中性粒细胞/淋巴细胞比值与急性缺血性卒中患者脑微出血的相关性

目的 探讨急性缺血性卒中患者中性粒细胞/淋巴细胞比值(neutrophil to lymphocyte ratio, NLR)与脑微出血(cerebral microbleeds, CMBs)的相关性.方法 连续纳入住院的急性缺血性卒中患者.采用梯度回波T2*加权成像评估CMBs及其数量.采用单变量分析比较CMBs组与非CMBs组的基线资料,利用多变量logistic回归分析确定NLR与CMBs的独立相关性.结果 共纳入218例急性缺血性卒中患者,其中66例(30.3%)伴有CMBs.非CMBs组年龄[(64.7 ± 6.6)岁对(66.9 ± 8.6)岁;t=2.052,P=0.041]、高敏C反应蛋白水平[7.0(2.3~13.9)mg/L对8.9(4.0~28.1)mg/L;Z=2.008,P=0.045]和NLR[1.9(1.4~2.9)对2.3(1.7~3.6);Z=2.071,P=0.038]显著低于CMBs组.多变量logistic回归分析显示,NLR(优势比1.276,95%可信区间1.008~1.670;P=0.045)和年龄(优势比1.044,95%可信区间1.002~1.087;P=0.040)是CMBs的独立危险因素.Spearman相关分析显示,NLR与CMBs严重程度呈显著正相关(r=0.210,P=0.007).结论 在急性缺血性卒中患者中,NLR与CMBs及其严重程度相关,提示炎性反应可能参与了CMBs的发生.     

椎动脉起始部狭窄支架置入与药物治疗的对比研究

目的比较椎动脉起始部狭窄患者支架置入与单纯药物治疗的疗效。方法回顾性分析2011年1月至2013年1月82例椎动脉起始部中重度狭窄(狭窄率>50%)患者的临床资料,按治疗方法的不同分为支架+药物组40例和药物组42例。记录患者治疗后1年DSA或CT血管成像复查时狭窄血管的狭窄程度、再狭窄率、脑缺血事件发生率、美国国立卫生研究院卒中量表(NIHSS),并进行综合分析。结果 (1)对40例支架置入患者共置入44枚支架,其中1例因狭窄部斑块较硬,虽经2次球囊后扩张,仍残余狭窄60%;围手术期间无严重并发症发生,手术成功率为97.5%(39/40)。支架置入1年时,支架+药物组患者椎动脉起始部的狭窄率显著改善,由(73±13)%降至中位数11%(8%,50%)(P<0.01)。(2)支架置入后1年,支架+药物组有11例(27.5%)患者出现支架内狭窄,其中有2例患者同时存在支架断裂;药物组有4例(9.5%)患者椎动脉完全闭塞,但仅2例患者出现相应的临床症状。(3)支架+药物组患者与药物组相比,治疗后两组NIHSS评分的差异无统计学意义(Z=1.678,P=0.093)。支架+药物组患者总的缺血性事件为7例(17.5%),与单纯药物组的16例(38.1%)比较,差异有统计学意义(χ2=4.306,P=0.038)。结论支架置入治疗椎动脉起始部狭窄患者安全、有效,可以明显改善椎动脉狭窄,并且对预防后循环缺血性事件优于单纯药物治疗,但椎动脉起始部支架置入较高的再狭窄率仍是亟待解决的重要问题。     

Effects of Peripheral Blood Mononuclear Cells Morphology on Vascular Calcification in Uremic Patients on Maintenance Hemodialysis

We used high‐resolution atomic force microscopy (AFM) to examine possible changes in the morphology of peripheral blood mononuclear cells (PBMCs), and to investigate their influence on vascular calcification in uremic patients on maintenance hemodialysis (MHD). 36 uremic patients had cardiovascular diseases after MHD (MHD group1) and 30 uremic patients did not (MHD group 2), and 20 healthy volunteers were the control group. The extent of coronary artery calcification was assessed with coronary artery calcification score (CACS). AFM was used to analyze PBMCs nuances. Concentrations of bone morphogenetic protein‐2 (BMP‐2) in PBMC supernatants were detected by ELISA. Protein expressions of BMP‐2 were measured by Western blot. No significant differences in PBMC morphology were observed among groups by light microscopy. AFM images revealed that uremic patients exhibited significant differences of PBMC morphology and vascular calcification when compared with healthy volunteers. The PBMCs in uremic patients were larger in volume, mean height, half‐maximum amplitude, average roughness and higher concentrations and expression of BMP‐2 and CACS (P < 0.05), with granular processes or caveolae of uneven size distributed over cell surfaces. These differences were also significant between MHD group 1 and group 2 (P < 0.05). PBMC volume, mean height, half‐maximum amplitude, and average roughness were positively correlated with BMP‐2 and CACS. Moreover, the correlation PBMC with BMP‐2 was higher than with CACS. PBMC morphology in MHD patients was related to the degree of vascular calcification. The larger mean height, half‐maximum amplitude, average roughness and cell volume were, the higher degree of vascular calcification was.     

