Inflation in Supersymmetric SU(5)

We analyze the adjoint field inflation in supersymmetric (SUSY) SU(5) model. In minimal SUSY SU(5) hybrid inflation monopoles are produced at the end of inflation. We therefore explore the non-minimal model of inflation based on SUSY SU(5), like shifted hybrid, which provides a natural solution for the monopole problem. We find that the supergravity corrections with non-minimal Kahler potential are crucial to realize the central value of the scalar spectral index n_s ~ 0.96 consistent with the seven year WMAP data. The tensor to scalar ratio r is quite small, taking on values r < 10^{-5}. Due to R-symmetry massless SU(3) octet and SU(2) triplet Higgs bosons are present and could spoil for gauge coupling unification. To keep gauge coupling unification intact, light vector-like particles are added which are expected to be observed at LHC.Comment: 16 page

Spin contributions to the gravitational-waveform modes for spin-aligned binaries at the 3.5PN order

We complete the post-Newtonian (PN) prediction at the 3.5PN order for the spin contributions to the gravitational waveforms emitted by inspiraling compact binaries, in the case of quasi-circular, equatorial orbits, where both spins are aligned with the orbital angular momentum. Using results from the multipolar post-Minkowskian wave generation formalism, we extend previous works that derived the dynamics and gravitational-wave energy flux and phasing, by computing the full waveform decomposed in spin-weighted spherical harmonics. This new calculation requires the computation of multipolar moments of higher multipolar order, new quadratic-in-spin contributions to the hereditary tail terms entering at the 3.5PN order, as well as other non-linear interactions between moments. When specialized to the test-mass limit, our results are equivalent to those obtained in the literature for the waveform emitted by a test-mass in equatorial, circular orbits around a Kerr black hole. We also compute the factorized modes for use in effective-one-body waveform models, correcting the 2.5PN nonspinning and 3PN quadratic-in-spin terms in the (2,1) mode used in current models

Microencapsulated 3-Dimensional Sensor for the Measurement of Oxygen in Single Isolated Pancreatic Islets

Background: Oxygen consumption reflects multiple processes in pancreatic islets including mechanisms contributing to insulin secretion, oxidative stress and viability, providing an important readout in studies of islet function, islet viability and drug testing. Due to the scarcity, heterogeneity, and intrinsic kinetic properties of individual islets, it would be of great benefit to detect oxygen consumption by single islets. We present a novel method we have developed to image oxygen in single islets. Methodology/Principal Findings: Using a microfluidics system, individual islets and a fluorescent oxygen-sensitive dye were encased within a thin alginate polymer layer. Insulin secretion by the encapsulated islets was normal. Fluorescent signal from the encased dye, detected using a standard inverted fluorescence microscope and digital camera, was stable and proportional to the amount of oxygen in the media. When integrated into a perifusion system, the sensing system detected changes in response to metabolic substrates, mitochondrial poisons, and induced-oscillations. Glucose responses averaged 30.167.1 % of the response to a metabolic inhibitor (cyanide), increases were observed in all cases (n = 6), and the system was able to resolve changes in oxygen consumption that had a period greater than 0.5 minutes. The sensing system operated similarly from 2–48 hours following encapsulation, and viability and function of the islets were not significantly affected by the encapsulation process

Global synchronization for delayed complex networks with randomly occurring nonlinearities and multiple stochastic disturbances

This is the post print version of the article. The official published version can be obained from the link - Copyright 2009 IOP Publishing LtdThis paper is concerned with the synchronization problem for a new class of continuous time delayed complex networks with stochastic nonlinearities (randomly occurring nonlinearities), interval time-varying delays, unbounded distributed delays as well as multiple stochastic disturbances. The stochastic nonlinearities and multiple stochastic disturbances are investigated here in order to reflect more realistic dynamical behaviors of the complex networks that are affected by the noisy environment. By utilizing a new matrix functional with the idea of partitioning the lower bound h1 of the time-varying delay, we employ the stochastic analysis techniques and the properties of the Kronecker product to establish delay-dependent synchronization criteria that ensure the globally asymptotically mean-square synchronization of the addressed stochastic delayed complex networks. The sufficient conditions obtained are in the form of linear matrix inequalities (LMIs) whose solutions can be readily solved by using the standard numerical software. A numerical example is exploited to show the applicability of the proposed results.This work was supported in part by the Engineering and Physical Sciences Research Council (EPSRC) of the UK under Grant GR/S27658/01, an International Joint Project sponsored by the Royal Society of the UK, the National 973 Program of China under Grant 2009CB320600, the National Natural Science Foundation of China under Grant 60804028, the Specialized Research Fund for the Doctoral Program of Higher Education for New Teachers under Grant 200802861044, the Teaching and Research Fund for Excellent Young Teachers at Southeast University of China, and the Alexander von Humboldt Foundation of Germany

