Early and long-term effects of radiation on intercellular adhesion molecule 1 (ICAM-1) expression in mouse urinary bladder endothelium

The aim was to assess the effect of irradiation on intercellular adhesion molecule 1 (ICAM-1) expression in endothelial cells of vessels in mouse urinary bladder and to compare endothelial ICAM-1 expression with changes in bladder function (storage capacity) during the early and late radiation response phases. Female C3H/Neu mice were irradiated with doses of either 20 or 0?Gy. For assessment of ICAM-1 expression, which was measured by the intensity of the immunohistochemical staining signal in bladder endothelium, an arbitrary semiquantitative score (0?–?3) was applied. Bladder storage function was assessed by transurethral cystotonometry. A positive functional radiation response, defined as a reduction in bladder capacity by >?50%, between days 0 and 15 or 16 and 30 was found in 40 and 64% of the animals, respectively. A late functional response was observed in 71% of the animals sacrificed after day 180. Minor constitutive expression of ICAM-1 was observed in bladder endothelial cells. After irradiation, an increase in staining signal by day 2, with a maximum on day 4, and on days 16?–?28 was found, which preceded the functional radiation effects. A permanent increase in ICAM-1 staining signal was observed in the late phase on top of an age-related rise. ICAM-1 expression was significantly higher in animals with a positive late response on day 90, i.e. during the initial late phase. Irradiation induces significant early and chronic variations in ICAM-1 expression in bladder endothelium, which preceded the functional response. This suggests that endothelial ICAM-1 is involved in the pathogenesis of both the early and late phases of radiation-induced urinary bladder effects.     

Early and long-term effects of radiation on intercellular adhesion molecule 1 (ICAM-1) expression in mouse urinary bladder endothelium

The aim was to assess the effect of irradiation on intercellular adhesion molecule 1 (ICAM-1) expression in endothelial cells of vessels in mouse urinary bladder and to compare endothelial ICAM-1 expression with changes in bladder function (storage capacity) during the early and late radiation response phases. Female C3H/Neu mice were irradiated with doses of either 20 or 0 Gy. For assessment of ICAM-1 expression, which was measured by the intensity of the immunohistochemical staining signal in bladder endothelium, an arbitrary semiquantitative score (0 - 3) was applied. Bladder storage function was assessed by transurethral cystotonometry. A positive functional radiation response, defined as a reduction in bladder capacity by > 50%, between days 0 and 15 or 16 and 30 was found in 40 and 64% of the animals, respectively. A late functional response was observed in 71% of the animals sacrificed after day 180. Minor constitutive expression of ICAM-1 was observed in bladder endothelial cells. After irradiation, an increase in staining signal by day 2, with a maximum on day 4, and on days 16 - 28 was found, which preceded the functional radiation effects. A permanent increase in ICAM-1 staining signal was observed in the late phase on top of an age-related rise. ICAM-1 expression was significantly higher in animals with a positive late response on day 90, i.e. during the initial late phase. Irradiation induces significant early and chronic variations in ICAM-1 expression in bladder endothelium, which preceded the functional response. This suggests that endothelial ICAM-1 is involved in the pathogenesis of both the early and late phases of radiation-induced urinary bladder effects.     

Cerebrospinal fluid and plasma concentration of soluble intercellular adhesion molecule 1, vascular cell adhesion molecule 1 and endothelial leukocyte adhesion molecule in patients with acute ischemic brain disease

