Objective: Bilateral facial palsy (BFP) has been identified as a possible neurological complication of human immunodeficiency virus (HIV) infection, but only a limited number of cases have been reported in the literature. The purpose of this study was to deepen our understanding of the etiology of BFP. Case report: We report the case of a 46-year-old married bisexual man with BFP associated with HIV infection. The patient underwent serological testing for HIV and was positive. In the absence of any other evidence of underlying systemic disease, facial palsy is thought to be secondary to HIV infection. After antiretroviral therapy, the patient recovered completely from facial palsy within 3 months. Results: HIV infection often involves BFP. The pathophysiology of this clinical presentation is thought to be related to the immune response to the systemic transmission of the virus. Conclusions: Most patients with BFP have underlying systemic causes, particularly autoimmune diseases. The exclusion of HIV infection in patients with BFP is essential for the early diagnosis and management of HIV.

目的 探讨达比加群酯对急性缺血性脑卒中并发心房颤动(AF)患者治疗的有效性及安全性.方法 选取本院 2018 年 3 月至 2020 年 5 月收治的 104 例急性缺血性脑卒中并发AF患者,按照随机数字表法划分成A、B组,每组 52 例.2 组入院后均给予神经内科常规治疗,在此基础上A应用华法林治疗,B组应用达比加群酯治疗.于治疗前、治疗 3 个月后测定 2 组凝血功能指标活化部分凝血活酶时间(APTT)、凝血酶原时间(PT)、D-二聚体(D-D)、采用美国国立卫生研究院卒中量表(NIHSS)评定 2 组神经功能缺损情况,并统计 2 组治疗 3 个月内血栓栓塞及不良反应发生率.结果 治疗 3 个月后,2 组APTT、PT与治疗前相比均升高(P＜0.05),且APTT、PT水平B组明显较A组高(P＜0.05);2 组D-D水平及NIHSS评分与治疗前相比均降低(P＜0.05),且B组均明显较A组低(P＜0.05);2 组血栓栓塞发生率比较差异无统计学意义(P＞0.05),B组出血事件发生率明显低于A组(P＜0.05).结论 对急性缺血性脑卒中并发AF患者应用达比加群酯治疗,可有效延长APTT、PT,降低D-D,且显著减轻神经功能损伤,降低血栓栓塞发生率,且出血风险低,用药安全性高.

Objective: Orolingual angioedema (OA) is a rare but life-threatening complication of intravenous thrombolysis using alteplase. Angioedema can be caused by almost any medication. Administration of recombinant tissue plasminogen activator causes atypical angioedema. This study aimed to investigate factors related to and treatment of OA after thrombolysis with alteplase. Case report: We describe the case of a 53-year-old man with a history of hypertension managed with enalapril, who presented with ischemic cerebrovascular stroke. Intravenous alteplase was administered, and within 54 minutes, the patient developed severe orolingual edema requiring emergent intubation. Subsequent imaging revealed an acute-to-subacute infarct in the left occipital lobe of the posterior cerebral artery. Results: The most common factor for increased risk of OA after recombinant tissue plasminogen activator was concomitant use of angiotensin-converting enzyme inhibitors (ACEI). Conclusion: Before intravenous thrombolytic therapy, patients should be asked if they have a history of allergies, are currently using ACEI, and try to avoid using ACEI antihypertensive drugs before and after thrombolytic therapy.

INTRODUCTION:Cerebral infarction (CI) is one of the leading causes of serious long-term disability and mortality.OBJECTIVE:We aimed to identify potential miRNAs and target mRNAs and assess the involvement of immunocyte infiltration in the process of CI.METHODS:First, miRNA and mRNA data were downloaded from the Gene Expression Omnibus database, followed by differential expression analysis. Second, correlation analysis between differentially expressed mRNAs and differential immunocyte subtypes was performed through the CIBERSORT algorithm. Third, the regulatory network between miRNAs and immunocyte subtype-related mRNAs was constructed followed by the functional analysis of these target mRNAs. Fourth, correlation validation between differentially expressed mRNAs and differential immunocyte subtypes was performed in the GSE37587 dataset. Finally, the diagnostic ability of immunocyte subtype-related mRNAs was tested.RESULTS:Up to 17 differentially expressed miRNAs and 3,267 differentially expressed mRNAs were identified, among which 310 differentially expressed mRNAs were significantly associated with immunocyte subtypes. Several miRNA-target mRNA-immunocyte subtype networks including hsa-miR-671-3p-ZC3HC1-neutrophils, hsa-miR-625-CD5-monocytes, hsa-miR-122-ACOX1/DUSP1/NEDD9-neutrophils, hsa-miR-455-5p-SLC24A4-monocytes, and hsa-miR-455-5p-SORL1-neutrophils were identified. LAT, ACOX1, DUSP1, NEDD9, ZC3HC1, BIN1, AKT1, DNMT1, SLC24A4, and SORL1 had a potential diagnostic value for CI.CONCLUSIONS:The network including miRNA, target mRNA, and immunocyte subtype may be novel regulators and diagnostic and therapeutic targets in CI.

