Race/ethnic discrimination in hiring can be measured under controlled conditions using matched pairs of minority and nonminority research assistants posing as applicants for the same job. In 149 in-person job applications in the Washington, D.C., labor market, African American applicants were treated less favorably than equally qualified nonminorities more than one-fifth of the time. Employer behavior during these interactions suggest that, within continued public and private efforts against discrimination, particular attention should be accorded to the cognitive underpinnings of bias.

Anglos and Latinos posing as job seekers applied for 468 job vacancies advertised in the Washington, D.C. area. Latino applicants received less favorable treatment than equally qualified Anglos more than 20% of the time. Discrimination was particularly prevalent for males and for jobs located in the center city, not requiring a college degree, and not widely advertised.

Thiamine deficiency causes Wernicke's encephalopathy, although the precise mechanism is unknown. We used a low-thiamine diet in conjunction with a thiamine analog, pyrithiamine, as a model of severe thiamine deficiency in rats. We investigated the function of intact, coupled mitochondria isolated from both brain and liver. State 4 respiration did not change in the thiamine-deficient animals. Brain state 3 rates fell in thiamine-deficient animals when pyruvate/malate, alpha-ketoglutarate, or glutamate were used as substrate. Liver state 3 rates were depressed only when pyruvate/malate was substrate. Activities of brain and liver pyruvate dehydrogenase complex and alpha-ketoglutarate dehydrogenase complex were depressed in the thiamine-deficient group. We conclude that the mitochondrial abnormalities resulting from thiamine deficiency are secondary to depression of thiamine-mediated enzyme activity, rather than from a putative role of thiamine in chemiosmotic coupling, and that the resulting abnormalities in ATP synthesis and perhaps in glutamate catabolism result in the irreversible neurologic defect seen in this disease.

Pairs of resumes, one for a 57-year-old and the other for a 32-year-old, were mailed to 775 large firms and employment agencies across the United States. Although the resumes presented equal qualifications, the older job seeker received a less favorable employer response 26.5% of times when a position appeared to be vacant. Vigorous enforcement of equal opportunity laws as well as initiatives to change employer attitudes are appropriate responses to such discrimination. The technique of employment testing, demonstrated in this research, can be useful in both efforts.

Neuroprotective agents administered post cerebral ischemia have failed so far in the clinic to promote significant recovery. Thus, numerous efforts were redirected towards prophylactic approaches such as preconditioning as an alternative therapeutic strategy. Our lab has revealed a novel long-term window of cerebral ischemic tolerance mediated by resveratrol preconditioning (RPC) that lasts for two weeks in mice. To identify its mediators, we conducted an RNA-seq experiment on the cortex of mice two weeks post RPC, which revealed 136 differentially expressed genes. The majority of genes (116/136) were downregulated upon RPC and clustered into biological processes involved in transcription, synaptic signaling, and neurotransmission. The downregulation in these processes was reminiscent of metabolic depression, an adaptation used by hibernating animals to survive severe ischemic states by downregulating energy-consuming pathways. Thus to assess metabolism, we used a neuronal-astrocytic co-culture model and measured the cellular respiration rate at the long-term window post RPC. Remarkably, we observed an increase in glycolysis and mitochondrial respiration efficiency upon RPC. We also observed an increase in the expression of genes involved in pyruvate uptake, TCA cycle, and oxidative phosphorylation, all of which indicated an increased reliance on energy-producing pathways. We then revealed that these nuclear and mitochondrial adaptations, which reduce the reliance on energy-consuming pathways and increase the reliance on energy-producing pathways, are epigenetically coupled through acetyl-CoA metabolism and ultimately increase