Jove
Visualize
联系我们
JoVE
x logofacebook logolinkedin logoyoutube logo
关于 JoVE
概览领导团队博客JoVE 帮助中心
作者
出版流程编辑委员会范围与政策同行评审常见问题投稿
图书馆员
用户评价订阅访问资源图书馆顾问委员会常见问题
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experiments存档
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教师资源中心教师网站
使用条款与条件
隐私政策
政策

相关概念视频

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...

您也可能阅读

相关文章

通过共同作者、期刊和引用图与本文相关的文章。

排序
Same author

<sup>18</sup>F- FDG PET Reveals a Nucleus Accumbens-Centered Metabolic Network Correlating With Clinical Severity in Anti-LGI1 Encephalitis.

MedComm·2025
Same author

Deficiency of FRMD5 results in neurodevelopmental dysfunction and autistic-like behavior in mice.

Molecular psychiatry·2024
Same author

Somatic mutation contributing to clonal haematopoiesis is a risk factor of recurrent stroke in first-ever acute ischaemic stroke: a prospective cohort study.

Stroke and vascular neurology·2022
Same author

GRP per capita and hospital characteristics associated with intravenous tissue plasminogen activator adherence rate: evidence from the Chinese Stroke Center Alliance.

Stroke and vascular neurology·2021
Same author

Comparison of frequency-resolved optical polarization gating induced by molecular alignment and Kerr effects.

Optics letters·2012
Same author

Direct transformation of simple enals to 3,4-disubstituted benzaldehydes under mild reaction conditions via an organocatalytic regio- and chemoselective dimerization cascade.

Chemistry (Weinheim an der Bergstrasse, Germany)·2012

相关实验视频

Updated: May 12, 2026

PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
12:01

PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke

Published on: June 14, 2018

12.8K

DNMT3A功能障碍促进神经炎症,并加剧急性缺血性中风.

Tian-Jie Lyu1,2, Xin Qiu1,2, Yubo Wang1,2

  • 1Department of Neurology Beijing Tiantan Hospital Capital Medical University Beijing China.

MedComm
|July 15, 2024
PubMed
概括

与克隆性血液形成 (CHIP) 相关的DNMT3A基因的体质突变,在急性缺血性中风 (AIS) 患者中恶化了结果. 在小鼠中,DNMT3A的抑制增加了中风的严重程度,这表明它在神经炎症和组织损伤中发挥了作用.

关键词:
在DNMT3A中,它是DNMT3A.在RG108中,我们可以使用RG108.克隆性血液形成 (clonal hematopoiesis) 是一种细胞形成的过程.功能性结果的结果.这是一种亲炎症性炎症.

更多相关视频

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia
11:36

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia

Published on: November 14, 2020

9.4K
AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke
05:40

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

Published on: November 29, 2024

437

相关实验视频

Last Updated: May 12, 2026

PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke
12:01

PET Imaging of Neuroinflammation Using [11C]DPA-713 in a Mouse Model of Ischemic Stroke

Published on: June 14, 2018

12.8K
A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia
11:36

A Cell Culture Model for Studying the Role of Neuron-Glia Interactions in Ischemia

Published on: November 14, 2020

9.4K
AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke
05:40

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

Published on: November 29, 2024

437

科学领域:

  • 神经科学是一个神经科学.
  • 遗传学 遗传学 是一个
  • 心血管科学 心血管科学

背景情况:

  • 不确定的潜力 (CHIP) 的克隆性血液形成与中风风险有关.
  • 在CHIP中DNMT3A突变对急性缺血性中风 (AIS) 结果的作用尚不清楚.

研究的目的:

  • 研究DNMT3A驱动的CHIP与AIS患者的神经障碍之间的关联.
  • 探索DNMT3A在缺血性中风小鼠模型中的机械作用.

主要方法:

  • 对8524名AIS患者进行DNMT3A突变和神经结果的分析.
  • 使用过渡性中脑动脉阻塞 (tMCAO) 的小鼠模型.

主要成果:

  • 在AIS患者中,DNMT3A驱动的CHIP与增加的神经障碍相关.
  • 在tMCAO小鼠中抑制DNMT3A增强了中性粒细胞的增殖和脑透.
  • 在雄性小鼠中,DNMT3A抑制恶化了心脏病发作量和神经行为功能.

结论:

  • DNMT3A体质突变与AIS中较差的神经结果有关.
  • 潜在的机制包括中性粒细胞活性增加和神经炎症.
  • 需要进一步的研究来了解DNMT3A在中风病理生理学中的作用.