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{"title":"Application of hyperbaric oxygen therapy in the treatment of spinal cord injury: insights from preclinical to clinical evidence.","authors":"Songyang Peng, Lin Zeng, Bing Lu, Qizheng Li","doi":"10.4103/mgr.MEDGASRES-D-24-00111","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00111","url":null,"abstract":"<p><p>Spinal cord injury (SCI) is a severe trauma that leads to significant motor, sensory, and autonomic dysfunction, imposing a substantial disease burden and economic costs globally. The pathophysiology of SCI involves primary and secondary injury stages, with the latter characterized by inflammatory responses, apoptosis, and tissue necrosis. Current therapeutic interventions, including pharmacological treatments and stem cell therapies, provide limited benefits and do not fully address the therapeutic effects on SCI. Hyperbaric oxygen therapy (HBOT), which delivers 100% oxygen at pressures exceeding 1 atmosphere absolute, has shown potential in SCI animal models due to its antiapoptotic, antioxidant, anti-inflammatory, and angiogenesis-promoting effects, thereby limiting secondary injury. Clinical studies have also demonstrated some efficacy of HBOT in treating SCI; however, the optimal timing, duration, and treatment cycles of HBOT remain contentious, and long-term efficacy has yet to be assessed. This review synthesizes the basic research and clinical practice of HBOT for SCI, thereby summarizing the main mechanistic pathways and demonstrating its clinical effects. Future large-scale, multicenter clinical studies are warranted to determine the efficacy and safety of HBOT in treating SCI and explore combined therapeutic modalities for a more comprehensive treatment approach.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"16 1","pages":"33-40"},"PeriodicalIF":3.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined carbon monoxide poisoning and smoke inhalational injury in a case of severe underlying lung disease.","authors":"Youmna Abdelghany, Nirav G Shah, Andrea Levine, Jason J Rose","doi":"10.4103/mgr.MEDGASRES-D-25-00083","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-25-00083","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"16 1","pages":"90-91"},"PeriodicalIF":3.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synapses and dendritic spines are eliminated in the primary visual cortex of mice subjected to chronic intraocular pressure elevation.","authors":"Xinyi Zhang, Deling Li, Weiting Zeng, Yiru Huang, Zongyi Zhan, Yuning Zhang, Qinyuan Hu, Lianyan Huang, Minbin Yu","doi":"10.4103/NRR.NRR-D-24-00394","DOIUrl":"10.4103/NRR.NRR-D-24-00394","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202603000-00046/figure1/v/2025-06-16T082406Z/r/image-tiff Synaptic plasticity is essential for maintaining neuronal function in the central nervous system and serves as a critical indicator of the effects of neurodegenerative disease. Glaucoma directly impairs retinal ganglion cells and their axons, leading to axonal transport dysfuntion, subsequently causing secondary damage to anterior or posterior ends of the visual system. Accordingly, recent evidence indicates that glaucoma is a degenerative disease of the central nervous system that causes damage throughout the visual pathway. However, the effects of glaucoma on synaptic plasticity in the primary visual cortex remain unclear. In this study, we established a mouse model of unilateral chronic ocular hypertension by injecting magnetic microbeads into the anterior chamber of one eye. We found that, after 4 weeks of chronic ocular hypertension, the neuronal somas were smaller in the superior colliculus and lateral geniculate body regions of the brain contralateral to the affected eye. This was accompanied by glial cell activation and increased expression of inflammatory factors. After 8 weeks of ocular hypertension, we observed a reduction in the number of excitatory and inhibitory synapses, dendritic spines, and activation of glial cells in the primary visual cortex contralateral to the affected eye. These findings suggest that glaucoma not only directly damages the retina but also induces alterations in synapses and dendritic spines in the primary visual cortex, providing new insights into the pathogenesis of glaucoma.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1236-1248"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Porcine decellularized nerve matrix hydrogel attenuates neuroinflammation after peripheral nerve injury by inhibiting the TLR4/MyD88/NF-κB axis.","authors":"Rui Li, Jianquan Liu, Liuxun Li, Guotian Luo, Xinrong Yuan, Shichao Shen, Yongpeng Shi, Jianlong Wu, Bin Yan, Lei Yang","doi":"10.4103/NRR.NRR-D-24-00302","DOIUrl":"10.4103/NRR.NRR-D-24-00302","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202603000-00045/figure1/v/2025-06-16T082406Z/r/image-tiff Peripheral nerve injury causes severe neuroinflammation and has become a global medical challenge. Previous research has demonstrated that porcine decellularized nerve matrix hydrogel exhibits excellent biological properties and tissue specificity, highlighting its potential as a biomedical material for the repair of severe peripheral nerve injury; however, its role in modulating neuroinflammation post-peripheral nerve injury remains unknown. Here, we aimed to characterize the anti-inflammatory properties of porcine decellularized nerve matrix hydrogel and their underlying molecular mechanisms. Using peripheral nerve injury model rats treated with porcine decellularized nerve matrix hydrogel, we evaluated structural and functional recovery, macrophage phenotype alteration, specific cytokine expression, and changes in related signaling molecules in vivo . Similar parameters were evaluated in vitro using monocyte/macrophage cell lines stimulated with lipopolysaccharide and cultured on porcine decellularized nerve matrix hydrogel-coated plates in complete medium. These comprehensive analyses revealed that porcine decellularized nerve matrix hydrogel attenuated the activation of excessive inflammation at the early stage of peripheral nerve injury and increased the proportion of the M2 subtype in monocytes/macrophages. Additionally, porcine decellularized nerve matrix hydrogel negatively regulated the Toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-κB axis both in vivo and in vitro . Our findings suggest that the efficacious anti-inflammatory properties of porcine decellularized nerve matrix hydrogel induce M2 macrophage polarization via suppression of the Toll-like receptor 4/myeloid differentiation factor 88/nuclear factor-κB pathway, providing new insights into the therapeutic mechanism of porcine decellularized nerve matrix hydrogel in peripheral nerve injury.