University of Nevada, Reno

About: University of Nevada, Reno is a education organization based out in Reno, Nevada, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 13561 authors who have published 28217 publications receiving 882002 citations. The organization is also known as: University of Nevada & Nevada State University.

Improving the nutrient composition of plants to enhance human nutrition and health1

Abstract: Plant foods contain almost all of the mineral and organic nutrients established as essential for human nutrition, as well as a number of unique organic phytochemicals that have been linked to the promotion of good health. Because the concentrations of many of these dietary constituents are often low in edible plant sources, research is under way to understand the physiological, biochemical, and molecular mechanisms that contribute to their transport, synthesis and accumulation in plants. This knowledge can be used to develop strategies with which to manipulate crop plants, and thereby improve their nutritional quality. Improvement strategies will differ between various nutrients, but generalizations can be made for mineral or organic nutrients. This review focuses on the plant nutritional physiology and biochemistry of two essential human nutrients, iron and vitamin E, to provide examples of the type of information that is needed, and the strategies that can be used, to improve the mineral or organic nutrient composition of plants.

Cumulative trauma: The impact of child sexual abuse, adult sexual assault, and spouse abuse

Abstract: The present study investigated the relationship between trauma symptoms and a history of child sexual abuse, adult sexual assault, and physical abuse by a partner as an adult. While there has been some research examining the correlation between individual victimization experiences and traumatic stress, the cumulative impact of multiple victimization experiences has not been addressed. Subjects were recruited from psychological clinics and community advocacy agencies. Additionally, a nonclinical undergraduate student sample was evaluated. The results of this study indicate not only that victimization and revictimization experiences are frequent, but also that the level of trauma specific symptoms are significantly related to the number of different types of reported victimization experiences. The research and clinical implications of these findings are discussed.

Interstitial cells of Cajal mediate inhibitory neurotransmission in the stomach.

Abstract: The structural relationships between interstitial cells of Cajal (ICC), varicose nerve fibers, and smooth muscle cells in the gastrointestinal tract have led to the suggestion that ICC may be involved in or mediate enteric neurotransmission. We characterized the distribution of ICC in the murine stomach and found two distinct classes on the basis of morphology and immunoreactivity to antibodies against c-Kit receptors. ICC with multiple processes formed a network in the myenteric plexus region from corpus to pylorus. Spindle-shaped ICC were found within the circular and longitudinal muscle layers (IC-IM) throughout the stomach. The density of these cells was greatest in the proximal stomach. IC-IM ran along nerve fibers and were closely associated with nerve terminals and adjacent smooth muscle cells. IC-IM failed to develop in mice with mutations in c-kit. Therefore, we used W/W(V) mutants to test whether IC-IM mediate neural inputs in muscles of the gastric fundus. The distribution of inhibitory nerves in the stomachs of c-kit mutants was normal, but NO-dependent inhibitory neuro-regulation was greatly reduced. Smooth muscle tissues of W/W(V) mutants relaxed in response to exogenous sodium nitroprusside, but the membrane potential effects of sodium nitroprusside were attenuated. These data suggest that IC-IM play a critical serial role in NO-dependent neurotransmission: the cellular mechanism(s) responsible for transducing NO into electrical responses may be expressed in IC-IM. Loss of these cells causes loss of electrical responsiveness and greatly reduces responses to nitrergic nerve stimulation.