全部最新文献

Background: This review and meta-analysis examined the effectiveness of non-pharmacological therapies delivered through school-based interventions for smoking cessation among adolescents in South and Southeast Asian countries.

Methods: A systematic search was conducted across PubMed, Scopus, Science Direct, BioMed Central, the Cochrane Library, and ProQuest Dissertations & Theses Global from inception to October 2024. Eligible studies comprised randomized controlled trials and quasi-experimental studies that compared non-pharmacological smoking cessation interventions delivered in schools or other educational institutions. Data on smoking abstinence outcomes were extracted from published studies, and odds ratios (ORs) with 95% confidence intervals (CIs) were pooled using a random-effects model via the Mantel-Haenszel estimator.

Results: Seven studies involving 1,260 participants were included. The meta-analysis demonstrated that non-pharmacological school-based therapies significantly increased smoking abstinence compared to controls (OR, 2.83; 95% CI, 1.83-4.40; p<0.001. Subgroup analyzes revealed benefits across both randomized controlled trials and quasi-experimental studies with varying abstinence rates. Studies utilizing biochemical verification showed significant positive effects despite substantial heterogeneity, and short-term (<3 months) abstinence was significantly higher in intervention groups compared to controls. Overall, no differences were found between subgroups regarding intervention effectiveness.

Conclusion: This meta-analysis indicates that non-pharmacological school-based interventions positively impact smoking abstinence rates, although effectiveness may vary based on study design, follow-up duration, and use of biochemical verification. The findings underscore the need for further research with larger sample sizes, extended follow-up periods, and improved methodological rigor in these regions.

For diverse neurodegenerative disorders, microglial cells are activated. Furthermore, dysfunctional and hyperactivated microglia initiate mitochondrial autophagy, oxidative stress, and pathological protein accumulation, ending with neuroinflammation that exacerbates damage to dopaminergic neurons and contributes significantly to the pathology of neurodegenerative disorder. Microglial over-activation is closely associated with the secretion of pro-inflammatory cytokines, the phagocytosis of injured neurons, and the modulation of neurotoxic environments. This review summarizes the role of microglia neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, multiple system atrophy, amyotrophic lateral sclerosis, frontotemporal dementia, progressive supranuclear palsy, cortical degeneration, Lewy body dementia, and Huntington's disease. It also discusses novel forms of cell death such as ferroptosis, cuproptosis, disulfidptosis, and parthanatos (poly(adenosine diphosphate ribose) polymerase 1-dependent cell death), as well as the impact of regulatory factors related to microglial inflammation on microglial activation and neuroinflammation. The aim is to identify potential targets for microglial cell therapy in neurodegenerative diseases.

Nerve trauma commonly results in chronic neuropathic pain. This is by triggering the release of pro-inflammatory mediators from local and invading cells that induce inflammation and nociceptive neuron hyperexcitability. Even without apparent inflammation, injury sites are associated with increased inflammatory markers. This review focuses on how it might be possible to reduce neuropathic pain by reducing inflammation. Physiologically, pain is resolved by a combination of the out-migration of pro-inflammatory cells from the injury site, the down-regulation of the genes underlying the inflammation, up-regulating genes for anti-inflammatory mediators, and reducing nociceptive neuron hyperexcitability. While various techniques reduce chronic neuropathic pain, the best are effective on < 50% of patients, no technique reliably or permanently eliminates neuropathic pain. This is because most techniques are predominantly aimed at reducing pain, not inflammation. In addition, while single factors reduce pain, increasing evidence indicates significant and longer-lasting pain relief requires multiple factors acting simultaneously. Therefore, it is not surprising that extensive data indicate that the application of platelet-rich plasma provides more significant and longer-lasting pain suppression than other techniques, although its analgesia is neither complete nor permanent. However, several case reports indicate that platelet-rich plasma can induce permanent neuropathic pain elimination when the platelet concentration is significantly increased and is applied to longer nerve lengths. This review examines the primary triggers of the development and maintenance of neuropathic pain and techniques that reduce chronic neuropathic pain. The application of platelet-rich plasma holds great promise for providing complete and permanent chronic neuropathic pain elimination.

