三种血管内皮损伤指标血清水平与冠心病病变范围的关系

目的:探讨血清可溶性血管细胞黏附分子-1(sVCAM-1)、可溶性细胞间黏附分子-1(sICAM-1)、血管性血友病因子(vWF)水平与冠心病(CHD)病变范围的相关性。方法:根据冠脉造影结果将87例患者分为CHD组(63例)和对照组(24例)。采用ELISA平行检测两组血清sVCAM-1、sICAM-1和vWF水平,酶法测定血脂水平,比较两组患者sVCAM-1、sICAM-1、vWF及血脂水平的差异,并进行相关性分析;以冠脉狭窄支数作为判断CHD病变范围的依据,探讨不同病变范围患者血清sVCAM-1、sICAM-1和vWF的水平变化。结果:CHD组血清sVCAM-1、sI-CAM-1、vWF水平显著高于对照组(P<0.01);血清sVCAM-1、sICAM-1和vWF水平与血脂水平之间无明显相关性(P>0.05);单支冠脉狭窄组血清sVCAM-1、sICAM-1水平显著低于多支冠脉狭窄组(P<0.05)。结论:CHD患者血清sV-CAM-1、sICAM-1和vWF水平升高,sVCAM-1、sICAM-1水平与CHD病变范围有关。     

阿托伐他汀对冠心病患者外周血单核细胞/巨噬细胞清道夫受体的影响

目的：观察冠心病患者外周血单核细胞（PBMs）转化巨噬细胞清道夫受体活性及血清炎性因子(包括CRP、sICAM-1 、sVCAM-1)的变化及阿托伐他汀对清道夫受体活性的影响，探讨炎性因子水平与清道夫受体活性关系及他汀类药物稳定粥样硬化斑块的可能机制。 方法： 75例血脂正常冠心病患者分为稳定性心绞痛组、不稳定性心绞痛组、急性心肌梗死3组，29例健康人作为对照。测定所有观察对象血清C反应蛋白、可溶性细胞间黏附分子（sICAM-1）、血管细胞黏附分子（sVCAM-1）水平；并在体外分离培养PBMs并转化为巨噬细胞, 观察阿托伐他汀对其表达清道夫受体的影响。 结果： 巨噬细胞清道夫受体活性及血清C反应蛋白、sICAM-1、sVCAM-1水平，急性心肌梗死组>不稳定性心绞痛组>稳定性心绞痛组>对照组。阿托伐他汀能下调冠心病患者PBMs源性巨噬细胞清道夫受体活性。冠心病患者PBMs源性巨噬细胞清道夫受体活性与C反应蛋白、sICAM-1、sVCAM-1呈正相关。 结论： PBMs源性巨噬细胞清道夫受体活性可作为易损斑块活动程度的监测指标；阿托伐他汀可抑制冠心病患者血PBMs源性巨噬细胞清道夫受体活性。     

氟伐他丁对CHD患者血清Hcy、IL-6和IL-8水平的影响

目的:探讨了氟伐他丁对冠心病(CHD)患者血清Hcy、IL-5和IL-8水平的影响。方法:采用随机、对照的方法将88例CHD患者分为氟伐他丁组(35例)和常规治疗组(53例)。另选50例健康人作为正常对照组。测定治疗前、治疗后2个月血清Hcy、IL-6和IL-8的变化。结果:①CHD患者血清Hcy、IL-6和IL-8水平非常显著地高于正常人组(P<0.01);②氟伐他丁组治疗2个月后血清Hcy、IL-6和IL-8水平非常显著地降低(P<0.01),而常规治疗组治疗后则无显著性变化。结论:氟伐他丁对CHD患者具有抗炎治疗作用。     

