Cerebral ischemia/reperfusion injury (CI/RI) is a common complication of cerebrovascular diseases such as stroke, characterized by mitochondrial dysfunction. This study investigates the function of proliferation-associated protein 2G4 (PA2G4) released by neural stem cells (NSCs)-derived exosomes (NSC-Exo) in treating middle cerebral artery occlusion/reperfusion (MCAO/R) by regulating mitophagy. NSC-Exo were extracted and identified. Treatment of NSC-Exo alleviated neurofunctional impairments in MCAO/R-induced mice, reduced oxidative stress and inflammatory responses in hippocampal tissues, and decreased neuronal apoptosis. We analyzed the alteration of molecular mechanisms under the effect of NSC-Exo treatment using bioinformatics analysis and RNA sequencing. PA2G4 was enriched in NSC-Exo, and the absence of PA2G4 in neurons impaired the mitigating effect of NSC-Exo on hippocampal neuronal injury and inhibited mitophagy. NSC-Exo delivered PA2G4 to recruit WW domain-containing protein 2 (WWP2), thereby mediating ubiquitination and degradation of Annexin A2 (ANXA2), and overexpression of PA2G4 or WWP2 reversed the accentuating effect of ANXA2 overexpression on MCAO injury. These findings indicate that PA2G4 delivered by NSC-Exo recruits WWP2 to mediate ubiquitination of ANXA2, thereby activating mitophagy to alleviate oxidative stress in hippocampal neurons in MCAO/R. This study offers a novel target for the treatment of CI/RI. PA2G4 delivered by NSC-Exo recruits WWP2 and mediates ubiquitination modification of ANXA2 to activate mitophagy and mitigate oxidative stress in hippocampal neurons in mice challenged by MCAO/R.

Objective Post-stroke cognitive impairment (PSCI) diagnosis primarily relies on scales, which are highly subjective. CDKN2B-AS1 is highly expressed in stroke patients. This study aims to investigate the clinical value and potential regulatory mechanisms of CDKN2B-AS1 in PSCI. Methods This study included 86 patients with PSCI. Cognitive function was assessed using the MoCA scales. A mouse PSCI model was established by treating mice with MCAO using the filament occlusion method. An in vitro PSCI model was constructed by treating HT22 cells with OGD/R. RT-qPCR was used to detect the expression of CDKN2B-AS1, miR-140-3p, Bax, Caspase-3, and Bcl-2 mRNA. ROC analysis evaluated the diagnostic value of CDKN2B-AS1. The Morris water maze assessed spatial learning and memory in mice. Cell proliferation, apoptosis, and inflammatory factors were measured using CCK-8 assay, flow cytometry, and ELISA, respectively. Results CDKN2B-AS1 is significantly upregulated in PSCI patients, with an AUC of 0.877 in ROC analysis. Its expression level is negatively correlated with MoCA scores. CDKN2B-AS1 has been demonstrated to directly bind and negatively regulate miR-140-3p. Knockdown of CDKN2B-AS1 alleviates OGD/R-induced neuronal apoptosis, inflammatory cytokine (IL-1β, IL-6, TNF-α) release, and oxidative stress levels by elevating miR-140-3p level. It also improves cognitive function in MCAO mice. These protective effects are reversed by miR-140-3p inhibition. Conclusion Silencing CDKN2B-AS1 may alleviate neuroinflammation and oxidative stress by upregulating miR-140-3p, thereby improving cognitive impairment. CDKN2B-AS1 holds potential as a diagnostic biomarker and therapeutic target for PSCI.

