Objective To explore the independent risk factors for complicated coronary heart disease (CHD) in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and to construct a risk prediction model. Methods A retrospective study was performed to analyze the clinical data of 308 OSAHS patients who visited Jiangsu Provincial People's Hospital from January 2021 to June 2025. The patients were divided into the CHD group (n=80) and non-CHD group (n=228) according to the presence or absence of complicated CHD. Independent risk factors were identified using univariate analysis and multivariate logistic regression, and a nomogram prediction model was constructed. The model was evaluated using the calibration curve, Hosmer-Lemeshow test, Decision Curve Analysis (DCA) curve, and Receiver Operating Characteristic (ROC) curve. Results The incidence of CHD in OSAHS patients was 25.97%. Age, history of hypertension, oxygen desaturation index (ODI), severe polysomnography (PSG) grade, decreased high-density lipoprotein cholesterol, elevated homocysteine, and elevated troponin I were independent risk factors for OSAHS complicated with CHD (P<0.05). The nomogram model demonstrated good calibration (Hosmer-Lemeshow test, P=0.995), and the DCA curve showed high clinical net benefit. The area under the ROC curve was 0.940 (95% CI: 0.908~0.972), with a sensitivity of 0.842 and a specificity of 0.900. Conclusion Age, history of hypertension, ODI, PSG grade, high-density lipoprotein cholesterol, homocysteine, and troponin I are independent risk factors for CHD in OSAHS patients. The prediction model constructed based on these factors can provide a reliable tool for clinical nurses to early identify high-risk individuals and formulate targeted intervention strategies.

BACKGROUND:Rheumatoid arthritis is an inflammatory disease.Many studies have shown that wogonin has a good anti-inflammatory effect on rheumatoid arthritis,but its exact efficacy and specific mechanism of action remain to be clarified. OBJECTIVE:To investigate the mechanism of wogonin ameliorating joint inflammation by regulating endoplasmic reticulum stress pathway in rats with collagen-induced arthritis. METHODS:(1)At the animal level:Female Wistar rats were divided into healthy control group,arthritis model group and wogonin treatment group.Rat models of arthritis in the latter two groups were established by subcutaneous injection of bovine type Ⅱ collagen and adjuvant.In the wogonin group,wogonin was given by gavage for 28 consecutive days after modeling.During this period,the rats in each group were weighed,and arthritis score and ankle swelling were measured every 7 days.After the experiment,the pathological changes of the joint were observed,the mRNA and protein levels of endoplasmic reticulum stress pathway GRP78 and CHOP were detected by qRT-PCR,western blot,and immunohistochemistry.(2)At the cellular level,cell counting kit-8 was used to detect the cytotoxic effect of wogonin on fibroblast-like synoviocytes from rats with collagen-induced arthritis.The fibroblast-like synoviocytes induced by thapsigargin were treated with different concentrations of wogonin.The levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant were detected by ELISA,and the intracellular reactive oxygen species in each group were determined by DCFH-DA probe method.The mRNA and protein levels of GRP78,IRE1α,XBP1s and CHOP were detected by qRT-PCR and western blot,respectively. RESULTS AND CONCLUSION:Compared with the healthy control group,arthritis index score and ankle swelling degree in the arthritis model group were increased(P<0.01),synovial hyperplasia,inflammatory cell infiltration,cartilage destruction and bone erosion were observed in pathological sections,and the mRNA and protein expressions of GRP78 and CHOP in the ankle were significantly increased(P<0.01),which were mainly located in synovial tissue and articular surface.Compared with the arthritis model group,the arthritis index score and ankle swelling degree in the wogonin treatment group were decreased(P<0.05),synovial hyperplasia and the number of inflammatory cells were decreased,cartilage destruction and bone erosion were alleviated,the mRNA and protein expression levels of GRP78 and CHOP in the ankle were decreased(P<0.05),particularly in synovial tissue and on the articular surface.There was no significant difference in body mass among the three groups(P>0.05).In the cell experiment,200 μmol/L wogonin significantly reduced the survival rate of fibroblast-like synoviocytes(P<0.01).Compared with the blank control group,the levels of interleukin-1β,tumor necrosis factor-α,content of reactive oxygen species,and mRNA and protein expression of GRP78,IRE1α,XBP1s,and CHOP in the thapsigargin group were significantly increased(P<0.05);compared with the thapsigargin group,50 and 100 μmol/L wogonin significantly reduced the levels of interleukin-1β and tumor necrosis factor-α in the cell supernatant(P<0.05,P<0.01),and 100 μmol/L wogonin significantly reduced the content of reactive oxygen species(P<0.01)and down-regulated the mRNA and protein expression levels of GRP78,IRE1α,XBP1s and CHOP(all P<0.05).These results suggest that wogonin can effectively alleviate joint inflammatory responses in rats with collagen-induced arthritis,and the endoplasmic reticulum stress pathway may be the key target of its intervention.

