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.

Instability, turbulence, and enhanced transport in accretion disks

Abstract: Recent years have witnessed dramatic progress in our understanding of how turbulence arises and transports angular momentum in astrophysical accretion disks. The key conceptual point has its origins in work dating from the 1950s, but its implications have been fully understood only in the last several years: the combination of a subthermal magnetic field (any nonpathological configuration will do) and outwardly decreasing differential rotation rapidly generates magnetohydrodynamic (MHD) turbulence via a remarkably simple linear instability. The result is a greatly enhanced effective viscosity, the origin of which had been a long-standing problem. The MHD nature of disk turbulence has linked two broad domains of magnetized fluid research: accretion theory and dynamos. The understanding that weak magnetic fields are not merely passively acted upon by turbulence, but actively generate it, means that the assumptions of classical dynamo theory break down in disks. Paralleling the new conceptual understanding has been the development of powerful numerical MHD codes. These have taught us that disks truly are turbulent, transporting angular momentum at greatly enhanced rates. We have also learned, however, that not all forms of disk turbulence do this. Purely hydrodynamic turbulence, when it is imposed, simply causes fluctuations without a significant increase in transport. The interplay between numerical simulation and analytic arguments has been particularly fruitful in accretion disk theory and is a major focus of this article. The authors conclude with a summary of what is now known of disk turbulence and mention some knotty outstanding questions (e.g., what is the physics behind nonlinear field saturation?) for which we may soon begin to develop answers.

Range-free localization schemes for large scale sensor networks

Abstract: Wireless Sensor Networks have been proposed for a multitude of location-dependent applications. For such systems, the cost and limitations of the hardware on sensing nodes prevent the use of range-based localization schemes that depend on absolute point-to-point distance estimates. Because coarse accuracy is sufficient for most sensor network applications, solutions in range-free localization are being pursued as a cost-effective alternative to more expensive range-based approaches. In this paper, we present APIT, a novel localization algorithm that is range-free. We show that our APIT scheme performs best when an irregular radio pattern and random node placement are considered, and low communication overhead is desired. We compare our work via extensive simulation, with three state-of-the-art range-free localization schemes to identify the preferable system configurations of each. In addition, we study the effect of location error on routing and tracking performance. We show that routing performance and tracking accuracy are not significantly affected by localization error when the error is less than 0.4 times the communication radio radius.

Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo.

Abstract: Skeletal muscles adapt to changes in their workload by regulating fibre size by unknown mechanisms. The roles of two signalling pathways implicated in muscle hypertrophy on the basis of findings in vitro, Akt/mTOR (mammalian target of rapamycin) and calcineurin/NFAT (nuclear factor of activated T cells), were investigated in several models of skeletal muscle hypertrophy and atrophy in vivo. The Akt/mTOR pathway was upregulated during hypertrophy and downregulated during muscle atrophy. Furthermore, rapamycin, a selective blocker of mTOR, blocked hypertrophy in all models tested, without causing atrophy in control muscles. In contrast, the calcineurin pathway was not activated during hypertrophy in vivo, and inhibitors of calcineurin, cyclosporin A and FK506 did not blunt hypertrophy. Finally, genetic activation of the Akt/mTOR pathway was sufficient to cause hypertrophy and prevent atrophy in vivo, whereas genetic blockade of this pathway blocked hypertrophy in vivo. We conclude that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of the Akt/mTOR pathway can oppose muscle atrophy induced by disuse.

Modulation of NF-κB-dependent transcription and cell survival by the SIRT1 deacetylase

Abstract: NF‐κB is responsible for upregulating gene products that control cell survival. In this study, we demonstrate that SIRT1, a nicotinamide adenosine dinucleotide‐dependent histone deacetylase, regulates the transcriptional activity of NF‐κB. SIRT1, the mammalian ortholog of the yeast SIR2 (Silencing Information Regulator) and a member of the Sirtuin family, has been implicated in modulating transcriptional silencing and cell survival. SIRT1 physically interacts with the RelA/p65 subunit of NF‐κB and inhibits transcription by deacetylating RelA/p65 at lysine 310. Treatment of cells with resveratrol, a small‐molecule agonist of Sirtuin activity, potentiates chromatin‐associated SIRT1 protein on the cIAP‐2 promoter region, an effect that correlates with a loss of NF‐κB‐regulated gene expression and sensitization of cells to TNFα‐induced apoptosis. While SIRT1 is capable of protecting cells from p53‐induced apoptosis, our work provides evidence that SIRT1 activity augments apoptosis in response to TNFα by the ability of the deacetylase to inhibit the transactivation potential of the RelA/p65 protein.

Autism as a strongly genetic disorder: evidence from a British twin study.

Abstract: Two previous epidemiological studies of autistic twins suggested that autism was predominantly genetically determined, although the findings with regard to a broader phenotype of cognitive, and possibly social, abnormalities were contradictory. Obstetric and perinatal hazards were also invoked as environmentally determined aetiological factors. The first British twin sample has been re-examined and a second total population sample of autistic twins recruited. In the combined sample 60% of monozygotic (MZ) pairs were concordant for autism versus no dizygotic (DZ) pairs; 92% of MZ pairs were concordant for a broader spectrum of related cognitive or social abnormalities versus 10% of DZ pairs. The findings indicate that autism is under a high degree of genetic control and suggest the involvement of multiple genetic loci. Obstetric hazards usually appear to be consequences of genetically influenced abnormal development, rather than independent aetiological factors. Few new cases had possible medical aetiologies, refuting claims that recognized disorders are common aetiological influences.