The study addressed the role for aldose reductase (AR) in 1) retinal oxidative stress and vascular endothelial growth factor (VEGF) overexpression in early diabetes, and 2) high glucose-induced oxidative stress in retinal endothelial cells. In vivo experiments were performed on control rats and diabetic rats treated with or without low or high dose of the AR inhibitor (ARI) fidarestat (2 or 16 mg ⅐ kg ؊1 ⅐ day ؊1 ). In vitro studies were performed on bovine retinal endothelial cells (BREC) cultured in either 5 or 30 mmol/l glucose with or without 1 mol/l fidarestat. Intracellular reactive oxygen species were assessed using the 5-(and-6)-chloromethyl-2,7-dichlorodihydrofluorescein diacetate (H 2 DCFDA) probe and flow cytometry. Both low and high doses of fidarestat (i.e., the doses that partially and completely inhibited sorbitol pathway hyperactivity) arrested diabetesinduced retinal lipid peroxidation. This was achieved due to upregulation of the key antioxidative defense enzyme activities rather than changes in reduced glutathione, oxidized glutathione, ascorbate and dehydroascorbate concentrations, and the glutathione and ascorbate redox states. Diabetes-associated 2.1-fold VEGF protein overexpression (enzyme-linked immunosorbent assay; ELISA) was dose-dependently prevented by fidarestat, whereas total VEGF mRNA and VEGF-164 mRNA (RT-PCR) abundance were not affected by either diabetes or the ARI. In BREC, fidarestat corrected hyperglycemiainduced increase in H 2 DCFDA fluorescence but not oxidative stress caused by three different pro-oxidants in normoglycemic conditions. In conclusion, increased AR activity contributes to retinal oxidative stress and VEGF protein overexpression in early diabetes. The findings justify the rationale for evaluation of fidarestat on diabetic retinopathy. Diabetes 52:864 -871, 2003

The current paper presents a lifespan model of ethnic-racial identity (ERI) from infancy into adulthood. We conceptualize that ethnic-racial priming during infancy prompts nascent awareness of ethnicity/race that becomes differentiated across childhood and through adulthood. We propose that the components of ERI that have been tested to date fall within five dimensions across the lifespan: ethnic-racial awareness, affiliation, attitudes, behaviors, and knowledge. Further, ERI evolves in a bidirectional process informed by an interplay of influencers (i.e., contextual, individual, and developmental factors, as well as meaning-making and identity-relevant experiences). It is our goal that the lifespan model of ERI will provide important future direction to theory, research, and interventions. Ethnic-racial identity (ERI) encompasses the process and content that defines an individual's sense of self related to ethnic heritage and racial background. It includes labels individuals use to define themselves according to ethnicity/race; awareness, beliefs, attitudes, and knowledge they have about their ethnic-racial background; enactment of their identity; and processes by which each of these dimensions evolve (Umaña-Taylor et al., 2014). ERI is recognized as an important developmental competency (Williams et al., 2012) that can promote positive adjustment in the face of risk or adversity (Neblett et al., 2012). Scholars emphasize that ERI development is dynamic and evolves throughout the lifespan (Syed et al., 2007). However, most conceptual models of ERI have focused independently on distinct developmental periods, such as childhood (e.g., Bernal et al., 1990) or adolescence (see Umaña-Taylor et al., 2014 for review), without an explicit lifespan perspective. This relatively piecemeal approach makes it difficult to chart continuity across developmental periods when identity components are defined specific to a single developmental period, with little effort tracing either the origin or maturation of components beyond a single developmental period. The resulting scholarship gives the impression of disjointed development of ethnic-racial identity. To piece together disparate scholarship in the field's conceptual understanding of ERI, [Adriana Umaña-Taylor and Esther Calzada] assembled a work group funded by the National Science Foundation. The goal of our work group was to develop an integrated model of ERI development that would describe when components of ERI first emerge, how they unfold from one developmental period to another, which components have 2 WILLIAMS ET AL.

We hypothesize that poly (ADP-ribosyl)ation, that is, poly (ADP-ribose) polymerase (PARP)-dependent transfer of ADP-ribose moieties from NAD to nuclear proteins, plays a role in diabetic nephropathy. We evaluated whether PARP activation is present and whether two unrelated PARP inhibitors, 3-aminobenzamide (ABA) and 1,5-isoquinolinediol (ISO), counteract overexpression of endothelin-1 (ET-1) and ET receptors in the renal cortex in short-term diabetes. The studies were performed in control rats and streptozotocin-diabetic rats treated with/without ABA or ISO (30 and 3 mg x kg(-1) x day(-1), intraperitoneally, for 2 weeks after 2 weeks of diabetes). Poly (ADP-ribose) immunoreactivity was increased in tubuli, but not glomeruli, of diabetic rats and this increase was corrected by ISO, whereas ABA had a weaker effect. ET-1 concentration (ELISA) was increased in diabetic rats, and this elevation was blunted by ISO. ET-1, ET(A), and ET(B) mRNA (ribonuclease protection assay), but not ET-3 mRNA (RT/PCR), abundance was increased in diabetic rats, and three variables were, at least, partially corrected by ISO. ABA produced a trend towards normalization of ET-1 concentration and ET-1, ET(A), and ET(B) mRNA abundance, but the differences with untreated diabetic group were not significant. Poly(ADP-ribosyl)ation is involved in diabetes-induced renal overexpression of ET-1 and ET receptors. PARP inhibitors could provide a novel therapeutic approach for diabetic complications including nephropathy, and other diseases that involve the endothelin system.

When does ERI development begin and end? 2. How do we account for age-dependent and contextually-initiated factors in ERI? 3. Should there be a reference point for healthy ERI, and if so, what is it? 4. How do the multiplicities of identity (intersectionality, multiracialism, whiteness) figure into our conceptualization of ERI? 5. How do we understand the role of ERI in pursuit of equity, diversity, and social justice? 2 ROGERS ET AL.

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