Inflammation and cerebral small vessel disease: A systematic review

Inflammation is increasingly implicated as a risk factor for dementia, stroke, and small vessel disease (SVD). However, the underlying mechanisms and causative pathways remain unclear. We systematically reviewed the existing literature on the associations between markers of inflammation and SVD (i.e., white matter hyperintensities (WMH), lacunes, enlarged perivascular spaces (EPVS), cerebral microbleeds (CMB)) in cohorts of older people with good health, cerebrovascular disease, or cognitive impairment. Based on distinctions made in the literature, markers of inflammation were classified as systemic inflammation (e.g. C-reactive protein, interleukin-6, fibrinogen) or vascular inflammation/endothelial dysfunction (e.g. homocysteine, von Willebrand factor, Lp-PLA2). Evidence from 82 articles revealed relatively robust associations between SVD and markers of vascular inflammation, especially amongst stroke patients, suggesting that alterations to the endothelium and blood-brain barrier may be a driving force behind SVD. Conversely, cross-sectional findings on systemic inflammation were mixed, although longitudinal investigations demonstrated that elevated levels of systemic inflammatory markers at baseline predicted subsequent SVD severity and progression. Importantly, regional analysis revealed that systemic and vascular inflammation were differentially related to two distinct forms of SVD. Specifically, markers of vascular inflammation tended to be associated with SVD in areas typical of hypertensive arteriopathy (e.g., basal ganglia), while systemic inflammation appeared to be involved in CAA-related vascular damage (e.g., centrum semiovale). Nonetheless, there is insufficient data to establish whether inflammation is causal of, or secondary to, SVD. Findings have important implications on interventions, suggesting the potential utility of treatments targeting the brain endothelium and blood brain barrier to combat SVD and associated neurodegenerative diseases.     

A Study on Four Antioxidation Effects of Lycium Barbarum Polysaccharides In Vitro

The objective of the study was to investigate the in vitro antioxidation activity of lycium barbarum polysaccharides (LBP). Ultraviolet spectrophotometry was adopted to determine the capability of LBP to clear superoxide anions, hydroxyl radicals, DPPH free radicals and ABTS free radicals. The result showed that the law for LBP to clear superoxide anions, hydroxyl radicals and DPPH free radicals was that the clearance rate increased gradually with the increase of the concentration, and when the concentration reached a certain value, the clearance rate leveled off, while the IC₅₀ for clearing ABTS free radicals was 47.158±6.231 µg/ml. The study concluded that LBP is a good in vitro antioxidant.     

原发性甲状旁腺机能亢进性骨病CT、MRI与病理对照的实验研究

目的研究原发性甲状旁腺机能亢进(PHPT)骨骼病变的CT、MRI特征性表现及诊断价值.方法健康成年中国白兔80只,随机分成两组,对照组40只以正常饮食(Ca:P,1:0.7)喂养,实验组40只以高磷饮食(Ca:P,1:7)喂养诱发原发性甲状旁腺机能亢进动物模型.在第3、4、5、6个月,分别对实验组和对照组动物行高场MR及螺旋CT骨扫描分析影像学特征.同时对所有动物甲状旁腺及骨标本行病理学检查,评价影像诊断的准确性.结果送检的甲状旁腺明显增生.骨骼均存在骨质疏松和骨皮质吸收的表现,MR T1WI表现不同程度局限性低信号改变,T2WI早期表现为不同程度的局限性低信号或中等信号改变,如骨髓水肿表现为高信号改变,随病情进展纤维组织取代骨组织则为低信号改变.相应螺旋CT扫描依次为阴性,可疑,骨质疏松,骨膜下皮质吸收表现.而对照组动物甲状旁腺及骨骼均未见异常.结论高场MR结合螺旋.CT扫描既可发现早期病变又可进行分期,是研究早期PHPT骨骼病变的可靠手段.     

经胸超声心动图对非体外循环房间隔缺损封堵术的作用

目的评价经胸超声心动图(TTE)对非体外循环房间隔缺损(ASD)封堵术的指导作用。方法应用心脏彩色多普勒超声诊断仪术前经胸测量房间隔缺损最大直径以及周缘情况;TTE法指导非体外循环经右胸ASD封堵术,评价封堵器牢固程度以及有无残余分流;术后即刻、术后1周及术后3个月TTE观察封堵器位置及有无分流。结果术前TTE测量ASD最大直径为11~48mm[(26.76±10.53)mm],封堵器大小为16~58mm[(34.35±11.54)mm]。除2例术后三天及术后1h脱落改行直视修补术外,其余38例均一次封堵成功,成功率95%。应用此方法,缺损最大直径大于30mm的病例的疗效与小于30mm的病例疗效无差别。结论在非体外循环房间隔缺损封堵术中经胸超声心动图在术前筛选病例、测量缺损大小、术中指导手术全过程以及术后追踪随访病例均具有重要的指导作用。     

