急性冠状动脉综合征病人VEGF与VCAM-1水平及其与斑块稳定性的研究

目的观察急性冠状动脉综合征病人血清血管内皮生长因子(VEGF)和血管细胞黏附分子-1(VCAM-1)等指标的水平,探讨两者与斑块稳定性的关系及其临床意义.方法根据临床诊断将研究对象分为急性冠状动脉综合征组(ACS组,30例)和稳定劳累性心绞痛组(SAP组,25例),另设健康对照组(30名),测定上述观测者入院血清VEGF、VCAM-1、肌酸激酶(CK)及其同工酶(CK-MB)的水平.结果 ACS组病人血清VEGF、VCAM-1、CK﹑CK-MB水平均显著高于SAP组和健康对照组.血清VEGF的水平与血清VCAM-1水平和CK-MB水平之间有相关性(r＝0.233,P＜0.05;r＝0.547,P＜0.01),与CK水平之间无相关性(r＝-0.139,P>0.05).结论急性冠状动脉综合征的早期VEGF和VCAM-1血管水平明显升高,对判定斑块稳定性具有一定价值.     

老年急性髓系白血病患者周围血清血管内皮生长因子水平的检测及意义

目的探讨血管内皮生长因子(VEGF)与老年急性髓系白血病(AML)发病及预后的关系。方法利用ELISA方法测定37例老年急性髓系白血病(AML)和12例健康对照者血清中VEGF水平。结果AML患者血清VEGF的含量(925.71±363.63)ng/L明显高于正常对照组(105.62±34.63)ng/L(P<0.001),VEGF水平高的AML患者与VEGF水平低的AML患者比较其CR率低、CR平均持续时间短(P<0.01)。结论VEGF与老年AML发病关系密切,血清VEGF水平的高低可预测老年AML治疗效果和预后。     

流式细胞术检测VEGF在急性冠状动脉综合征诊断中的应用

目的对健康对照组和急性冠状动脉综合征病例组血清中的血管内皮生长因子(VEGF)进行检测,观察VEGF在健康对照组和病例组以及不同病例类型中的变化情况。方法使用BD Aria流式细胞仪及配套试剂、标准品按使用说明进行检查。结果 VEGF含量在健康对照组及病例组血清中含量有显著差异(P0.05),病例组内稳定型心绞痛、不稳定型心绞痛和急性心肌梗死患者VEGF含量也存在显著性的差异(P0.05)。结论 VEGF浓度随着稳定型心绞痛、不稳定型心绞痛和心肌梗死的病程发展而逐渐增加,VEGF的检测对冠状动脉综合征的诊断和病程的判断具有一定的临床应用价值。     

HIF-1对大鼠急性缺血心肌的保护作用

目的研究HIF-1对大鼠急性缺血心肌的保护作用及其作用机制。方法应用HIF-1活性诱导剂氯化钴预处理大鼠,观察预处理对大鼠急性心肌梗死面积和心肌VEGF、iNOS蛋白表达的影响。结果氯化钴预处理组大鼠较对照组和假手术组急性心肌梗死面积显著减少(P<0.01),VEGF、iNOS蛋白表达显著增高(P<0.01)。结论HIF-1可以减少大鼠急性心肌梗死面积,对大鼠急性缺血心肌具有保护作用,其机制可能与HIF-1促进VEGF、iNOS蛋白表达增加有关。     

