川崎病509例分析与比较

川崎病自1967年日本川崎富作先生首次报告至今已30年有余，日本每二年1次流行病学调查已进行14次，发现川崎病10万人次。据北京梁翊常教授在全国12所大城市儿童医院住院者中统计，川崎病已取代风湿病成为我国小儿后天性心脏病主要病因之一。为此，我们对’全省509例患儿进行分析并与日本资料进行比较，以发现共同点与不同点。一材料与方法3对象为全省有儿科病床的县、市、部队所属医院及有条件的厂矿职工医院共197所，1993年1月至1997年12月期间住院的患儿。调查方法是通过举办J；贿病学习班，统一认识、统一标准，调查表寄给医院的负责人…     

南京市结核病流行病学调查分析

目的 调查2000年－2001年南京市人群结核病患病率、儿童结核免疫水平、死亡率；并对近年来南京市结核病防制规划执行情况和结核病项目实施效果进行评价；了解南京市结核病的流行状况和人群危害程度，为制订未来几年南京市结核病预防控制规划提供科学依据。方法 采用分层整群随机抽样方法，在南京市江宁区农村、溧水县农村、鼓楼区、六合县农村、哺口区城郊共抽样调查8051人。结果 南京市结核病患病率为522．4／10万；肺结核患病率为509．6／10万，男女比为2．33：1，涂阳患病率为216．6／10万，菌阳患病率为293．0／10万，空洞性患病率为63．7／10万；儿童结核菌素试验（PPD）阴性反应为69．2％，强阳性反应为12．8％；死亡率为12．2／10万；62．5％的肺结核病人为本次流调新发现，已知肺结核病人的治理管理率为53．3％。结论 本次调查初步了解了南京市结核病的流行情况，有关资料及其研究分析结果为政府制订控制结核病流行的决策和相关研究提供了科学依据。     

云南省川崎病患病情况调查

目的　了解云南省川崎病的发病、分布和流行病学特征。方法　采用日本中国川崎病流行病调查表 ,对云南省 12 6家县级以上有儿科病床的医院、妇幼保健院进行填表调查。结果　 5年间共报告患儿 594例 ,发病率 4 45 10万 ;男女之比为 1 50∶1(3 56 2 3 8) ,发病年龄以 5岁以下为主 (86 2 % )。以城市患儿居多为 3 98例(67 0 % )。少数民族患儿 45例 (7 6% )。 3 99例中发生心脏后遗症者 114例 (2 8 6% )。无死亡病例。复发病例4例 (0 7% )。结论　云南省川崎病发病明显低于日本 ,而与国内部分省份相近。心脏后遗症者高于日本与国内一些省份。基层医院应提高对川崎病的认识和提高诊断治疗水平     

川崎病患儿炎症因子和免疫功能指标检测的临床意义

目的:探讨川崎病患儿炎症因子和免疫功能指标的变化及意义。方法:选取2013年1月至2017年1月在我院儿科住院治疗的川崎病患儿78例作为川崎病组,同期在我院儿科住院的非川崎病患儿82例作为非川崎病组,同期在我院门诊体检的健康儿童75例作为对照组。检测三组儿童的炎症因子及免疫功能指标,其中川崎病组患儿分别在急性期和亚急性期各检测一次,比较分析检测结果。结果:川崎病组患儿急性期CRP、IL-1β、IL-6、IL-8、TNF-α水平明显升高,亚急性期开始降低,但仍均高于对照组(P均<0。05);亚急性期CRP、IL-1β、IL-6、IL-8、TNF-α水平与非川崎病组比较,差异均无统计学意义(P均>0.05);急性期CD3+、CD8+、NK细胞水平明显降低,亚急性期开始升高,但仍均低于对照组和非川崎病组(P均<0.05);急性期CD4+、CD4+/CD8+、IgG、IgA、IgM水平明显升高,亚急性期开始降低,但仍高于对照组和非川崎病组(P均<0.05)。结论:川崎病患儿存在炎症因子和免疫功能指标异常,CD3+、CD8+、NK细胞、CD4+、CD4+/CD8+、IgG、IgA、IgM可以作为诊断川崎病的实验室指标,而CRP、IL-1β、IL-6、IL-8、TNF-α仅可考虑作为川崎病患儿急性期的实验室诊断指标。     