Post-stroke cognitive impairment (PSCI) is a common sequela that occurs after ischaemic stroke (IS). This study aimed to investigate whether miR-409-3p is related to PSCI. Patients with IS were divided into two subgroups: PSCI and post-stroke cognitive normality (PSCN). The plasma level of miR-409-3p was determined by RT-qPCR. The association between PSCI and miR-409-3p was evaluated through binary logistic regression and by analysing the correlation between miR-409-3p and the MoCA score. In mice with middle cerebral artery occlusion (MCAO), the effects of miR-409-3p on cognitive function were explored through mNSS score and Morris water maze. In OGD/R-induced SH-SY5Y cells, the effects of miR-409-3p on cell viability, apoptosis and neuronal inflammation were evaluated using CCK-8, flow cytometry and ELISA. The content of miR-409-3p in patients with IS and those with PSCI was both increased, and its content showed a significant negative correlation with the MoCA score. The binary logistic regression analysis showed that a high risk of PSCI was associated with miR-409-3p. In MCAO mice, inhibition of miR-409-3p can significantly reduce the mNSS score and shorten the escape latency in the Morris water maze. Further-more, in neurons induced by OGD/R, down-regulation of miR-409-3p can exert a significant protective effect on neurons, manifested by enhanced cell viability, reduced apoptosis rate and inhibition of the synthesis of inflammatory factors. We conclude that miR-409-3p is a risk factor associated with PSCI. In MCAO mice and neurons induced by OGD/R, inhibition of miR-409-3p significantly alleviated neurological deficits and suppres-sed neuronal apoptosis and neuronal inflammation.

NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome plays a pivotal role in the progression of cerebral ischemia/reperfusion injury (CI/RI). We aimed to investigate the implication of WW domain-containing protein 2 (WWP2), an E3 ubiquitin ligase, in CI/RI and its mechanism. Microglia were subjected to oxygen-glucose deprivation/reoxygenation, and mice were subjected to middle cerebral artery occlusion (MCAO) for modeling. WWP2 was reduced in the brain tissues of mice with MCAO/R. WWP2 overexpression in microglia inhibited the NLRP3 inflammasome activation to alleviate MCAO/R-induced injury and microglia-induced neurotoxicity. WWP2 inhibited the mitochondrial translocation of NLRP3 by degrading mitochondrial antiviral-signaling protein (MAVS) to block its interaction with NLRP3, and MAVS overexpression in microglia promoted the NLRP3 activation to exacerbate MCAO/R and neurotoxicity. The nuclear export of TAR DNA-binding protein 43 (TDP-43) in MCAO/R promoted the WWP2 degradation via the (UG)n element of the 3'UTR of WWP2. TDP-43 overexpression also impaired the blockade of NLRP3 activation and exacerbated neurotoxicity in the presence of WWP2. Overall, our investigations demonstrate that nuclear export of TDP-43 in microglia activates NLRP3 inflammasome and exacerbates CI/RI by blocking MAVS degradation through (UG)n element-mediated instability of WWP2.

Even though long-term immunosuppressant drugs (ISD) are employed to inhibit immune system activity, enhancing graft functionality and patient survival in solid organ transplantation (SOT), these transplants often lead to immune complications, with post-transplant autoimmune diseases of the central nervous system (CNS) being uncommon. Here, we detail the case of a 66-year-old woman who underwent a renal transplantation 8 months prior, who was admitted with subacute onset of encephalomyelitis, accompanied by headaches, paraplegia, weakness, vomiting, and abdominal pain, with a positive COVID-19 nasopharyngeal swab test 1 month before admission. MRI scans of the brain revealed multiple lesions in the white matter of the bilateral deep frontal lobe, the left temporal lobe and insula lobe. Additionally, there were multiple short segment lesions in the spinal cord and subdural hematoma at T1, T6-T7 posterior. The serum revealed a positive result for GlyR-IgG. Following the administration of corticosteroid and intravenous immunoglobulin, there was a significant improvement in the patient’s symptoms within 2 weeks, and her brain MRI showed a reduction in the lesion. Despite its rarity, we believe this to be the inaugural documentation of anti-GlyR encephalomyelitis occurring during renal transplantation. A full panel of antibodies for autoimmune encephalomyelitis is the key leading to the diagnosis.

A-synuclein (α-syn) is a protein associated with the pathogenesis of Parkinson's disease (PD), a neurodegenerative disease with no effective treatment. Therefore, there has been a strong drive to clarify the pathology of PD associated with α-syn. Several mechanisms have been proposed to unravel the pathological cascade of this disease, and most of them share a particular similarity: cell-to-cell communication through exosomes (EXO). Here, we show that tumor necrosis factor receptor superfamily member 10B (TNFRSF10B) promotes the secretion of α-syn-containing EXO by microglia, resulting in motor dysfunction in PD. Upregulation of TNFRSF10B predicted severer condition in PD patients. In response to α-syn preformed fibrils (PFF), the expression of TNFRSF10B was increased in microglia. PFF-treated microglia exhibited a pro-inflammatory phenotype and caused neuronal damage by secreting α-syn-containing EXO. TNFRSF10B downregulation in microglia inhibited the secretion of α-syn-containing EXO and the release of pro-inflammatory factors, and ameliorated neuronal injury. PFF induced motor dysfunction in mice, which was ameliorated by inhibiting TNFRSF10B to suppress microglia-mediated α-syn communication or by directly depleting microglia. Taken together, these results indicate that TNFRSF10B promotes neuronal injury and motor dysfunction by delivery of α-syn-containing EXO and highlight the TNFRSF10B knockdown as a potential therapeutic target in PD.

