Coronavirus disease 2019 (COVID‐19) is a health emergency worldwide, and gastrointestinal (GI) symptoms are increasingly reported in COVID‐19 patients. However, sample size was small and the incidence of GI symptoms in patients was variable across studies, and the correlation between these symptoms and clinical outcomes remains incompletely understood. The objective of this study is to compare clinical characteristics and outcomes between patients with and without GI symptoms admitted to Jianghan Fangcang Shelter Hospital in Wuhan. This retrospective study recruited 1320 COVID‐19 patients admitted to hospital from 5 February 2020 to 9 March 2020. On the basis of the presence of GI symptoms, the sample was divided into a GI group (n = 192) and a non‐GI group (n = 1128). The three most common GI symptoms were diarrhea (8.1%), anorexia (4.7%), and nausea and vomiting (4.3%). The rate of clinical deterioration was significantly higher in the GI group than in the non‐GI group (15.6% vs. 10.1%, P = .032). GI symptoms (P = .045), male gender P < .001), and increased C‐reactive protein (P = .008) were independent risk factors for clinical worsening. This study demonstrated that the rate of clinical deterioration was significantly higher in the GI group. Furthermore, potential risk factors for developing GI symptoms, male gender, and increased C‐reactive protein can help clinicians predict clinical outcomes in COVID‐19 patients.

Background and purpose: Mitophagy plays a significant role in the progression of diabetic nephropathy (DN), although the regulatory mechanisms remain unclear. Recently, accumulating evidence demonstrated that impaired mitochondrial function and mitophagy are involved in DN. Here, we are aimed to explore the role of c-Src (Src) and FUNDC1-related mitophagy in the development of DN.Methods: The db/db mice were used to establish a DN mice model. The mice accepted PP2 (Src inhibitor) treatment to study the role of Src in DN. Kidney function was measured via biochemical testing. Renal histopathology and morphometric analysis were conducted via hematoxylin-eosin (HE), periodic acid-Schiff (PAS), Masson’s staining, and transmission electron microscopy (TEM). We measured degree of apoptosis in kidney by TUNEL assay. Indices of mitophagy (LC3 and p62) were evaluated by Western blotting and immunofluorescence. Complementary in vitro assays were conducted using human podocytes subjected to high glucose in combination with PP2 treatment or FUNDC1 small interfering RNAs (siRNAs). Flow cytometry was used to detect the apoptotic cells. Mitochondrial function was evaluated by JC-1 staining. Double immunofluorescence labeling of LC3 and TOMM20 used to assess the degree of mitophagy.Results: Increased Src activation was detected in the kidneys of db/db mice, and its expression was positively correlated with mitochondrial damage, podocyte apoptosis, and renal dysfunction. Inhibition of Src activation with PP2 protected against mitochondrial damage and podocyte apoptosis. In vitro experiments in podocytes established that high glucose increased Src activation, promoting FUNDC1 phosphorylation and inhibiting mitophagy. Consistent with the mouse model, inhibiting Src activity protected podocytes against mitochondrial damage. FUNDC1 silencing negated the actions of PP2, indicating that FUNDC1-mediated mitophagy is downstream pathway of Src.Conclusion: In summary, our data indicated that Src is a culprit factor in diabetic renal damage via suppression of FUNDC1-mediated mitophagy, promoting the development of DN.

Background: There is no clear conclusion on the relationship between thyroid disease and obesity and lifestyle factors such as smoking and drinking. In this study, we analysed the association of body mass index (BMI), smoking and drinking with subclinical hypothyroidism (SHO) and thyroid nodules (TNs) with the results of a cross-sectional survey of urban residents in central China and discussed the potential mechanism linking these predictive factors and the two diseases. Methods: This study included 1279 participants who were recruited from a Chinese community in 2011 and 2012. A questionnaire, laboratory examination and ultrasound diagnosis were conducted on these participants. Binary logistic regression analysis was used to analyse these factors. Results: Overweight (BMI ≥ 25 kg/m²) was closely related to SHO and TNs in univariate and multivariate logistic regression analyses. Smoking had a protective effect on SHO and TNs, while drinking had a protective effect on TNs in univariate logistic regression and multivariate logistic regression with some covariates, but there was no significant difference between smoking and drinking and the two kinds of thyroid diseases in multivariate logistic regression analysis with all the covariates. In subgroup analysis, BMI ≥ 25 kg/m2 was significantly associated with SHO in people with positive thyroid antibodies (odds ratio (OR) = 2.221, 95 % confidence interval (CI): 1.168–4.184, P = 0.015) and smokers (OR = 2.179, 95 % CI: 1.041–4.561, P = 0.039). BMI ≥ 25 kg/m2 was significantly associated with TNs in people over 60 years old (OR = 2.069, 95 % CI: 1.149–3.724, P = 0.015) and drinkers (OR = 3.065, 95 % CI: 1.413–6.648, P = 0.005). Drinking alcohol had a protective effect on TNs in smokers (OR = 0.456, 95 % CI: 0.240–0.865, P = 0.016) and people with BMI ≥ 25 kg/m² (OR = 0.467, 95 % CI: 0.236–0.925, P = 0.029). No significant association was found between smoking and the two thyroid diseases in different subgroups. Conclusions: Obesity is a risk factor for both TNs and SHO, especially in elderly individuals and people with positive thyroid autoantibodies. Obesity and metabolic syndrome may be more associated with TNs than SHO. Smoking may have a protective effect on thyroid disease, while drinking may have a protective effect only on TNs.

