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Biomedical subjects

H Amos

Publications and source records attributed to H Amos.

At least 19 recordsLinked to original sources
PubMed1998

Minority faculty and academic rank in medicine.

CONTEXT: Previous studies have found that fewer minority medical school faculty hold senior professorial ranks than do majority faculty and may not be promoted as rapidly. OBJECTIVE: To determine whether minority faculty were as likely as majority faculty to have attained senior rank (associate professor or full professor) after adjusting for other factors that typically influence promotion. DESIGN: A self-administered mailed survey of US medical school faculty using the Association of American Medical Colleges database. The sample was stratified by department, graduation cohort, and sex. PARTICIPANTS: A stratified random sample of 3013 full-time faculty at 24 representative US medical schools. All underrepresented minority faculty at these schools were sampled. MAIN OUTCOME MEASURE: Attainment of senior academic rank (associate professor or full professor). RESULTS: Of 3013 faculty surveyed, 1807 (60.0%) responded, including 1463 white (81.0%), 154 black (8.5%), 136 Asian (7.5%), and 54 Hispanic (3.0%). Overall, 980 faculty (54%) had attained senior academic rank, including 47 (30.5%) of 154 black faculty, 59 (43.4%) of 136 Asian faculty, 22 (40.8%) of 54 Hispanic faculty, and 852 (58.3%) of 1463 white faculty. White faculty had significantly more first-authored and total peer-reviewed publications than the other groups. After adjusting for the medical school, department, years as medical school faculty, number of peer-reviewed publications, receipt of research grant funding, proportion of time in clinical activities, sex, and tenure status, we found that the odds ratios of holding senior rank relative to white faculty were 0.33 (95% confidence interval [CI], 0.17-0.63) for black faculty, 0.36 (95% CI, 0.12-1.08) for Hispanic faculty, and 0.58 (95% CI, 0.30-1.12) for Asian faculty. CONCLUSIONS: Minority faculty were less likely than white faculty to hold senior academic rank. This finding was not explained by potential confounders such as years as a faculty member or measures of academic productivity.

Career Mobility↗
PubMed1985

Heat-shock treatment lethal for mammalian cells deprived of glucose and glutamine: protection by alpha-keto acids.

Nil and Nilpy hamster cells exposed to temperatures of 44 degrees C to induce the heat-shock proteins survive such exposure for 2 h or more when incubated in Eagle's Minimum Essential Medium with 10% undialyzed fetal calf serum. If D-glucose and L-glutamine are withdrawn from the medium during heat treatment, nearly all the cells are killed by as little as 20 min at 44 degrees C. Several alpha-keto acids, pyruvate, alpha-ketobutyrate, oxaloacetate, and alpha-ketoglutarate, protect cells from the lethal action of the heat treatment in the absence of D-glucose and L-glutamine. L-Glucose and D-glutamine are without effect. Efforts to reverse lethal effects have not been successful.

Animals↗
PubMed1984

Deprival of nicotinamide leads to enhanced glucose transport in chick embryo fibroblasts.

Chick embryo fibroblasts growing in medium free of pyridine ring precursors of NADH and NADPH replicate several times before multiplication ceases. The rate of glucose transport is progressively enhanced, finally reaching levels several times higher than those normally observed in cells severely depleted of NADH. Whereas normal cells respond to additional glucose by further reducing transport, the NADH-depleted cell is refractory to glucose even at five times the normal glucose concentration. Readdition of nicotinamide does little to restore normal transport within 24 h. On the other hand NAD+ or NADP+ provided simultaneously with glucose results in a sharp decline in measurable transport within 2-4 h. The role of the pyridine nucleotides in this reduction of transport function is for the moment unknown.

3-O-Methylglucose↗
PubMed1984

Hexose transport derepressed and refractory to purine regulation in NAD(H)-Depleted Nil cells.

