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Biomedical subjects

M Karon

Publications and source records attributed to M Karon.

At least 19 recordsLinked to original sources
PubMed1984

Post-traumatic subdural hygromas: observations concerning a surgical enigma.

Four per cent (38) of 881 head injured patients developed known subdural hygromas. Their times of onset and course were variable. However, only two large hygromas seemed clinically significant. Hygromas were more frequent when intracranial pressure monitors were placed, possibly due to opening of the arachnoid, particularly if intracranial pressure was low. But, of course, monitors were only inserted in more severely injured patients. The use of Richmond bolts to drain subdural hygromas in a controlled fashion while monitoring intracranial pressure is suggested.

Adult↗
PubMed1981

Three-dimensional subgross morphology of the human endometrium.

A method is described for subgross, structural assessment of endometrial configuration. Human uteri from autopsy and surgical pathology were preserved in formalin and sectioned at 1-mm intervals. A procedure for staining, dehydration, and clearing was developed to achieve three-dimensional resolution of endometrial morphology. Processed specimens were sealed in translucent heavy plastic bags for the purpose of storage, easy manipulation under the dissecting microscope, and for photographic documentation. For simultaneous comparison with standard histological preparations, selected areas of sealed specimens were punched-out and paraffin sections made. This simple method can easily be applied to the future investigation and classification of focal premalignant, dysplastic, anaplastic, and atypical changes in the endometrium. The significance of this approach and its possible application to specimens obtained at dilatation and curettage is discussed.

Endometrium↗
PubMed1979

Evaluation of intramuscular versus intravenous administration of L-asparaginase in childhood leukemia.

A study was done to evaluate intramuscular versus intravenous administration of L-asparaginase in childhood leukemia. The results of this study demonstrate that the intramuscular method of administering L-asparaginase is as effective, but less toxic, than the intravenous method for children with advanced leukemia. The utilization of L-asparaginase in the initial induction of children with lymphoblastic and undifferentiated leukemia should be investigated. Its addition to the standard inducing agents may increase the percentage and ease of remission without significantly increasing toxicity.

Asparaginase↗
PubMed1977

L-Asparaginase, vincristine, and prednisone for induction of first remission in acute lymphocytic leukemia.

L-Asparaginase was added to vincristine and prednisone for induction of first remission in 815 children with acute lymphocytic or acute undifferentiated leukemia. This combination resulted in an overall remission rate of 93%. The addition of L-asparaginse to the standard induction regimen using prednisone and vincristine did not significantly increase the morbidity or mortality rate during the induction period. The most common side effect was transient L-asparaginase-induced hyperglycemia. The safe administration of L-asparaginase i.m. and the dose efficacy of 6000 I.U./sq m were confirmed. For these reasons, L-asparaginase should be combined with vincristine and prednisone for the initial induction of children with acute lymphocytic or acute undifferentiated leukemia.

Adolescent↗
PubMed1976

Effect of adriamycin on DNA, RNA, and protein synthesis in cell-free systems and intact cells.

The effect of adriamycin on DNA, RNA, and protein synthesis was investigated in cell-free systems and intact cells. In studies with purified mammalian cell enzymes, adriamycin produced a greater inhibition of DNA-dependent DNA polymerase than of RNA polymerase. The extent of inhibition of both these enzymes was decreased by increasing the concentration of the DNA template in the reaction mixture. In studies with isolated nuclei, adriamycin was also a more potent inhibitor of DNA synthesis than RNA synthesis. However, with intact cells, adriamycin inhibited both DNA and RNA synthesis to about the same extent. The inhibition produced by adriamycin on RNA synthesis in intact cells was greater than that observed in the cell-free systems. Adriamycin inhibited protein synthesis in a cell-free system consisting of polyribosomes, transfer RNA, and enzymes but did not inhibit protein synthesis in intact cells. These differences in the pattern of inhibition may be due to biotransformation of the drug and/or preferential binding to chromosomal DNA in the intact cell.

Binding Sites↗
PubMed1976

Detection of bacterial endotoxin in antitumor agents.

The Limulus amebocyte lysate assay was used to detect the presence of bacterial endotoxin in a variety of chemotherapeutic agents currently in use. Results were quantitated using a standard Escherichia coli endotoxin curve. Relative concentrations of endotoxin ranging from 0.1 to 63 ng/ml were detected in individual lots of L-asparaginase, 5-azacytidine, bleomycin, DTIC, actinomycin D, adriamycin, and vinblastine diluted to normal concentrations for injection. When multiple lots of a given drug were tested, at least one lot produced a negative assay, indicating less than 0.1 ng/ml of endotoxin in 50% of these drugs. All lots of cytosine arabinoside, cyclophosphamide, daunorubicin, vincristine, and streptozotocin tested had less than 0.1 ng/ml of endotoxin. Inactivation kinetics of the Limulus-positive drug material in dilute alkali solutions were identical to those of E. coli endotoxin. The Limulus lysate test is a rapid and specific method for the detection of small amounts of bacterial endotoxin contaminating parenteral preparations of antitumor agents.

Animals↗
PubMed1975

The treatment of acute childhood leukemia: predictions for the future based on extrapolations from the past.

Further progress in the treatment of acute leukemia involves a careful assessment of host and disease factors in each child and the selection of a therapeutic regimen which interacts with these factors to provide the maximum chance for survival. For some children, this therapy can be carried out in the community by expertly trained hematologist-oncologists; for others, the best treatment will involve clinical research at a center. Such a general approach has the best chance of fulfilling the optimistic survival projections made by the President's Cancer Panel in 1973 for acute lymphocytic leukemia.

