University of Oklahoma

About: University of Oklahoma is a education organization based out in Norman, Oklahoma, United States. It is known for research contribution in the topics: Population & Radar. The organization has 25269 authors who have published 52609 publications receiving 1821706 citations. The organization is also known as: OU & Oklahoma University.

A nonsynonymous functional variant in integrin-alpha(M) (encoded by ITGAM) is associated with systemic lupus erythematosus.

Abstract: We identified and replicated an association between ITGAM (CD11b) at 16p11.2 and risk of systemic lupus erythematosus (SLE) in 3,818 individuals of European descent. The strongest association was at a nonsynonymous SNP, rs1143679 (P = 1.7 x 10(-17), odds ratio = 1.78). We further replicated this association in two independent samples of individuals of African descent (P = 0.0002 and 0.003; overall meta-analysis P = 6.9 x 10(-22)). The genetic association between ITGAM and SLE implicates the alpha(M)beta2-integrin adhesion pathway in disease development.

Research issues in data stream association rule mining

Abstract: There exist emerging applications of data streams that require association rule mining, such as network traffic monitoring and web click streams analysis. Different from data in traditional static databases, data streams typically arrive continuously in high speed with huge amount and changing data distribution. This raises new issues that need to be considered when developing association rule mining techniques for stream data. This paper discusses those issues and how they are addressed in the existing literature.

Epigenetic remodeling of the fungal secondary metabolome

Abstract: Fungi treated with DNA methyltransferase and histone deacetylase inhibitors exhibited natural product profiles with enhanced chemical diversity demonstrating that small-molecule epigenetic modifiers are effective tools for rationally controlling the native expression of fungal biosynthetic pathways and generating new biomolecules.

Physiology of spinal cord stimulation: review and update.

Abstract: Spinal cord stimulation (SCS) was an outgrowth of the well-known gate control theory presented by Melzack and Wall in 1965. Although the method has been used to treat chronic severe pain for more than three decades, very little was known about the physiological and biochemical mechanisms behind the beneficial effects until recently. We now know that SCS activates several different mechanisms to treat different types of pain such as neuropathic and ischemic. In general, these mechanisms seem most dependent on activation of only a few segments of the spinal cord. However, both animal studies and human observations have indicated that supraspinal circuits may contribute as well. In the treatment of neuropathic pain, intermittent SCS may give several hours of pain relief after cessation of the stimulation. This protracted effect indicates long-lasting modulation of neural activity involving changes in the local transmitter systems in the dorsal horns. In ischemic pain, animal experiments demonstrate that inhibition of afferent activity in the spinothalamic tracts, long-term suppression of sympathetic activity, and antidromic effects on peripheral reflex circuits may take part in the pain alleviation. Moderate SCS intensities seem to evoke sympathetic inhibition, but higher stimulation intensities may induce antidromically mediated release of vasoactive substances, eg, the calcitonin gene-related peptide (CGRP), resulting in peripheral vasodilation. The anti-ischemic effect of SCS in angina pectoris due to intermittent coronary ischemia probably occurs because application of SCS appears to result in a redistribution of cardiac blood supply, as well as a decrease in tissue oxygen demand. Recent studies indicate that SCS modulates the activity of cardiac intrinsic neurons thereby restricting the arrythmogenic consequences of intermittent local coronary ischemia. The present state of knowledge is briefly reviewed and recent research directions outlined.