Environmentally Persistent Free Radicals Cause Apoptosis in HL-1 Cardiomyocytes.

Samples of environmental particulate matter contain environmentally persistent free radicals (EPFRs) capable of sustained generation of oxygen radicals. While exposure to EPFRs produces cardiac toxicity and oxidative stress in experimental animals, the underlying mechanisms are largely unknown. To determine whether EPFRs could directly damage cardiomyocytes, cultured mouse cardiomyocytes (HL-1) and primary rat adult left ventricular myocytes (ALVM) were incubated with an EPFR consisting of 1,2-dichlorobenzene chemisorbed to CuO-coated silica beads (DCB230).

Environmentally persistent free radicals decrease cardiac function and increase pulmonary artery pressure.

Epidemiological studies have consistently linked inhalation of particulate matter (PM) to increased cardiac morbidity and mortality, especially in at risk populations. However, few studies have examined the effect of PM on baseline cardiac function in otherwise healthy individuals. In addition, airborne PM contain environmentally persistent free radicals (EPFR) capable of redox cycling in biological systems.

Role of TRIB3 in regulation of insulin sensitivity and nutrient metabolism during short-term fasting and nutrient excess.

We have suggested previously that Tribbles homolog 3 (TRIB3), a negative regulator of Akt activity in insulin-sensitive tissues, could mediate glucose-induced insulin resistance in muscle under conditions of chronic hyperglycemia (Liu J, Wu X, Franklin JL, Messina JL, Hill HS, Moellering DR, Walton RG, Martin M, Garvey WT. Am J Physiol Endocrinol Metab 298: E565-E576, 2010). In the current study, we have assessed short-term physiological regulation of TRIB3 in skeletal muscle and adipose tissues by nutrient excess and fasting as well as TRIB3's ability to modulate glucose transport and mitochondrial oxidation.

Increasing Asian American women's research participation: the Asian grocery store-based cancer education program.

Background: Research study participants with diverse characteristics produce the most generalizable outcomes, but recruiting heterogeneous samples is difficult.

Methods: This pilot study tests whether Asian women (N=1079) with diverse language proficiencies, who were personally recruited to one study by a linguistically and culturally aligned recruiter, would enroll in another study with a single mailed invitation in English.

Results: The 134 participants in the second study represented 17.

Pulmonary ozone exposure induces vascular dysfunction, mitochondrial damage, and atherogenesis.

More than 100 million people in the United States live in areas that exceed current ozone air quality standards. In addition to its known pulmonary effects, environmental ozone exposures have been associated with increased hospital admissions related to cardiovascular events, but to date, no studies have elucidated the potential molecular mechanisms that may account for exposure-related vascular impacts. Because of the known pulmonary redox and immune biology stemming from ozone exposure, we hypothesized that ozone inhalation would initiate oxidant stress, mitochondrial damage, and dysfunction within the vasculature.

The role of tobacco smoke induced mitochondrial damage in vascular dysfunction and atherosclerosis.

The majority of individuals chronically exposed to tobacco smoke will eventually succumb to cardiovascular disease (CVD). However, despite the major cardiovascular health implications of tobacco smoke exposure, concepts of how such exposure specifically results in cardiovascular cell dysfunction that leads to CVD development are still being explored. Moreover, surprisingly little is known about the effects of prenatal and childhood tobacco smoke exposure on adult CVD development.