Bridging Gaps in Oncology Nutrition Education and Teaching: A Comprehensive Analysis of Resident Physicians in China.

Residents are actively involved in patient assessment and all aspects of patient care, and they are critical in providing nutritional support education and treatment for patients with cancer. This study aims to assess the nutritional knowledge and performance of resident physicians, providing insights into existing gaps in awareness and practices related to cancer nutrition. A total of 300 resident physicians undergoing standardized residency training in China participated in this study. An anonymous online questionnaire covering demographic characteristics, nutritional knowledge, clinical practice, and training requirements was designed and administered through the "Wenjuanxing" platform. Data were collected from June 1, 2023, to July 31, 2023. Among the participants, only 40.00% demonstrated adequate knowledge of cancer nutrition, and merely 32.00% exhibited proficient performance in nutritional care. Socio-demographic analysis revealed that residents without affiliations and those specializing in obstetrics and gynecology had superior knowledge, while surgery specialists showed significantly worse performance. Most participants expressed a lack of exposure to cancer nutrition education during academic and standardized residency training. The study highlights the demand for enhanced education and the preference for case-based teaching methods. The findings underscore an urgent need for comprehensive oncology nutrition education within China's standardized residency training. Targeted interventions and curriculum enhancements are essential to improve medical talent development and enhance patient care outcomes in oncology. The study emphasizes the critical role of practical, case-based teaching methods in addressing identified gaps in nutritional knowledge and practices among resident physicians.

Role of m6A RNA methylation in the development of hepatitis B virus-associated hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) is the most common liver malignancy that can be developed from hepatitis B and cirrhosis. Many pathophysiological alterations, including hepatitis B virus (HBV) DNA integration, oxidative stress, cytokine release, telomerase homeostasis, mitochondrial damage, epigenetic modification, and tumor microenvironment, are involved in the biological process from hepatitis B to cirrhosis and HCC. N6-methyladenosine (m6A), as an epitranscriptomic modification of RNAs, can regulate the stability, splicing, degradation, transcription, and translation of downstream target RNAs in HBV and liver cancer cells. m6A regulators (writers, erasers, and readers) play an important role in the pathogenesis of HBV-associated HCC by regulating cell proliferation, apoptosis, migration, autophagy, differentiation, inflammation, angiogenesis, and tumor microenvironment. This review summarizes the current progress of m6A methylation in the molecular mechanisms, biological functions, and potential clinical implications of HBV-associated HCC.

ß-catenin represses miR455-3p to stimulate m6A modification of HSF1 mRNA and promote its translation in colorectal cancer.

BACKGROUND: Heat shock transcription factor1 (HSF1) was overexpressed to promote glutaminolysis and activate mTOR in colorectal cancer (CRC). Here, we investigated the mechanism for cancer-specific overexpression of HSF1. METHODS: HSF1 expression was analyzed by chromatin immunoprecipitation, qRT-PCR, immunohistochemistry staining and immunoblotting. HSF1 translation was explored by polysome profiling and nascent protein analysis. Biotin pulldown and m6A RNA immunoprecipitation were applied to investigate RNA/RNA interaction and m6A modification. The relevance of HSF1 to CRC was analyzed in APCmin/+ and APCmin/+ HSF1+/-mice. RESULTS: HSF1 expression and activity were reduced after the inhibition of WNT/ß-catenin signaling by pyrvinium or ß-catenin knockdown, but elevated upon its activation by lithium chloride (LiCl) or ß-catenin overexpression. There are much less upregulated genes in HSF1-KO MEF treated with LiCl when compared with LiCl-treated WT MEF. HSF1 protein expression was positively correlated with ß-catenin expression in cell lines and primary tissues. After ß-catenin depletion, HSF1 mRNA translation was impaired, accompanied by the reduction of its m6A modification and the upregulation of miR455-3p, which can interact with 3'-UTR of HSF1 mRNA to repress its translation. Interestingly, inhibition of miR455-3p rescued ß-catenin depletion-induced reduction of HSF1 m6A modification and METTL3 interaction. Both the size and number of tumors were significantly reduced in APCmin/+ mice when HSF1 was genetically knocked-out or chemically inhibited. CONCLUSIONS: ß-catenin suppresses miR455-3p generation to stimulate m6A modification and subsequent translation of HSF1 mRNA. HSF1 is important for ß-catenin to promote CRC development. Targeting HSF1 could be a potential strategy for the intervention of ß-catenin-driven cancers.

Visit-to-visit variability of glycated albumin was associated with incidence or progression of lower extremity atherosclerotic disease.