We show that down-regulation of circular ribonucleic acid 0001588 with small interfering-circular ribonucleic acid 0001588 mimics promoted caspase-3 and caspase-9 activity levels, increased lactate dehydrogenase activity levels, and reduced cell growth of in vitro model. Circular ribonucleic acid 0001588 plasmids increased circular ribonucleic acid 0001588 expressions and promoted cell growth and reduced activity levels of lactate dehydrogenase, caspase-3, and caspase-9 activity levels in vitro model of Alzheimer's disease. Then, circular ribonucleic acid 0001588 down-regulation also promoted reactive oxygen species production and oxidative stress (malonaldehyde), and reduced superoxide dismutase, glutathione, and glutathione peroxidase levels by suppressing of silent information regulator 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 in vitro. However, over-expression of circular ribonucleic acid 0001588 reduced reactive oxygen species production and malonaldehyde levels and increased superoxide dismutase, glutathione, and levels via activation signal pathway of silent information regulator 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling pathway by miR-211-5p up-regulation in vitro. Overexpression of miR-211-5p attenuated the role of circular ribonucleic acid 0001588 on Alzheimer's disease-induced oxidative stress. Also, activation of the silent information regulator 1 pathway attenuated the antioxidative effects of circular ribonucleic acid 0001588 down-regulation on oxidative stress by activating silent information regulator 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 in vitro. In conclusion, our findings indicated that circular ribonucleic acid 0001588 induced the silent information regulator 1/nuclear factor erythroid 2-related factor 2-dependent heme oxygenase-1 pathway to prevent oxidative stress by miR-211-5p in the rat model or in vitro model of a sporadic type of Alzheimer's disease. Therefore, the expression of the circular ribonucleic acid 0001588 gene was inhibited in rodent Alzheimer's disease model.

目的 检测脑梗塞患者血脂、血尿酸水平并分析其临床意义,为临床脑梗塞的诊断提供依据.方法 选取我院神经内科收治的脑梗塞患者80例为观察组.并选取同期健康查体中心,查体的健康人群80例为对照组.所有的患者均行血脂及尿酸检查.对比两组患者血脂、血尿酸等危险因素指标,通过单因素及多因素Logistic回归分析确定尿酸是否为脑梗塞的独立危险因素,并通过直线相关与回归分析:血脂与血尿酸的相关性.结果 糖尿病、高血压、TG、TC、尿酸均为脑梗塞的独立危险因素.结论 尿酸可以独立影响脑梗塞的发生.

目的 研究缺血性脑梗死预后与磁共振成像的相关性.方法 选取我院神经内科收治的缺血性脑梗死患者80 例.根据mRS评分结果 分为两组:预后良好组(36例)及预后不良组(44例).对比两组患者的磁共振检查结果 ,判断病灶的血流量与mRS的相关性.结果 血流动力学参数rCBF与mRS 评分呈正相关,(OR＝1 .21 ;95%可信区间,1 .02-1 .45;P＜0.05).结论 磁共振灌注成像结果 可以作为缺血性脑梗死预后判断的相关指标,为临床缺血性脑梗死预后提供依据.

目的 研究马来酸左旋氨氯地平与贝那普利治疗高血压患者合并新发脑卒中长期降压疗效及卒中复发情况.方法 选择83例新发脑卒中合并高血压患者,按入组顺序随机分组.左旋氨氯地平组42例,给予氨氯地平降压治疗;贝那普利组41例,给予贝那普利降压治疗.观察2组患者血压水平及脑卒中复发情况.结果 2组患者收缩压及舒张压较治疗前均降低(P<0.05),左旋氨氯地平组收缩压和舒张压与贝那普利组比较差异无统计学意义(P>0.05).氨氯地平组脑卒中复发率为7.14％低于贝那普利组的24.39％,差异有统计学意义(P=0.031).结论 在新发脑卒中合并高血压患者的治疗中,氨氯地平和贝那普利均有较好的降压效果,但在脑卒中复发率控制上,左旋氨氯地平则优于贝那普利.

Amyotrophic lateral sclerosis (ALS) is a chronic, fatal neurodegenerative disorder characterized by the progressive loss of upper and lower motor neurons. Currently, there is no effective drug for ALS. Recent studies in ALS model mice have shown that insulin-like growth factor-1 (IGF1) may be a promising therapeutic drug. We demonstrate that self-complementary adeno-associated virus serum type 9 encoding the human IGF1 (scAAV9-hIGF1) could significantly postpone the onset and slow down the progression of the disease owning to inhibiting the NF-κB signaling pathway. Furthermore, the results were supported by experiments in which the CRISPR/Cas9 system was used to knock-down IGF1 in ALS mice (mIGF1). Our data indicate that IGF1-mediated suppression of NF-κB activation in microglia is a novel molecular mechanism underlying MN death in ALS. It provides new insight into IGF1 and points toward novel therapeutic targets of IGF1 in ALS.