sICAM-1和sVCAM-1与乙肝病毒标志物关系的研究

目的探讨可溶性血管内皮细胞问黏附分子1(sVCAM-1)和可溶性细胞问黏附分子1(sICAM-1)的水平与乙肝病毒标志物之间的关系。方法用ELISA法测定乙肝病毒标志物、sVCAM-1、sICAM-1，用PER法定量测定HBV-DNA的含量。结果HBVM阳性者，除HBsAb阳性者外，其血清sVCAM-1、sICAM-1水平较全阴性者均有较明显的升高，但升高的各组间无明显差异；sICAM-1与ALT呈正相关(r=0．652)，与HBA-DNA呈负相关(r=-0．498)；sVCAM-1与ALT、HBV-DNA的相关系数r分别为0．191、-0．027。结论1、乙肝病毒感染者血清sVCAM-1、sICAM-1有明显的升高，各组间无明显差异。2、sICAM-1的水平可以反应肝脏的损害程度和HBV-DNA的复制情况。     

丁二磺酸腺苷蛋氨酸辅助治疗胆汁淤积性肝炎的疗效评价

目的:探究丁二磺酸腺苷蛋氨酸辅助治疗胆汁淤积性肝炎(Cholestatic hepatitis,CH)的效果.方法:选取2019年1月至2020年12月我院收治的100例CH患者,随机分2组(n=50).对照组静滴门冬氨酸钾镁20 mL Qd治疗,研究组在此基础上静滴丁二磺酸腺苷蛋氨酸1000 mg Qd治疗.对比2组治疗28 d后总有效率,并于治疗前、治疗28 d后以全自动生化分析仪测定肝功能及肝纤维化指标,酶联免疫吸附法测定血清可溶性细胞间黏附分子-1(Serum soluble intercellular adhesionmolecule-1,sICAM-1)、血管细胞黏附分子-1(Soluble vascular cell adhesion molecule-1,sVCAM-1,sVCAM-1)水平.结果:与对照组相比,研究组总有效率更高(P<0.05);与治疗前相比,各治疗组血清GGT、AST、TBIL、ALT、sICAM-1、sVCAM-1、IV-C、PCIII、HA水平均明显降低(P<0.05),其中研究组效果更为显著(P<0.05).结论:丁二磺酸腺苷蛋氨酸对CH患者具有显著的辅助治疗作用,可改善肝功能及肝纤维化,利于患者恢复.     

肾移植术后血清sICAM-1和sVCAM-1的动态监测及临床意义

目的：探讨肾移植术后监测血清可溶性细胞问粘附分子-1(sICAM-1)和可溶性血管细胞粘附分子-1(sVCAM-1)的临床意义。方法：采用ELISA法，动态监测86例肾移植患者手术前后血清sICAM-l和sVCAM-1的变化。结果：移植术前sICAM-1、sVCAM-l与对照组无显著性差别，术后均明显升高，于第3天时达到高峰，l周至2周后降至术前水平。发生急性排斥反应前l-3天血清sICAM-1、sVCAM-1即开始升高，抗排斥治疗有效后逐渐下降。并发感染时sICAM-1、sVCAM-l显著升高，CsA中毒时无明显变化。结论：动态监测血清sICAM-1、sVCAM-l可做为早期辅助诊断急性排斥反应的免疫学指标，有助于急性排斥反应与CsA肾中毒的鉴别。     

慢性乙型肝炎患者血清黏附分子和肝功能关系的研究

<正>目的:研究慢性乙型肝炎患者血清黏附分子和肝功能的关系,探索黏附分子对慢性乙肝发病的作用。方法:选用180例慢性乙型肝炎患者,清晨空腹采取肘静脉血,分离血清,采用ELISA检测血清中循环黏附分子sICAM-1和sVCAM-1水平,同时检测血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)等     