川崎病患儿血清白细胞介素-6、-10、-1水平变化及意义

目的 观察川崎病患儿血清白细胞介素-6(IL-6)、白细胞介素-10(IL-10)、白细胞介素-1(IL-1)水平变化及其临床意义.方法 选取38例川崎病患儿(观察组)和38例健康儿童(对照组)血清IL-6、IL-10和IL-1水平,观察两组差异及对治疗效果的影响.结果 观察组IL-6、IL-10和IL-1水平均高于对照组(t=10.3877、15.1010、15.1243,均P＜0.05),观察组急性期IL-6、IL-10、IL-1等水平明显高于亚急性期患儿(t=9.7594、11.6486、11.6622,均P＜0.05)及对照组(t=11.7032、11.7718、11.8267,均P＜0.05).对照组48 h内细胞凋亡率为(2.8±0.8)％,明显低于川崎病患儿的(38.3±7.9)％(t=38.59,P＜0.01).血小板升高[(464.0±110.2)×109/L]的川崎病患儿IL-1水平(663±94) ng/L,明显高于无血小板升高[(307.0±104.9)×109/L]的患儿(492±92) ng/L(t =13.1044,P＜0.05).结论 检测川崎病患儿血清IL-6、IL-10和IL-1水平,有助于临床判断的病情、并发症情况及治疗效果,具有重要的临床意义.     

川崎病患儿血浆吲哚胺2,3双加氧酶含量的研究

目的:探究川崎病(KD)患儿血浆吲哚胺2,3双加氧酶(IDO)含量变化与其发病的相关性。方法:选取2015年1月—2015年3月心血管内科住院的KD患儿20例作为观察组,另选择20例健康体检儿童作为对照组,采用酶联免疫吸附试验(ELISA)分别检测观察组急性期及恢复期血浆IDO含量以及对照组血浆IDO含量,并进行比较。结果:观察组KD患儿急性期IDO含量明显增高,与对照组及恢复期IDO含量比较,差异有统计学意义(P<0.01)。观察组恢复期IDO含量与对照组比较差异无统计学意义(P>0.05)。各组内男女不同性别之间血浆IDO含量比较差异无统计学意义(P>0.05)。结论:血浆IDO在川崎病患儿急性期含量增高,可能参与了KD患儿急性期免疫性炎症反应。IDO的表达水平与性别无关。     

阿仑膦酸钠对绝经后骨质疏松的应用

目的 探讨流行性乙型脑炎(以下简称乙脑)在临沂市的流行规律，制定有效的防治措施。方法 收集我市1960-2002年乙脑疫情报告及流行病学调查资料，并进行汇总分析。结果 1960-2002年临沂市共发生乙脑43385例，死亡5451例，年平均发病率为12．14／10万。病死率9．77％；发病均有严格的季节性；年龄主要集中在1。9岁年龄段，占发病总数的74.48％；散居儿童和小学生是主要的发病人群，占88．66％。结论 人群疫苗免疫、媒介蚊虫控制及动物宿主管理是减少乙脑发病流行的3项有效措施。     

免疫球蛋白对川崎病患儿一氧化氮及白细胞介素-6的影响

目的：了解一氧化氮(NO)、白细胞介素-6(IL- 6)在静脉滴注免疫球蛋白(IVIG)治疗川崎病(KD)患儿中的作用及意义。方法：收集38例川崎病患儿,用IVIG治疗前、治疗3 d后血液、尿液标本,以30例正常体检同龄儿童作对照;以酶联免疫吸附法测定血清及尿液中NO、IL-6水平。结果：治疗前KD急性期患儿血清及尿液NO、IL-6较对照组显著增高,经IVIG治疗后,KD患儿血清NO、IL-6及尿液IL-6含量较治疗前显著降低,尿液NO含量无显著变化。结论：KD患儿急性期经IVIG治疗后,通过抑制NO、IL-6等递质的产生,从而减轻炎症损害,使患儿迅速恢复。     

肺炎支原体感染在川崎病及冠状动脉病变中的作用

目的：探讨支原体肺炎感染在川崎病（KD）及其冠状动脉病变（CAD）发生中的作用。方法：采用回顾性病例对照研究,分析2007年1月～2008年12月入院治疗的川崎病患儿资料。并以同期其他病因的患儿为对照。结果：KD组患儿支原体阳性率为24．7％（19／77）,对照组阳性率为10．0％（8／80）。KD组MP感染率较高（x0=5．934,P=0．015）,其OR值为2．948,95％CI为1．126～8．318。77例KD患儿中,31例CAD患儿阳性率38．7％（12／31）;46例非CAD阳性率15．2％（7,46）。CAD组MP感染率高于非CAD组（x^2=5．499,P=0．019）,其OR值为3．519,95％CI为1．057-12．208。31例CAD患儿中．22例冠状动脉扩张组NP阳性率31．8％（7／22）;7例中小型冠状动脉瘤组阳性率42．9％（3／7）;2例巨大型冠状动脉瘤组阳性率100．0％（2／2）,组间差异无统计学意义。结论：支原体肺炎感染在川崎病及其冠状动脉病变发生中的作用,但其与冠状动脉病变程度的关系尚待进一步探讨。     

