See no evil: color blindness and perceptions of subtle racial discrimination in the workplace.

Workplace discrimination has grown more ambiguous, with interracial interactions often perceived differently by different people. The present study adds to the literature by examining a key individual difference variable in the perception of discrimination at work, namely individual color-blind attitudes. We examined relationships between 3 dimensions of color-blind attitudes (Racial Privilege, Institutional Discrimination, and Blatant Racial Issues) and perceptions of racial microaggressions in the workplace as enacted by a White supervisor toward a Black employee (i.e., discriminatory actions ranging from subtle to overt). Findings showed that observer views on institutional discrimination fully mediated, and blatant racial issues partially mediated, the relationships between racial group membership and the perception of workplace microaggressions. Non-Hispanic Whites endorsed color blindness as institutional discrimination and blatant racial issues significantly more than members of racioethnic minority groups, and higher levels of color-blind worldviews were associated with lower likelihoods of perceiving microaggressions. Views on racial privilege did not differ significantly between members of different racial groups or affect microaggression perceptions. Implications for organizations concerned about promoting more inclusive workplaces are discussed.

Storage media effect on bond strength of orthodontic brackets.

INTRODUCTION: In testing bond strengths, various storage media are used. The purpose of this study was to determine the effect of 6 storage media and rinsing on the shear bond strength of bonded orthodontic brackets. METHODS: Bovine teeth were stored in 6 storage media for 7 months before bonding: dry (no medium), filtered water, 10% formalin, 1% chloramine T, 10% chloramine T, isotonic saline solution, and 70% ethanol. These teeth were further subdivided into 2 groups; 1 group was rinsed with oil-free air and water spray before bonding orthodontic brackets, and the other group not rinsed. All specimens were tested in the shear-peel mode to failure. RESULTS: The 10% formalin rinsed sample had statistically significantly higher bond strength (16.9 +/- 6.56 MPa), and storage in ethanol (rinsed, 9.04 +/- 5.61 MPa; not rinsed, 9.08 +/- 3.5 MPa) and dry (8.34 +/- 3.80 MPa) produced significantly lower bond strengths. No difference was found between the other modes of storage or rinsing. The adhesive remnant index values showed no statistically significant difference between any groups. CONCLUSIONS: For bond strength studies, storage media can have an effect on bond strength results. Dry, formalin, and ethanol storage should be avoided. Water, isotonic saline solution, and chloramine T storage produced comparable bond strengths. Rinsing or not rinsing had no effect on bond strength with these storage media.

Development of a human neuronal cell model for human immunodeficiency virus (HIV)-infected macrophage-induced neurotoxicity: apoptosis induced by HIV type 1 primary isolates and evidence for involvement of the Bcl-2/Bcl-xL-sensitive intrinsic apoptosis pathway.

Neuronal apoptosis within the central nervous system (CNS) is a characteristic feature of AIDS dementia, and it represents a common mechanism of neuronal death induced by neurotoxins (e.g., glutamate) released from human immunodeficiency virus (HIV)-infected macrophages (HIV/macrophage-induced neurotoxicity). Neuronal apoptosis may result from activation of the intrinsic (mitochondrial/bcl-2 regulated) or extrinsic (death receptor) pathways, although which pathway predominates in CNS HIV infection is unknown. Apoptosis initiated by the intrinsic pathway is typically blocked by antiapoptosis Bcl-2 family proteins, such as Bcl-2 and Bcl-xL, but whether these can block HIV/macrophage-induced neuronal apoptosis is unknown. To determine the potential role of the Bcl-2 family in HIV/macrophage-induced neuronal apoptosis, we developed a unique in vitro model, utilizing the NT2 neuronal cell line, primary astrocytes and macrophages, and primary CNS HIV type 1 (HIV-1) isolates. We validated our model by demonstrating that NT2.N neurons are protected against HIV-infected macrophages by N-methyl-D-aspartate (NMDA) glutamate receptor antagonists, similar to effects seen in primary neurons. We then established stable NT2.N neuronal lines that overexpress Bcl-2 or Bcl-xL (NT2.N/bcl-2 and NT2.N/bcl-xL, respectively) and determined their sensitivity to macrophages infected with primary R5, X4, and R5/X4 HIV-1 isolates. We found that NT2.N/bcl-2 and NT2.N/bcl-xL neurons were resistant to apoptosis induced by either R5, X4, or R5/X4 isolates and that resistance was abrogated by a Bcl-2 antagonist. Thus, the NMDA receptor/bcl-2-regulated apoptotic pathway contributes significantly to HIV/macrophage-induced neuronal apoptosis, and Bcl-2 family proteins protect neurons against the spectrum of primary HIV-1 isolates. Modulation of bcl-2 gene expression may therefore offer adjunctive neuroprotection against development of AIDS dementia.