BACKGROUND: Leukocyte migration into the ischemic area is a complex process, controlled by adhesion molecules (AM) in leukocytes and endothelium, by migratory capacity of leukocytes and the presence of hemotaxic agents in the tissue. In this research it was supposed that in the blood and cerebrospinal fluid (CSF) of patients in the acute phase of ischemic brain disease (IBD) there were relevant changes in the concentration of soluble AM (sICAM-1, sVCAM-1 and sE-selectin), that could have been the indicators of the intensity of damaging processes in central nervous system (CNS). METHODS: The study included 45 IBD patients, 15 with transient ischemic attack (TIA), 15 with reversible ischemic attack (RIA), and 15 with brain infarction (BI), of both sexes, mean age 66 +/- 7. Control group consisted of 15 patients with radicular lesions of discal origin, subjected to diagnostic radiculography, without the signs of interruption in the passage of CSF. Changes of selected biochemical parameters were determined in all patients in frame 72 hours since the occurrence of an ischemic episode. Concentrations of soluble AM were determined in plasma and CSF by ELISA. Total number of leukocytes (TNL) in peripheral blood was determined by hematological analyzer. RESULTS: The results showed that during the first 72 hrs of IBD significant increases occurred in TNL and that the increase was progressive compared to the severeness of the disease. Significant increase of soluble AM concentration was shown in plasma of IBD patients. The increase was highest in BI, somewhat lower in RIA and the lowest in TIA patients compared to the control. In CSF concentrations of sICAM-1, sVCAM-1 and sE-selectin demonstrated similar increasing trend as in plasma. CONCLUSION: TNL, as well as the soluble AM concentrations in plasma and CSF, were increased during the acute IBD phase and progressive in relation to the severeness of the disease, so that they might have been the indicators of CNS inflammatory reaction intensity. Furthermore, the results indicated their role in IBD pathogenesis and offered the possibility of researching the application of antagonists and/or activity modulators of some of them in IBD therapy.     

恒磁场对脂多糖诱导内皮细胞与中性粒细胞黏附及细胞间黏附分子表达影响的研究

目的研究恒磁场对脂多糖(LPS)诱导中性粒细胞与内皮细胞黏附及内皮细胞表达细胞间黏附分子的影响。方法人脐静脉内皮细胞于0·05、0·1、1mT的磁场中曝磁,用LPS刺激内皮细胞,内皮细胞与中性粒细胞黏附用细胞计数法评估,内皮细胞表面细胞间黏附分子表达用流式细胞仪及酶联免疫吸附法测定。结果LPS刺激后,中性粒细胞的黏附率为58%;0·05、0·1mT磁场条件下中性粒细胞黏附率下降为40%及38%,与单纯LPS组比较明显下降(P<0·05),而1mT组中性粒细胞黏附率为65%,与单纯LPS组相近。单纯LPS组细胞间黏附分子表达为10·34±0·33/0·89±0·16;0·05、0·1mT磁场条件下细胞黏附分子表达为6·61±0·17/0·53±0·18、6·98±0·15/0·46±0·10,与单纯LPS组比较明显下降(P<0·05);1mT组为10·99±0·41/0·78±0·15,与单纯LPS组比较无明显差异。结论0·05、0·1mT可以抑制LPS刺激下内皮细胞与中性粒细胞的黏附及内皮细胞表面细胞间黏附分子的表达。     

严重烧伤后早期大鼠肾脏细胞粘附分子1和白介素6的表达

目的:观察严重烧伤早期大鼠肾脏细胞粘附分子l(Intercellulal adhesion molecule-1,ICAM-1)、白细胞介素6(Interleukin 6,IL-6)在不同时间点的表达及早期病理变化,为阐明伤后早期肾脏损伤机制及为伤后早期损伤的防治打下基础。方法:①光镜和电镜观察大鼠在烧伤后早期(5min至72h)肾脏的病理变化;②免疫组织化学、原位杂交和图像分析技术对伤后不同时间点肾脏ICAM-1进行染色和分析;③免疫组织化学、原位杂交和图像分析技术对伤后不同时间点肾脏IL-6进行染色和分析。结果:①伤后早期主要病理变化为出血、充血和水肿;电镜显示:肾脏毛细血管内皮细胞受损;②伤后30min,免疫组化和原位杂交显示ICAM-1、IL-6表达增强,伤后2-24h明显增强,呈阳性或强阳性;伤后 72h,表达逐渐减弱。结论:伤后早期肾脏的损伤可能与内皮细胞损伤有关,ICAM-1、IL-6在伤后早期肾脏损害机制中占有重要地位。     