肝癌高发区人群中丙型肝炎抗体的检出率

对肝癌病发区内的三批人群应用国产试剂测定抗-HCV，结果肝癌病人检出率为8.8％（8／91），献血员为1．8％（2／111），急性肝炎病人为10．3％（6／58）；应用第一代Ortho试剂测定，肝癌病人为8．9％（10／112），自然人群为2．2％（5／225），献血员为4．0％（4／100），HBsAg携带者为2．6％（3／116）；应用第二代Ortho试剂测定，65例肝癌仅有1例阳性，227例自然人群中也仅1例阳性，120例HBsAg携带者中竟无一阳性。研究表明，HCV与肝癌的关系值得重视，但远不如HBV重要。     

儿童川崎病115例临床分析

目的：探讨儿童川崎病（KD）的临床特征、实验室检查、冠状动脉病变（CAL）的相关危险因素及治疗方法。方法：对2003年1月至2013年6月入住我院的115例KD患儿的临床资料进行回顾性分析。结果：（1）男73例（63.5%）,女42例（36.5%）,5岁以内96例（83.5%）。（2）典型KD 90例,不完全性KD（IKD）25例;IKD组婴儿（〈1岁）比例和CAL发生率均高于典型KD组（44.0%vs 7.8%,40.0%vs 17.8%,P均〈0.05）;除肛周脱屑、卡疤红肿外,IKD组其他临床症状发生率低于典型KD组,出现时间晚于KD组（P均〈0.05）;除血红蛋白外,两组实验室检查指标比较差异无统计学意义（P〉0.05）。（3）CAL组男性比例、婴儿比例、发热时间、血小板计数（PLT）、血红胞沉降率（ESR）、C反应蛋白（CRP）水平均大（高）于非CAL组（P均〈0.05）。（4）KD发病10 d内的CAL发生率低于发病10 d后,且治疗2周后复查发病10 d内给予静脉用免疫球蛋白组新CAL发生率低于发病10 d后给予IVIG组（P〈0.05）。结论：IKD多发于婴儿,且其CAL发生率较高,肛周脱屑、卡疤红肿有助于其早期诊断;CAL发生率与男性、年龄〈1岁、发热时间、PLT、ESR、CRP有关;KD发病10 d内应用静脉用免疫球蛋白效果较好。     

417 例川崎病患儿单中心回顾性研究

目的:总结川崎病(KD)患儿的临床资料,分析其临床特点及变化趋势。方法:对2011-2016 年在荆州市中心医院确诊的417 例KD 住院患儿的临床资料进行回顾性分析,按照入院时间分为三组:A 组(2011-2012 年)70 例,B 组(2013-2014 年)139 例,C 组(2015-2016 年)208 例,比较三组KD 患儿的临床特点及变化情况。结果:KD 患儿的入院构成比从2011 年的3.18/10 000 上升至2016 年7.86/10 000, 呈逐年上升的趋势( P <0.05)。0 ~ 1 岁组49 例(11.8%), >1 ~ 2 组岁173 例(41.6%),>2 ~5 岁组170 例(40.7%),>5 ~14 岁组25 例(5.9%)。冠状动脉损害(CAL)发生率31.2%。不完全KD(IKD)早 期易诊断为急性化脓性淋巴结炎、脓毒症、呼吸道感染等导致KD 延迟诊断。IVIG 耐受组KD 应用糖皮质激素(GC) 治疗可较快退热,缓解病情。结论:2011-2016 年荆州市中心医院KD 患儿的入院构成比呈逐渐增高的趋势,1 ~5 岁为高发年龄,CAL 发生率明显增高,IKD 早期易误诊为其他疾病。GC 对IVIG 耐受KD 患儿治疗有效。     

