BACKGROUND:Alzheimer's disease has been associated with sarcopenia,but a causal relationship has not been established.Exploring the causal relationship between the two most common disability-burdening diseases in the aging population-Alzheimer's disease and sarcopenia-and their potential mediating factors holds certain implications for further alleviating the healthcare costs and socioeconomic burden for older adults in China.OBJECTIVE:To explore the potential causal relationship between Alzheimer's disease and sarcopenia in the general population using a Mendelian randomization study and to explore the role of body mass index in this context.METHODS:Two-sample Mendelian randomization analysis based on published genome-wide association studies(GWAS)were used to infer causality,and univariate Mendelian randomization and mediation analyses were used in the study design.Through the Integrative Epidemiology Unit(IEU)database,ieu-b-2 was selected as the Alzheimer's disease dataset(sample size:63 926),ieu-b-4816 as the body mass index dataset(99 998),ebi-a-GCST90000027 as the appendicular lean mass dataset(244 730),ukb-b-7478 as the left hand grip strength dataset(461 026),ukb-b-10215 as the right hand grip strength dataset(461 089)and ukb-b-4711 as the walking pace dataset(459 915).Inverse-variance weighting was used as the primary analysis method,and the results were validated by pleiotropy and heterogeneity analysis.The Steiger Directionality Test was performed to validate the reasonableness of the causal direction.RESULTS AND CONCLUSION:(1)The Mendelian randomization analyses provided evidence that Alzheimer's disease predicted the risk of appendicular lean mass[odds ratio(OR)=1.009;95％confidence interval(Cl),1.001-1.017;P=0.023),and walking pace(OR=1.010;95％Cl,1.003-1.017;P=0.008).No correlation with hand grip strength was observed.(2)Alzheimer's disease was negatively correlated with body mass index(OR=0.893;95％Cl,0.811-0.984;P=0.022);body mass index was positively correlated with appendicular lean mass(OR=1.084;95％Cl,1.031-1.141;P=0.002)and negatively correlated with walking pace(OR=0.975;95％Cl,0.969-0.980;P＜0.001).(3)Mediation analyses showed that the causal relationship between Alzheimer's disease and appendicular lean mass and walking pace was partially mediated by body mass index,with the proportion of mediations being 50.25％and 32.11％,respectively.(4)The results of this study suggest that based on large-scale population studies,genetic prediction of Alzheimer's disease is a potential risk factor for sarcopenia,in which body mass index plays an important mediating role.This suggests that in clinical practice,attention should be paid to the muscle condition of patients with Alzheimer's disease,and weight management should be implemented,as maintaining a body mass index within the normal high range may have a preventive effect on the occurrence of sarcopenia in patients with Alzheimer's disease.However,further research is needed to verify the applicability of this conclusion to other ethnic groups.This study utilized an international public database for analysis,providing a reference for research on the correlation between Alzheimer's disease and sarcopenia in the Chinese population.It also highlights the significant mediating role of body mass index,offering insights for further prevention and treatment of sarcopenia among Chinese individuals.

ObjectiveTo analyze the characteristics of 150 patients with spinal cord injury complicated with spasticity. MethodsA cross-sectional survey was conducted on 150 patients with spinal cord injury accompanied by spasticity from September, 2019 to December, 2024. Their age, gender, cause of injury, injury site, severity of injury, spasticity severity and other indicators were recorded. The relationships between different characteristics were analyzed, and a correlation analysis of disease duration, spasticity grade, injury level, injury severity and age were conducted. ResultsThere was no significant difference in age distribution between patients with tetraplegia and paraplegia (Z = 0.806, P = 0.420). The proportions of trauma (χ² = 3.982, P = 0.046) and tetraplegia (χ² = 10.559, P = 0.010) were higher in males than in females. Trauma was the main cause of injury in both tetraplegia and paraplegia patients; the proportion of tetraplegia was higher than paraplegia in trauma patients, while paraplegia was higher than tetraplegia in non-trauma patients (χ² = 11.885, P < 0.001). Patients with tetraplegia was dominated by incomplete injury, whereas patients with paraplegia was dominated by complete injury (χ² = 10.885, P = 0.012). Grade A injury was predominant in trauma patients (P = 0.003). Spasticity grade showed a very weak positive correlation with disease duration (r = 0.175, P = 0.032) and age (r = 0.168, P = 0.040). Injury severity showed a very weak positive correlation with age (r = 0.183, P = 0.025). ConclusionCharacteristics of patients with spinal cord injury complicated with spasticity is different with gender, cause of injury, injury level, injury severity.