Cerebral ischaemia/reperfusion (I/R) injury is caused by blood flow restoration after an ischaemic insult, and effective treatments targeting I/R injury are still insufficient. Oxidative stress plays a critical role in the pathogenesis of cerebral I/R injury. This study investigated whether vitamin D receptor (VDR) could inhibit oxidative stress caused by cerebral I/R injury and explored the detailed mechanism. VDR was highly expressed in brain tissues of mice with cerebral I/R injury. Pretreatment with the active vitamin D calcitriol and synthetic vitamin D analogue paricalcitol (PC) reduced autophagy and apoptosis, improved neurological deficits and decreased infarct size in mice after cerebral I/R. Calcitriol or PC upregulated VDR expression to prevent cerebral I/R injury by affecting oxidative stress. Silencing of VDR reversed the protective effects of calcitriol or PC on brain tissues in mice with cerebral I/R. The bioinformatics analysis revealed that VDR interacted with SMAD family member 3 (SMAD3). It was validated through the chromatin immunoprecipitation assay that SMAD3 can bind to the VDR promoter and VDR can bind to the SMAD3 promoter. Collectively, these findings provide evidence that reciprocal activation between SMAD3 and VDR transcription factors defines vitamin D-mediated oxidative stress to prevent cerebral I/R injury.

BACKGROUND:Trigeminal neuralgia (TN) is a type of transient and paroxysmal recurrent severe pain confined to the trigeminal nerve region. This study systematically evaluated the efficacy and safety of microvascular decompression (MVD) and percutaneous balloon compression (PBC) in the treatment of TN.METHODS:PubMed, Embase, The Cochrane Library, China National Knowledge Infrastructure, Wanfang, and Weipu databases were searched for articles published on the use of MVD and PBC in the treatment of TN from the dates of inception of the databases to October 2019. Articles on MVD and PBC in the treatment of TN were selected, and a meta-analysis was performed using RevMan 5.2 software.RESULTS:Eighteen studies (comprising 1,932 patients) were included in the study. MVD and PBC had similar overall effective rates in treating TN [odds ratio (OR) =0.79, 95% confidence interval (CI): 0.55-1.13, P=0.19]. Patients treated with PBC had a higher recurrence rate of TN than those treated MVD (OR =3.50, 95% CI: 2.25-5.44; P<0.00001), and patients treated with PBC experienced more adverse reactions than those treated with MVD (OR =17.79, 95% CI: 10.17-31.11; P<0.00001).DISCUSSION:The overall effective rates of PBC and MVD in the treatment of TN ewer similar, but MVD was associated with better recurrence and a lower rate of adverse reactions. Thus, both MVD and PBC can be used to effectively treat TN patients.

Purpose:NAD(P)H: Quinone Oxidoreductase 1 gene (NQO1) polymorphism is associated with the risk of cardiovascular disease. This study was designed to investigate the relationship between NQO1 gene polymorphism and ischemic stroke susceptibility in Chinese Han nationality.Patients and Methods:One hundred and forty-one patients diagnosed with ischemic stroke and 139 matched control groups were recruited in this study. The polymorphism distribution of rsl800566 locus and rs10517 locus of NQO1 gene was genotyped via TaqMan assay, and the concentration of Oxidized low-density lipoprotein (ox-LDL) in the blood of the subjects was detected by enzyme linked immunosorbent assay (ELISA). The relationship between the polymorphism distribution and the susceptibility to ischemic stroke was evaluated.Results:The frequency distribution of the three genotypes of NQO1 rs1800566 between the case group and the control group was statistically significant, and cases carrying CT and TT genotype were less likely to suffer from ischemic stroke. Compared with individuals carrying T allele, C allele carriers have higher risk of ischemic stroke. However, there was no significant difference in frequency distribution among the three genotypes of NQO1 rs10517 between controls and patients.Conclusion:The NQO1 rs1800566 C allele may be a novel marker associated with ischemic stroke susceptibility in Chinese Han population. Polymorphism of rsl800566 locus in NQO1 gene may be protective against ischemic stroke risk.

