The neural network hypothesis is one of the important pathogenesis of drug-resistant epilepsy. Axons guide molecules through synaptic remodeling and brain tissue remodeling, which may result in the formation of abnormal neural networks. Therefore, axon guidance plays a crucial role in disease progression. However, although Robo1 is one of the important components of axon guidance, the role of Robo1 in epilepsy remains unclear. In this study, we aimed to explore the mechanism of Robo1 in epilepsy. Male adult C57BL/6 mice were intraperitoneally injected with pentylenetetrazol to establish an epilepsy model. Lentivirus (LV) was given via intracranial injection 2 weeks before pentylenetetrazol injection. Different expressions of Robo1 between the control group, LV-mediated Robo1 short hairpin RNA group, empty vector control LV group, and normal saline group were analyzed using Western blot, immunofluorescence staining, Golgi staining, and video monitoring. Robo1 was increased in the hippocampus in the pentylenetetrazol-induced epilepsy mouse model; lentiviral Robo1 knockdown prolonged the latency of seizure and reduced the seizure grade in mice and resulted in a decrease in dendritic spine density, while the number of mature dendritic spines was maintained. We speculate that Robo1 has been implicated in the development and progression of epilepsy through its effects on dendritic spine morphology and density. Epileptic mice with Robo1 knockdown virus intervention had lower seizure grade and longer latency. Follow-up findings suggest that Robo1 may modulate seizures by affecting dendritic spine density and morphology. Downregulation of Robo1 may negatively regulate epileptogenesis by decreasing the density of dendritic spines and maintaining a greater number of mature dendritic spines.
{"title":"Mechanism of Robo1 in the pentylenetetrazol-kindled epilepsy mouse model","authors":"Zheng Liu, Wei Huang, Man-Min Zhu, Zhong-Xiang Xu, Zu-Cai Xu, Chang-Yin Yu, Hao Huang","doi":"10.1002/ibra.12127","DOIUrl":"10.1002/ibra.12127","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 <p>The neural network hypothesis is one of the important pathogenesis of drug-resistant epilepsy. Axons guide molecules through synaptic remodeling and brain tissue remodeling, which may result in the formation of abnormal neural networks. Therefore, axon guidance plays a crucial role in disease progression. However, although Robo1 is one of the important components of axon guidance, the role of Robo1 in epilepsy remains unclear. In this study, we aimed to explore the mechanism of Robo1 in epilepsy. Male adult C57BL/6 mice were intraperitoneally injected with pentylenetetrazol to establish an epilepsy model. Lentivirus (LV) was given via intracranial injection 2 weeks before pentylenetetrazol injection. Different expressions of Robo1 between the control group, LV-mediated Robo1 short hairpin RNA group, empty vector control LV group, and normal saline group were analyzed using Western blot, immunofluorescence staining, Golgi staining, and video monitoring. Robo1 was increased in the hippocampus in the pentylenetetrazol-induced epilepsy mouse model; lentiviral Robo1 knockdown prolonged the latency of seizure and reduced the seizure grade in mice and resulted in a decrease in dendritic spine density, while the number of mature dendritic spines was maintained. We speculate that Robo1 has been implicated in the development and progression of epilepsy through its effects on dendritic spine morphology and density. Epileptic mice with Robo1 knockdown virus intervention had lower seizure grade and longer latency. Follow-up findings suggest that Robo1 may modulate seizures by affecting dendritic spine density and morphology. Downregulation of Robo1 may negatively regulate epileptogenesis by decreasing the density of dendritic spines and maintaining a greater number of mature dendritic spines.</p>\u0000 </section>\u0000 </div>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12127","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81339762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yingzhu Zhuang, Jiyan Xu, Kunying Zheng, Hong Zhang
Cardiopulmonary bypass (CPB) is often used in cardiothoracic surgery because its nonphysiological state causes pathophysiological changes in the body, causing multiorgan and multitissue damage to varying degrees. Postoperative cognitive dysfunction (POCD) is a common central nervous system complication after cardiac surgery. The etiology and mechanism of POCD are not clear. Neuroinflammation, brain mitochondrial dysfunction, cerebral embolism, ischemia, hypoxia, and other factors are related to the pathogenesis of POCD. There is a close relationship between CPB and POCD, as CPB can cause inflammation, hypoxia and reperfusion injury, and microemboli formation, all of which can trigger POCD. POCD increases medical costs, seriously affects patients' quality of life, and increases mortality. Currently, there is a lack of effective treatment methods for POCD. Commonly used methods include preoperative health management, reducing inflammation response during surgery, preventing microemboli formation, and implementing individualized rehabilitation programs after surgery. Strengthening preventive measures can minimize the occurrence of POCD and its adverse effects.