血清胱抑素C水平与高血压性脑出血风险

目的：探讨血清胱抑素C（cystatinC,CysC）水平与高血压性脑出血（hypertensive intracerebral hemorrhage, HICH）的关系。方法纳入HICH患者和健康对照者,收集人口统计学和临床资料,采用免疫比浊法检测血清CysC水平。结果共纳入连续的94例HICH患者和131名健康对照者。 HICH组基线收缩压[（168.57±28.64）mmHg对（128.13±16.23）mmHg;t=－13.442,P<0.001;1 mmHg=0.133 kPa]、舒张压[（95.56±14.68）mmHg对（76.80±8.76）mmHg;t=－11.965, P<0.001]、空腹血糖[（6.24±1.83）mmol/L对（5.22±1.13）mmol/L;t=－5.169,P<0.001]和血清CysC水平[（1.02±0.26）mg/L对（0.91±0.13）mg/L;t=－4.234,P<0.001]显著高于对照组。多变量logistic回归分析显示,基线收缩压≥140 mmHg [优势比（odds ratio, OR）12.523,95％可信区间（confidence interval, CI）5.353~29.299;P<0.01]、舒张压≥90 mmHg（OR 3.968,95％CI 1.792~8.784;P<0.01）、血清CysC水平≥1.09 mg/L（OR 3.279,95％CI 1.336~8.050;P<0.05）是HICH的独立危险因素。在HICH患者中,出血量≥30 ml组血清CysC水平[（1.13±0.26）mg/L]高于出血量<30 ml组[（0.99±0.25）mg/L;P<0.001]和对照组[（0.91±0.13）mg/L;P<0.001],出血量<30 ml组血清CysC水平高于对照组（P=0.004）。血清CysC与年龄、肌酐、尿素、尿酸之间呈正相关（P均＜0.01）,与估算的肾小球滤过率之间呈负相关（P＜0.01）。多变量线性回归分析显示,年龄、肌酐、尿素和尿酸与血清CysC水平独立相关（P均＜0.05）。结论 HICH患者血清CysC水平升高与出血量有关,血清CysC水平增高是HICH的独立危险因素。     

人源性促甲状腺激素受体抗体Fab段抗体库的构建

目的 通过噬菌体表面展示技术,构建人源性促甲状腺激素受体抗体(TRAb)Fab片段抗体库.方法 从甲状腺功能亢进症患者外周血单个核细胞抽提总RNA,PCR法扩增免疫球蛋白分子轻链K、λ基因及重链Fd基因.构建轻链文库及组合文库.一个随机的组合文库在噬菌体表面表达.结果 从外周血单个核细胞中抽提得到总RNA,并反转录获得cDNA文库.PCR法扩增了大小约为680 bp的轻链K、λ基因及重链Fd基因,并构建了库容为1.32×105基因抗体库(轻链库)和库容为2.28×105 Fab抗体库(组合文库).Fab组合文库转化到大肠杆菌XL1-Blue感受态细胞,在辅助噬菌体M13K07的辅助下,扩增得到噬菌体抗体库.结论 噬菌体表面展示技术可成功构建人源性TRAb Fab片段组合文库.     

中老年血管免疫母细胞性T细胞淋巴瘤患者临床特征及预后影响因素分析

目的 探讨中老年血管免疫母细胞性T细胞淋巴瘤(AITL)患者的临床特征、诊断及治疗.方法 回顾性分析,纳入北京医院2008年5月至2017年3月收治的45岁及以上(年龄47?85岁)中老年AITL患者33例,中位年龄64岁,男性54.5％(18例).收集临床表现、病理、影像及生存资料,分析不同治疗方案的客观有效率(OR...     

402例混合性病感染情况分析

对402例性病病例感染病原进行分析,结果显示,同一STD患者可以同时感染两种以上性病,其中男性前4位混合感染病原依次为:NG CT,118例;NG UU,42例;CT UU,24例;NG CA,17例。女性前4位混合感染病原依次为:NG CA,37例;NG CT,16例;NG UU,14例,CA CT,14例。男性混合性病感染高于女性2.4倍(P<0.005)。以21～50岁居多,占94.03％,经性接触传染达95.03％。     

Prenatal hypoxia may aggravate the cognitive impairment and Alzheimer’s disease neuropathology in APP/PS1 transgenic mice

Most cases of Alzheimer's disease (AD) arise through interactions between genetic and environmental factors. It is believed that hypoxia is an important environmental factor influencing the development of AD. Our group has previously demonstrated that hypoxia increased β-amyloid (Aβ) generation in aged AD mice. Here, we further investigate the pathological role of prenatal hypoxia in AD. We exposed the pregnant APP^Swe/PS1^A246E transgenic mice to high-altitude hypoxia in a hypobaric chamber during days 7–20 of gestation. We found that prenatal hypoxic mice exhibited a remarkable deficit in spatial learning and memory and a significant decrease in synapses. We also documented a significantly higher level of amyloid precursor protein, lower level of the Aβ-degrading enzyme neprilysin, and increased Aβ accumulation in the brain of prenatal hypoxic mice. Finally, we demonstrated striking neuropathologic changes in prenatal hypoxic AD mice, showing increased phosphorylation of tau, decreased hypoxia-induced factor, and enhanced activation of astrocytes and microglia. These data suggest that although the characteristic features of AD appear later in life, hypoxemia in the prenatal stage may contribute to the pathogenesis of the disease, supporting the notion that environmental factors can trigger or aggravate AD.