Appropriate autophagy has protective effects on ischemic nerve tissue,while excessive autophagy may cause cell death.The inflammatory response plays an important role in the survival of nerve cells and the recovery of...Appropriate autophagy has protective effects on ischemic nerve tissue,while excessive autophagy may cause cell death.The inflammatory response plays an important role in the survival of nerve cells and the recovery of neural tissue after ischemia.Many studies have found an interaction between autophagy and inflammation in the pathogenesis of ischemic stroke.This study outlines recent advances regarding the role of autophagy in the post-stroke inflammatory response as follows.(1)Autophagy inhibits inflammatory responses caused by ischemic stimulation through mTOR,the AMPK pathway,and inhibition of inflammasome activation.(2)Activation of inflammation triggers the formation of autophagosomes,and the upregulation of autophagy levels is marked by a significant increase in the autophagy-forming markers LC3-II and Beclin-1.Lipopolysaccharide stimulates microglia and inhibits ULK1 activity by direct phosphorylation of p38 MAPK,reducing the flux and autophagy level,thereby inducing inflammatory activity.(3)By blocking the activation of autophagy,the activation of inflammasomes can alleviate cerebral ischemic injury.Autophagy can also regulate the phenotypic alternation of microglia through the nuclear factor-κB pathway,which is beneficial to the recovery of neural tissue after ischemia.Studies have shown that some drugs such as resveratrol can exert neuroprotective effects by regulating the autophagy-inflammatory pathway.These studies suggest that the autophagy-inflammatory pathway may provide a new direction for the treatment of ischemic stroke.展开更多
Ischemic stroke is a leading cause of morbidity and mortality worldwide. Resident microglia are the principal immune cells of the brain, and the first to respond to the pathophysiological changes induced by ischemic s...Ischemic stroke is a leading cause of morbidity and mortality worldwide. Resident microglia are the principal immune cells of the brain, and the first to respond to the pathophysiological changes induced by ischemic stroke. Traditionally, it has been thought that microglial activation is deleterious in ischemic stroke, and therapies to suppress it have been intensively explored. However,increasing evidence suggests that microglial activation is also critical for neurogenesis, angiogenesis, and synaptic remodeling, thereby promoting functional recovery after cerebral ischemia. Here, we comprehensively review the dual role of microglia during the different phases of ischemic stroke, and the possible mechanisms controlling the post-ischemic activity of microglia. In addition, we discuss the dynamic interactions between microglia and other cells, such as neurons, astrocytes, oligodendrocytes,and endothelial cells within the brain parenchyma and the neurovascular unit.展开更多
Background DI-3-n-butylphthalide （NBP）, first isolated from the seeds of celery, showed efficacy in animal models of stroke. This study was a clinical trial to assess the efficacy and safety of NBP with a continuous...Background DI-3-n-butylphthalide （NBP）, first isolated from the seeds of celery, showed efficacy in animal models of stroke. This study was a clinical trial to assess the efficacy and safety of NBP with a continuous dose regimen among patients with acute ischemic stroke. Methods A randomized, double-blind, double-dummy trial enrolled 573 patients within 48 hours of onset of ischemic stroke in China. Patients were randomly assigned to receive a 14-day infusion of NBP followed by an NBP capsule, a 14- day infusion of NBP followed by aspirin, or a 14-day infusion of ozagrel followed by aspirin. The efficacy measures were Barthel index score and the modified Rankin scale （mRS） at day 90. Differences among the three groups on mRS were compared using X2 test of proportions （with two-sided e=0.05） and Logistic regression analysis was conducted to take the baseline National Institutes of Health Stroke Scale （NIHSS） score into consideration. Results Among the 535 subjects included in the efficacy analysis, 90-day treatment with NBP was associated with a significantly favorable outcome than 14-day treatment with ozagrel as measured by mRS （P 〈0.001）. No significant difference was found among the three groups on Barthel index at day 90. The rate of adverse events was similar among the three groups. Conclusions The 90-day treatment with NBP could improve outcomes at the third month after stroke. The NBP treatment （both intravenous and oral） is safe （ChiCTR-TRC-09000483）.展开更多
Objective To investigate whether pretreatment with repeated electroacupuncture (EA)at the Baihui acupoint could induce ischemic tolerance against transient focal cerebral ischemic injury in rats. Methods Thirty mal...Objective To investigate whether pretreatment with repeated electroacupuncture (EA)at the Baihui acupoint could induce ischemic tolerance against transient focal cerebral ischemic injury in rats. Methods Thirty male Sprague-Dawley (SD) rats were randomly divided into 3 groups (n=10 for each): the control group consisted of animals receiving no treatment, the isoflurane (ISO) group had animals that inhaled 1.5% isoflurane for 30 min a day for 5 days, and animals in the EA group received electroacupuncture at the Baihui acupoint for 30 min a day for 5 days under 1.5% isoflurane anesthesia. Twenty-four hours after the last treatment, the middle cerebral artery was occluded with No. 3 nylon monofilament for 120 min. The neurological outcomes were evaluated 24 h after reperfusion. The infarct volumes were then assessed using 2% triphenyltetrazolium chloride staining after the neurological outcome evaluation. Results The neurological deficit score (NDS) of the EA group was lower than that of the ISO group and the control group , P<0.05. The infarct volume of the EA group (38.3±25.4 mm 3) was significantly smaller than that of the control group (220.5±66.0 mm 3) and the ISO group (168.6±57.6 mm 3) 24 h after reperfusion. Conclusion Electroacupuncture at the Baihui acupoint 30 min a day for 5 days significantly reduces neurological injury induced by transient middle cerebral artery occlusion.展开更多
Ischemic stroke is a common disease with high mortality and morbidity worldwide.One of the important pathophysiological effects of ischemic stroke is apoptosis.A neuroprotective effect is defined as the inhibition of ...Ischemic stroke is a common disease with high mortality and morbidity worldwide.One of the important pathophysiological effects of ischemic stroke is apoptosis.A neuroprotective effect is defined as the inhibition of neuronal apoptosis to rescue or delay the infarction in the surviving ischemic penumbra.Resveratrol is a natural polyphenol that reportedly prevents cerebral ischemia injury by regulating the expression of PI3K/AKT/mTOR.Therefore,this study aimed to elucidate the neuroprotective effect of resveratrol on cerebral ischemia/reperfusion injury and to investigate the signaling pathways and mechanisms through which resveratrol regulates apoptosis in the ischemic penumbra.Rats were subjected to middle cerebral artery occlusion for 2 h followed by 24 h reperfusion.Cerebral infarct volume was measured using 2%TTC staining.TUNEL staining was conducted to evaluate neuronal apoptosis.Western blotting and immunohistochemistry were used to detect the proteins involved in the JAK2/STAT3/PI3K/AKT/mTOR pathway.The results suggested that resveratrol significantly improved neurological function,reduced cerebral infarct volume,decreased neuronal damage,and markedly attenuated neuronal apoptosis;these effects were attenuated by the inhibition of PI3K/AKT with LY294002 and JAK2/STAT3 with AG490.We also found that resveratrol significantly upregulated the expression of p-JAK2,p-STAT3,p-AKT,p-mTOR,and BCL-2 and downregulated expression of cleaved caspase-3 and BAX,which was partially reversed by LY294002 and AG490.These results suggested that resveratrol provides a neuroprotective effect against cerebral ischemia/reperfusion injury,which is partially mediated by the activation of JAK2/STAT3 and PI3K/AKT/mTOR.Resveratrol may indirectly upregulate the PI3K/AKT/mTOR pathway by activating JAK2/STAT3.展开更多
