Controlled glass bead peening Patent

Method and apparatus for inducing compressive stresses in pressure vessel to prevent stress corrosio

Is Reisprosa Joernalistiek?

Om na ’n bekende land te reis, om die aard van die landskap, die mense en hul lewenswyse daar te leer ken, bly nog steeds ’n opwindende ervaring. Die revolusie wat die moderne tegniek ten opsigte van lugvervoer teweeggebring het, het die wêreld benouend klein gemaak. Wat vroeer ’n onbereikbare wêrelddeel was, het nou skokkend naby gekom, intiem bekend geword. Om dié rede is die merkwaardige opbloei van reisprosa in die eietydse wêreldliteratuur verstaanbaar

Structural and electrical transport properties of superconducting Au{0.7}In{0.3} films: A random array of superconductor-normal metal-superconductor (SNS) Josephson junctions

The structural and superconducting properties of Au{0.7}In{0.3} films, grown by interdiffusion of alternating Au and In layers, have been studied. The films were found to consist of a uniform solid solution of Au{0.9}In{0.1}, with excess In precipitated in the form of In-rich grains of various Au-In phases (with distinct atomic compositions), including intermetallic compounds. As the temperature was lowered, these individual grains became superconducting at a particular transition temperature (Tc), determined primarily by the atomic composition of the grain, before a fully superconducting state of zero resistance was established. From the observed onset Tc, it was inferred that up to three different superconducting phases could have formed in these Au{0.7}In{0.3} films, all of which were embedded in a uniform Au{0.9}In{0.1} matrix. Among these phases, the Tc of a particular one, 0.8 K, is higher than any previously reported for the Au-In system. The electrical transport properties were studied down to low temperatures. The transport results were found to be well correlated with those of the structural studies. The present work suggests that Au{0.7}In{0.3} can be modeled as a random array of superconductor-normal metal-superconductor (SNS) Josephson junctions. The effect of disorder and the nature of the superconducting transition in these Au{0.7}In{0.3} films are discussed.Comment: 8 text pages, 10 figures in one separate PDF file, submitted to PR

Precious Metals in SDSS Quasar Spectra. II. Tracking the Evolution of Strong, 0.4 < z < 2.3 Mg II Absorbers with Thousands of Systems

We have performed an analysis of over 34,000 Mg II doublets at 0.36 < z < 2.29 in Sloan Digital Sky Survey (SDSS) Data Release 7 quasar spectra; the catalog, advanced data products, and tools for analysis are publicly available. The catalog was divided into 14 small redshift bins with roughly 2500 doublets in each and from Monte Carlo simulations, we estimate 50% completeness at rest equivalent width W_r ≈ 0.8 Å. The equivalent width frequency distribution is described well by an exponential model at all redshifts, and the distribution becomes flatter with increasing redshift, i.e., there are more strong systems relative to weak ones. Direct comparison with previous SDSS Mg II surveys reveals that we recover at least 70% of the doublets in these other catalogs, in addition to detecting thousands of new systems. We discuss how these surveys came by their different results, which qualitatively agree but because of the very small uncertainties, differ by a statistically significant amount. The estimated physical cross section of Mg II-absorbing galaxy halos increased approximately threefold from z = 0.4 to z = 2.3, while the W_r ≥ 1 Å absorber line density, dN_(Mg II)/dX, grew by roughly 45%. Finally, we explore the different evolution of various absorber populations—damped Lyα absorbers, Lyman limit systems, strong C IV absorbers, and strong and weaker Mg II systems—across cosmic time (0 < z < 6)

Brucella abortus Infection of Placental Trophoblasts Triggers Endoplasmic Reticulum Stress-Mediated Cell Death and Fetal Loss via Type IV Secretion System-Dependent Activation of CHOP.

Subversion of endoplasmic reticulum (ER) function is a feature shared by multiple intracellular bacteria and viruses, and in many cases this disruption of cellular function activates pathways of the unfolded protein response (UPR). In the case of infection with Brucella abortus, the etiologic agent of brucellosis, the unfolded protein response in the infected placenta contributes to placentitis and abortion, leading to pathogen transmission. Here we show that B. abortus infection of pregnant mice led to death of infected placental trophoblasts in a manner that depended on the VirB type IV secretion system (T4SS) and its effector VceC. The trophoblast death program required the ER stress-induced transcription factor CHOP. While NOD1/NOD2 expression in macrophages contributed to ER stress-induced inflammation, these receptors did not play a role in trophoblast death. Both placentitis and abortion were independent of apoptosis-associated Speck-like protein containing a caspase activation and recruitment domain (ASC). These studies show that B. abortus uses its T4SS to induce cell-type-specific responses to ER stress in trophoblasts that trigger placental inflammation and abortion. Our results suggest further that in B. abortus the T4SS and its effectors are under selection as bacterial transmission factors.IMPORTANCE Brucella abortus infects the placenta of pregnant cows, where it replicates to high levels and triggers abortion of the calf. The aborted material is highly infectious and transmits infection to both cows and humans, but very little is known about how B. abortus causes abortion. By studying this infection in pregnant mice, we discovered that B. abortus kills trophoblasts, which are important cells for maintaining pregnancy. This killing required an injected bacterial protein (VceC) that triggered an endoplasmic reticulum (ER) stress response in the trophoblast. By inhibiting ER stress or infecting mice that lack CHOP, a protein induced by ER stress, we could prevent death of trophoblasts, reduce inflammation, and increase the viability of the pups. Our results suggest that B. abortus injects VceC into placental trophoblasts to promote its transmission by abortion

Interferon-γ inducible factor 16 (IFI16) restricts adeno-associated virus type 2 (AAV2) transduction in an immune-modulatory independent way

We determined the transcription profile of adeno-associated virus type 2 (AAV2)-infected primary human fibroblasts. Subsequent analysis revealed that cells respond to AAV infection through changes in several significantly affected pathways, including cell cycle regulation, chromatin modulation, and innate immune responses. Various assays were performed to validate selected differentially expressed genes and to confirm not only the quality but also the robustness of the raw data. One of the genes upregulated in AAV2-infected cells was interferon-γ inducible factor 16 (IFI16). IFI16 is known as a multifunctional cytosolic and nuclear innate immune sensor for double-stranded as well as single-stranded DNA, exerting its effects through various mechanisms, such as interferon response, epigenetic modifications, or transcriptional regulation. IFI16 thereby constitutes a restriction factor for many different viruses among them, as shown here, AAV2 and thereof derived vectors. Indeed, the post-transcriptional silencing of IFI16 significantly increased AAV2 transduction efficiency, independent of the structure of the virus/vector genome. We also show that IFI16 exerts its inhibitory effect on AAV2 transduction in an immune-modulatory independent way by interfering with Sp1-dependent transactivation of wild-type AAV2 and AAV2 vector promoters. IMPORTANCE Adeno-associated virus (AAV) vectors are among the most frequently used viral vectors for gene therapy. The lack of pathogenicity of the parental virus, the long-term persistence as episomes in non-proliferating cells, and the availability of a variety of AAV serotypes differing in their cellular tropism are advantageous features of this biological nanoparticle. To deepen our understanding of virus-host interactions, especially in terms of antiviral responses, we present here the first transcriptome analysis of AAV serotype 2 (AAV2)-infected human primary fibroblasts. Our findings indicate that interferon-γ inducible factor 16 acts as an antiviral factor in AAV2 infection and AAV2 vector-mediated cell transduction in an immune-modulatory independent way by interrupting the Sp1-dependent gene expression from viral or vector genomes