Our Health Is in Our Hands: A Social Marketing Campaign to Combat Obesity and Diabetes.

PURPOSE: Design, implement, and evaluate a 6-week social marketing campaign (SMC) to raise awareness of obesity and increase involvement in type 2 diabetes prevention, nutrition, and fitness programs offered by the Brooklyn Partnership to Drive Down Diabetes (BP3D) in two low-income, urban communities. DESIGN: This was a nonexperimental, formative research, mixed-methods study. SETTING: The study took place in Central Brooklyn and East New York, two of the most impoverished, high-need communities in New York City. SUBJECTS: Participants were black and Hispanic adults, who were 18+ years of age and residing in the priority communities. INTERVENTION: Advertisements in English and Spanish encouraging healthier eating habits and advocating for better food options were displayed on New York City bus shelters, buses, and subway cars operating in the priority communities. Social media, Web sites, and print material were used to promote the campaign message. MEASURES: Social media metrics and a street intercept postsurvey informed the campaign's success. ANALYSIS: Quantitative data were analyzed using descriptive statistics. RESULTS: One hundred advertisements in English and Spanish were posted. After an 18-month followup, there were over 11,000 visits to the Facebook page. Results from the postsurvey (n = 171) suggest the SMC motivated participants who recognized the advertisements to improve their health behaviors. CONCLUSION: A multifaceted SMC that coincides with prevention programs can effectively raise attention to health issues and activities in a high-risk population at a relatively low cost.

Lipid raft: A floating island of death or survival.

Lipid rafts are microdomains of the plasma membrane enriched in cholesterol and sphingolipids, and play an important role in the initiation of many pharmacological agent-induced signaling pathways and toxicological effects. The structure of lipid rafts is dynamic, resulting in an ever-changing content of both lipids and proteins. Cholesterol, as a major component of lipid rafts, is critical for the formation and configuration of lipid raft microdomains, which provide signaling platforms capable of activating both pro-apoptotic and anti-apoptotic signaling pathways. A change of cholesterol level can result in lipid raft disruption and activate or deactivate raft-associated proteins, such as death receptor proteins, protein kinases, and calcium channels. Several anti-cancer drugs are able to suppress growth and induce apoptosis of tumor cells through alteration of lipid raft contents via disrupting lipid raft integrity.

The role of cholesterol in UV light B-induced apoptosis.

Modification of major lipid raft components, such as cholesterol and ceramide, plays a role in regulation of programmed cell death under various stimuli. However, the relationship between cholesterol level modification and the activation of apoptotic signaling cascades upon UVB light has not been established. In this report, we demonstrate that upon UVB irradiation cholesterol levels in membrane rafts of skin cells increase, which leads to Fas-receptor (Fas) aggregation in the rafts. Utilizing a continuous velocity floatation technique, we show that Fas accumulated in the lipid rafts of human melanoma M624 cells after UVB irradiation. The subsequent events of death-inducing signaling complex formation were also detected in the lipid raft fractions. Depletion of cholesterol by methyl-ß-cyclodextrin reduces Fas aggregation, while overloading increases. Disruption of lipid rafts also prevents Fas death domain-associated protein (Daxx) from dissociating from Fas in the lipid rafts, which is accompanied with a reduced apoptotic, but increased nonapoptotic death of UVB-irradiated human keratinocytes, HaCaT cells. Results indicate that cholesterol located in the plasma membrane of skin cells is required for lipid raft domain formation and activation of UVB-induced apoptosis.

The role of translational regulation in ultraviolet C light-induced cyclooxygenase-2 expression.

