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A national survey of social work educators teaching in CSWE-accredited social work education programs in the United States was conducted to explore their perceptions about integrating social justice content into their teaching. A content analysis of written commentary provided by 139 educators revealed four key areas relevant to their efforts: (a) the effect of program mission and integration, (b) the effect of faculty preparation and engagement, (c) the effect of students' positionality, and (d) the challenge of connecting an abstract concept to concrete practices. Findings from this study have highlighted not only the difficulties educators face trying to make this abstract concept more concrete for students but also the significance of the educational context as relevant to the challenges of meeting this obligation. Practical implications for social work education programs and educators as well as areas of further research are provided.

This study explored the needs and preferences of older gay and lesbian adults regarding their care in later life. Using a phenomenological case study approach, 15 participants were interviewed regarding their anticipated practical needs, including housing and finances, and their psychological needs, such as support and quality of life. Fearing prejudice from providers in later life, participants expressed a preference for personal care by friends and family and residence in a gay-affirmative care environment. However, few had developed a long-term financial plan for their older adulthood. Recommendations include improving guidance to older gays and lesbians regarding their long-term care preparations, nurturance of social networks in later life, and the need for more gay-affirmative residential care facilities. (Contains 1 table.)

Atherosclerotic plaques can lead to partial vascular occlusions that produce abnormally high levels of arterial wall shear stress. Such pathophysiological shear stress can promote shear-induced platelet aggregation (SIPA), which has been linked to acute myocardial infarction, unstable angina, and stroke. This study investigated the role of the tyrosine kinase Syk in shear-induced human platelet signaling. The extent of Syk tyrosine phosphorylation induced by pathophysiological levels of shear stress (100 dyn/[cm.sup.2]) was significantly greater than that resulting from physiological shear stress (10 dyn/[cm.sup.2]). With the use of phospho-Syk specific antibodies, these data are the first to show that key regulatory sites of Syk at tyrosines 525/526 (Y525/526) and tyrosine 352 (Y352) were phosphorylated in response to pathophysiological shear stress. Increased phosphorylation at both sites was attenuated by pharmacological inhibition of Syk using two different Syk inhibitors, piceatannol and 3-(1-methyl-1H-indol-3-yl-methylene)-2-oxo-2,3-dihydro-1H-indole-5-sulfonamide (OXSI-2), and by inhibition of upstream Src-family kinases (SFKs). Shear-induced response at the Syk 525/ 526 site was ADP dependent but not contingent on glycoprotein (GP) IIb-IIIa ligation or the generation of thromboxane (Tx) [A.sub.2]. Pretreatment with Syk inhibitors not only reduced SIPA and Syk phosphorylation in isolated platelets, but also diminished, up to 50%, the platelet-mediated thrombus formation when whole blood was perfused over type-III collagen. In summary, this study demonstrated that Syk is a key molecule in both SIPA and thrombus formation under flow. Pharmacological regulation of Syk may prove efficacious in treating occlusive vascular disease. GPIb; GPIIb-IIIa; signal transduction; thrombosis; collagen

Increased oxidative stress is a major characteristic of restenosis after angioplasty. The oxidative stress is mainly created by oxidants such as reactive oxygen species (ROS), which are assumed to play an important role in neointima formation after angioplasty. DNA is a sensitive target for oxidants; however, oxidative DNA damage remains a poorly examined field in the pathogenesis of restenosis. In the present study, we demonstrated that the expression of the oxidative DNA damage marker 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxo-dG) was quickly increased in rat carotid arteries after balloon injury. It reached its peak at 14 days after injury and still kept high expression at 28 days after injury. The immunostaining of 8-oxo-dG was present predominantly in the neointima. In response to oxidative DNA damage, the DNA repair enzyme poly(ADP-ribose) polymerase-1 (PARP-1) was significantly increased after balloon injury. The time course change and location of PARP-1 is similar to that of 8-oxo-dG. Daily injections of the PARP-1 inhibitor PJ34 (5 mg x [kg.sup.-1] x [day.sup.-1] ip) attenuated neointima formation by ~40% at 7, 14, and 28 days after balloon injury. Treatment with PJ34 inhibited leukocyte infiltration and improved both anatomic (reendothelialization) and functional (endothelial function) recovery of endothelial cells after balloon injury. In conclusion, levels of oxidative DNA damage and the DNA repair enzyme PARP-1 are increased in vessels after balloon injury. Inhibition of PARP-I attenuates neointima formation through inhibition of leukocyte infiltration and improvement of endothelial cell recovery after balloon injury. Targeting of the DNA repair enzyme might be a therapeutic strategy for restenosis. angioplasty; DNA damage; oxidative stress; restenosis

Vascular NAD(P)H oxidase-derived reactive oxygen species (ROS) such as hydrogen peroxide ([H.sub.2][O.sub.2]) have emerged as important molecules in the pathogenesis of atherosclerosis, hypertension, and diabetic vascular complications. Additionally, myeloperoxidase (MPO), a transcytosable heme protein that is derived from leukocytes, is also believed to play important roles in the above-mentioned inflammatory vascular diseases. Previous studies have shown that MPO-induced vascular injury responses are [H.sub.2][O.sub.2] dependent. It is well known that MPO can use leukocyte-derived [H.sub.2][O.sub.2]; however, it is unknown whether the vascular-bound MPO can use vascular nonleukocyte oxidasederived [H.sub.2][O.sub.2] to induce vascular injury. In the present study, ANG II was used to stimulate vascular NAD(P)H oxidases and increase their [H.sub.2][O.sub.2] production in the vascular wall, and vascular dysfunction was used as the vascular injury parameter. We demonstrated that vascular-bound MPO has sustained activity in the vasculature. MPO could use the vascular NAD(P)H oxidase-derived [H.sub.2][O.sub.2] to produce hypochlorus acid (HOCl) and its chlorinating species. More importantly, MPO derived HOCl and chlorinating species amplified the [H.sub.2][O.sub.2]-induced vascular injury by additional impairment of endothelium-dependent relaxation. HOCl-modified low-density lipoprotein protein (LDL), a specific biomarker for the MPO-HOCl-chlorinating species pathway, was expressed in LDL and MPO-bound vessels with vascular NAD(P)H oxidase-derived [H.sub.2][O.sub.2]. MPO-vascular NAD(P)H oxidase-HOCl-chlorinating species may represent a common pathogenic pathway in vascular diseases and a new mechanism involved in exacerbation of vascular diseases under inflammatory conditions. endothelial dysfunction; atherosclerosis; inflammation; leukocyte