This study was designed to determine if repeated hyperbaric oxygen (HBO) exposure induces ischemic tolerance in focal cerebral ischemia Methods Sixty male SD rats were used in this study Thirty animals underw...This study was designed to determine if repeated hyperbaric oxygen (HBO) exposure induces ischemic tolerance in focal cerebral ischemia Methods Sixty male SD rats were used in this study Thirty animals underwent transient middle cerebral artery occlusion (MCAO) and the other thirty permanent MCAO model The rats were randomly allocated to 3 sub-groups: control group (n=10), HBO-3 group (n=10), and HBO-5 group (n=10) The animals in HBO-3 and HBO-5 groups received 1*!hour hyperbaric oxygenation at 2 5 atmosphere absolute (ATA) in 100% oxygen every day for 3 and 5 days, respectively The animals in the control group received sham treatments 24*!hours after the last HBO, transient MCAO (120 min) and permanent MCAO were induced by introducing a 3-0 nylon monofilament suture through internal carotid artery based on the Koizumi technique The neurological outcome was evaluated until 24*!hours after reperfusion in transient MCAO rats and ischemia in permanent MCAO rats The infarct volume was then assessed by TTC staining Results In transient MCAO rats, the neurological outcome in both the HBO-3 and HBO-5 groups was better than that of the control group ( P <0 05 and 0 001) The infarct volume decreased from 171 5±113*!mm 3 to 40 6±49 9*!mm 3 ( P <0 05) in the HBO-3 group and 16 2±28 8*!mm 3 ( P <0 01) in the HBO-5 group There were no significant differences in neurological outcome and infarct volume among the three groups in permanent MCAO rats Conclusions The present study demonstrated that HBO preconditioning can induce ischemic tolerance in transient not permanent MCAO rats in a “dose-dependent' manner展开更多
Objective To investigate the rule of the aquaporin 4 (AQP4) expression in acute ischemic brain edema, and to study the correlation between AQP4 expression and diffusion weighted imaging (DWI) Methods Thirty ...Objective To investigate the rule of the aquaporin 4 (AQP4) expression in acute ischemic brain edema, and to study the correlation between AQP4 expression and diffusion weighted imaging (DWI) Methods Thirty six Wistar rats were divided into 2 groups randomly, control group (n=12) and operation group (n=24) in which right middle cerebral artery of each animal had been occluded unilaterally (MCAO) at interval times of: 15 minutes, 30 minutes, 1 hours, 3 hours, 6 hours and 24 hours, respectively The operation process of the control group was the same as the operation group except for the MCAO All groups were examined using DWI The apparent diffusion coefficient (ADC), relative density (rd) and relative area (rs) of the biggest hyperintensity signal layer on DWI were measured After that the animals were sacrificed and perfused with the mixture solution consisting of TTC The biggest layers of the ischemic cerebral tissues in each rat corresponding to the DWI were stained with TTC and examined with immunochemistry (△S) , in situ hybridization (α) and histology Results There was no significant change in the control group In the operation group, a hyperintensity signal was found in the DWI of the right MAC territory at 15 minutes after MCAO The ADC value decreased quickly within one hour after MCAO, while the AQP4 expression, rd DWI and rs DWI increased rapidly during this stage As time progressed, the ADC value decreased further to (2 1±0 6)×10 4 mm 2/s at 3 hours, and then began to increase slowly till 24 hours But the AQP4 expression (△S and α) and rd as well as the rs continuously increased slowly between 1 hour and 6 hours after MCAO, followed a peak after 6 hours The AQP4 expression (α) showed a positive relationship with the rs DWI, they all presented two peaks and a plateau The corresponding sequential pathologic changes were a gradual increase of intracellular edema (within one hour), then an emergence of vasogenic edema (1-6 hours), and fin展开更多
Objective: The 3-N-butylphthalide (NBP) comprises one of the chemical constituents of celery oil. It has a series of pharmacologic mechanisms including reconstructing microcirculation, protecting mitochondrial functio...Objective: The 3-N-butylphthalide (NBP) comprises one of the chemical constituents of celery oil. It has a series of pharmacologic mechanisms including reconstructing microcirculation, protecting mitochondrial function, inhibiting oxidative stress, inhibiting neuronal apoptosis, etc. Based on the complex multi-targets of pharmacologic mechanisms of NBP, the clinical application of NBP is increasing and more clinical researches and animal experiments are also focused on NBP. The aim of this review was to comprehensively and systematically summarize the application of NBP on neurologic diseases and briefly summarize its application to non-neurologic diseases. Moreover, recent progress in experimental models of NBP on animals was summarized. Data sources: Literature was collected from PubMed and Wangfang database until November 2018, using the search terms including "3-N-butylphthalide,""microcirculation,""mitochondria,""ischemic stroke,""Alzheimer disease,""vascular dementia,""Parkinson disease,""brain edema,""CO poisoning,""traumatic central nervous system injury,""autoimmune disease,""amyotrophic lateral sclerosis,""seizures,""diabetes,""diabetic cataract," and "atherosclerosis." Study selection: Literature was mainly derived from English articles or articles that could be obtained with English abstracts and partly derived from Chinese articles. Article type was not limited. References were also identified from the bibliographies of identified articles and the authors’ files. Results: NBP has become an important adjunct for ischemic stroke. In vascular dementia, the clinical application of NBP to treat severe cognitive dysfunction syndrome caused by the hypoperfusion of brain tissue during cerebrovascular disease is also increasing. Evidence also suggests that NBP has a therapeutic effect for neurodegenerative diseases. Many animal experiments have found that it can also improve symptoms in other neurologic diseases such as epilepsy, cerebral edema, and decreased cognitive function caused by severe acute carbon展开更多
