Search PubMed⌕ Search

Biomedical subjects

A M Miller

Publications and source records attributed to A M Miller.

At least 91 records · Page 5Linked to original sources
PubMed1982

Training health professionals in the care of the elderly.

Twenty-seven projects for the development of interdisciplinary geriatric curricula were supported by the Health Resources Administration's Bureau of Health Professions in fiscal 1979. A variety of clinical training sites were used (e.g., university gerontology centers, VA medical centers, senior citizen facilities, adult health care centers), and innovative teaching approaches were developed. For example, a combined medical/dental/optometry clinic is conducted by students at the three professional schools; medical students accompany volunteers serving Meals on Wheels; and dental students treat patients in nursing homes in a mobile dental unit. Students have gained insights into the problems of the elderly and the roles of other health professionals through the interdisciplinary-team training courses. Nurse-practitioner programs to prepare nurses to provide primary health care to the elderly were also supported by the Bureau, as were special projects to develop short-term in-service basic training programs for nurses' aides and orderlies in nursing homes, to upgrade the skills of the paraprofessionals who care for the elderly. In other projects, the geriatric educational needs of pharmacy students were assessed, and dental schools promoted remote-site training to improve access to dental care for the elderly.

Aged↗
PubMed1982

Nitroso-chloramphenicol: cell cycle specificity of action.

We have examined the ability of the nitroso derivative of chloramphenicol (NO-CAP) to inhibit subsequent growth of logarithmically growing or plateau phase cell cultures after short-term drug exposure. Raji cells taken from log growth cultures exhibited complete inhibition after 6-hour preincubation with 2-3 x 10(-5)M NO-CAP, while similarly treated cells taken from plateau populations demonstrated 90-100% of expected growth on replating. Flow-cytometric studies indicate that the irreversible effects of NO-CAP are greatest as cells proceed into and through the DNA synthetic portion (S phase) of the cell cycle.

Cell Cycle↗
PubMed1982

Purification of human granulocyte-macrophage progenitor cells (CFU-C) using indirect immunofluorescence and cell sorting.

We have attempted to purify human bone marrow granulocyte-macrophage progenitor cells utilizing purified stimulating factor, indirect immunofluorescence and cell sorting. These cells can be labelled by sequential incubation with colony-stimulating factor (CSF), rabbit anti-CSF antibody and fluorescently labelled goat anti-rabbit gamma globulin. Flow photometry demonstrated that binding of CSF to marrow cells varied with CSF concentration and duration of incubation. Marrow cells were pre-concentrated by incubation with carbonyl iron followed by Percoll gradient centrifugation and then labelled by this indirect immunofluorescence method. Sorting of these cells yielded up to 95-fold purification of colony-forming cells and fractions containing in excess of 10% colony- and cluster-forming cells.

Bone Marrow Cells↗
PubMed1981

Control of hepatitis B infection. The role of surveillance and an isolation hemodialysis center.

A 3 1/4-year study assessed intervention approaches for hemodialysis-associated hepatitis. A 12-month retrospective study was followed by one year of prospective surveillance (during which attention to hygienic techniques was encouraged) and then by a 15-month period during which antigen-positive cases were transferred from study centers to an isolation hemodialysis center (IHL). The incidence of hepatitis B infection (HBI) fell 35.9% in study centers during surveillance; this was followed by a 50.0% drop during the IHC phase. The total 67.9% drop during the entire study period was statistically highly significant; the IHC contributed significantly more to the total drop than did surveillance alone. At comparison units, HBI increased 97.9% during the same period. This study indicates that HBI incidence can be markedly reduced by a combination of surveillance and assignment of antigen-positive patients to a separate dialysis unit.

Communicable Disease Control↗
PubMed1981

Immunological and functional differences between human type I and II colony-stimulating factors.

Two distinct types of colony-stimulating factor (CSF) have recently been described in human tissues and cultured cell lines. Antisera to purified type I and II CSF were prepared in rabbits. Anti-CSF I antibody inhibits CSF I, but has no effect on CSF II. It cross-inhibits CSF I from several other human sources, but does not inhibit CSF from mouse lung or mouse L cells. Anti-CSF II antibody inhibits the activity of CSF II, but has no effect on CSF I. A radioimmunoassay for CSF I has been established. Competitive binding assay further demonstrated the immunological differences between CSF I and II. When CSF II is used to stimulate human marrow cells fractionated by sedimentation velocity, two populations of CFU-C are separated, one sedimenting at 8 mm/h and forming colonies by day 7, and a second sedimenting at 6.8 mm/h and forming colonies by day 13. In contrast, CSF I does nt stimulate colony growth by day 7 but does do so by day 13 in cells sedimenting between 7.2-8.5 mm/h. These results indicate that CSF I and II are distinct in their biochemical, immunological, and functional properties.