碱性成纤维细胞生长因子对大鼠弥漫性脑损伤组织细胞间黏附分子-1表达的影响

目的 观察碱性成纤维细胞生长因子(bFGF)对弥漫性脑损伤(DBI)组织细胞问黏附分子-1(ICAM一1)表达的影响,探讨bFGF的脑保护机制.方法 按照Marmarou法建立大鼠DBI模型.干湿重法和荧光实时定量PCR分别测定脑外伤及bFGF预处理大鼠脑组织含水量和ICAM-1 mRNA的表达. 结果 bFGF预处理组伤后不同时问点的脑组织含水量和ICAM-1 mRNA表达趋势与外伤组类似.同一时间点预处理组含水量比外伤组下降,但高峰期延迟至48 h出现.在6,12,24,48和72 h时间点外伤组和预处理组含水量差异有统计学意义(P<0.05).在6,12,24,48,72 h和7 d时间点两组ICAM-1mRNA的表达差异有统计学意义(P<0.05或P<0.01). 结论 bFGF预处理能下调外伤后ICAM-1mRNA的表达,这可能足其脑保护作用机制之一.     

高压氧对老年脑梗死患者血清细胞间粘附分子-1表达的影响

目的 探讨老年脑梗死患者高压氧（HBO）治疗前后体内可溶性细胞间粘附分子-1（sICAM-1）表达水平的变化及其与疾病变化相关性。方法 选择老年脑梗死患者及老年健康体检者各20例，通过ELISA法分别检测其血清sICAM-1水平并进行组间比较。结果 脑梗死组sICAM-1值高于正常对照组，其组间差别具有统计学意义（P〈0．01）。HBO治疗后脑梗死组sICAM-1水平显著降低（P〈0．01），与正常对照组比较差别无统计学意义（P〉0．05）。结论 HBO可明显抑制老年脑梗死患者体内sICAM-1的表达。     

Time dependence of the expression of ICAM-1 (CD 54) in human skin wounds

To characterize the vitality and age of skin wounds by means of the ICAM-1 pattern, 157 intravital human skin wounds (time since injury ranging from 5 min to 730 days) were immunohistochemically investigated. ICAM-1 was detected in paraffin sections after autoclaving and using the ABC technique in 86% of the wounds investigated. The correlation between ICAM-1 expression and the degree of wound inflammation is weak. Strong positive staining was observed 1.5 h at the earliest and 3.5 days at the latest after the time of injury. ICAM-1 also appeared at low concentrations in samples of uninjured skin (n = 65), on keratinocytes and the endothelial cells of blood vessels. Moderate to strong ICAM-1 expression is a valuable indication of the vitality of the wound. However, at present the detection of ICAM-1 alone is not sufficient to fix the wound age with the accuracy which is required for forensics applications. Received: 2 July 1996 / Received in revised form: 16 April 1997     

Early detection of oleic acid-induced lung injury in rats using (111)In-labeled anti-rat intercellular adhesion molecule-1.

Previous study of the bleomycin-induced lung injury model suggested that (111)In-labeled antirat intercellular adhesion molecule-1 (aICAM-1) might be a useful acute respiratory distress syndrome (ARDS) diagnostic agent. We further investigated the ability of (111)In-aICAM-1 to detect inflammation in another ARDS lung injury model. METHODS: (111)In-labeled rat polymorphonuclear leukocytes (PMNs), (111)In-aICAM-1, (111)In-labeled normal mouse IgG (nmIgG), and (111)In-labeled rat serum albumin (RSA) were injected into rats 18-24 h before kill. Biodistributions, scintigraphic images, and lung ICAM-1 upregulation were obtained in uninjured rats and in rats after injury with oleic acid. RESULTS: (111)In-RSA and (111)In-nmIgG localized in inflamed lung at 5 min postinjury (PI). (111)In-PMN uptake increased significantly only at 24 h PI. (111)In-aICAM-1 localization increased significantly (30%-60%) at 1 h PI and remained elevated up to 24 h PI. Lung/blood ratios (L/B) at 1 and 4 h PI were very low (<0.6) for (111)In-nmIgG and (111)In-PMN rats; however, for (111)In-aICAM-1 rats, they were >1 and 25%-60% higher than those for the control samples. A low L/B suggests poor inflammation detection on the images. Images and region-of-interest analysis confirmed that only (111)In-aICAM-1 could distinguish inflamed lungs at 4 h PI. ICAM-1 was upregulated at 4 and 24 h PI. CONCLUSION: In this model, (111)In-aICAM-1 detected lung inflammation very early in the course of the disease. These results support the suggestion that (111)In-aICAM-1 could be a very early, highly specific ARDS diagnostic agent and may be useful to detect a wide range of inflammations.     

