Microdeformation in Vredefort rocks; evidence for shock metamorphism

Planar microdeformations in quartz from basement or collar rocks of the Vredefort Dome have been cited for years as the main microtextural evidence for shock metamorphism in this structure. In addition, Schreyer describes feldspar recrystallization in rocks from the center of the Dome as the result of transformation of diaplectic glass, and Lilly reported the sighting of mosaicism in quartz. These textural observations are widely believed to indicate either an impact or an internally produced shock origin for the Vredefort Dome. Two types of (mostly sub) planar microdeformations are displayed in quartz grains from Vredefort rocks: (1) fluid inclusion trails, and (2) straight optical discontinuities that sometimes resemble lamellae. Both types occur as single features or as single or multiple sets in quartz grains. Besides qualitative descriptions of cleavage and recrystallization in feldspar and kinkbands in mica, no further microtextural evidence for shock metamorphism at Vredefort has been reported to date. Some 150 thin sections of Vredefort basement rocks were re-examined for potential shock and other deformation effects in all rock-forming minerals. This included petrographic study of two drill cores from the immediate vicinity of the center of the Dome. Observations recorded throughout the granitic core are given along with conclusions

Ar-40 to Ar-39 dating of pseudotachylites from the Witwatersrand basin, South Africa, with implications for the formation of the Vredefort Dome

The formation of the Vredefort Dome, a structure in excess of 100 km in diameter and located in the approximate center of the Witwatersrand basin, is still the subject of lively geological controversy. It is widely accepted that its formation seems to have taken place in a single sudden event, herein referred to as the Vredefort event, accompanied by the release of gigantic amounts of energy. It is debated, however, whether this central event was an internal one, i.e., a cryptoexplosion triggered by volcanic or tectonic processes, or the impact of an extraterrestrial body. The results of this debate are presented

Suppression of anomalous impurity transport in NBI-heated W7-X plasmas

Radial impurity density profiles in two Wendelstein 7-X (W7-X) experiments heated by neutral beam injection (NBI) are analyzed with respect to their impurity transport properties. Local impurity densities are derived from charge exchange reactions with the W7-X NBI system using simulated neutral densities cross-validated with beam emission spectroscopy. Impurity profiles of argon and carbon are found to show an evolving central accumulation inside half radius. The properties of the underlying impurity transport are assessed using the one-dimensional transport code pySTRAHL. Comparisons between simulation and experiment indicate transport dominated by anomalous diffusion outside half radius. The observed central impurity accumulation is found to match best simulations with purely (neo-)classical transport in the accumulation region. This data implies a suppression of the anomalous impurity transport channel to below 35% of the (neo-)classical one. Experimental data is found to be matched best when invoking a time evolving, inward propagating zone where anomalous impurity transport is suppressed. An additional central power deposition into a plasma with central impurity accumulation via electron cyclotron resonance heating is found to affect the (neo-)classical transport components in case of operation times below 200 ms only. For longer operation times, it is found to re-introduce an altered level of anomalous diffusion. The existence of an inward directed anomalous pinch as an alternative explanation for the central impurity accumulation cannot explain the observed profiles

Rheumatoid Factor as a Potentiator of Anti–Citrullinated Protein Antibody–Mediated Inflammation in Rheumatoid Arthritis

Objective. The co-occurrence of rheumatoid factor (RF) and anti–citrullinated protein antibody (ACPA) positivity in rheumatoid arthritis (RA) is well described. However, the mechanisms underlying the potential interaction between these 2 distinct autoantibodies have not been well defined. The aim of this study was to evaluate the epidemiologic and molecular interaction of ACPAs and RF and its association with both disease activity and measures of RA-associated inflammation. Methods. In a cohort of 1,488 US veterans with RA, measures of disease activity and serum levels of cytokines and multiplex ACPAs were compared between the following groups of patients: double-negative (anti–cyclic citrullinated peptide [anti-CCP]-/RF-), anti-CCP+/RF-, anti-CCP-/RF+, or double-positive (anti-CCP+/RF+). Additional studies were performed using an in vitro immune complex (IC) stimulation assay in which macrophages were incubated with ACPA ICs in the presence or absence of monoclonal IgM-RF, and tumor necrosis factor α production measured as a readout of macrophage activation. Results. Compared with the double-negative subgroup (as well as each single-positive subgroup), the double-positive subgroup exhibited higher disease activity as well as higher levels of C-reactive protein and inflammatory cytokines (all P \u3c 0.001). In vitro stimulation of macrophages by ACPA ICs increased cytokine production, and the addition of monoclonal IgM-RF significantly increased macrophage tumor necrosis factor α production (P = 0.003 versus ACPA ICs alone). Conclusion. The combined presence of ACPAs and IgM-RF mediates increased proinflammatory cytokine production in vitro and is associated with increased systemic inflammation and disease activity in RA. Our data suggest that IgM-RF enhances the capacity of ACPA ICs to stimulate macrophage cytokine production, thereby providing a mechanistic link by which RF enhances the pathogenicity of ACPA ICs in RA

X-Box Binding Protein 1 Is Essential for the Anti-Oxidant Defense and Cell Survival in the Retinal Pigment Epithelium

Damage to the retinal pigment epithelium (RPE) is an early event in the pathogenesis of age-related macular degeneration (AMD). X-box binding protein 1 (XBP1) is a key transcription factor that regulates endoplasmic reticulum (ER) homeostasis and cell survival. This study aimed to delineate the role of endogenous XBP1 in the RPE. Our results show that in a rat model of light-induced retinal degeneration, XBP1 activation was suppressed in the RPE/choroid complex, accompanied by decreased anti-oxidant genes and increased oxidative stress. Knockdown of XBP1 by siRNA resulted in reduced expression of SOD1, SOD2, catalase, and glutathione synthase and sensitized RPE cells to oxidative damage. Using Cre/LoxP system, we generated a mouse line that lacks XBP1 only in RPE cells. Compared to wildtype littermates, RPE-XBP1 KO mice expressed less SOD1, SOD2, and catalase in the RPE, and had increased oxidative stress. At age 3 months and older, these mice exhibited apoptosis of RPE cells, decreased number of cone photoreceptors, shortened photoreceptor outer segment, reduced ONL thickness, and deficit in retinal function. Electron microscopy showed abnormal ultrastructure, Bruch's membrane thickening, and disrupted basal membrane infolding in XBP1-deficient RPE. These results indicate that XBP1 is an important gene involved in regulation of the anti-oxidant defense in the RPE, and that impaired activation of XBP1 may contribute to RPE dysfunction and cell death during retinal degeneration and AMD