Puerarin suppresses autophagy to alleviate cerebral ischemia/reperfusion injury, and accumulating evidence indicates that the AMPKm TOR signaling pathway regulates the activation of the autophagy pathway through the c...Puerarin suppresses autophagy to alleviate cerebral ischemia/reperfusion injury, and accumulating evidence indicates that the AMPKm TOR signaling pathway regulates the activation of the autophagy pathway through the coordinated phosphorylation of ULK1. In this study, we investigated the mechanisms underlying the neuroprotective effect of puerarin and its role in modulating autophagy via the AMPK-m TOR-ULK1 signaling pathway in the rat middle cerebral artery occlusion model of cerebral ischemia/reperfusion injury. Rats were intraperitoneally injected with puerarin, 50 or 100 mg/kg, daily for 7 days. Then, 30 minutes after the final administration, rats were subjected to transient middle cerebral artery occlusion for 90 minutes. Then, after 24 hours of reperfusion, the Longa score and infarct volume were evaluated in each group. Autophagosome formation was observed by transmission electron microscopy. LC3, Beclin-1 p62, AMPK, m TOR and ULK1 protein expression levels were examined by immunofluorescence and western blot assay. Puerarin substantially reduced the Longa score and infarct volume, and it lessened autophagosome formation in the hippocampal CA1 area following cerebral ischemia/reperfusion injury in a dose-dependent manner. Pretreatment with puerarin（50 or 100 mg/kg） reduced Beclin-1 expression and the LC3-II/LC3-I ratio, as well as p-AMPK and p S317-ULK1 levels. In comparison, it increased p62 expression. Furthermore, puerarin at 100 mg/kg dramatically increased the levels of p-m TOR and p S757-ULK1 in the hippocampus on the ischemic side. Our findings suggest that puerarin alleviates autophagy by activating the APMK-m TOR-ULK1 signaling pathway. Thus, puerarin might have therapeutic potential for treating cerebral ischemia/reperfusion injury.展开更多
The inflammatory response after cerebral ischemia/reperfusion is an important cause of neurological damage and repair.After cerebral ischemia/reperfusion,microglia are activated,and a large number of circulating infla...The inflammatory response after cerebral ischemia/reperfusion is an important cause of neurological damage and repair.After cerebral ischemia/reperfusion,microglia are activated,and a large number of circulating inflammatory cells infiltrate the affected area.This leads to the secretion of inflammatory mediators and an inflammatory cascade that eventually causes secondary brain damage,including neuron necrosis,blood-brain barrier destruction,cerebral edema,and an oxidative stress response.Activation of inflammatory signaling pathways plays a key role in the pathological process of ischemic stroke.Increasing evidence suggests that acupuncture can reduce the inflammatory response after cerebral ischemia/reperfusion and promote repair of the injured nervous system.Acupuncture can not only inhibit the activation and infiltration of inflammatory cells,but can also regulate the expression of inflammation-related cytokines,balance the effects of pro-inflammatory and anti-inflammatory factors,and interfere with inflammatory signaling pathways.Therefore,it is important to study the transmission and regulatory mechanism of inflammatory signaling pathways after acupuncture treatment for cerebral ischemia/reperfusion injury to provide a theoretical basis for clinical treatment of this type of injury using acupuncture.Our review summarizes the overall conditions of inflammatory cells,mediators,and pathways after cerebral ischemia/reperfusion,and discusses the possible synergistic intervention of acupuncture in the inflammatory signaling pathway network to provide a foundation to explore the multiple molecular mechanisms by which acupuncture promotes nerve function restoration.展开更多
Objective:Our previous research showed that Naotaifang(a compound traditional Chinese herbal medicine)extract(NTE)has clinically beneficial effects on neurological improvement of patients with acute cerebral ischemia....Objective:Our previous research showed that Naotaifang(a compound traditional Chinese herbal medicine)extract(NTE)has clinically beneficial effects on neurological improvement of patients with acute cerebral ischemia.In this study,we investigated whether NTE protected acute brain injury in rats and whether its effects on ferroptosis could be linked to the dysfunction of glutathione peroxidase 4(GPX4)and iron metabolism.Methods:We established an acute brain injury model of middle cerebral artery occlusion(MCAO)in rats,in which we could observe the accumulation of iron in neurons,as detected by Perl’s staining.Using assay kits,we measured expression levels of ferroptosis biomarkers,such as iron,glutathione(GSH),reactive oxygen species(ROS)and malonaldehyde(MDA);further the expression levels of transferrin receptor1(TFR1),divalent metal transporter 1(DMT1),solute carrier family 7 member 11(SLC7 A11)and GPX4 were determined using immunohistochemical analysis,real-time quantitative polymerase chain reaction and Western blot assays.Results:We found that treatment with NTE reduced the expression levels of TFR1 and DMT1,reduced ROS,MDA and iron accumulation and reduced neurobehavioral scores,relative to untreated MCAO rats.Treatment with NTE increased the expression levels of SLC7 A11,GPX4 and GSH,and the number of Nissl bodies in the MCAO rats.Conclusion:Taken together,our data suggest that acute cerebral ischemia induces neuronal ferroptosis and the effects of treating MCAO rats with NTE involved inhibition of ferroptosis through the TFR1/DMT1 and SCL7 A11/GPX4 pathways.展开更多
OBJECTIVE： To investigate the association of E-selectin $128R polymorphisms with ischemic stroke. DATA SOURCES： A computer-based online search was conducted in PubMed, Elsevier, Ovid Database, the China National Kno...OBJECTIVE： To investigate the association of E-selectin $128R polymorphisms with ischemic stroke. DATA SOURCES： A computer-based online search was conducted in PubMed, Elsevier, Ovid Database, the China National Knowledge Infrastructure, and Wanfang Database between January 1998 and December 2010. STUDY SELECTION： Case-controlled studies addressing the association of the E-selectin polymorphism and ischemic stroke were included in this review. The genotype distribution complied with the Hardy-Weinberg genetic equilibrium. The included reports were evaluated by two authors for strict quality screening. Meta-analysis software, REVMAN 5.1, was used to investigate heterogeneity, pooled odds ratio （OR） and 95% confidence interval （CO in individual studies. MAIN OUTCOME MEASURES： Genotype and allele distributions at the E-selectin $128R site. RESULTS： Six case-controlled studies were included after screening and application of inclusion and exclusion criteria. There was no heterogeneity in the genotype and allele frequencies, and no publication bias was found. Meta-analysis of the pooled data showed that the OR value of the （AC＋CC）/AA genotype was 1.93 （95% CI： 1.55 2.41, Z= 5.80, P 〈 0.000 01）, and the ORfor the C/A allele was 1.80 （95% CI： 1.47 2.22, Z= 5.59, P 〈 0.000 01） in the ischemic stroke group, compared with control group. Results of pooled data in Chinese subjects showed that the ORvalue of （AC＋CC）/AA was 2.36 （95% CI： 1.68 3.31, Z = 4.99, P 〈 0.000 01）, and the OR value of the C/A allele was 2.25 （95% CI： 1.63 3.12, Z= 4.89, P 〈 0.000 01）. CONCLUSION： Polymorphism of E-selectin S128R was significantly associated with susceptibility to ischemic stroke; the AC and CC genotypes as well as the C allele may be factors associated with susceptibility to ischemic stroke.展开更多
Objective: To study the effect of contralateral acupuncture(CAT) at acupoints of Quchi(LI 11) and Zusanli(ST 36) on the unaffected limbs of ischemic stroke patients with left hemiplegia based on regional homogeneity(R...Objective: To study the effect of contralateral acupuncture(CAT) at acupoints of Quchi(LI 11) and Zusanli(ST 36) on the unaffected limbs of ischemic stroke patients with left hemiplegia based on regional homogeneity(ReHo) indices. Methods: Ten ischemic stroke patients with left hemiplegia received CAT on right side at LI 11 and ST 36. Functional magnetic resonance imaging(fMRI) was performed before and after acupuncture. A ReHo analytical method was used to compare brain responses of patients before and after CAT operated by REST software. Results: The stimulation at both LI 11 and ST 36 on the unaffected limbs produced significantly different neural activities. CAT elicited increased ReHo values at the right precentral gyrus and superior frontal gyrus, decreased ReHo value at right superior parietal lobule, left fusiform gyrus and left supplementary motor area. Conclusions: Acupuncture at one side could stimulate bilateral regions. CAT could evoke the gyrus which was possibly related to motor recovery from stroke. A promising indicator of neurobiological deficiencies could be represented by ReHo values in post-stroke patients.展开更多
Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protec...Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway.The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion.Nicotiflorin（10 mg/kg） was administered by tail vein injection.Cell apoptosis in the ischemic cerebral cortex was examined by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase d UTP nick end labeling assay.Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining.Additionally,p-JAK2,p-STAT3,Bcl-2,Bax,and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay.Nicotiflorin altered the shape and structure of injured neurons,decreased the number of apoptotic cells,down-regulates expression of p-JAK2,p-STAT3,caspase-3,and Bax,decreased Bax immunoredactivity,and increased Bcl-2 protein expression and immunoreactivity.These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway.展开更多
Background In-hospital medical complications are associated with poorer clinical outcomes for stroke patients after disease onset. However, few studies from China have reported the effect of these complications on the...Background In-hospital medical complications are associated with poorer clinical outcomes for stroke patients after disease onset. However, few studies from China have reported the effect of these complications on the mortality of patients with acute ischemic stroke. In this prospective work, the China National Stroke Registry Study, we investigated the effect of medical complications on the case fatality of patients with acute ischemic stroke. Methods From September 2007 to August 2008, we prospectively obtained the data of patients with acute stroke from 132 clinical centers in China. Medical complications, case fatality and other information recorded at baseline, during hospitalisation, and at 3, 6, and 12 months after stroke onset. Multivariable Logistic regression was performed to analyze the effect of medical complications on the case fatality of patients with acute ischemic stroke. Results There were 39741 patients screened, 14526 patients with acute ischemic stroke recruited, and 11 560 ischemic stroke patients without missing data identified during the 12-month follow-up. Of the 11 560 ischemic patients, 15.8% （1826） had in-hospital medical complications. The most common complication was pneumonia （1373; 11.9% of patients）, followed by urinary tract infection and gastrointestinal bleeding. In comparison with patients without complications, stroke patients with complications had a significantly higher risk of death during their hospitalization, and at 3, 6 and 12 months post-stroke. Having any one in-hospital medical complication was an independent risk factor for death in patients with acute ischemic stroke during hospital period （adjusted OR=6.946; 95% CI 5.181 to 9.314）, at 3 months （adjusted OR=3.843; 95% C/3.221 to 4.584）, 6 months （adjusted OR=3.492; 95% CI 2.970 to 4.106）, and 12 months （adjusted OR= 3.511; 95% CI 3.021 to 4.080）. Having multiple complications strongly increased the death risk of patients. Conclusion Short-term and long-term outcomes of acute stroke patients展开更多
BACKGROUND:Cerebral stroke is a disease with a high disability rate and a high fatality rate.This study was undertaken to assess the risk of stroke associated pneumonia(SAP) in patients with ischemic stroke using A2DS...BACKGROUND:Cerebral stroke is a disease with a high disability rate and a high fatality rate.This study was undertaken to assess the risk of stroke associated pneumonia(SAP) in patients with ischemic stroke using A2DS2 score.METHODS:Altogether 1 279 patients with ischemic stroke who were treated in our department from 2009 to 2011 were retrospectively analyzed with A2DS2 score. A2DS2 score was calculated as follows:age ≥75 years=1,atrial fi brillation=1,dysphagia=2,male sex=1; stroke severity:NIHSS score 0–4=0,5–15=3,≥16=5. The patients were divided into three groups according to A2DS2 score:620 in score 0 group,383 in score 1–9 group,and 276 in score ≥10 group. The three groups were comparatively analyzed. The diagnostic criteria for SAP were as follows:newly emerging lesions or progressively infiltrating lesions on post-stroke chest images combined with more than two of the following clinical symptoms of infection:(1) fever ≥38 °C;(2) newly occurred cough,productive cough or exacerbation of preexisting respiratory tract symptoms with or without chest pain;(3) signs of pulmonary consolidation and/or wet rales;(4) peripheral white blood cell count ≥10×109/L or ≤4×109/L with or without nuclear shift to left,while excluding some diseases with clinical manifestations similar to pneumonia,such as tuberculosis,pulmonary tumors,non-infectious interstitial lung disease,pulmonary edema,pulmonary embolism and atelectasis. The incidence and mortality of SAP as well as the correlation with ischemic stroke site were analyzed in the three groups respectively. Mean± standard deviation was used to represent measurement data with normal distribution and Student's t test was used. The chi-square test was used to calculate the percentage for enumeration data.RESULTS:The incidence of SAP was significantly higher in the A2DS2 score≥10 group than that in the score 1–9 and score 0 groups(71.7% vs. 22.7%,71.7% vs. 3.7%,respectively),whereas the mortality in the score≥10 group was significantly higher than th展开更多
基金supported by the Natural Science Foundation of Shanghai of China,No.17ZR1425800(to KYL)the Shanghai Pudong District Health Bureau of China,No.PDZX2017-25(to KYL)
文摘Appropriate autophagy has protective effects on ischemic nerve tissue,while excessive autophagy may cause cell death.The inflammatory response plays an important role in the survival of nerve cells and the recovery of neural tissue after ischemia.Many studies have found an interaction between autophagy and inflammation in the pathogenesis of ischemic stroke.This study outlines recent advances regarding the role of autophagy in the post-stroke inflammatory response as follows.(1)Autophagy inhibits inflammatory responses caused by ischemic stimulation through mTOR,the AMPK pathway,and inhibition of inflammasome activation.(2)Activation of inflammation triggers the formation of autophagosomes,and the upregulation of autophagy levels is marked by a significant increase in the autophagy-forming markers LC3-II and Beclin-1.Lipopolysaccharide stimulates microglia and inhibits ULK1 activity by direct phosphorylation of p38 MAPK,reducing the flux and autophagy level,thereby inducing inflammatory activity.(3)By blocking the activation of autophagy,the activation of inflammasomes can alleviate cerebral ischemic injury.Autophagy can also regulate the phenotypic alternation of microglia through the nuclear factor-κB pathway,which is beneficial to the recovery of neural tissue after ischemia.Studies have shown that some drugs such as resveratrol can exert neuroprotective effects by regulating the autophagy-inflammatory pathway.These studies suggest that the autophagy-inflammatory pathway may provide a new direction for the treatment of ischemic stroke.
