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Biomedical subjects

A A MacKinney

Publications and source records attributed to A A MacKinney.

At least 19 recordsLinked to original sources
PubMed1994

On teaching bedside diagnostic and therapeutic procedures to medical students: an annotated bibliography of audiovisual materials.

OBJECTIVE: The teaching of procedures that involve risk of pain or morbidity deserves special care. The author set out to develop a teaching program for medical students to ensure quality control of bedside diagnostic and therapeutic procedures. DESIGN: A bibliography of available videotapes and related audiovisual teaching materials on 15 common bedside procedures was assembled following requests for materials from all U.S. medical schools. Audiovisual materials from nine institutions were reviewed. SETTING: Medical schools and teaching institutions. PARTICIPANTS: Medical schools and libraries. MAIN RESULTS: Seventy-three percent (24/33) of responding schools had no visual material on the procedures. There was ten times more material on physical diagnosis than on bedside procedures. About 20 videotapes were reviewed in an annotated bibliography. Some videos contained valuable insights on how to make good teaching materials. A set of criteria for quality videotapes is listed. CONCLUSIONS: Considerable work needs to be done to develop audiovisual materials and curricula for teaching bedside procedures. Videotape is a valuable medium for introducing procedures and ensuring uniformity of technique. After reviewing all available videotapes, the author decided that videotapes should be the initial part of a multidimensional program for teaching procedures.

Audiovisual Aids↗
PubMed1993

Simultaneous demonstration of the Philadelphia chromosome in T, B, and myeloid cells.

A patient presented with lymphoblastic lymphoma in lymph-nodes and chronic myelogenous leukemia (CML) in narrow and peripheral blood. All marrow and unstimulated peripheral blood cells contained the Philadelphia chromosome[t(9:22)]. Lymphoma cells were analyzed by flow cytometry and were identified as T cells (CD2+CD5+CD7+CD34+). All fresh lymphoma cells contained the t(9:22) translocation. Cultures of purified peripheral blood T and B cells and specifically stimulated NK cells revealed that 59% of the B cells, 10% of the NK cells, and none of the normal T cells contained the translocation. The lack of translocation in normal peripheral T cells is attributed to their long lifespan. No rearrangement of immunoglobulin or T cell receptor beta or gamma genes was found in either the leukemia or lymphoma cells. Analysis of the DNA from cryopreserved lymphoma biopsy showed clonal rearrangement within the common breakpoint cluster region of the bcr gene identical to the bcr rearrangement in DNA from leukemia blood cells. The data support the concept that T and B cells originate in the patient's totipotent stem cell from which the CML is also derived.

Antigens, CD↗
PubMed1988

The effect of diphenylhydantoin and cortisol on the cell cycle.

Normal human lymphocytes cultured in the presence of phytohemagglutinin were blocked in G0G1 when diphenylhydantoin (DPH) or cortisol 3.6 X 10(-4) M was added at the beginning of culture. The suppression of culture growth was analyzed by flow cytometry and confirmed by [3H]thymidine incorporation and mitotic rate analysis. The correlation of these measurements with flow cytometry was good for DNA synthesis and excellent for mitosis. There was an additive effect on the G0G1 retention of cells when both drugs were present in the culture. These data may partially explain the suppression of cell-mediated immunity which occurs in DPH-treated patients.

Cell Cycle↗
PubMed1986

Diphenylhydantoin inhibits cortisol-induced lysis of thymocytes.

Diphenylhydantoin (DPH) shares two features with cortisol: immunosuppression and cleft palate formation. We tested the hypothesis that DPH would have effects on lymphocytes in vitro similar to those induced by cortisol, and the corollary that DPH would inhibit those cortisol effects. We found that DPH lysed rat thymocytes, although at higher concentrations than cortisol. When combined, DPH inhibited cortisol lysis of thymocytes. Neither drug lysed human phytohemagglutinin (PHA)-stimulated cells, but both drugs depressed DNA and RNA syntheses in PHA cells. DPH augmented cortisol inhibition of DNA and RNA syntheses in PHA cells and DNA synthesis in rat thymocytes. It had no effect on cortisol inhibition of RNA synthesis in rat thymocytes. It appears that DPH has a cortisol-like action (lysis of rat thymocytes). The actions of this drug enable us to show that cortisol lysis and the inhibition of DNA or RNA synthesis can be associated. These phenomena may explain some immunosuppressive effects of DPH in the human.

Animals↗
PubMed1984

1-Acetyl-3-acetoxy-5'5-diphenylhydantoin has colchicine-like activity.

1-Acetyl-3-acetoxy-5'5-diphenylhydantoin (Ac-DPH) is a synthetic derivative of diphenylhydantoin with unusual properties: 1) it inhibits microtubular polymerization and depolymerizes established microtubules; 2) it blocks colchicine binding and displaces colchicine from microtubular protein, although it bears no resemblance to colchicine; and 3) it does not arrest human lymphocytes in metaphase, in contrast to diphenylhydantoin or its metabolite, 5-(4-hydroxyphenyl)-5-phenylhydantoin (HPPH).

Animals↗
PubMed1982

A comparison of diphenylhydantoin metabolism in different tissues using high performance liquid chromatography.

