Molecular Neurobiology最新文献_第10页

Functional Outcome Prediction of Acute Ischemic Stroke Based on the Oral and Gut Microbiota. 根据口腔和肠道微生物群预测急性缺血性脑卒中的功能预后

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-15 DOI: 10.1007/s12035-024-04618-2

Jingru Liang, Yueran Ren, Yifeng Zheng, Xiaofei Lin, Wei Song, Jiajia Zhu, Xiaomei Zhang, Hongwei Zhou, Qiheng Wu, Yan He, Jia Yin

{"title":"Functional Outcome Prediction of Acute Ischemic Stroke Based on the Oral and Gut Microbiota.","authors":"Jingru Liang, Yueran Ren, Yifeng Zheng, Xiaofei Lin, Wei Song, Jiajia Zhu, Xiaomei Zhang, Hongwei Zhou, Qiheng Wu, Yan He, Jia Yin","doi":"10.1007/s12035-024-04618-2","DOIUrl":"https://doi.org/10.1007/s12035-024-04618-2","url":null,"abstract":"Although several studies have identified a distinct gut microbiota in individuals with acute ischemic stroke (AIS), there is a limited amount of research that has simultaneously investigated alterations in the oral and intestinal microbiota in AIS patients and their correlation with clinical prognosis. This was a prospective and observational single-center cohort study in which we included 160 AIS patients who were admitted within 24 h after a stroke event. We collected oral and rectal swab samples for analysis using 16S rRNA high-throughput sequencing. Our study revealed that patients with unfavorable outcomes after AIS showed early disruptions in their oral and intestinal microbiota. Rectal swabs showed increased levels of facultatively anaerobic bacteria in patients with a poor prognosis, while the oral cavity exhibited higher levels of anaerobic and opportunistic pathogenic bacteria. By employing machine learning analysis, we found that the microbiota composition at both rectal and oral sites could predict early and long-term outcomes. Moreover, patients with a poor prognosis displayed increased oral bacterial colonization in the rectal microbiota and altered interactions between the oral and gut microbiota. This study reveals distinct rectal and oral bacteria that could predict unfavorable outcomes for AIS patients. Monitoring the microbiota of various body sites during the early stages after admission may hold prognostic value and inform personalized treatment strategies. The presence of oral bacteria colonizing the intestines during the acute phase of stroke could serve as an early indication of poor outcomes for AIS patients.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639314","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}

引用次数: 0

Sodium Danshensu Inhibits Macrophage Inflammation in Atherosclerosis via the miR-200a-3p/MEKK3/NF-κB Signaling Pathway. 丹参素钠通过 miR-200a-3p/MEKK3/NF-κB 信号通路抑制动脉粥样硬化中巨噬细胞的炎症反应

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-15 DOI: 10.1007/s12035-024-04626-2

Xiaolu Zhang, Yilin Zhang, Miao Zeng, Qun Yu, Jiali Gan, Yijing Wang, Xijuan Jiang

{"title":"Sodium Danshensu Inhibits Macrophage Inflammation in Atherosclerosis via the miR-200a-3p/MEKK3/NF-κB Signaling Pathway.","authors":"Xiaolu Zhang, Yilin Zhang, Miao Zeng, Qun Yu, Jiali Gan, Yijing Wang, Xijuan Jiang","doi":"10.1007/s12035-024-04626-2","DOIUrl":"https://doi.org/10.1007/s12035-024-04626-2","url":null,"abstract":"Macrophages are fundamental cellular components of atherosclerotic plaques, and inhibition of macrophage inflammation can delay the development of atherosclerotic plaques. Sodium danshensu (SDSS) can inhibit inflammatory responses and thus delay atherosclerosis, but the specific mechanism remains unclear. The effect of SDSS in inhibiting atherosclerosis was confirmed by observing and detecting atherosclerotic plaque area, morphology and lipid levels in the aorta. The mechanism by which SDSS attenuated atherosclerotic plaques was elucidated by in vivo and in vitro detection of inflammation-related mRNA and protein expression. In addition, bioinformatics analysis, RT-qPCR and dual-luciferase assays were used to predict and validate the potential miRNAs of SDSS to attenuate atherosclerosis. miR-200a-2p mimic and inhibitor were then compared for their effects on the efficacy of SDSS. SDSS inhibited atherosclerotic plaque formation and suppressed the expression of MEKK3, TNF-α, and IL-1β as well as nuclear factor-κB (NF-κB) phosphorylation and nuclear translocation to attenuate inflammatory responses. Bioinformatic predictions combined with RT-qPCR results and dual-luciferase assays indicated that miR-200a-3p negatively regulated MEKK3 expression by directly targeting the 3'UTR region of MEKK3, thereby blocking MEKK3. Further studies showed that miR-200a-3p inhibitor, but not miR-200a-3p mimic, reversed the beneficial effects of SDSS on inflammation. SDSS inhibited macrophage inflammation by modulating the miR-200a-3p/MEKK3/NF-κB signaling pathway.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639320","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}