基金the National Natural Science Foundation of China (81571132, 81873743, and 81801223)Fundamental Research Funds for the Central Universities, China (2017KFYXJJ107 and 2017KFYXJJ124)the National Institutes of Health, USA (R01NS088627)
文摘Ischemic stroke is a leading cause of morbidity and mortality worldwide. Resident microglia are the principal immune cells of the brain, and the first to respond to the pathophysiological changes induced by ischemic stroke. Traditionally, it has been thought that microglial activation is deleterious in ischemic stroke, and therapies to suppress it have been intensively explored. However,increasing evidence suggests that microglial activation is also critical for neurogenesis, angiogenesis, and synaptic remodeling, thereby promoting functional recovery after cerebral ischemia. Here, we comprehensively review the dual role of microglia during the different phases of ischemic stroke, and the possible mechanisms controlling the post-ischemic activity of microglia. In addition, we discuss the dynamic interactions between microglia and other cells, such as neurons, astrocytes, oligodendrocytes,and endothelial cells within the brain parenchyma and the neurovascular unit.
文摘Background DI-3-n-butylphthalide （NBP）, first isolated from the seeds of celery, showed efficacy in animal models of stroke. This study was a clinical trial to assess the efficacy and safety of NBP with a continuous dose regimen among patients with acute ischemic stroke. Methods A randomized, double-blind, double-dummy trial enrolled 573 patients within 48 hours of onset of ischemic stroke in China. Patients were randomly assigned to receive a 14-day infusion of NBP followed by an NBP capsule, a 14- day infusion of NBP followed by aspirin, or a 14-day infusion of ozagrel followed by aspirin. The efficacy measures were Barthel index score and the modified Rankin scale （mRS） at day 90. Differences among the three groups on mRS were compared using X2 test of proportions （with two-sided e=0.05） and Logistic regression analysis was conducted to take the baseline National Institutes of Health Stroke Scale （NIHSS） score into consideration. Results Among the 535 subjects included in the efficacy analysis, 90-day treatment with NBP was associated with a significantly favorable outcome than 14-day treatment with ozagrel as measured by mRS （P 〈0.001）. No significant difference was found among the three groups on Barthel index at day 90. The rate of adverse events was similar among the three groups. Conclusions The 90-day treatment with NBP could improve outcomes at the third month after stroke. The NBP treatment （both intravenous and oral） is safe （ChiCTR-TRC-09000483）.
基金ThisstudywassupportedinpartbyagrantfromtheNationalNaturalScienceFoundationofChina (No 30 170 90 7)
文摘Objective To investigate whether pretreatment with repeated electroacupuncture (EA)at the Baihui acupoint could induce ischemic tolerance against transient focal cerebral ischemic injury in rats. Methods Thirty male Sprague-Dawley (SD) rats were randomly divided into 3 groups (n=10 for each): the control group consisted of animals receiving no treatment, the isoflurane (ISO) group had animals that inhaled 1.5% isoflurane for 30 min a day for 5 days, and animals in the EA group received electroacupuncture at the Baihui acupoint for 30 min a day for 5 days under 1.5% isoflurane anesthesia. Twenty-four hours after the last treatment, the middle cerebral artery was occluded with No. 3 nylon monofilament for 120 min. The neurological outcomes were evaluated 24 h after reperfusion. The infarct volumes were then assessed using 2% triphenyltetrazolium chloride staining after the neurological outcome evaluation. Results The neurological deficit score (NDS) of the EA group was lower than that of the ISO group and the control group , P<0.05. The infarct volume of the EA group (38.3±25.4 mm 3) was significantly smaller than that of the control group (220.5±66.0 mm 3) and the ISO group (168.6±57.6 mm 3) 24 h after reperfusion. Conclusion Electroacupuncture at the Baihui acupoint 30 min a day for 5 days significantly reduces neurological injury induced by transient middle cerebral artery occlusion.
基金supported by the Foundation for Science and Technology Research Project of Chongqing(cstc2012ggB1002).
