Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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The aim of the present study was to evaluate levels of neutrophil gelatinase-associated lipocalin (NGAL), a stress protein increased after renal and systemic stimuli, in a cohort of 15 patients with severe proteinuria secondary to idiopathic membranous nephropathy and conserved renal function. Neutrophil gelatinase-associated lipocalin levels and the fractional excretion of this protein were higher in patients than in healthy controls. Furthermore, a close correlation was found between serum NGAL and urinary (uNGAL) (r = 0.81; P < 0.01) and between uNGAL and daily proteinuria (r = 0.44; P < 0.03). ⋯ The findings made suggest that the NGAL balance is altered in patients with severe proteinuria who have not yet developed overt chronic renal failure, thus confirming the potential use of this protein as an early biomarker of kidney damage preceding the increase in serum creatinine levels. Furthermore, also extra-renal cells (neutrophils, endothelium) may hyper-release NGAL, expressing systemic stress related to severe proteinuria. This would explain the impressive decrease occurring in NGAL values after intravenous immunoglobulin infusion, thus providing further evidence of the antiinflammatory properties of this particular therapeutic approach and indicating the possible value of NGAL measurement in monitoring the efficacy of treatment of renal diseases.
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Adenosine (ADO) is an endogenous nucleoside, which has been involved in blood pressure failure during severe systemic inflammatory response syndrome (severe SIRS) after cardiac surgery with cardiopulmonary bypass (CPB). Adenosine acts via its receptor subtypes, namely A1, A2A, A2B, or A3. Because A2A receptors are implicated in vascular tone, their expression might contribute to severe SIRS. We compared adenosine plasma levels (APLs) and A2A ADO receptor expression (ie, B, K, and mRNA amount) in patients with or without postoperative SIRS. ⋯ High expression of A2A ADO receptor and high APLs may be a predictive factor of postoperative severe SIRS after CPB.
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Cholesteryl ester transfer protein (CETP) plays an important role in lipoprotein metabolism. The present study was undertaken to compare the difference in the CETP TaqIB gene polymorphism and its association with serum lipid levels between the Guangxi Hei Yi Zhuang and Han populations. ⋯ There were significant differences in the interactions between the CETP TaqIB genotypes and several environmental factors in the Hei Yi Zhuang and Han populations. The polymorphism predicted differences in HDL-C and ApoAI in the Hei Yi Zhuang but not in the Han Chinese, even after adjustment for confounding variables. This means that the gene may not be truly involved in regulation of high-density lipoprotein metabolism or that there is an ethnic-specific effect.
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In October 2006, the Society for Women's Health Research convened a workshop that focused on the behavioral and social influences on obesity in women across the life span with an emphasis on ethnicity, socioeconomic status, and mental health. The purposes of the workshop were to examine the current state of the science related to behavioral influences on obesity in women across the life span; to determine the mechanisms, methods, and technical advances required for research progress in this area; and to develop an agenda for future research on behavioral influences on obesity in women. ⋯ Discussions during the workshop focused on 4 specific topics: (1) the relationship between mental or emotional health and obesity in women; (2) the impact of social, cultural, and environmental factors on obesity in women; (3) the improvement of obesity research methodology; and (4) the development of obesity prevention and intervention strategies. Based on these discussions, participants proposed recommendations for future research.
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Since the emergence of highly active antiretroviral therapy (HAART), human immunodeficiency virus-1 (HIV-1)-infected patients have demonstrated dramatic decreases in viral burden and opportunistic infections, and an overall increase in life expectancy. Despite these positive HAART-associated outcomes, it has become increasingly clear that HIV-1 patients have an enhanced risk of developing cardiovascular disease over time. Clinical studies are instrumental in our understanding of vascular dysfunction in the context of HIV-1 infection. ⋯ We analyze recent in vitro and in vivo studies examining endothelial toxicity in response to HIV-1 proteins or in response to the various classes of antiretroviral drugs. Furthermore, we discuss the multiple mechanisms by which HIV-1 proteins and HAART injure the vascular endothelium in HIV-1 patients. By understanding the molecular mechanisms of HIV-1 protein- and antiretroviral-induced cardiovascular disease, we may ultimately improve the quality of life of HIV-1 patients through better drug design and the discovery of new pharmacological targets.