Stroke patients have a high incidence of venous thromboembolism (VTE). Improving the prevention and control rates of VTE in stroke patients can enhance their quality of life. The aim of this study was to analyze the effect of 4R crisis management combined with the health belief model in the prevention and control of VTE in stroke patients.

A randomized controlled trial was conducted on 86 stroke patients in the neurosurgery department of a tertiary hospital in Wuhan. The control group was treated with the routine VTE prevention and control strategy, while the experimental group was treated with 4R crisis management combined with the health belief model. The primary outcome measures were the incidence rates of deep vein thrombosis and pulmonary thromboembolism, while the secondary outcome measures were the Short Form Health Belief Model Scale score, medical quality evaluation, and stroke patients’ health behavior scale score. The statistical analysis methods included t-tests and non-parametric tests.

After the intervention, the incidence rate of deep vein thrombosis in the control group was 14.6% (6/41), while in the experimental group it was 2.4% (1/41). The difference was statistically significant (χ2 = 3.905, P = 0.048). The incidence rates of pulmonary thromboembolism in both groups were 0%. The scores of all dimensions of the Short Form Health Belief Model Scale in the experimental group were higher than those in the control group, and the difference was statistically significant (P < 0.05, P < 0.01). The medical quality for each item showed that the experimental group performed better than the control group, with the difference being statistically significant (P < 0.05, P < 0.01). The scores on the stroke patients’ health behavior scale in the experimental group were higher than in the control group, except for responsibility, tobacco, and alcohol (P < 0.01).

The application of 4R crisis management combined with the health belief model can effectively improve the health beliefs and health behaviors of stroke patients to prevent VTE, thereby reducing the incidence of VTE.

Accumulating evidence indicates that fecal syndecan-2 (SDC2) methylation is a promising biomarker for early detection of colorectal cancer. This study aimed to investigate the diagnostic efficacy of fecal SDC2 methylation testing for adenomas and evaluate the risk stratification efficacy of the Asia-Pacific Colorectal Screening Scoring (APCS) combined with SDC2 methylation status.

This was a prospective, multicenter diagnostic study. Adult participants with no history of colonoscopy within the past three years were enrolled. Demographic data were collected, and APCS scores were evaluated. All participants underwent fecal SDC2 methylation testing and colonoscopy. Colonoscopy outcomes and pathological results of any polyps served as reference standards. The fecal SDC2 methylation test and reference standard assessments were conducted in a blinded manner. The APCS-SDC2 scoring system was developed by integrating fecal SDC2 methylation results with APCS scores, and its efficacy was assessed.

In total, 985 participants were enrolled, among whom 62 (6.3%) tested positive for fecal SDC2 methylation. The sensitivity and specificity of fecal SDC2 methylation in detecting advanced adenomas were 31.3% (95% confidence interval (CI): 21.6–42.7%) and 96.1% (95% CI: 94.6–97.2%), respectively. The APCS-SDC2 scoring system demonstrated superior discriminatory performance for advanced adenomas (area under the curve: 0.7032; 95% CI: 0.5869–0.8195). For advanced adenoma screening, the specificity of the APCS-SDC2 score was higher than that of the APCS score (86.7% vs. 66.7%; P < 0.001).

A positive fecal SDC2 methylation test indicated a higher risk of advanced adenoma, and colonoscopy should be prioritized. The APCS-SDC2 scoring system demonstrated superior risk stratification performance for advanced adenomas.

Artificial intelligence (AI) is transforming the diagnosis, treatment, monitoring, and research of soft tissue disorders, which include muscles, tendons, ligaments, fascia, nerves, and blood vessels. Traditional diagnostic methods often rely on imaging, histopathology, and clinical evaluation, which can be time-consuming and prone to human error. This review aims to explore the impact of AI on enhancing soft tissue care. The review examines the application of deep learning algorithms in medical imaging, pathology, predictive analytics, and treatment planning. It also evaluates AI’s role in monitoring and rehabilitation, as well as its contributions to research in soft tissue disorders. AI significantly improves the accuracy of medical imaging analysis, facilitating the detection of abnormalities such as tumors and tears. AI-powered pathology tools automate slide analysis, enhancing diagnostic consistency and efficiency. Predictive analytics enable early risk assessment and personalized patient management. In surgical contexts, AI supports preoperative simulations and robotic-assisted procedures, leading to improved outcomes. Additionally, AI enhances patient monitoring through wearable devices and telemedicine. The integration of AI into soft tissue diagnostics and therapeutics presents transformative potential for personalized and efficient healthcare. However, challenges related to data security, algorithm bias, interpretability, and ethical considerations must be addressed. Overall, AI holds promise for improving patient outcomes and advancing medical science in the field of soft tissue disorders.

Endometrial polyp (EMP) is one of the most common diagnoses in the evaluation of women with abnormal uterine bleeding. Understanding the malignancy risk associated with EMPs and related risk factors is essential for guiding both pathology practice and clinical management. This study aimed to explore risk factors for malignancy in EMPs.

The pathology database was searched for women diagnosed with EMP between 2021 and 2022. Patient age, polyp size, background endometrium, recurrence, and (if applicable) cancer types were recorded. Immunohistochemistry (IHC) for p53 and p16 was performed on selected cases. Risk factors for malignancy were analyzed using Chi-square and analysis of variance tests.