Autosomal dominant tubulointerstitial kidney disease (ADTKD) is a rare autosomal dominant hereditary disorder characterized by hyperuricemia, gout, impaired urinary concentration, and progressive renal failure. It is primarily caused by mutations in uromodulin (UMOD) gene. This study reports a family with ADTKD in which whole-exome sequencing and Sanger sequencing identified a missense mutation in the UMOD gene, c.761A>C (p.H254P), present in both the proband and affected relatives. According to American College of Medical Genetics and Genomics (ACMG) guidelines, this variant is classified as likely pathogenic. The mutation results in an amino acid substitution that may impair UMOD protein folding and intracellular trafficking. UMOD gene mutations are associated with ADTKD, and genetic testing plays a vital role in the early diagnosis and treatment of this condition, highlighting its importance in the diagnosis of rare kidney diseases.
Adult ; Humans ; Male ; Exome Sequencing ; Mutation ; Mutation, Missense ; Nephritis, Interstitial/genetics* ; Pedigree ; Uromodulin/genetics*

Long-term spaceflight exposes astronauts to multiple extreme environmental factors, such as cosmic radiation, microgravity, social isolation, and circadian rhythm disruption, that markedly increase the risk of depressive symptoms, posing a direct threat to mental health and mission safety. However, the underlying biological mechanisms remain complex and incompletely understood. The potential mechanisms of spaceflight-induced depressive symptoms involve multiple domains, including alterations in brain structure and function, dysregulation of neurotransmitters and neurotrophic factors, oxidative stress, neuroinflammation, neuroendocrine system imbalance, and gut microbiota disturbances. Collectively, these changes may constitute the biological foundation of depressive in astronauts during spaceflight. Space-related stressors may increase the risk of depressive symptoms through several pathways: impairing hippocampal neuroplasticity, suppressing dopaminergic and serotonergic system function, reducing neurotrophic factor expression, triggering oxidative stress and inflammatory responses, activating the hypothalamic-pituitary-adrenal axis, and disrupting gut microbiota homeostasis. Future research should integrate advanced technologies such as brain-computer interfaces to develop individualized monitoring and intervention strategies, enabling real-time detection and effective prevention of depressive symptoms to safeguard astronauts' psychological well-being and mission safety.
Space Flight ; Humans ; Astronauts/psychology* ; Depression/physiopathology* ; Gastrointestinal Microbiome ; Weightlessness/adverse effects* ; Oxidative Stress ; Brain/physiopathology* ; Hypothalamo-Hypophyseal System ; Neuronal Plasticity ; Pituitary-Adrenal System