IL-17、IL-10在急性期和亚急性期川崎病患儿血清中浓度变化及意义

目的探讨急性期和亚急性期川崎病（kawasaki disease,KD）患儿血清IL-17及IL-10水平的变化,并进一步分析其临床意义。方法采用ELISA方法检测31例急性期及亚急性期KD患儿血清IL-17及IL-10的水平,并与同期22例健康儿童对照。结果急性期、亚急性期KD患儿组血清IL-17及IL-10水平均高于正常对照组（P〈0．01）;急性期KD患儿组血清IL-17及IL-10水平均高于亚急性期KD患儿组（P〈0．01）;急性期KD患儿血清IL-17水平与血清IL-10水平呈正相关。（r=0．630,P〈0．05）。亚急性期KD患儿血清IL-17水平与血清IL-10水平呈负相关。（r=-0．810,P〈0．05）。结论急性期KD患儿血清IL-17水平和IL-10水平均明显增高,亚急性期KD患儿血清IL-17水平显著下降,而亚急性期血清IL—10水平虽较急性期下降,但仍维持较高水平。IL-17是一种强的促炎细胞因子,而IL-10是一种抑炎细胞因子,二者血清水平的变化提示它们分别在KD发生和发展的不同阶段发挥着各自重要作用。在临床上可以通过检测血清IL-17和IL-10的水平为KD的诊断和治疗提供依据。     

川崎病61例临床分析

目的分析川崎病（KD）尤其是不完全川崎病（IKD）的临床表现及实验室检查特点,以早期诊治,减少冠状动脉损害的发生。方法对2003年7月～2011年7月我院儿科收治住院的川崎病患儿61例,其中典型川崎病（KD）45例和不完全川崎病（IKD）16例临床资料进行回顾性分析。结果 61例KD中男36例,女25例,男女比例为1.44：1,其中5岁以下发病占80.3%I,KD占26.2%。典型KD和IKD 2组病例在皮疹、眼球结膜充血、口唇及口腔黏膜改变、四肢硬肿脱皮、颈淋巴结肿大方面比较,差异有统计学意义;在实验室检查及冠状动脉损害方面,差异无统计学意义。结论 IKD与典型病例的冠状动脉损害发生率相近,一旦疑为川崎病,应尽早做超声心动图检查。     

Kinetic and equilibrium studies of Ah receptor-ligand binding: use of [125I]2-iodo-7,8-dibromodibenzo-p-dioxin

In this report, we have used the radioligand [125I]2-iodo-7,8-dibromo-dibenzo-p-dioxin to describe the kinetics of ligand binding to the Ah receptor prepared from C57BL/6J mouse liver. The higher specific activity of this radioligand (2176 Ci/mmol), compared with the usual tritiated ligand [1,6-3H]2,3,7,8-tetrachloro-dibenzo-p-dioxin (58 Ci/mmol) permitted the study of ligand-receptor interactions at much lower component concentrations. For this radioiodinated ligand, Scatchard analysis of saturation binding curves, determined at six different protein concentrations, indicated that the apparent equilibrium dissociation constant, KD, was directly related to the dilution of the receptor preparation; for example, at 1160 micrograms of protein/ml, KD = 1.6 x 10(-10) M; at 36 micrograms of protein/ml, KD = 1.2 x 10(-11) M. Extrapolation of this function to infinite receptor dilution yielded KD = 6 x 10(-12) M. The addition of 70 micrograms/ml of bovine serum albumin to a receptor preparation of 30 micrograms of protein/ml produced a 10-fold decrease in the slope of the Scatchard plot (i.e., 10-fold increase in the apparent KD). Conversely, enrichment of the receptor by high performance liquid chromatography led to an increased slope and thus decreased estimate of KD. The association rate constant (k1), calculated from the integrated second-order rate equation, was 2.8 x 10(10) M-1 hr-1 and, from the initial velocity equation, had a value of 5.25 x 10(10) M-1 hr-1. The dissociation rate constant was biphasic, consisting of a predominant fast component with a rate constant of 0.36 hr-1 (k-1) and a slower component with a rate constant of 4.2-9.4 x 10(-3) hr-1 (k-2). Higher protein concentrations produced a decrease in estimates of k1 but not k-1 or k-2. The KD determined from the ratio of the kinetic rate constant, k-1/k1 = 6.9 x 10(-12) M, is in excellent agreement with that derived from the results of equilibrium binding experiments extrapolated to infinite dilution, KD = 6 x 10(-12) M. The decrease in KD, observed in equilibrium binding studies upon dilution of the receptor preparation, is best explained by a more accurate classification of "free" radioligand at lower protein concentrations. Finally, ligand binding to the Ah receptor is best described by a two-step process, the formation of an initial complex, characterized by rapid ligand dissociation, which undergoes transformation to a second distinct complex displaying a much slower ligand dissociation rate.     

