Theoretical approach to oxygen atom degradation of silver

Based on available Rutherford backscattering spectrometry (RBS), proton induced X-ray emission (PIXE) and ellipsometry data obtained on silver specimens subjected to atomic oxygen attack in low Earth orbit STS flight 41-G, a theory was developed to model the oxygen atom degradation of silver. The diffusion of atomic oxygen in a microscopically nonuniform medium is an essential constituent of the theory. The driving force for diffusion is the macroscopic electrochemical potential gradient developed between the specimen surface exposed to the ambient and the bulk of the silver specimen. The longitudinal electric effect developed parallel to the gradient is modified by space charge of the diffusing charged species. Lateral electric fields and concentration differences also exist due to the nonuniform nature of the medium. The lateral concentration differences are found to be more important than the lateral electric fields in modifying the diffusion rate. The model was evaluated numerically. Qualitative agreement exists between the kinetics predicted by the theory and kinetic data taken in ground-based experiments utilizing a plasma asher

Direct sampling of exponential phase moments of smoothed Wigner functions

We investigate exponential phase moments of the s-parametrized quasidistributions (smoothed Wigner functions). We show that the knowledge of these moments as functions of s provides, together with photon-number statistics, a complete description of the quantum state. We demonstrate that the exponential phase moments can be directly sampled from the data recorded in balanced homodyne detection and we present simple expressions for the sampling kernels. The phase moments are Fourier coefficients of phase distributions obtained from the quasidistributions via integration over the radial variable in polar coordinates. We performed Monte Carlo simulations of the homodyne detection and we demonstrate the feasibility of direct sampling of the moments and subsequent reconstruction of the phase distribution.Comment: RevTeX, 8 pages, 6 figures, accepted Phys. Rev.

Non-monotonic magnetic field and density dependence of in-plane magnetoresistance in dilute two-dimensional holes in GaAs/AlGaAs

We studied low temperature (T=50mK) in-plane magnetoresistance of a dilute two-dimensional hole system in GaAs/AlGaAs heterostructure that exhibits an apparent metal-insulator transition. We found an anisotropic magnetoresistance, which changes dramatically at high in-plane fields (B_{\parallel}\agt5T) as the hole density is varied. At high densities where the system behaves metallic at $B_{\parallel}=0$, the transverse magnetoresistance is larger than the longitudinal magnetoresistance. With decreasing the hole density the difference becomes progressively smaller, and at densities near the "critical" density and lower, the longitudinal magnetoresistance becomes larger than the transverse magnetoresistance

Energy-Momentum Tensor of Cosmological Fluctuations during Inflation

We study the renormalized energy-momentum tensor (EMT) of cosmological scalar fluctuations during the slow-rollover regime for chaotic inflation with a quadratic potential and find that it is characterized by a negative energy density which grows during slow-rollover. We also approach the back-reaction problem as a second-order calculation in perturbation theory finding no evidence that the back-reaction of cosmological fluctuations is a gauge artifact. In agreement with the results on the EMT, the average expansion rate is decreased by the back-reaction of cosmological fluctuations.Comment: 19 pages, no figures.An appendix and references added, conclusions unchanged, version accepted for publication in PR

Field-induced Ordering in Critical Antiferromagnets

Transfer-matrix scaling methods have been used to study critical properties of field-induced phase transitions of two distinct two-dimensional antiferromagnets with discrete-symmetry order parameters: triangular-lattice Ising systems (TIAF) and the square-lattice three-state Potts model (SPAF-3). Our main findings are summarised as follows. For TIAF, we have shown that the critical line leaves the zero-temperature, zero -field fixed point at a finite angle. Our best estimate of the slope at the origin is $(dT_c/dH)_{T=H=0} = 4.74 \pm 0.15$. For SPAF-3 we provided evidence that the zero-field correlation length diverges as $\xi(T \to 0, H=0) \simeq \exp (a/T^{x})$, with $x=1.08 \pm 0.13$, through analysis of the critical curve at $H \neq 0$ plus crossover arguments. For SPAF-3 we have also ascertained that the conformal anomaly and decay-of-correlations exponent behave as: (a) H=0: $c=1, \eta=1/3$; (b) $H \neq 0: c=1/2, \eta=1/4$.Comment: RevTex, 7 pages, 4 eps figures, to be published in Phys. Rev.

Mechanically Powered Motion Imaging Phantoms: Proof of Concept

Motion imaging phantoms are expensive, bulky and difficult to transport and set-up. The purpose of this paper is to demonstrate a simple approach to the design of multi-modality motion imaging phantoms that use mechanically stored energy to produce motion. We propose two phantom designs that use mainsprings and elastic bands to store energy. A rectangular piece was attached to an axle at the end of the transmission chain of each phantom, and underwent a rotary motion upon release of the mechanical motor. The phantoms were imaged with MRI and US, and the image sequences were embedded in a 1D non linear manifold (Laplacian Eigenmap) and the spectrogram of the embedding was used to derive the angular velocity over time. The derived velocities were consistent and reproducible within a small error. The proposed motion phantom concept showed great potential for the construction of simple and affordable motion phantomsComment: Accepted for publication at IEEE EMBC (41st International Engineering in Medicine and Biology Conference) 201

