缺氧缺血性脑病新生儿的颅脑超声参数变化及与病情严重程度和预后的关系分析

目的 观察缺氧缺血性脑病新生儿(HIE)颅脑超声参数变化情况,并分析其颅脑超声参数变化与病情严重程度和预后的关系。方法 选取2022年2月-2022年11月本院新生儿重症监护病房收治的75例HIE患儿,根据其病情分度分为轻度组(38例) ,中度组(24例),重度组(13例)。并选取同期健康新生儿75例作为对照组。均于出生48h及72h分别行经颅彩色多普勒超声(TCD),收集其脑血流动力学相关参数,比较各组间差异。对HIE患儿进行28d的随访,再次进行TCD复查及预后评估,利用Peason相关性分析相关性。结果 出生48h 收缩期血流速度峰值(Vs)、舒张末期血流速度(Vd)、平均流速(Vm)：对照组>轻度组>中度组>重度组(均P<0.05);出生48h 阻力指数(RI)：对照组<轻度组<中度组<重度组(均P<0.05)。轻度组出生72h各参数均与对照组比较无差异(均P<0.05);出生72h Vs、Vd、Vm：对照组>中度组>重度组(均P<0.05);出生72h RI：对照组<中度组<重度组(均P<0.05)。预后不良者出生28d的新生儿行为神经测定(NBNA)量表评分、Vs、Vd、Vm均低于预后良好者,RI高于预后良好者(均P<0.05)。HIE患儿出生28d后的Vs、Vd、Vm均与NBNA评分呈正相关(r=0.493,0.434,0.432,P<0.05),RI与NBNA评分呈负相关(r=-0.478,P<0.05)。结论 HIE患儿TCD脑血流动力学参数Vs、Vd、Vm随着病情程度的加重呈降低趋势,RI呈升高趋势;TCD脑血流动力学参数监测可较为客观的反映HIE患儿脑血流灌注变化情况,且对其预后评价均具有一定的指导意义。     

基于网络药理学和分子对接探讨补阳还五汤治疗糖尿病脑病的作用机制

目的：基于网络药理学方法和分子对接技术,探讨补阳还五汤有效成分治疗糖尿病脑病潜在作用机制。方法：从中药系统药理学数据库与分析平台(TCMSP)和中科院化学专业数据库筛选出补阳还五汤有效化学成分及其靶点,通过GeneCards、在线人类孟德尔遗传(OMIM)数据库收集糖尿病脑病靶点,运用STRING数据库构建蛋白质-蛋白质相互作用(PPI)网络图并通过Cytoscape 3.8.0软件中CytoNCA插件筛选关键靶点。利用ClusterProfiler程序包进行基因本体(GO)和京都基因和基因组百科全书(KEGG)富集分析,并通过Cytoscape 3.8.0软件构建补阳还五汤药物-成分-靶点-通路网络,最后利用AutoDock软件进行分子对接验证。结果：筛选得到补阳还五汤中活性成分108种,对应潜在靶点469个,网络图显示槲皮素、甘氨酸、洋川芎醌等是补阳还五汤治疗糖尿病脑病的关键成分,蛋白激酶、P53蛋白、肿瘤坏死因子等是该方治疗糖尿病脑病的关键靶点。GO富集分析显示该方可能通过对氧化应激的反应、对药物的反应、对金属离子的反应等生物过程发挥作用,与膜筏、膜微域、膜区域等细胞组分有关,与...     

尿毒症脑病和血管内皮功能障碍关系的研究进展

心脑血管系统疾病是慢性肾病最常见的并发症,也是导致患者终末期肾脏病死亡的主要原因.大量研究表明尿毒症引起的脑病和尿毒症素的蓄积、氧化应激、炎症等因素有关.尿毒症毒素引起的脑血管内皮受损,血脑屏障功能破坏是引起尿毒症脑病的病理原因之一.因此修复脑血管内皮可作为防治本病的一种治疗策略.本文就慢性肾病导致的尿毒症脑病和血管内...     

肝性脑病误诊1例报道及文献复习

探讨肝性脑病(HE)的临床特征及误诊原因。对我科收治的1例HE误诊病例资料进行回顾性分析。本例患者主因乏力伴纳差1年,加重2个月,意识不清约2 h就诊,经过详细询问病史,完善有特征性意义的辅助检查而确诊,因患者病情重、家庭经济条件差,家属放弃治疗。凡以性格改变或行为失常、睡眠障碍等为突出表现的肝病患者,应警惕HE的可能。加强认识、提高诊治水平是尽早确诊、改善预后的关键。     

The Absence of HIV Mutations in Cerebrospinal Fluid and in Peripheral Blood Mononuclear Cells During a Regimen Containing Trizivir Plus Tenofovir

Abstract

Methotrexate (MTX) is widely used in the treatment of hematological diseases. The typical side-effects of high-dose MTX chemotherapy on the CNS range from asymptomatic white matter changes to severe CNS demyelination. MTX neuro - toxicity has been described to be associated with homocysteine and folate levels as well as genetic variants affecting methionine metabolism. Here we describe a case of severe, acute MTX-induced encephalopathy in a patient who was found to be homozygous for the rare missense variant methionine synthase (MTR) c.2756A>G (D919G), which may have modified the effect of MTX on homocysteine metabolism. This finding encourages further studies to determine to what extent the individual conditions of folate and methionine metabolism influence the effects or side-effects of MTX treatment.     