ObjectiveTo establish an ultra-performance liquid fingerprint and multi-components determination method for Naomaili granules. To evaluate the quality of different batches by chemometrics， and the anti-neuroinflammatory effects of water extract and main components of Naomaili granules were tested in vitro. MethodsThe similarity and common peaks of 27 batches of Naomaili granules were evaluated by using Ultra performance liquid chromatography （UPLC） fingerprint detection. Ultra-performance liquid chromatography-tandem mass spectrometry （UPLC-MS/MS） technology was used to determine the content of the index components in Naomaili granules and to evaluate the quality of different batches of Naomaili granules by chemometrics. LPS-induced BV-2 cell inflammation model was used to investigate the anti-neuroinflammatory effects of the water extract and main components of Naomaili granules. ResultsThe similarity of fingerprints of 27 batches of samples was > 0.90. A total of 32 common peaks were calibrated， and 23 of them were identified and assigned. In 27 batches of Naomaili granules， the mass fractions of 14 components that were stachydrine hydrochloride， leonurine hydrochloride， calycosin-7-O-glucoside， calycosin，tanshinoneⅠ， cryptotanshinone， tanshinoneⅡ_A， ginsenoside Rb₁， notoginsenoside R₁， ginsenoside Rg₁， paeoniflorin， albiflorin， lactiflorin， and salvianolic acid B were found to be 2.902-3.498， 0.233-0.343， 0.111-0.301， 0.07-0.152， 0.136-0.228， 0.195-0.390， 0.324-0.482， 1.056-1.435， 0.271-0.397， 1.318-1.649， 3.038-4.059， 2.263-3.455， 0.152-0.232， 2.931-3.991 mg∙g^-1， respectively. Multivariate statistical analysis showed that paeoniflorin， ginsenoside Rg₁， ginsenoside Rb₁ and staphylline hydrochloride were quality difference markers to control the stability of the preparation. The results of bioactive experiment showed that the water extract of Naomaili granules and the eight main components with high content in the prescription had a dose-dependent inhibitory effect on the release of NO in the cell supernatant. Among them， salvianolic acid B and ginsenoside Rb₁ had strong anti-inflammatory activity， with IC₅₀ values of （36.11±0.15） mg∙L^-1 and （27.24±0.54） mg∙L^-1， respectively. ConclusionThe quality evaluation method of Naomaili granules established in this study was accurate and reproducible. Four quality difference markers were screened out， and eight key pharmacodynamic substances of Naomaili granules against neuroinflammation were screened out by in vitro cell experiments.

