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Biomedical subjects

B Ramot

Publications and source records attributed to B Ramot.

At least 55 records · Page 3Linked to original sources
PubMed1990

Dental extraction for patients on oral anticoagulant therapy.

Dental extraction in patients receiving long-term oral anticoagulant therapy is a controversial issue. Continuation of anticoagulation exposes the patient to serious hemorrhage, whereas cessation of therapy increases the risk of thromboembolism. Forty patients treated by coumarin underwent 63 tooth extractions, without a change in the therapeutic protocol of anticoagulation. The biologic adhesive Beriplast was used successfully to achieve local hemostasis at the site of the surgical wound. Apart from one patient who had mild oozing, there were no incidences of postsurgical hemorrhage.

Administration, Oral↗
PubMed1990

Ultrasonic attenuation maps of liver based on a conventional B-scan and an amplitude loss technique.

The authors present a novel ultrasonic amplitude loss technique, using image processing techniques and designed for computation of local attenuation estimates. Three different estimation approaches were evaluated: the extended Prony, the maximum likelihood, and the least squares approaches. The latter two approaches were found to result in a much higher estimation error than that observed for the Prony method. The attenuation values in the normal population (49 subjects) were 0.44 +/- 0.03 dB/MHz/cm. Three hundred sixty-seven liver scans from 266 patients were evaluated. Hodgkin's lymphoma patients with liver involvement had attenuation values of 0.22 +/- 0.07 dB/MHz/cm. Low attenuation values also were observed for four patients with viral hepatitis (0.31 +/- 0.08 dB/MHz/cm). The detectability of other disease states was not increased by these global attenuation estimates; however, the results demonstrate possible potential uses for the proposed technique for the diagnosis of diffuse liver disease.

Adult↗
PubMed1990

Tranexamic acid therapy in acute myeloid leukemia: possible reduction of platelet transfusions.

We studied the clinical efficacy and safety of the antifibrinolytic drug tranexamic acid (TA) in patients undergoing chemotherapy for acute leukemia. 54 newley diagnosed AML patients were treated with 1 g of TA every 6 hours until the platelet count rose to above 20 x 10(9)/l. Platelet transfusions were given, irrespective of the count, only when oral, mucosal or significant skin bleeding manifestations were observed. During induction, the average number of days with thrombocytopenia below 20 x 10(9)/l was 14.4 +/- 7.4 and 4.6 +/- 4.1 transfusions were given in each course. During consolidation, the average number of thrombocytopenic days was 8.4 +/- 8.5 and only 1.7 +/- 1.8 transfusions were administered. In 11.5% of the induction and 32.1% of the consolidation courses, no platelet support was required. TA was tolerated very well and no side effects or thromboembolic complications were observed. Only in 6 of the 78 induction courses did a major bleeding event occur and there were none in any of the 53 consolidation courses. Thus it seems that TA therapy allowed a significant reduction in the use of platelet transfusions without submitting the patients to greater bleeding risks.

Acute Disease↗
PubMed1990

Effect of excess parathyroid hormone on human bone marrow fibroblasts.

Patients with uremia have excess levels of parathyroid hormone (PTH). It has been reported that excess PTH is associated with bone marrow fibrosis. The present study was undertaken to examine the in vitro effect of intact 1-34 PTH and the active 1-34 N-terminal fragment on human bone-marrow-derived fibroblasts. Proliferation of fibroblasts was not stimulated by PTH in concentrations present in uremia (5-30 U/ml) nor by uremic sera which contained either high or low PTH levels. The lack of stimulation contrasted with the activity of both PTH preparations in other systems, i.e., inhibitory to erythroid colonies and stimulatory to heart muscle cells.

Bone Marrow↗
PubMed1990

Is transfusion of fresh plasma after cardiac operations indicated?

Patients undergoing cardiac operations constitute the majority of recipients of fresh frozen plasma. In most centers the reason for transfusing fresh frozen plasma is to replace clotting factors. However, the decrease of clotting factors during cardiopulmonary bypass is not sufficient in most patients to cause abnormal bleeding. One of the major causes of nonsurgical bleeding after cardiac operations is acquired platelet dysfunction, which can be corrected by transfusion of 1 unit of fresh whole blood. Because plasmatic factors in fresh whole blood may be responsible for this improvement, a study was designated to evaluate the effect of transfusing fresh plasma on platelet function after cardiac operations. Forty patients undergoing cardiopulmonary bypass were randomized to receive either fresh plasma or the fresh packed cell fraction. Administration of packed cells increased platelet number (118 +/- 8.5 to 154 +/- 7.6 x 10(9)/L, p less than 0.05), shortened bleeding time (7.57 +/- 0.4 to 4.0 +/- 0.3 minutes, p less than 0.05), and improved platelet aggregation in response to collagen and epinephrine (32% +/- 4.7% to 50% +/- 5.6% and 37% +/- 5.8% to 50% +/- 5.8%, respectively, p less than 0.05). Fresh plasma, however, neither increased platelet number nor improved bleeding time or platelet aggregation. Each group later received the remainder of the blood unit, with similar results. The results suggest that improvement of platelet function in patients receiving fresh whole blood after cardiac operations is not related to plasmatic factors. Therefore the massive use of fresh frozen plasma in patients after cardiopulmonary bypass should be reconsidered.