文摘Ischemic stroke is a common disease with high mortality and morbidity worldwide.One of the important pathophysiological effects of ischemic stroke is apoptosis.A neuroprotective effect is defined as the inhibition of neuronal apoptosis to rescue or delay the infarction in the surviving ischemic penumbra.Resveratrol is a natural polyphenol that reportedly prevents cerebral ischemia injury by regulating the expression of PI3K/AKT/mTOR.Therefore,this study aimed to elucidate the neuroprotective effect of resveratrol on cerebral ischemia/reperfusion injury and to investigate the signaling pathways and mechanisms through which resveratrol regulates apoptosis in the ischemic penumbra.Rats were subjected to middle cerebral artery occlusion for 2 h followed by 24 h reperfusion.Cerebral infarct volume was measured using 2%TTC staining.TUNEL staining was conducted to evaluate neuronal apoptosis.Western blotting and immunohistochemistry were used to detect the proteins involved in the JAK2/STAT3/PI3K/AKT/mTOR pathway.The results suggested that resveratrol significantly improved neurological function,reduced cerebral infarct volume,decreased neuronal damage,and markedly attenuated neuronal apoptosis;these effects were attenuated by the inhibition of PI3K/AKT with LY294002 and JAK2/STAT3 with AG490.We also found that resveratrol significantly upregulated the expression of p-JAK2,p-STAT3,p-AKT,p-mTOR,and BCL-2 and downregulated expression of cleaved caspase-3 and BAX,which was partially reversed by LY294002 and AG490.These results suggested that resveratrol provides a neuroprotective effect against cerebral ischemia/reperfusion injury,which is partially mediated by the activation of JAK2/STAT3 and PI3K/AKT/mTOR.Resveratrol may indirectly upregulate the PI3K/AKT/mTOR pathway by activating JAK2/STAT3.
基金ThisstudywassupportedinpartbyagrantfromtheNationalNaturalScienceFoundationofChina (No 396 70 6 99)
文摘This study was designed to determine if repeated hyperbaric oxygen (HBO) exposure induces ischemic tolerance in focal cerebral ischemia Methods Sixty male SD rats were used in this study Thirty animals underwent transient middle cerebral artery occlusion (MCAO) and the other thirty permanent MCAO model The rats were randomly allocated to 3 sub-groups: control group (n=10), HBO-3 group (n=10), and HBO-5 group (n=10) The animals in HBO-3 and HBO-5 groups received 1*!hour hyperbaric oxygenation at 2 5 atmosphere absolute (ATA) in 100% oxygen every day for 3 and 5 days, respectively The animals in the control group received sham treatments 24*!hours after the last HBO, transient MCAO (120 min) and permanent MCAO were induced by introducing a 3-0 nylon monofilament suture through internal carotid artery based on the Koizumi technique The neurological outcome was evaluated until 24*!hours after reperfusion in transient MCAO rats and ischemia in permanent MCAO rats The infarct volume was then assessed by TTC staining Results In transient MCAO rats, the neurological outcome in both the HBO-3 and HBO-5 groups was better than that of the control group ( P <0 05 and 0 001) The infarct volume decreased from 171 5±113*!mm 3 to 40 6±49 9*!mm 3 ( P <0 05) in the HBO-3 group and 16 2±28 8*!mm 3 ( P <0 01) in the HBO-5 group There were no significant differences in neurological outcome and infarct volume among the three groups in permanent MCAO rats Conclusions The present study demonstrated that HBO preconditioning can induce ischemic tolerance in transient not permanent MCAO rats in a “dose-dependent' manner
基金theNationalNaturalScienceFoundationofChina (No 3 0 0 70 2 47)
文摘Objective To investigate the rule of the aquaporin 4 (AQP4) expression in acute ischemic brain edema, and to study the correlation between AQP4 expression and diffusion weighted imaging (DWI) Methods Thirty six Wistar rats were divided into 2 groups randomly, control group (n=12) and operation group (n=24) in which right middle cerebral artery of each animal had been occluded unilaterally (MCAO) at interval times of: 15 minutes, 30 minutes, 1 hours, 3 hours, 6 hours and 24 hours, respectively The operation process of the control group was the same as the operation group except for the MCAO All groups were examined using DWI The apparent diffusion coefficient (ADC), relative density (rd) and relative area (rs) of the biggest hyperintensity signal layer on DWI were measured After that the animals were sacrificed and perfused with the mixture solution consisting of TTC The biggest layers of the ischemic cerebral tissues in each rat corresponding to the DWI were stained with TTC and examined with immunochemistry (△S) , in situ hybridization (α) and histology Results There was no significant change in the control group In the operation group, a hyperintensity signal was found in the DWI of the right MAC territory at 15 minutes after MCAO The ADC value decreased quickly within one hour after MCAO, while the AQP4 expression, rd DWI and rs DWI increased rapidly during this stage As time progressed, the ADC value decreased further to (2 1±0 6)×10 4 mm 2/s at 3 hours, and then began to increase slowly till 24 hours But the AQP4 expression (△S and α) and rd as well as the rs continuously increased slowly between 1 hour and 6 hours after MCAO, followed a peak after 6 hours The AQP4 expression (α) showed a positive relationship with the rs DWI, they all presented two peaks and a plateau The corresponding sequential pathologic changes were a gradual increase of intracellular edema (within one hour), then an emergence of vasogenic edema (1-6 hours), and fin
文摘Objective: The 3-N-butylphthalide (NBP) comprises one of the chemical constituents of celery oil. It has a series of pharmacologic mechanisms including reconstructing microcirculation, protecting mitochondrial function, inhibiting oxidative stress, inhibiting neuronal apoptosis, etc. Based on the complex multi-targets of pharmacologic mechanisms of NBP, the clinical application of NBP is increasing and more clinical researches and animal experiments are also focused on NBP. The aim of this review was to comprehensively and systematically summarize the application of NBP on neurologic diseases and briefly summarize its application to non-neurologic diseases. Moreover, recent progress in experimental models of NBP on animals was summarized. Data sources: Literature was collected from PubMed and Wangfang database until November 2018, using the search terms including "3-N-butylphthalide,""microcirculation,""mitochondria,""ischemic stroke,""Alzheimer disease,""vascular dementia,""Parkinson disease,""brain edema,""CO poisoning,""traumatic central nervous system injury,""autoimmune disease,""amyotrophic lateral sclerosis,""seizures,""diabetes,""diabetic cataract," and "atherosclerosis." Study selection: Literature was mainly derived from English articles or articles that could be obtained with English abstracts and partly derived from Chinese articles. Article type was not limited. References were also identified from the bibliographies of identified articles and the authors’ files. Results: NBP has become an important adjunct for ischemic stroke. In vascular dementia, the clinical application of NBP to treat severe cognitive dysfunction syndrome caused by the hypoperfusion of brain tissue during cerebrovascular disease is also increasing. Evidence also suggests that NBP has a therapeutic effect for neurodegenerative diseases. Many animal experiments have found that it can also improve symptoms in other neurologic diseases such as epilepsy, cerebral edema, and decreased cognitive function caused by severe acute carbon
基金supported by the National Natural Science Foundation of China,No.81202625the Open Fund of Key Laboratory of Cardiovascular and Cerebrovascular Diseases Translational Medicine,China Three Gorges University,China,No.2016xnxg101
文摘Puerarin suppresses autophagy to alleviate cerebral ischemia/reperfusion injury, and accumulating evidence indicates that the AMPKm TOR signaling pathway regulates the activation of the autophagy pathway through the coordinated phosphorylation of ULK1. In this study, we investigated the mechanisms underlying the neuroprotective effect of puerarin and its role in modulating autophagy via the AMPK-m TOR-ULK1 signaling pathway in the rat middle cerebral artery occlusion model of cerebral ischemia/reperfusion injury. Rats were intraperitoneally injected with puerarin, 50 or 100 mg/kg, daily for 7 days. Then, 30 minutes after the final administration, rats were subjected to transient middle cerebral artery occlusion for 90 minutes. Then, after 24 hours of reperfusion, the Longa score and infarct volume were evaluated in each group. Autophagosome formation was observed by transmission electron microscopy. LC3, Beclin-1 p62, AMPK, m TOR and ULK1 protein expression levels were examined by immunofluorescence and western blot assay. Puerarin substantially reduced the Longa score and infarct volume, and it lessened autophagosome formation in the hippocampal CA1 area following cerebral ischemia/reperfusion injury in a dose-dependent manner. Pretreatment with puerarin（50 or 100 mg/kg） reduced Beclin-1 expression and the LC3-II/LC3-I ratio, as well as p-AMPK and p S317-ULK1 levels. In comparison, it increased p62 expression. Furthermore, puerarin at 100 mg/kg dramatically increased the levels of p-m TOR and p S757-ULK1 in the hippocampus on the ischemic side. Our findings suggest that puerarin alleviates autophagy by activating the APMK-m TOR-ULK1 signaling pathway. Thus, puerarin might have therapeutic potential for treating cerebral ischemia/reperfusion injury.
