Background: Cardiometabolic index (CMI), a novel indicator that combines abdominal obesity and lipid levels, has been confirmed to correlate with non-alcoholic fatty liver disease (NAFLD). However, limited research has been conducted on the relationship between CMI and controlled attenuation parameter (CAP), a parameter measured by transient elastography and reflecting the extent of fat accumulation in the liver. The objective of our study was to investigate the relationship between the two variables. Methods: This was a cross-sectional study with a sample size of 1,759 U.S. adults with NAFLD sourced from the NHANES 2017–2020. Participants with a median CAP ≥ 248 dB/m were considered to have hepatic steatosis. CMI was calculated as [waist circumference (cm)/height(cm)]×[TG (mmol/L)/HDL-C (mmol/L)]. Multivariate linear regression, generalized additive model and subgroup analysis were employed to examine the association of CMI and CAP. Results: The average age of the 1,759 participants was 50.2 years, with males accounting for 50.76% and females 49.24%. The average BMI was 32.23 kg/m². The multivariate linear regression model indicated that with every 1-unit increase in CMI, there was an associated rise of 10.40 dB/m in CAP (95% CI, 7.14–13.67) after adjusting for covariates and a p for trend < 0.05 suggested the existence of a linear association between the two variables. Similarly, generalized additive model also found it a roughly linear relationship between the two. Subgroup analysis revealed a positive correlation in the majority of subgroups. Conclusions: CMI was positively associated with CAP in U.S. adults with NAFLD. Our findings indicated that CMI may serve as an ideal indicator for monitoring the degree of hepatic steatosis among patients with NAFLD.

J Indian Prosthodont Soc, Official publication of Indian Prosthodontic Society

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Helicobacter pylori is an extremely common cause of gastritis that can lead to gastric adenocarcinoma over time. Approximately half of the world's population is infected with H. pylori, making gastric cancer the fourth leading cause of cancer‐related deaths worldwide. Innate immunity significantly contributes to systemic and local immune responses, maintains homeostasis, and serves as the vital link to adaptive immunity, and in doing so, mediates H. pylori infection outcomes and consequent cancer risk and development. The gastric innate immune system, composed of gastric epithelial and myeloid cells, is uniquely challenged by its need to interact simultaneously and precisely with commensal microbiota, exogenous pathogens, ingested substances, and endogenous exfoliated cells. Additionally, innate immunity can be detrimental by promoting chronic infection and fibrosis, creating an environment conducive to tumor development. This review summarizes and discusses the complex role of innate immunity in H. pylori infection and subsequent gastric oncogenesis, and in doing so, provides insights into how these pathways can be exploited to improve prevention and treatment.