No abstract

The isolation and establishment in vitro of a hitherto undescribed type of lymphocyte designated D.G.-75 is reported. The original inoculum was derived from the pleural effusion of a child with a primary abdominal lymphoma, which clinically and histologically resembled Burkitt's lymphoma. In addition to the absence of the EBV genome and EBV receptors, this line possesses a number of other properties which distinguish it from previously described lymphoblastoid cell lines. It has different growth characteristics and morphology; does not form EAC or E rosettes (representative of B and T) cell surface markers, respectively); possesses IgM-kappa immunoglobulins on the cell surface (B lymphocyte), has an unusually high cap-forming ability and low agglutinability with fluorescent concanavalin A. One homologue of the No.14 chromosome pair possesses extra chromatin material as revealed on chromosome banding. This abnormal chromosome marker is similar to that described in biopsies and cultured tumor cells from patients with African Burkitt's lymphoma.

No abstract

Rosenthal, Dreskin and Rosenthal (1953) described a familial haemorrhagic disorder due to plasma thromboplastin antecedent (PTA) deficiency. Further studies have established the properties of this factor and its action in the early phase of thromboplastin generation (Rosenthal, 1954; Rosenthal, Dreskin and Rosenthal, 1955; Ramot, Angelopoulos and Singer, 1955; Campbell, Mednikoff and Dameshek, 1957; Cavins and Wall, 1960). The mode of hereditary transmission of this deficiency has been discussed by various authors (Cavins and Wall, 1960; Campbell et al., 1957; Rosenthal et al., 1955). Recently Rapaport, Proctor, Patch and Yettra (1961), using a quantitative assay of PTA, suggested that this deficiency is transmitted by an intermediate gene, which produces major PTA deficiency in the homozygote and minor PTA deficiency in the heterozygote. In the present communication, 10 families with PTA deficiency will be described and the mode of its inheritance will be discussed.

In order to determine the efficacy of the antifibrinolytic agent tranexamic acid (TA) in reducing bleeding and platelet transfusions during the treatment of acute myeloid leukemia (AML), we conducted a randomized placebo-controlled double-blind study. Patients with AML undergoing induction or postremission consolidation chemotherapy were randomized into TA or placebo groups. Patients were not given platelet transfusions prophylactically but only when bleeding occurred. The severity of any bleeding event was scored. Thirty eight patients were randomized during induction. There were no significant differences between the two groups in the number of bleeding events and their severity or in the number of platelet transfusions given. Eighteen patients were studied during consolidation. In contrast, to the induction period, during consolidation there was a significantly less severe bleeding tendency in the TA group resulting in a lower platelet transfusion requirement [3.7 +/- 4.1 vs. 9.3 +/- 3.3 platelet units (p < .05)]. TA was well tolerated and no side effects were seen and no specific thromboembolic events were noticed. We conclude that giving TA during the thrombocytopenic period of AML patients undergoing consolidation chemotherapy is beneficial and safely reduces platelet transfusions.