Nil hamster fibroblasts depleted of NAD(H) by growth in medium devoid of nicotinamide (NAm-MEM) exhibit up to 2-3-fold higher rates of glucose transport. Derepression of glucose transport is observed only when Nil cells have become severely depleted of both intracellular NAD(H) and ATP, despite the continued presence of 5.5 mM D-glucose in the growth medium. Neither the initial rate of transport, approximated from 3-O-methylglucose uptake, nor accumulation of D-glucose itself is repressed upon restoring nicotinamide to the medium. Exposure of the cells to NAD+ (10(-5) M), however, leads to a sharp curtailment of transport within 2 to 3 hours. The purines, hypoxanthine and guanine, that sharply reduce glucose transport capacity of normal cells, have no significant effect upon transport activity of NAD(H)-depleted cells.

Adenosine Triphosphate↗
PubMed1984

Transaminase inhibitors block glycolysis and G1 to S phase progression in chick embryo fibroblasts: reversal by alpha-keto acids.

Two transaminase inhibitors, aminooxyacetate and cycloserine, inhibited the initiation of insulin-stimulated DNA synthesis in chick embryo fibroblasts. This inhibition was overcome when pyruvate (4 mM), oxaloacetate (4 mM), or alpha-ketobutyrate (10 mM) was included in the culture medium with hormone and inhibitor. Aminooxyacetate also inhibited lactate production in insulin-treated cultures in the absence of added alpha-keto acid.

Acetates↗
PubMed1983

Purines as 'hyper-repressors' of glucose transport. A role for phosphoribosyl diphosphate.

Under selected conditions the rate of glucose transport and the intracellular phosphoribosyl diphosphate (PPRibP) concentrations of chick-embryo fibroblasts are inversely correlated. This relationship holds when cells are incubated with mannose, fructose, xylose or various concentrations of glucose. The metabolic inhibitors 2,4-dinitrophenol, rotenone and Methylene Blue increased glucose transport and decreased PPRibP. The addition of any pyrimidine or purine base or ribonucleoside dramatically depleted PPRibP pools, regardless of the carbon source. Addition of guanine (10 microM) or hypoxanthine (100 microM) decreased transport in glucose-grown chick cells to barely detectable values, but did not affect increases observed in cells depressed by substitution of xylose for glucose. Guanosine, inosine and the purine analogues 6-thioguanine, 6-thioguanosine, 8-azaguanine and 6-methylmercaptopurine riboside sharply decreased transport in glucose-grown cells and blocked the increase in transport resulting from the replacement of glucose by fructose or xylose in the culture medium.

3-O-Methylglucose↗
PubMed1983

Reactivation of NAD(H) biosynthetic pathway by exogenous NAD+ in Nil cells severely depleted of NAD(H).

The culture of Nil hamster fibroblasts in MEM lacking nicotinamide (NAm-MEM) leads to: (1) the rapid loss of intracellular total nicotinamide adenine dinucleotide (NAD(H)) content in these cells from a level of 150-200 pmoles/10(5) cells to less than 20 pmoles/10(5) cells; (2) the cessation of cell division and inhibition of DNA synthesis; and (3) a reduction of glucose consumption and lactic acid production. In most situations, following nicotinamide starvation, the restoration of intracellular NAD(H) follows rapidly the readdition of NAD+ (oxidized), nicotinamide mononucleotide (NMN), nicotinamide, or nicotinic acid. Resumption of cell division occurs after only a lag of about 24 hours. Nil cells subcultured for three consecutive times in the absence of nicotinamide (3(0) NAm- cells) exhibit different behavior. These severely starved cells are incapable of quickly restoring their intracellular NAD(H) content to normal levels when provided with any pyridine ring compound except NAD+. One-hour exposure of such cells to NAD+ allows utilization of nicotinamide to rapidly restore intracellular NAD(H). This short incubation with NAD+ does not result in any significant restoration of intracellular NAD(H) or lead to the accumulation of an intracellular pool of some precursor. This function of NAD+ as a stimulatory signal to the NAD(H)-biosynthetic pathway in severely starved Nil cells is a previously unreported role of NAD+, and does not require protein synthesis.

Animals↗
PubMed1982

Counter-transport in chick embryo fibroblasts. A significant factor in measurement of glucose entry.