Brain microvascular endothelial cells (BMECs) injury is one of the main causes of cerebrovascular diseases. Circular RNA (circRNA) has been found to be involved in the regulation of cerebrovascular diseases progression. However, the role and mechanism of circ_0003423 in cerebrovascular diseases is still unclear. In our study, oxidized low density lipoprotein (ox-LDL)-induced HBMEC-IM cells were used to construct cerebrovascular cell injury model in vitro. Quantitative real-time PCR was used to determine the expression levels of circ_0003423, miR-589-5p and Ten-eleven translocation 2 (TET2). The interactions between miR-589-5p and circ_0003423 or TET2 were confirmed by dual-luciferase reporter assay, RIP assay and RNA pull-down assay. Cell viability, angiogenesis and apoptosis were measured using cell counting kit 8 assay, tube formation assay and flow cytometry. Cell oxidative stress was evaluated by detecting the levels of reactive oxygen species and lactate dehydrogenase. The protein levels were examined by western blot analysis. Our results showed that circ_0003423 was a downregulated circRNA in ox-LDL-induced HBMEC-IM cells. In the terms of mechanism, circ_0003423 was found to be a sponge of miR-589-5p. Function analysis showed that circ_0003423 overexpression could relieve ox-LDL-induced HBMEC-IM cell injury, and this effect could be reversed by miR-589-5p mimic. In addition, TET2 was confirmed to be a target of miR-589-5p, and its overexpression could alleviate ox-LDL-induced HBMEC-IM cell injury. Moreover, the rescue experiments also confirmed that TET2 silencing could abolish the inhibition effect of anti-miR-589-5p on ox-LDL-induced HBMEC-IM cell injury. In summary, our data showed that circ_0003423 alleviated ox-LDL-induced HBMEC-IM cells injury through regulating the miR-589-5p/TET2 axis.

Therapeutic hypothermia (TH) is a promising neuroprotective agent for treating stroke. However, its clinical application was limited by the impractical duration. Icariin (ICA) were reported to have therapeutic effect on cerebral ischemia. In this research, our aim was to investigate whether the combination of TH and ICA had better neuroprotective effects on ischemic stroke. An ischemia-reperfusion rat model was established and treated with mild hypothermia, ICA or JSH-23 (inhibitor of NF-κB). Thermistor probe, 2′3’5′-triphenyl tetrazolium chloride (TTC), 5/12-score system, and ELISA were used to detect temperature (rectum, cortex, striatum), infarct volume, neurological deficit, and cerebral cell death of these rats. The expressions of tumor necrosis factor (TNF)-α, Interleukin- 6 (IL-6), nuclear factor-kappa B (NF-κB), nuclear factor erythroid2-related factor (Nrf2), peroxisome proliferator activated receptor gamma (PPARα), PPARγ, Janus kinase 2 (JAK2), p-JAK2, signal transducers and activators of transduction-3 (STAT3), and p-STAT3 were detected by Western blot or q-PCR. Mild hypothermia, ICA, and JSH-23 reduced the cerebral infarct volume, neurological deficit, cerebral cell death of rats, downregulated the expressions of TNF-α, IL-6, C-Caspase 3 and Bax, and the activation of PPARs/Nrf2/NF-κB and JAK2/STAT3 pathways, but elevated the expression of Bcl-2. ICA promoted the effect of mild hypothermia on infarct volume, neurological deficit, and cerebral cell death. Moreover, ICA also enhanced the regulatory effect of mild hypothermia on apoptosis/inflammation factors expressions and activation of PPARs/Nrf2/NF-κB and JAK2/STAT3 pathways. ICA could promote mild hypothermia-induced neuroprotection by inhibiting the activation of NF-κB through the PPARs/Nrf2/NF-κB and JAK2/STAT3/NF-κB pathways in experimental stroke.