{"title":"Research progress of postoperative cognitive dysfunction in cardiac surgery under cardiopulmonary bypass","authors":"Yingzhu Zhuang, Jiyan Xu, Kunying Zheng, Hong Zhang","doi":"10.1002/ibra.12123","DOIUrl":"https://doi.org/10.1002/ibra.12123","url":null,"abstract":"Cardiopulmonary bypass (CPB) is often used in cardiothoracic surgery because its nonphysiological state causes pathophysiological changes in the body, causing multiorgan and multitissue damage to varying degrees. Postoperative cognitive dysfunction (POCD) is a common central nervous system complication after cardiac surgery. The etiology and mechanism of POCD are not clear. Neuroinflammation, brain mitochondrial dysfunction, cerebral embolism, ischemia, hypoxia, and other factors are related to the pathogenesis of POCD. There is a close relationship between CPB and POCD, as CPB can cause inflammation, hypoxia and reperfusion injury, and microemboli formation, all of which can trigger POCD. POCD increases medical costs, seriously affects patients' quality of life, and increases mortality. Currently, there is a lack of effective treatment methods for POCD. Commonly used methods include preoperative health management, reducing inflammation response during surgery, preventing microemboli formation, and implementing individualized rehabilitation programs after surgery. Strengthening preventive measures can minimize the occurrence of POCD and its adverse effects.","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75458583","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}
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective degeneration of upper and lower motor neurons. Although dyskinesia is the most prominent clinical manifestation of ALS, with an in‐depth understanding of disease pathogenesis and clinical detection, more and more ALS patients are found to have nonmotor symptoms, such as sensory impairment. Genetic testing technology has developed rapidly in recent years. New genes have been proven to be involved in the pathogenesis of ALS. However, according to the existing research evidence, no literature has reported that patients with ALS have leucine‐rich repeats and sterility α mutations in motif 1 (LRSAM1) and receptor expression accessory protein 1 (REEP1). The mutation sites of REEP1 gene have not been reported, and the simultaneous mutations of two genes have not been reported. In the largest human gene mutation frequency database gnomad, the mutation sites of two genes are currently defined as new heterozygous variants with unclear clinical significance. Therefore, this article reports the clinical data of this case to further deepen the clinicians' understanding of the disease, and may provide evidence for further study of the new genotype–phenotype of LRSAM1 and REEP1.
{"title":"Double gene mutations of LRSAM1 and REEP1 and a new REEP1 mutation site found in a patient with amyotrophic lateral sclerosis with subjective paresthesia: A case report","authors":"Jiahui Qin, Zun‐Lin Zhou, Yuankun Zhou, Ya Chen, Xiao‐Yan Yang, Hai‐Qing Zhang, Zucai Xu","doi":"10.1002/ibra.12125","DOIUrl":"https://doi.org/10.1002/ibra.12125","url":null,"abstract":"Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by selective degeneration of upper and lower motor neurons. Although dyskinesia is the most prominent clinical manifestation of ALS, with an in‐depth understanding of disease pathogenesis and clinical detection, more and more ALS patients are found to have nonmotor symptoms, such as sensory impairment. Genetic testing technology has developed rapidly in recent years. New genes have been proven to be involved in the pathogenesis of ALS. However, according to the existing research evidence, no literature has reported that patients with ALS have leucine‐rich repeats and sterility α mutations in motif 1 (LRSAM1) and receptor expression accessory protein 1 (REEP1). The mutation sites of REEP1 gene have not been reported, and the simultaneous mutations of two genes have not been reported. In the largest human gene mutation frequency database gnomad, the mutation sites of two genes are currently defined as new heterozygous variants with unclear clinical significance. Therefore, this article reports the clinical data of this case to further deepen the clinicians' understanding of the disease, and may provide evidence for further study of the new genotype–phenotype of LRSAM1 and REEP1.","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86594547","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}
Edoardo Scarpa, Mariafrancesca Cascione, Anna Griego, Paolo Pellegrino, Giorgia Moschetti, Valeria De Matteis
Neurodegenerative diseases (NDs) impose substantial medical and public health burdens on people worldwide and represent one of the major threats to human health. The prevalence of these age-dependent disorders is dramatically increasing over time, a process intrinsically related to a constantly rising percentage of the elderly population in recent years. Among all the NDs, Alzheimer's and Parkinson's are considered the most debilitating as they cause memory and cognitive loss, as well as severely affecting basic physiological conditions such as the ability to move, speak, and breathe. There is an extreme need for new and more effective therapies to counteract these devastating diseases, as the available treatments are only able to slow down the pathogenic process without really stopping or resolving it. This review aims to elucidate the current nanotechnology-based tools representing a future hope for NDs treatment. Noble metal nano-systems, that is, gold and silver nanoparticles (NPs), have indeed unique physicochemical characteristics enabling them to deliver any pharmacological treatment in a more effective way within the central nervous system. This can potentially make NPs a new hope for reversing the actual therapeutic strategy based on slowing down an irreversible process into a more effective and permanent treatment.
