393 research outputs found
Molecular simulations of sliding on SDS surfactant films
We use molecular dynamics simulations to study the frictional response of the
anionic surfactant sodium dodecyl sulfate (SDS) monolayers and hemicylindrical
aggregates physisorbed on gold. Our simulations of a sliding spherical asperity
reveals two friction regimes: At low loads, the films show Amontons' friction
with a friction force that rises linearly with normal load. At high loads, the
friction force is independent of load as long as no direct solid-solid contact
occurs. The transition between these two regimes happens when only a single
molecular layer is confined in the gap between the sliding bodies. The friction
force at high loads on a monolayer rises monotonically with film density and
drops slightly with the transition to hemicylindrical aggregates. This
monotonous increase of friction force is compatible with a traditional plowing
model of sliding friction. At low loads, the friction coefficient reaches a
minimum at intermediate surface concentrations. We attribute this behavior to a
competition between adhesive forces, repulsion of the compressed film, and the
onset of plowing.Comment: 14 pages, 10 figure
Spatial Structures in a Generalized Ginzburg-Landau Free Energy
Searching for characteristic signatures of a higher order phase transition
(specifically of order three or four), we have calculated the spatial profiles
and the energies of a spatially varying order parameter in one dimension. In
the case of a order phase transition to a superconducting ground
state, the free energy density depends on temperature as , where is the reduced temperature. The energy of a domain wall between
two degenerate ground states is . We have also
investigated the effects of a supercurrent in a narrow wire. These effects are
limited by a critical current which has a temperature dependence . The phase slip center profiles and their energies are also
calculated. Given the suggestion that the superconducting transtion in \bkbox,
for , may be of order four, these predictions have relevance for
future experiments.Comment: 7 pages, 5 figure
High Altitude test of RPCs for the ARGO-YBJ experiment
A 50 m**2 RPC carpet was operated at the YangBaJing Cosmic Ray Laboratory
(Tibet) located 4300 m a.s.l. The performance of RPCs in detecting Extensive
Air Showers was studied. Efficiency and time resolution measurements at the
pressure and temperature conditions typical of high mountain laboratories, are
reported.Comment: 16 pages, 10 figures, submitted to Nucl. Instr. Met
Negative Elongation Factor Controls Energy Homeostasis in Cardiomyocytes
SummaryNegative elongation factor (NELF) is known to enforce promoter-proximal pausing of RNA polymerase II (Pol II), a pervasive phenomenon observed across multicellular genomes. However, the physiological impact of NELF on tissue homeostasis remains unclear. Here, we show that whole-body conditional deletion of the B subunit of NELF (NELF-B) in adult mice results in cardiomyopathy and impaired response to cardiac stress. Tissue-specific knockout of NELF-B confirms its cell-autonomous function in cardiomyocytes. NELF directly supports transcription of those genes encoding rate-limiting enzymes in fatty acid oxidation (FAO) and the tricarboxylic acid (TCA) cycle. NELF also shares extensively transcriptional target genes with peroxisome proliferator-activated receptor α (PPARα), a master regulator of energy metabolism in the myocardium. Mechanistically, NELF helps stabilize the transcription initiation complex at the metabolism-related genes. Our findings strongly indicate that NELF is part of the PPARα-mediated transcription regulatory network that maintains metabolic homeostasis in cardiomyocytes
The Alternating Access Transport Mechanism in LacY
Lactose permease of Escherichia coli (LacY) is highly dynamic, and sugar binding causes closing of a large inward-facing cavity with opening of a wide outward-facing hydrophilic cavity. Therefore, lactose/H+ symport via LacY very likely involves a global conformational change that allows alternating access of single sugar- and H+-binding sites to either side of the membrane. Here, in honor of Stephan H. White’s seventieth birthday, we review in camera the various biochemical/biophysical approaches that provide experimental evidence for the alternating access mechanism
Forced Notch Signaling Inhibits Commissural Axon Outgrowth in the Developing Chick Central Nerve System
BACKGROUND: A collection of in vitro evidence has demonstrated that Notch signaling plays a key role in the growth of neurites in differentiated neurons. However, the effects of Notch signaling on axon outgrowth in an in vivo condition remain largely unknown. METHODOLOGY/PRINCIPAL FINDINGS: In this study, the neural tubes of HH10-11 chick embryos were in ovo electroporated with various Notch transgenes of activating or inhibiting Notch signaling, and then their effects on commissural axon outgrowth across the floor plate midline in the chick developing central nerve system were investigated. Our results showed that forced expression of Notch intracellular domain, constitutively active form of RBPJ, or full-length Hes1 in the rostral hindbrain, diencephalon and spinal cord at stage HH10-11 significantly inhibited commissural axon outgrowth. On the other hand, inhibition of Notch signaling by ectopically expressing a dominant-negative form of RBPJ promoted commissural axonal growth along the circumferential axis. Further results revealed that these Notch signaling-mediated axon outgrowth defects may be not due to the alteration of axon guidance since commissural axon marker TAG1 was present in the axons in floor plate midline, and also not result from the changes in cell fate determination of commissural neurons since the expression of postmitotic neuron marker Tuj1 and specific commissural markers TAG1 and Pax7 was unchanged. CONCLUSIONS/SIGNIFICANCE: We first used an in vivo system to provide evidence that forced Notch signaling negatively regulates commissural axon outgrowth
The insertion/deletion (I/D) polymorphism in the Angiotensin-converting enzyme gene and cancer risk: a meta-analysis
<p>Abstract</p> <p>Background</p> <p>The insertion/deletion (I/D) polymorphism in the <it>Angiotensin-converting enzyme </it>(<it>ACE</it>) gene has been implicated in susceptibility to cancer, but a large number of studies have reported inconclusive results. The aim of this study is to assess the association between the I/D polymorphism in the <it>ACE </it>gene and cancer risk by meta-analysis.</p> <p>Methods</p> <p>A search was performed in Pubmed database, Embase database, Chinese Biomedical (CBM) database, China National Knowledge Infrastructure (CNKI) database and Weipu database, covering all studies until August 31, 2010. Statistical analysis was performed by using Revman4.2 and STATA 10.0.</p> <p>Results</p> <p>A total of 25 case-control studies comprising 3914 cancer patients and 11391 controls were identified. No significant association was found between the I/D polymorphism and over all cancer risks (OR = 0.88, 95%CI = 0.73-1.06, P = 0.17 for DD+DI vs. II). In the subgroup analysis by ethnicity, no significant association was found among Asians and Europeans for the comparison of DD+DI vs. II. In the subgroup analysis by cancer types, no significant associations were found among lung cancer, breast cancer, prostate cancer, colorectal cancer, gastric cancer for the comparison of DD+DI vs. II. Results from other comparative genetic models also indicated the lack of associations between this polymorphism and cancer risks.</p> <p>Conclusions</p> <p>This meta-analysis suggested that the <it>ACE </it>D/I polymorphism might not contribute to the risk of cancer.</p
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