Coronary vasospasm is an unlikely cause of Takotsubo syndrome,although we should keep an open mind

This viewpoint pertains to the still elusive pathophysiology of the Takotsubo syndrome (TTS), maintaining the position that this affliction is not the result of coronary vasospasm (CV) involving one or more coronary arteries. Although CV has been rarely encountered in the acute stage of TTS, or elicited via provocative testing in the subacute stage of the disease, it does not appear to be the cause of TTS as shown by the bulk of the published relevant literature. The author provides some speculations to explain the spontaneous appearance of CV, or its artificial elicitation, in some patients with TTS. However while we are striving to unravel the pathophysiology of TTS, we should keep an open mind about a possible role for CV in the causation of TTS.     

2型糖尿病（T2DM）患者血细胞形态的异常与其合并微血管病变的相关性研究

目的：通过对血细胞形态的异常的监测,探讨其与2型糖尿病(T2DM)患者合并微血管病变之间的相关性。方法通过对2013年2月—2014年6月该院收治的对合并组、无合并组2组糖尿病患者,共71例2型糖尿病(T2DM)患者及对照组60例健康人的血细胞形态参数（血红蛋白量Hb、红细胞压积HCT、平均红细胞体积MCV、平均红细胞血红蛋白含量MCH、平均红细胞血红蛋白浓度MCHC以及平均血小板体积MPV）的对比,通过对比评价分析血细胞形态的异常情况。结果与对照组相比较,合并组红细胞压积（43.23±4.00）%、平均红细胞体积（92.96±4.17） fl、平均血小板体积（9.13±4.56） fl都有所增加,平均红细胞血红蛋白浓度(329.01±11.21) g/l则有所降低降低,各组的血红蛋白量、平均红细胞血红蛋白含量处于相近的水平。结论血液流变学障碍是导致糖尿病患者微血管病变的重要影响因子,控制血细胞处于一个稳态平衡,对于控制诱发糖尿病慢性并发性疾病具有重要意义,同时也对患者及家人的生活质量具有正向的积极意义。     

血管内皮生长因子及其受体与肺癌血管新生的研究

目的：研究血管内皮生长因子及其受体促进肺癌血管新生的机制，探讨肺癌治疗的新策略。方法：共收集49份原发性支气管肺癌标本，用免疫组织化学技术检测微血管密度（MVD），血管内皮生长因子（VEGF），受体1（Flt1)受体2（KDR）在肺癌组织不同细胞成份中的表达程度。用Kaplan-Meier方法比较不同血管密度患者的生存情况。结果：（1）VEGF，Flt1和KDR在肿瘤细胞，基质成纤维细胞和血管内皮细胞上均有表达。（2）肺癌组织MVD与肿瘤TNM分期，临床分期，病理类型和分化程度等关联不明显，但微血管高密度组患者生存时间短，预后差（P＜0．05）。而Flt1和KDR在血管高密度组的表达程度均明显高于低密度组（P＜0．01）。（4）肿瘤细胞与基质成纤维细胞VEGF的表达程度有密切关联并且具有良好的一到场生。（5）肿瘤细胞VEGF与肿瘤细胞和血管内皮细胞KDR的表达均具有一致性，而与Flt1的表达却不具有一致性。结论：（1）肺癌组织MVD不受或较少受其它临床因素干扰，是肺中层得评估疗效，推测预后的一个独立和良好的指标。（2）VEGF促进血管新生的作用不单取决于其自身，还必须通过受体Flt1和KDR的介导才能实现，VEGF及其受体是抗肿瘤治疗良好的新靶点。（3）肿瘤细胞和基质成纤维细胞可能都分泌VEGF。（4）VEGF通过受体介导的机制均包含旁分泌和自分泌，但两种受体的重要性不同，KDR可能起主要作用。     

关木通致急性肾小管坏死患者肾间质微血管病变的研究

目的探讨肾间质微血管病变在关木通致急性肾小管坏死肾间质纤维化中的作用及发生机制。方法取4例关木通致急性肾小管坏死患者(A组)、5例抗生素致急性肾小管坏死患者(B组)、5例非IgA型轻度系膜增生性肾小球肾炎患者(C组)肾活检标本,免疫组化SP法观察肾小管上皮血管内皮生长因子(VEGF)表达及肾小管周围毛细血管(PTC)密度及形态改变,电镜观察微血管内皮细胞和基底膜的结构变化。结果(1)A组PTC数目明显少于B组及C组(P<0.01),并可见管腔扩张变形或缩小、血管壁断裂。(2)A组电镜见PTC内皮细胞肿胀,有胞质空泡、致密颗粒,细胞局部与基底膜分离。基底膜有皱缩及增厚。(3)A组肾小管上皮VEGF表达明显少于B组,但2组VEGF表达均多于C组。(4)A、B组PTC密度与肾小管VEGF表达呈正相关(均r=0.793,P<0.01),与肾小管上皮再生呈正相关(r分别为0.880、0.802,P值均小于0.01)。结论关木通致急性肾小管坏死存在原发性肾间质微血管损伤,肾小管VEGF低表达可能参与了损伤过程。关木通致急性肾小管坏死中的微血管病变可能是肾小管中毒性损伤后修复不良及病变慢性化进展的原因之一。     

Pancreatic B-cell function in relation to diabetic retinopathy in Asian Indian NIDDM patients

Summary Pancreatic B-cell function in relation to diabetic retinopathy was studied in 195 NIDDM patients with long-standing diabetes. Background diabetic retinopathy (BDR) was present in 95 (48.7%) and proliferative retinopathy (PDR) in 17 (8.7%) of the subjects. There was no significant difference between the BDR, PDR, and non-retinopathy groups with respect to age, age at diagnosis of diabetes and HbA₁ values. Mean duration of diabetes was higher in the PDR group (p<0.05). Serum C-peptide values showed no correlation with the presence of retinopathy or with the duration of diabetes. The C-peptide values were widely scattered in patients with BDR and PDR showing no association between pancreatic B-cell reserve and occurrence or severity of retinopathy in NIDDM patients. Thus, decreased pancreatic B-cell reserve does not appear to be a risk factor for diabetic retinopathy in NIDDM patients.     

Impact of different topical negative pressure levels on myocardial microvascular blood flow

BACKGROUND: We have previously shown that a myocardial topical negative pressure (TNP) of -50 mmHg significantly increases microvascular blood flow in the underlying myocardium in normal, ischemic, and reperfused porcine myocardium. The present study was designed to elucidate the effect of different TNP levels between -50 and -150 mmHg on microvascular flow in normal and ischemic myocardium. MATERIALS AND METHODS: Seven pigs underwent median sternotomy. The microvascular blood flow in the myocardium was recorded, before and after the application of TNP, using laser Doppler velocimetry. Analyses were performed before left anterior descending artery (LAD) occlusion (normal myocardium) and after 20 min of LAD occlusion (ischemic myocardium). RESULTS: A TNP of -50 mmHg significantly increased microvascular blood flow in both normal (from 320.0+/-56.1 PU before TNP application to 435.7+/-65.5 PU after TNP application, P=.028) and ischemic myocardium (from 110.0+/-36.7 PU before TNP application to 194.3+/-56.2 PU after TNP application, P=.012). TNP between -75 and -150 mmHg showed no significant increase in microvascular blood flow in normal or ischemic myocardium. CONCLUSIONS: Of pressures between -50 and -150 mmHg, a TNP of -50 mmHg seems to be the most effective negative pressure concerning significant increase in microvascular blood flow in both normal and ischemic myocardium.