This article examines the effect that postsecondary education has on earnings and the duration of time spent in the Social Security disability programs for young persons who are deaf or hard of hearing. Our hypothesis is that investments in postsecondary training increase the likelihood of employment for persons who are deaf or hard of hearing and thus reduce dependency on disability-related income support programs. A longitudinal data set based upon records from the National Technical Institute for the Deaf and Social Security administrative records is used for this analysis. We find that those who graduate, even those who graduate with vocational degrees, experience significant earnings benefits and reductions in the duration of time spent on federal disability programs when compared with those who do not graduate with a degree. This finding suggests that reductions in the duration of time spent on Social Security programs are not limited to those with the highest level of scholastic aptitude and that investments in post-secondary education can benefit a broad group of deaf and hard-of-hearing persons. In addition, the data show that individuals who attend college, but withdraw before graduation, fair no better economically than individuals who never attended college.

Studies of homozygous PAR2 gene knockout mice have described a mix of phenotypic effects in vitro and in vivo. However, there have been few studies of PAR2 heterozygous (wild-type/knockout; PAR2-HET) mice. The phenotypes of many hemi and heterozygous transgenic mice have been described as intermediates between those of wild-type and knockout animals. In our study we aimed to determine the effects of intermediary par2 gene zygosity on vascular tissue responses to PAR2 activation. Specifically, we compared the vasodilator effectiveness of the PAR2 activating peptide 2-furoyl-LIGRLO-amide in aortas of wild-type PAR2 homozygous (PAR2-WT) and PAR2-HET mice. In myographs under isometric tension conditions, isolated aortic rings were contracted by alpha 1-adrenoeceptor agonist (phenylephrine), and thromboxane receptor agonist (U46619) and then relaxation responses by the additions of 2-furoyl-LIGRLO-amide, acetylcholine, and nitroprusside were recorded. A Schild regression analysis of the inhibition by a PAR2 antagonist (GB-83) of PAR2 agonist-induced aortic ring relaxations was used to compare receptor expression in PAR2-WT to PAR2-HET. PAR2 mRNA in aortas was measured by quantitative real-time PCR. In aortas contracted by either phenylephrine or U46619, the maximum relaxations induced by 2-furoyl-LIGRLO-amide were less in PAR2-HET than in the gender-matched PAR2-WT. GB-83 was 3- to 4-fold more potent for inhibition of 2fly in PAR2-HET than in PAR2-WT. PAR2 mRNA content of aortas from PAR2-HET was not significantly different than in PAR2-WT. Acetylcholine- and nitroprusside-induced relaxations of aortas from PAR2-HET were not significantly different than in PAR2-WT and PAR2 knockout. An interesting secondary finding was that relaxations induced by agonists of PAR2 and muscarinic receptors were larger in females than in males. We conclude that the lower PAR2-mediated responses in PAR2-HET aortas are consistent with evidence of a lower quantity of functional receptor expression, despite the apparently normal PAR2 mRNA content in PAR2-HET aortas.

Endothelial cell (EC)-dependent vasodilation by proteinase-activated receptor 2 (PAR2) is preserved in small caliber arteries in disease states where vasodilation by muscarinic receptors is decreased. In this study, we identified and characterized the PAR2-mediated intracellular calcium (Ca2+)-release mechanisms in EC from small caliber arteries in healthy and diseased states. Mesenteric arterial EC were isolated from PAR2 wild-type (WT) and null mice, after saline (controls) or angiotensin II (AngII) infusion, for imaging intracellular calcium and characterizing the calcium-release system by immunofluorescence. EC Ca2+ signals comprised two forms of Ca2+-release events that had distinct spatial-temporal properties and occurred near either the plasmalemma (peripheral) or center of EC. In healthy EC, PAR2-dependent increases in the densities and firing rates of both forms of Ca2+-release were abolished by inositol 1,4,5- trisphosphate receptor (IP3R) inhibitor, but partially reduced by transient potential vanilloid channels inhibitor ruthenium red (RR). Acetylcholine (ACh)-induced less overall Ca2+-release than PAR2 activation, but enhanced selectively the incidence of central events. PAR2-dependent Ca2+-activity, inhibitors sensitivities, IP3R, small- and intermediate-conductance Ca2+-activated potassium channels expressions were unchanged in EC from AngII WT. However, the same cells exhibited decreases in ACh-induced Ca2+-release, RR sensitivity, and endothelial nitric oxide synthase expression, indicating AngII-induced dysfunction was differentiated by receptor, Ca2+-release, and downstream targets of EC activation. We conclude that PAR2 and muscarinic receptors selectively elicit two elementary Ca2+ signals in single EC. PAR2-selective IP3R-dependent peripheral Ca2+-release mechanisms are identical between healthy and diseased states. Further study of PAR2-selective Ca2+-release for eliciting pathological and/or normal EC functions is warranted.

No abstract

In hypertension where other signal transduction pathways are attenuated, protease‐activated receptor 2 (PAR2)‐mediated vascular relaxation is preserved. Despite this difference, PAR2 calcium events in vascular endothelium are not understood. We hypothesize that PAR2‐mediated calcium events are preserved in isolated mesenteric endothelial cells from hypertensive mice. Calcium activity was measured by spinning‐disk confocal microscopy in PAR2 wild type (PAR2‐WT) and PAR2 deficient (PAR2‐KO) mice treated subcutaneously with saline or angiotensin II (hypertensive). Isolated endothelial cells were incubated with fluorescent calcium indicator, fluo‐4 AM, and then exposed to a PAR2‐activating peptide 2‐furoyl LIGRLO‐amide (2fly) or muscarinic M3 agonist acetylcholine. Our results show the number of calcium release sites and event rate are preserved in hypertensive PAR2‐WT exposed to 2fly. Acetylcholine‐induced calcium release sites and event rate were attenuated by 21% and 24% respectively. Similar results were found in hypertensive PAR2‐KO. Two types of calcium event were identified; small peripheral and repetitive, large central amplitude events. We conclude that PAR2‐mediated calcium signaling in isolated resistance endothelial cells is preserved in hypertension. Research funded by Canadian Institutes of Health Research and Research & Development Corporation Newfoundland and Labrador.