Enhanced rates of carrier-mediated 3-O-methyl-D-glucose (0.1 mM) transport were observed in primary cell cultures of chicken embryo fibroblasts deprived of glucose for 1 day. The addition of 5.5 mM-glucose, glucosamine or 2-deoxy-D-glucose for 15 min (37 degrees C) to glucose-starved cultures followed by washing and immediate measurement of 3-O-methyl-D-glucose transport resulted in an apparent further stimulation of transport. Transport stimulation increased with increasing concentrations of the added preincubation sugar and was observed at test concentrations ranging from 0.1 mM- to 10 mM-3-O-methyl-D-glucose. This enhancement occurred when the preloaded sugar was rapidly effluxing from cells and was eliminated by allowing cultures to incubate in buffer without sugar for 30 min (37 degrees C) after the removal of hexose and before measuring transport. A transient overshoot in the cumulative uptake of 3-O-methyl-D-glucose was observed in glucose-starved cultures that were pre-incubated in the presence of 55 mM-glucose or -glucosamine for 15 min (37 degrees C). These data suggest that counter-transport accounts for the apparent enhancement of glucose-transport capability observed in glucose-starved cells when they are briefly re-exposed to hexose.

3-O-Methylglucose↗
PubMed1982

Effects of pyruvate on the growth of normal and transformed hamster embryo fibroblasts.

The growth of NIL and NILpy hamster embryo fibroblasts was determined in the presence and absence of pyruvate as a component of the growth medium. It was demonstrated that NIL cells respond to the presence of pyruvate by decreasing cell doubling time, glucose utilization, glutamine utilization, and increasing lactate production with the effects being more pronounced at low inoculum densities. Polyoma-virus transformed NIL cells (NILpy) demonstrate none of the above effects upon pyruvate addition regardless of initial cell inoculum density.

Animals↗
PubMed1982

Starvation, deoxy-sugars, ouabain, and ATP metabolism in normal and malignant cells.

When starved of a carbon source, early passage normal cells such as chick embryo fibroblasts, human fibroblasts, mixed culture of splenic lymphocytes as well as "normal" cell lines (Nil or CHO cells grown as monolayer cultures) maintain their ATP levels for 8 to 24 h at essentially those characteristic of cells fed glucose. Several malignant or transformed cells (Py6, PyNil, Ehrlich ascites tumor cells, CHO cells in suspension and P388 lymphoblasts) exhibit a dramatic lowering in their ATP within a few hours of the removal of glucose. Normal cells exposed to 2-deoxy-D-glucose (2-DOG) in the absence of glucose lose ATP as rapidly as starved transformed cells. The loss of ATP by transformed cells on starvation is also accelerated by 2-DOG as is cell death. 2-deoxy-D-galactose (2-DOGAL) slows the loss of ATP in glucose starved transformed cells (growing as monolayer cultures) observed when the cultures are shifted to sugar-free medium. Finally, normal cells in culture are able to maintain both their ATP levels and their viability even after prolonged cultivation in a nutrient-free medium. Cultivation of malignant cells in a nutrient-free medium causes rapid loss in their ATP, a phenomenon not preventable by the presence of ouabain.

Adenosine Triphosphate↗
PubMed1981

Regulation of glucose utilization in chick embryo fibroblasts by bicarbonate ion.

The amount of glucose consumed by chick embryo fibroblasts in primary culture is strongly influenced by the presence of bicarbonate ion in the culture medium. Cells grown on glucose at physiologic concentration (5.5 mm) and in the absence of bicarbonate ion have a reduced rate of glucose utilization when compared to their counterparts cultivated in medium containing the usual 25 mM bicarbonate. The presence or absence of bicarbonate is without effect on chick embryo fibroblast proliferation over a 6-day growth period. Both lactic acid accumulation per mole of glucose consumed and the utilization of glutamine increase as a function of bicarbonate ion in the growth medium.

Animals↗
PubMed1979

Regulation of the G1 leads to S phase transition in chick embryo fibroblasts with alpha-keto acids and L-alanine.