Dll4 Suppresses Transcytosis for Arterial Blood-Retinal Barrier Homeostasis

Rationale: Central nervous system has low vascular permeability by organizing tight junction (TJ) and limiting endothelial transcytosis. While TJ has long been considered to be responsible for vascular barrier in central nervous system, suppressed transcytosis in endothelial cells is now emerging as a complementary mechanism. Whether transcytosis regulation is independent of TJ and its dysregulation dominantly causes diseases associated with edema remain elusive. Dll4 signaling is important for various vascular contexts, but its role in the maintenance of vascular barrier in central nervous system remains unknown. / Objective: To find a TJ-independent regulatory mechanism selective for transcytosis and identify its dysregulation as a cause of pathological leakage. / Methods and Results: We studied transcytosis in the adult mouse retina with low vascular permeability and employed a hypertension-induced retinal edema model for its pathological implication. Both antibody-based and genetic inactivation of Dll4 or Notch1 induce hyperpermeability by increasing transcytosis without junctional destabilization in arterial endothelial cells, leading to nonhemorrhagic leakage predominantly in the superficial retinal layer. Endothelial Sox17 deletion represses Dll4 in retinal arteries, phenocopying Dll4 blocking-driven vascular leakage. Ang II (angiotensin II)–induced hypertension represses arterial Sox17 and Dll4, followed by transcytosis-driven retinal edema, which is rescued by a gain of Notch activity. Transcriptomic profiling of retinal endothelial cells suggests that Dll4 blocking activates SREBP1 (sterol regulatory element-binding protein 1)-mediated lipogenic transcription and enriches gene sets favorable for caveolae formation. Profiling also predicts the activation of VEGF (vascular endothelial growth factor) signaling by Dll4 blockade. Inhibition of SREBP1 or VEGF-VEGFR2 (VEGF receptor 2) signaling attenuates both Dll4 blockade–driven and hypertension-induced retinal leakage. / Conclusions: In the retina, Sox17-Dll4-SREBP1 signaling axis controls transcytosis independently of TJ in superficial arteries among heterogeneous regulations for the whole vessels. Uncontrolled transcytosis via dysregulated Dll4 underlies pathological leakage in hypertensive retina and could be a therapeutic target for treating hypertension-associated retinal edema

The role of mTOR and phospho-p70S6K in pathogenesis and progression of gastric carcinomas: an immunohistochemical study on tissue microarray

<p>Abstract</p> <p>Background</p> <p>mTOR signaling pathway and its downstream serine/threonine kinase p70S6k were frequently activated in human cancers. The dysregulation of the mTOR pathway has been found to be a contributing factor of a variety of different cancer. To investigate the role of mTOR signal pathway in the stepwise development of gastric carcinomas, we analyzed the correlations between the mTOR and P70S6K expression and clinic pathological factors and studied its prognostic role in gastric carcinomas.</p> <p>Methods</p> <p>mTOR and phospho-p70S6K proteins were examined by immunohistochemistry on tissue microarray containing gastric carcinomas (n = 412), adenomas (n = 47) and non-neoplastic mucosa (NNM, n = 197) with a comparison of their expression with clinicopathological parameters of carcinomas.</p> <p>Results</p> <p>There was no difference of mTOR expression between these three tissues (p > 0.05). Cytoplasmic phospho(p)-P706SK was highly expressed in adenoma, compared with ANNMs (p < 0.05), whereas its nuclear expression was lower in gastric carcinomas than gastric adenoma and ANNMs (p < 0.05). These three markers were preferably expressed in the older patients with gastric cancer and intestinal-type carcinoma (p < 0.05). mTOR expression was positively correlated with the cytoplasmic and nuclear expression of p-P70S6K(p < 0.05). Nuclear P70S6K was inversely linked to tumor size, depth of invasion, lymph node metastasis and UICC staging (p < 0.05). Univariate analysis indicated that expression of mTOR and nuclear p-P70S6K was closely linked to favorable prognosis of the carcinoma patients (p < 0.05). Multivariate analysis showed that age, depth of invasion, lymphatic invasion, lymph node metastasis, Lauren's classification and mTOR expression were independent prognostic factors for overall gastric carcinomas (p < 0.05).</p> <p>Conclusion</p> <p>Aberrant expression of p-P70S6K possibly contributes to pathogenesis, growth, invasion and metastasis of gastric carcinomas. It was considered as a promising marker to indicate the aggressive behaviors and prognosis of gastric carcinomas.</p

HDAC1 Inactivation Induces Mitotic Defect and Caspase-Independent Autophagic Cell Death in Liver Cancer

Histone deacetylases (HDACs) are known to play a central role in the regulation of several cellular properties interlinked with the development and progression of cancer. Recently, HDAC1 has been reported to be overexpressed in hepatocellular carcinoma (HCC), but its biological roles in hepatocarcinogenesis remain to be elucidated. In this study, we demonstrated overexpression of HDAC1 in a subset of human HCCs and liver cancer cell lines. HDAC1 inactivation resulted in regression of tumor cell growth and activation of caspase-independent autophagic cell death, via LC3B-II activation pathway in Hep3B cells. In cell cycle regulation, HDAC1 inactivation selectively induced both p21WAF1/Cip1 and p27Kip1 expressions, and simultaneously suppressed the expression of cyclin D1 and CDK2. Consequently, HDAC1 inactivation led to the hypophosphorylation of pRb in G1/S transition, and thereby inactivated E2F/DP1 transcription activity. In addition, we demonstrated that HDAC1 suppresses p21WAF1/Cip1 transcriptional activity through Sp1-binding sites in the p21WAF1/Cip1 promoter. Furthermore, sustained suppression of HDAC1 attenuated in vitro colony formation and in vivo tumor growth in a mouse xenograft model. Taken together, we suggest the aberrant regulation of HDAC1 in HCC and its epigenetic regulation of gene transcription of autophagy and cell cycle components. Overexpression of HDAC1 may play a pivotal role through the systemic regulation of mitotic effectors in the development of HCC, providing a particularly relevant potential target in cancer therapy