{"title":"Gold and silver nanoparticles in Alzheimer's and Parkinson's diagnostics and treatments","authors":"Edoardo Scarpa, Mariafrancesca Cascione, Anna Griego, Paolo Pellegrino, Giorgia Moschetti, Valeria De Matteis","doi":"10.1002/ibra.12126","DOIUrl":"10.1002/ibra.12126","url":null,"abstract":"<p>Neurodegenerative diseases (NDs) impose substantial medical and public health burdens on people worldwide and represent one of the major threats to human health. The prevalence of these age-dependent disorders is dramatically increasing over time, a process intrinsically related to a constantly rising percentage of the elderly population in recent years. Among all the NDs, Alzheimer's and Parkinson's are considered the most debilitating as they cause memory and cognitive loss, as well as severely affecting basic physiological conditions such as the ability to move, speak, and breathe. There is an extreme need for new and more effective therapies to counteract these devastating diseases, as the available treatments are only able to slow down the pathogenic process without really stopping or resolving it. This review aims to elucidate the current nanotechnology-based tools representing a future hope for NDs treatment. Noble metal nano-systems, that is, gold and silver nanoparticles (NPs), have indeed unique physicochemical characteristics enabling them to deliver any pharmacological treatment in a more effective way within the central nervous system. This can potentially make NPs a new hope for reversing the actual therapeutic strategy based on slowing down an irreversible process into a more effective and permanent treatment.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12126","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41180784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Nowadays, with the development of the social health care system, there is an increasing trend towards an aging society. The incidence of Alzheimer's disease (AD) is also on the rise. AD is a kind of neurodegenerative disease that can be found in any age group. For years, scientists have been committing to discovering the cause of AD. DNA methylation is one of the most common epigenetic mechanisms in mammals and plays a vital role in the pathogenesis of several diseases, including tumors. Studying chemical changes in the epigenome, or DNA methylation can help us understand the effects of our environment and life on diseases, such as smoking, depression, and menopause, which may affect people's chances of developing Alzheimer's or other diseases. Recent studies have identified some crucial genes like ANK1, RHBDF2, ABCA7, and BIN1, linking DNA methylation to AD. This review focuses on elucidating the relationship between DNA methylation and the pathogenesis of AD and provides an outlook on possible targeted therapeutic modalities.
如今，随着社会医疗体系的发展，老龄化社会的趋势日益明显。阿尔茨海默病（AD）的发病率也呈上升趋势。阿尔茨海默病是一种神经退行性疾病，任何年龄段的人都有可能患病。多年来，科学家们一直致力于发现阿尔茨海默病的病因。DNA 甲基化是哺乳动物最常见的表观遗传机制之一，在包括肿瘤在内的多种疾病的发病机制中发挥着重要作用。研究表观基因组或DNA甲基化的化学变化，可以帮助我们了解环境和生活对疾病的影响，如吸烟、抑郁和更年期，这可能会影响人们患老年痴呆症或其他疾病的几率。最近的研究发现了一些关键基因，如 ANK1、RHBDF2、ABCA7 和 BIN1，它们将 DNA 甲基化与阿兹海默症联系起来。本综述将重点阐明DNA甲基化与AD发病机制之间的关系，并对可能的靶向治疗方法进行展望。
{"title":"DNA methylation: The epigenetic mechanism of Alzheimer's disease","authors":"Hao-Yue Qin, Jiao-Yan Liu, Chang-Le Fang, Yan-Ping Deng, Ying Zhang","doi":"10.1002/ibra.12121","DOIUrl":"10.1002/ibra.12121","url":null,"abstract":"<p>Nowadays, with the development of the social health care system, there is an increasing trend towards an aging society. The incidence of Alzheimer's disease (AD) is also on the rise. AD is a kind of neurodegenerative disease that can be found in any age group. For years, scientists have been committing to discovering the cause of AD. DNA methylation is one of the most common epigenetic mechanisms in mammals and plays a vital role in the pathogenesis of several diseases, including tumors. Studying chemical changes in the epigenome, or DNA methylation can help us understand the effects of our environment and life on diseases, such as smoking, depression, and menopause, which may affect people's chances of developing Alzheimer's or other diseases. Recent studies have identified some crucial genes like <i>ANK1</i>, <i>RHBDF2</i>, <i>ABCA7</i>, and <i>BIN1</i>, linking DNA methylation to AD. This review focuses on elucidating the relationship between DNA methylation and the pathogenesis of AD and provides an outlook on possible targeted therapeutic modalities.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135553755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
