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Biomedical subjects

D L Becton

Publications and source records attributed to D L Becton.

At least 37 records · Page 2Linked to original sources
PubMed1988

Deferoxamine inhibition of human neuroblastoma viability and proliferation.

Patients with widespread neuroblastoma (NB) frequently have elevated serum ferritin levels, and recently anti-NB effects of the iron chelator deferoxamine (DFO) have been reported. We have investigated the effect of DFO on human bone marrow NB cells from two untreated children with Evans Stage IV disease. DFO treatment caused dose- and time-dependent cytotoxicity of NB cells, with maximal killing at exposure to 50 micron DFO for 72 h. Cytotoxicity was prevented by cotreatment with stoichiometric amounts of iron salts and reversible by removal of DFO or addition of iron salts within 48 h of treatment. Additionally, DFO inhibited clonal growth of human bone marrow NB cells in methylcellulose in a time- and dose-dependent manner. These effects were also prevented by cotreatment with iron salts. Thus, DFO has potent antitumor effects on human NB cells which appear to be related to iron deprivation. DFO should be considered for further preclinical evaluation as an anti-NB agent.

Bone Marrow↗
PubMed1988

An experience with an implanted port system in 66 children with cancer.

Totally implanted port catheter systems have a lower incidence of infection and are more easily used in home care that external catheters in adult cancer patients. Experience with this method in children has been limited. During the past 2 years, we have implanted 71 ports in 66 children with cancer. Our experience demonstrates an infection rate (0.15 episodes of bacteremia per 100 patient days) slightly lower than that reported for children with Broviac or Hickman catheters, but not as low as that seen in adults with implanted systems. Patients and families have been extremely satisfied with the devices. Our experience supports further use of implanted systems in children with cancer.

Adolescent↗
PubMed1988

Thrombotic thrombocytopenic purpura in an asplenic patient with hereditary spherocytosis: failure of plasmapheresis, antiplatelet therapy, and corticosteroids.

Thrombotic thrombocytopenic purpura (TTP) is a severe multisystem disorder characterized by microangiopathic hemolysis, central nervous system and renal dysfunction, and a very poor prognosis. Recently, however, plasma exchange or infusion therapy has proven effective in the majority of patients with TTP. We report a patient who developed TTP several years after splenectomy for hereditary spherocytosis. Despite aggressive therapy with plasmapheresis (PP), plasma infusion, antiplatelet drugs, and corticosteroids, the patient had progression of TTP that eventually resulted in his death. The occurrence of TTP in an asplenic patient with an intrinsic red cell disorder, a previously unreported association, may predict a poor prognosis.

Adrenal Cortex Hormones↗
PubMed1987

Treatment of lymphohistiocytic erythrophagocytosis with VP-16 and aziridinylbenzoquinone.

Lymphohistiocytic erythrophagocytosis (LE) is a usually fatal disease characterized by fever, organomegaly, hyperlipidemia, central nervous system involvement, and cellular immunodeficiency. Treatment with corticosteroids, cytotoxic chemotherapy, and blood exchange is unsuccessful. We have treated two children with the epipodophyllotoxin VP-16 and with intrathecal chemotherapy. Each patient had an initial complete response, and one remains in remission 36 months after therapy began. Aziridinylbenzoquinone (AZQ) therapy induced a complete response in a patient who relapsed during VP-16 therapy. A combination of VP-16 and intrathecal chemotherapy appears to be the most effective therapy for LE, and further evaluation of the role of AZQ is indicated.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1987

Isolated vocal cord hematoma in a child with severe factor VIII deficiency.

We have reported the first case of isolated submucosal hematoma of the true vocal cord in a hemophilic patient. He was managed with factor VIII replacement therapy as an outpatient for five consecutive days, without complication. Similar but more serious cases usually require more aggressive intervention by the pediatrician and the otolaryngologist.

Acute Disease↗
PubMed1987

Bacterial endocarditis in a child with a Broviac catheter.

Broviac and Hickman catheters facilitate the care of children with cancer but provide a source of potential infection. We describe a child with a Broviac catheter who developed left-sided bacterial endocarditis in whom right-to-left atrial shunting was documented following catheter flushing. Following removal of the catheter and administration of prolonged intravenous antibiotics, recovery was complete and cardiac function returned to normal.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1987

Natural history of histiocytosis-X.

Histiocytosis-X can involve many organs and tissues in all age groups and in both sexes and occurs most often in caucasians. The signs and symptoms observed in the patient are directly related to the infiltration of Langerhans histiocytes, which compress or displace normal tissues and cause destruction of the tissues and organs involved. The disease tends to be benign and self-limiting when the involvement is limited to only one site. When more than one site is involved, the disease course can be chronic or acute. The chronic course tends to smolder for years, causing significant morbidity and disability but not death. The acute form tends to cause significant morbidity and early mortality.

Histiocytosis, Langerhans-Cell↗
PubMed1986

Analysis of deficiencies in IFN-gamma-mediated priming for tumor cytotoxicity in peritoneal macrophages from A/J mice.

