University of Virginia

About: University of Virginia is a education organization based out in Charlottesville, Virginia, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 52543 authors who have published 113268 publications receiving 5220506 citations. The organization is also known as: U of V & UVa.

Teacher-Child Relationships and Children's Success in the First Years of School.

Abstract: This work examines associations between closeness and conflict in teacher-child relationships and children's social and academic skills in first grade in a sample of 490 children. Assessments of te...

The cell-polarity protein Par6 links Par3 and atypical protein kinase C to Cdc42.

Abstract: PAR (partitioning-defective) proteins, which were first identified in the nematode Caenorhabditis elegans, are essential for asymmetric cell division and polarized growth, whereas Cdc42 mediates establishment of cell polarity. Here we describe an unexpected link between these two systems. We have identified a family of mammalian Par6 proteins that are similar to the C. elegans PDZ-domain protein PAR-6. Par6 forms a complex with Cdc42-GTP, with a human homologue of the multi-PDZ protein PAR-3 and with the regulatory domains of atypical protein kinase C (PKC) proteins. This assembly is implicated in the formation of normal tight junctions at epithelial cell-cell contacts. Thus, Par6 is a key adaptor that links Cdc42 and atypical PKCs to Par3.

Generalized KYP lemma: unified frequency domain inequalities with design applications

Abstract: The celebrated Kalman-Yakubovic/spl caron/-Popov (KYP) lemma establishes the equivalence between a frequency domain inequality (FDI) and a linear matrix inequality, and has played one of the most fundamental roles in systems and control theory. This paper first develops a necessary and sufficient condition for an S-procedure to be lossless, and uses the result to generalize the KYP lemma in two aspects-the frequency range and the class of systems-and to unify various existing versions by a single theorem. In particular, our result covers FDIs in finite frequency intervals for both continuous/discrete-time settings as opposed to the standard infinite frequency range. The class of systems for which FDIs are considered is no longer constrained to be proper, and nonproper transfer functions including polynomials can also be treated. We study implications of this generalization, and develop a proper interface between the basic result and various engineering applications. Specifically, it is shown that our result allows us to solve a certain class of system design problems with multiple specifications on the gain/phase properties in several frequency ranges. The method is illustrated by numerical design examples of digital filters and proportional-integral-derivative controllers.

Characterization of the human cysteinyl leukotriene CysLT1 receptor.

Abstract: The cysteinyl leukotrienes-leukotriene C4(LTC4), leukotriene D4(LTD4) and leukotriene E4(LTE4)-are important mediators of human bronchial asthma. Pharmacological studies have determined that cysteinyl leukotrienes activate at least two receptors, designated CysLT1 and CysLT2. The CysLT1-selective antagonists, such as montelukast (Singulair), zafirlukast (Accolate) and pranlukast (Onon), are important in the treatment of asthma. Previous biochemical characterization of CysLT1 antagonists and the CysLT1 receptor has been in membrane preparations from tissues enriched for this receptor. Here we report the molecular and pharmacological characterization of the cloned human CysLT1 receptor. We describe the functional activation (calcium mobilization) of this receptor by LTD4 and LTC4, and competition for radiolabelled LTD4 binding to this receptor by the cysteinyl leukotrienes and three structurally distinct classes of CysLT1-receptor antagonists. We detected CysLT1-receptor messenger RNA in spleen, peripheral blood leukocytes and lung. In normal human lung, expression of the CysLT1-receptor mRNA was confined to smooth muscle cells and tissue macrophages. Finally, we mapped the human CysLT1-receptor gene to the X chromosome.

Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline.

Abstract: Background Parkinson disease (PD) is a degenerative neurological disorder for which no treatment has been shown to slow the progression. Objective To determine whether a range of dosages of coenzyme Q10is safe and well tolerated and could slow the functional decline in PD. Design Multicenter, randomized, parallel-group, placebo-controlled, double-blind, dosage-ranging trial. Setting Academic movement disorders clinics. Patients Eighty subjects with early PD who did not require treatment for their disability. Interventions Random assignment to placebo or coenzyme Q10at dosages of 300, 600, or 1200 mg/d. Main Outcome Measure The subjects underwent evaluation with the Unified Parkinson Disease Rating Scale (UPDRS) at the screening, baseline, and 1-, 4-, 8-, 12-, and 16-month visits. They were followed up for 16 months or until disability requiring treatment with levodopa had developed. The primary response variable was the change in the total score on the UPDRS from baseline to the last visit. Results The adjusted mean total UPDRS changes were +11.99 for the placebo group, +8.81 for the 300-mg/d group, +10.82 for the 600-mg/d group, and +6.69 for the 1200-mg/d group. ThePvalue for the primary analysis, a test for a linear trend between the dosage and the mean change in the total UPDRS score, was .09, which met our prespecified criteria for a positive trend for the trial. A prespecified, secondary analysis was the comparison of each treatment group with the placebo group, and the difference between the 1200-mg/d and placebo groups was significant (P= .04). Conclusions Coenzyme Q10was safe and well tolerated at dosages of up to 1200 mg/d. Less disability developed in subjects assigned to coenzyme Q10than in those assigned to placebo, and the benefit was greatest in subjects receiving the highest dosage. Coenzyme Q10appears to slow the progressive deterioration of function in PD, but these results need to be confirmed in a larger study.