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{"title":"Hippocampal damage through foreign body placement in organotypic cultures leads to plastic responses in newly born granule cells.","authors":"Tassilo Jungenitz, Lukas Frey, Sophia Kirscht, Stephan W Schwarzacher, Angélica Zepeda","doi":"10.4103/NRR.NRR-D-24-00783","DOIUrl":"10.4103/NRR.NRR-D-24-00783","url":null,"abstract":"<p><p>JOURNAL/nrgr/04.03/01300535-202603000-00038/figure1/v/2025-06-16T082406Z/r/image-tiff The dentate gyrus of the hippocampus is a plastic structure that displays modifications at different levels in response to positive stimuli as well as to negative conditions such as brain damage. The latter involves global alterations, making understanding plastic responses triggered by local damage difficult. One key feature of the dentate gyrus is that it contains a well-defined neurogenic niche, the subgranular zone, and beyond neurogenesis, newly born granule cells may maintain a \"young\" phenotype throughout life, adding to the plastic nature of the structure. Here, we present a novel experimental model of local brain damage in organotypic entorhino-hippocampal cultures that results in the activation of adjacent newly born granule cells. A small piece of filter paper was placed on the surface of the granule cell layer of the dentate gyrus, which evoked a foreign body reaction of astrocytes, along with the activation of local young neurons expressing doublecortin. Forty-eight hours after foreign body placement, the number of doublecortin-immunoreactive cells increased in the subgranular zone in the direct vicinity of the foreign body, whereas overall increased doublecortin immunoreactivity was observed in the granule cell layer and molecular layer of the dentate gyrus. Foreign body placement in the pyramidal layer of the CA1 region evoked a comparable local astroglial reaction but did not lead to an increase in doublecortin-immunoreactive in either the CA1 region or the adjacent dentate gyrus. Seven days after foreign body placement in the dentate gyrus, the increase in doublecortin-immunoreactivity was no longer observed, indicating the transient activation of young cells. However, 7 days after foreign body placement, the number of doublecortin-immunoreactive granule cells coimmunoreactive for calbindin was lower than that under the control conditions. As calbindin is a marker for mature granule cells, this result suggests that activated young cells remain at a more immature stage following foreign body placement. Live imaging of retrovirally green fluorescent protein-labeled newly born granule cells revealed the orientation and growth of their dendrites toward the foreign body placement. This novel experimental model of foreign body placement in organotypic entorhino-hippocampal cultures could serve as a valuable tool for studying both glial reactivity and neuronal plasticity, specifically of newly born neurons under controlled in vitro conditions.</p>","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":" ","pages":"1142-1150"},"PeriodicalIF":6.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296414/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","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":"10.4103/mgr.MEDGASRES-D-25-00083","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"16 1","pages":"90-91"},"PeriodicalIF":2.9,"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":"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}

{"title":"Mechanism by which hydrogen-rich water mitigates exercise-induced fatigue: activation of the immunoresponsive gene 1-itaconate/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 pathway.","authors":"Yinyin Zhang, Yajing Ying, Xianpeng Zu, Lingling Ding, Xuan Shi, Jing Wang, Xiangtong Li, Chujian Li, Qicheng Zhou, Hui Shen, Hongxia Li, Hongtao Lu, Jin Cheng","doi":"10.4103/mgr.MEDGASRES-D-24-00148","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00148","url":null,"abstract":"<p><p>JOURNAL/mgres/04.03/01612956-202603000-00005/figure1/v/2025-06-28T140100Z/r/image-tiff Exercise-induced fatigue limits athletic performance. Molecular hydrogen is an effective treatment for relieving fatigue, but the exact mechanism is not clear. In our study, a mouse model of fatigue was established to explore the molecular mechanism by which hydrogen-rich water reduces exercise-induced fatigue. The results showed that hydrogen-rich water improved the motor function of fatigue mice, reduced the levels of fatigue-related biomarkers (blood urea nitrogen, lactate, and creatine kinase), and alleviated gastrocnemius muscle injury. Furthermore, ultrahigh-performance liquid chromatography-mass spectrometry revealed that hydrogen-rich water upregulated the expression of immune response gene 1 (IRG1), increased the abnormally reduced levels of itaconic acid due to fatigue, and subsequently activated the downstream nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway. Finally, C2C12 cells exposed to an IRG1 inhibitor (IRG1-IN) or 4-octyl itaconic acid (4-OI) were treated with hydrogen-rich water, indicating that hydrogen-rich water effectively upregulated the expression of Nrf2 and HO-1 in cells. In summary, hydrogen-rich water alleviates exercise-induced fatigue by activating the IRG1-itaconic acid/Nrf2/HO-1 pathway and inhibiting oxidative stress.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"16 1","pages":"26-32"},"PeriodicalIF":3.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528825","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":6.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296469/pdf/","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":"OA","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":6.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296486/pdf/","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":"OA","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":6.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296471/pdf/","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":"OA","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":6.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296399/pdf/","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":"OA","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":"10.4103/NRR.NRR-D-24-01074","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 3","pages":"1140-1141"},"PeriodicalIF":6.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296444/pdf/","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":"OA","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":"10.4103/NRR.NRR-D-24-01336","url":null,"abstract":"","PeriodicalId":19113,"journal":{"name":"Neural Regeneration Research","volume":"21 3","pages":"1122-1123"},"PeriodicalIF":6.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296408/pdf/","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":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}