A review of mentoring deaf and hard-of-hearing scholars.

Diversification of the scientific workforce usually focuses on recruitment and retention of women and underrepresented racial and ethnic minorities but often overlooks deaf and hard-of hearing (D/HH) persons. Usually classified as a disability group, such persons are often members of their own sociocultural linguistic minority and deserve unique support. For them, access to technical and social information is often hindered by communication- and/or language-centered barriers, but securing and using communication access services is just a start. Critical aspects of training D/HH scientists as part of a diversified workforce necessitates: (a) educating hearing persons in cross-cultural dynamics pertaining to deafness, sign language, and Deaf culture; (b) ensuring access to formal and incidental information to support development of professional soft skills; and (c) understanding that institutional infrastructure change may be necessary to ensure success. Mentorship and training programs that implement these criteria are now creating a new generation of D/HH scientists.

Fatty acids differentially modulate insulin-stimulated endothelial nitric oxide production by an Akt-independent pathway.

BACKGROUND: Insulin increases endothelial nitric oxide (NO) production by activating endothelial nitric oxide synthase (eNOS) through protein kinase B (Akt)-mediated phosphorylation of serine residue 1179 (p-eNOS serine 1179). Because fatty acids modulate insulin-stimulated Akt signaling cascades in smooth muscle cells, we hypothesized that fatty acids would differentially regulate endothelial Akt signaling, eNOS phosphorylation, and NO production. METHODS: Porcine pulmonary artery endothelial cells (PAECs) were treated for 3 hours with 100 microM oleic (18:1) or eicosapentaenoic (20:5) acids or with an equivalent volume of ethanol vehicle (0.1%). PAECs were then treated with graded concentrations (10(9)-10(-5) M) of insulin or incubated overnight (24 hours) in culture medium without fatty acids before insulin treatment. Activation and phosphorylation of Akt and eNOS were determined by immunoblotting. NO production was measured with a chemiluminescence NO analyzer or with a NO-selective carbon fiber microelectrode. RESULTS: Insulin-stimulated Akt phosphorylation, eNOS phosphorylation, and NO production. The phosphatidylinositol-3 kinase inhibitor wortmannin attenuated insulin-stimulated Akt activation and NO production. Treatment with the omega-3 fatty acid 20:5, but not 18:1, enhanced insulin-stimulated NO production but failed to alter insulin-stimulated Akt activation or eNOS serine 1179 phosphorylation. CONCLUSION: Individual fatty acyl species have distinct effects on insulin-stimulated endothelial NO production. Although fatty acids alter Akt signaling in muscle cells, the current results indicate that fatty acids do not modulate endothelial NO production through alterations in insulin-stimulated, Akt-mediated eNOS phosphorylation.