甲状腺疾病患者血清可溶性细胞间粘附分子-1的研究

目的 探讨血清可溶性细胞间粘附分子-1(sICAM-1)水平与甲状腺疾病的关系.方法 采用125I-sICAM-1 RIA方法,检测了健康人273名(对照组),Graves(GD)病患者557例,初诊慢性淋巴细胞性甲状腺炎(HT)患者33例,初诊单纯性甲状腺肿(SG)患者17例,初诊非毒性结节性甲状腺肿(NTNG)患者9例的血清sICAM-1水平,比较各组间差异及其与其他指标的相关性.变量资料为正态分布时,应用ANOVA或t检验进行组间比较;不满足条件时,应用秩和检验(Kruskal-Wallis或Mann-Whitney)进行分析.结果 初诊GD组[58例,(255.04±82.40)μg/L]和HT组[(227.22±77.08)μg/L]sICAM-1水平均高于对照组[(149.89±39.45)μg/L](GD:Z=-9.401,HT:Z=-5.902;P均＜0.01),而sG组[(173.82±59.50)μg/L]和NTNG组[(159.31±28.73)μg/L]与对照组差别无统计学意义(SG:Z=-1.9,NTNG:Z=-0.949;P均＞0.05).初诊及各治疗阶段GD伴突眼组sI-CAM-1水平均高于非突眼组,但仅在治疗≥19个月组差异有统计学意义[(211.58±53.58)与(189.50±39.99)μg/L;t=2.004,P＜0.05].复发GD突眼及非突眼组sICAM-1水平亦显著高于对照组(X2=88.257,P＜0.01).在经抗甲状腺药物(ATD)治疗后甲状腺功能恢复正常且病情稳定的GD患者中,sICAM-1水平随疗程延长逐步缓慢降低,且当疗程≥19个月时,GD组在非突眼及突眼患者中,其血清sICAM-1[(189.50±39.99),(211.58±53.58)μg/L]与各自初诊组[(244.75±81.58),(287.36±79.20)μg/L]差异有统计学意义(F=9.986和3.398,P＜0.01和P＜0.05),但直至停药时仍高于对照组[(185.25±39.64)与(149.89±39.45)μg/L;Z=-3.813,P＜0.05].结论 血清sICAM-1可反映自身免疫性甲状腺疾病(AITD)患者体内的自身免疫状态,其测定对GD、HT有辅助诊断价值,这对于了解GD患者的自身免疫活动程度、预测GD眼病的发生和GD复发、确定合理的疗程和停药时机可能具有重要意义.     

+GZ重复暴露对大鼠脑组织细胞间粘附因子-1基因表达的影响

目的：了解＋Gz重复暴露后大鼠脑组织细胞间粘附因子－1（ICAM－1）基因表达的变化,探讨＋Gz引起脑损伤的分子机制。方法：24只SD大鼠随机分成对照组,＋Gz重复暴露后30min,6h和24h四组,6h和24h四组,每组6只。实验组大鼠在动脉离心机上经历了3次＋10Gz/3min（两次中间间隔30min)作用,对照组大鼠G值为＋1Gz。分别于暴露后30min,6h和24h处死大鼠取脑,提取总RNA,用半定量反转录聚合酶链反应（RT－PCR）检测方法检测＋Gz重复暴露后大鼠脑组织ICAM－1 mNRA表达水平。结果：＋Gz重复暴露后30min,6h和24h大鼠脑组织ICAM－1 mRNA均明显升高,分别是对照组的1,7倍,3．0倍和1．9倍。结论：＋Gz重复暴露可诱导大鼠组织ICAM－1 mRNA的表达,介导了白细胞,脑微血管内皮细胞的粘附增强,在＋Gz所致脑损害的病理过程中起一定作用。     

