PurposeThis study aimed to identify independent risk factors for carotid atherosclerosis (CAS) and construct and validate a CAS risk prediction model based on the Chinese population.MethodsThis retrospective study included 4,570 Chinese adults who underwent health checkups (including carotid ultrasound) at the Zhenhai Lianhua Hospital, Ningbo, China, in 2020. All the participants were randomly assigned to the training and validation sets at a ratio of 7:3. Independent risk factors associated with CAS were identified using multivariate logistic regression analysis. The least absolute shrinkage and selection operator combined with 10-fold cross-validation were screened for characteristic variables, and nomograms were plotted to demonstrate the risk prediction model. C-index and receiver operating characteristic curves, calibration plots, and decision curve analysis (DCA) were used to evaluate the risk model’s discrimination, calibration, and clinical applicability.ResultsAge, body mass index, diastolic blood pressure, white blood cell count, mean platelet volume, alanine transaminase, aspartate transaminase, and gamma-glutamyl transferase were identified as independent risk factors for CAS. In the training, internal validation, and external validation sets, the risk model showed good discriminatory power with C-indices of 0.961 (0.953–0.969), 0.953 (0.939–0.967), and 0.930 (0.920–0.940), respectively, and excellent calibration. The results of DCA showed that the prediction model could be beneficial when the risk threshold probabilities were 1–100% in all sets. Finally, a network computer (dynamic nomogram) was developed to facilitate the physicians’ clinical operations. The website is https://nbuhgq.shinyapps.io/DynNomapp/.ConclusionThe development of risk models contributes to the early identification and prevention of CAS, which is important for preventing and reducing adverse cardiovascular and cerebrovascular events.

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Objective: To elaborate the link of thyroid hormones and metabolic syndrome in a Chinese euthyroid employee population with metabolic syndrome component(s). Methods: An annual health check-up was performed on employees in 2019. Anthropometric parameters, metabolic parameters and thyroid function were measured. A questionnaire was used in conjunction with Zhenhai Lianhua Hospital database to receive employees' medication records and thyroid surgical history records. Results: A total of 5486 eligible employees were included, the prevalence of metabolic syndrome was generally higher in males than in females (38.9% vs. 30.4%, P < 0.001). Among employees with central obesity, hypertriglyceridemia, hyperglycemia, hypertension, and low high density lipoprotein cholesterol, the prevalence of metabolic syndrome was 68.8%, 63.6%, 68.2%, 48.8% and 60.0% in males and 72.6%, 63.3%, 61.3%, 42.3% and 42.3% in females, respectively. Logistic regression analysis showed that thyroid stimulating hormone (TSH) and Free thyroxine (FT4) quartiles had no significant impact on metabolic syndrome; Free Triiodothyronine / Free thyroxine (FT3/FT4), and Free Triiodothyronine (FT3) quartiles were positively associated with the increased odds ratio for metabolic syndrome and dyslipidemia (hypertriglyceridemia, low HDL-C), regardless of gender. In males, FT3, FT3/FT4 quartiles were positively associated with the odds ratio for central obesity, whereas FT4 quartiles were negatively associated; both FT3 and FT4 quartiles were positively associated with increased odds ratio of hyperglycemia, while similar results were not observed in females. Interaction analysis indicated no significant effect of gender and thyroid hormone interactions on risk of metabolic syndrome. Conclusion: High FT3, FT3/FT4 were strongly linked with metabolic syndrome and dyslipidemia in our study, even in the euthyroid individuals. Tighter control of thyroid function was necessary for those with pre-existing metabolic syndrome component(s).

Diabetes mellitus is a metabolic disease caused by a combination of genetics and environmental factors. The importance of the inflammatory response occurring in the pancreas and adipose tissue in the occurrence and progression of diabetes has been gradually accepted. Excess blood glucose and free fatty acids produce large amounts of inflammatory cytokines and chemokines through oxidative stress and endoplasmic reticulum stress. There is sufficient evidence that proinflammatory mediators, such as interleukin (IL)-1β, IL-6, macrophage chemotactic protein-1, and tumor necrosis factor-α, are engaged in the insulin resistance in peripheral adipose tissue and the apoptosis of pancreatic β-cells. IL-36, IL-37, and IL-38, as new members of the IL-1 family, play an indispensable effect in the regulation of immune system homeostasis and are involved in the pathogenesis of inflammatory and autoimmune diseases. Recently, the abnormal expression of IL-36, IL-37, and IL-38 in diabetes has been reported. In this review, we discuss the emerging functions, potential mechanisms, and future research directions on the role of IL-36, IL-37, and IL-38 in diabetes mellitus and its complications.