Bleeding Time↗
PubMed1989

Immunoglobulin heavy chain gene rearrangements in chronic lymphocytic leukaemia: correlation with clinical stage.

A search for a correlation between the clinical stage of chronic lymphocytic leukaemia (CLL) and the pattern of immunoglobulin heavy chain gene rearrangements was undertaken. DNA samples from the leukaemic cells of 38 CLL patients were analysed by Southern blot hybridization. Using probes for the immunoglobulin heavy chain J (JH) and C mu regions a marked heterogeneity of the hybridization patterns was observed in both regions. The number of JH hybridization bands varied from one to four and more than two were found in 58% of the patients. In 42% of the patients no germline JH genes were found. One to three additional C mu bands were observed in 34%, but the germline was preserved in all samples. There was no correlation between the clinical stage and the number of hybridizing JH bands; however, a significant correlation was found between the loss of JH germline band or a C mu multiband pattern and advanced stage of the disease. The genetic events in the immunoglobulin genes observed in advanced CLL patients are assumed to result from clonal evolution and tumour progression.

Adult↗
PubMed1989

Effect in vivo of recombinant GM-CSF on neutropenia and survival in mice treated by high-dose melphalan.

High doses of melphalan cause severe neutropenia and may irreversibly damage hematopoietic stem cells. Treatment of mice with recombinant murine GM-CSF (GM-CSF) for 5 days immediately after 400 micrograms of melphalan did not prevent the severe neutropenia. However, GM-CSF accelerated the neutrophil recovery and reduced the mortality rate during the neutropenic period compared to melphalan-only treated mice. CFU-GM levels measured 6 d after melphalan treatment without GM-CSF were markedly reduced in the bone marrow while being elevated in the spleen. In comparison, GM-CSF further reduced the total CFU-GM population in melphalan-treated mice including the levels in the bone marrow and in the spleen. On d 14 after melphalan, the spleen regained its active CFU-GM production. By d 90, the number of circulating neutrophils, the number of bone marrow CFU-GM and splenic CFU-GM were the same in GM-CSF-treated and -untreated mice. The results suggest that GM-CSF could be used to shorten the neutropenic period and reduce mortality caused by a high dose of melphalan. Though this effect could be at the expense of a temporary reduction in CFU-GM population, GM-CSF did not induce more long-term damage to myelopoiesis than that already caused by melphalan alone.

Agranulocytosis↗
PubMed1989

A search for bcl1, bcl2, and c-myc oncogene rearrangements in chronic lymphocytic leukemia.

Three cellular or putative oncogenes: c-myc, bcl1, and bcl2 were previously found to be rearranged in some B cell malignancies due to chromosomal translocations. Data concerning the role of such genetic rearrangements in B-CLL are very scanty and limited to few cases in which bcl1 rearrangements were found. We studied DNA samples from 38 cases of B-CLL by Southern blot technique in order to find out the existence and frequency of such events. No bcl1 or bcl2 rearrangements were found in any of the studied cases; thus, involvement of these genes in CLL must be rare. In one patient who had an aggressive and resistant disease, c-myc rearrangement was found.

Adult↗
PubMed1989

Effect of alpha interferon on growth of leukemic and normal hematopoietic progenitors. Synergism with H2 histamine receptor antagonists.

