Dietary Factors and the Risk of Colorectal Cancer: A Mendelian Randomization Study.

OBJECTIVE: To examine the causal association between 15 dietary factors and the incidence of colorectal cancer through the application of Mendelian randomization methodology. METHODS: The data associated with 15 dietary factors were derived from the IEU OPEN GWAS database, and the colorectal cancer data were sourced from the FinnGen database. The Inverse Variance Weighting method was the principal research method. Sensitivity analyses were implemented to affirm the robustness of the findings. Additionally, we conducted multivariable Mendelian randomization analyses to adjust for the intake of ω-3 and ω-6 polyunsaturated fatty acids. RESULTS: In our research, we observed suggestive causal relationships between genetically predicted water intake and the reduced risk of colorectal cancer (OR = 0.54; 95% CI= 0.31 ∼ 0.93; p = 0.028); genetically predicted ω-3 PUFA intake (OR = 1.17; 95% CI= 1.05 ∼ 1.30; p = 0.005) were suggestively associated with the increased risk of colorectal cancer. In the multivariable Mendelian randomization analysis, the effect of ω-3 PUFA intake remains significant after adjusting for the influence of ω-6 PUFA intake. Horizontal pleiotropy was not present in this study. CONCLUSIONS: There exists a suggestive causal association between increased water intake and decreased risk of colorectal cancer, while ω-3 PUFA intake are suggestive linked to the increased risk of colorectal cancer.

Unhealthy lifestyle factors and the risk of colorectal cancer: a Mendelian randomization study.

The purpose of this study was to investigate the causal association between unhealthy lifestyle style factors and the risk of colorectal cancer, with the aim of preventing the occurrence of colorectal cancer by modifying unhealthy lifestyles. A two-sample Mendelian randomization (MR) approach was employed in this study, utilizing the inverse-variance weighted method as the primary research method. This MR analysis analyzed data of 3022 colorectal cancer cases and 174,006 controls from the FinnGen database. Single nucleotide polymorphisms (SNPs) associated with unhealthy lifestyle factors were selected as instrumental variables (IVs), including two obesity-related indicators, BMI (body mass index) and WHR (waist-to-hip ratio). Four phenotypes of smoking (smoking initiation, ever smoked, smoking per day, smoking cessation) and one phenotype of alcohol consumption (drinks per week). Four phenotypes of physical activity (accelerometer-based physical activity, moderate-to-vigorous physical activity, vigorous physical activity, strenuous sports or other exercises). All SNPs were obtained from published genome-wide association studies. The study found that the obesity-related indicator, higher WHR (OR = 1.38, 95% CI 1.12-1.70; P = 0.002) were associated with an increased risk of colorectal cancer, and two smoking phenotypes, cigarettes per day(OR = 1.30, 95% CI 1.01-1.68; P = 0.042)and smoking initiation (OR = 3.48, 95% CI 1.15-10.55; P = 0.028), were potentially associated with an increased risk of colorectal cancer. However, there was no evidence to suggest that physical activities and alcohol consumption were associated with colorectal cancer (all p > 0.05). In addition, the study detected no pleiotropy (all p > 0.05). This MR analysis indicates a causal association between a higher waist-to-hip ratio and the risk of colorectal cancer and a suggestive association between smoking and the risk of colorectal cancer among Europeans. These findings contribute to the understanding of the etiology of colorectal cancer and have potential implications for its prevention.

Predictive Value of Annenxin A1 for Disease Severity and Prognosis in Patients with Community-Acquired Pneumonia.

This prospective, single-center study evaluated the clinical utility of annenxin (Anx)A1 level as a biomarker for determining the severity of illness and predicting the risk of death in hospitalized patients with community-acquired pneumonia (CAP). A total of 105 patients (53 with severe [S]CAP, 52 with non-SCAP) were enrolled from December 2020 to June 2021. Demographic and clinical data were recorded. Serum AnxA1 concentration on days one and six after admission was measured by enzyme-linked immunosorbent assay. AnxA1 level at admission was significantly higher in SCAP patients than in non-SCAP patients (p < 0.001) irrespective of CAP etiology and was positively correlated with Pneumonia Severity Index and Confusion, Uremia, Respiratory Rate, Blood Pressure, and Age ≥ 65 Years score. AnxA1 level was significantly lower on day six after treatment than on day one (p = 0.01). Disease severity was significantly higher in patents with AnxA1 level ≥254.13 ng/mL than in those with a level <254.13 ng/mL (p < 0.001). Kaplan-Meier analysis of 30-day mortality showed that AnxA1 level ≤670.84 ng/mL was associated with a significantly higher survival rate than a level >670.84 ng/mL. These results indicate that AnxA1 is a useful biomarker for early diagnosis and prognostic assessment of CAP.

Contrast-Associated Acute Kidney Injury: Advances and Challenges.

A decrease in renal function that follows intravascular administration of contrast medium (CM) within a few days is reported as contrast-induced acute kidney injury (CI-AKI). In clinical practice, the imaging procedure is frequently deferred when clinicians consider that the renal risks caused by CM outweigh the benefits of enhanced imaging. However, with an in-depth understanding of AKI and contrast medium, scholars have realized that the decrease in renal function after CM is caused by contrast medium factors and noncontrast medium factors (such as anemia and hemodynamic instability). Therefore, acute kidney injury caused by CM has been overestimated in the past. The term "contrast-associated acute kidney injury (CA-AKI)" has been increasingly used to indicate AKI after intravascular administration of contrast medium compared with CI-AKI. CA-AKI can increase the risk of death and chronic kidney disease. However, its pathophysiological mechanism has not been fully elucidated, and the effectiveness of various preventive and therapeutic measures have been questioned. These present challenges for us. In this article, we will review the diagnostic criteria, epidemiology, risk factors, pathophysiological mechanisms and treatment of CA-AKI to provide optimized imaging procedures in clinical practice.

Modulator effect of mangiferin on biochemical characterization in 7,12-dimethylbenz[a]anthracene induced oral cancer in experimental hamsters.

BACKGROUND: Newly, chemo-preventive technique might be a hopeful advancement in developing countries for treating cancers with the aid of toxic less natural based constituents. Malignancy urges to augment effectual chemo-preventive agents that are look forward to suppress the tumours which may be stimulated by chewing and smoking of tobacco and over alcohol consumption related with the high prevalence of human oral cancer (OC) patients. METHODS: In the present research, we examined to assess antioxidants, lipid peroxidation (LPO) and detoxification enzymes levels of anticancer activity of mangiferin on 0.5% 7.12-dimethylbenz[a]anthracene (DMBA) provoked hamster cheek pouch carcinoma (HCPC). OC on hamster buccal pouch (HBP) was incited by DMBA treatment for thrice per week for over 14 weeks. RESULTS: 100% well defined OC establishment with body weight (bw), tumour burden (TB), antioxidant, LPO and liver marker enzymes and also histological changes were observed on DMBA-challenged buccal pouch carcinoma (BPC) in hamsters. Orally treated mangiferin at an effective dosage of 50 mg/kg bw, to DMBA painted hamsters were significantly averted the body weight, succession of tumour, the biochemical as well as histopathological changes. CONCLUSION: Findings of this work clearly suggest that the anti-carcinoma effect of mangiferin possesses the modulator effects on potent antioxidant, anti-LPO and detoxification agents to expel the metabolites of malignant cells, on DMBA-provoked BPC in hamsters.