引用次数: 0

Correction: Vilazodone, a Novel SSRI Antidepressant with 5-HT1A Partial Agonist Properties: Diminished Potentiation of Chronic Oral Methylphenidate-Induced Dynorphin Expression in the Striatum in Adolescent Male Rats. 更正：具有 5-HT1A 部分激动剂特性的新型 SSRI 抗抑郁剂维拉唑酮：减弱慢性口服哌醋甲酯诱导的青春期雄性大鼠纹状体中Dynorphin表达的增效作用。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-14 DOI: 10.1007/s12035-024-04621-7

Michael Hrabak, Rania Ahmed, Michelle G Soriano, Aidan Powell, Panayotis K Thanos, Heinz Steiner

引用次数: 0

Deletion of the Transient Receptor Potential Melastatin 2 Gene Mitigates the 6-Hydroxydopamine-Induced Parkinson's Disease-Like Pathology. 瞬时受体电位美拉汀 2 基因缺失可减轻 6-羟基多巴胺诱发的帕金森病样病理变化

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-14 DOI: 10.1007/s12035-024-04611-9

Ana Flavia F Ferreira, Henning Ulrich, Yasuo Mori, Zhong-Ping Feng, Hong-Shuo Sun, Luiz Roberto Britto

{"title":"Deletion of the Transient Receptor Potential Melastatin 2 Gene Mitigates the 6-Hydroxydopamine-Induced Parkinson's Disease-Like Pathology.","authors":"Ana Flavia F Ferreira, Henning Ulrich, Yasuo Mori, Zhong-Ping Feng, Hong-Shuo Sun, Luiz Roberto Britto","doi":"10.1007/s12035-024-04611-9","DOIUrl":"https://doi.org/10.1007/s12035-024-04611-9","url":null,"abstract":"Pharmacological inhibition of the transient receptor potential melastatin 2 (TRPM2), an oxidative stress-activated calcium channel, was previously reported to be protective in Parkinson's disease (PD). However, the inhibitors used were not TRPM2 specific, so the involvement of this channel in PD remains unclear. Here, for the first time, Trpm2 partial (+ / -) and complete (- / -) knockout mice underwent stereotaxic surgery for PD induction. Six-hydroxydopamine was injected in the right striatum. On days 3 and 6, motor behavior tests (cylinder, apomorphine, and pole test) were performed. On day 7, brains were collected for dopaminergic neuron immunostaining. Our results showed that Trpm2 + / - male and female mice had reduced motor impairment and dopaminergic neuron death after PD induction. In addition, Trpm2 - / - male and female mice showed absent or lesser motor deficit and the dopaminergic neuronal loss was no longer observed. These findings suggest that TRPM2 is involved in the PD-like pathology and that targeting TRPM2 may possibly represent a potential neuroprotective strategy for PD.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622738","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}

引用次数: 0

Lactylation and Ischemic Stroke: Research Progress and Potential Relationship. 乳化与缺血性中风：研究进展和潜在关系。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-14 DOI: 10.1007/s12035-024-04624-4

