Jialong Chen

Parkinson’s Disease (PD) is characterized by selective loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). PANoptosis, a

Calcium dysregulation is closely associated with cancer cell proliferation, migration, and invasion. Transient receptor potential canonical 1 (TRPC1) plays an essential role in regulating calcium homeostasis. However, the role of TRPC1 in calcium dysregulation in gliomas remains incompletely understood. In this study, we demonstrate that TRPC1 promotes glioma cell migration by increasing Signal transduction and transcription activator 3 (STAT3) protein levels. Furthermore, we show that TRPC1 modulates STAT3 stability by inhibiting chaperone‐mediated autophagy (CMA), and we identify STAT3 as a novel substrate of CMA. Additionally, TRPC1 modulates the interaction between HDAC6 and Heat Shock Cognate 70 through intracellular Ca ²⁺ homeostasis, which is associated with changes in CMA activity. These changes prevent STAT3 degradation, highlighting the TRPC1‐HDAC6 axis as a regulator of glioma progression. Thus, the TRPC1‐HDAC6 axis inhibits STAT3 degradation by suppressing CMA activity, contributing to glioma progression. This pathway may represent a potential therapeutic target.

Background: Stroke is a leading cause of death and long-term disability worldwide and is increasingly recognized as a neuroinflammatory, immune-mediated disease. Acute ischemia triggers robust activation and infiltration of innate immune cells, exacerbating neuronal injury. Zinc is an essential micronutrient with known immunomodulatory and autophagy-regulating roles, but its impact on stroke-driven neuroinflammation remains unclear. We aimed to investigate whether zinc protects against ischemic brain injury by modulating autophagy and the immune microenvironment.Methods: Genome-wide association (GWAS) and NHANES cohort analyses were performed to assess the association between zinc intake levels and stroke risk. Pathway enrichment analysis, PPI network construction, and diagnostic modeling were undertaken to identify ZIARs (zinc-responsive immuno-autophagic regulators). Immune infiltration analysis was used to assess immune cell infiltration levels in stroke. Cell-based ischemia-reperfusion experiments were conducted to evaluate zinc’s effects on autophagy and neuronal cell injury.Results: Higher zinc levels were associated with lower stroke prevalence, as supported by GWAS results (OR ~0.141) and NHANES findings (adjusted OR ~0.96). Zinc-associated genes were predominantly enriched in autophagy and inflammatory signaling pathways, including PI3K-Akt and NF-κB. The diagnostic model identified ZIARs whose expression was closely linked to immune cell composition, particularly neutrophil infiltration, in stroke. In vitro experiment, zinc pretreatment of hypoxia-stressed neurons reduced cell death and oxidative damage, whereas autophagy inhibition abolished zinc’s neuroprotective effect. qPCR and Western blot analyses further confirmed that zinc attenuates RELA-driven autophagy overactivation, thereby promoting neuronal survival.Conclusion: Zinc confers neuroprotection in ischemic stroke by restoring autophagic flux and suppressing excessive innate inflammation through regulation of ZIARs. These findings underscore zinc’s neuroprotective role via immune-autophagy crosstalk and position it as a potential strategy for stroke prevention and intervention.

Background: Peer support is increasingly recognized as a valuable method for managing blood glucose levels and reducing the risk of chronic complications in patients with diabetes. This systematic review and meta-analysis specifically evaluated the effect of peer support on HbA1c levels in middle-aged and elderly patients with type 2 diabetes and explored the potential benefits of peer interactions on glycemic control. Methodology: A comprehensive search was conducted across six databases from January 2018 to July 2023, with a focus on randomized controlled trials (RCTs) that compared peer support interventions to standard diabetic care in adults. Among the 3,395 articles identified, eleven studies involving 2,187 participants were included. The quality of each study was assessed using the Cochrane risk of bias tool. A random-effects model was employed to calculate the mean difference (MD) in HbA1c changes, with additional subgroup analyses for specific contexts. Results: The findings revealed a modest but statistically significant improvement in HbA1c levels in groups receiving peer support (MD: −0.20; 95% CI [−0.37 to −0.02]; p = 0.03). More pronounced benefits were observed in interventions conducted within formal medical settings, those involving high-frequency contact, and those in group sessions, particularly among elderly patients. Conclusions: The results suggest that while peer support provides a slight improvement in HbA1c levels, other intervention strategies—such as frequent contact, group sessions, and formal medical settings—may offer greater glycemic control benefits in elderly patients with type 2 diabetes. These findings support incorporating peer support into diabetes care and underscore the need for further research with larger samples and standardized protocols.

