Structure and phase stability of nanocrystalline Ce1−xLnxO2−x/2−δ (Ln = Yb, Lu) in oxidizing and reducing atmosphere

The structure and phase evolution of nanocrystalline Ce1−xLnxO2−x/2−δ (Ln = Yb, Lu, x = 0 − 1) oxides upon heating in H2 was studied for the first time. Up to 950 °C the samples were single-phase, with structure changing smoothly with x from fluorite type (F) to bixbyite type (C). For the Lu-doped samples heated at 1100 °C in the air and H2, phase separation into coexisting F- and C-type structures was observed for ~0.40 < x < ~0.70 and ~0.25 < x < ~0.70, respectively. It was found also that addition of Lu3+ and Yb3+ strongly hinders the crystallite growth of ceria during heat treatment at 800 and 950 °C in both atmospheres. Valency of Ce and Yb in Ce0.1Lu0.9O1.55−δ and Ce0.95Yb0.05O1.975−δ samples heated at 1100 °C was studied by XANES and magnetic measurements. In the former Ce was dominated by Ce4+, with small contribution of Ce3+ after heating in H2. In the latter, Yb existed exclusively as 3+ in both O2 and H2

Functional characterization of the trans-membrane domain interactions of the Sec61 protein translocation complex beta-subunit

<p>Abstract</p> <p>Background</p> <p>In eukaryotic cells co- and post-translational protein translocation is mediated by the trimeric Sec61 complex. Currently, the role of the Sec61 complex β-subunit in protein translocation is poorly understood. We have shown previously that in <it>Saccharomyces cerevisiae </it>the trans-membrane domain alone is sufficient for the function of the β-subunit Sbh1p in co-translational protein translocation. In addition, Sbh1p co-purifies not only with the protein translocation channel subunits Sec61p and Sss1p, but also with the reticulon family protein Rtn1p.</p> <p>Results</p> <p>We used random mutagenesis to generate novel Sbh1p mutants in order to functionally map the Sbh1p trans-membrane domain. These mutants were analyzed for their interactions with Sec61p and how they support co-translational protein translocation. The distribution of mutations identifies one side of the Sbh1p trans-membrane domain α-helix that is involved in interactions with Sec61p and that is important for Sbh1p function in protein translocation. At the same time, these mutations do not affect Sbh1p interaction with Rtn1p. Furthermore we show that Sbh1p is found in protein complexes containing not only Rtn1p, but also the two other reticulon-like proteins Rtn2p and Yop1p.</p> <p>Conclusion</p> <p>Our results identify functionally important amino acids in the Sbh1p trans-membrane domain. In addition, our results provide additional support for the involvement of Sec61β in processes unlinked to protein translocation.</p

Shifting the Paradigm: The Putative Mitochondrial Protein ABCB6 Resides in the Lysosomes of Cells and in the Plasma Membrane of Erythrocytes

ABCB6, a member of the adenosine triphosphate–binding cassette (ABC) transporter family, has been proposed to be responsible for the mitochondrial uptake of porphyrins. Here we show that ABCB6 is a glycoprotein present in the membrane of mature erythrocytes and in exosomes released from reticulocytes during the final steps of erythroid maturation. Consistent with its presence in exosomes, endogenous ABCB6 is localized to the endo/lysosomal compartment, and is absent from the mitochondria of cells. Knock-down studies demonstrate that ABCB6 function is not required for de novo heme biosynthesis in differentiating K562 cells, excluding this ABC transporter as a key regulator of porphyrin synthesis. We confirm the mitochondrial localization of ABCB7, ABCB8 and ABCB10, suggesting that only three ABC transporters should be classified as mitochondrial proteins. Taken together, our results challenge the current paradigm linking the expression and function of ABCB6 to mitochondria

Prognostic model to predict postoperative acute kidney injury in patients undergoing major gastrointestinal surgery based on a national prospective observational cohort study.

Background: Acute illness, existing co-morbidities and surgical stress response can all contribute to postoperative acute kidney injury (AKI) in patients undergoing major gastrointestinal surgery. The aim of this study was prospectively to develop a pragmatic prognostic model to stratify patients according to risk of developing AKI after major gastrointestinal surgery. Methods: This prospective multicentre cohort study included consecutive adults undergoing elective or emergency gastrointestinal resection, liver resection or stoma reversal in 2-week blocks over a continuous 3-month period. The primary outcome was the rate of AKI within 7 days of surgery. Bootstrap stability was used to select clinically plausible risk factors into the model. Internal model validation was carried out by bootstrap validation. Results: A total of 4544 patients were included across 173 centres in the UK and Ireland. The overall rate of AKI was 14·2 per cent (646 of 4544) and the 30-day mortality rate was 1·8 per cent (84 of 4544). Stage 1 AKI was significantly associated with 30-day mortality (unadjusted odds ratio 7·61, 95 per cent c.i. 4·49 to 12·90; P < 0·001), with increasing odds of death with each AKI stage. Six variables were selected for inclusion in the prognostic model: age, sex, ASA grade, preoperative estimated glomerular filtration rate, planned open surgery and preoperative use of either an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker. Internal validation demonstrated good model discrimination (c-statistic 0·65). Discussion: Following major gastrointestinal surgery, AKI occurred in one in seven patients. This preoperative prognostic model identified patients at high risk of postoperative AKI. Validation in an independent data set is required to ensure generalizability

E-W strike slip shearing of Kinwat granitoid at South East Deccan Volcanic Province, Kinwat, Maharashtra, India

We study the margin of South East Deccan Volcanic Province around Kinwat lineament, Maharashtra, India, which is NW extension of the Kaddam Fault. Structural field studies document similar to E-W strike-slip mostly brittle faults from the basement granite. We designate this as ` Western boundary East Dharwar Craton Strike-slip Zone' (WBEDCSZ). At local level, the deformation regime from Kinwat, Kaddam Fault, micro-seismically active Nanded and seismically active Killari corroborate with the nearby lineaments. Morphometric analyses suggest that the region is moderately tectonically active. The region of intense strike-slip deformation lies between seismically active fault along Tapi in NW and Bhadrachalam in the SE part of the Kaddam Fault/lineament. The WBEDCSZ with the surface evidences of faulting, presence of a major lineaments and intersection of faults could be a zone of intraplate earthquake