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Re-directing human T cell specificity by functional expression of a chimeric T cell receptor
No full textRe-directing human T cell specificity by functional expression of a chimeric T cell receptor
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T-cell-based immunotherapy in multiple sclerosis: induction of regulatory immune networks by T-cell vaccination
No full textMultiple sclerosis (MS) is a chronic inflammatory disease of the CNS with presumed autoimmune origin. Pathogenic autoimmune responses in MS are thought to be the result of a breakdown of self tolerance. Several mechanisms account for the natural state of immunological tolerance to self antigens, including clonal deletion of self-reactive T cells in the thymus. However, autoimmune T cells are also part of the normal T-cell repertoire, supporting the existence of peripheral regulatory mechanisms that keep these potentially pathogenic T cells under control. One such mechanism involves active suppression by regulatory T cells. It has been indicated that regulatory T cells do not function properly in autoimmune disease. Immunization with attenuated autoreactive T cells, T-cell vaccination, may enhance or restore the regulatory immune networks to specifically suppress autoreactive T cells, as shown in experimental autoimmune encephalomyelitis, an animal model for MS. In the past decade, T-cell vaccination has been tested for MS in several clinical trials. This review summarizes these clinical trials and updates our current knowledge on the induction of regulatory immune networks by T cell vaccination.We thank J Zhang, R Medaer, A Van der Aa and G Hermans for their contribution to the above-reviewed results of our laboratory. This work was funded by grants from the Belgian Instituut voor de bevordering van het Wetenschappelijk Technologisch Onderzoek in de Industrie, the Belgian Charcot Foundation, the Belgian WOMS Foundation and Hasselt University (UHasselt)
Rapid identification of PKU‐associated mutations by multiplex DGGE analysis of the PAH gene
No full textA system of five sets of multiplex polymerase chain reaction amplifications followed by denaturing gel electrophoresis analysis allows rapid analysis of all 13 exons of the phenylalanine hydroxylase gene
High prevalence and incidence of vertebral deformities in ankylosing spondylitis patients with hyperkyphosis
No full texts-Posters IBMS/ECTS 2001-First Joint Meeting S118 metabolism in uremic patients. Thus circulating OPG may be an uremic toxin to develop uremic bone and parathyroid diseases through increasing skeletal resistance to PTH. Ji Shui Tan Hospital Objectives: To observe change of the serum TNF-alpha concentration when patients with osteodystrophy have been treated by 1-alpha(OH)D3. Methods: Twelve patients with chronic renal failure and renal osteodystrophy treated with 1-alpha(OH)D 3 , 0.5µg /day for 2 weeks and 4 weeks individually. Results: The serum TNF-alpha concentration descended obviously after 1-alpha(OH)D3 treatment. Conclusions: 1-alpha(OH)D3 may regulate TNF-alpha producting and secreting in mononuclear leukocyte. Objective To investigate the characteristic of bone metabolism in type 2 diabetes mellitus. Methods The levels of serum 25OHD, IBGP and urine HOP, Crosslaps were determined in 64 type 2 diabetes mellitus patient. Results (1) The levels of serum 25OHD in type 2 diabetes mellitus group were lower than that in normal controls (Male and premenopause women vs controls P0.05). The relevant analysis suggests there was no significant relativity among age | duration of diabetes and the BMD | serum BGP | ALK-B | Pyr-D | calcium | phosphorus and urine calcium in diabetic group. There were obvious positive relations between bodyweight index and serum phosphorus and BMD (P<0.05 and P<0.01). Conclusions: Low body weight is a risk for diabetic patients to get OP. BMD in diabetic patients is a bit higher than in normal elder, but no significant difference. The nature of ectopic bone and depositions of amorpheous calcifications in advanced atherosclerosic lesions is not well understood. Accumulating evidence suggests that atherosclerotic calcification shares features with bone calcification. We studied the presence of osteoprotegerin (OPG) and osteoprotegerin ligand (OPGL) in ectopic bone and amorpheous calcifications of type Vb human atherosclerotic lesions derived from the abdominal aorta. The localization of OPG and OPGL was determined by immunohistochemistry in 5 patients with ectopic bone formation (Group 1) and in 7 patients with amorpheous calcified depositions without bone structure (Group 2). In group 1, areas of lamellar bone were found containing lining cells, osteoblasts, osteoid, trabecular bone with cement lines, osteocytes and osteoclasts. In some areas cartilage structures were found containing matrix, lacunas and chondrocytes. In group 2, amorphous calcium deposits were found. OPGL was absent in and around the bone matrix in group 1. Faint OPGL depositions were