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BackgroundThe effect of tea consumption on conditions such as hypertension, diabetes, and obesity has attracted significant global interest. However, the results of various studies on this topic have been mixed and somewhat contentious. Therefore, we conducted a Mendelian randomization (MR) analysis to investigate the causal relationships between tea consumption and the aforementioned health conditions.MethodsA bidirectional two-sample MR analysis was used to systematically explores the associations between tea consumption and hypertension, diabetes, and obesity. MR-Egger regression, weighted median, inverse variance weighted, and weighted mode methods were used to evaluate the potential causal associations. Leave-one-out sensitivity test was used to check the robustness of the IVW estimates.ResultsMR analysis indicated that genetically predicted tea consumption is associated with a protective effect against hypertension, with an odds ratio (OR) of 0.78 and a 95% confidence interval (CI) ranging from 0.64 to 0.95. Additionally, tea consumption appeared to have a potential protective effect on type 2 diabetes and obesity related to excessive calorie intake, influenced by specific single nucleotide polymorphisms (SNPs), namely “rs57462170” and “rs17685.” No causal link was observed between the consumption of green or herbal tea and hypertension, diabetes, or obesity. However, there was a marginal negative association between type 2 diabetes and tea consumption and (OR = 0.99; 95% CI: 0.97–1.00) and a significant negative correlation between obesity due to excessive calorie intake and green tea consumption (OR = 0.35; 95% CI: 0.16–0.78).ConclusionThis study demonstrates a protective causal relationship between the consumption of tea (including black and green teas) and reduced risk of hypertension. Furthermore, our results suggest that tea intake may also have a protective effect on type 2 diabetes and obesity. The results recommend further research to verify or refine these findings.

Abstract Mitochondrial DNA plays a critical role in the pathophysiological process of inflammation. However, the relationship between mitochondrial DNA copy number (mtDNA-CN) and inflammatory bowel diseases (IBD) remains poorly understood. We conducted a comprehensive Mendelian randomization (MR) using three instrumental variables (IVs) to explore the causal associations between mtDNA-CN and IBD, including Crohn's disease (CD), ulcerative colitis (UC). MR-Egger regression, weighted median, inverse-variance weighted (IVW), and weighted mode methods were used to evaluate the potential causal associations. The robustness of the IVW estimates was determined using the leave-one-out sensitivity test. A meta-analysis was conducted to pool the results from the three sets of IVs. Upon analysis, the findings of the current study revealed that genetically predicted mtDNA-CN was not associated with IBD (CD + UC) and UC. The results of MR analyses between mtDNA-CN and CD risk were inconsistent by using three sets of IVs. After a meta-analysis, we found that genetically predicted mtDNA-CN was associated with CD risk (odds ratio = 2.09; 95% confidence interval: 1.37–3.18). This finding was also confirmed by multivariable MR analyses and remained robust when tested with the leave-one-out sensitivity test. In conclusion, genetically predicted mtDNA-CN was found to be associated with CD risk. Therefore, mtDNA levels in the blood could potentially be used as a marker for CD risk assessment. Further studies are needed to elucidate the underlying mechanisms and validate the results of this study.

Abstract Elastomeric nanostructures are normally expected to fulfill an explicit mechanical role and therefore their mechanical properties are pivotal to affect material performance. Their versatile applications demand a thorough understanding of the mechanical properties. In particular, the time dependent mechanical response of low-density polyolefin (LDPE) has not been fully elucidated. Here, utilizing state-of-the-art PeakForce quantitative nanomechanical mapping jointly with force volume and fast force volume, the elastic moduli of LDPE samples were assessed in a time-dependent fashion. Specifically, the acquisition frequency was discretely changed four orders of magnitude from 0.1 up to 2 k Hz. Force data were fitted with a linearized DMT contact mechanics model considering surface adhesion force. Increased Young’s modulus was discovered with increasing acquisition frequency. It was measured 11.7 ± 5.2 MPa at 0.1 Hz and increased to 89.6 ± 17.3 MPa at 2 kHz. Moreover, creep compliance experiment showed that instantaneous elastic modulus E 1 , delayed elastic modulus E 2 , viscosity η, retardation time τ were 22.3 ± 3.5 MPa, 43.3 ± 4.8 MPa, 38.7 ± 5.6 MPa s and 0.89 ± 0.22 s, respectively. The multiparametric, multifunctional local probing of mechanical measurement along with exceptional high spatial resolution imaging open new opportunities for quantitative nanomechanical mapping of soft polymers, and can potentially be extended to biological systems.

