4,054 research outputs found
Sponsored by ASABE Galt House
Abstract. Several studies were conducted by Forest Service researchers and University and Industrial collaborators that investigated the potential for lessening soil surface disturbances and compaction in forest operations through modifications of machine components or harvest systems. Specific machine modifications included change in tire size, use of dual tire systems, reduction of tire inflation pressures, reductions in load size and ground pressure. Soil surface disturbances were most evident in sites with high soil moisture content that were lessened by lowering tire inflation pressures or using a dual tire configuration. Traffic intensity increased rutting potential of harvest sites, especially with the use of narrow tires. Traffic intensities varied spatially and in intensity in clear cut harvest operations with intensities that ranged between none to 100 or more. Soil physical properties responded to choice of tire size and inflation pressure with narrower tires and/or higher inflation pressures associated with increased soil compaction. Soil disturbance data collected in three clear cut operations in Alabama indicated no differences among the operations by location, but soil response varied depending on site properties. Soil physical properties did not necessarily reflect the intensity of soil disturbance
Cosmic D-Strings and Vortons in Supergravity
Recent developments in string inspired models of inflation suggest that
D-strings are formed at the end of inflation. Within the supergravity model of
D-strings there are 2(n-1) chiral fermion zero modes for a D-string of winding
n. Using the bounds on the relic vorton density, we show that D-strings with
winding number n>1 are more strongly constrained than cosmic strings arising in
cosmological phase transitions. The D-string tension of such vortons, if they
survive until the present, has to satisfy 8\pi G_N \mu \lesssim p 10^{-26}
where p is the intercommutation probability. Similarly, D-strings coupled with
spectator fermions carry currents and also need to respect the above bound.
D-strings with n=1 do not carry currents and evade the bound. We discuss the
coupling of D-strings to supersymmetry breaking. When a single U(1) gauge group
is present, we show that there is an incompatibility between spontaneous
supersymmetry breaking and cosmic D-strings. We propose an alternative
mechanism for supersymmetry breaking, which includes an additional U(1), and
might alleviate the problem. We conjecture what effect this would have on the
fermion zero modes.Comment: 11 page
Mouse models for preeclampsia: disruption of redox-regulated signaling
The concept that oxidative stress contributes to the development of human preeclampsia has never been tested in genetically-defined animal models. Homozygous deletion of catechol-Omethyl transferase (Comt-/-) in pregnant mice leads to human preeclampsia-like symptoms (high
blood pressure, albuminurea and preterm birth) resulting from extensive vasculo-endothelial pathology, primarily at the utero-fetal interface where maternal cardiac output is dramatically increased during pregnancy. Comt converts estradiol to 2-methoxyestradiol 2 (2ME2) which
counters angiogenesis by depleting hypoxia inducible factor-1 alpha (HIF-1 alpha) at late pregnancy. We propose that in wild type (Comt++) pregnant mice, 2ME2 destabilizes HIF-1 alpha by inhibiting mitochondrial superoxide dismutase (MnSOD). Thus, 2ME2 acts as a pro-oxidant, disrupting
redox-regulated signaling which blocks angiogenesis in wild type (WT) animals in physiological pregnancy. Further, we suggest that a lack of this inhibition under normoxic conditions in mutant animals (Comt-/-) stabilises HIF-1 alpha by inactivating prolyl hydroxlases (PHD). We predict that a lack of inhibition of MnSOD, leading to persistent accumulation of HIF-1 alpha, would trigger
inflammatory infiltration and endothelial damage in mutant animals. Critical tests of this hypothesis  would be to recreate preeclampsia symptoms by inducing oxidative stress in WT animals or to ameliorate by treating mutant mice with Mn-SOD-catalase mimetics or activators of PHD
Can We Really Prevent Suicide?
Every year, suicide is among the top 20 leading causes of death globally for all ages. Unfortunately, suicide is difficult to prevent, in large part because the prevalence of risk factors is high among the general population. In this review, clinical and psychological risk factors are examined and methods for suicide prevention are discussed. Prevention strategies found to be effective in suicide prevention
include means restriction, responsible media coverage, and general public education, as well identification methods such as screening, gatekeeper training, and primary care physician education. Although the treatment for preventing suicide is difficult, follow-up that includes pharmacotherapy, psychotherapy, or both may be useful. However, prevention methods cannot be restricted to the individual. Community, social, and policy interventions will also be essentia
Orbital state and magnetic properties of LiV_2 O_4
LiV_2 O_4 is one of the most puzzling compounds among transition metal oxides
because of its heavy fermion like behavior at low temperatures. In this paper
we present results for the orbital state and magnetic properties of LiV_2 O_4
obtained from a combination of density functional theory within the local
density approximation and dynamical mean-field theory (DMFT). The DMFT
equations are solved by quantum Monte Carlo simulations. The trigonal crystal
field splits the V 3d orbitals such that the a_{1g} and e_{g}^{pi} orbitals
cross the Fermi level, with the former being slightly lower in energy and
narrower in bandwidth. In this situation, the d-d Coulomb interaction leads to
an almost localization of one electron per V ion in the a_{1g} orbital, while
the e_{g}^{pi} orbitals form relatively broad bands with 1/8 filling. 2The
theoretical high-temperature paramagnetic susceptibility chi(T) follows a
Curie-Weiss law with an effective paramagnetic moment p_{eff}=1.65 in agreement
with the experimental results.Comment: 11 pages, 10 figures, 2 table
