ischemia

摘要： β2-Microglobulin(β2M),a component of the major histocompatibility complex class I molecule,is associated with aging-related cognitive impairment and Alzheimer’s disease.Although upregulation ofβ2M is considered to be highly related to ischemic stroke,the specific role and underlying mechanistic action ofβ2M are poorly understood.In this study,we established a rat model of focal cerebral ischemia by occlusion of the middle cerebral artery.We found thatβ2M levels in the cerebral spinal fluid,serum,and brain tissue were significantly increased in the acute period but gradually decreased during the recovery period.RNA interference was used to inhibitβ2M expression in the acute period of cerebral stroke.Tissue staining with 2,3,5-triphenyltetrazolium chloride and evaluation of cognitive function using the Morris water maze test demonstrated that decreasedβ2M expression in the ischemic penumbra reduced infarct volume and alleviated cognitive deficits,respectively.Notably,glial cell,caspase-1(p20),and Nod-like receptor pyrin domain containing 3(NLRP3)inflammasome activation as well as production of the inflammatory cytokines interleukin-1β,interleukin-6,and tumor necrosis factor-αwere also effectively inhibited byβ2M silencing.These findings suggest thatβ2M participates in brain injury and cognitive impairment in a rat model of ischemic stroke through activation of neuroinflammation associated with the NLRP3 inflammasome.

摘要： Retraction:Resveratrol inhibits matrix metalloproteinases to attenuate neuronal damage in cerebral ischemia:a molecular docking study exploring possible neuroprotection https://doi.org/10.4103/1673-5374.310702 The editors of Neural Regeneration Research(NRR)has retracted the publication entitled“Resveratrol inhibits matrix metalloproteinases to attenuate neuronal damage in cerebral ischemia:a molecular docking study exploring possible neuroprotection”(Pandey et al.,2015;doi:10.4103/1673-5374.155429)according to NRR Policy on Article Retraction(https://journals.lww.com/nrronline/Pages/instructionsforauthors.aspx).

摘要： Cervical spondylotic myelopathy is the main cause of non-traumatic spinal cord injury,with chronic static and/or dynamic compressive spinal cord injury as the unique pathogenesis.In the progression of this condition,the microvascular network is compressed and destroyed,resulting in ischemia and hypoxia.The main pathological changes are inflammation,damage to the blood spinal cord barriers,and cell apoptosis at the site of compression.Studies have confirmed that vascular regeneration and remodeling contribute to neural repair by promoting blood flow and the reconstruction of effective circulation to meet the nutrient and oxygen requirements for nerve repair.Surgical decompression is the most effective clinical treatment for this condition;however,in some patients,residual neurological dysfunction remains after decompression.Facilitating revascularization during compression and after decompression is therefore complementary to surgical treatment.In this review,we summarize the progress in research on chronic compressive spinal cord injury,covering both physiological and pathological changes after compression and decompression,and the regulatory mechanisms of vascular injury and repair.

摘要： The adult cortex has long been regarded as non-neurogenic.Whether injury can induce neurogenesis in the adult cortex is still controversial.Here,we report that focal ischemia stimulates a transient wave of local neurogenesis.Using 5′-bromo-2′-deoxyuridine labeling,we demonstrated a rapid generation of doublecortin-positive neuroblasts that died quickly in mouse cerebral cortex following ischemia.Nestin-Cre^(ER)-based cell ablation and fate mapping showed a small contribution of neuroblasts by subventricular zone neural stem cells.Using a mini-photothrombotic ischemia mouse model and retrovirus expressing green fluorescent protein labeling,we observed maturation of locally generated new neurons.Furthermore,fate tracing analyses using PDGFRα-,GFAP-,and Sox2-Cre^(ER) mice showed a transient wave of neuroblast generation in mild ischemic cortex and identified that Sox2-positive astrocytes were the major neurogenic cells in adult cortex.In addition,a similar upregulation of Sox2 and appearance of neuroblasts were observed in the focal ischemic cortex of Macaca mulatta.Our findings demonstrated a transient neurogenic response of Sox2-positive astrocytes in ischemic cortex,which suggests the possibility of inducing neuronal regeneration by amplifying this intrinsic response in the future.

摘要： In“Offspring of rats with cerebral hypoxia-ischemia manifest cognitive dysfunction in learning and memory abilities”,which was published on pages 1662-1670,Issue 9,Volume 15 of Neural Regeneration Research(Xue et al.,2020),Figure 1A appears incorrectly because of the author’s error made in image selection.

摘要： 心肌缺血再灌注损伤(myocardial ischemia-reperfu-sion injury,MIRI),是指在冠状动脉发生完全或部分梗阻之后,在一段时间内又重新获得血流时,这部分心肌组织的损伤反而会进行性加重[1]。临床上常见的心肌梗死、心脏骤停等疾病都存在心肌缺血再灌注损伤的问题。在减少再灌注损伤的风险问题上。

摘要： 肢深静脉血栓(deep vein thrombosis,DVT)彩色多普勒超声(color doppler ultrasound,CDUS)缺血/再灌注损伤(ischemia reperfusion injury,IRI)急性肾损伤(acute kidney injury,AKI)亚临床急性排斥反应(subclinical acute rejection,subAR)。

摘要： Objective: Ischemic conditioning (IC) limits myocyte necrosis after acute myocardial ischemia-reperfusion;however, controversy persists regarding its potential to attenuate LV contractile dysfunction. Pressure-volume (P-V) loop analysis, via the load-insensitive conductance catheter method, was used to evaluate LV contractility, diastolic function, and ventriculo-arterial coupling. The goal of this study was to evaluate the ability of IC to improve post-ischemic recovery of LV contractile function. Methods: Twelve anesthetized dogs were randomly distributed to either the IC or the non-IC group;all dogs were subject to 60-min acute coronary occlusion followed by 180-min reperfusion. IC consisted of 4 repeated cycles of 5-min occlusion and 5-min reperfusion of the left main coronary artery. LV P-V relations were constructed under steady-state conditions (by inferior vena cava occlusion) at the beginning and end of the experiments;P-V loops were acquired at different time points before and during ischemia-reperfusion. Results: During ischemia and reperfusion, dP/dtmax decreased significantly compared to baseline in both groups;dP/dtmin, an indicator of the rate of LV relaxation rate was not affected for either group. Significant changes in several parameters of LV function including LVEF, SW, tPFR, ESV, and EDV caused by ischemia were also identified;none of these negative effects were resorbed, even in part, during reperfusion. Conclusions: Diminished LV contractile efficiency during systole and diastole produced by ischemia-reperfusion did not improve with IC pre-treatment despite significant endogenous protection against tissue necrosis.

摘要： Retraction:Ki20227 aggravates apoptosis,inflammatory response,and oxidative stress after focal cerebral ischemia injury https://doi.org/10.4103/1673-5374.337056 This article has been retracted:please see NRR Policy on Article Retraction(http://www.nrronline.org/contributors.asp).

摘要： To the Editor:Hepatic ischemia-reperfusion(I/R)injury is the component of liver injury related to liver transplantation and liver surgery[1-3].The hepatic sinus microcirculation injury is a central part of hep-atic I/R injury,which eventually leads to hepatocyte injury.This process is closely associated with the participation of liver non-parenchymal cells such as Kuffer cells,hepatic stellate cells,liver sinusoidal endothelial cells(LSECs),and cytokines.