Jingyuan Zhang, Feng Lin, Yue Xu, Jiaxin Sun, Lei Zhang, Wenli Chen

{"title":"Lactylation and Ischemic Stroke: Research Progress and Potential Relationship.","authors":"Jingyuan Zhang, Feng Lin, Yue Xu, Jiaxin Sun, Lei Zhang, Wenli Chen","doi":"10.1007/s12035-024-04624-4","DOIUrl":"https://doi.org/10.1007/s12035-024-04624-4","url":null,"abstract":"Ischemic stroke is caused by interrupted cerebral blood flow and is a leading cause of mortality and disability worldwide. Significant advancements have been achieved in comprehending the pathophysiology of stroke and the fundamental mechanisms responsible for ischemic damage. Lactylation, as a newly discovered post-translational modification, has been reported to participate in several physiological and pathological processes. However, research on lactylation and ischemic stroke is scarce. This review summarized the current function of protein lactylation in other diseases or normal physiological processes and explored their potential link with the pathophysiological process and the reparative mechanism of ischemic stroke. We proposed that neuroinflammation, regulation of metabolism, regulation of messenger RNA translation, angiogenesis, and neurogenesis might be the bridge linking lactylation and ischemic stroke. Our study provided a novel perspective for comprehending the role of protein lactylation in the pathophysiological processes underlying ischemic stroke. Lactylation might be a promising target in drug development of ischemic stroke.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142623520","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}

引用次数: 0

Early-Life Stress Influences the Transcriptional Activation of Alpha-2A Adrenergic Receptor and Associated Protein Kinase A Signaling Molecules in the Frontal Cortex of Rats. 早期生活压力影响大鼠额叶皮层中α-2A肾上腺素能受体及相关蛋白激酶A信号分子的转录激活

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-13 DOI: 10.1007/s12035-024-04578-7

Sarah Ali, Yogesh Dwivedi

{"title":"Early-Life Stress Influences the Transcriptional Activation of Alpha-2A Adrenergic Receptor and Associated Protein Kinase A Signaling Molecules in the Frontal Cortex of Rats.","authors":"Sarah Ali, Yogesh Dwivedi","doi":"10.1007/s12035-024-04578-7","DOIUrl":"https://doi.org/10.1007/s12035-024-04578-7","url":null,"abstract":"Early life is a highly sensitive period associated with profound changes in brain structure and function. Adverse experiences of early-life stress (ELS) are prominent risk factors for the precipitation of major depressive disorder (MDD). In recent years, dysfunction of the central noradrenergic (NA) system and subsequent deficits in norepinephrine (NE) signaling have gained increasing attention in the pathophysiology of MDD. However, the role of the α-2A adrenergic receptor and its downstream second messenger signaling system has not been investigated in connection to early-life stress-induced depression, limiting valuable insights into neurobiological mechanisms underlying this disorder. In this study, we used maternal separation (MS) as a rodent model of ELS to investigate whether ELS-induced depressive behavior is related to the α-2A adrenergic receptor and its associated second messenger signaling cascade. To do so, we studied expression levels of the α-2A adrenergic receptor (Adra2a), G alpha proteins (stimulatory subunit-Gαs [Gnas] and inhibitory subunit-Gαi [Gnai1 and Gnai2]), and downstream protein kinase A (PKA) catalytic [Prkarcα and Prkarcβ] and regulatory subunits [Prkar1α, Prkar1β, Prkar2α, and Prkar2β]) in the frontal cortex (FC) of MS rats. We found reduced sucrose preference in MS animals, along with reduced transcript levels of Adra2a, Gnai2, Prkar1β, and Prkarcβ. These findings suggest that ELS exposure may contribute to depression symptomatology via alterations in the expression of key genes involved in the NA system, highlighting potential mechanisms underlying ELS-induced depressive behavior.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622746","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}

引用次数: 0

Microglia Sing the Prelude of Neuroinflammation-Associated Depression. 小胶质细胞唱响神经炎症相关抑郁症的序曲

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-13 DOI: 10.1007/s12035-024-04575-w