Antigen-Antibody Complex↗
PubMed1980

Mechanisms of levamisole-induced granulocytopenia in breast cancer patients.

Five of 39 (13%) women treated with adjuvant combination chemotherapy plus levamisole immunotherapy after mastectomy for Stage II or III breast cancer developed levamisole-induced granulocytopenia. This complication occurred in each of the women between six and ten weeks after the completion of six months of combination chemoimmunotherapy when they were taking levamisole alone. Although none of the patients had an HLA B-27 locus and leukoagglutinins could not be demonstrated, complement-dependent, IgM mediated, peripheral destruction of granulocytes was documented using a microgranulocytotoxicity assay. In addition, a factor(s) present in serum from patients developing levamisole-induced granulocytopenia caused suppression of bone marrow granulocyte progenitor cells (CFU-C). The possible relationships between levamisole-induced peripheral granulocyte destruction and bone marrow CFU-C suppression are discussed.

Acute Disease↗
PubMed1980

An evaluation of 99Tcm-labelled HIDA in hepatobiliary scanning.

99Tcm-labelled HIDA administered intravenously is promptly taken up by the liver and excreted into the bile duct and gallbladder. In this study the use of this agent in hepatoscintigraphy was evaluated. Thirty patients with a variety of hepatobiliary pathology were studied. After an overnight fast 2 mCi of 99Tcm HIDA were given intravenously and the patient was scanned continuously for 1 h. A rapid outline of the liver and biliary tract was usually obtained and the T 1/2 of the tracer in the blood stream was 20 min. In total obstructive jaundice, isotope was excreted through the renal tract without visualization of the liver. Hepatoscintigraphy was compared with conventional radiographs and ultrasonography in 19 patients presenting an emergencies with suspected hepatobiliary disease and was found to be comparable to the latter modes of investigation. In the jaundiced patients hepatoscintigraphy was inferior to percutaneous transhepatic cholangiography and to ultrasonography. No adverse side effects have followed the use of the radiopharmaceutical.

Adolescent↗
PubMed1980

Heterogeneity of human colony-forming cells (CFUc) with respect to their sensitivity to chloramphenicol.

Human granulocyte-macrophage progenitor cells (CFUc) fractionated by velocity sedimentation at unit gravity exhibit heterogeneity with respect to inhibition by the drug chloramphenicol (CAP). An inverse correlation is observed between sedimentation velocity and sensitivity to CAP, e.g., increasing sensitivity with decreasing velocity. This heterogeneity is not a result of protection by endogenously produced colony stimulating factor since the same result obtains after removal of adherent cell populations. This heterogeneity in CFUc sensitivity to CAP may be a determining factor on the variability of bone marrow suppression by the drug.

Cell Separation↗
PubMed1980

Antibody to purified human colony-stimulating factor: use in the identification and isolation of granulocyte macrophage progenitor cells.

Conditioned media prepared from human lung, placenta, peripheral leukocytes, cultured human pancreatic carcinoma cells, and cultured cervical carcinoma cells exhibit a common pattern of two distinct types of colony-stimulating factors (CSF) separable by isoelectrofocusing. Type I and type II CSF differ in MW, isoelectric point, CFU-C specificity, and the morphologic type of colonies they stimulate. Type I CSF exhibits higher activity in mouse than in human marrow while type II is more active in human marrow. Type I and II CSF from cultured human pancreatic carcinoma have been purified, type I to apparent homogeneity, and antibody has been prepared against them in rabbits. We have utilized purified CSF and anti-CSF antibodies to label CFU-C fluorescently for the purpose of cell sorting via flow photometry. Human bone marrow cells preincubated with CSF and then treated first with anti-CSF antibody then fluorescein-labeled goat antirabbit globulin retain their ability to grow and form aggregates in the presence of additional CSF. Colonies thus formed exhibit fluorescence, the intensity of which diminishes with increase in aggregate size. These observations provide new insight into the biology of CFU-C and suggest the following: (1) Incubation of marrow cells with CSF for 2 h results in binding of CSF or an antigenic component of CSF to membranes of CFU-C. (2) Bound CSF-anti CSF complex remains on CFU-C membranes through at least 5-6 cell divisions. (3) The approach described offers great potential for the preparation of highly purified CFU-C populations by fluorescence cell sorting.

Antibodies↗
PubMed1980

Nitroso-chloramphenicol: possible mediator in chloramphenicol-induced aplastic anemia.