Brain Neoplasms↗
PubMed1975

Intensive chemotherapy as primary treatment for rhabdomyosarcoma of the pelvis.

Twenty-six cases of childhood rhabdomyosarcoma involving the pelvis were treated at Childrens Hospital of Los Angeles between 1950 and 1972. The median survival of 17 patients treated up to 1970 was 6 months. Of a group of 9 patients treated with intensive chemotherapy (ICG) prior to surgery and/or x-ray therapy, 5 are surviving from 12 to 60 months and have a relative survival rate of 4.5 times that of the mixed therapy group (MTG) (p = 0.01). Deaths have occurred only in patients with Stage IV disease. The use of preoperative chemotherapy with or without x-ray therapy followed by local surgical excision when necessary can be as effective in prolonging the survival of children with pelvic rhabdomyosarcoma as those obtained with more traditional approaches; this limitation in use of surgery is likely to preserve the quality of life, should the child live to adulthood.

Adolescent↗
PubMed1975

Inhibitory effects of mitogens on adenoidal lymphocytes in vitro.

Cultures of human adenoidal lymphocytes exposed briefly to either phytohemagglutinin (PHA), Staphylococcus filtrate (Staph-F), concanavalin-A (Con-A), or pokeweed mitogen (PWM) incorporate increased amounts of thymidine earlier than replicate cultures exposed continuously to the mitogens. These effects can begin in the first 24 hr of culture and are seen maximally between 36 and 72 hr. Once a blastogenic response is established, PHA or PWM can diminish that response. Inhibition with PWM requires that the initial stimulation was with this mitogen, while PHA can inhibit blastogenesis to both PHA and PWM-stimulated cells. Because these mitogens can have a paradoxical effect on adenoidal lymphocytes, being capable of both initiating and inhibiting DNA synthesis, this phenomena should be kept in mind when such systems are utilized for the evaluation of antigens and drug effects.

Adenoids↗
PubMed1975

BCG in the treatment of acute lymphocytic leukemia.

Children with acute lymphocytic leukemia, who were in remission after induction with prednisone and vincristine and consolidation with intravenous methotrexate, were randomized into three groups receiving (1) no further therapy, (2) BCG, and (3) chemotherapy with biweekly methotrexate and monthly prednisone and vincristine. Children continuing in remission after 8 mo on chemotherapy in group 3 were rerandomized into three similar groups, i.e., no therapy, BCG, and chemotherapy. In the primary randomization, the median duration of remission was identical in the groups receiving no therapy or BCG, (4 and 4.3 mo respectively), and both were significantly less than the median duration of remission on chemotherapy which had not been reached prior to secondary randomization at 8 mo. Results of secondary randomization were similar to those of primary randomization. As used in this study, BCG was ineffective in prolonging drug-induced remissions either early in remission or when the leukemic cell population might have been further reduced after 8 mo of maintenance chemotherapy.

Adolescent↗
PubMed1975

Cellular phosphorylation of 1-beta-D-arabinofuranosylcytosine 5-azacytidine with intact fibrosarcoma and leukemic cells.

The phosphorylation of 1-beta-D-arabinofuranosylcytosine (ara-C) and 5-azacytidine (5-aza-C) by A(T1)C1-3 hamster fibrosarcoma cells and L5178Y murine leukemic cells was studied, using intact cells. The cellular phosphorylation of both these nucleoside analogs appears to follow Michaelis-Menton kinetics. The apparent Km value for ara-C in the fibrosarcoma and leukemic cells was about 40 muM, whereas the apparent Km values for 5-aza-C in these cells were about 1.3 and 0.41 mM, respectively. Deoxycytidine and cytidine were found to be potent competitive inhibitors of the phosphorylation of ara-C and 5-aza-C, respectively, ara-C and 5-aza-C were found to be weak competitive inhibitors of the phosphorylation of deoxycytidine and cytidine, respectively. A clone isolated from the fibrosarcoma cells that was partially resistant to the cytotoxic effects of ara-C exhibited a higher Km value for both ara-C and deoxycytidine than the wild-type fibrosarcoma cells.

Animals↗
PubMed1975

In vitro biochemical and cytotoxicity studies with 1-beta-D-arabinofuranosylcytosine and 5-azacytidine in combination.

The effect of 1-beta-D-arabinofuranosylcytosine (ara-C) and 5-azacytidine (5-aza-C), alone and in combination, on DNA synthesis and cytotoxicity in hamster fibrosarcoma cells has been studied. After a 2-hr exposure of S-phase cells to ara-C at concentrations of 2 to 200 muM, the cells required about 4 to 6 hr to recover from inhibition of DNA synthesis. When 2 exposures to ara-C were used, maximal cytotoxicity occurred when the 2nd dose of ara-C was administered at the time when the cells recovered from the inhibition of DNA synthesis. When the S-phase cells were exposed to ara-C, the maximal killing effect of 5-aza-C occurred when this agent was administered 6 hr later, at the time when the cells had recovered from the inhibition of DNA synthesis. When S-phase cells were exposed to 5-aza-C, the maximal cell kill produced by ara-C also occurred 5 to 6 hr later. When the S-phase cells were exposed simultaneously to both ara-C and 5-aza-C, significant antagonism with respect to cytotoxicity was observed between these 2 agents. When cells in G1 were exposed to 5-aza-C, the cytotoxicity produced by ara-C on these cells when they entered S phase was additive with respect to the cytotoxicity produced by 5-aza-C exposure alone.

Antineoplastic Agents↗