To explore the interaction of instrumental activities of daily living (IADLs) and dual sensory function on cognition in the elderly. A cross-sectional survey was conducted in six general hospitals in China, from October 2022 to December 2022. Data collection included general information, IADLs scale, self-reported sensory function questionnaire, and mini-mental state examination (MMSE). Binary logistic regression was used to examine the association between factors and cognition. The interactive effect was evaluated by synergy index (S), relative excess risk due to interaction (RERI), and attributable proportion due to interaction (AP). The odds ratio (OR) of IADLs decline in cognition is 4.412 (95% confidence interval [CI]: 3.633–5.358, p < 0.001); the OR of dual sensory difficulty on cognition is 2.502 (95% CI: 1.272–4.921, p = 0.008). The OR of interaction between IADLs decline and dual sensory difficulty on cognition is 13.737 (95% CI: 9.726–19.400, p < 0.001). RERI (95% CI) = 7.823 (3.230–12.417), AP (95% CI) = 0.570 (0.392–0.747), S (95% CI) = 2.593 (1.616–4.160). IADLs decline and dual sensory difficulty are associated with cognitive decline. IADLs decline and dual sensory difficulty have interaction with cognitive decline; the interaction is greater than the sum effect of those two on cognitive decline independently. Sensory and IADLs assessment can be used as early screening items for cognition among the elderly. In addition, protecting sensory function and maintaining IADLs in the elderly can help protect their cognition.
探讨老年人日常生活工具性活动与双重感觉功能对认知的影响。2022年10月至2022年12月，在中国六家综合医院进行了横断面调查。数据收集包括一般信息、IADL量表、自我报告的感觉功能问卷和迷你精神状态检查（MMSE）。二元逻辑回归用于检验因素与认知之间的关系。交互效应通过协同指数（S）、交互作用引起的相对超额风险（RERI）和交互作用造成的可归因比例（AP）来评估。IADL认知能力下降的比值比（OR）为4.412（95%置信区间[CI]:3.633-5.358，p p = 二者交互作用的OR为13.737（95%CI:9.726-19.400，p
{"title":"The interaction between instrumental activities of daily living and dual sensory function on cognition among the elderly in China: A cross-sectional survey","authors":"Heting Liang, Zhixia Jiang, Xiaoling Yang, Shuang Li, Xiaoling Zhao, Yongya Dai, Siqin Liu, Yumeng Zhang, Xiaoli Yuan","doi":"10.1002/ibra.12124","DOIUrl":"10.1002/ibra.12124","url":null,"abstract":"<p>To explore the interaction of instrumental activities of daily living (IADLs) and dual sensory function on cognition in the elderly. A cross-sectional survey was conducted in six general hospitals in China, from October 2022 to December 2022. Data collection included general information, IADLs scale, self-reported sensory function questionnaire, and mini-mental state examination (MMSE). Binary logistic regression was used to examine the association between factors and cognition. The interactive effect was evaluated by synergy index (S), relative excess risk due to interaction (RERI), and attributable proportion due to interaction (AP). The odds ratio (OR) of IADLs decline in cognition is 4.412 (95% confidence interval [CI]: 3.633–5.358, <i>p</i> < 0.001); the OR of dual sensory difficulty on cognition is 2.502 (95% CI: 1.272–4.921, <i>p</i> = 0.008). The OR of interaction between IADLs decline and dual sensory difficulty on cognition is 13.737 (95% CI: 9.726–19.400, <i>p</i> < 0.001). RERI (95% CI) = 7.823 (3.230–12.417), AP (95% CI) = 0.570 (0.392–0.747), S (95% CI) = 2.593 (1.616–4.160). IADLs decline and dual sensory difficulty are associated with cognitive decline. IADLs decline and dual sensory difficulty have interaction with cognitive decline; the interaction is greater than the sum effect of those two on cognitive decline independently. Sensory and IADLs assessment can be used as early screening items for cognition among the elderly. In addition, protecting sensory function and maintaining IADLs in the elderly can help protect their cognition.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12124","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41163400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xing-Yu Yang, Xiao Zhang, Jun-Feng Cao, Mei Wu, Sheng-Yan Chen, Li Chen
Cerebral ischemia is a serious cerebrovascular disease with the characteristics of high morbidity, disability, and mortality. Currently, stem cell therapy has been extensively applied to a wide range of diseases, including neurological disorders, autoimmune deficits, and other diseases. Transplantation therapy with neural stem cells (NSCs) is a very promising treatment method, which not only has anti-inflammatory, antiapoptotic, promoting angiogenesis, and neurogenesis effects, but also can improve some side effects related to thrombolytic therapy. NSCs treatment could exert protective effects in alleviating cerebral ischemia-induced brain damage and neurological dysfunctions. However, the different injection routes and doses of NSCs determine diverse therapeutic efficacy. This review mainly summarizes the various injection methods and injection effects of NSCs in cerebral ischemia, as well as proposes the existing problems and prospects of NSCs transplantation.