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1222-1235"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Somatostatin interneurons and the pathogenesis of Alzheimer's disease.","authors":"Victor N Almeida, Guilherme S V Higa","doi":"10.4103/NRR.NRR-D-24-01277","DOIUrl":"10.4103/NRR.NRR-D-24-01277","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1128-1129"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143493021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Illusion of inactivity: Revisiting progressive multiple sclerosis treatment paradigms.","authors":"Tal Ganz, Tamir Ben-Hur","doi":"10.4103/NRR.NRR-D-24-01308","DOIUrl":"10.4103/NRR.NRR-D-24-01308","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1134-1135"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are emerging electroconductive biomaterials for spinal cord injury repair the future?","authors":"Aleksandra Serafin, Maurice N Collins","doi":"10.4103/NRR.NRR-D-24-01074","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01074","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 3","pages":"1140-1141"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain-computer interfaces re-shape functional neurosurgery.","authors":"Thomas Kinfe, Steffen Brenner, Nima Etminan","doi":"10.4103/NRR.NRR-D-24-01336","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01336","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 3","pages":"1122-1123"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential common pathogenesis of several neurodegenerative diseases.","authors":"Ting Fan, Jiaman Peng, Huiting Liang, Wenzhi Chen, Junlin Wang, Renshi Xu","doi":"10.4103/NRR.NRR-D-24-01054","DOIUrl":"https://doi.org/10.4103/NRR.NRR-D-24-01054","url":null,"abstract":"<p><p>With the gradual advancement of research methods and technologies, various biological processes have been identified as playing roles in the pathogenesis of neurodegenerative diseases. However, current descriptions of these biological processes do not fully explain the onset, progression, and development of these conditions. Therefore, exploration of the pathogenesis of neurodegenerative diseases remains a valuable area of research. This review summarizes the potential common pathogeneses of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, frontotemporal lobar dementia, and Lewy body disease. Research findings have indicated that several common biological processes, including aging, genetic factors, progressive neuronal dysfunction, neuronal death and apoptosis, protein misfolding and aggregation, neuroinflammation, mitochondrial dysfunction, axonal transport defects, and gut microbiota dysbiosis, are involved in the pathogenesis of these six neurodegenerative diseases. Based on current information derived from diverse areas of research, these biological processes may form complex pathogenic networks that lead to distinctive types of neuronal death in neurodegenerative diseases. Furthermore, promoting the regeneration of damaged neurons may be achievable through the repair of affected neural cells if the underlying pathogenesis can be prevented or reversed. Hence, these potential common biological processes may represent only very small, limited elements within numerous intricate pathogenic networks associated with neurodegenerative diseases. In clinical treatment, interfering with any single biological process has proven insufficient to completely halt the progression of neurodegenerative diseases. Therefore, future research on the pathogenesis of neurodegenerative diseases should focus on uncovering the complex pathogenic networks, rather than isolating individual biological processes. Based on this, therapies that aim to block or reverse various targets involved in the potential pathogenic mechanisms of neurodegenerative diseases may be promising directions, as current treatment methods that focus on halting a single pathogenic factor have not achieved satisfactory efficacy.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 3","pages":"972-988"},"PeriodicalIF":5.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144310175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperbaric oxygen for paroxysmal sympathetic hyperactivity syndrome after acute carbon monoxide poisoning.","authors":"Lu Yang, Ding Nan, Xuehua Liu, Jing Zhang, Yi Zhang, Fang Liang, Wanqiu Zhu, Jing Yang","doi":"10.4103/mgr.MEDGASRES-D-25-00109","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-25-00109","url":null,"abstract":"<p><p>JOURNAL/mgres/04.03/01612956-202603000-00002/figure1/v/2025-06-28T140100Z/r/image-tiff Paroxysmal sympathetic hyperactivity syndrome (PSH) is common in patients with severe craniocerebral injuries. Carbon monoxide poisoning (ACOP) may lead to secondary PSH, and hyperbaric oxygen (HBO) is an important treatment method for ACOP that can promote the dissociation of carboxyhemoglobin and reduce the long-term sequelae of ACOP. To explore the risk factors and clinical characteristics of PSH secondary to acute ACOP and to investigate the efficacy of HBO treatment, a retrospective analysis was performed on patients with moderate to severe ACOP admitted to the Hyperbaric Oxygen Department of Beijing Chaoyang Hospital, Capital Medical University, from January 1, 2018 to December 31, 2024. Three patients developed PSH during hospitalization and were classified into the PSH group, while the remaining 50 patients were in the non-PSH group. Univariate Fisher's exact test indicated that a coma duration of more than 72 hours was related to the occurrence of PSH after ACOP, and irregular HBO treatment after onset might be associated with the occurrence of PSH after ACOP. All three PSH patients developed paroxysmal postural or dystonic disorders after onset, accompanied by sympathetic excitation manifestations such as increased heart rate, respiratory rate, elevated blood pressure, and fever. Antiepileptic drugs had poor effects, and the attacks were effectively controlled after HBO treatment combined with adjusted drug therapy. The results indicate that for patients with severe carbon monoxide poisoning, especially those with a long coma duration or irregular HBO treatment after onset, if epileptic seizures occur during the disease course and are accompanied by sympathetic excitation manifestations, the possibility of PSH should be considered. Regular HBO treatment is of great significance for controlling the onset of symptoms.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"16 1","pages":"6-11"},"PeriodicalIF":3.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}