BACKGROUND: The aim of this study was to investigate the association of visit-to-visit variability of hemoglobin A1c (HbA1c) and glycated albumin (GA) with the risk of lower extremity atherosclerotic disease (LEAD). METHOD: We performed a prospective cohort study of 436 patients with type 2 diabetes (258 men and 178 women) with at least 3 measurements of HbA1c and GA prior to baseline investigation from the Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital. Different HbA1c and GA variability markers were calculated. Multivariable Cox proportional hazard regression models were used to demonstrate the association between visit-to-visit HbA1c and GA variability and the risk of incident or progressive LEAD. RESULTS: During a mean follow-up period of 3.77 years, 112 participants developed LEAD. Multivariate-adjusted hazard ratios (HRs) of LEAD across tertiles of GA-CV values were 1.00, 1.06 (95% confidence interval [CI] 0.65-1.75), and 1.71 (95% CI 1.07-2.73) (P for trend = 0.042), respectively. When we used GA-VIM and GA-ARV values as exposures, similar positive associations with the risk of LEAD primary were found. Multivariate-adjusted HRs of LEAD for each 1 unit increase in GA-CV, GA-VIM and GA-ARV were 1.03 (95% CI 1.01-1.06), 1.32 (95% CI 1.03-1.69), and 1.07 (95%CI 1.01-1.15), respectively. However, there was no significant association between visit-to-visit variability of HbA1c and the risk of LEAD. CONCLUSIONS: Visit-to-visit variability of GA may be an optimal biomarker in relation to LEAD risk among patients with type 2 diabetes.

High precision line-of-sight angle measuring and large ranging laser radar system for deep-space rendezvous and docking.

With the development of automatic rendezvous and docking missions from Earth orbit to deep space, new sensors are needed to perceive precise ranging and bearing information of the target at a longer distance. A new type of laser line-of-sight (LOS) deviation measuring and ranging system is developed, which is characterized by an operational range of 0.5 m to 20 km with a precision of 0.4 m (far) and 0.025 m (near), and a scanning range of up to 120∘×145∘ with an precision of LOS angle up to 0.025°. In addition, gaze-tracking capability enables the system to capture and track high-speed targets. The scheme of the designed system is presented in detail, including optical path design, scanning strategy for tracking, ranging signal processing, and LOS measurement. Meanwhile, the performance of the designed system is verified by extensive indoor and outdoor experiments, including ground simulated rendezvous and docking experiments from about 20 km to 0.5 m.

Heat Shock Factor 1 Epigenetically Stimulates Glutaminase-1-Dependent mTOR Activation to Promote Colorectal Carcinogenesis.

Heat shock factor 1 (HSF1) generally exhibits its properties under stress conditions. In tumors, HSF1 has a pleiotropic feature in regulating growth, survival, and aggressiveness of cancer cells. In this study, we found HSF1 was increased in colorectal cancer (CRC) and had a positive correlation with shorter disease-free survival (DFS). Knockdown of HSF1 in CRC cells attenuated their growth while inhibiting mTOR activation and glutamine metabolism. HSF1 inhibited the expression of microRNA137 (MIR137), which targeted GLS1 (glutaminase 1), thus stimulating GLS1 protein expression to promote glutaminolysis and mTOR activation. HSF1 bound DNA methyltransferase DNMT3a and recruited it to the promoter of lncRNA MIR137 host gene (MIR137HG), suppressing the generation of primary MIR137. The chemical inhibitor of HSF1 also reduced cell growth, increased apoptosis, and impaired glutamine metabolism in vitro. Moreover, both chemical inhibition and genetic knockout of HSF1 succeeded in increasing MIR137 expression, reducing GLS1 expression, and alleviating colorectal tumorigenesis in azoxymethane (AOM)/dextran sulfate sodium (DSS) mice. In conclusion, HSF1 expression was increased and associated with poor prognosis in CRC. By recruiting DNMT3a to suppress the expression of MIR137 that targets GLS1 mRNA, HSF1 stimulated GLS1-dependent mTOR activation to promote colorectal carcinogenesis. Therefore, targeting HSF1 to attenuate glutaminolysis and mTOR activation could be a promising approach for CRC treatment.

Growth differentiation factor-15 predicts the prognoses of patients with acute coronary syndrome: a meta-analysis.