During long-duration manned space missions, the complex and extreme space environment exerts significant impacts on astronauts' physiological, psychological, and cognitive functions, thereby posing direct risks to mission safety and operational efficiency. As a key bridge between the brain and external devices, brain-computer interface (BCI) technology enables precise acquisition and interpretation of neural signals, offering a novel paradigm for human-machine collaboration in manned spaceflight. Non-invasive BCI technology shows broad application prospects across astronaut selection, mission training, in-orbit task execution, and post-mission rehabilitation. During mission preparation, multimodal signal assessment and neurofeedback training based on BCI can effectively enhance cognitive performance and psychological resilience. During mission execution, BCI can provide real-time monitoring of physiological and psychological states and enable intention-based device control, thereby improving operational efficiency and safety. In the post-mission rehabilitation phase, non-invasive BCI combined with neuromodulation may improve emotional and cognitive functions, support motor and cognitive recovery, and contribute to long-term health management. However, the application of BCI in space still faces challenges, including insufficient signal robustness, limited system adaptability, and suboptimal data processing efficiency. Looking forward, integrating multimodal physiological sensors with deep learning algorithms to achieve accurate monitoring and individualized intervention, and combining BCI with virtual reality and robotics to develop intelligent human-machine collaboration models, will provide more efficient support for space missions.
Brain-Computer Interfaces ; Humans ; Space Flight ; Astronauts/psychology* ; Neurofeedback ; Cognition ; Electroencephalography ; Man-Machine Systems

OBJECTIVES: Mobile phone dependence has become increasingly prominent among university students, posing significant risks to their social functioning and mental health. Previous studies suggest that perfectionistic personality traits may be key psychological predictors of mobile phone dependence, but the underlying mechanisms remain unclear. This study aims to identify core symptoms of mobile phone dependence among university students and to examine the pattern of associations between different dimensions of perfectionism and mobile phone dependence. METHODS: A cross-sectional questionnaire survey was conducted among 1404 university students nationwide. The Mobile Phone Involvement Questionnaire (MPIQ) and the Forst Multidimensional Perfectionism Scale (FMPS) were used to assess mobile phone use and perfectionism traits. The EBIC-GLASSO network model was constructed to analyze the network structure linking perfectionism and mobile phone dependence. RESULTS: A total of 56.48% of university students in the sample met the criteria for mobile phone dependence. The total FMPS score was positively correlated with the total MPIQ score (r=0.47, P<0.001). Results of multiple linear regression controlling for demographic variables showed that dimensions of FMPS score significantly predicted MPIQ score (all P<0.05). Network analysis revealed that the central dimension in perfectionism is "organization" (expected influence=2.69) and the core symptom of mobile phone dependence was "I lose track of how much I am using my smartphone" (expected influence= 0.78). Bridge centrality analysis identified "organization" as a key bridging factor linking perfectionism and mobile phone dependence (bridge strength=1.96). Among the symptom-to-symptom connections, "parental expectations" showed the strongest positive association with "arguments have arisen with others because of my mobile phone use" (partial correlation coefficient=0.15), serving as a risk factor. In contrast, "organization" was most strongly negatively associated with the same symptom (partial correlation coefficient=-0.13), serving as a protective factor, suggesting a protective effect. CONCLUSIONS Mobile phone dependence is common among college students and is primarily characterized by a lack of self-control in phone use. Although perfectionism is generally positively associated with mobile phone dependence, its internal dimensions appear to exert a dual effect. Specifically, "parental expectations" and "doubt over actions" may increase the risk of mobile phone dependence, whereas "organization" serves as a protective factor, particularly against interpersonal conflicts related to phone dependency.
Humans ; Perfectionism ; Students/psychology* ; Cell Phone ; Universities ; Cross-Sectional Studies ; Male ; Female ; Surveys and Questionnaires ; China ; Young Adult ; Adult ; Adolescent ; Personality

