analyses by study design, sites of lesions, regions and follow‐up time. Although Publication bias was observed for AG, the association remained significant after trim‐and‐fill adjustment. Conclusions: H. pylori eradication could significantly improve AG and IM at early stage. [ABSTRACT FROM AUTHOR]

Context Mitochondrial DNA (mtDNA) plays a key role in diabetes mellitus and metabolic syndrome (MetS). An increasing number of studies have reported the association between mtDNA copy number (mtDNA-CN) and the risk of diabetes mellitus and MetS; however, the associations remain conflicted and a systematic review and meta-analysis on the association between mtDNA-CN and diabetes mellitus and MetS is lacking. Objective We aimed to investigate the association of mtDNA-CN and diabetes mellitus and MetS using a systematic review and meta-analysis of observational studies. Methods PubMed, EMBASE, and Web of Science were searched up to December 15, 2022. Random-effect models were used to summarize the relative risks (RRs) and 95% CIs. Results A total of 19 articles were included in the systematic review and 6 articles (12 studies) in the meta-analysis involving 21 714 patients with diabetes (318 870 participants) and 5031 MetS (15 040 participants). Compared to the highest mtDNA-CN, the summary RR (95% CIs) for the lowest mtDNA-CN were 1.06 (95% CI, 1.01-1.12; I2 = 79.4%; n = 8) for diabetes (prospective study: 1.11 (1.02-1.21); I2 = 22.6%; n = 4; case-control: 1.27 (0.66-2.43); I2 = 81.8%; n = 2; cross-sectional: 1.01 (0.99-1.03); I2 = 74.7%; n = 2), and 1.03 (0.99-1.07; I2 = 70.6%; n = 4) for MetS (prospective: 2.87 (1.51-5.48); I2 = 0; n = 2; cross-sectional: 1.02 (1.01-1.04); I2 = 0; n = 2). Conclusion Decreased mtDNA-CN was associated with increased risk of diabetes mellitus and MetS when limited to prospective studies. More longitudinal studies are warranted. [ABSTRACT FROM AUTHOR]