AIMS: The role of ultraviolet C light (UVC)-induced phosphorylation of the eukaryotic initiation factor 2 (eIF2) in the regulation of cyclooxygenase-2 (COX-2) expression at both transcriptional and translational levels is investigated. MAIN METHODS: Western analysis was used to determine COX expressions. Immunoprecipitation after [(35)S]-Met/Cys metabolic labeling was used to determine the rate for COX-2 synthesis and turnover. Quantitative real-time PCR was used to determine COX-2 mRNA levels. Ingenuity Pathways Analysis 6 was used for mapping COX-2 activation network. KEY FINDINGS: UVC induces COX-2 expression in wild-type mouse embryo fibroblasts (MEF(S/S)) and that the inducibility is reduced in MEF(A/A) cells in which the phosphorylation site, Ser-51 in the eIF2alpha, is replaced with a nonphosphorylatable Ala (S51A). UVC-induced transcription of COX-2 is delayed in MEF(A/A) cells, which correlates with NF-kappaB activation as previously reported (Wu, S, Tan, M, Hu, Y, Wang, JL, Scheuner, D, Kaufman, RJ, Ultraviolet light activates NFkappaB through translational inhibition of IkappaBalpha synthesis. The Journal of Biological Chemistry, 279, 34898-34902, 2004). The translational efficiency of COX-2 is higher in MEF(A/A) cells than in MEF(S/S) cells at 4 h, but not at 24 h post-UVC. The translation efficiency is correlated to the ratio of activated COX-2 binding protein HuR/TIAR. In addition, the newly synthesized COX-2 protein is more stable in MEF(A/A) cells than in MEF(S/S) cells. The results demonstrated a complex and dynamic regulation of COX-2 expression. SIGNIFICANCE: UVC induces a prolonged expression of COX-2. While transcriptional regulation of COX-2 expression is intensively studied, the role of translational regulation of COX-2 synthesis upon UVC-irradiation is not yet clear. This study elucidated a novel eIF2alpha phosphorylation-centered network for the regulation of COX-2 expression after UVC-irradiation.

Training community health workers to be advocates for health promotion: efforts taken by a community-based organization to reduce health disparities in cardiovascular disease.

Compared to white adults, blacks are less likely to be aware of their cardiovascular risk factors and are less likely to respond appropriately to signs and symptoms of a myocardial infarction or stroke. This fact highlights the need for better dissemination of health information about cardiovascular disease among communities of color. Community health workers (CHWs) are important resources for disseminating health information. Recognizing this important role of CHWs, the Greater Southern Brooklyn Health Coalition and its community and academic partners developed a workshop designed to educate CHWs about the risk factors, signs and symptoms of cardiovascular disease. The purpose of this workshop was to educate CHWs so that they themselves could be better informed and thus, be in a better position to educate their respective clients. The resulting workshop, Taking Action Against Cardiovascular Disease in Our Communities: A Training for Service Providers, was a half-day workshop attended by 70 CHWs from various community service organizations. Approximately 97% of attendees said that the workshop met their expectations. More than half said they learned the signs and symptoms of cardiovascular disease and about 90% said that they received clear and concrete information that they could use with their clients. These evaluations also provided critiques regarding aspects of the workshop that could be improved upon and other information which will be used as a formative tool in developing future educational initiatives. In conclusion, this workshop demonstrated that it was feasible to develop effective community programs targeted at educating CHWs about cardiovascular disease.

The roles of translation initiation regulation in ultraviolet light-induced apoptosis.

Ultraviolet light (UV) inhibits translation initiation through activation of kinases that phosphorylate the alpha-subunit of eukaryotic initiation factor 2 (eIF2alpha). Two eIF2alpha kinases, PERK and GCN2, are known to phosphorylate the Serine-51 of eIF2alpha in response to UV-irradiation. In this report, we present evidence that phosphorylation of eIF2alpha plays a role in UV-induced apoptosis. Our data show that wild-type mouse embryo fibroblasts (MEF(s/s)) are less sensitive to UV-induced apoptosis than MEF(A/A) cells in which the phosphorylation site, Ser51, of eIF2alpha is replaced with a non-phosphorylatable Ala (Ser51Ala). PARP expression in MEF(A/A) cells is reduced without being cleaved after UV-irradiation. In contrast, PARP is cleaved without a significant decrease in parental PARP in MEF(S/S) cells after UV-irradiation. Our data also show that MEF(GCN2-/-) cells, in which GCN2 is knocked out, are more sensitive to UV-irradiation, agreeing with the observation from MEF(A/A) cells. However, MEF(PERK-/-) cells, in which PERK is knocked out, are less sensitive to UV-irradiation. In addition, MCF-7-PERKDeltaC cells, which are stably transfected with a kinase domain deleted mutant of PERK (PERKDeltaC), are more resistant to UV-induced apoptosis than parental MCF-7 cells. Overexpression of wild-type PERK sensitizes MCF-7 cells to UV-induced apoptosis without directly inducing cell death. These results suggest that the level of eIF2alpha phosphorylation impacts PARP expression upon UV-irradiation. The eIF2alpha kinases may mediate UV-induced apoptosis via an eIF2alpha dependent or independent signaling pathway.