We studied whether the histamine H2 receptor antagonist, cimetidine, potentiates antiproliferative effects of recombinant alpha interferon (IFN alpha) on in vitro clonal growth of certain normal and malignant hematopoietic cells. Cimetidine alone, at therapeutic serum concentrations, was not inhibitory to the cells studied. IFN alpha alone inhibited the growth of HL-60 leukemic cells only at concentrations greater than 1000 U/ml, whereas with cimetidine, inhibition was seen at greater than 1 U/ml of IFN alpha. The enhancing effect of cimetidine on IFN alpha inhibition of clonal growth was neutralized by histamine and was not seen with histamine H1 receptor antagonist. In HL-60 cells, cimetidine also increased the enzymatic activity of (2'-5')-oligoadenylate synthetase, induced by IFN alpha. The combination of cimetidine and IFN alpha had a synergistic inhibitory effect on the growth of leukemic granulocyte-macrophage colony-forming units (CFU-GM) from chronic myeloid leukemia patients, normal CFU-GM, and normal erythroid burst-forming unit (BFU-E) progenitors. These data suggest that cimetidine may play a role in overcoming resistance to IFN alpha therapy in leukemia, but may also increase IFN alpha hematopoietic toxicity.

2',5'-Oligoadenylate Synthetase↗
PubMed1988

Recombinant interferon alpha-C for advanced hairy cell leukemia. An Israeli multicenter study.

Thirteen patients with advanced hairy cell leukemia were treated with a new subspecies of interferon (IFN): recombinant IFN (rIFN)-alpha-C. The timing of the peripheral hematologic remission of individual blood elements was similar to that reported for other interferons, and 60% of patients attained a complete peripheral hematologic remission at 9 months. Two patients relapsed despite a good initial response to IFN. No anti-IFN antibodies could be detected in their sera. In vitro studies of colony formation from the peripheral blood of all responding patients showed that rIFN-alpha-C did not inhibit the growth of colonies but favorably affected the maturation of their elements towards monocytes, granulocytes, and erythroid elements. The relapsing patient examined initially experienced a similar beneficial in vitro response which paralleled his in vivo improvement. During relapse, rIFN-alpha-C inhibited both the colony formation and the myelomonocytic differentiation in the in vitro cultures. These findings may suggest that the acquired resistance to IFN in our patient could be due either to an acquired stem cell maturation arrest in response to IFN or to emergence of a new clone indifferent to IFN-alpha-C differentiation effect.

Age Factors↗
PubMed1988

Non-Hodgkin's lymphoma complicating acute lymphoblastic leukemia in remission.

Second malignancies occurring in patients cured of childhood acute lymphoblastic leukemia (ALL) are rare but increasingly recognized. There are only three reported cases of non-Hodgkin's lymphoma complicating ALL in remission. We report here another case of B-cell-type large-cell lymphoma, presenting in the uterus of a 24-year-old woman, 16.5 years after the diagnosis of ALL was made. Although immune markers of the ALL were not available, it was thought to be unlikely that the second malignancy was a relapse of the original tumor. Due to the long latency period and the minimal exposure to alkylating agents, the role of chemotherapy seems to be insignificant in this case. The development of a second malignancy could be a manifestation of the basic susceptibility to cancer.

Adult↗
PubMed1988

Late immune and haemopoietic functions in plasmacytoma-bearing mice cured by melphalan.

Alkylating agents can cause latent and permanent damage to the bone marrow. We compared the long term effects of melphalan on a number of immune and haemopoietic functions of plasmacytoma bearing BALB/c mice with that of normal mice treated with a similar dose of melphalan. The drug administered orally at a dose of 250 micrograms and 400 micrograms on day 14 and 24 following i.m. inoculation of MOPC-315 plasmacytoma cells resulted in cure of the mice. Their spleen cells showed a permanent impairment of MLR activity, T-cell number and IL-2 production as well as a mild suppression of NK activity for one year after cessation of melphalan therapy. The number of B cells was elevated. In contrast, plasmacytoma-free mice treated with melphalan retained long term normal immune functions, although shortly after melphalan therapy a temporary suppression was noted. On the other hand, melphalan was responsible for bone marrow myeloid stem cell damage since the number of myeloid progenitor cell (CFU-GM) colonies was reduced in both melphalan-treated groups compared to untreated normal controls. Plasmacytoma bearing mice had a shorter survival. These results demonstrate that some late sequelae of alkylating agents are not due to the drug alone; shorter survival and T-cell deficiency are related to the previous presence of the tumour.

Animals↗
PubMed1988

T-cell acute lymphoblastic leukemia with severe leukopenia: evidence for suppression of myeloid progenitor cells by leukemic blasts.

A patient with T-cell acute lymphoblastic leukemia presented with leukopenia due to neutropenia, no circulating blasts and normal hemoglobin level. Marrow leukemic T lymphoblasts inhibited in vitro normal CFU-GM colony growth and released an activity that stimulated normal BFU-E growth. This patient demonstrates that immature T cells may modify hematopoietic stem cell growth both in vitro and in vivo.

Adult↗