Search PubMed⌕ Search

Biomedical subjects

A Gorski

Publications and source records attributed to A Gorski.

28 records · Page 2Linked to original sources
PubMed1986

Abnormal B-cell function in hemophiliacs treated with cryoprecipitate and factor VIII and IX concentrates.

B-Cell function was evaluated in a group of 43 patients with factor VIII or factor IX deficiency. Thirty had been treated primarily with cryoprecipitate and 13 with concentrates of factor VIII or IX. Serum immunoglobulin G levels were found to be diffusely elevated; however, the absolute number of mature B cells in peripheral blood was normal. B-Cell function as measured by testing mitogen-induced proliferation and and immunoglobulin secretion by plaque-forming cells (PFC) in vitro was reduced. Coculture experiments suggested that these abnormal B-cell responses might be secondary to increased suppressor T-cell activity, which was found more frequently in patients seropositive for antibody to lymphadenopathy-associated virus. Both seronegative and seropositive patients had reduced responses in the proliferative and PFC assays, but the lowest PFC responses occurred in the seropositive group.

Adolescent↗
PubMed1984

Inhibition of human B lymphocyte differentiation by a stable metabolite of cyclophosphamide (ASTA Z 7557, INN mafosfamide).

We have evaluated the immunosuppressive effect of a new stable derivative of cyclophosphamide (ASTA Z 7557) on human lymphocyte immunoglobulin biosynthesis in vitro. When graded amounts of the drug are added to lymphocyte cultures stimulated with the helper T cell-dependent activator (PWM), a marked inhibition of B cell proliferation and differentiation occurs. Lymph node cells are particularly sensitive to the drug, while splenocytes are relatively resistant. The agent exerts only a minor effect on immunoglobulin synthesis triggered by a direct B cell stimulant (S. paratyphi bacteria).

B-Lymphocytes↗
PubMedDate not supplied

Increased mRNA expression of transforming growth factor beta in the arterial wall of chronically rejected renal allografts in humans.

INTRODUCTION: Transforming growth factor beta (TGF-beta) has an established role in interstitial damage of renal transplants during chronic rejection (CR). However, its involvement in transplant vasculopathy is not clear. The aim of the study was to assess TGF-beta gene expression in the walls of large-caliber arteries within chronically rejecting renal allografts. We evaluated associations between gene expression of this factor and intimal thickness or clinical data. MATERIAL AND METHODS: Renal artery samples of kidney allografts were obtained from 20 hemodialysis patients with end-stage renal graft disease due to CR, who were undergoing graftectomy. The control group included 32 hemodialysis patients with end-stage renal disease, undergoing nephrectomy due to autosomal dominant polycystic kidney disease (n = 12), chronic pyelonephritis (n = 13), or kidney limited tumor (n = 7). Gene expression of TGF-beta was measured using real-time PCR. RESULTS: TGF-beta mRNA expression was 3.25-fold higher in CR than in control patients (P < .001). Expression of mRNA for this cytokine was not influenced by the following factors: intimal thickness; age; serum cholesterol, triglycerides and glucose; BMI; graft survival; time of dialysis before transplantation; total ischemic time; immunosuppressive regimen; incidence of acute rejection episode; panel reactive antibodies; and period of dialysis before graftectomy. TGF-beta is involved in neointimal formation in CR.

Adult↗