T-cell acute lymphoblastic leukemia (T-ALL) is a highly aggressive hematologic malignancy with a poor prognosis, despite advancements in treatment. Many patients struggle with relapse or refractory disease. Investigating the role of the super-enhancer (SE) regulated gene ubiquitin-specific protease 20 (USP20) in T-ALL could enhance targeted therapies and improve clinical outcomes. Analysis of histone H3 lysine 27 acetylation (H3K27ac) chromatin immunoprecipitation sequencing (ChIP-seq) data from six T-ALL cell lines and seven pediatric samples identified USP20 as an SE-regulated driver gene. Utilizing the Cancer Cell Line Encyclopedia (CCLE) and BloodSpot databases, it was found that USP20 is specifically highly expressed in T-ALL. Knocking down USP20 with short hairpin RNA (shRNA) increased apoptosis and inhibited proliferation in T-ALL cells. In vivo studies showed that USP20 knockdown reduced tumor growth and improved survival. The USP20 inhibitor GSK2643943A demonstrated similar anti-tumor effects. Mass spectrometry, RNA-Seq, and immunoprecipitation revealed that USP20 interacted with hypoxia-inducible factor 1 subunit alpha (HIF1A) and stabilized it by deubiquitination. Cleavage under targets and tagmentation (CUT&Tag) results indicated that USP20 co-localized with HIF1A, jointly modulating target genes in T-ALL. This study identifies USP20 as a therapeutic target in T-ALL and suggests GSK2643943A as a potential treatment strategy.

Alzheimer's disease (AD) is the leading neurodegenerative disorder in the nervous system, and there is still a lack of effective therapeutic drugs. Protecting neurons and synapses is crucial in reversing AD progression. Mesenchymal stem cell-derived exosome (MSC-Exo) is rich in various stem cell components such as proteins, RNAs, and DNAs; due to its strong ability in promoting nerve repair and inhibiting neuroinflammation, MSC-Exo is expected to become a potential choice for AD treatment. This article elaborates on the biological characteristics of MSC-Exo and its application and progress in AD treatment, aiming to provide reference for translational medicine research and clinical application of MSC-Exo in AD.

Thyroid cancer is the only non reproductive tumor that mainly occurs in women.The morbidity rate of female thyroid cancer is three times higher than that of male thyroid cancer.However,the ex-isting studies have not systematically summarized the factors that contribute to the high incidence of thyroid cancer in women.This paper reviews all the literatures that mention the high incidence of thyroid cancer in women,and sorts out the main reasons,such as estrogen,obesity,reproductive factors,oxidation antioxidant system imbalance,X chromosome,etc.,which are the main reasons for the current research finding that the in-cidence rate of thyroid cancer in women is higher than that in men.This paper makes a vivid graphic analysis and summary of the reasons,providing a research direction for future researchers to research on gender duality of thyroid cancer,and providing a certain reference for the clinical diagnosis and treatment of gender differences in thyroid cancer.

Tumour neoantigen sprimarily refer to a specific group of tumour antigens derived from tumour mutant proteins, but also including antigens generated by the oncogenic viruses integrated into the genome, which are not expressed by normal cells in the human body but are specifically expressed in tumor cells, and are capable of triggering the tumour-specific cellular and humoral immunity in the host. In recent years, significant advances in tumor immunotherapy such as therapeutic oncology vaccines, and adoptive cell therapy (ACT) have been acquired. However, standalone tumor therapeutic vaccines exhibit several drawbacks. They possess low immunogenicity, face a substantial tumor burden, and are highly susceptible to the immunosuppressive microenvironment. Consequently, when applied in isolation during clinical practice, their therapeutic efficacy remains limited. Compared with immunotherapies such as immune checkpoint inhibitors and tumor vaccines, ACT is less affected by the immunosuppressive microenvironment in the body and can generate a sufficient number of killer cells. The crux of ACT lies in the generation of immunogenic tumor-specific killer cells. Neoantigens enhance the immunogenicity and anti-tumor specificity of ACT. Among them, the ACT targeting mutant gene mutations, including ERBB2IP, KRAS and TP53, as well as those derived from viruses such as Epstein-Barr virus (EBV) and human papillomavirus (HPV), is primarily summarized. Moreover, the existing issues of neoantigen-specific ACT and corresponding countermeasures are summarized and discussed.