Joint marketing as a framework for targeting men who have sex with men in China: A pilot intervention study

To apply the joint marketing principle as a new intervention approach for targeting men who have sex with men (MSM) who are often difficult to reach in societies with discrimination towards homosexuality and HIV/ AIDS. A pilot intervention according to the principles of joint marketing was carried out by the CDC in Shenzhen, China, in MSM social venues. A self-designed questionnaire of HIV knowledge, condom use, and access to HIV-related services was used before and after the pilot intervention to evaluate its effectiveness. The CDC supported gatekeepers of MSM social venues in running their business and thereby increasing their respectability and income. In return, the gatekeepers cooperated with the CDC in reaching the MSM at the venues with health promotion messages and materials. Thus a win-win situation was created, bringing together two noncompetitive parties in reaching out to a shared customer, the MSM. The pilot intervention succeeded in demonstrating acceptability and feasibility of the joint marketing approach targeting MSM. HIV knowledge, the rate of condom use, and access to HIV-related services of pa\rticipants in the pilot intervention increased significantly. The joint marketing intervention is an innovative way to create synergies between the gatekeepers of MSM social venues and public health officials for reaching and potentially changing HIV high-risk behaviors among MSM

Extracellular superoxide dismutase deficiency exacerbates pressure overload-induced left ventricular hypertrophy and dysfunction

Extracellular superoxide dismutase (SOD) contributes only a small fraction to total SOD activity in the normal heart but is strategically located to scavenge free radicals in the extracellular compartment. To examine the physiological significance of extracellular SOD in the response of the heart to hemodynamic stress, we studied the effect of extracellular SOD deficiency on transverse aortic constriction (TAC)-induced left ventricular remodeling. Under unstressed conditions extracellular SOD deficiency had no effect on myocardial total SOD activity, the ratio of glutathione:glutathione disulfide, nitrotyrosine content, or superoxide anion production but resulted in small but significant increases in myocardial fibrosis and ventricular mass. In response to TAC for 6 weeks, extracellular SOD-deficient mice developed more severe left ventricular hypertrophy (heart weight increased 2.56-fold in extracellular SOD-deficient mice as compared with 1.99-fold in wild-type mice) and pulmonary congestion (lung weight increased 2.92-fold in extracellular SOD-deficient mice as compared with 1.84-fold in wild-type mice). Extracellular SOD-deficient mice also had more ventricular fibrosis, dilation, and a greater reduction of left ventricular fractional shortening and rate of pressure development after TAC. TAC resulted in greater increases of ventricular collagen I, collagen III, matrix metalloproteinase-2, matrix metalloproteinase-9, nitrotyrosine, and superoxide anion production. TAC also resulted in a greater decrease of the ratio of glutathione:glutathione disulfide in extracellular SOD-deficient mice. The finding that extracellular SOD deficiency had minimal impact on myocardial overall SOD activity but exacerbated TAC induced myocardial oxidative stress, hypertrophy, fibrosis, and dysfunction indicates that the distribution of extracellular SOD in the extracellular space is critically important in protecting the heart against pressure overload