Id-1表达与膀胱癌浸润性关系的研究

 目的 研究Id-1(分化抑制因子1)mRNA在正常膀胱黏膜和不同阶段膀胱移行细胞癌(BTCC)中的表达,分析其与膀胱癌的浸润性和复发的关系.方法 RT-PCR方法检测30例人BTCC和12例正常膀胱组织Id-1表达.结果 在mRNA水平,膀胱癌Id-1表达阳性率约73.3%,其中浅表性膀胱癌阳性率为66.7%,浸润性膀胱癌阳性率为83.3%,正常膀胱黏膜无表达.正常膀胱黏膜与BTCC的Id-1 mRNA表达比较差异有统计学意义(P<0.01),浅表性和浸润性膀胱癌Id-1表达差异有统计学意义(P<0.01).结论 浸润性膀胱癌Id-1 mRNA高表达,膀胱癌的侵袭性和复发与Id-1的mRNA表达呈正相关关系.     

艾塞那肽对载脂蛋白E基因敲除小鼠动脉粥样硬化模型中VCAM-1、ICAM-1表达的影响

目的 探讨胰高血糖素样肽1(GLP-1)受体激动剂艾塞那肽对ApoE-/-小鼠动脉粥样硬化模型中主动脉病变的影响.方法 ApoE-/-小鼠随机分为普通饮食组(n=14)和高脂饮食组(n=68),喂养12周后随机抽取普通饮食组4只和高脂饮食组8只小鼠检测造模情况.将高脂饮食组小鼠再分为非药物干预组、阿托伐他汀钙片组、艾塞那肽小剂量组、艾塞那肽大剂量组、阿托伐他汀+艾塞那肽小剂量组、阿托伐他汀+艾塞那肽大剂量组(每组10只).药物干预6周后,各组小鼠眶周静脉丛取血,并取主动脉弓行石蜡切片,HE染色观察.ELISA法检测血清血脂水平,Western blotting检测主动脉血管细胞黏附分子-1(VCAM-1)、细胞间黏附分子-1(ICAM-1)的蛋白表达水平.结果 HE染色结果显示:普通饮食组及阿托伐他汀+艾塞那肽大剂量组镜下观察未见异常;阿托伐他汀钙片组,艾塞那肽小、大剂量组,阿托伐他汀+艾塞那肽小剂量组可见广泛的病理性内膜增厚;非药物干预组有脂质斑块形成,可见脂核.单独应用艾塞那肽或联合阿托伐他汀可不同程度降低血清血脂(TC、TG、LDL-C)水平(p＜0.05).艾塞那肽不同剂量单独或联合阿托伐他汀可降低主动脉VCAM-1、ICAM-1的表达(P＜0.05).结论 艾塞那肽可能通过下调ApoE-/-小鼠主动脉VCAM-1、ICAM-1的表达,抑制ApoE-/-小鼠动脉粥样硬化病变的形成.     

脑创伤早期大鼠肺组织细胞间黏附分子-1mRNA的表达及其意义

目的 观察脑创伤后早期大鼠细胞间黏附分子－1（ICAM－1）mRAN的表达及细胞定位,探讨其病理生理意义。方法 Wistar大鼠104只,随机分为假致伤组（8只）、致伤组（48只）、致伤加N－乙酰半胱氨酸（NAC）处理组（48只）。用牙科钻在大鼠冠状缝后缘、中线左侧开骨窗、保持颅脑膜完整,再用落体撞击装置撞击硬度,按各时相点麻醉成功后,取相同部位肺组织制作标本,采用原位杂交、计算机图像分析技术及病理学观察等方法,研究脑创伤后肺组织ICAM－1mRNA的表达和分布情况,以及病理学改变。结果 假致伤动物ICAM－1mRNA在肺组织中仅有少量表达。脑创伤后,大鼠肺组织ICAM－1mRNA表达强度明显增加;阳性细胞主要定位于支气管内皮细胞、肺间质细胞、血管内皮细胞及血管壁组织细胞。腹腔注射N－乙酰半胱氨酸（NAC）显著抑制脑伤后肺组织ICAM－1mRNA表达。结论 脑创伤后肺内ICAM－1mRNA表达分泌增加,可能是脑外伤后急性肺损伤发病的分子基础之一。     

