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排序方式: 共有906条查询结果,搜索用时 15 毫秒
71.
Aseptic meningitis associated with high dose intravenous immunoglobulin therapy. 总被引:1,自引:1,他引:0
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![点击此处可从《Journal of neurology, neurosurgery, and psychiatry》网站下载免费的PDF全文](/ch/ext_images/free.gif)
J D Watson J Gibson D E Joshua H Kronenberg 《Journal of neurology, neurosurgery, and psychiatry》1991,54(3):275-276
Two cases of aseptic meningitis occurred in temporal association with high dose intravenous immunoglobulin therapy to treat thrombocytopenia. In neither case was any other aetiological agent identified and both patients completely recovered within a few days. This phenomenon has been reported in only one previous paediatric case. 相似文献
72.
Mutation of the signal peptide-encoding region of the preproparathyroid hormone gene in familial isolated hypoparathyroidism. 总被引:15,自引:5,他引:10
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![点击此处可从《The Journal of clinical investigation》网站下载免费的PDF全文](/ch/ext_images/free.gif)
A Arnold S A Horst T J Gardella H Baba M A Levine H M Kronenberg 《The Journal of clinical investigation》1990,86(4):1084-1087
Preproparathyroid hormone (preproPTH) gene mutation has been proposed as a cause of familial isolated hypoparathyroidism (FIH). We cloned the preproPTH alleles of a patient with autosomal dominant FIH and sequenced the coding regions, 5' flanking regions, and splice junctions. The putatively abnormal (based on previous linkage studies) allele differed from the other allele's normal sequence at only one nucleotide. This T to C point mutation changes the codon for position 18 of the 31 amino acid prepro sequence from cysteine to arginine, disrupting the hydrophobic core of the signal sequence. Because the hydrophobic core is required by secreted proteins for efficient translocation across the endoplasmic reticulum, the mutant protein is likely to be inefficiently processed. Indeed, in vitro studies demonstrated dramatically impaired processing of the mutant preproPTH to proPTH. In summary, we observed a point mutation in the signal peptide-encoding region of a preproPTH gene in one FIH kindred and demonstrated a functional defect caused by the mutation. Mutation of the signal sequence constitutes a novel pathophysiologic mechanism in man, and further study may yield important insights both into this form of hormone deficiency and into the role of signal sequences in human physiology. 相似文献
73.
Polyadenylated RNA, extracted from rat hypothalami, cross-hybridized with a RNA probe complementary in sequence to rat PTH (rPTH) messenger RNA (mRNA). Amplification of complementary DNA (cDNA) by the polymerase chain reaction also demonstrated the presence of rPTH mRNA in the rat hypothalamus and parathyroid gland. rPTH mRNA was localized by in situ hybridization in the paraventricular and supraoptic nuclei of the rat hypothalamus. These results demonstrate the expression of the PTH gene in the central nervous system of the rat in areas which suggest roles for PTH in neuroendocrine function. 相似文献
74.
Spanaus KS Kronenberg F Ritz E Schlapbach R Fliser D Hersberger M Kollerits B König P von Eckardstein A;Mild-to-Moderate Kidney Disease Study Group 《Clinical chemistry》2007,53(7):1264-1272
BACKGROUND: Plasma concentrations of B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) are diagnostic and prognostic biomarkers of heart failure and are also increased in patients with chronic kidney disease (CKD). We examined the relevance of BNP and NT-proBNP as predictors of CKD progression. METHODS: Of 227 nondiabetic patients with mild-to-moderate renal insufficiency, 177 patients ages 18-65 years were followed in a prospective multicenter cohort study for a period of < or = 7 years. CKD progression was assessed by recording renal endpoints, defined as doubling of baseline serum creatinine or end-stage renal disease (ESRD) requiring renal replacement therapy. RESULTS: BNP and NT-proBNP were significantly higher among 65 patients who reached the combined renal endpoint than among the 112 who did not [median (interquartile range) 61 (27-98) ng/L vs 39 (20-70) ng/L, P = 0.023, for BNP; 320 (117-745) ng/L vs 84 (44-176) ng/L, P <0.001, for NT-proBNP)]. Each increment of 1 SD in log-transformed BNP and NT-proBNP increased the risk of CKD progression by hazard ratios of 1.38 (95% CI 1.09-1.76, P = 0.009) and 2.28 (1.76-2.95, P <0.001), respectively. After adjustment for other established prognostic factors of CKD progression, NT-proBNP but not BNP remained a significant independent predictor of the combined renal endpoint. CONCLUSIONS: Increased BNP and NT-proBNP concentrations indicate an increased risk for accelerated progression of CKD to ESRD and may prove to be valuable biomarkers for the assessment of prognosis in patients with CKD. 相似文献
75.