JOURNAL/nrgr/04.03/01300535-202604000-00038/figure1/v/2025-06-30T060627Z/r/image-tiff Recombinant tissue plasminogen activator is commonly used for hematoma evacuation in minimally invasive surgery following intracerebral hemorrhage. However, during minimally invasive surgery, recombinant tissue plasminogen activator may come into contact with brain tissue. Therefore, a thorough assessment of its safety is required. In this study, we established a mouse model of intracerebral hemorrhage induced by type VII collagenase. We observed that the administration of recombinant tissue plasminogen activator without hematoma aspiration significantly improved the neurological function of mice with intracerebral hemorrhage, reduced pathological damage, and lowered the levels of apoptosis and autophagy in the tissue surrounding the hematoma. In an in vitro model of intracerebral hemorrhage using primary cortical neurons induced by hemin, the administration of recombinant tissue plasminogen activator suppressed neuronal apoptosis, autophagy, and endoplasmic reticulum stress. Transcriptome sequencing analysis revealed that recombinant tissue plasminogen activator upregulated the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway in neurons. Moreover, the phosphoinositide 3-kinase inhibitor LY294002 abrogated the neuroprotective effects of recombinant tissue plasminogen activator in inhibiting excessive apoptosis, autophagy, and endoplasmic reticulum stress. Furthermore, to specify the domain of recombinant tissue plasminogen activator responsible for its neuroprotective effects, various inhibitors were used to target distinct domains. It has been revealed that the epidermal growth factor receptor inhibitor AG-1478 reversed the effect of recombinant tissue plasminogen activator on the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway. These findings suggest that recombinant tissue plasminogen activator exerts a direct neuroprotective effect on neurons following intracerebral hemorrhage, possibly through activation of the phosphoinositide 3-kinase/RAC-alpha serine/threonine-protein kinase/mammalian target of rapamycin pathway.

Regulatory T cells, a subset of CD4 + T cells, play a critical role in maintaining immune tolerance and tissue homeostasis due to their potent immunosuppressive properties. Recent advances in research have highlighted the important therapeutic potential of Tregs in neurological diseases and tissue repair, emphasizing their multifaceted roles in immune regulation. This review aims to summarize and analyze the mechanisms of action and therapeutic potential of Tregs in relation to neurological diseases and neural regeneration. Beyond their classical immune-regulatory functions, emerging evidence points to non-immune mechanisms of regulatory T cells, particularly their interactions with stem cells and other non-immune cells. These interactions contribute to optimizing the repair microenvironment and promoting tissue repair and nerve regeneration, positioning non-immune pathways as a promising direction for future research. By modulating immune and non-immune cells, including neurons and glia within neural tissues, Tregs have demonstrated remarkable efficacy in enhancing regeneration in the central and peripheral nervous systems. Preclinical studies have revealed that Treg cells interact with neurons, glial cells, and other neural components to mitigate inflammatory damage and support functional recovery. Current mechanistic studies show that Tregs can significantly promote neural repair and functional recovery by regulating inflammatory responses and the local immune microenvironment. However, research on the mechanistic roles of regulatory T cells in other diseases remains limited, highlighting substantial gaps and opportunities for exploration in this field. Laboratory and clinical studies have further advanced the application of regulatory T cells. Technical advances have enabled efficient isolation, ex vivo expansion and functionalization, and adoptive transfer of regulatory T cells, with efficacy validated in animal models. Innovative strategies, including gene editing, cell-free technologies, biomaterial-based recruitment, and in situ delivery have expanded the therapeutic potential of regulatory T cells. Gene editing enables precise functional optimization, while biomaterial and in situ delivery technologies enhance their accumulation and efficacy at target sites. These advancements not only improve the immune-regulatory capacity of regulatory T cells but also significantly enhance their role in tissue repair. By leveraging the pivotal and diverse functions of Tregs in immune modulation and tissue repair, regulatory T cells-based therapies may lead to transformative breakthroughs in the treatment of neurological diseases.