白血病,肾病综合征的外周血淋巴细胞糖皮质激素受体与糖皮质 …

用放射配本结合分析检测了急性白血病和肾病综合征（肾综）外周淋巴细胞的细胞的糖皮质激素受体（ＧＲ）的含量。结果显示：白血病和肾综多为糖皮质激素信赖性。急性淋巴细胞性白血病ＧＲ含量明显增高，对激素治疗的反应性较高；成人和小儿肾缩的ＧＲ含量均高于正常（Ｐ〈０．０５）。小儿肾综的ＧＲ含量大于正常值者，对激素治疗的反应敏感比率为７０．５９％；小于正常值者则为５０％，且易复发。这表明ＧＲ含量高的患者激素疗效较     

白血病、肾病综合征的外周血淋巴细胞糖皮质激素受体与糖皮质激素依赖性关系的临床意义

用放射配体结合分析检测了急性白血病和肾病综合征（肾综）外周淋巴细胞的糖皮质激素受体（ＧＲ）的含量。结果提示：白血病和肾综多为糖皮质激素依赖性。急性淋巴细胞性白血病ＧＲ含量明显增高，对激素治疗的反应性较高；成人和小儿肾综的ＧＲ含量均高于正常人（Ｐ＜０．０５）。小儿肾综的ＧＲ含量大于正常值者，对激素治疗的反应敏感比率为７０．５９％；小于正常值者则为５０％，且易复发，这表明ＧＲ含量高的患者激素疗效好，反之疗效低。本方法简便，用于观察激素疗效较灵敏，可多次取材重复检测，具有一定临床价值。     

外周血白细胞糖皮质激素受体与肝硬化关系的研究

为探讨外周血白细胞糖皮质激素受体在慢性肝病中的变化及其产，和放射本法和放射免疫法分别测定５０例肝硬化及１６例正常人外周血白细胞ＧＲ和血浆皮质醇水平。     

扩张型心肌病患者外周血白细胞糖皮质激素受体的测定

扩张型心肌病患者外周血白细胞糖皮质激素受体的测定赵以强（山东省立医院内科济南２５００２１）任忠水（济宁骨伤医院）周焰（枣庄矿务局医院）董波（山东省立医院内科济南２５００２１）糖皮质激素受体（ＧＲ）与许多疾病的病理过程及糖皮质激素（ＧＣ）的疗效有关。为...     

高、低亲和力糖皮质激素受体同源性的研究

我们以前的工作表明糖皮质激素(GC)靶细胞上除存在经典的高亲和力、低容量GC受体(GR_H)外,尚存在低亲和力GC受体(GR_L)。GR_L可介导大剂量GC的作用。本文初步探讨了GR_L与GR_H在分子结构以及基因水平上的相互关系。利用两种抗大鼠肝GR_H单克隆抗体(MabN250:为抗GR_H N端免疫活性区的单抗,MabBuGR_1:为抗GR_H DNA结合区的单抗)制备Mab-Sepharose 4 B亲和层析柱,将[~3H]曲安缩酮(TA)与大     

系统性红斑狼疮患者外周血白细胞糖皮质激素受体及血浆皮质醇测定

应用放射配体结合法测定了12例未用糖皮质激素的系统性红斑狼疮女性患者外周血糖皮质激素受体的变化,发现所有患者糖皮质激素受体少于正常人;同时应用放射免疫分析法测定了患者血浆皮质醇,结果与正常人无明显差异;提示系统性红斑狼疮时糖皮质激素—糖皮质激素受体系统异常,本文对这一异常的意义做了探讨。     

原发性癫痫患者糖皮质激素和糖皮质激素受体改变的研究

用放射配体结合分析，测定了４１例（男１６例，女２５例）原发性癫痫患者外周血白细胞糖皮质激素受体（ｇｌｕｃｏｃｏｒｔｉｃｏｉｄ ｒｅｃｅｐｔｏｒ ＧＲ），同时用放射免疫分析测定了患者血浆皮质醇（Ｆ），即糖皮质激素（ｇｌｕｃｏｃｒｔｉｃｏｉｄＧＣ），并与正常对照组比较。结果表明，无论年龄、性别及服用何种抗痫药物，原发性癫痫患者的ＧＣ都明显高于对照组（Ｐ〈０．０１）；ＧＲ都明显低于对照组，（Ｐ〈０．０     

脑出血患者外周血白细胞糖皮质激素受体及其效应指标的改变？…

应用放射配体结合法，测定了５６例脑出血患者外周血白细胞糖皮质激素受体（ＧＲ）的改变。结果发现脑出血组血浆皮质醇均明显升高，但白细胞ＧＲ随出血量的增多而降低超明显，并同时伴有氢化的可的松（Ｆ）对中性多形核白细胞（ＰＭＮ）趋化移动（ＣＨｔＭ）抑制率（ＦＩ）的降低。故测定ＣＲ有助于以对病情及预后的判断。     

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.     

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.     

The Rad9-Hus1-Rad1 (9-1-1) clamp activates checkpoint signaling via TopBP1

DNA replication stress triggers the activation of Checkpoint Kinase 1 (Chk1) in a pathway that requires the independent chromatin loading of the ATRIP-ATR (ATR-interacting protein/ATM [ataxia-telangiectasia mutated]-Rad3-related kinase) complex and the Rad9-Hus1-Rad1 (9-1-1) clamp. We show that Rad9's role in Chk1 activation is to bind TopBP1, which stimulates ATR-mediated Chk1 phosphorylation via TopBP1's activation domain (AD), a domain that binds and activates ATR. Notably, fusion of the AD to proliferating cell nuclear antigen (PCNA) or histone H2B bypasses the requirement for the 9-1-1 clamp, indicating that the 9-1-1 clamp's primary role in activating Chk1 is to localize the AD to a stalled replication fork.     

HLA-DRB1, -DQA1, -DQB1 and DPB1 susceptibility alleles in Cameroonian type 1 diabetes patients and controls

It is known that certain combinations of alleles within the human leucocyte antigen (HLA) complex are associated with susceptibility or resistance to type 1 diabetes. Variable associations of DR and DQ with type 1 diabetes are documented in Caucasians but rarely in African populations; however, the role of HLA-DP genes in type 1 diabetes remains uncertain. In order to investigate the HLA class II associations with type 1 diabetes in Cameroonians, we used sequence-specific oligonucleotide probing (SSOP) to identify DRB1, DQA1, DQB1 and DPB1 alleles in 10 unrelated C-peptide negative patients with type 1 diabetes and 90 controls from a homogeneous population of rural Cameroon. We found a significantly higher frequency of the alleles DRB1*03 (χ² = 17.9; P = 0.001), DRB1*1301 (χ² = 37.4; P < 0.0001), DQA1*0301 (χ² = 18.5; P = 0.001) and DQB1*0201 (χ² = 37.4; P < 0.001) in diabetes patients compared to the control group. The most frequent alleles in the control population were DQA1*01, DQB1*0602 and DRB1*15. The DRB1*04 allele was not significantly associated with type I diabetes in our study population. We observed no significant difference between patients and controls in DPB1 allele frequency. In conclusion, the data in Cameroonian diabetes patients suggest the existence of HLA class II predisposing and specific protective markers, but do not support previous reports of a primary association between HLA-DP polymorphism and development of type I diabetes .