BACKGROUND:Alzheimer's disease has been associated with sarcopenia,but a causal relationship has not been established.Exploring the causal relationship between the two most common disability-burdening diseases in the aging population-Alzheimer's disease and sarcopenia-and their potential mediating factors holds certain implications for further alleviating the healthcare costs and socioeconomic burden for older adults in China.OBJECTIVE:To explore the potential causal relationship between Alzheimer's disease and sarcopenia in the general population using a Mendelian randomization study and to explore the role of body mass index in this context.METHODS:Two-sample Mendelian randomization analysis based on published genome-wide association studies(GWAS)were used to infer causality,and univariate Mendelian randomization and mediation analyses were used in the study design.Through the Integrative Epidemiology Unit(IEU)database,ieu-b-2 was selected as the Alzheimer's disease dataset(sample size:63 926),ieu-b-4816 as the body mass index dataset(99 998),ebi-a-GCST90000027 as the appendicular lean mass dataset(244 730),ukb-b-7478 as the left hand grip strength dataset(461 026),ukb-b-10215 as the right hand grip strength dataset(461 089)and ukb-b-4711 as the walking pace dataset(459 915).Inverse-variance weighting was used as the primary analysis method,and the results were validated by pleiotropy and heterogeneity analysis.The Steiger Directionality Test was performed to validate the reasonableness of the causal direction.RESULTS AND CONCLUSION:(1)The Mendelian randomization analyses provided evidence that Alzheimer's disease predicted the risk of appendicular lean mass[odds ratio(OR)=1.009;95％confidence interval(Cl),1.001-1.017;P=0.023),and walking pace(OR=1.010;95％Cl,1.003-1.017;P=0.008).No correlation with hand grip strength was observed.(2)Alzheimer's disease was negatively correlated with body mass index(OR=0.893;95％Cl,0.811-0.984;P=0.022);body mass index was positively correlated with appendicular lean mass(OR=1.084;95％Cl,1.031-1.141;P=0.002)and negatively correlated with walking pace(OR=0.975;95％Cl,0.969-0.980;P＜0.001).(3)Mediation analyses showed that the causal relationship between Alzheimer's disease and appendicular lean mass and walking pace was partially mediated by body mass index,with the proportion of mediations being 50.25％and 32.11％,respectively.(4)The results of this study suggest that based on large-scale population studies,genetic prediction of Alzheimer's disease is a potential risk factor for sarcopenia,in which body mass index plays an important mediating role.This suggests that in clinical practice,attention should be paid to the muscle condition of patients with Alzheimer's disease,and weight management should be implemented,as maintaining a body mass index within the normal high range may have a preventive effect on the occurrence of sarcopenia in patients with Alzheimer's disease.However,further research is needed to verify the applicability of this conclusion to other ethnic groups.This study utilized an international public database for analysis,providing a reference for research on the correlation between Alzheimer's disease and sarcopenia in the Chinese population.It also highlights the significant mediating role of body mass index,offering insights for further prevention and treatment of sarcopenia among Chinese individuals.

Secondary rhabdoid tumors (RTs) with atypical teratoid/rhabdoid tumor-like features rarely arise from, or coexist with, pleomorphic xanthoastrocytomas (PXAs), and their clinicopathological and molecular characteristics remain poorly understood. We report a 17-year-old girl with a temporal lobe mass that, upon gross total resection, pathologically contained both RT and PXA components. Immunohistochemistry revealed loss of INI1 expression restricted to the RT component, while the PXA area retained INI1. Next-generation sequencing identified a shared BRAF::TRIM24 fusion and homozygous deletion of CDKN2A/2B in both components, indicating a shared clonal origin. Additionally, a germline ATM frameshift mutation (c.5288_5289insGA) was identified in both tumor components, making the first such report in central nervous system tumors. SMARCB1 loss was confined to the RT component, further supporting the hypotheses of clonal evolution and secondary transformation. Despite gross total resection, craniospinal irradiation, and chemotherapy, the patient developed rapid leptomeningeal dissemination and died 5 months after surgery. This case provides clinicopathological and molecular evidence for clonal evolution and secondary transformation of PXA into an RT. The presence of germline ATM mutation may have therapeutic and biological relevance. Further studies are required to clarify the pathogenesis and optimal management of these rare and aggressive tumors.

In patients with differentiated thyroid cancer (DTC), initial recurrence risk stratification based on clinical, histopathological, and perioperative data remains the key determinant for guiding management strategies during the first 1-2 years post-treatment. However, the adoption of ongoing risk stratification (ORS), which dynamically reassesses risk by integrating longitudinal clinical data and treatment response, enables more precise long-term prognostic assessment and facilitates highly individualized management. Building upon recent guidelines, the 2026 KTA guideline has been further refined by incorporating robust evidence from large-scale national cohorts and comprehensive systematic reviews. These updated recommendations outline contemporary concepts of ORS, risk-adapted TSH suppression targets, optimized surveillance modalities for recurrence detection, and disease-specific long-term follow-up strategies. Reflecting the paradigm shift toward de-escalated treatment, this revision integrates evolved perspectives on TSH suppression intensity, the clinical interpretation of thyroglobulin levels, and tailored follow-up intervals. These evidence-based recommendations aim to minimize unnecessary treatment and excessive surveillance in the large proportion of patients with excellent prognosis after initial therapy, while ensuring that each patient receives appropriately tailored and effective long-term management.