BackgroundOver recent decades, epidemiological studies have shown relationships between vitamins and Helicobacter pylori (H. pylori) infection and eradication, but the results are controversial.MethodsA comprehensive meta-analysis and systematic review were conducted to clarify the relationships between common types of vitamins and H. pylori. We applied meta-regression, subgroup analysis and sensitivity analysis to obtain available evidence. Articles published from January 1991 to June 2021 in PubMed, EMBASE, and the Cochrane Library were searched.ResultsIn total, we identified 48 studies. The results indicate that H. pylori -positive patients had lower serum vitamin B12 [standardized mean difference (SMD) = −0.30; 95% confidence interval (CI): −0.53 – −0.08], folate (SMD = −0.69; 95% CI: −1.34 – −0.04), vitamin C (SMD = −0.37; 95%CI: −0.57 – −0.18) and vitamin D (SMD = −0.34; 95% CI: −0.49 – −0.18) levels than H. pylori-negative patients. Patients in which H. pylori had been successfully eradicated had higher serum vitamin D levels (SMD = 1.37; 95% CI: 0.37–2.38) than in patients in which eradication had been unsuccessful. The serum vitamin B12 levels of H. pylori-positive patients improved after successful H. pylori eradication therapy (SMD = 1.85; 95% CI: 0.81–2.90), and antioxidant vitamin supplementation to an H. pylori eradication regimen improved the eradication rate (risk ratio = 1.22; 95% CI: 1.02–1.44 for per-protocol analysis; risk ratio = 1.25; 95% CI: 1.06–1.47 for intention-to-treat analysis).ConclusionsH. pylori infections decrease the serum levels of several types of vitamins, eradication of H. pylori could rescue its adverse effects, and antioxidant vitamin supplementation may improve the H. pylori eradication rate.Systematic Review Registrationidentifier: CRD42021268127.

Background. Metabolic reprogramming is associated with the carcinogenesis of hepatocellular carcinoma (HCC). The effects of metabolism-related genes on predicting survival and immune status in HCC remain unclear. Objectives. To develop and validate metabolic models for predicting the survival and immune status of HCC patients. Materials and methods. The metabolic core genes for overall survival (OS) and disease-free survival (DFS) were retrieved. Then, glycolysis and fatty acid metabolism prognostic models were constructed and validated using The Cancer Genome Atlas (TCGA) and the International Cancer Genome Consortium (ICGC) data. Decision trees based on machine learning were developed for classifying the prognostic risks of HCC patients. The associations between the metabolic signatures, immunotherapy and immune cell infiltration were investigated. Experimental validations were performed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and immunohistochemistry (IHC). Results. We identified 30 prognostic core genes for glycolysis metabolism and 12 prognostic core genes for fatty acid metabolism. Subsequently, 2 glycolysis models and 2 fatty acid metabolism models were developed to predict the OS and DFS of HCC patients, respectively. Two decision trees were constructed to classify the low-, intermediate- and high-risk groups of HCC patients for OS and DFS. Moreover, the patients in the high-risk groups of glycolysis and fatty acid metabolic models tended to have higher expression of programmed cell death ligand-1 (PD-L1 or CD274), programmed cell death 1 (PDCD1), cytotoxic T-lymphocyte-associated protein-4 (CTLA-4), and lymphocyte activating 3 (LAG3). Most of the metabolic core genes were significantly associated with immune cell infiltration. In addition, ATP-binding cassette subfamily B member 6 (ABCB6), peptidylprolyl isomerase A (PPIA), uroporphyrinogen decarboxylase (UROD), and non-SMC condensin II complex subunit H2 (NCAPH2) were positively correlated with both tumor mutational burden (TMB) and microsatellite instability (MSI) scores. The expression of ABCB6, PPIA, UROD, and NCAPH2 was validated using RT-qPCR and IHC. Conclusions. We established novel prognostic models based on metabolism-related genes to better predict the outcome and immune status of HCC patients. [ABSTRACT FROM AUTHOR]