阿托伐他汀对冠心病患者血清细胞因子水平影响的研究

目的探讨阿托伐他汀对冠心病患者血清细胞因子水平的影响.方法用酶联免疫吸附法和常规酶法测定45例常规治疗组和45例阿托伐他汀治疗组冠心病患者治疗前后血清可溶性细胞间粘附分子-1(sICAM-1)、肿瘤坏死因子-α(TNF-α)水平以及总胆固醇(TC)水平的变化.结果与常规治疗组相比,阿托伐他汀组病人治疗4、8周后sICAM-1、TNF-α以及TC水平均明显降低(p均<0.05),并且上述三个因子水平治疗4、8周后均呈逐渐下降趋势(p均<0.05).阿托伐他汀组sICAM-1水平降低与TNF-α水平降低呈相关性(p<0.05),但sICAM-1和TNF-α水平降低与TC降低无相关性(p均>0.05).结论阿托伐他汀可以降低冠心病患者血清sICAM-1和TNF-α水平,减轻冠心病的炎症反应,并且这种机制独立于降脂作用以外.     

急性冠脉综合征病人血清中E-选择素、可溶性细胞间粘附分子-1和可溶性血管细胞间粘附分子-1含量的变化

目的:探讨急性冠脉综合征病人血中粘附分子表达在识别不稳定冠脉粥样硬化斑块中的作用。方法:选取急性冠脉综合征病人80例, 其中急性心肌梗死病人40例, 不稳定心绞痛病人40例, 急性冠脉综合征病人经治疗4个月后进行随访, 同时选取正常对照40例。采用酶联免疫法(ELISA)测定血清中E-选择素、可溶性细胞间粘附分子-1(sICAM-1)和可溶性血管细胞间粘附分子-1(sVCAM-1)的水平。结果:外周血中E-选择素、sICAM-1、sVCAM-1水平在急性心肌梗死组、不稳定心绞痛组显著高于对照组, 除sVCAM-1外在随访时明显降低。结论:外周血中E-选择素、sICAM-1的水平可能作为诊断和预测急性冠脉综合征发生的敏感指标, 并可以反映冠脉粥样硬化斑块的稳定情况。     

胃癌患者手术治疗前后血清E-Cad、sICAM-1、L-selectin检测的临床意义

文献报告,细胞黏附分子家族是介导细胞黏附作用的一大类分子,其中以上皮钙黏蛋白（E—Cad）、可溶性细胞黏附分子（sICAM-1）和L选择素（L-selectin）在肿瘤的发生和发展中起着重要的作用。国内尚少见有胃癌患者手术治疗前后血清E-Cad、sICAM-1和L-selectin水平联检的报道。为此,我们进行探讨,现报道如下。     

先兆子痫患者HLA-DQA1、-DQB、-DPA1基因多态性

目的：探讨人类白细胞抗原HLA-DQA1、-DQB1、-DPA1基因多态性与先兆子痫发病的关系。方法：采用序列特异性引物技术（PCR-SSP） 对46例先兆子痫患者和105例正常孕妇及其新生儿进行HLA-DQ-DPA1等位基因分型。结果：所有标本共检出11种HLA-DQA1基因表型、16种HLA-DQB1基因表型、6种HLA-DPA1基因表型。先兆子痫患者HLA-DQB1＊0301基因频率高于正常孕妇，差异有显著性（Pc=0．032，RR=2．43，AR=0．30），其余各基因表型频率两组比较差异均无显著性。结论：HLA-DQB1＊0301基因可能是一种先兆子痫发病的易感基因。     

HLA-DRB1, -DQA1, -DQB1, -DPA1 and -DPB1 genes in Japanese multiple sclerosis patients

Japanese MS patients and controls were examined for the distribution of HLA-DRB1, -DQA1, -DQB1, -DPA1 and -DPB1 alleles using in vitro amplification of genomic DNA and probing with sequence-specific oligonucleotides. No significant difference in frequency of the examined alleles was observed among the two groups. This is in contrast to Norwegian MS patients, where an association to a combination of certain DQA1 and DQB1 alleles has previously been demonstrated.     