Among the 740 EMP cases analyzed, 94% were benign, 2% were premalignant, and 4% were malignant. The median patient age was 54 years (range: 19–92). Minimal serous carcinoma (n = 14, 2%) was the most prevalent cancer. Among the 52 cases with p53 IHC, 38 were diagnosed as benign, supported by a wild-type p53 pattern, while 14 were diagnosed as serous carcinoma, supported by a mutant p53 pattern. Malignant polyps were found to be significantly associated with advanced age and malignant background endometrium (p < 0.001). Large size and recurrence were not identified as significant risk factors.

EMPs carry a low risk of malignancy, which is not significantly influenced by the polyp’s size or its recurrence. Our findings highlight the significantly elevated risk of malignancy in elderly patients and the importance of p53 IHC in improving diagnostic accuracy.

Full or partial trisomy of human chromosome 21 results in dysregulation of gene expression, leading to the manifestation of specific phenotypes described in individuals with Down syndrome (DS). Defects in brain development, coupled with impairment in neurogenesis, are ultimately expressed as cognitive deficiency, Alzheimer disease (AD), and dementia. Amid the triplication of all human chromosome 21 (HSA21) genes, dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A)-mediated neurogenesis and dendritic development have been attributed to the learning and memory deficits and cognitive impairment in the DS population. Upregulated DYRK1A perturbs the development and function of the brain, collectively affecting neurogenesis, synaptogenesis, synaptic transmission, and cell signaling pathways, which might disproportionately produce inhibitory neurotransmission and contribute to the cognitive phenotype. However, the lack of distinct gene-phenotype associations acts as a potential barrier to therapeutic improvement of cognitive performance and amelioration of AD-related neurodegeneration. The present review aims to summarize the neurogenetic consequences of triplicated DYRK1A in the DS population in relation to sexual dimorphism and expression of the Apolipoprotein Eε4 (APOE ε4) genotype. Notably, normalization of trisomic DYRK1A demonstrated improved synaptic plasticity, glutamatergic/GABAergic (excitatory/inhibitory) balance, and learning and memory in DS mouse models. Therapeutic approaches using inhibitors of DYRK1A, including catechins present in green tea extract and several other natural and synthetic agents, produced variable outcomes in cognitive improvement, depending on age and dose of administration. Mitigation of impairment in neurogenetic differentiation and cognitive performance might help control AD-related dementia and enhance quality of life. This review highlights the consequences of upregulated DYRK1A kinase on impairment of neurogenesis and cognitive deficits, and the therapeutic challenges associated with DYRK1A inhibitors for ameliorating dysregulated gene expression in DS models and human DS.

ATP-binding cassette (ABC) transporters are transmembrane proteins involved in the translocation of bilirubin, bile acids, phospholipids, and cholesterol into bile canaliculi. Mutations in particular genes encoding these transporters—including BSEP (ABCB11 gene), MDR3 (ABCB4 gene), sterolin-1 and sterolin-2 (ABCG5/8 genes), and MRP2 (ABCC2 gene)—result in a wide spectrum of liver diseases, ranging from benign conditions such as Dubin-Johnson syndrome to more severe presentations like progressive familial intrahepatic cholestasis. The severity of disease is influenced by many factors, including zygosity, mutation type, and environmental modifiers such as hormones, consanguinity, and founder effects. Homozygous and compound heterozygous mutations typically result in severe and early-onset diseases, while heterozygous single-allelic mutants generally result in milder diseases. Next-generation genetic testing has proven to have high diagnostic value and is important for prognostication. With knowledge of the underlying specific mutations, there is also potential for future targeted therapy for many severe diseases. The aim of this review is to update and discuss the hepatic diseases associated with ABC transporter mutations, the genetic and environmental effects that influence the severity of disease, typical presentations of these cholestatic hepatic diseases, diagnostic considerations, and treatment options.

Hepatic iron deposition (HID) in the reticuloendothelial system (RES) is associated with histological severity in metabolic dysfunction-associated steatotic liver disease (MASLD). This study aimed to assess the interaction between the transferrin (TF)-rs1049296 C>T variant and HID patterns on the risk of significant liver fibrosis in MASLD.

We analyzed 406 adults with liver biopsy-confirmed MASLD. HID was categorized as hepatocellular, RES, or mixed, based on Perl's iron staining. The association between iron-related genetic variants and significant liver fibrosis (fibrosis stage ≥ F2) was analyzed, focusing on the interactions between single-nucleotide polymorphism genotypes and iron deposition patterns. Multivariable logistic regression analysis was used to adjust for potential confounders.

HID was detected in 271 (66.7%) patients, with hepatocellular, RES, and mixed patterns accounting for 11.1%, 18.0%, and 37.7%, respectively. A significant interaction was observed between HID and the TF-rs1049296 genotype (Pinteraction = 0.035). In multivariable analysis, male sex, hypertension, severe lobular inflammation, and mixed hepatocellular/RES iron deposition were independent predictors of significant liver fibrosis. RES deposition markedly increased the risk of significant liver fibrosis (adjusted odds ratio: 6.65; 95% confidence interval: 1.84–23.97, p < 0.05), particularly in men with isolated RES iron deposition (adjusted odds ratio: 5.26; 95% confidence interval: 1.21–22.81, p < 0.05).

The TF-rs1049296 T allele interacts with RES iron deposition to identify a MASLD subpopulation at elevated risk of progressive liver disease, providing opportunities for refined risk stratification and personalized management.