基金This work was supported by the National Natural Science Foundation of China,Nos.81072947,81473470,81774423,the Natural Science Foundation of Guangdong Province of China,No.2014A030311033(all to FT).
文摘The inflammatory response after cerebral ischemia/reperfusion is an important cause of neurological damage and repair.After cerebral ischemia/reperfusion,microglia are activated,and a large number of circulating inflammatory cells infiltrate the affected area.This leads to the secretion of inflammatory mediators and an inflammatory cascade that eventually causes secondary brain damage,including neuron necrosis,blood-brain barrier destruction,cerebral edema,and an oxidative stress response.Activation of inflammatory signaling pathways plays a key role in the pathological process of ischemic stroke.Increasing evidence suggests that acupuncture can reduce the inflammatory response after cerebral ischemia/reperfusion and promote repair of the injured nervous system.Acupuncture can not only inhibit the activation and infiltration of inflammatory cells,but can also regulate the expression of inflammation-related cytokines,balance the effects of pro-inflammatory and anti-inflammatory factors,and interfere with inflammatory signaling pathways.Therefore,it is important to study the transmission and regulatory mechanism of inflammatory signaling pathways after acupuncture treatment for cerebral ischemia/reperfusion injury to provide a theoretical basis for clinical treatment of this type of injury using acupuncture.Our review summarizes the overall conditions of inflammatory cells,mediators,and pathways after cerebral ischemia/reperfusion,and discusses the possible synergistic intervention of acupuncture in the inflammatory signaling pathway network to provide a foundation to explore the multiple molecular mechanisms by which acupuncture promotes nerve function restoration.
基金supported by the National Natural Science Foundation of China(No.81774033 and No.81773736)the Hunan Provincial Department of Education-funded Scientific Research Project(No.18C0379 and No.19A378)。
文摘Objective:Our previous research showed that Naotaifang(a compound traditional Chinese herbal medicine)extract(NTE)has clinically beneficial effects on neurological improvement of patients with acute cerebral ischemia.In this study,we investigated whether NTE protected acute brain injury in rats and whether its effects on ferroptosis could be linked to the dysfunction of glutathione peroxidase 4(GPX4)and iron metabolism.Methods:We established an acute brain injury model of middle cerebral artery occlusion(MCAO)in rats,in which we could observe the accumulation of iron in neurons,as detected by Perl’s staining.Using assay kits,we measured expression levels of ferroptosis biomarkers,such as iron,glutathione(GSH),reactive oxygen species(ROS)and malonaldehyde(MDA);further the expression levels of transferrin receptor1(TFR1),divalent metal transporter 1(DMT1),solute carrier family 7 member 11(SLC7 A11)and GPX4 were determined using immunohistochemical analysis,real-time quantitative polymerase chain reaction and Western blot assays.Results:We found that treatment with NTE reduced the expression levels of TFR1 and DMT1,reduced ROS,MDA and iron accumulation and reduced neurobehavioral scores,relative to untreated MCAO rats.Treatment with NTE increased the expression levels of SLC7 A11,GPX4 and GSH,and the number of Nissl bodies in the MCAO rats.Conclusion:Taken together,our data suggest that acute cerebral ischemia induces neuronal ferroptosis and the effects of treating MCAO rats with NTE involved inhibition of ferroptosis through the TFR1/DMT1 and SCL7 A11/GPX4 pathways.
文摘OBJECTIVE： To investigate the association of E-selectin $128R polymorphisms with ischemic stroke. DATA SOURCES： A computer-based online search was conducted in PubMed, Elsevier, Ovid Database, the China National Knowledge Infrastructure, and Wanfang Database between January 1998 and December 2010. STUDY SELECTION： Case-controlled studies addressing the association of the E-selectin polymorphism and ischemic stroke were included in this review. The genotype distribution complied with the Hardy-Weinberg genetic equilibrium. The included reports were evaluated by two authors for strict quality screening. Meta-analysis software, REVMAN 5.1, was used to investigate heterogeneity, pooled odds ratio （OR） and 95% confidence interval （CO in individual studies. MAIN OUTCOME MEASURES： Genotype and allele distributions at the E-selectin $128R site. RESULTS： Six case-controlled studies were included after screening and application of inclusion and exclusion criteria. There was no heterogeneity in the genotype and allele frequencies, and no publication bias was found. Meta-analysis of the pooled data showed that the OR value of the （AC＋CC）/AA genotype was 1.93 （95% CI： 1.55 2.41, Z= 5.80, P 〈 0.000 01）, and the ORfor the C/A allele was 1.80 （95% CI： 1.47 2.22, Z= 5.59, P 〈 0.000 01） in the ischemic stroke group, compared with control group. Results of pooled data in Chinese subjects showed that the ORvalue of （AC＋CC）/AA was 2.36 （95% CI： 1.68 3.31, Z = 4.99, P 〈 0.000 01）, and the OR value of the C/A allele was 2.25 （95% CI： 1.63 3.12, Z= 4.89, P 〈 0.000 01）. CONCLUSION： Polymorphism of E-selectin S128R was significantly associated with susceptibility to ischemic stroke; the AC and CC genotypes as well as the C allele may be factors associated with susceptibility to ischemic stroke.