依达拉奉对大鼠肝I/R损伤的保护作用

目的探讨依达拉奉对大鼠肝缺血再灌注(I/R)损伤中的保护作用。方法将60只大鼠随机分为实验组和对照组,建立常温下部分肝脏I/R动物模型。在肝脏I/R开始时和1 h后对实验组大鼠给予依达拉奉注射液,对照组给予同等容量的生理盐水。再灌注0,2,4 h测定肝脏脂质过氧化反应物(LPO)浓度和肝脏酶学指标及TNF-α和E-selectin的mRNA,并行两组肝脏的病理学检查。结果再灌注2,4 h实验组大鼠肝脏LPO反应程度和肝脏酶指标检测值明显低于对照组(P0.05)。再灌注2 h肝TNF-αmRNA和E-selectinmRNA表达明显低于对照组(P0.05)。再灌注2 h实验组大鼠肝脏切片的E-selectin免疫反应性明显低于对照组。结论依达拉奉能抑制氧化应激反应,从而降低肝I/R损伤;并显著减少炎性细胞和黏附分子的产生,抑制炎性反应的发生。     

Thoracic juxtafacet cyst (JFC) as a rare cause of myelopathy – An additional reference to support the instability theory

Several causes for the development of a juxtafacet cyst (JFC) of the spine have been discussed, with a focus on instability with overload of the facet joints. In the thoracic spine, JFC is a very rare space-occupying lesion, which can lead to spinal canal stenosis with pain, myelopathic signs and neurological deficits. We report a case of a 70-year-old woman who had a posterolateral fusion of L2 to S1 and, six weeks later a L1 compression fracture. In the following period a thoracolumbar kyphosis has developed. Fourteen months after the fusion procedure a left-sided JFC T11/12 was identified on MRI and CT scans which led to myelopathic symptoms. This was not seen on former MRI scans. After surgical removal of the JFC the myelopathic symptoms were clearly reduced and the woman became pain free. This case report gives a strong support to the hypothesis that spinal instability can lead to overload of the facet joints and result in JFC.     

中药对缺血心肌血管内皮细胞生长因子、碱性成纤维细胞生长因子水平的影响

中药对缺血心肌血管新生的促进作用已成为心肌梗死治疗的又一途径。血管新生为多种细胞因子共同作用的结果,通过对其机制的探讨,发现在促进缺血心肌血管新生过程中血管内皮细胞生长因子（VEGF）、碱性成纤维细胞生长因子（bFGF）起到了重要的作用。     

系统性红斑狼疮合并溶血性贫血患者病情活动度脏器损害程度及相关实验室检查的特点

目的探讨系统性红斑狼疮(SLE)患者合并溶血性贫血(hemolytic anemia,HA)发生率与SLE病情活动指数(DAI)、脏器损伤指数(SDI)、抗心磷脂(aCL)抗体阳性率、抗双链DNA(ds-DNA)抗体阳性率及肾脏、神经精神系统受累率的关系。方法分析453例SLE患者的临床资料及相关实验室指标,应用χ2检验进行统计学分析。结果 453例SLE患者中,213例(占47%)无贫血,193例(占42%)合并非溶血性贫血,合并溶血性贫血者47例(占10.3%)。溶血性贫血组DAI(17.6分±6.1分)、SDI(1.83分±1.8分)、aCL抗体阳性率(33.8%)、肾脏、神经精神系统受累率(81.7%和32.6%)高于非贫血组(上述指标,分别为10.6分±5.3分、1.1分±1.3分、24.7%、43.9%和18.0%)及非溶血性贫血组(上述指标分别为13.7分±4.2分、1.2分±1.0分、24.1%、57.6%和19.1),且具有统计学意义(P<0.05)。溶血性贫血组抗dsD-NA抗体阳性率为73.4%高于非贫血组(55.7%)及非溶血性贫血组(61.2%),且与非贫血组的差异具有统计学意义(P<0.05)。结论 SLE发生HA者有更高的病情活动度、损伤指数、肾脏、神经精神系统受累率及抗ds-DNA抗体和aCL抗体阳性率。     

发病3～6h应用rt-PA静脉溶栓治疗急性脑梗死的有效性与安全性分析

目的探讨重组组织型纤溶酶原激活物(rt-PA)静脉溶栓治疗扩大时间窗至6 h的疗效与安全性。方法试验组选择发病3 h内的患者(A组)16例,3～6 h的患者(B组)10例做为观察对象,分别给予rt-PA(0.7 mg/kg)静脉溶栓治疗;另选择发病在0～6 h内未选择溶栓治疗的患者为对照组(16例)。试验组与对照组均给予奥扎格雷钠80 mg,1次/d,静点;舒雪宁20 mL,1次/d,静点;阿司匹林0.1 g,1次/d,口服治疗。评定患者治疗前、治疗后2 h、24 h、7 d、30 d的NIHSS评分及治疗后90 d的Barthel指数评分。治疗前、治疗后1 d查头部CT,判定是否出血(根据影像学判定是梗死后还是实质出血)并记录各组出血和死亡例数。结果试验组与对照组各自NIHSS评分治疗前无差别(P>0.05),治疗后各时间点比较有统计学意义(P<0.05),试验A组与B组治疗前后各时间点差别无统计学意义(P>0.05);试验组与对照组B I指数治疗前与治疗后90d比较差异有统计学意义。A组出血2例,1例为梗死后出血,1例为脑实质出血,死亡1例;B组出血1例,为梗死后出血,死亡0例;对照组出血1例,1例为梗死后出血,死亡1例。结论用rt-PA溶栓治疗,扩大时间窗至6 h,疗效确切,未增加出血几率。因此,将溶栓时间窗扩大至6 h可行。