Adenosine diphosphate-ribosylation (ADPRylation) is a reversible posttranslational modification that plays a crucial role in cellular homeostasis and disease development. ADPRylation is produced via nicotinamide adenine dinucleotide hydrolysis and modifies proteins via corresponding transferases, mainly poly(ADP-ribose) polymerases (PARPs), the inhibitors of which have been used in the clinical treatment of cancer. ADPRylation is involved in various physiological processes, including pathogen infection, inflammation, DNA repair, and neurological disorders. In neurodegenerative diseases (NDs), dysregulated ADPRylation contributes to protein aggregation, neuroinflammation, and metabolic disturbances, while targeted modulation shows therapeutic potential. ADPRylation differentially regulates neurodegenerative processes, and PARP inhibitors can reduce neuroinflammation, oxidative stress, and metabolic dysfunction. However, challenges such as poor blood–brain barrier penetration and cell type-specific responses limit clinical translation. This review summarizes recent findings on the role of ADPRylation and PARPs in NDs, highlighting their involvement in protein aggregation and cellular signaling. It emphasizes the importance of ADPRylation in neuronal cells and supports the development of precision therapies targeting this pathway to address current treatment challenges in NDs.

Background: The Health System Responsiveness Questionnaire has been an important tool for evaluating the quality of health services from non-clinical perspectives. However, there is a lack of reliable and valid tools to assess the responsiveness of the mental health system in China, despite the increasing attention to the quality of mental health services. Purpose: This study aimed to adapt a Chinese version of the Mental Health System Responsiveness Questionnaire based on the WHO Health System Responsiveness Questionnaire and assess its psychometric properties among psychiatric outpatients. Patients and Methods: We adapted the Health System Responsiveness Questionnaire into Chinese and used it on psychiatric outpatients through face-to-face interviews, resulting in 1067 valid responses. We conducted a reliability and validity analysis based on classical test theory (CTT) and applied the graded response model based on item response theory (IRT) to examine the performance of each item. Results: From the CTT analysis, values of Cronbach’s alpha, test-retest reliability, and split-half reliability of the questionnaire were all greater than 0.8. Confirmatory factor analysis exhibited a good fit; convergent and discriminant validity were achieved with average variance extracted > 0.5 and heterotrait-monotrait ratio < 0.9. Results from the IRT analysis showed that all items demonstrated acceptable discrimination (discrimination parameters ≥ 0.65) and appropriate difficulty parameters (ranging from − 4 to 4). Additionally, all items provided sufficient information, except for two items in the prompt attention domain. Conclusion: Our adapted Mental Health System Responsiveness Questionnaire possessed strong psychometric properties and could serve as an effective tool for assessing the responsiveness of mental health systems in China. However, improving two items in the domain of prompt attention may contribute to more optimal psychometric properties of the questionnaire.

Rationale: Tuberous sclerosis complex is a multisystem genetic disorder caused by variant of TSC1 or TSC2, which were defined as an independent diagnostic criterion for TSC. Patient concerns: We present a novel hereditary variant in a family. The family showed a phenomenon of familial aggregation in the Tuberous sclerosis complex. Diagnoses: The proband had the c.3974del (exon 33) (p.Gly1325Alafs*58) loss of heterozygosity frameshift in the TSC2 gene (chr16), which was 1 base deletion on the coding sequence of TSC2, leading to a frameshift mutation. Moreover, the novel variant occurred in the grandchildren (generation 3) also can be detected in the grandparental (generation 1) and parental (generation 2). Interventions: The proband had taken antiepileptic drugs (oxcarbazepine [30 mg/(kg·day)], depakine [28 mg/(kg·day)], levetiracetam [38 mg/(kg·day)], and lamotrigine [2 mg/(kg·day)]) and performed a right parietal resection of the epileptic lesion. Outcomes: The treatment received by the proband was ineffective. Lessons: The novel gene mutation sites to be found provide more research entry points for genetic diagnosis, providing new clinical data for tuberous sclerosis complex research.