Predictive significance of the six-minute walk distance for long-term survival in chronic hypercapnic respiratory failure
Background: The 6-min walk distance ( 6-MWD) is a global marker of functional capacity and prognosis in chronic obstructive pulmonary disease ( COPD), but less explored in other chronic respiratory diseases. Objective: To study the role of 6-MWD in chronic hypercapnic respiratory failure ( CHRF). Methods: In 424 stable patients with CHRF and non-invasive ventilation ( NIV) comprising COPD ( n = 197), restrictive diseases ( RD; n = 112) and obesity-hypoventilation- syndrome ( OHS; n = 115), the prognostic value of 6-MWD for long- term survival was assessed in relation to that of body mass index (BMI), lung function, respiratory muscle function and laboratory parameters. Results: 6-MWD was reduced in patients with COPD ( median 280 m; quartiles 204/350 m) and RD ( 290 m; 204/362 m) compared to OHS ( 360 m; 275/440 m; p <0.001 each). Overall mortality during 24.9 (13.1/40.5) months was 22.9%. In the 424 patients with CHRF, 6-MWD independently predicted mortality in addition to BMI, leukocytes and forced expiratory volume in 1 s ( p <0.05 each). In COPD, 6-MWD was strongly associated with mortality using the median {[} p <0.001, hazard ratio ( HR) = 3.75, 95% confidence interval (CI): 2.24-6.38] or quartiles as cutoff levels. In contrast, 6-MWD was only significantly associated with impaired survival in RD patients when it was reduced to 204 m or less (1st quartile; p = 0.003, HR = 3.31, 95% CI: 1.73-14.10), while in OHS 6-MWD had not any prognostic value. Conclusions: In patients with CHRF and NIV, 6-MWD was predictive for long- term survival particularly in COPD. In RD only severely reduced 6-MWD predicted mortality, while in OHS 6-MWD was relatively high and had no prognostic value. These results support a disease-specific use of 6-MWD in the routine assessment of patients with CHRF. Copyright (C) 2007 S. Karger AG, Basel
Singular values of the Dirac operator in dense QCD-like theories
We study the singular values of the Dirac operator in dense QCD-like theories
at zero temperature. The Dirac singular values are real and nonnegative at any
nonzero quark density. The scale of their spectrum is set by the diquark
condensate, in contrast to the complex Dirac eigenvalues whose scale is set by
the chiral condensate at low density and by the BCS gap at high density. We
identify three different low-energy effective theories with diquark sources
applicable at low, intermediate, and high density, together with their
overlapping domains of validity. We derive a number of exact formulas for the
Dirac singular values, including Banks-Casher-type relations for the diquark
condensate, Smilga-Stern-type relations for the slope of the singular value
density, and Leutwyler-Smilga-type sum rules for the inverse singular values.
We construct random matrix theories and determine the form of the microscopic
spectral correlation functions of the singular values for all nonzero quark
densities. We also derive a rigorous index theorem for non-Hermitian Dirac
operators. Our results can in principle be tested in lattice simulations.Comment: 3 references added, version published in JHE
Deriving a mutation index of carcinogenicity using protein structure and protein interfaces
With the advent of Next Generation Sequencing the identification of mutations in the genomes of healthy and diseased tissues has become commonplace. While much progress has been made to elucidate the aetiology of disease processes in cancer, the contributions to disease that many individual mutations make remain to be characterised and their downstream consequences on cancer phenotypes remain to be understood. Missense mutations commonly occur in cancers and their consequences remain challenging to predict. However, this knowledge is becoming more vital, for both assessing disease progression and for stratifying drug treatment regimes. Coupled with structural data, comprehensive genomic databases of mutations such as the 1000 Genomes project and COSMIC give an opportunity to investigate general principles of how cancer mutations disrupt proteins and their interactions at the molecular and network level. We describe a comprehensive comparison of cancer and neutral missense mutations; by combining features derived from structural and interface properties we have developed a carcinogenicity predictor, InCa (Index of Carcinogenicity). Upon comparison with other methods, we observe that InCa can predict mutations that might not be detected by other methods. We also discuss general limitations shared by all predictors that attempt to predict driver mutations and discuss how this could impact high-throughput predictions. A web interface to a server implementation is publicly available at http://inca.icr.ac.uk/
Molecular and cellular mechanisms underlying the evolution of form and function in the amniote jaw.
The amniote jaw complex is a remarkable amalgamation of derivatives from distinct embryonic cell lineages. During development, the cells in these lineages experience concerted movements, migrations, and signaling interactions that take them from their initial origins to their final destinations and imbue their derivatives with aspects of form including their axial orientation, anatomical identity, size, and shape. Perturbations along the way can produce defects and disease, but also generate the variation necessary for jaw evolution and adaptation. We focus on molecular and cellular mechanisms that regulate form in the amniote jaw complex, and that enable structural and functional integration. Special emphasis is placed on the role of cranial neural crest mesenchyme (NCM) during the species-specific patterning of bone, cartilage, tendon, muscle, and other jaw tissues. We also address the effects of biomechanical forces during jaw development and discuss ways in which certain molecular and cellular responses add adaptive and evolutionary plasticity to jaw morphology. Overall, we highlight how variation in molecular and cellular programs can promote the phenomenal diversity and functional morphology achieved during amniote jaw evolution or lead to the range of jaw defects and disease that affect the human condition
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