Binding of dihydrodigitoxin to beef and human cardiac (Na+ + K+)-ATPase: evidence for two binding sites in cell membranes

The specific binding of three cardiac glycosides, 3H-ouabain, 3H-digitoxin and 3H-dihydrodigitoxin, to beef cardiac (Na+ + K+)-ATPase was compared. Non-specific binding was defined as that in the presence of 0.1 mM unlabelled compound, or in the absence of ligands. The dissociation constants (KD-values) calculated from the inhibition of 3H-ouabain binding were: ouabain, 2.9 X 10(-9)M; digitoxin, 1.1 X 10(-9)M; and dihydrodigitoxin 2.7 X 10(-8)M. The concentrations which inhibited beef cardiac (Na+ + K+)-ATPase by 50% were: ouabain, 5.9 X 10(-9)M; digitoxin, 1.6 X 10(-9)M; and dihydrodigitoxin, 2.5 X 10(-8)M. Ouabain and digitoxin showed straight Scatchard plots for one site of high affinity (ouabain, KD = 2.6 X 10(-9)M; digitoxin, KD = 1.7 X 10(-9)M). However, dihydrodigitoxin gave a curved Scatchard plot. Analysis of this binding by the methods of M. J. Weidemann, H. Erdelt and M. Klingenberger (Eur. J. Biochem. 16, 313 (1970) for two binding sites gave the following results: for Mg2+,Pi-supported binding, the KD of the high affinity site was 1.6 X 10(-8)M with a capacity similar to that for ouabain of about 30 pmole/mg protein. For binding supported by Na+,ATP,Mg2+, the KD-value of the high affinity site was 5.3 X 10(-8)M of similar capacity. The low affinity binding site (KD = 4.0 X 10(-6)M for Mg2+,Pi; KD = 5.5 X 10(-6)M for Na+,ATP,Mg2+) bound about 350 pmole/mg protein. The low affinity site but not the high affinity site was also present in heat-denatured enzyme. Binding supported by Mg2+,Pi showed one low affinity site only for ouabain and dihydrodigitoxin in the presence of 200 mM Na+. The high affinity sites for these three cardiac glycosides were further characterized by measurement of the association and dissociation rate constants. The specific binding of 3H-ouabain and 3H-dihydrodigitoxin to human cardiac (Na+ + K+)-ATPase was measured. 3H-Ouabain showed a straight Scatchard plot for one high affinity site only (KD = 4.5 X 10(-9) M, capacity about 15 pmole/mg protein). 3H-Dihydrodigitoxin gave two binding sites: a high affinity site (KD = 1.8 X 10(-8) M) of similar capacity to ouabain, and a low affinity site (KD = 2.0 X 10(-6) M) of about 10-fold greater capacity.(ABSTRACT TRUNCATED AT 400 WORDS)     

The kinin B1 receptor antagonist des-Arg9-[Leu8]bradykinin: an antagonist of the angiotensin AT1 receptor which also binds to the AT2 receptor.

1. Agonists and antagonists of kinin B1 and B2 receptors were evaluated in vitro for their effects against angiotensin II (AII)-induced contractile responses in the rabbit aorta and for their binding properties to angiotensin AT1 and AT2 receptors from purified membrane of rat liver and lamb uterus respectively. 2. In aortic rings, the kinin B1 receptor antagonist, des-Arg9-[Leu8]bradykinin (BK) (3-100 microM) caused a concentration-dependent decrease in sensitivity and a depression of the maximum response to AII. Des-Arg10-[Leu9]kallidin (KD), des-Arg9-BK, des-Arg10-KD, BK or KD at 3 microM had no effect against AII-induced contractions. 3. Des-Arg9-[Leu8]BK (3 or 100 microM) did not affect contractions of aortic rings to histamine, potassium chloride, endothelin-1, 5-hydroxytryptamine, noradrenaline and the thromboxane A2-mimetic, U46619. 4. Des-Arg9-[Leu8]BK displaced [125I]-Sar1-AII binding to the AT1 subtype in rat liver membranes with a Ki value of 1.1 +/- 0.4 microM. Values of Ki for des-Arg9-BK and KD were 45 +/- 13 microM and 25 +/- 22 microM, respectively. The other kinin derivatives des-Arg10-KD, BK and des-Arg10-[Leu9]KD at concentrations up to 100 microM did not bind to the AT1 receptor. 5. All the kinin derivatives except BK bound to AT2 receptors in lamb uterus membranes. Values of Ki for des-Arg9-[Leu8]BK, des-Arg10-[Leu9]KD, des-Arg9-BK, des-Arg10-KD and KD were 0.3 +/- 0.1, 0.7 +/- 0.1, 1.2 +/- 0.3, 1.5 +/- 0.3 and 7.0 +/- 1.6 microM, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of KD3-671, an angiotensin II type 1 receptor antagonist,on anti-thy-1 nephritis in rats

