[Alveolar echinococcosis of the liver. New data. I. Biological and clinical study].
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Biomedical subjects
Publications and source records attributed to G Rifle.
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Donor-specific antibodies may play an important role in the development of chronic allograft rejection process. However, the mechanisms leading to intimal vascular proliferation and fibrosis remain poorly understood. The aim of this study was to examine whether donor-specific HLA antibodies induce overexpression of tissue factor (TF) by endothelial cells. HLA typed human umbilical vein endothelial cells (HUVEC) were incubated for 1 to 12 hours with LPS (10 microg/mL), and increasing concentrations (1 to 500 microg/mL) of anti-HLA A1 antibody specific for an antigen expressed by HUVEC and of an anti-HLA A2 antibody for which A2 was not expressed by the HUVEC. Expression of TF mRNA transcripts was quantified using real time Q-RT PCR and TF activity was tested in cell lysates of cultured HUVEC using a chromogenic TF activity assay. HUVEC-specific anti-HLA A1 antibody at low concentrations (10 microg/mL) induced both a significant increase of TF mRNA transcripts after 1 hour of incubation and TF activity after 3 hours incubation compared to incubation with medium alone or with the nonspecific anti-HLA A2 antibody (n = 4 for all experiments, P < .05). These data show for the first time that specific anti-HLA antibody can induce overexpression of TF on endothelial cells. TF, a transmembrane glycoprotein involved not only in the onset of the coagulation cascade, but also in cell proliferation and anti-apoptotic processes, may play a role in the development of alloantibody-induced chronic rejection.
The place of plasma exchange in treating systemic lupus erythematosus remains to be discussed. Currently available clinical data suggest that PE may be a useful additional therapy only in certain subsets of some severe lupus manifestations such as CNS involvement, crescentic glomerulonephritis, and lupus vasculitis. Using PE could also be of interest in certain manifestations of the anti-phospholipid syndrome. The conflict between the rapid improvement seen in some biological abnormalities (circulating immune complexes, ds-DNA antibodies) and the lack of obvious parallel clinical benefits remains a field of stimulating investigation. Next to plasma exchange associated with conventional corticosteroid or immunosuppressive therapies, other approaches could be of value such as the synchronization of plasma exchange and cyclophosphamide pulses, or the selective removal of assumed pathogenetic antibodies or immune complexes. Insufficient data are presently available to interpret the results of the former. The latter methods could offer the advantage of more precisely establishing the role of selectively removed substances in the pathogenesis of SLE.
A case of retro-peritoneal lymphoid angio-follicular hyperplasia or Castleman's pseudo-tumour with normochromic hormocytic anemia and membrano-proliferative glomerulonephritis is reported in a 53 year-old man. Since the first description by Castleman in 1954, 259 other cases have been published. The anatomo-clinical study of our observation and of 198 cases collected in the literature bears out 3 types of clinical forms, according to the location of the pseudo-tumour: mediastinal, superficial and abdominal. The first ones generally asymptomatic are the most frequent whereas the last ones, less common, are often associated with biological abnormalities. In spite of these differences such neoformations present the same morphologic features. They are round or ovoid and well delimited by a capsule. Under this capsule a lymphoid vascular tissue surrounds follicules with central capillaries or arterioles. When plasma cells infiltrate the stroma, perturbations such as anemia or hypoalbunemia appear. Besides a nephrotic syndrome has been discovered in our observation and in that of Humpherys. In all the cases the removal of the pseudo-tumour induces the retrogression of the biological abnormalities and of the nephrotic syndrome. Neither a recidive nor another location of the disease are noticed later on. This evolution is probably the fact of a benign hyperplatic process which grows after an antigenic stimulation.
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By analogy with desmoid tumours, tamoxifen has been used in the treatment of idiopathic retroperitoneal fibrosis. The authors report the 6th case of retroperitoneal fibrosis treated by tamoxifen alone, which had not recurred 11 months after stopping treatment.
Low grade CLL/SLL can evolve to a spectrum of various morphologic higher grade malignancies showing Reed-Sternberg like cells. The evolution towards Hodgkin's disease is rare but frequently associated with the presence of scattered RSL cells within the small lymphocyte proliferation of the CLL/SLL. The evolution towards a Richter's syndrome is more frequent and it can exhibit CD30 positive Reed-Sternberg like cells. In these Richter's syndrome cases, regarding the morphology and the phenotype, it seems likely that there is a spectrum of lesions between true HD and large cell NHL. In the present study, the authors report two cases of transformation of CLL/SLL in non immuno-suppressed patients; one evolved to a morphological and immunohistochemical Hodgkin's disease and the second to a NHL (Richter's syndrome) with numerous Reed-Sternberg like cells. In both cases, EBV has been detected within RSL cells by immunohistochemistry and in-situ hybridization (ISH). So, the role of EBV is suggested in that kind of transformation.