Qingqing Li, Ying Xie, Jinyi Lin, Miaomiao Li, Ziyan Gu, Tianli Xin, Yang Zhang, Qixia Lu, Yihui Guo, Yanhong Xing, Wuyang Wang

引用次数: 0

Alpha‑Asarone Ameliorates Neuronal Injury After Ischemic Stroke and Hemorrhagic Transformation by Attenuating Blood-Brain Barrier Destruction, Promoting Neurogenesis, and Inhibiting Neuroinflammation. α-阿沙隆通过减轻血脑屏障破坏、促进神经元生成和抑制神经炎症，改善缺血性脑卒中和出血转化后的神经元损伤。

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-12 DOI: 10.1007/s12035-024-04596-5

Lijun Luo, Qinrui Hu, Ruijie Yan, Xiaofeng Gao, Di Zhang, Yi Yan, Qi Liu, Shengjun Mao

{"title":"Alpha‑Asarone Ameliorates Neuronal Injury After Ischemic Stroke and Hemorrhagic Transformation by Attenuating Blood-Brain Barrier Destruction, Promoting Neurogenesis, and Inhibiting Neuroinflammation.","authors":"Lijun Luo, Qinrui Hu, Ruijie Yan, Xiaofeng Gao, Di Zhang, Yi Yan, Qi Liu, Shengjun Mao","doi":"10.1007/s12035-024-04596-5","DOIUrl":"https://doi.org/10.1007/s12035-024-04596-5","url":null,"abstract":"Recombinant tissue-type plasminogen activator (rt-PA), the primary drug for acute ischemic stroke (IS), has a narrow therapeutic window and carries a potential risk of hemorrhagic transformation (HT). Without rt-PA administration, patients may suffer permanent cerebral ischemia. Alpha-asarone (ASA), a natural compound derived from Acorus tatarinowii Schott, exhibits diverse neuropharmacological effects. This study aims to investigate whether ASA could improve outcomes in IS and be used to mitigate HT induced by rt-PA. We employed models of permanent middle cerebral artery occlusion (pMCAO) and photothrombotic cortical injury (PCI) to investigate both the therapeutic efficacy and underlying mechanisms of ASA during the acute and recovery periods following IS, respectively. Additionally, Sprague-Dawley rats were subjected to rt-PA treatment at 6-h post-PCI to mimic HT (rt-PA-HT). Our results revealed three key findings: (1) ASA demonstrated therapeutic effects in the acute phase of pMCAO rats by alleviating blood-brain barrier damage through inhibition of glial cell-mediated neuroinflammation; (2) administration of ASA 24 h after stroke ameliorated the neurological damage during the recovery phase in PCI mice by promoting neurogenesis via activation of the BDNF/ERK/CREB signaling pathway; (3) ASA attenuated rt-PA-HT injury by modulating the NLRP3/Caspase1/IL-1β and IL-18 pathways. Overall, our findings suggest that ASA mitigates neuronal injury following IS and HT, positioning it as a promising candidate for treating these conditions.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142622487","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}

引用次数: 0

Upregulation of C1QC as a Mediator of Blood-Brain Barrier Damage in Type 2 Diabetes Mellitus. 作为 2 型糖尿病血脑屏障损伤介质的 C1QC 上调

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-12 DOI: 10.1007/s12035-024-04615-5