We have quantified diphenylhydantoin metabolism in vitro using high performance liquid chromatography. Five metabolites from rat liver post-mitochondrial supernates were assayed (in order of concentrations): pHPPH, dihydrodiol, pHPPHglucuronide, mHPPH, and an unknown. Catechol was rarely identified and 3-0-methyl catechol was not found. Induction of DPH metabolism by phenobarbital, beta-naphthoflavone, and DPH was studied. While phenobarbital increased synthesis of all the products, beta-naphthoflavone decreased DPH metabolism. DPH itself stimulated only dihydrodiol formation. Studies of dog liver showed that microsomes were more efficient metabolizers of DPH than post-mitochondrial supernatants, with predominance of mHPPH over pHPPH. This finding differed from that with rat liver. Rat thymus lymphocytes and cultured human peripheral blood lymphocytes converted less than 1% of DPH and yielded HPLC profiles indistinguishable from cell-free blanks.

Animals↗
PubMed1978

Cytosine arabinoside modulation of the mitotic index in treatment of adult acute leukemia.

Twenty-three unselected adult acute leukemic patients were treated with an initial intravenous pulse of cytosine arabinoside (Ara-C) 5 mg/kg. The mean mitotic index dropped from 7.7/1,000 to 2.8/1,000 at 4 hours after Ara-C pulse and rebounded to 6.7/1,000 at 18 hours. Infusions of Ara-C 7--10 mg/kg were given for 9 or 12 hours, depending on changes in the mitotic index. The group of responders (M1 or M2 marrows) could be predicted by the initial blast count in the marrow and the change in the mitotic index 18 hours after the Ara-C pulse. There were 9 (39%) complete and partial remissions. Six patients remained in remission more than 200 days. Since the changes in the mitotic indices induced by Ara-C were indistinguishable from those of another more successful trial, we infer that factors other than modulation of the cell cycle are critical to the success of this mode of therapy.

Acute Disease↗
PubMed1978

Age and treatment response in acute nonlymphoblastic leukemia.

Treatment of older acute leukemia patients has been the subject of recent debate. We treated 101 acute leukemia patients in a prospective randomized trial. Fifty-seven per cent of the population was over 50. Half were treated with a mild induction program (VAMP) and half with a vigorous program (CAT). The older patients who received vigorous treatment did better than those who received mild treatment. We suggest that patients over 50 should be regarded as a separate category in design of treatment protocols in order to further maximize the benefits of therapy.

Age Factors↗
PubMed1978

Effect of aging on the peripheral blood lymphocyte count.

Analysis of 1684 inpatient and 884 outpatient peripheral blood counts revealed the following: (1) The absolute lymphocyte count declines sharply from 5000/microletre to 2000/microletre in the first two decades, remains constant for three decades, then declines at an accelerated rate beginning in the 40s, to reach 1500/microletre at age 90. (2) The absolute granulocyte count does not show age-dependent variation, remaining essentially constant throughout life. (3) The values of absolute lymphocytes are indistinguishable for ambulatory or hospitalized subjects except for higher absolute lymphocyte counts in hospitalized children in the first decade. (4) The data support other evidence for declining cellular and humoral immunity in aging man.

Adolescent↗
PubMed1978

Hydantoin drugs inhibit polymerization of pure microtubular protein.

5,5-Diphenylhydantoin or 5-(4-hydroxyphenyl)-5-phenylhydantoin, 3.6 X 10(-4) M, inhibited polymerization of purified pig brain tubulin 50% as measured by viscosometric assay and estimation of tubulin length by electron microscopy. 5,5-Diphenylhydantoin did not bind to the low molecular weight fraction of tubulin or to guanosinetriphosphate; it displaced colchicine weakly from its binding site. 5,5-Diphenylhydantoin did not depolymerize established microtubules, indicating that it differs from colchicine in site and mode of action.

Animals↗
PubMed1978

Morphologic effect of hydantoin drugs on mitosis and microtubules of cultured human lymphocytes.

A new class of mitotic inhibitors is described. Diphenylhydantoin and 5-(4-hydroxyphenyl)-5-phenylhydantoin (HPPH), its metabolite, increase the mitotic index of cultured human lymphocytes without affecting the second resting phase (G2). Mitotic inhibition by these compounds is time dependent, and not a property of hydantoins in general. HPPH proved to be more potent than diphenylhydantoin. Electron micrographs of HPPH-treated human lymphocytes showed changes in 45% of the cells in metaphase: a decrease in microtubules or the appearance of 100 A microfilaments. These changes resemble those induced by colchicine.

Cells, Cultured↗
PubMed1975

The effect of parahydroxylation of diphenylhydantoin on metaphase accumulation.

DPH has a colchicine-like action on metaphase arrest of cultured human lymphocytes. The first step in detoxification of DPH increased its power to accumulate metaphases 3-fold. This hydroxy derivative [5-[4-hydroxyphenyl]-5-phenylhydantoin, HPPH] 3.6 X 10(-4) M was equivalent colchicine 1 x 10(-5) M in its power to inhibit metaphase completion. The effect of HPPH on mitosis was reversible; colchicine effect was not reversed and vincristine effect was partially reversed by washing drug from the medium. Hydroxylation of DPH did not change its inhibition of DNA synthesis and enhanced inhibition of protein synthesis to a minor degree. Detoxification increased the colchicine-like action of DPH.

Cells, Cultured↗
PubMed1975

Comparison of five radioimmunoassays and enzyme bioassay for measurement of digoxin in blood.

Digoxin-containing sera from 86 patients were analyzed for this drug by bioassay and radioimmunoassay. Each serum was analyzed in duplicate by six procedures: inhibition of Na+-K+-dependent ATPase and five "kit" radioimmunoassays from four different commercial sources. Mean values for two of the radioimmunoassays differed significantly from those for the bioassay. One radioimmunoassay mean value was significantly different from the other five mean values. We conclude that normal values for digoxin radioimmunoassay should be determined for each kit, and should not be adopted from published data.

Adenosine Triphosphatases↗