Asymmetrical Axillary Artery Deviations of the Brachial Plexus

Introduction: The relationship between the brachial plexus and other key axillary vascular structures have been explored extensively in medical literature highlighting different variations in the brachial plexus. Understanding variations provides valuable knowledge for surgical interventions. Typically at the axillary region, the lateral cord splits into the musculocutaneous nerve and the lateral root of the median nerve. The medial cord contributes the medial root to the median nerve where the axillary artery normally runs posteriorly. Objective: The goal of this case report is to highlight a bilateral anatomical variation of the brachial plexus in relation of the progression of the axillary artery in a 71 year-old male cadaver. Methods: During a routine dissection in a medical school Anatomy course, the axilla of a male cadaver was dissected bilaterally according to laboratory protocol. Digital photography was used to preserve visual observations. Results: In the right axilla, the joining of the lateral root and medial root to form the median nerve occurs proximally in the axillary region. This junction occurs more distally in the brachial region of the left arm. In the left axilla, the axillary artery is running between the superior anterior division and the middle anterior division from anteriorly to posteriorly. More distally, the axillary emerges from the posterior side coming over the median nerve. The right axillary region has an axillary artery running above the median nerve as well. Conclusion: Knowledge of anatomical variations in the brachial plexus is important for anatomists and surgeons during interventional procedures including nerve blocks and surgery. Here we report a unique variation of the brachial plexus and the position of the axillary artery in the left axilla as well as the right axilla

Silencing CD36 gene expression results in the inhibition of latent-TGF-β1 activation and suppression of silica-induced lung fibrosis in the rat

<p>Abstract</p> <p>Background</p> <p>The biologically active form of transforming growth factor-β1 (TGF-β1) plays a key role in the development of lung fibrosis. CD36 is involved in the transformation of latent TGF-β1 (L-TGF-β1) to active TGF-β1. To clarify the role of CD36 in the development of silica-induced lung fibrosis, a rat silicosis model was used to observe both the inhibition of L-TGF-β1 activation and the antifibrotic effect obtained by lentiviral vector silencing of CD36 expression.</p> <p>Methods</p> <p>The rat silicosis model was induced by intratracheal injection of 10 mg silica per rat and CD36 expression was silenced by administration of a lentiviral vector (Lv-shCD36). The inhibition of L-TGF-β1 activation was examined using a CCL-64 mink lung epithelial growth inhibition assay, while determination of hydroxyproline content along with pathological and immunohistochemical examinations were used for observation of the inhibition of silica-induced lung fibrosis.</p> <p>Results</p> <p>The lentiviral vector (Lv-shCD36) silenced expression of CD36 in alveolar macrophages (AMs) obtained from bronchoalveolar lavage fluid (BALF) and the activation of L-TGF-β1 in the BALF was inhibited by Lv-shCD36. The hydroxyproline content of silica+Lv-shCD36 treated groups was significantly lower than in other experimental groups. The degree of fibrosis in the silica+Lv-shCD36-treated groups was less than observed in other experimental groups. The expression of collagen I and III in the silica+Lv-shCD36-treated group was significantly lower than in the other experimental groups.</p> <p>Conclusion</p> <p>These results indicate that silencing expression of CD36 can result in the inhibition of L-TGF-β1 activation in a rat silicosis model, thus further preventing the development of silica-induced lung fibrosis.</p

Mitochondria matter: Systemic aspects of nonalcoholic fatty liver disease (nafld) and diagnostic assessment of liver function by stable isotope dynamic breath tests

The liver plays a key role in systemic metabolic processes, which include detoxification, synthesis, storage, and export of carbohydrates, lipids, and proteins. The raising trends of obesity and metabolic disorders worldwide is often associated with the nonalcoholic fatty liver disease (NAFLD), which has become the most frequent type of chronic liver disorder with risk of progression to cirrhosis and hepatocellular carcinoma. Liver mitochondria play a key role in degrading the pathways of carbohydrates, proteins, lipids, and xenobiotics, and to provide energy for the body cells. The morphological and functional integrity of mitochondria guarantee the proper functioning of β‐oxidation of free fatty acids and of the tricarboxylic acid cycle. Evaluation of the liver in clinical medicine needs to be accurate in NAFLD patients and includes history, physical exam, imaging, and laboratory assays. Evaluation of mitochondrial function in chronic liver disease and NAFLD is now possible by novel diagnostic tools. “Dynamic” liver function tests include the breath test (BT) based on the use of substrates marked with the non‐radioactive, naturally occurring stable isotope13C. Hepatocellular metabolization of the substrate will generate13CO2, which is excreted in breath and measured by mass spectrometry or infrared spectroscopy. Breath levels of 13 CO2 are biomarkers of specific metabolic processes occurring in the hepatocyte cytosol, microsomes, and mitochondria.13 C‐BTs explore distinct chronic liver diseases including simple liver steatosis, non‐alcoholic steatohepatitis, liver fibrosis, cirrhosis, hepatocellular carcinoma, drug, and alcohol effects. In NAFLD,13C‐BT use substrates such as α‐ketoisocaproic acid, methionine, and octanoic acid to assess mitochondrial oxidation capacity which can be impaired at an early stage of disease.13C‐BTs represent an indirect, cost‐effective, and easy method to evaluate dynamic liver function. Further applications are expected in clinical medicine. In this review, we discuss the involvement of liver mitochondria in the progression of NAFLD, together with the role of13C‐BT in assessing mitochondrial function and its potential use in the prevention and management of NAFLD