基金Supported by the"Innovation and Strength of Hospital"grants from the First Affiliated Hospital of Guangzhou University of Chinese Medicine(No.2016QN09)
文摘Objective: To study the effect of contralateral acupuncture(CAT) at acupoints of Quchi(LI 11) and Zusanli(ST 36) on the unaffected limbs of ischemic stroke patients with left hemiplegia based on regional homogeneity(ReHo) indices. Methods: Ten ischemic stroke patients with left hemiplegia received CAT on right side at LI 11 and ST 36. Functional magnetic resonance imaging(fMRI) was performed before and after acupuncture. A ReHo analytical method was used to compare brain responses of patients before and after CAT operated by REST software. Results: The stimulation at both LI 11 and ST 36 on the unaffected limbs produced significantly different neural activities. CAT elicited increased ReHo values at the right precentral gyrus and superior frontal gyrus, decreased ReHo value at right superior parietal lobule, left fusiform gyrus and left supplementary motor area. Conclusions: Acupuncture at one side could stimulate bilateral regions. CAT could evoke the gyrus which was possibly related to motor recovery from stroke. A promising indicator of neurobiological deficiencies could be represented by ReHo values in post-stroke patients.
基金financially supported by the Natural Science Foundation of Education Department of Sichuan Province of China,No.14ZB0152the Joint Research Program of Luzhou and Southwest Medical University,in China,No.14JC0120
文摘Nicotiflorin is a flavonoid extracted from Carthamus tinctorius.Previous studies have shown its cerebral protective effect,but the mechanism is undefined.In this study,we aimed to determine whether nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis through the JAK2/STAT3 pathway.The cerebral ischemia/reperfusion injury model was established by middle cerebral artery occlusion/reperfusion.Nicotiflorin（10 mg/kg） was administered by tail vein injection.Cell apoptosis in the ischemic cerebral cortex was examined by hematoxylin-eosin staining and terminal deoxynucleotidyl transferase d UTP nick end labeling assay.Bcl-2 and Bax expression levels in ischemic cerebral cortex were examined by immunohistochemial staining.Additionally,p-JAK2,p-STAT3,Bcl-2,Bax,and caspase-3 levels in ischemic cerebral cortex were examined by western blot assay.Nicotiflorin altered the shape and structure of injured neurons,decreased the number of apoptotic cells,down-regulates expression of p-JAK2,p-STAT3,caspase-3,and Bax,decreased Bax immunoredactivity,and increased Bcl-2 protein expression and immunoreactivity.These results suggest that nicotiflorin protects against cerebral ischemia/reperfusion injury-induced apoptosis via the JAK2/STAT3 pathway.
文摘Background In-hospital medical complications are associated with poorer clinical outcomes for stroke patients after disease onset. However, few studies from China have reported the effect of these complications on the mortality of patients with acute ischemic stroke. In this prospective work, the China National Stroke Registry Study, we investigated the effect of medical complications on the case fatality of patients with acute ischemic stroke. Methods From September 2007 to August 2008, we prospectively obtained the data of patients with acute stroke from 132 clinical centers in China. Medical complications, case fatality and other information recorded at baseline, during hospitalisation, and at 3, 6, and 12 months after stroke onset. Multivariable Logistic regression was performed to analyze the effect of medical complications on the case fatality of patients with acute ischemic stroke. Results There were 39741 patients screened, 14526 patients with acute ischemic stroke recruited, and 11 560 ischemic stroke patients without missing data identified during the 12-month follow-up. Of the 11 560 ischemic patients, 15.8% （1826） had in-hospital medical complications. The most common complication was pneumonia （1373; 11.9% of patients）, followed by urinary tract infection and gastrointestinal bleeding. In comparison with patients without complications, stroke patients with complications had a significantly higher risk of death during their hospitalization, and at 3, 6 and 12 months post-stroke. Having any one in-hospital medical complication was an independent risk factor for death in patients with acute ischemic stroke during hospital period （adjusted OR=6.946; 95% CI 5.181 to 9.314）, at 3 months （adjusted OR=3.843; 95% C/3.221 to 4.584）, 6 months （adjusted OR=3.492; 95% CI 2.970 to 4.106）, and 12 months （adjusted OR= 3.511; 95% CI 3.021 to 4.080）. Having multiple complications strongly increased the death risk of patients. Conclusion Short-term and long-term outcomes of acute stroke patients
文摘BACKGROUND:Cerebral stroke is a disease with a high disability rate and a high fatality rate.This study was undertaken to assess the risk of stroke associated pneumonia(SAP) in patients with ischemic stroke using A2DS2 score.METHODS:Altogether 1 279 patients with ischemic stroke who were treated in our department from 2009 to 2011 were retrospectively analyzed with A2DS2 score. A2DS2 score was calculated as follows:age ≥75 years=1,atrial fi brillation=1,dysphagia=2,male sex=1; stroke severity:NIHSS score 0–4=0,5–15=3,≥16=5. The patients were divided into three groups according to A2DS2 score:620 in score 0 group,383 in score 1–9 group,and 276 in score ≥10 group. The three groups were comparatively analyzed. The diagnostic criteria for SAP were as follows:newly emerging lesions or progressively infiltrating lesions on post-stroke chest images combined with more than two of the following clinical symptoms of infection:(1) fever ≥38 °C;(2) newly occurred cough,productive cough or exacerbation of preexisting respiratory tract symptoms with or without chest pain;(3) signs of pulmonary consolidation and/or wet rales;(4) peripheral white blood cell count ≥10×109/L or ≤4×109/L with or without nuclear shift to left,while excluding some diseases with clinical manifestations similar to pneumonia,such as tuberculosis,pulmonary tumors,non-infectious interstitial lung disease,pulmonary edema,pulmonary embolism and atelectasis. The incidence and mortality of SAP as well as the correlation with ischemic stroke site were analyzed in the three groups respectively. Mean± standard deviation was used to represent measurement data with normal distribution and Student's t test was used. The chi-square test was used to calculate the percentage for enumeration data.RESULTS:The incidence of SAP was significantly higher in the A2DS2 score≥10 group than that in the score 1–9 and score 0 groups(71.7% vs. 22.7%,71.7% vs. 3.7%,respectively),whereas the mortality in the score≥10 group was significantly higher than th