血管内皮细胞生长因子在急性肺损伤大鼠中的表达及意义

目的探讨血管内皮细胞生长因子(VEGF)在脂多糖所致急性肺损伤大鼠中的表达及意义,为临床防治急性肺损伤提供参考依据。方法将40只SD大鼠随机分为LPS(脂多糖)组和NS(生理盐水)组,麻醉后气管插管,LPS组吸入LPS(3 mg/kg),NS组吸入等量NS。0h、2h、4h、6h时每组分别处死5只大鼠,抽血行血气分析,同时进行血浆VEGF水平、肺泡灌洗液(BALF)蛋白定量和VEGF水平、肺组织病理学、免疫组化以及VEGF mRNA表达水平检测。结果 LPS组2h、4h、6h时间点p H和Pa O2均明显低于NS组相应时间点,Pa CO2和肺损伤评分均明显高于NS组相应时间点(P0.05)。LPS组2h、4h、6h时间点BALF蛋白定量均明显高于NS组相应时间点(P0.05),LPS组2h、4h、6h时间点BALF和血浆VEGF定量均明显高于NS组相应时间点(P0.05)。LPS组BALF和血浆中VEGF水平与肺损伤评分均呈正相关(r=0.682和r=0.613,P0.001),BALF中VEGF水平与蛋白定量呈正相关(r=0.715,P0.001)。LPS组2h、4h、6h时间点肺组织中VEGF mRNA的表达均明显高于NS组相应时间点表达(P0.05)。结论 ALI大鼠血浆、BALF和肺组织中VEGF水平明显升高,血浆和BALF中VEGF水平与肺损伤程度呈正相关,BALF中VEGF水平与蛋白定量呈正相关,提示VEGF可能通过增加呼吸膜的通透性参与急性肺损伤发生过程。     

急性白血病患者血管内皮生长因子及其受体表达的临床意义

目的 :探讨血管内皮生长因子 (VEGF)及其受体 (VEGFR)在成人急性白血病 (AL)中的表达、对临床疗效和预后的影响以及与多药耐药的关系。方法 :采用逆转录 聚合酶链反应 (RT PCR)方法检测 6 4例成人AL患者VEGF、VEGFR 1、VEGFR 2、mdr 1mRNA表达水平。结果 :VEGF基因在AL组中表达的平均水平和阳性率均高于正常对照组 (P <0 .0 5 )。其中急性粒细胞白血病 (AML)组广泛表达 ,明显高于正常对照组 (P <0 .0 5 ) ,而急性淋巴细胞白血症 (ALL)组的表达与正常对照组相比差异无显著性意义 (P >0 .0 5 )。AL组VEG FR 1表达阳性率高于正常对照组 (P <0 .0 5 ) ;VEGFR 2表达阳性率与正常对照组相比无显著性意义 (P >0 .0 5 )。VEGF表达水平在临床耐药组高于临床敏感组 (P <0 .0 5 ) ,是影响缓解率和生存期的危险因素。VEGF与mdr 1表达无相关关系。结论 :VEGF及VEGFR 1基因在成人AL患者中有异常表达 ,是影响成人AL患者临床疗效和预后的因素之一。     

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。     

血管内皮生长因子对急性肺损伤大鼠的影响及地塞米松干预效果

目的 探讨血管内皮生长因子(VEGF)在急性肺损伤(ALI)中的动态变化和地塞米松的干预效果.方法 通过静脉注射脂多糖(LPS)2 h、4 h、6 h和气管内滴入大肠杆菌(E.coli)12 h、24 h、36 h复制大鼠ALI模型,观察不同时间点两种ALI模型血清和支气管肺泡灌洗液(BALF)中VEGF、肺组织VEG...     

老年急性脑梗死患者血清血管内皮生长因子和S100-β蛋白水平动态变化的临床评价

脑梗死的发病机制有多种学说,但确切的发病机制仍不清楚.目前发现一些多肽因子如成纤维细胞生长因子(bFGF)、血管内皮生长因子(VEGF)、转移生长因子(TGF-β)及炎性细胞因子如白介素-6(IL-6)、IL-8、肿瘤坏死因子-α(TNF-α)等在脑梗死急性期明显增加,但其作用仍不明确.本文老年急性脑梗死患者血清VEGF和S100-β蛋白进行检测,探讨VEGF和S100-β蛋白对老年急性脑梗死患者病情的判断和对神经功能恢复的预测价值,并为急性脑梗死的新的治疗提供理论依据.     

急性白血病患者血清血管内皮细胞生长因子测定及临床意义

目的探讨血管内皮细胞生长因子(VEGF)在急性白血病(AL)患者中的表达和临床意义.方法采用双抗体夹心ELISA法检测了41例AL初发患者(ANLL32例,其中是M14例、M24例、M38例、M44例、M512例和ALL9例)血清VEGF含量,并且检测了其中10例获得完全缓解后的AL患者血清VEGF水平;同时留取41例AL初发患者和10例获得完全缓解后AL患者骨髓涂片,进行瑞特染色后检测骨髓原始和幼稚细胞百分率.结果血清VEGF在ANLL和ALL中分别是(807.76±347.04)ng/L、(998.18±387.80)ng/L,均高于正常对照组(461.43±127.05)ng/L,均P＜0.01;ANLL和ALL之间血清VEGF水平差异无统计学意义(P＞0.05);10例完全缓解的AL患者,其血清VEGF含量为(495.28±102.79)ng/L明显低于初发时(1263.44±490.39)ng/L,P＜0.01;AL缓解组血清VEGF含量与其骨髓中原始幼稚白细胞百分率具有一定相关性,r=0.57,P＜0.01.结论血清VEGF在AL患者中明显升高,且血清VEGF水平与病情和预后密切相关.     