先兆子痫患者HLA-DQA1、-DQB1、-DPA1基因多态性

目的:探讨人类白细胞抗原HLA-DQ-A1、DQB1、DPA1基因多态性与先兆子痫发病的关系。方法:采用序列特异性引物技术(PCRSSP)对46例先兆子痫患者和105例正常孕妇及其新生儿进行HLA-DQ-DPA1等位基因分型。结果:所有标本共检出11种HLADQA1基因表型、16种HLADQB1基因表型、6种HLADPA1基因表型。先兆子痫患者HLA-DQ-B10301基因频率高于正常孕妇,差异有显著性(Pc=0.032,RR=2.43,AR=0.30),其余各基因表型频率两组比较差异均无显著性。结论:HLADQB10301基因可能是一种先兆子痫发病的易感基因。     

Initial Changes of Rat Leukemia Induced by 1-Ethyl-1-Nitrosourea and 1-Butyl-1-Nitrosourea

The initial histological changes of leukemia were investigated in rats to which 1-ethyl- 1-nitrosourea and 1 butyl 1 nitrosourea were orally administered. The appearance of orthochromatic erythroblasts in the peripheral blood was used as the index of the initial stage of leukemia. The rat leukemia progressed from solitary lesions to scattered and further diffuse lesions. These leukemias are thought to begin as one, or only a few nodular foci, mainly in the bone marrow and partly in the spleen. Acta Pathol Jpn 42: 158–165, 1992.     

Comprehensive sequence analysis of HLA-DQA1 and -DQB1 alleles and characterization of DRB1-QAP-DQA1-DQB1 haplotypes

It is well known that both chain and β chain of HLA-DQ are highly polymorphic. However the polymorphisms outside the hypervariable region were not fully examined so far. To further clarify the polymorphisms in DQ genes, we determined the nucleotide sequences of full length cDNA, spanning from the leader sequence to the stop codon, from 15 DQA1 alleles and 15 DQB1 alleles. We identified several new DQ alleles which had identical exon 2 sequence and were different in other exons. On the basis of the sequence analyses, a comprehensive PCR-based oligotyping system for DQA1 gene was established. We then characterized DRB1-QAP(DQA1 promoter)-DQA1-DQB1 haplotypes of B-lymphoblastoid cell lines homozygous for HLA and healthy unrelated Japanese and Norwegian populations. It was revealed that DQA1 alleles, which were identical in exon 2 but different in other exons, showed close linkage disequilibrium with diferent characteristic DRB1, QAP and DQB1 alleles. These results suggest that DR-DQ haplotypes have been generated in the early stage of molecular evolution.     

Interleukin-1, Interleukin-1 Receptors and Interleukin-1 Receptor Antagonist

IL-1 (IL-1α or IL-1β) is the prototypic “multifunctional” cytokine. Unlike the lymphocyte and colony stimulating growth factors, IL-1 affects nearly every cell type, and often in concert with other cytokines or small mediator molecules. Although some lymphocyte and colony stimulating growth factors may be therapeutically useful, IL-1 is a highly inflammatory cytokine and the margin between clinical benefit and unacceptable toxicity in humans is exceedingly narrow. In contrast, agents that reduce the production and/or activity of IL-1 are likely to have an impact on clinical medicine. In support of this concept, there is growing evidence that the production and activity of IL-1, particularly IL-1β, are tightly regulated events as if nature has placed specific “road blocks” to reduce the response to IL-1 during disease. In addition to controlling gene expression, synthesis and secretion, this regulation extends to surface receptors, soluble receptors and a receptor antagonist. Investigators have studied how production of the different members of the IL-1 family is controlled, the various biological activities of IL-1, the distinct and various functions of the IL-1 receptor (IL-1R) family and the complexity of intracellular signaling. Mice deficient in IL-1β, IL-1β converting enzyme (ICE) and IL-1R type I have also been studied. Humans have been injected with IL-1 (either IL-1α or IL-1β) for enhancing bone marrow recovery and for cancer treatment. The IL-1 specific receptor antagonist (IL-IRa) has also been tested in clinical trials.