彩色多普勒用于足月新生儿缺氧缺血性脑病颅内静脉系统检查

目的 观察缺氧缺血新生儿的颅内静脉系统的血流特点,为临床判定缺氧缺血性脑病提供新的参考依据.方法 实验组缺氧缺血新生儿52例,对照组正常足月新生儿52例,通过前囟门应用彩色多普勒观察颅内静脉系统中直窦(SS)、上矢状窦(sss)、双侧横窦(Ts)、双侧室管膜下静脉(SV)及双侧大脑内静脉(ICV)的最大平均血流速度及频谱形态.结果 与对照组相比较,实验组SSS、双侧ICV及双侧SV平均最大血流速度减低.对照组SSS频谱为搏动型,双侧ICV及双侧SV频谱为连续平坦型.实验组SSS的频谱形态可见连续平坦型,SS及双侧TS的频谱形态存在搏动型及连续平坦型.颅内双侧ICV及双侧SV的频谱为连续乎坦型.结论 颅内静脉系统中,SSS、双侧ICV及双侧SV为提示缺氧缺血性脑病的合适观察对象.     

A Pilot Study for Targeted Surveillance of Bovine Spongiform Encephalopathy in Nigeria

Bovine spongiform encephalopathy (BSE), popularly known as ‘mad cow disease’, led to an epidemic in Europe that peaked in the mid‐1990s. Its impact on developing countries, such as Nigeria, has not been fully established as information on livestock and surveillance has eluded those in charge of this task. The BSE risk to Nigeria’s cattle population currently remains undetermined, which has resulted in international trade restrictions on commodities from the cattle population. This is mainly because of a lack of updated BSE risk assessments and disease surveillance data. To evaluate the feasibility of BSE surveillance in Nigeria, we carried out a pilot study targeting cattle that were presented for emergency or casualty slaughter. In total, 1551 cattle of local breeds, aged 24 months and above were clinically examined. Ataxia, recumbency and other neurological signs were topmost on our list of criteria. A total of 96 cattle, which correspond to 6.2%, presented clinical signs that supported a suspect of BSE. The caudal brainstem tissues of these animals were collected post‐mortem and analysed for the disease‐specific form of the prion protein using a rapid test approved by the International Animal Health Organization (OIE). None of the samples were positive for BSE. Although our findings do not exclude the presence of BSE in Nigeria, they do demonstrate that targeted sampling of clinically suspected cases of BSE is feasible in developing countries. In addition, these findings point to the possibility of implementing clinical monitoring schemes for BSE and potentially other diseases with grave economic and public health consequences.     

桥本脑病伴帕金森综合征1例并文献复习

目的加深临床对桥本脑病的认识,提高临床诊出率。方法分析1例临床诊断为桥本脑病患者的临床表现、神经系统体征、实验室检查、电生理、影像学资料及治疗效果。结果患者神经系统表现为认知功能下降、帕金森综合征和癫痫发作,脑脊液IgG合成率增高,头MRI颅内多发病灶,脑电图示慢波增多。糖皮质激素治疗有效。结论桥本脑病临床表现多样,还可伴随帕金森综合征,临床上对脑病患者应想到此病的可能性,避免误诊、漏诊。     

Valproate-Induced Hyperammonemic Encephalopathy Treated by Hemodialysis

Valproate-induced hyperammonemic encephalopathy is an unusual but serious complication that may occur in people with normal liver-associated enzyme levels, despite normal therapeutic doses and serum levels of valproate. Here, we describe an adolescent girl who had absence seizure and complained about progressive dizziness and general malaise several days after restarting valproate. Then, she presented vomiting and decreased consciousness three weeks after valproate use. Notably, her serum ammonia level was five times the upper limit of normal (184 μmmol/L), with normal liver-associated enzyme and supra-therapeutic valproate level. EEG showed continuous generalized slowing. The tandem mass analysis revealed carnitine deficiency. Consciousness improved after emergent hemodialysis. Ammonia level and EEG also returned to normal. Possible mechanisms, risk factors and the treatments of valproate-induced hyperammonemic encephalopathy are described. Physicians should consider this possibility when consciousness disturbance occurs in patients treated with valproate.     

Pathological Role for Exocytotic Glutamate Release from Astrocytes in Hepatic Encephalopathy

Liver failure can lead to generalized hyperammonemia, which is thought to be the underlying cause of hepatic encephalopathy. This neuropsychiatric syndrome is accompanied by functional changes of astrocytes. These glial cells enter ammonia-induced self-amplifying cycle characterized by brain oedema, oxidative and osmotic stress that causes modification of proteins and RNA. Consequently, protein expression and function are affected, including that of glutamine synthetase and plasmalemmal glutamate transporters, leading to glutamate excitotoxicity; Ca²⁺-dependent exocytotic glutamate release from astrocytes contributes to this extracellular glutamate overload.