Temporal inhibition of protein synthesis with cycloheximide prevents subsequent insulin, but not serum-stimulated DNA synthesis in G1-arrested chick embryo fibroblasts (CEF). The inhibition is measured by the incorporation of 3H-thymidine into acid insoluble material and confirmed by chemical estimate of the DNA content of inhibited and uninhibited cells. Cycloheximide treatment is without effect if the cell cultures are maintained at 4 degrees C while exposed to the drug. Several alpha-keto acids (pyruvate, oxaloacetate, alpha-ketobutyrate) at 0.5-1 mM concentrations restore DNA synthesis in previously inhibited cells when combined with insulin. L-alanine (D-alanine is inert) is even more effective than the keto acids in stimulating DNA synthesis after cycloheximide treatment. Glucose transport was unaffected by cycloheximide treatment while lactate levels in medium from inhibited, insulin-stimulated CEF were reduced 70% compared to uninhibited counterparts. We speculate that cycloheximide treatment may lead to the decay of a glycolytic enzyme which compromises the ability of inhibited cells to synthesize pyruvate from glucose, and thus induces an exogenous requirement for alpha-keto acid or L-alanine. A serum component(s) with a molecular weight of about 100 permitted insulin-stimulated DNA synthesis in inhibited cells.

Alanine↗
PubMed1977

Transport enhancement and reversal: glucose and 3-O-methyl glucose.

In chick embryo fibroblast cultures the 15- to 30-fold enhancement of D-glucose uptake observed when cells are starved of glucose for 24 hours is not duplicated for derivatives of glucose that compete effectively for uptake and have generally been considered to use the same carrier. 2-deoxy-D-glucose, D-mannose, D-galactose and D-glucosamine are derepressed progressively less sharply in that order with glucosamine uptake never more than doubled by starvation. D-glucose at a concentration of 5.5 mM in the 24-hour conditioning medium is a strong "repressor" resulting in low "transport" behavior for each of the five sugars cited. D-glucosamine is equally effective at the same concentration. A 10-fold reduction in the concentration of glucosamine (0.55 mM) allows for the escape from repression of mannose, glucose, and deoxyglucose uptake while the others remain repressed. Mannose uptake escapes as well when the glucose concentration in the "conditioning" medium is similarly reduced. Under certain conditions of starvation and cell density dramatic effects of supplemental stimulation by insulin can be achieved. Insulin withdrawal interrupts the supplemental stimulation process. Cycloheximide, actinomycin D and cordycepin block both non-insulin and insulin-induced derepression. Short exposure (15-30 minutes) of 24-hour starved cells to glucose (5.5 mM) reduces glucose sharply but does not affect 3-O-methyl glucose uptake. If the exposure is to 2-deoxyglucose (5.5 mM) further derepression of glucose uptake results.

Animals↗
PubMed1977

Regulation of glucose carriers in chick fibroblasts.

The derepression of glucose transport initiated by removing glucose from the incubation medium requires both protein and RNA synthesis. The synthesis and accumulation of putative mRNA for the carrier protein(s) can be demonstrated by inhibiting protein synthesis with cycloheximide (2 microgram/ml). Release from inhibition with simultaneous addition of actinomycin D (1-5 microgram/ml) results in a burst of carrier synthesis that achieves virtually maximal derepression in 4-6 h. An external energy source provided by a "nonrepressive" sugar (D-fructose, D-xylose) or by pyruvate is required to accomplish carrier synthesis. Previous failure to demonstrate mRNA accumulation was due to the depletion of energy in the starved cells. Glucose acts as a repressor at a posttranscriptional step, probably at the level of turnover of formed carrier. The protection of formed carrier in the absence of glucose and by inhibitors of protein synthesis even in the presence of glucose has encouraged conjecture that a protease is activated by a metabolic product of glucose that is analogous to a corepressor. The glucose metabolite either activates the protease by direct interaction with it or alters the conformation of the carrier to expose a critical region to protease attack. Indeed the regulation of carrier density in the membrane of chick fibroblasts may be achieved entirely by carrier inactivation, the rate of which is a function of glucose concentration in the culture medium.

Animals↗