{"title":"Routes and methods of neural stem cells injection in cerebral ischemia","authors":"Xing-Yu Yang, Xiao Zhang, Jun-Feng Cao, Mei Wu, Sheng-Yan Chen, Li Chen","doi":"10.1002/ibra.12122","DOIUrl":"10.1002/ibra.12122","url":null,"abstract":"<p>Cerebral ischemia is a serious cerebrovascular disease with the characteristics of high morbidity, disability, and mortality. Currently, stem cell therapy has been extensively applied to a wide range of diseases, including neurological disorders, autoimmune deficits, and other diseases. Transplantation therapy with neural stem cells (NSCs) is a very promising treatment method, which not only has anti-inflammatory, antiapoptotic, promoting angiogenesis, and neurogenesis effects, but also can improve some side effects related to thrombolytic therapy. NSCs treatment could exert protective effects in alleviating cerebral ischemia-induced brain damage and neurological dysfunctions. However, the different injection routes and doses of NSCs determine diverse therapeutic efficacy. This review mainly summarizes the various injection methods and injection effects of NSCs in cerebral ischemia, as well as proposes the existing problems and prospects of NSCs transplantation.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12122","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41170259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ya Chen, Xia Zhang, Hai‐Qing Zhang, Zhong Luo, Xueyan Zhou, Tao Liang, Fei Yang, Jun Zhang, Zucai Xu
{"title":"Study on the efficacy of compound porcine cerebroside and ganglioside injection in patients with ischemic stroke: A randomized, single‐center, open‐label, prospective study","authors":"Ya Chen, Xia Zhang, Hai‐Qing Zhang, Zhong Luo, Xueyan Zhou, Tao Liang, Fei Yang, Jun Zhang, Zucai Xu","doi":"10.1002/ibra.12120","DOIUrl":"https://doi.org/10.1002/ibra.12120","url":null,"abstract":"","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80607080","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":"Progress of research on antiferroptosis and antipyroptosis effects of gastrodin","authors":"Xue Zheng, Jing Li, Zhao‐Qiong Zhu","doi":"10.1002/ibra.12118","DOIUrl":"https://doi.org/10.1002/ibra.12118","url":null,"abstract":"","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75080195","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}
Spinal cord injury (SCI) animal models have been widely created and utilized for repair therapy research, but more suitable experimental animals and accurate modeling methodologies are required to achieve the desired results. In this experiment, we constructed an innovative dorsal 1/4 spinal cord transection macaque model that had fewer severe problems, facilitating postoperative care and recovery. In essence, given that monkeys and humans share similar genetics and physiology, the efficacy of this strategy in a nonhuman primate SCI model basically serves as a good basis for its prospective therapeutic use in human SCI.
{"title":"Development of an innovative minimally invasive primate spinal cord injury model: A case report","authors":"Yong-Min Niu, Jin-Xiang Liu, Hao-Yue Qin, Yi-Fan Liu, Ni-Jiao Huang, Ji-Li Jiang, Yan-Qiu Chen, Si-Jing Chen, Tao Bai, Chang-Wei Yang, Yu Cao, Sheng Liu, Hao Yuan","doi":"10.1002/ibra.12117","DOIUrl":"10.1002/ibra.12117","url":null,"abstract":"<p>Spinal cord injury (SCI) animal models have been widely created and utilized for repair therapy research, but more suitable experimental animals and accurate modeling methodologies are required to achieve the desired results. In this experiment, we constructed an innovative dorsal 1/4 spinal cord transection macaque model that had fewer severe problems, facilitating postoperative care and recovery. In essence, given that monkeys and humans share similar genetics and physiology, the efficacy of this strategy in a nonhuman primate SCI model basically serves as a good basis for its prospective therapeutic use in human SCI.</p>","PeriodicalId":94030,"journal":{"name":"Ibrain","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/ibra.12117","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41165732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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