We examined the effects of KD3-671 (2-propyl-8-oxo-1-[(2'-(H-tetrazole-5-yl)biphenyl-4-yl)methyl]-4,5,6,7-tetrahydrocycloheptimidazole), an angiotensin II type1 receptor antagonist, on an experimental rat model of mesangioproliferative glomerulonephritis, anti-Thy-1 nephritis. Anti-Thy-1 nephritis was induced by intravenous injection of 300 microg/kg of anti-Thy-1.1 monoclonal antibody into rats. KD3-671 (3, 10, 30 mg/kg per day) or enalapril (30 mg/kg per day), an angiotensin II converting enzyme inhibitor, was given p.o. once daily from the day before the antibody injection (the 1st day) to the 15th day after. KD3-671 significantly inhibited an increase in the number of total and proliferating cell nuclear antigen-positive cells and the deposition of alpha-smooth muscle actin and fibronectin in the glomeruli of nephritic rats, but enalapril (30 mg/kg per day) suppressed only the number of total cells and the deposition of alpha-smooth muscle actin in the glomeruli. Moreover, to elucidate the effect of KD3-671 on matrix deposition in the glomeruli, we measured the production of fibronectin in isolated glomeruli obtained from anti-Thy-1 nephritic rats. The glomeruli in anti-Thy-1 nephritic rats produced more fibronectin than that in control rats. KD3-671 (10(-8), 10(-7), 10(-6) M) dose-dependently attenuated fibronectin production in isolated nephritic glomeruli. These findings suggest that KD3-671 may be an effective agent for the treatment of mesangioproliferative glomerulonephritis.     

Autoregulation of bradykinin receptors: agonists in the presence of interleukin-1beta shift the repertoire of receptor subtypes from B2 to B1 in human lung fibroblasts.

Elevated formation of bradykinin (BK) and Lys-BK or kallidin (KD) and their carboxypeptidase metabolites desArg(9)BK and desArg(10)KD is evident at sites of inflammation. Moreover, B2 receptors (B2R), which mediate the action of BK and KD, participates in the acute stage of the inflammatory and pain response, whereas B1 receptors (B1R), through which desArg(9)BK and desArg(10)KD act, partake in the chronic stage. We hypothesized that kinins autoregulate B2R and B1R expression in favor of B1R. Incubation of IMR-90 cells with BK (100 nM) led to a loss (89%) of B2R with a half-life (T(1/2)) of 7.0 min. Concomitantly, BK increased B1R (2- to 3-fold) with a T(1/2) of 120 min. DesArg(10)KD (100 nM) had no effect on B2R but increased B1R (3- to 4-fold) with the same rate as BK. Interleukin-1beta (IL-1beta; 500 pg/ml) also increased B1R (4- to 6-fold). Although both desArg(10)KD and BK increased the level of IL-1beta mRNA, IL-1beta receptor antagonist inhibited the increase in B1R only in response to BK. DesArg(10)KD and BK synergistically increased B1R (9-fold), which was further increased by inclusion of IL-1beta (36-fold). Therefore, kinin metabolism and kinin-stimulated production of cytokines may play a pivotal role in shifting the repertoire of kinin receptor subtypes in favor of B1R during inflammation.     

Binding studies of platelet alpha 2- and lymphocyte beta 2-adrenoceptors in patients with cirrhosis.

Radioligand binding studies were performed on 10 patients with cirrhosis and 10 healthy subjects. Bmax and KD of platelet alpha 2-adrenoceptors, studied using [3H]-yohimbine, were similar in both groups (Bmax 24.9 vs 22.1 fmol/10(9) platelets, P = 0.47; KD 4.6 vs 5.5 nmol 1-1, P = 0.56). Bmax and KD of lymphocyte beta 2-adrenoceptors, studied using [125I]-iodocyanopindolol, were also similar in both groups (Bmax 24.0 vs 27.2 fmol mg-1 protein, P = 0.55; KD 49.6 vs 55.3 pmol 1-1, P = 0.65). In this model there is no evidence of adrenoceptor down-regulation in cirrhosis despite the increased sympathetic activity in this condition.