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21.
22.
为了研究不同HLA B分子对NK细胞杀伤活性的影响 ,我们分别构建pcDNA3 HLA B 390 5 2、B 2 70 4、B 5 1 0 2 2基因真核表达载体 ;借助脂质体将各质粒转染入K5 6 2细胞 ,经G4 1 8筛选 ,分别获得阳性表达细胞株 ;并应用LDH法检测转染细胞对不同个体外周血NK细胞杀伤活性的抑制效应。结果显示 :与转染了空质粒的对照组相比 ,外周血NK细胞对K5 6 2 B39的杀伤率无明显影响 ,而对K5 6 2 B2 7,K5 6 2 B5 1的杀伤率降低。当使用针对NK细胞受体KIR3DL1的单抗DX9封闭NK细胞后 ,此抑制效应大部分消失。提示靶细胞表达HLA Bw4分子可明显抑制NK细胞的杀伤效应 ,而表达HLA Bw6分子对NK细胞杀伤功能无明显影响 相似文献
23.
Quantitation of muscle glycogen synthesis in normal subjects and subjects with non-insulin-dependent diabetes by 13C nuclear magnetic resonance spectroscopy 总被引:58,自引:0,他引:58
G I Shulman D L Rothman T Jue P Stein R A DeFronzo R G Shulman 《The New England journal of medicine》1990,322(4):223-228
To examine the extent to which the defect in insulin action in subjects with non-insulin-dependent diabetes mellitus (NIDDM) can be accounted for by impairment of muscle glycogen synthesis, we performed combined hyperglycemic-hyperinsulinemic clamp studies with [13C]glucose in five subjects with NIDDM and in six age- and weight-matched healthy subjects. The rate of incorporation of intravenously infused [1-13C]glucose into muscle glycogen was measured directly in the gastrocnemius muscle by means of a nuclear magnetic resonance (NMR) spectrometer with a 15.5-minute time resolution and a 13C surface coil. The steady-state plasma concentrations of insulin (approximately 400 pmol per liter) and glucose (approximately 10 mmol per liter) were similar in both study groups. The mean (+/- SE) rate of glycogen synthesis, as determined by 13C NMR, was 78 +/- 28 and 183 +/- 39 mumol-glucosyl units per kilogram of muscle tissue (wet weight) per minute in the diabetic and normal subjects, respectively (P less than 0.05). The mean glucose uptake was markedly reduced in the diabetic (30 +/- 4 mumol per kilogram per minute) as compared with the normal subjects (51 +/- 3 mumol per kilogram per minute; P less than 0.005). The mean rate of nonoxidative glucose metabolism was 22 +/- 4 mumol per kilogram per minute in the diabetic subjects and 42 +/- 4 mumol per kilogram per minute in the normal subjects (P less than 0.005). When these rates are extrapolated to apply to the whole body, the synthesis of muscle glycogen would account for most of the total-body glucose uptake and all of the nonoxidative glucose metabolism in both normal and diabetic subjects. We conclude that muscle glycogen synthesis is the principal pathway of glucose disposal in both normal and diabetic subjects and that defects in muscle glycogen synthesis have a dominant role in the insulin resistance that occurs in persons with NIDDM. 相似文献
24.
25.
Creutzfeldt-Jakob disease (CJD) with a mutation at codon 148 of prion protein gene: relationship with sporadic CJD 总被引:1,自引:0,他引:1
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Pastore M Chin SS Bell KL Dong Z Yang Q Yang L Yuan J Chen SG Gambetti P Zou WQ 《The American journal of pathology》2005,167(6):1729-1738
Creutzfeldt-Jakob disease (CJD), the most common human prion disease, includes sporadic (s) and familial (f) forms. Regardless of etiology, both forms are thought to share the pathogenic mechanism whereby the cellular prion protein (PrP(C)) converts into its pathogenic isoform (PrP(Sc)). While PrP(C) conversion is thought to be random in sCJD, conversion in fCJD is facilitated by the congenital presence of mutated PrP. Differences in PrP genotype (PRNP) and in conversion circumstances lead to PrP(Sc) with distinct characteristics that elicit different disease phenotypes. Here, we describe a case of fCJD with a substitution of histidine (H) for arginine (R) at codon 148 (R148H) and heterozygosity of the methionine/valine (M/V) polymorphic codon 129, with the 129M allele coupled with the mutation. The disease phenotype and all major characteristics of PrP(Sc) of fCJD(R148H) were virtually indistinguishable from those of sCJDMV2, which has features different from those of any other sCJD. Therefore, despite the differences in etiology, PRNP, and conversion process, the two forms of PrP(Sc) had similar characteristics. Furthermore, comparison of fCJD(R148H) with a recently reported case carrying R148H and homozygosity at codon 129 suggests that codon 129 coupled with the mutation as well as that located on the normal allele can modify major phenotypic and PrP(Sc) features of fCJD(R148H). 相似文献
26.
27.
243例健康人血红细胞悬浮液射频介电特性的研究 总被引:8,自引:0,他引:8
本文应用同轴传输线反射法建立的细胞悬浮液介电测量系统,测量了243例健康人(男120,女123名)血红细胞悬浮液在1~500MHz频率范围的介电常数和电导率。结果表明不同性别和不同血型之间的红细胞悬浮液的介电参数无显著差异。将19~80岁之间的受试者按10岁年龄间隔分成六个组,探讨年龄差别对介电参数的影响;发现50岁左右是人红细胞介电参数有显著差异的临界年龄,49岁后三个高年龄组的介电参数显著地低于49岁前的三个低年龄组的数值(P<0.05)。本文的结果证明年龄对人血红细胞的介电参数有明确的影响。 相似文献
28.
29.
Isolation of a new clathrin heavy chain gene with muscle-specific expression from the region commonly deleted in velo-cardio-facial syndrome 总被引:3,自引:4,他引:3
Sirotkin H; Morrow B; DasGupta R; Goldberg R; Patanjali SR; Shi G; Cannizzaro L; Shprintzen R; Weissman SM; Kucherlapati R 《Human molecular genetics》1996,5(5):617-624
Velo-cardio-facial syndrome (VCFS) and DiGeorge syndrome (DGS) are
developmental disorders characterized by a spectrum of phenotypes including
velopharyngeal insufficiency, conotruncal heart defects and facial
dysmorphology among others. Eighty to eighty-five percent of VCFS/DGS
patients are hemizygous for a portion of chromosome 22. It is likely that
the genes encoded by this region play a role in the etiology of the
phenotypes associated with the disorders. Using a cDNA selection protocol,
we isolated a novel clathrin heavy chain cDNA (CLTD) from the VCFS/DGS
minimally deleted interval. The cDNA encodes a protein of 1638 amino acids.
CLTD shares significant homology, but is not identical to the ubiquitously
expressed clathrin heavy chain gene. The CLTD gene also shows a unique
pattern of expression, having its maximal level of expression in skeletal
muscle. Velopharyngeal insufficiency and muscle weakness are common
features of VCFS patients. Based on the location and expression pattern of
CLTD, we suggest hemizygosity at this locus may play a role in the etiology
of one of the VCFS-associated phenotypes.
相似文献
30.
A new factor in pathogenesis of edema of cardiac origin 总被引:1,自引:0,他引:1