Severe acute pancreatitis in acute hepatitis E.

We report an 18-year-old boy with severe acute pancreatitis developing during acute hepatitis E and complicated by sepsis and acute renal failure. The patient recovered on supportive management.     

Myocarditis associated with acute nasopharyngitis and acute tonsillitis

Thirty-five instances of fatal myocarditis atributable to acute nasopharyngeal and tonsillar infections have been reported. The available evidence indicates that these are samples of a not uncommon type of cardiac disease which fortunately has a relatively good prognosis. Further investigation should be carried on to establish fully the etiological agent and the pathogenesis of the lesion. Although the pathologic observations indicated that all patients died of cardiac failure, heart disease was suspected clinically in only three, and in fifteen patients death was unexpected. Significant clinical observations which would seem to be of importance in the recognition of the process were: disproportion of the temperature and pulse rate, hypotension, thready or feeble pulse, and substernal oppression. Cyanosis, dyspnea, and orthopnea occurred frequently.Autopsy findings included significant enlargement of the heart in many cases. The microscopic changes, similar in both nasopharyngeal and tonsillar infections, have been classified in three overlapping groups. In all of these the inflammatory process was observed to be patchy, frequently showing considerable variation in intensity from one area to another and having no predilection for a particular portion of the myocardium. Significant (moderate or marked) degrees of muscle degeneration observed in the diffuse type of myocardial lesion were not present in the interstitial form. The cellular reaction, which was characteristically more intense than that observed in diphtheritic myocarditis, was predominantly mononuclear, but significant numbers of polymorphonuclear leucocytes accumulated at sites of more severe inflammation.Although the figures are too small to justify conclusions, there appears to be significant correlation between the clinical occurrence of hypotension and the estimated severity of the myocarditis, since it was a feature in every severe case in which the blood pressure was recorded. The only available electrocardiograms (four), abnormal in every case, were from patients whose hearts showed muscle degeneration of moderate or marked degree. Anginal pains were related to the presence of hypotension. Fibrosis of the heart muscle was related both to the muscle degeneration and to duration of illness.In therapy, attention is called to the danger involved in the administration of intravenous fluids.     

Philadelphia chromosome-positive acute lymphoblastic leukemia preceded by acute pleuropericarditis

A 69-year-old woman was admitted with sudden chest pain and high fever. Electrocardiography showed negative T waves in the precordial leads. Subsequently, pleural and pericardial effusion developed, but the symptoms and signs subsided without specific therapy. On day 31, fever, left shoulder pain and pleural effusion reappeared. 67Ga scintigraphy showed abnormal uptake in the chest and left shoulder. Blasts were detected in the peripheral blood on day 44, and in the pleural effusion and bone marrow on day 45. The blasts were positive for Philadelphia chromosome, CD10, CD19, CD33, CD34 and IgH-chain rearrangement and negative for myeloperoxidase. The clinical picture of the preceding pleuropericarditis was that of viral or idiopathic origin, but its relationship with acute lymphoblastic leukemia was unclear. Inflammatory chemokines in the pleural space may have induced invasion of the leukemic cells.     

Fatal idiopathic acute eosinophilic pneumonia with acute lung injury

A fatal case of idiopathic eosinophilic pneumonia with acute lung injury is described. The patient required treatment with mechanical ventilation and intravenous corticosteroids, however, she died on the third hospital day. At autopsy, both exudative and proliferative phases of diffuse alveolar damage were observed bilaterally. Marked eosinophilic infiltrate was noted in the alveolar wall and within the alveolar cavities with occasional abscess-like features. To our knowledge, this is the first report of fatal acute eosinophilic pneumonia, and provides important information for the management of this condition.