University of Missouri

About: University of Missouri is a education organization based out in Columbia, Missouri, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 41427 authors who have published 83598 publications receiving 2911437 citations. The organization is also known as: Mizzou & Missouri-Columbia.

Parental control in Latino families : An integrated review of the literature

Abstract: Using social information processing and cultural change models as explanatory frameworks, this article reviews the literature on Latino parental control and its implications for child development. It is argued that the use of parental control in Latino families may have motivational roots in cultural childrearing goals such as familismo (familism), respeto (respect), and educacion (moral education). Consideration of these underpinnings, in conjunction with psychological and methodological issues, helps to explain variability in the use of Latino parental control and its effect on child development. Recommendations for future research include refinement of control and acculturation instruments, and attention to both contextual and individual variables.

Role of TNF-α in vascular dysfunction

Abstract: Healthy vascular function is primarily regulated by several factors including EDRF (endothelium-dependent relaxing factor), EDCF (endothelium-dependent contracting factor) and EDHF (endothelium-dependent hyperpolarizing factor). Vascular dysfunction or injury induced by aging, smoking, inflammation, trauma, hyperlipidaemia and hyperglycaemia are among a myriad of risk factors that may contribute to the pathogenesis of many cardiovascular diseases, such as hypertension, diabetes and atherosclerosis. However, the exact mechanisms underlying the impaired vascular activity remain unresolved and there is no current scientific consensus. Accumulating evidence suggests that the inflammatory cytokine TNF (tumour necrosis factor)-α plays a pivotal role in the disruption of macrovascular and microvascular circulation both in vivo and in vitro. AGEs (advanced glycation end-products)/RAGE (receptor for AGEs), LOX-1 [lectin-like oxidized low-density lipoprotein receptor-1) and NF-κB (nuclear factor κB) signalling play key roles in TNF-α expression through an increase in circulating and/or local vascular TNF-α production. The increase in TNF-α expression induces the production of ROS (reactive oxygen species), resulting in endothelial dysfunction in many pathophysiological conditions. Lipid metabolism, dietary supplements and physical activity affect TNF-α expression. The interaction between TNF-α and stem cells is also important in terms of vascular repair or regeneration. Careful scrutiny of these factors may help elucidate the mechanisms that induce vascular dysfunction. The focus of the present review is to summarize recent evidence showing the role of TNF-α in vascular dysfunction in cardiovascular disease. We believe these findings may prompt new directions for targeting inflammation in future therapies.

Ventricular dysfunction and the risk of stroke after myocardial infarction

Abstract: Background In patients who have had a myocardial infarction, the long-term risk of stroke and its relation to the extent of left ventricular dysfunction have not been determined. We studied whether a reduced left ventricular ejection fraction is associated with an increased risk of stroke after myocardial infarction and whether other factors such as older age and therapy with anticoagulants, thrombolytic agents, or captopril affect long-term rates of stroke. Methods We performed an observational analysis of prospectively collected data on 2231 patients who had left ventricular dysfunction after acute myocardial infarction who were enrolled in the Survival and Ventricular Enlargement trial. The mean follow-up was 42 months. Risk factors for stroke were assessed by both univariate and multivariate Cox proportional-hazards analysis. Results Among these patients, 103 (4.6 percent) had fatal or nonfatal strokes during the study (rate of stroke per year of follow-up, 1.5 percent). The estimated five-year rate o...

A motivational perspective on risky behaviors: the role of personality and affect regulatory processes.

Abstract: The present study tested a motivational model in which personality influences on risky behaviors were hypothesized to be primarily indirectly mediated, by shaping the nature and quality of emotional experience as well as characteristic styles of coping with these emotions. This model was tested in a representative community sample of 1,666 young adults, aged 18 to 25 years old. Results revealed strong support for the model, indicating that broad traits related to neuroticism and extraversion promote involvement in alcohol use and risky sex via distinct pathways. Neurotic individuals were prone to engage in risky behaviors as a way to cope with aversive mood states, whereas extraverted individuals were more likely to engage in risky behaviors as a way to enhance positive affective experience. In contrast, impulsivity directly predicted some forms of risk taking, and interacted with extraversion and neuroticism to predict motives for risky behaviors. The model provides a highly general though not complete account of risky behaviors.

Mitochondrial reactive oxygen species: A double edged sword in ischemia/reperfusion vs preconditioning

Abstract: Reductions in the blood supply produce considerable injury if the duration of ischemia is prolonged. Paradoxically, restoration of perfusion to ischemic organs can exacerbate tissue damage and extend the size of an evolving infarct. Being highly metabolic organs, the heart and brain are particularly vulnerable to the deleterious effects of ischemia/reperfusion (I/R). While the pathogenetic mechanisms contributing to I/R-induced tissue injury and infarction are multifactorial, the relative importance of each contributing factor remains unclear. However, an emerging body of evidence indicates that the generation of reactive oxygen species (ROS) by mitochondria plays a critical role in damaging cellular components and initiating cell death. In this review, we summarize our current understanding of the mechanisms whereby mitochondrial ROS generation occurs in I/R and contributes to myocardial infarction and stroke. In addition, mitochondrial ROS have been shown to participate in preconditioning by several pharmacologic agents that target potassium channels (e.g., ATP-sensitive potassium (mKATP) channels or large conductance, calcium-activated potassium (mBKCa) channels) to activate cell survival programs that render tissues and organs more resistant to the deleterious effects of I/R. Finally, we review novel therapeutic approaches that selectively target mROS production to reduce postischemic tissue injury, which may prove efficacious in limiting myocardial dysfunction and infarction and abrogating neurocognitive deficits and neuronal cell death in stroke.