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.

Glucose entry, as measured by 5-min uptake into the acid-soluble fraction, is enhanced 15-30 times by long-term (12-24 hr) hexose starvation of chick fibroblasts. The rate of galactose accumulation in the cells increases only 5 times under the same conditions of starvation. Several carbon and energy sources that were tested for their effect on this "derepression" can be classified as: (i) those resembling glucose in blocking the "stimulation," (ii) those permitting full "derepresssion"; and (iii) those partially preventing the enhanced entry. Inhibitors of protein synthesis block enhancement under conditions otherwise conducive to it. We conclude that the glucose and galactose carrier systems are not identical, based largely on the asymmetric "repression" observed when glucose and galactose are compared as "repressors."The mechanism of glucose entry into vertebrate cells has received considerable attention (1-5). It is now generally agreed that glucose is transported into cells (2-4) by carriermediated facilitated diffusion unlinked to energy-generating processes. Illiano and Cuatrecasas (4), using membrane preparations from fat cells, were able to stimulate entry by exposure of the membranes to insulin in a system uncomplicated by the problems of metabolism of the transported glucose.In studies to determine whether D-glucose entry into chick fibroblasts was subject to modification by insulin (unpublished data), a marked enhancement of the rate of entry of D-glucose and D-galactose into the acid-soluble pool after prolonged starvation for a carbon and energy source was observed. Indeed, glucose starvation also rendered the cells responsive to insulin, whereas "fed" cells were unresponsive.The experiments reported in this paper deal exclusively with evidence for asymmetric "derepression" of transport activity in chick fibroblasts dependent upon starvation of the cells. The results lead to the tentative proposal that glucose and galactose entry are not totally dependent on a common carrier. MATERIALS AND METHODSCell Cultures. Chick embryo monolayer cultures were prepared by trypsinization of whole 10-to 12-day embryos (6). Culture vessels were inoculated to obtain initial cell densities of 104 to 5 X 104 cells per cm2. After 48-72 hr the monolayers were washed with Hanks' balanced salt solution (7) and incubated in Eagle's basal medium (8) supplemented with 3% calf serum or unsupplemented as indicated for each experiment.Glucose or Galactose Entry into Cells. Trichloroacetic acidsoluble D-glucose, 2-deoxy-D-glucose, or D-galactose contained in monolayer cells was determined after exposure to radioactive (14C or 3H) sugars for 5, 10, or 20 min. The following procedure was generally used: (1) Experiments were conducted at 370; all reagents were equilibrated to that temperature at the start of the experiment. The incubation medium was decanted from the monolayers to be used, and the last drops were removed with a Pasteur pipette. (2f) The monolayers were washed twice with 15 ml of balanced salt solution (with...

The rate of D-glucose uptake by cells that had been deprived of sugar for 18-24h was consistently observed to be 15-20 times higher than that in control cells maintained for the same length of time in medium containing glucose. This increased rate of glucose transport by sugar-starved cells was due to a 3-5-fold increase in the Vmax. value of a low-affinity system (Km 1 mM) combined with an increase in the Vmax of a separate high-affinity system (Km 0.05-0.2 mM). The high-affinity system, which was most characteristic of starved cells, was particularly sensitive to low concentrations of the thiol reagent N-ethylmaleimide; 50% inhibition of uptake occurred at approx. 0.01 mM-N-ethylmaleimide. In contrast with the high-affinity system, the low-affinity system of either the fed cells or the starved cells was unaffected by N-ethylmaleimide. In addition to the increases in the rate of D-glucose transport, cells deprived of sugar had increased rates of transport of 3-O-methyl-D-glucose and 2-deoxy-D-glucose. No measurable high-affinity transport system could be demonstrated for the transport of 3-O-methylgucose, and N-ethylmaleimide did not alter the initial rate. Thus the transport of 3-O-methyglucose by both fed and starved cells was exclusively by the N-ethylmaleimide-insensitive low-affinity system. The low-affinity system also appeared to be the primary means for the transport of 2-deoxyglucose by fed and starved cells. However, some of the transport of 2-deoxyglucose by starved cells was inhibited by N-ethylmaleimide, suggesting that 2-deoxyglucose may also be transported by a high-affinity system. The results of experiments that measured transport kinetics strongly suggest that glucose can be transported by a least two separate systems, and 3-O-methylglucose and 2-deoxyglucose by one. Support for these interpretations comes from the analysis of the effects of N-ethylmaleimide and cycloheximide as well as from the results of competition experiments. The uptake of glucose is quite different from that of 2-deoxyglucose and 3-O-methylglucose. The net result of sugar starvation serves to emphasize these differences. The apparent de-repression of the transport systems studied presents an interesting basis for further studies of the regulation of transport in a variety of cells.

Normal primary chick embryo fibroblast cultures product a nerve growth-promoting factor which cross-reacts with monospecfic antibody to pure male mouse submaxillary gland nerve growth factor (NGF). When taken together with the earlier demonstration that mouse L2 CELLS AND 3T3 cells also produce an NGF-like protein, these findings suggest that secretion of this factor may be a general property of fibroblast.

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