A wave of medical student activism is shining a spotlight on medical educators' sometimes maladroit handling of racial categories in teaching about health disparities. Coinciding with recent critiques, primarily by social scientists, regarding the imprecise and inappropriate use of race as a biological or epidemiological risk factor in genetics research, medical student activism has triggered new collaborations among students, faculty, and administrators to rethink how race is addressed in the medical curriculum. Intensifying critiques of racial essentialism are a crucial concern for educators since bioscientific knowledge grounds the authority of health professionals. Central ethical issues-racial bias and social justice-cannot be properly addressed without confronting the epistemological problem of racial essentialism in bioscience teaching. Thus, educators now face an ethical imperative to improve academic capacities for robust interdisciplinary teaching about the conceptual apparatus of race and the recalibration of its use in teaching both genetics and the more pervasive and urgent social causes of health inequalities.

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The axonal transport and metabolism of glycoproteins in sciatic nerve sensory axons were examined from 2 h to 7 weeks following injection of [3H]fucose into the 5th lumbar dorsal root ganglion of adult rats. Incorporation of fucose into glycoproteins was prolonged; only half of the 3H label in the ganglion was acid‐insoluble after 4 h, and maximal labeling did not occur until approximately 24 h after injection. [3H]Glycoproteins were transported distally at a rate of approximately 310 mm per day after a synthesis and/or processing lag of approximately 40 min. Gel electrophoresis demonstrated that many glycoproteins were transported, including prominent labeled species having apparent M.W. of approximately 49,000, 90,000, 118,000, and 132,000. With increasing time after injection, a peak with an apparent M.W. of 49,000 accounted for an increasing proportion of the total label in the nerve. The accumulation of this glycoprotein (possibly a subunit of Na+,K+‐ATPase, an enzyme known to be present in axolemma) was due in part to its preferential deposition in the axons, while other glycoproteins passed through the axons directly to the nerve terminals. Radioactivity in another labeled glycoprotein, with an apparent M.W. of 30,000, also increased preferentially in the nerve relative to other labeled glycoproteins. This was shown to be the myelin P0 protein. This protein was not transported from the ganglion; rather, its increased prominence with time in the nerve was due both to a decrease in amounts of other labeled species and to an absolute increase in labeling of the P0 protein, possibly due to reutilization by the Schwann cells of fucose released during turnover of labeled glycoproteins delivered to the axons by axonal transport.

Lipid precursors ([2-3H]glycerol for phospholipids and [3H]acetate for cholesterol) were injected into the L-5 dorsal root ganglion of adult rats. At various times, animals were killed, the ganglion and consecutive 5-mm segments of sciatic nerve were dissected, and lipids were extracted and analyzed by TLC. Individual lipid classes exhibited markedly different transport patterns. The crest of radioactive phosphatidylcholine moved as a sharply defined front at about 300 mm/day, with a relatively flat plateau behind the moving crest. Although some radioactive phosphatidylethanolamine also moved at the same rate, the crest was continually attenuated as it moved so that a gradient of radioactive phosphatidylethanolamine along the axon was maintained for several days. Transported diphosphatidylglycerol exhibited a defined crest, as did phosphatidylcholine, but moved at about half the rate. Labeled cholesterol was transported at a rapid rate similar to that for phosphatidylcholine and phosphatidylethanolamine, but like phosphatidylethanolamine, the initial moving crest of radioactivity was continually attenuated. Relative to the phospholipids, cholesterol showed a more prolonged period of accumulation in the axons and was more metabolically stable. We propose that most labeled phosphatidylcholine, phosphatidylethanolamine, and cholesterol is transported in similar (or the same) rapidly moving membranous particles. Once incorporated into these particles, molecules of phosphatidylcholine tend to maintain associated with them during transport. In contrast, molecules of phosphatidylethanolamine and cholesterol in these transported particles exchange extensively with unlabeled molecules in stationary axonal structures. Diphosphatidylglycerol, localized in a specialized organelle, the mitochondrion, is transported at a slower rate than other phospholipids, and does not exchange with other structures.

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