We report a case of genetic Creutzfeldt-Jakob disease (gCJD), which has a clinical phenotype that is highly similar to Fatal Family Insomnia (FFI) and has a triad of Wernicke-Korsakoff syndrome (WKs) at the developmental stage of the disease. The 51-year-old male complained of sleep disorder and imbalance who had visited five different hospitals before diagnosed. A neurological examination revealed a triad of symptoms characteristic for WKs such as gaze paresis, ataxia of limbs and trunk, and memory disturbances. The disturbances increased during the course of the disease, which led to the death of the patient 18 months after the appearance of the signs. Although the patient show negative in brain magnetic resonance imaging (MRI) and 14-3-3 protein of cerebrospinal fluid (CSF), he was finally diagnosed with gCJD disease by the human prion protein (PRNP) gene mutations.

Mild hypothermia (MH) and edaravone (EDA) exert neuroprotective effects against cerebral ischemia/reperfusion (I/R) injury through activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. However, whether MH and EDA exert synergistic effects against cerebral I/R injury remains unknown. The aim of the present study was to investigate the effects and mechanism of action of MH in combination with EDA in cerebral I/R injury. A rat cerebral I/R injury model was constructed by middle cerebral artery occlusion (MCAO) followed by reperfusion, and the mice were treated by MH, EDA or the inhibitor of the Nrf2 signaling pathway brusatol (Bru). It was observed that mice treated by MCAO had higher neurological deficit scores and oxidative stress levels, and low spatial learning and memory capacity; moreover, the CA1 region of the hippocampi of the mice exhibited reduced neuronal density and viability, and reduced mitochondrial dysfunction. However, MH in combination with EDA reversed the effects of MCAO, which were blocked by Bru injection. The levels of glutathione (GSH), GSH peroxidase, catalase and superoxide dismutase in rat ischemic hemisphere tissues were reduced by Bru. Western blotting demonstrated that the combined treatment with MH and EDA promoted the nuclear localization of Nrf2, and increased the levels of NAD(P)H quinone oxidoreductase and heme oxygenase (HO)-1. In conclusion, MH combined with EDA exerted synergistic neuroprotective effects against cerebral I/R injury involving changes in the Nrf2/HO-1 pathway.

目的 随访观察颈动脉狭窄脑梗死患者支架置入术后的颅内血流动力学及脑血管反应性(cerebral vascular reactivity,CVR)的变化,比较介入治疗对颈动脉狭窄患者临床预后的影响.方法 选取本院收治的103例颈动脉狭窄的脑梗死患者,根据患者及家属的治疗意愿分为手术组50例和药物组53例;手术组均接受颈动脉支架置入术(carotid artery stenting,CAS)及药物的治疗,药物组仅接受药物治疗,记录2组的NIHSS评分变化、脑卒中和死亡事件;所有手术患者均在术前、术后3d、1、3、6、12个月进行CDFI和TCD检查,测量颈动脉狭窄局部管径、狭窄段收缩期峰值流速(peak systolic velocity,PSV)、阻力指数(resistance index,RI)及同侧大脑中动脉(MCA)的PSV、搏动指数(pulsatilityt index,PID及CVR,比较手术前后的血流动力学变化.结果 2组NIHSS评分变化均呈下降趋势(P＜0.05),术后3、6、12个月手术组NIHSS评分明显低于药物组(P＜0.05);术后颈动脉原狭窄处内径明显增宽,PSV及RI低于术前,患侧大脑中动脉PSV、PI及CVR高于术前(P均＜0.05);手术组手术前后的CVR与美国国立卫生研究院卒中量表评分呈负相关(r=-0.84,-0.75,-0.66,-0.78,-0.61,P＜0.05).结论 CAS治疗后颈动脉狭窄患者颈部血管结构及血流动力学明显改善,可有效改善脑梗死患者的中远期预后,且术后CVR的改变可用于预测CAS治疗后的中远期疗效.