In modern society， the comorbidity of insomnia with amnesia has shown a significantly increasing incidence and become increasingly severe， emerging as a public health issue that endangers people's physical and mental health and quality of life. Anmei Dan （AMD）， originally recorded in the Shishi Milu by CHEN Shiduo in the Qing Dynasty， possesses profound theoretical foundations and distinct clinical advantages in ameliorating insomnia with amnesia. Basic research has unequivocally confirmed its definite therapeutic effects on insomnia with amnesia and revealed partial mechanisms. AMD is therefore a veritable classic prescription embodying the principle of treating different diseases with the same method for insomnia and amnesia. However， few researchers have reviewed the related research progress. This article systematically summarized the theoretical connotations of traditional Chinese medicine in treating insomnia with amnesia， delineated the multi-component material basis of AMD in ameliorating insomnia with amnesia （including various chemical components such as ginsenosides， jujubosides， and salvianolic acids）， and evaluate its multi-dimensional clinical efficacy （e.g.， prolonging total sleep time， improving sleep efficiency， and enhancing memory）. Moreover， it systematically summarizes the multi-pathway mechanisms of action. The results indicate that AMD has a clear material basis， definite clinical efficacy， and a favorable safety profile in ameliorating insomnia and amnesia. AMD may exert the therapeutic effect by regulating sleep-wake rhythms， enhancing synaptic plasticity， inhibiting neuroimmune inflammation， and modulating autophagy， oxidative stress， and energy metabolism. In conclusion， AMD exerts synergistic effects through multi-component， multi-dimensional， and multi-pathway approaches， serving as an important prescription for enriching and developing the theory of treating different diseases with the same method for insomnia with amnesia.

Tissue repair requires the reconstruction of functional vascular networks to restore oxygen and nutrient delivery, eliminate metabolic waste, and maintain tissue homeostasis. Although biochemical factors such as growth factors and cytokines have been extensively studied in vascular regeneration, increasing evidence indicates that mechanical signals from the extracellular matrix (ECM) are equally important regulators of angiogenesis. Matrix stiffness, as a major biomechanical property of the tissue microenvironment, provides critical information that influences endothelial cell (EC) behavior and vascular remodeling through mechanotransduction. However, the biological effects of matrix stiffness are not universally defined as either pro- or anti-angiogenic, but are highly dependent on tissue context, cellular composition, disease progression, and the dynamic changes occurring during tissue repair. Therefore, understanding how matrix stiffness regulates vascular regeneration is essential for developing more precise strategies for tissue engineering and regenerative medicine. In this review, we summarize recent advances in the regulation of angiogenesis by matrix stiffness during tissue repair from multiple perspectives. First, we discuss the direct effects of matrix stiffness on EC behaviors, including differentiation, morphological remodeling, migration, proliferation, barrier maintenance, and vascular network formation. ECs sense mechanical alterations in the surrounding matrix through various mechanosensitive structures, including integrins, focal adhesion complexes, and mechanosensitive ion channels such as Piezo1 and TRPV proteins. These mechanical signals are subsequently transmitted through intracellular pathways involving FAK, RhoA/ROCK, MAPK, and Hippo-YAP/TAZ signaling, leading to cytoskeletal reorganization and transcriptional regulation. Through these mechanisms, matrix stiffness regulates endothelial functional states and determines the balance between regenerative vascular formation and pathological vascular remodeling. Beyond the direct regulation of ECs, we further highlight the importance of stiffness-mediated intercellular communication within the regenerative microenvironment. Matrix stiffness can regulate the behavior and secretory profiles of vascular-associated cells, including mesenchymal stem cells and macrophages, thereby indirectly affecting endothelial function through paracrine mechanisms. Changes in matrix mechanics influence the secretion of angiogenic factors, inflammatory cytokines, and extracellular vesicles from these cells, creating a mechanical regulation network that coordinates vascular regeneration. This perspective extends the traditional concept of matrix stiffness from a physical support structure to an active regulatory signal that integrates multiple cellular responses during tissue repair. Furthermore, we discuss the tissue-specific effects of matrix stiffness in vascular regeneration across different organs, including the aorta, lung, liver, and heart. Although excessive matrix stiffening is frequently associated with fibrosis and vascular dysfunction, the consequences of mechanical changes vary considerably among tissues. Moderate stiffness alterations may support endothelial activation and vascular stabilization in certain regenerative contexts, whereas persistent pathological stiffening can promote inflammation, endothelial dysfunction, and impaired vascular repair. These findings emphasize that the biological meaning of “soft” and “stiff” microenvironments should be interpreted according to specific tissue and experimental conditions rather than as universal mechanical classifications. Finally, we summarize current challenges and future perspectives in this field. A major limitation is the lack of standardized mechanical characterization among different studies, as stiffness measurements are influenced by material properties, testing methods, and experimental conditions, limiting direct comparison across research systems. Moreover, most existing models fail to fully reproduce the dynamic and viscoelastic properties of native ECM during tissue regeneration. Future studies should combine advanced biomaterials with standardized mechanical analysis, organoid models, and multi-omics approaches to establish more accurate mechanical regulatory maps. Overall, this review proposes that matrix stiffness is not merely a structural feature of tissues, but an active biological signal that regulates vascular regeneration through coordinated mechanotransduction and multicellular interactions. A deeper understanding of stiffness-mediated vascular regulation will provide new theoretical insights and therapeutic opportunities for improving tissue repair outcomes.

