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J Bas

Researcher at University of Barcelona

Publications -  32
Citations -  2394

J Bas is an academic researcher from University of Barcelona. The author has contributed to research in topics: Transplantation & Immune system. The author has an hindex of 13, co-authored 31 publications receiving 2267 citations. Previous affiliations of J Bas include Bellvitge University Hospital.

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Goodpasture syndrome during the course of a Schönlein-Henoch purpura

TL;DR: The presence of an IgA linear pattern on the kidney biopsy specimen and circulating anti-glomerular basement membrane (GBM) IgA antibodies led to the diagnosis of Goodpasture syndrome, which implies the possibility that the well-known pulmonary involvement during the course of Schönlein-Henoch purpura could be caused by Good Pasture syndrome in certain cases.
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Lymphocyte populations in Parkinson's disease and in rat models of parkinsonism.

TL;DR: In this article, the involvement of the immune system in Parkinson's disease was assessed using the phenotype of circulating lymphocytes in 30 untreated and 34 treated patients, and they found a numeric decrease in helper T cells (higher in CD4+CD45RA(+) than in CD+CD29(+)) and B cells, and a rise in activated, CD4(+)CD25(+) lymphocytes that was correlated with lymphocyte depletion.
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Achieving Donor-Specific Hyporesponsiveness Is Associated with FOXP3+ Regulatory T Cell Recruitment in Human Renal Allograft Infiltrates

TL;DR: Reaching donor-specific hyporesponsiveness is feasible after renal transplantation and associated with Treg recruitment in the graft, suggesting that the recruitment of Tregs in the allograft plays an important role for renal acceptance.
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Lymphocyte immunophenotyping by flow cytometry in normal adults. Comparison of fresh whole blood lysis technique, Ficoll-Paque separation and cryopreservation.

TL;DR: Standard Ficoll-Paque separation and cryopreservation of mononuclear cells alter the measurement of lymphocyte subsets by flow cytometry, which increased the percentage of CD4+, CD19+ and CD4+CD45RA+ cells, as well as decreasing that of CD8+, and CD3+CD29+ cells compared to the fresh whole blood lysis technique.
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Hepatitis C virus-associated membranoproliferative glomerulonephritis in renal allografts.

TL;DR: In renal transplantation, chronic allograft nephropathy is the leading cause of long-term graft losses, transplant glomerulopathy being its glomerular form, and hepatitis C virus infection may be associated with type II cryoglobulinemia which may lead to membranoproliferativeglomerulonephritis.