close to areas of inflammation, which included T cells. In the lesions with cartilage structure, no OPG or OPGL could be identified. In group 2, deposition of OPGL was found in areas immediately around amorphous calcium depositions. OPG was found in the lining cells and in some of the smooth muscle cells in group 1 but could not be detected in group 2. These results indicate that OPG and OPGL are involved in ectopic bone formation and in the deposition of amorpheous calcium in atherosclerosis. This could provide a base for the study of the effect of bone-specific agents on the progression of atherosclerosis. Inflammatory Bowel Disease (IBD) is often followed by a loss of bone mass and bone quality. The resulting metabolic osteopathy should be characterized using laboratory and bone histomorphometric parameters. We investigated 19 patients (9 men, 10 women, age 23-68 years) suffering from Crohn's disease (16) or ulcerative colitis (3). The mean duration of the disease was 5,2 years (0,5-23). At the time of investigation, 16 patients were treated with corticosteroids (for a mean of 1,9 ys.). As serologic parameters we determined ESR, CRP, calcium, 25-OH-vitamin-D3, PTH and osteocalcin. After tetracycline labelling, bone biopsies were taken from the right anterior iliac crest applying a vertical technique. The samples were embedded in methylmetacrylate, sectioned on a heavy-duty microtome and stained (Masson-Goldner, Gomori, Giemsa). The following histomorphometric parameters were obtained using a Merz grid: bone volume (BV, in % of total bone volume), osteoid surface (OS), eroded surface (ES), osteoblast-(ObS) and osteoclast-covered surface (OcS), mineralized surface (MS, each in % of bone surface) and mineral apposition rate (MAR in microm). Patients with IBD showed increased CRP-levels (30,2±39,1 mg/l) and normal levels of calcium (2,32±0,21 mmol/l), 25-OH-vitamin-D3 (20,0±10,3 ng/ml) and PTH (25,6±10,9 ng/l), with a tendency towards low osteocalcin-levels (5,7±3,1 ng/ ml, reference 5-12). Histomorphometric parameters of IBD-patients were as follows (reference value of healthy young adults in parenthesis): 0,73±0,29microm (0,75). Osteopathy in IBD may be caused by a reduced calcium and vitamin-D resorption, the systemic action of inflammatory cytokines and the effect of corticosteriod treatment on bone. The normal levels of calcium, vitamin D and PTH in our patients do not support the hypothesis of a calcium deficiency as a main pathogenetic aspect. Small osteoid surface and low osteocalcin levels reflect a reduced bone formation, which is likely to be caused by the effects of corticosteriods on bone. In contrast, both the elevation of eroded surface and osteoclast-covered bone surface point to an increased bone resorption. According to our histomorphometric parameters, reduced bone formation and increased bone resorption seem to be characteristic features of osteopathy in patients with IBD
Type I alfa 1 collagen gene polymorphism is associated with bone density, muscle strength and susceptibility for fractures in elderly women.
No full textPrognosis of very young breast cancer patients
No full textThe relation between age of breast cancer patients at presentation and prognosis remains a matter of debate. Despite this controversy, more aggressive systemic treatments are claimed for younger patients. The population consisted of 1285 patients, which were divided in three age groups: (A) under the age of 35 (n = 63), (B) between 36 and 49 (448) and (C) older than 49 years (774). Clinical and pathological parameters, known to be related to prognosis, were recorded prospectively between 1983 and 1996 and related to the site of recurrence, disease free survival and survival. 41,27% of the patients from group A had recurrent disease compared to 25,7% for older patients (p=0,01). Confounding prognostic parameters were diameter, TNM-classification, location of the tumor within the breast, type of treatment and nodal status. However, these prognostic parameters did not explain why young patients did worse. The diameter of the tumor was even smaller with a mean of 2,49 cm within group A, compared to 2,74 and 3,21 cm for groups B and C respectively (p=0,001). Although the rate of locoregional relapse was identical in the three age groups, the younger age group had significantly more and earlier systemic recurrences (p=0,017). Overall survival was 73,53 (A), 84,65% (B) and 72,76 (C – p=0,004) at 5 years of follow-up. No prognostic parameter was significantly related to the risk of recurrence or survival. Younger breast cancer patients under the age of 35 have a significantly higher and earlier systemic recurrence compared to older age groups. This translates in a decreased survival 3 to 8 years after diagnosis. This poor prognosis can neither be explained nor predicted by routine clinical and pathological prognostic parameter
Routine clinical prognostic parameters do not explain the outcome of very young breast cancer patients
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