The functional and biochemical responses of macrophages derived from the A/J mouse strain to IFN-gamma have been studied. As compared to macrophages obtained from C57BL/6 strain mice, cells from mice of the A/J strain are deficient in their response to IFN-gamma for acquisition of tumoricidal competence. This deficiency was not due to reduced expression of surface receptors for IFN-gamma or to altered affinity of the receptor for its ligand. IFN-gamma recently has been shown to enhance the potential activity of protein kinase C (PKc) and to modulate the efflux of intracellular Ca2+ in macrophages from C57BL/6 mice. Neither of these two biochemical changes were induced in macrophages derived from A/J mice. Functional competence could, however, be pharmacologically induced in both C57BL/6- and A/J-derived macrophages by combined treatment with an ionophore plus phorbol myristic acetate, which increase intracellular Ca2+ and stimulate PKc, respectively. Although the exact nature of the deficit in A/J strain mice has not been defined, the present findings indicate that it lies between the expression of receptor and the modulation of PKc activity and Ca2+ levels. Furthermore, the data provide support for the notion that these molecular changes are important components of the stimulus-response coupling process in IFN-gamma-mediated activation of macrophages.

Animals↗
PubMed1986

An infant girl with severe autoimmune hemolytic anemia: apparent anti-Vel specificity.

Autoantibodies directed against the common red-cell antigen Vel are unusual, with only 2 previous cases reported. This report describes an infant girl with steroid-resistant autoimmune hemolytic anemia whose serum contained an antibody with apparent specificity for Vel antigen. Transfusion with Vel-positive cells resulted in a massive hemolytic transfusion reaction. Survival of labelled Vel-negative cells was normal up to 8 h following transfusion, and no transfusion reaction followed subsequent use of Vel-negative cells. There was no evidence of a collagen vascular disease, an immunodeficiency syndrome, or a malignancy. Although rare, anti-Vel should be considered in unexplained autoimmune hemolytic anemia.

Anemia, Hemolytic, Autoimmune↗
PubMed1986

Severe Mycoplasma pneumonia in three sisters with sickle cell disease.

Mycoplasma pneumoniae, which usually causes mild infections in normal children, has been shown to cause isolated cases of severe pneumonia in children with sickle cell disease. We recently observed an outbreak of Mycoplasma pneumonia in three sisters with homozygous sickle cell disease. Two of them required hospitalization, and one progressed to respiratory failure requiring prolonged ventilatory assistance. All eventually recovered without long-term pulmonary complications. Familial outbreaks are not uncommon in Mycoplasma infection, but they have not been described previously in siblings with sickle cell disease. It is assumed that local or systemic host defense abnormalities predispose patients with sickling syndromes to more severe courses of Mycoplasma infections.

Anemia, Sickle Cell↗
PubMed1985

Interferon-gamma modulates protein kinase C activity in murine peritoneal macrophages.

The content of Ca2+-, phospholipid-dependent protein kinase activity (protein kinase C) in murine peritoneal macrophages treated with recombinant interferon-gamma (IFN-gamma) has been investigated. Protein kinase C activity was solubilized by nonionic detergent extraction of sonicated cells and separated by high performance liquid chromatography on a TSK 4000 SW gel filtration column. The enzyme eluted from the column in a molecular weight range of 60-80 X 10(3) and was identified by virtue of Ca2+ and phospholipid requirements. Macrophages treated with recombinant IFN-gamma exhibited a substantial increase in total protein kinase activity which could be accounted for entirely by increased protein kinase C activity. This activity was enhanced as much as 5-fold over that seen in untreated macrophages and was specific for IFN-gamma in that other agents known to signal changes in macrophage function had no effect. The time required for the elevation of kinase activity was identical to that required for induction of other functions by IFN-gamma in macrophages. These observations suggest that protein kinase C may be a focus of regulatory action in IFN-gamma-mediated macrophage activation.

Animals↗
PubMed1985

Characterization of protein kinase C activity in interferon gamma treated murine peritoneal macrophages.

Macrophage activation for tumoricidal and microbicidal functions can be achieved in part by treatment with recombinant interferon gamma (IFN gamma) in vitro. We have previously demonstrated that IFN gamma treatment of murine peritoneal macrophages results in a two- to five-fold increase in the activity of Ca++, phospholipid dependent protein kinase C (Hamilton et al., J. Biol. Chem., 260:1378, 1985). We now report that this effect was not dependent upon continuing protein synthesis since treatment with cycloheximide under conditions where normal protein synthesis was inhibited by greater than 95% had no effect upon the development of increased enzyme activity. Examination of Ca++ and phospholipid requirements revealed no differences between enzyme isolated from control or IFN gamma treated cells. Similarly, protein kinase C from control and IFN gamma-treated cells could not be distinguished in terms of the diacylglycerol (DG) or phorbol diester (PMA) concentration required for stimulation of activity. Kinetic analysis of the ATP (as substrate) concentration dependence revealed that both control and treated enzyme preparations (either basal or stimulated) had comparable Km values. Maximum velocity (Vmax) was increased both by IFN gamma treatment and also by stimulation with DG or PMA. The major difference which could be discerned between protein kinase C derived from control versus IFN gamma-treated macrophages was the magnitude of the response to DG or PMA; IFN gamma treatment increased the stimulation index (i.e., ratio of basal to stimulated activity) by a factor of two to four fold. These results suggest that IFN gamma treatment leads to reversible modulation of existing protein kinase C resulting in increased catalytic efficiency when exposed to an appropriate stimulant.

Adenosine Triphosphate↗