Objective Based on Chinese guidelines for the management of ischemic stroke, a standardized stroke management program was performed to provide intensive education and training for medical physicians, aiming to enhance their knowledge and ability for ischemic stroke prevention and treatment, thereby reducing patients′ in-hospital cost and length of stay, and improving patients′ clinical prognosis. Methods This study was conducted in 20 general hospitals throughout Hainan province. A total of 163 physicians from 20 hospitals involved in the management of stroke patients were trained by highly experienced physicians based on the Chinese guidelines for diagnosis and treatment of acute ischemic stroke 2014 and the Chinese guidelines for secondary prevention of ischemic stroke and transient ischemic attack 2014. Prior to and post the standardized stroke management training, the data of 3218 and 3367 patients with ischemic stroke were respectively collected. Quality of life assessments including the Barthel index (BI) and the modified Rankin Scale (mRS) score of all patients were recorded at baseline and after discharge. The length of stay and in-hospital cost were directly collected from the hospital information system. Results Physicians′ knowledge and ability manifested as testing scores were significantly improved after training (78.2 ± 15.5 vs 55.6 ± 10.7, t=69.1, P<0.01). The average length of stay of post-training patients was significantly shorter than that of pre-training patients ((8.7 ± 0.9) vs (11.7 ± 1.5) days, t=97.9, P<0.01). The average in-hospital cost of post-training patients was significantly less than that of pre-training patients ((7681.7 ± 1397.7) vs (11846.2 ± 2514.6) Yuan, t=82.5, P<0.01). Both BI (68.2 ± 3.2 vs 43.5 ± 5.3, t=227.7, P<0.01) and mRS score (2.74±0.51 vs 3.65±0.71, t=59.5, P<0.01) were significantly improved for post-training patients. Multivariate linear regression analysis illustrated that standardized stroke management was negatively associated with in-hospital cost (r=-0.461, P<0.01), length of stay (r=-0.357, P<0.01) and mRS score (r=-0.298, P<0.01), and was positively associated with levels of BI (r=0.376, P<0.01). Conclusion Standardized stroke management program might be a cost-effective choice for the management of ischemic stroke as it reduces the in-hospital cost and improves patients′BI and mRS levels.

Ischemic stroke (IS) is the main cause of mortality and disability in China; thus, this study aimed to examine the association between six variants and their haplotypes within the transferrin (TF) gene and the risk of IS in the Southern Chinese Han population. Genotyping was performed using the Sequenom MassARRAY platform for 249 IS patients and 249 age- and sex-matched controls. The association between polymorphisms and IS risk was tested by Chi squared test and haplotype and stratification analysis. Odds ratios (ORs) and confidence intervals (CIs) were estimated by unconditional logistic regression analysis. The results of genetic model analyses indicated that the two SNPs (rs1880669 and rs2692695) were associated with decreased IS risk under the co-dominant, dominant, and additive models. Additionally, rs4525863 was also associated with decreased IS risk both under the dominant and additive models in males. Moreover, the CG haplotype of TF (rs1880669 and rs2692695) was significantly associated with a decreased risk of IS in the total population and males. Our findings suggested that polymorphisms (rs4525863, rs1880669, and rs2692695) of the TF gene might be a protective factor for IS in Southern Chinese Han population. Further large prospective studies are required to confirm these findings.

目的 探讨经颅多普勒超声(TCD)评价重度颈内动脉狭窄患者接受颈动脉支架植入术(CAS)后脑血流动力学参数的变化情况及对术后近期转归的预测效果.方法 纳入接受CAS的50例颈内动脉狭窄患者为对象,采用TCD技术检测手术前后患者脑血流动力学参数.对患者持续随访1年,观察不良转归事件发生情况,测评脑血流动力学参数对预测不良转归事件的效能.结果 50例患者中12例在术后1年内出现不良转归.不良转归组患侧大脑中动脉(MCA)平均血流速度(Vm)及搏动指数(PI)在手术前后的变化量均明显低于转归良好组,差异有统计学意义(P＜0.05).手术前后MCA Vm和MCA PI均与美国国立卫生研究院卒中量表(NIHSS)评分呈正相关(P＜0.05).手术前后MCA Vm和MCA PI的增加量均能够有效预测不良转归,ROC曲线下面积分别为0.656、0.884.结论 动脉狭窄患者经CAS治疗后,患侧MCA Vm和MCA PI明显提升,且提升量能够预测患者的近期转归.