H Dieplinger C Lackner F Kronenberg C Sandholzer K Lhotta F Hoppichler H Graf P Knig 《The Journal of clinical investigation》1993,91(2):397-401
Patients with terminal renal insufficiency suffer from an increased incidence of atherosclerotic diseases. Elevated plasma concentrations of lipoprotein(a) [Lp(a)] have been established as a genetically controlled risk factor for these diseases. Variable alleles at the apo(a) gene locus determine to a large extent the Lp(a) concentration in the general population. In addition, other genetic and nongenetic factors also contribute to the plasma concentrations of Lp(a). We therefore investigated Apo(a) phenotypes and Lp(a) plasma concentrations in a large group of patients with end-stage renal disease (ESRD) and in a control group. Lp(a) concentrations were significantly elevated in ESRD patients (20.1 +/- 20.3 mg/dl) as compared with the controls (12.1 +/- 15.5 mg/dl, P < 0.001). However, no difference was found in apo(a) isoform frequency between the ESRD group and the controls. Interestingly, only patients with large size apo(a) isoforms exhibited two- to fourfold elevated levels of Lp(a), whereas the small-size isoforms had similar concentrations in ESRD patients and controls. Beside elevated Lp(a) concentrations, ESRD patients had lower levels of plasma cholesterol and apolipoprotein B. These results show that elevated Lp(a) plasma levels might significantly contribute to the risk for atherosclerotic diseases in ESRD. They further indicate that nongenetic factors related to renal insufficiency or other genes beside the apo(a) structural gene locus must be responsible for the high Lp(a) levels. 相似文献
76.
77.
Nattermann J Nischalke HD Hofmeister V Kupfer B Ahlenstiel G Feldmann G Rockstroh J Weiss EH Sauerbruch T Spengler U 《Antiviral therapy》2005,10(1):95-107
HIV has evolved several strategies to evade recognition by the host immune system including down-regulation of major histocompatibility complex (MHC) class I molecules. However, reduced expression of MHC class I molecules may stimulate natural killer (NK) cell lysis in cells of haematopoietic lineage. Here, we describe how HIV counteracts stimulation of NK cells by stabilizing surface expression of the non-classical MHC class I molecule, HLA-E. We demonstrate enhanced expression of HLA-E on lymphocytes from HIV-infected patients and show that in vitro infection of lymphocytes with HIV results in up-regulation of HLA-E expression and reduced susceptibility to NK cell cytotoxicity. Using HLA-E transfected K-562 cells, we identified the well-known HIV T-cell epitope p24 aa14-22a as a ligand for HLA-E that stabilizes surface expression of HLA-E, favouring inhibition of NK cell cytotoxicity. These results propose HIV-mediated up-regulation of HLA-E expression as an additional evasion strategy targeting the antiviral activities of NK cells, which may contribute to the capability of the virus in establishing chronic infection. 相似文献
78.
Invariant natural killer T (iNKT) cells are T lymphocytes that behave similarly to cells of the innate immune system. The glycolipid alpha-galactosylceramide (alpha-GalCer) is a potent and specific activator of mouse and human iNKT cells and has been used in cancer clinical trials to drive NKT cell-mediated immune responses. However, little is known about the dynamics of the iNKT cell response to alpha-GalCer in vivo. In this issue of the JCI, Parekh and colleagues demonstrate that administration of alpha-GalCer causes iNKT cells to become unresponsive, for at least 1 month, in mice. This leads us to ask, should sequential administration of alpha-GalCer still be used to activate iNKT cells given the anergic state it has been shown here to induce? This intriguing article raises the issue of the avoidance of anergy induction in the design of treatment regimens that use alpha-GalCer as a specific activator of iNKT cells. 相似文献
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