Lily Y. Wong

Alteration of gene expression during progression of hypertension-induced cardiac dysfunction in rats

Hypertension induced by high-salt diet in Dahl salt-sensitive rats leads to compensatory cardiac hypertrophy by approximately 11 wk, cardiac dysfunction at approximately 17 wk, and death from cardiac dysfunction at approximately 21 wk. It is unclear what molecular hallmarks distinguish the compensatory hypertrophy from the decompensated cardiac dysfunction phase. Here we compared the gene expression in rat cardiac tissue from the compensatory hypertrophic phase (11 wk, n = 6) with the cardiac dysfunction phase (17 wk, n = 6) and with age-matched normotensive controls. Messenger RNA levels of 93 genes, selected based on predicted association with cardiac dysfunction, were measured by quantitative real-time PCR. In the hypertrophic phase, the expression of three genes, atrial natriuretic peptide (ANP; P = 0.0089), brain natriuretic peptide (P = 0.0012), and endothelin-1 precursor (P = 0.028), significantly increased, whereas there was decreased expression of 24 other genes including SOD2 (P = 0.0148), sarco(endo)plasmic reticulum Ca(2+)-ATPase 2a (P = 0.0002), and ryanodine receptor 2 (P = 0.0319). In the subsequent heart cardiac dysfunction phase, the expression of an additional 20 genes including inducible nitric oxide synthase (NOS; P = 0.0135), angiotensin I-converting enzyme (P = 0.0082), and IL-1beta (P < 0.0001) increased, whereas the expression of seven genes decreased compared with those of age-matched controls. Furthermore, the expression of 22 genes, including prepro-endothelin-1, ANP, angiotensin I-converting enzyme, beta(1)-adrenergic receptor, SOD2, and endothelial NOS, significantly changed in the cardiac dysfunction phase compared with the compensatory hypertrophic phase. Finally, principal component analysis successfully segregated animals with decompensatory cardiac dysfunction from controls, as well as from animals at the compensated hypertrophy phase, suggesting that we have identified molecular markers for each stage of the disease.

Molecular Technologies for Salmonella Detection

Salmonella has been associated with some of the most devastating foodborne outbreaks in recent history. Salmonella outbreaks have been linked to a variety of foods including produce [Alfalfa Sprouts2009, 2010, 2011; pistachios-2009; cantaloupes-2008, 2011 etc.], processed foods [peanuts – 2009], and prepared foods [turkey burgers2011, Banquet Pot Pies – 2007]. The contamination of commercial shell eggs with Salmonella Enteriditis in 2010 led to the recall of over a half a billion eggs, and the contamination of peanut-containing products with Salmonella Typhimurium in 2008-2009 led to one of the largest recalls in U.S. history with over 3,900 products being recalled. The Peanut Corporation of America, responsible for the Salmonella outbreak in peanuts, was forced into bankruptcy. Multiple lawsuits were filed against Wright County Egg and Hillandale Farms responsible for the Salmonella outbreak in eggs. Despite their own internal testing which showed Salmonella contamination, these facilities still shipped product. The 2008 outbreak of Salmonella in jalapeno peppers resulted in 1442 persons infected with Salmonella Saintpaul across 43 states, the District of Columbia, and Canada. Unfortunately, the tomato industry was implicated early in the investigation, which resulted in economic losses to the tomato industry in hundreds of millions of dollars. Because Salmonella is widespread in the environment (in such places as chicken houses), vegetable plants and animals (as well as meat samples, eggs etc.), rapid, reliable, and validated pathogen detection methods are needed for use in production facilities, public health labs, as well as in the regulatory and monitoring agencies. To provide comprehensive rapid food testing solutions, all components of a pathogen detection system should be addressed: sample preparation, detection and data analysis.