Cheng Huang, Jiaxing Lin, Lan Chen, Wenzhe Sun, Jinjun Xia, Min Wu

{"title":"Upregulation of C1QC as a Mediator of Blood-Brain Barrier Damage in Type 2 Diabetes Mellitus.","authors":"Cheng Huang, Jiaxing Lin, Lan Chen, Wenzhe Sun, Jinjun Xia, Min Wu","doi":"10.1007/s12035-024-04615-5","DOIUrl":"https://doi.org/10.1007/s12035-024-04615-5","url":null,"abstract":"The blood-brain barrier (BBB) is a neurovascular structure that safeguards the brain by inhibiting the passage of harmful substances. In individuals with type 2 diabetes mellitus (T2DM), the heightened blood glucose may cause damage to endothelial cells and neurons, increase collagen protein content, and elevate BBB permeability. Although the impact of blood glucose regulation on the structure and function of BBB has been documented, the exact mechanism remains incompletely elucidated. The primary aim of this investigation was to uncover the pivotal dysregulation of specific genes observed within the cerebral microvascular endothelial cells of diabetic patients, with a particular focus on understanding its biological implications in the disruption of the BBB. By integrating bioinformatics analysis, we identified C1QC as a potential upregulated marker. The expression level of C1QC was subsequently verified in both in vivo and in vitro models. Our experiments have discovered that, under diabetic conditions, suppressing C1QC leads to the mitigation of BBB damage. The presence of a high level of C1QC, through its binding to discoidin domain receptor 2 (DDR2), may trigger the activation of its downstream MMP9, a calcium-dependent enzyme that is capable of degrading protein components in the extracellular matrix, consequently leading to the structural and functional disruption of BBB. In summary, the findings of this study indicate that the aberrantly upregulated expression of C1QC may exert deleterious effects on the BBB under diabetes. To alleviate neurological impairments in individuals with T2DM, C1QC may emerge as a promising therapeutic target worthy of further investigation.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142623724","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}

引用次数: 0

The Impact of the Histone Deacetylase Inhibitor-Sodium Butyrate on Complement-Mediated Synapse Loss in a Rat Model of Neonatal Hypoxia-Ischemia. 组蛋白去乙酰化酶抑制剂-丁酸钠对新生儿缺氧缺血大鼠模型中补体介导的突触丢失的影响

IF 4.6 2区医学

Molecular Neurobiology Pub Date : 2024-11-12 DOI: 10.1007/s12035-024-04591-w

Karolina Ziabska, Magdalena Gewartowska, Malgorzata Frontczak-Baniewicz, Joanna Sypecka, Malgorzata Ziemka-Nalecz

{"title":"The Impact of the Histone Deacetylase Inhibitor-Sodium Butyrate on Complement-Mediated Synapse Loss in a Rat Model of Neonatal Hypoxia-Ischemia.","authors":"Karolina Ziabska, Magdalena Gewartowska, Malgorzata Frontczak-Baniewicz, Joanna Sypecka, Malgorzata Ziemka-Nalecz","doi":"10.1007/s12035-024-04591-w","DOIUrl":"https://doi.org/10.1007/s12035-024-04591-w","url":null,"abstract":"Perinatal asphyxia is one of the most important causes of morbidity and mortality in newborns. One of the key pathogenic factors in hypoxic-ischemic (HI) brain injury is the inflammatory reaction including complement system activation. Over-activated complement stimulates cells to release inflammatory molecules and is involved in the post-ischemic degradation of synaptic connections. On the other hand, complement is also involved in regenerative processes. The histone deacetylase inhibitor (HDACi)-sodium butyrate (SB)-provides reduction of inflammation by decreasing the expression of the proinflammatory factors. The main purpose of this study was to examine the effect of SB treatment on complement activation and synapse elimination after HI. Neonatal HI was induced in Wistar rats pups by unilateral ligation of the common carotid artery followed by 60-min hypoxia (7.6% O2). SB (300 mg/kg) was administered on a 5-day regimen. Our study has shown decreased levels of synapsin I, synaptophysin, and PSD-95 in the hypoxic-ischemic hemisphere, indicating synaptic loss after neonatal HI. Transmission electron microscopy revealed injury of the synaptic structures in the brain after HI. SB treatment increased the level of the synaptic proteins, improved tissue ultrastructure, and reduced degradation of the synapses. Neonatal HI induced mRNA expression of the complement C1q, C3, C5, and C9, and their receptors C3aR and C5aR. The effect of SB was different depending on the time after induction of hypoxic-ischemic damage. Our study demonstrated that neuroprotective effect of SB may be related to the modulation of complement activity after HI brain injury.","PeriodicalId":18762,"journal":{"name":"Molecular Neurobiology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142623616","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}

引用次数: 0