Publications

BACKGROUND

The 2006 Centers for Disease Control and Prevention (CDC) HIV testing guidelines recommend screening for HIV infection in all healthcare settings, including the emergency department (ED). In urban areas with a high background prevalence of HIV, the ED has become an increasingly important site for identifying HIV infection. However, this public health policy has been operationalized using different models. We sought to describe the development and implementation of HIV testing programs in three EDs, assess factors shaping the adoption and evolution of specific program elements, and identify barriers and facilitators to testing.

METHODS

We performed a qualitative evaluation using in-depth interviews with fifteen 'key informants' involved in the development and implementation of HIV testing in three urban EDs serving sizable racial/ethnic minority and socioeconomically disadvantaged populations. Testing program HIV prevalence ranged from 0.4% to 3.0%.

RESULTS

Three testing models were identified, reflecting differences in the use of existing ED staff to offer and perform the test and disclose results. Factors influencing the adoption of a particular model included: whether program developers were ED providers, HIV providers, or both; whether programs took a targeted or non-targeted approach to patient selection; and the extent to which linkage to care was viewed as the responsibility of the ED. A common barrier was discomfort among ED providers about disclosing a positive HIV test result. Common facilitators were a commitment to underserved populations, the perception that testing was an opportunity to re-engage previously HIV-infected patients in care, and the support and resources offered by the medical setting for HIV-infected patients.

CONCLUSIONS

ED HIV testing is occurring under a range of models that emerge from local realities and are tailored to institutional strengths to optimize implementation and overcome provider barriers.

Inhibition of adipocyte triglyceride biosynthesis is required for fatty acid mobilization during inflammation. Triglyceride biosynthesis requires glycerol 3-phosphate and phosphoenolpyruvate carboxykinase (PEPCK) plays a key role. We demonstrate that LPS, zymosan, and TNF-α decrease PEPCK in liver and fat. Turpentine decreases PEPCK in liver, but not in fat. The LPS-induced decrease in PEPCK does not occur in TLR4 deficient animals, indicating that this receptor is required. The LPS-induced decrease in hepatic PEPCK does not occur in TNF receptor/IL-1 receptor knockout mice, but occurs in fat, indicating that TNF-α/IL-1 is essential for the decrease in liver but not fat. In 3T3-L1 adipocytes TNF-α, IL-1, IL-6, and IFNγ inhibit PEPCK indicating that there are multiple pathways by which PEPCK is decreased in adipocytes. The binding of PPARγ and RXRα to the PPARγ response element in the PEPCK promoter is markedly decreased in adipose tissue nuclear extracts from LPS treated animals. Lipopolysaccharide and zymosan reduce PPARγ and RXRα expression in fat, suggesting that a decrease in PPARγ and RXRα accounts for the decrease in PEPCK. Thus, there are multiple cytokine pathways by which inflammation inhibits PEPCK expression in adipose tissue which could contribute to the increased mobilization of fatty acids during inflammation.

This article assessed the relationship between breast and cervical cancer screening rates and health beliefs in African American women participating in Witness Project of Harlem (WPH) education sessions. WPH is a culturally sensitive, faith-based breast and cervical cancer screening education program targeting African American women in medically underserved New York City communities. A questionnaire administered to women participating for the first time in a Witness Project education session collected demographics, adherence to breast and cervical cancer screening, and information about health beliefs related to cancer worry, medical mistrust, and religious faith. Screening adherence guidelines applied were as per the American Cancer Society recommendations. No statistically significant relationship was found between worry about getting breast or cervical cancer and screening adherence, or between screening adherence and agreement with statements about medical mistrust and religious beliefs. The low screening mammography and monthly breast self-exam rates emphasize the utility of programs like WPH that teach the importance of screening mammography and breast self-exam and point to the need for increased access to quality health care and cancer screening in underserved populations.

Primary ovarian insufficiency (POI) resulting from ovarian autoimmunity is a poorly understood clinical condition lacking in effective treatments. Understanding the targets of the autoimmune response and induction of ovarian-specific tolerance would allow development of focused therapies to preserve fertility in an at-risk population. MATER (maternal antigen that embryos require) is a known ovarian autoantigen targeted in autoimmune syndromes of POI. We attempt to induce ovarian-specific tolerance via transgenic expression of the MATER antigen on potentially tolerogenic antigen-presenting cells (APC), which typically present antigen via the major histocompatibility complex (MHC) class II molecule. We hypothesize that expression of MATER in a MHC class II-dependent manner on APC can mediate induction of ovarian tolerance. We utilized a well-characterized murine model of ovarian autoimmunity, whereby oophoritis develops after d 3 neonatal thymectomy (NTx). Wild-type and transgenic mice, carrying an MHC Class II-driven Mater gene (IE-Mater), were subjected to NTx and assessed for evidence of autoimmune oophoritis. After disease induction by NTx, female mice carrying the IE-Mater transgene had significant reductions in histological oophoritis (56%) and circulating ovarian autoantibodies (28%) compared with wild-type females (94% and 82%, respectively). Incidence of other autoimmunity was unaffected as assessed by antinuclear autoantibodies. Transgenic expression of MATER in APC can induce antigen-specific tolerance with a significant reduction in ovarian autoimmunity. Lack of complete disease protection suggests that other antigens may also play a role in autoimmune oophoritis. As a known autoantigen in the human APS1 (autoimmune polyglandular syndrome type 1), which is associated with POI, MATER may represent a relevant target for future diagnostic and therapeutic clinical interventions.