Artificial intelligence (AI) has been used to study thyroid diseases since the 1990s. Previously, it mainly concentrated on the diagnosis of thyroid function and distinguishing benign from malignant thyroid nodules. With the rapid development of machine and deep learning, AI has been widely used in multiple areas of thyroid disease management, including image analysis, pathological diagnosis, personalized treatment, patient monitoring, and follow-up. This review systematically examines the evolution of AI applications in thyroid disease management since the 1990s, with a focus on diagnostic innovations, therapeutic personalization, and emerging challenges in clinical implementation. AI not only reduces the subjectivity associated with ultrasound examinations but also enhances the differentiation rate of benign and malignant thyroid nodules, thereby reducing the frequency of unnecessary fine-needle aspirations. AI synthesizes multimodal data, such as ultrasound, electronic health records, and wearable sensors, for continuous health monitoring. This integration facilitates the early detection of subclinical recurrence risk, particularly in patients who have undergone thyroidectomy. Despite the broad prospects of AI applications, challenges related to data privacy, model interpretability, and clinical applicability remain. This review critically evaluates studies across the ultrasound, CT/MRI, and histopathology domains, while addressing barriers to clinical translation, such as data heterogeneity and ethical concerns.

Purpose: The expressions of antibodies against thyroid peroxidase (TPOAb) and thyroglobulin (TgAb) are very common in the sera of patients with autoimmune thyroid diseases (AITD). The relationship between thyroid autoantibodies and the occurrence of glucose and lipid metabolic disorders remains unclear. This study was performed to investigate the correlation between the presence of serum TPOAb/TgAb and those metabolic disorders in euthyroid general population. Methods: The data of this study were derived from the Thyroid Disease, Iodine status, and Diabetes National epidemiological (TIDE) survey from all 31 provinces of mainland China. A total of 17,964 euthyroid subjects including 5,802 males (4,000 with TPOAb⁻TgAb⁻ and 1,802 with TPOAb⁺/TgAb⁺) and 12,162 females (8,000 with TPOAb⁻TgAb⁻ and 4,162 with TPOAb⁺/TgAb⁺) were enrolled in this study. The blood glucose and lipid levels were compared between individuals with TPOAb⁻TgAb⁻ and those with TPOAb⁺TgAb⁻, TPOAb⁻TgAb⁺, TPOAb⁺TgAb⁺. Results: Both fasting blood glucose (FBG) concentration and the proportion of individuals with impaired FBG (IFG) showed the decreased trends in TPOAb⁻TgAb⁺ males as compared with TPOAb⁻TgAb⁻ men. There were significantly lower FBG and higher HDL-C levels as well as tendencies toward decreased incidences of IGT and hypertriglyceridemia in TPOAb⁻TgAb⁺ females when compared with TPOAb⁻TgAb⁻ women. Binary logistic regression analysis further showed that serum TgAb single positivity in males was an independent protective factor for IFG with an OR of 0.691 (95% CI, 0.503–0.949). For females, serum TgAb single positivity was an independent protective factor for hypertriglyceridemia with an OR of 0.859 (95% CI, 0.748–0.987). Trend test showed that with the increase of serum TgAb level, there were significant decreases in the prevalence of IFG among the men with TSH ≤ 2.5 mIU/L and that of hypertriglyceridemia in the women, especially among non-obese females. Conclusion: Serum TgAb single positivity may imply a reduced risk of IFG in euthyroid men and that of hypertriglyceridemia in euthyroid women. The mechanisms for the independent protective roles of TgAb await further investigation.