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D Straus

Publications and source records attributed to D Straus.

8 recordsLinked to original sources
PubMed1992

High incidence of disseminated intravascular coagulation during remission induction of adult patients with acute lymphoblastic leukemia.

We determined the incidence and complications of disseminated intravascular coagulation (DIC) at presentation and during remission induction of previously untreated adults with acute lymphoblastic leukemia (ALL) or de novo Philadelphia chromosome-positive ALL (PCALL) seen at Memorial Hospital between January 1, 1978 and December 31, 1989. DIC was diagnosed in the presence of (1) low fibrinogen (less than or equal to 160 mg/dL), (2) prolonged prothrombin time (PT) and falling fibrinogen, or (3) prolonged PT and positive fibrin split products (FSP). L-Asparaginase was not used during remission induction. Among adequately screened patients with ALL, DIC was detected in 7 of 58 (12%) before initiation of chemotherapy and in 35 of 45 (78%) during remission induction. DIC was not simply the result of infection because clinical and laboratory signs of infection were absent in 16 patients, whereas only 2 of the 22 febrile patients with DIC had positive cultures. Among the 38 patients with DIC at presentation or during remission induction, serious complications were seen in 13 in temporal association with DIC (pulmonary embolus in one, sagittal sinus thrombosis in three, and serious hemorrhage in nine) and were major factors in the deaths of three patients. Among the 10 patients with thorough screening but no evidence of DIC there was only one hemorrhage during the same time interval. In patients with PCALL, DIC was detected in 9% at presentation and in 80% during remission induction. We conclude that DIC is rare at presentation but common during remission induction of adult ALL and PCALL and may be associated with significant thrombotic and hemorrhagic complications. We suggest daily screening for DIC during the first 14 days of remission induction. The treatment of DIC in ALL and PCALL should be a subject of future clinical studies.

Adult↗
PubMed1979

Studies in acute leukemia. I. Antibody-dependent and spontaneous cellular cytotoxicity by leukemic blasts from patients with acute nonlymphoid leukemia.

Leukemic blasts from patients with acute nonlymphoid leukemia were examined for the presence of Ig, receptors for IgGFc, and for their capacity to mediate antibody-dependent cellular cytotoxicity (ADCC) against chicken red blood cells (RBC) coated with IgG and spontaneous cell-mediated cytotoxicity (SCMC) against cells of K562 cell line. Leukemic blasts from acute myeloblastic leukemia (AML) patients lacked both Fc receptors and Ig on their surface, had no SCMC activity and majority, but not all of them, lacked ADCC activity. Leukemic blasts from patients with acute monocytic leukemia (AMOL) had Fc receptors, and 50% had IgG on their surface. IgG was cytophilic and appeared not to be directed against cell-surface antigens. This antibody did not interfere with the ADCC activity of leukemic cells. Leukemic blasts from majority of patients with AMOL mediated ADCC, but had no SCMC activity. An association between ADCC and presence of Fc receptor was observed.

Adult↗
PubMed1977

Cell marker analysis in acute monocytic leukemias.

Leukemic cells from nine cases of acute monocytic leukemia (AMoL) were characterized by multiple differentiation markers. Cells in most cases were phagocytic, carried an Fc receptor, and stained positively for alpha-naphthyl acetate esterase but negatively for naphthol AS-D chloroacetate esterase. However, subtle differences in marker expression were observed which suggested different degrees of leukemic cellular maturation or activation. Cell marker analysis proved to be a useful adjunct to conventional morphology in confirming the diagnosis and the recognition of the neoplastic cells in AMoL, and may ultimately provide insight into the functional state of these cells.

Esterases↗
PubMed1977

Enhancement of carrier-mediated transport after immunologic activation of peritoneal macrophages.

Immunologically activated peritoneal macrophages from inbred mice and Hartley strain guinea pigs demonstrate a markedly greater than normal transport of 2-deoxy-D-glucose and L-leucine. The degree of nutrilite transport enhancement was greatest when animals were injected with the appropriate eliciting antigens before harvesting and also, if antigen was included in the tissue culture medium during the initial hours of in vitro culture. Enhanced hexose and amino acid uptake could also be achieved by exposure of macrophages from nonimmunized animals for 48 hr to supernatants of sensitized splenic lymphocyte cultures incubated with specific antigens. The animal systems in which this phenomenon was observed included CBA/J and C57BL/6J mice immunized with Staphylococcus aureus or sub-lethal doses of Listeria monocytogens, and the Hartley strain, albino guinea pig immunized with S. aureus or BCG. In all cases, immunization resulted in a state of delayed hypersensitivity as measured by skin testing or footpad swelling. Splenic cell supernatants contained lymphokines as detected by the presence of macrophage inhibitory factor (MIF), and by the supernatants' capacity to stimulate incorporation of 14C-glucosamine by macrophages in vitro. No increase of glucose or leucine transport by macrophages was observed in the absence of appropriate antigen stimulation in vivo or in vitro. We previously showed that a phagocytic stimulus results in a significant increase in hexose transport by normal macrophages; leucine transport by these same cells was unaltered after phagocytosis. In contrast, immunologically activated macrophages do not transport measurably more 2-deoxy-C-glucose after particle ingestion; activation or the phagocytic stimulus enhance 2-deoxy-C-glucose uptake to approximately the same extent. Analysis of nutrilite transport kinetics revealed that immunologic activation of macrophages increases the initial velocity (V1) and Vmax but does not change the Km values of hexose or amino acid transport. The kinetics of transport by the immunologically activated macrophages do not change measurably after phagocytosis. We conclude that either immunological activation or phagocytosis results in augmented 2-deoxy-D-glucose transport via identical or related mechanisms and that transport of the sugar can't be increased above that level induced by either event. The reasons why immunologic activation increases both glucose and leucine transport but phagocytosis increases only the former are not yet understood.

Animals↗
PubMed1976

Uptake of diphtheria toxin and its fragment A moiety by mammalian cells in culture.

Evidence suggesting that diphtheria toxin reaches the cytoplasm of susceptible mammalian cells by two independent mechanisms is presented. A schematic model describing the two processes of toxin entry into the cell is developed. One process of toxin uptake considered to by physiologically significant is passage of the protein toxin through the plasma membrane. This most likely happens by binding of fragment B to receptors on the membrane and by subsequent toxin-membrane interaction so that ultimately fragment A, the enzymatically active moiety, is transported tothe cell interior. This process, which ultimately leads to cessation of protein synthesis and cell death, involves a comparatively small number of toxin molecules. A second mechanism of toxin uptake is by classical pinocytosis. The majority of toxin taken into the cell is accomplished by this process. The fate of toxin taken into HEp-2 cells via pinocytosis is proteolysis by lysosomal enzymes. Thus, such vesicle-bound toxin is ordinarily not expressed biologically. Evidence suggesting that ammonium chloride provides total protection to diphtheria toxin-susceptible cells by preventing entry of toxin by the specific receptor-associated process is also provided; data showing that the ammonium salt immobilizes bound toxin on the plasma membrane of HEp-2 cells are presented. Finally, it is suggested that actively endocytic cells such as guinea pig macrophages interact with toxin in a significantly different manner than do nonphagocytic cells.

Ammonium Chloride↗