We compared the effects of CAP and its nitroso derivative on DNA synthesis, CFU-C growth, and cell viability in human bone marrow and on mouse CFU-S viability in vitro. As previously reported from this laboratory, CAP inhibited DNA synthesis only when used in high concentrations (greater than 3 x 10(-4)M), and the inhibition was largely reversible. It also caused a reversible concentration-dependent inhibition of CFU-C growth but did not affect marrow cell viability. In sharp contrast, nitroso-CAP inhibited DNA synthesis in much lower concentrations and caused irreversible inhibition of CFU-C growth and cell death at 5 x 10(-5)M as well as irreversible mouse CFU-S damage. In a rapidly growing human lymphoid cell line, nitroso-CAP caused accumulation of cells in the G2M phase and increasing cell death within the arrested population. We have postulated from these and other observations that CAP-induced aplastic anemia occurs in the predisposed host who provides the milieu for the transformation of the p-NO2 group of the drug to toxic intermediates.

Anemia, Aplastic↗
PubMed1978

In vitro evidence for genetically determined variations in marrow erythroid cell sensitivity to chloramphenicol.

The effect of chloramphenicol (CAP) was examined on the in vitro growth of CFU-E and CFU-C from four strains of mice: C57L/J, A/HEJ and their first generation hybrid LAF1, and the inbred strain C57BL/6J. The growth of marrow CFU-E from C57L/J and the hybrid LAF1 was inhibited by 82--96% at a CAP concentration of 10 microgram/ml compared to only 22--39% for CFU-E from A/HEJ and C57BL/6J. There was little difference in the degree of inhibition of CFU-C growth by CAP among the four strains, with that of C57L/J showing a slightly greater sensitivity to the drug. These results indicate a genetically-determined variation in the sensitivity of marrow erythroid cells to CAP.

Animals↗
PubMed1978

Heterogeneity of human colony-forming cells (CFU-C): differences in size, rate of colony formation, and responsiveness to colony-stimulating factor.

Human bone marrow cells have been fractionated by velocity sedimentation at unit gravity. Fractions were analyzed for cell morphology, number of nucleated cells and myeloid colony-forming cells (CFU-C's). Colony formation was assayed with the following CSF preparations: serum-free HLCM and two electrophoretically distinct CSF fractions (CSF-A and CSF-B) purified from the same source. Two distinct CFU-C populations were found. One, a rapidly sedimenting (7.2 to 8.0 mm/hr), population exhibited colonies after 7 days of culture in response to HLCM and CSF-A only. The second, a more slowly sedimenting (6.5 mm/hr) CFU-C peak, did not exhibit colonies until 11 days of culture and did so in response to all three CSF's tested. The results indicate that human bone marrow CFU-C's are heterogeneous and that the two purified CSF fractions from human lung have different CFU-C specificity.

Bone Marrow↗
PubMed1978

Modulation of granulopoiesis: opposing roles of prostaglandins F and E.

CSF-dependent myeloid colony growth can be augmented or inhibited by a number of modulating factors. PGs of the E series are known to inhibit colony formation. The antagonistic actions of PGE and PGF in many biological systems prompted us to compare their effects on myelopoiesis in vitro. PGF2alpha at an optimal concentration of 1 x 10(-9)M increased colony formation by 50% over that stimulated by CSF alone. Similar augmentation was also observed from 16,16-dimethyl PGF2alpha, PGF1alpha, 6-keto PGF1alpha, and MIX. In contrast PGE1, PGE2, and 15(S),15-methyl PGE1 inhibited colony growth. Simulation by PGF reflected an absolute increase in granulocytic colonies, whereas inhibition by PGE affected both granulocyte and macrophage colony formation. The relative levels of PGE and PGF may play a determining role in the modulation of granulopoiesis.

Animals↗
PubMed1977

Determination of an anti-inflammatory methanesulfonanilide in plasma by high-speed liquid chromatography.

A sensitive and chemically specific high-speed liquid chromatographic method was developed for the determination of 4-nitro 2-phenoxymethanesulfonanilide in plasma. The method includes selective extraction of the anti-inflammatory drug and an internal standard, 2-(4'-chlorophenoxy)-4-nitromethanesulfonanilide, into benzene from acidified plasma followed by reextraction into 0.2 N NaOH. The aqueous layer is acidified, and the drug is reextracted into benzene. The benzene is evaporated, and the residue is dissolved in a small volume of acetonitrile. A 10-microliter aliquot is analyzed on a reversed-phase column. The mean overall extraction recovery, after correction for aliquot factors, is 99%. The accuracy, expressed as the relative error, is 4, 0.3, and -3% at 0.60, 1.50, and 3.00 microgram/ml, respectively. Repeated analysis of reference standards indicates that the precision, expressed as the relative standard deviation, is 3% or less. The lower sensitivity limit is 0.2 microgram/ml with a 2-ml plasma sample. The method was applied successfully to the determination of plasma levels of 4-nitro-2-phenoxymethanesulfonanilide in humans and rats in metabolic experiments at pharmacological doses.

Animals↗