Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.1.1.69 (BMT)
 2,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The (NZW x BXSB)F1 (W/BF1) mouse is known to be an animal model of systemic lupus erythematosus (SLE) and immune thrombocytopenic purpura (ITP). These mice produce not only anti-DNA antibodies but also anti-platelet antibodies, resulting in decreased platelet counts. They show a high level of proteinuria, increased white blood cell (WBC) counts, hypertension, and myocardial infarction due to the high levels of anti-cardiolipin antibodies. When W/BF1 mice (4-5 months) were lethally irradiated and then reconstituted with T cell-depleted bone marrow cells of normal BALB/c mice (8 weeks), 60% of the mice survived more than one year. The WBC and platelet counts in the mice were normalized, and the levels of anti-DNA and anti-platelet antibodies decreased. The renal dysfunction was also ameliorated as indicated by a lower level of proteinuria, lower levels of serum creatinine (S-CRTN) and blood urea nitrogen (BUN), and by improved histology. The blood pressure (BP) of the treated W/BF1 mice decreased due to the improved renal functions. In contrast to the non-treated W/BF1 mice which died of myocardial infarction or renal failure by the age of 7 months, the treated W/BF1 mice showed no evidence of myocardial infarction even one year after BMT. This was due to the lower cardiolipin levels.
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PMID:Effect of bone marrow transplantation on antiphospholipid antibody syndrome in murine lupus mice. 778 96

We compared the efficacy of three dual and two triple therapies for eradication of Helicobacter pylori (HP), and evaluated the influence of smoking and omeprazole pretreatment on HP eradication. 220 patients with proven HP infection (histology and 13C-urea breath test [UBT]) were randomly allocated to one of the following regimes: BMT (bismuth subsalicylate 600 mg t. i. d. for 28 days, metronidazole 400 mg t. i. d. and tetracycline 500 mg q. i. d. for ten days). OA (omeprazole 40 mg o. d. and amoxicillin 750 mq q. i. d. for 14 days), OC (omeprazole 40 mg o. d. and clarithromycin 500 mg b. i. d. for 14 days), OT (omeprazole 40 mg o. d. and tetracycline 500 mg q. i. d. for 14 days), OMC (omeprazole 40 mg o. d., metroinidazole 400 mg t. i. d. and clarithromycin 250 mg b. i. d. for seven days). Eradication was defined as negative UBT six weeks after completion of the therapy. In an "all-patients-treated" ("per-protocol") analysis, the eradication rates were: BMT, 91% (93%); OA, 84% (90%); OC, 74% (74%); OT, 24% (24%); and OMC, 90% (93%). Smoking impaired the success of OA and OT (p < 0.05), but the efficacy of the triple regimens was not affected. Omeprazole pretreatment did not influence eradication rates. Thus, highest eradication rates were achieved with the two triple therapies tested. However, OA, given at a daily antibiotic dose of 3 g amoxicillin for 14 d, was also highly effective. After failure of triple therapy, OA was successful in seven of ten patients (70%). The efficacy of OC was lower than that of the triple therapies (p < 0.05). In conclusion, metronidazole- and clarithromycin-based triple therapies are highly effective first line therapies. OA, given at a dose of 3 g per day over 14 days, should be considered as a possible second line therapy, e.g. in retherapy after failed triple therapy.
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PMID:Dual versus triple therapy: comparison of five antibiotic regimens for eradication of Helicobacter pylori in a prospective, randomized study. 979 9

Thrombotic thrombocytopenic purpura(TTP) is a multisystem disorders characterized by thrombocytopenia, microangiopathic hemolytic anemia associated with red cell fragmentation, and neurological and renal symptoms. Plasma of patients with TTP has been shown to contain unusually large von Willebrand factor(vWF) multimers that may cause platelet agglutination in vivo. Recently, a metalloprotease responsible for cleavage of vWF multimers has been isolated from normal human plasma and was found to be deficient in some patients with TTP. We examined the activity of the vWF-cleaving protease(vWF-CP), by modified Furlan's method, in plasma from patients with a familial TTP, 3 acquired TTP, 4 thrombotic microangiopathy(TMA) and 2 veno-occlusive disease(VOD) associated after allo-BMT. Diluted plasma samples of patients were incubated with protease-free vWF purified from normal human plasma, in the presence of urea and barium ions. The extent of vWF degradation was assayed by electrophoresis in SDS-agarose gels and immunoblotting. Activity of vWF-CP from 12 normal plasma have been shown as 77-180%(average 115%), whereas, no vWF-CP(below 5%) was observed in plasma from familial TTP, before and after plasma exchange, although FFP infusion therapy has been effective for this patient to recover thrombocytopenia. In 3 acquired TTP, 2 patients showed lack of vWF-CP activity in plasma, and inhibitors against vWF-CP have been elucidated by plasma cross-mixing test. After extensive plasma exchange and FFP infusion followed by corticosteroid therapy, normal vWF-CP was recovered in plasma from 2 acquired TTP patients. Among BMT patients, plasma from 4 BMT-TMA showed normal vWF-CP activities as 55-111%, whereas plasma from 2 BMT-VOD revealed low vWF-CP activity, as 24% and 37%, respectively. Thus, measurement of vWF-CP is crucial to predict differentiation of primary forms of TMA to establish the pathogenesis in varied endothelial dysfunction.
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PMID:[Measurement of plasma von Willebrand factor cleaving protease in patients with varied thrombotic microangiopathy]. 1288 37

INK4A/ARF mutations are acquired in bcr/abl(+) lymphoid blast phase chronic myelogenous leukemia (CML) and bcr/abl(+) acute lymphoblastic leukemia (ALL). Donor lymphocyte infusion and graft-versus-leukemia (GVL) are generally ineffective in such ALLs, whereas GVL is highly active against bcr/abl(+) CML, which does not have a lesion in the INK4A/ARF locus. The mechanisms for the ineffectiveness of GVL are not fully known, and it is possible that intrinsic resistance of acute lymphoid leukemias to immune effectors associated with allogeneic GVL may contribute to ineffectiveness. This work tested the hypothesis that INK4A/ARF mutations that are associated with transformation of bcr/abl(+) CML to an ALL phenotype, and that are associated with increased resistance to apoptosis render ALL cells insensitive to allogeneic immune responses to minor histocompatibility antigens (mHA). Murine acute pre-B ALLs were induced by transfer of the human p210 bcr/abl gene into bone marrow of INK4A/ARF null mice. These ALL lines were then studied in a murine model of MHC-matched, mHA-mismatched allogeneic BMT. In vivo growth of these ALLs was inhibited in allogeneic transplants characterized by active allogeneic immune responses compared to their behavior in syngeneic transplants. In vitro ALLs with INK4A/ARF, p210 bcr/abl, or p190 bcr/abl mutations remained sensitive to anti-mHA cytolytic T cells. In addition, the ALLs were capable of inducing primary immune responses to mHAs in vivo. Thus, ALLs with INK4A/ARF or bcr/abl mutations are not intrinsically resistant to allogeneic T cell responses, suggesting that active immunotherapies against mHA have the potential to control such acute lymphoblastic leukemias.
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PMID:High-risk acute lymphoblastic leukemia cells with bcr-abl and INK4A/ARF mutations retain susceptibility to alloreactive T cells. 1848 87