Objective To explore the efficacy of arthroscopic reduction combined with percutaneous screw fixation in the treatment of Sanders types Ⅱ and Ⅲ calcaneal fractures.Methods Forty-eight patients with Sanders types Ⅱ and Ⅲcalcaneal fractures were divided into the arthroscopic reduction combined with percutaneous screw fixation(arthroscopy)group(n=23)and the tarsal sinus approach open reduction combined with screw internal fixation(tarsal sinus approach)group(n=25)according to different surgical methods and plans.The operative time,incision length,postoperative complications and secondary removal of internal fixation were compared between the two groups.Changes in B?hler's angle and Gissane's angle were evaluated and compared between the two groups at 3 months,6 months after operation and at the last follow-up.Additionally,the American Orthopaedic Foot&Ankle Society(AOFAS)ankle-hindfoot score and the visual analog scale(VAS)for pain were used to assess outcomes at the last follow-up.Results Compared with the tarsal sinus approach group,the incision length was reduced,the operation time was prolonged and the incidence of complications was decreased in the arthroscopic group(P＜0.05).At 3 months,6 months after the operation and the last follow-up,there were no significant differences in the B?hler Angle,Gissanes Angle,AOFAS and VAS scores between the arthroscopic group and the tarsal sinus approach group(P＞0.05).Conclusion Both groups of regimens can enable patients to achieve good postoperative therapeutic efficacy.However,under arthroscopic assistance,surgical incisions inherently possess minimally invasive advantages,while the incidence of postoperative complications is lower compared to the sinus tarsi approach.

Ethanol (EtOH) is a common trigger for gastric mucosal diseases, and mitigating oxidative stress is essential for attenuating gastric mucosal damage. Capsaicin (CAP) has been identified as a potential agent to counteract oxidative damage in the gastric mucosa; however, its precise mechanism remains unclear. This study demonstrates that CAP alleviates EtOH-induced gastric mucosal injuries through two primary pathways: by suppressing the chemokine receptor 4 (CCR4)/Src/p47phox axis, thereby reducing oxidative stress, and by inhibiting the phosphorylation and nuclear translocation of nuclear factor-κB p65 (NF-κB) p65, resulting in diminished inflammatory responses. These findings elucidate the mechanistic pathways of CAP and provide a theoretical foundation for its potential therapeutic application in the treatment of gastric mucosal injuries.
Ethanol/toxicity* ; Animals ; Gastric Mucosa/metabolism* ; Signal Transduction/drug effects* ; Oxidative Stress/drug effects* ; Capsaicin/pharmacology* ; Male ; NADPH Oxidases/genetics* ; Mice ; Humans ; src-Family Kinases/genetics*