白细胞-内皮细胞间黏附分子-1基因多态性与2型糖尿病肾病的关系

目的：研究白细胞-内皮细胞间黏附分子-1（LECAM-1）在P213S位点的基因多态性与2型糖尿病肾病的关系。方法：应用聚合酶链反应和限制性内切酶方法检测28～76岁2型糖尿病肾病55例、2型糖尿病非肾病64例和正常对照组112例的LECAM-1基因的多态性。结果：糖尿病肾病组LECAM-1213PP基因型和P等位基因频率显著高于非糖尿病肾病组及对照组（P〈0.05）。结论：LECAM-1基因多态性与2型糖尿病肾病发病有明显的相关性，213PP基因型可能是2型糖尿病肾病的遗传危险因素。     

高压氧治疗对大鼠脑外伤后P-选择素和细胞间粘附分子表达的影响

目的探讨脑外伤后P-选择素（CD62p）和细胞间粘附分子（ICAM-1，CD54）与继发性损伤的关系及高压氧（hyperbaric oxygen，HBO）治疗对其表达的影响。方法采用Feeney动物模型，将Wislar大鼠分成假手术组、损伤对照组和HBO治疗组。在脑外伤后1、6、2448、72h5个时间点，每个时间点分3组，共15组，每组6只，应用FACScan流式细胞仪测定各组脑组织标本内CD62p的表达和CD54的阳性细胞数量。结果外伤后6hCD62p和CD54的表达升高（P〈0．05），伤后48h达到高峰，然后逐渐降低。HBO可明显降低CD62p和CD54的表达，HBO治疗组在脑外伤6h后各个时间点两种粘附分子的表达均低于损伤对照组。结论CD62p和CD54在脑外伤后的继发性损伤中起重要作用，HBO治疗可抑制脑外伤后脑组织CD62p和CD54表达。     

Distention of the posterior urethra: association with nonneurogenic neurogenic bladder (Hinman syndrome).

In nonneurogenic neurogenic bladder (NNNB), or Hinman syndrome, a functional bladder outlet obstruction is produced by voluntary contraction of the external sphincter during voiding. To determine whether any radiographic findings are diagnostic of this condition, the authors reviewed the genitourinary images of six boys in whom NNNB was diagnosed in the past 5 years. In contrast to true neurogenic bladder, findings of elongated, trabeculated, high-volume bladders with substantial postvoid residuals, obstructive uropathy, and vesicoureteral reflux were not associated with clinical, radiographic, or urodynamic evidence of an underlying neurologic abnormality. Furthermore, four boys had distention of the posterior urethra that the authors believe is suggestive of this condition. In these patients, the posterior urethra appeared entirely normal during early voiding, but distended after contraction of the external sphincter as voiding progressed. This posterior urethral distention may worsen the symptoms of enuresis, but may also reduce or retard the damage to the proximal urinary tract.     

缺氧对牙周炎大鼠龈沟液中可溶性细胞间黏附分子-1变化的影响

目的研究平原常氧和模拟高原缺氧条件下慢性牙周炎SD大鼠模型龈沟液(GCF)中可溶性细胞间黏附分子-1(sICAM-1)浓度的变化,以探讨sICAM-1与高原牙周炎的关系。方法选取40只SD大鼠,雌雄各半,分为平原对照组(A组)、平原牙周炎组(B组)、缺氧对照组(C组)、缺氧牙周炎组(D组),每组10只。B、D组大鼠分别建立平原、高原牙周炎模型,A、C组分别作为平原、高原对照组。8周后采用ELISA法检测4组大鼠GCF中sICAM-1浓度变化,并进行比较。结果A、B、C、D组GCF中sICAM-1浓度分别为21.98±2.93、32.20±3.80、23.44±3.81、36.64±2.64ng/ml,B组与A组、D组与C组、C组与A组、D组与B组比较,差异均有统计学意义(P<0.05),其中D组显著高于其他三组(P<0.05)。结论缺氧牙周炎组大鼠GCF中的sICAM-1水平高于平原牙周炎组,提示高原缺氧环境对机体的免疫黏附能力有一定影响。