Self-complementary adeno-associated viral vector 9 (scAAV9) has been confirmed to be an efficient AAV serotype for gene transfer to the central nervous system (CNS). Neurotrophic factors have been considered to be therapeutic targets for amyotrophic lateral sclerosis (ALS). In the present study, we intramuscularly injected scAAV9 encoding human insulin-like growth factor 1 (hIGF1) into an hSOD1G93A ALS mouse model. We observed that scAAV9-hIGF1 significantly reduced the loss of motor neurons of the anterior horn in the lumbar spinal cord and delayed muscle atrophy in ALS mice. Importantly, IGF1 significantly delayed disease onset and prolonged the life span of ALS mice. In addition, scAAV9-hIGF1 protected motor neurons from apoptosis through upregulation of D-amino acid oxidase (DAO), which controls the level of D-serine. Moreover, to further verify these results, we used CRISPR-Cas9 system to target the central nervous system knockdown of IGF1. This experiment supported the continued investigation of neurotrophic factor gene therapies targeting the central nervous system as a potential treatment for ALS.

Amyotrophic lateral sclerosis (ALS) is an adult-onset, irreversible neurodegenerative disease that leads to progressive paralysis and inevitable death 3–5 years after diagnosis. The mechanisms underlying this process remain unknown, but new evidence indicates that accumulating levels of d -serine result from the downregulation of d -amino acid oxidase (DAO) and that this is a novel mechanism that leads to motoneuronal death in ALS via N -methyl- d -aspartate receptor-mediated cell toxicity. Here, we explored a new therapeutic approach to ALS by overexpressing DAO in the lumbar region of the mouse spinal cord using a single stranded adeno-associated virus serotype 9 (ssAAV9) vector. A single intrathecal injection of ssAAV9-DAO was made in SOD1 G93A mice, a well-established mouse model of ALS. Treatment resulted in moderate expression of exogenous DAO in motorneurons in the lumbar spinal cord, reduced immunoreactivity of d -serine, alleviated motoneuronal loss and glial activation, and extended survival. The potential mechanisms underlying these effects were associated with the down-regulation of NF-κB and the restoration of the phosphorylation of Akt. In conclusion, administering ssAAV9-DAO may be an effective complementary approach to gene therapy to extend lifespans in symptomatic ALS.

Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease that leads to paralysis and death three to five years after diagnosis in most patients. The disease is incurable, and the mechanism of motoneuron degeneration remains unknown, although research has demonstrated that activated microglia are involved in motor neuron death. Here, we used a simple method to deliver AAV9 virus by direct intrathecal injection and found that scAAV9-VEGF-165 improved the motor performance and prolonged the life span of SOD1-G93A mice. Furthermore, scAAV9-VEGF-165 activated the PI3K/Akt survival pathway and increased the level of Bcl-2, which contributed to the protection of motor neurons. Additionally, scAAV9-VEGF-165 attenuated the expression of classically activated (M1) microglial markers and enhanced the expression of alternatively activated (M2) microglial markers. Taken together, the results of our study suggest that simple, direct intrathecal injection of scAAV9-VEGF-165 may have a curative effect for ALS.

Objective To observe the variation of regulatory CD4+ CD25+ Foxp3+T cell(Treg) of thymus in different courses of experimental autoimmune encephalomyelitis(EAE) group,alpha lipoic acid(ALA) group and investigate the immune effect of ALA on the thymus of EAE.Methods Flow cytometry was used to analyze the expression rate of CD4+ CD25+ Foxp3+ Treg cells in the course of control group,EAE group and ALA group.Results In acute course and relapse course of EAE group,the expression of CD4+ CD25+ Foxp3+ Treg cells decreased significantly than that in the control group(P0.05).In recovery course CD4+CD25+Foxp3+ Treg cells raised.No significant difference was found in the expression rate of CD4+ CD25+ Foxp3+ Treg cells between the EAE group and the ALA group.The three groups in half-year course,CD4+ CD25+ Foxp3+ Treg cells reduced to a low level significantly,but there was no significant difference among the three groups(P0.05).Conclusion CD4+ CD25+ Foxp3+ Treg cells may play a role in the occurrence of EAE.There is significant relation between the development of EAE and CD4+ CD25+ Foxp3+Treg cells.The function of ALA may not play through CD4+ CD25+ Foxp3+Treg cells in immune adjustment at EAE.As the age added,the thymus may not be the main immune organ.

短暂性脑缺血发作(TIA)是局灶性脑缺血导致突发短暂性可逆性神经功能障碍[1].TIA是中老年人群中的常见病、多发病.我国的人群患病率约为每年180/10万,男女比率3∶1[2].频繁发作的TIA是脑梗死的特级警报[1].据统计,TIA后90 d内发生卒中的危险性大约10%,其中半数发生在头2 d内,若TIA是由颈内动脉狭窄引起者,90 d内发生卒中的危险性甚至更大[3].因此,TIA是发生脑卒中的危险信号,及时识别TIA的病因,积极采取有效的预防和治疗措施,并在常规治疗的同时,大胆应用新技术、新方法及新药物,是临床上诊治短暂性脑缺血发作的关键.