BACKGROUND: Recent studies have shown Growth differentiation factor-15 (GDF-15) that is a member of the transforming growth factor ß (TGF-ß) superfamily might be a potential predictive cytokine for the prognosis of Acute coronary syndrome (ACS). However, there are discrepancies in these studies. METHODS: Publication searches of the PubMed/Medline and EMBASE databases were performed without any time or ethnicity restrictions. The inclusion and exclusion criteria, when clear, were addressed. Random effects models were used for all analyses. Publication bias was tested using funnel plots and the Egger test. RESULTS: We identified eight eligible studies that provided mortality data. Five of these studies provided recurrent myocardial infarction (MI) data. The maximal duration of follow-up ranged from 6 months to 6 years. A significant association was found between the patients with the highest and lowest GDF-15 levels (overall analyses) in terms of mortality (p < 0.00001; RR = 6.08; 95 % CI = 4.79-7.71) and recurrent MI (p < 0.00001; RR = 1.76; 95 % CI = 1.49-2.07). We also found significant associations between the subgroup analyses stratified by ACS types, cutoff points and follow-up durations (p < 0.001). The combined hazard ratio was high for GDF-15 to ACS (HR = 1.656, 95 % CI = 1.467-1.871). CONCLUSION: High plasma GDF-15 levels are associated with an increased risk of mortality and recurrent MI in patients with ACS.

Meta-analyses of methylation markers for prostate cancer.

Prostate cancer (PCa) is the most frequently diagnosed non-cutaneous cancer that has become the sixth leading cause of mortality in both the developed and developing countries. Accumulating evidence showed a number of genes with aberrant DNA methylation in the pathogenesis of PCa. Here, we conducted a systematic meta-analysis to evaluate the contribution of aberrantly methylated genes to the risk of PCa. Relevant methylation studies were retrieved from PubMed and Wanfang literature databases. In the meta-analysis, Mantel-Haenszel odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated for each methylation event under appropriate models. A total of 594 publications were initially retrieved from PubMed and Wanfang literature database. After a three-step filtration, we harvested 39 case-control articles investigating the role of gene methylation in the prediction of PCa risk. Among the 31 genes involved, 24 genes were shown to be significantly hypermethylated in the PCa patients. Our meta-analyses identified strong associations of four aberrantly methylated genes (GSTP1, RASSF1, p16, and RARB) with PCa. Further research is needed to strengthen our findings in the future.

A novel PCR-based approach to discover miRNA target genes.

MiRNAs are potent regulators of gene expression, and most miRNAs have from several to several thousands of gene targets. Validating the numerous gene targets of a given miRNA remains challenging despite the existence of various tools and databases that predict candidate gene-miRNA pairs. In the present study, we present a high-throughput but flexible method that applies a PCR-based application to simulate the binding of miRNAs to their gene targets. Using hsa-miR-377 as an illustrative example, our method was able to identify 13 potential targets of hsa-miR-377. Moreover, our results include 2 genes (SOD2 and PPM1A) that have already been verified as targets of hsa-miR-377. Our method may provide an alternative way of identifying the gene targets of miRNAs for future research.

Association of CDKN2BAS polymorphism rs4977574 with coronary heart disease: a case-control study and a meta-analysis.

The goal of our study was to explore the significant association between a non-protein coding single nucleotide polymorphism (SNP) rs4977574 of CDKN2BAS gene and coronary heart disease (CHD). A total of 590 CHD cases and 482 non-CHD controls were involved in the present association study. A strong association of rs4977574 with CHD was observed in females (genotype: p=0.002; allele: p=0.002, odd ratio (OR)=1.57, 95% confidential interval (CI)=1.18-2.08). Moreover, rs4977574 was more likely to be a risk variant of CHD under the recessive model in females (χ2=10.29, p=0.003, OR=2.14, 95% CI=1.31-2.77). A breakdown analysis by age had shown that there was an 87% increased risk of CHD for females younger than 65 years (genotype: χ2=14.64, degrees of freedom (df)=2, p=0.0002; allele: χ2=11.31, df=1, p=0.0008, OR=1.87, 95% CI=1.30-2.70). Similar observation was also found in males younger than 65 years (genotype: χ2=8.63, df=2, p=0.04; allele: χ2=7.55, df=1, p=0.006, OR=1.45, 95% CI=1.11-1.90). p values were adjusted by age, sex, smoking, high density lipoprotein cholesterol (HDL-C) and low density lipoprotein cholesterol (LDL-C). Meta-analysis of 23 studies among 36,452 cases and 39,781 controls showed a strong association between rs4977574 and the risk of CHD (p<0.0001, OR=1.27, 95% CI=1.22-1.31).