[objective]To study effect of cerebral blood perfusion and cognitive function of carotid artery stenting com-bined with medical therapy for patients with severe internal carotid stenosis.[Methods]124 patients with severe internal ca-rotid stenosis from June 2014 to June 2016 were divided into observed group and the treatment group,The treatment group given pure medical therapy,observation group given carotid artery stenting combined with medical therapy.One year follow-upr,cerebral blood flow perfusion,cognitive function,adverse events were compared between two groups.[Result]The ob-servation group rTTP,rMTT,rCBV,rCBF were significantly lower than treatment group(P<0.05,P<0.01);MMSE,MoCA score were significantly higher than treatment group(P<0.05);Vascular Occlusion,vascular restenosis,cerebral ischemic stroke,transient cerebral ischemia were significantly lower than treatment group(1.61% vs 11.29%,4.84% vs 19.35%, 1.61% vs 14.52%,4.84% vs 17.74,P<0.05).[Conclusion]Carotid artery stenting combined with medical therapy help to improve cerebral blood flow perfusion in patients with severe internal carotid stenosi,improve cognitive function,and pre-vent adverse events.

Objective: To analyze the clinical efficacy of Naogengtong decoction combined with Shuxuening injection in the treatment of patients with cerebral infarction and its effects on levels of IL-6, IL-10, TNF-α and MMP-9. Methods: 176 cases of cerebral infarction in the first affiliated hospital of Nanchang University from February 2014 to February 2017 were devided into two groups according to the order of admission, each with 88 cases. Patients were all treated with routine treatment, in addition, patients in the control group were treated with Shuxuening injection, and those in the observation group were treated with Naogengtong decoction combined with Shuxuening injection. All patients were treated for 4 weeks. The Barther Index, the Foggel's score (FMMS), the modified Ashworth score (Ashwoeth), IL-6, TNF-α, and MMP-9 scores before and after the treatment in two groups were compared. Results: The clinical efficacy in the observation group was significantly better than that in the control group (P ＜0. 05). BI score and FMMS score in the observation group were higher than those in the control group (P ＜0. 05). After the treatment, the ashworth score and CSS score in the observation group were lower than those in the control group (P ＜0. 05). Levels of IL-6, IL-10, TNF-α and MMP-9 in the observation group were lower than those in the control group (P ＜0.05). Conclusion: The clinical efficacy of Naogengtong decoction combined with Shuxuening injection in the treatment of cerebral infarction is significant, which can effectively improve levels of IL-6, IL-10, TNF-α and MMP-9 in patients.

Population Health ManagementVol. 21, No. 3 Letter to the EditorCost-Effectiveness Analysis of a Standardized Management Program for Ischemic Stroke Patients in Hainan Province, ChinaZhongqin Wan, Chaoyun Li, Faqing Long, Yuhui Zhang, Bufei Wang, Yingman Wu, Mingming Dai, Desheng Wang, Bin Chen, Yangyang Duan, and Qingjie SuZhongqin WanSearch for more papers by this author, Chaoyun LiSearch for more papers by this author, Faqing LongSearch for more papers by this author, Yuhui ZhangSearch for more papers by this author, Bufei WangSearch for more papers by this author, Yingman WuSearch for more papers by this author, Mingming DaiSearch for more papers by this author, Desheng WangSearch for more papers by this author, Bin ChenSearch for more papers by this author, Yangyang DuanSearch for more papers by this author, and Qingjie SuSearch for more papers by this authorPublished Online:1 Jun 2018https://doi.org/10.1089/pop.2017.0205AboutSectionsView articleView Full TextPDF/EPUB Permissions & CitationsPermissionsDownload CitationsTrack CitationsAdd to favorites Back To Publication ShareShare onFacebookTwitterLinked InRedditEmail View article"Cost-Effectiveness Analysis of a Standardized Management Program for Ischemic Stroke Patients in Hainan Province, China." Population Health Management, 21(3), pp. 253–254FiguresReferencesRelatedDetailsCited byReview of cost-effectiveness of antithrombotic alternatives in patients with atrial fibrillation1 July 2021 | Revista da Associação Médica Brasileira, Vol. 67, No. 7 Volume 21Issue 3Jun 2018 InformationCopyright 2018, Mary Ann Liebert, Inc.To cite this article:Zhongqin Wan, Chaoyun Li, Faqing Long, Yuhui Zhang, Bufei Wang, Yingman Wu, Mingming Dai, Desheng Wang, Bin Chen, Yangyang Duan, and Qingjie Su.Cost-Effectiveness Analysis of a Standardized Management Program for Ischemic Stroke Patients in Hainan Province, China.Population Health Management.Jun 2018.253-254.http://doi.org/10.1089/pop.2017.0205Published in Volume: 21 Issue 3: June 1, 2018Online Ahead of Print:March 12, 2018PDF download