Twin-Free GaAs Nanosheets by Selective Area Growth: Implications for Defect-Free Nanostructures

Highly perfect, twin-free GaAs nanosheets grown on (111)B surfaces by selective area growth (SAG) are demonstrated. In contrast to GaAs nanowires grown by (SAG) in which rotational twins and stacking faults are almost universally observed, twin formation is either suppressed or eliminated within properly oriented nanosheets are grown under a range of growth conditions. A morphology transition in the nanosheets due to twinning results in surface energy reduction, which may also explain the high twin-defect density that occurs within some III–V semiconductor nanostructures, such as GaAs nanowires. Calculations suggest that the surface energy is significantly reduced by the formation of {111}-plane bounded tetrahedra after the morphology transition of nanowire structures. By contrast, owing to the formation of two vertical {11̅0} planes which comprise the majority of the total surface energy of nanosheet structures, the energy reduction effect due to the morphology transition is not as dramatic as that for nanowire structures. Furthermore, the surface energy reduction effect is mitigated in longer nanosheets which, in turn, suppresses twinning

Cutting Edge: Inflammasome Activation by Alum and Alum's Adjuvant Effect Are Mediated by NLRP3

Alum is the only adjuvant approved for routine use in humans, although the basis for its adjuvanticity remains poorly understood. We have recently shown that Alum activates caspase-1 and induces secretion of mature IL-1β and IL-18. Here we show that in human and mice macrophages, alum-induced IL-1β, IL-18, and IL-33 secretion is mediated by the NLR protein NLRP3 and its adaptor ASC, but not by NLRC4. Other particulate adjuvants, such as QuilA and chitosan, induce inflammasome activation in a NLRP3-dependent fashion, suggesting that activation of the NLRP3-inflammasome may be a common mechanism of action of particulate adjuvants. Importantly, we demonstrate that antigen-specific antibody production elicited by vaccines that contain alum is significantly impaired in NLRP3-deficient mice. Our results demonstrate for the first time a role for the NLRP3-inflammasome during development of the immune response elicited by alum-enhanced vaccination. and suggest that therapeutic intervention aimed at NLRP3 may improve adjuvant efficacy

α-Klotho Expression in Human Tissues.

CONTEXT: α-Klotho has emerged as a powerful regulator of the aging process. To date, the expression profile of α-Klotho in human tissues is unknown, and its existence in some human tissue types is subject to much controversy. OBJECTIVE: This is the first study to characterize systemwide tissue expression of transmembrane α-Klotho in humans. We have employed next-generation targeted proteomic analysis using parallel reaction monitoring in parallel with conventional antibody-based methods to determine the expression and spatial distribution of human α-Klotho expression in health. RESULTS: The distribution of α-Klotho in human tissues from various organ systems, including arterial, epithelial, endocrine, reproductive, and neuronal tissues, was first identified by immunohistochemistry. Kidney tissues showed strong α-Klotho expression, whereas liver did not reveal a detectable signal. These results were next confirmed by Western blotting of both whole tissues and primary cells. To validate our antibody-based results, α-Klotho-expressing tissues were subjected to parallel reaction monitoring mass spectrometry (data deposited at ProteomeXchange, PXD002775) identifying peptides specific for the full-length, transmembrane α-Klotho isoform. CONCLUSIONS: The data presented confirm α-Klotho expression in the kidney tubule and in the artery and provide evidence of α-Klotho expression across organ systems and cell types that has not previously been described in humans.K.L. received a Genzyme-Sanofi Fellowship in Nephrology grant. T.F.H. is funded by the NIHR award to the Cambridge Biomedical Research Centre and by NIHR grant 14/49/147. The Cambridge Aorta Study is funded by the British Heart Foundation.This is the author accepted manuscript. The final version is available from the Endocrine Society via http://dx.doi.org/10.1210/jc.2015-1800

The Center for Independent Experts: The National External Peer Review Program of NOAA's National Marine Fisheries Service

Requirements are growing for peer review of the science used for governmental management decisions. This is particularly true for fisheries science, where management decisions are often controversial. The National Oceanic and Atmospheric Administration's National Marine Fisheries Service instituted the Center for Independent Experts (CIE) in 1998 as a national peer-review program. Operations of the CIE, run under a contract with the University of Miami, maintain the independence of reviewers from the agency, and follow strict conflict of interest guidelines. Reviews by the CIE fulfill the requirements of the Information Quality Act and the Office of Management and Budget's Peer Review Bulletin. The CIE completed 101 reviews between 1999 and September 2006. Ninety-eight reviewers have participated in CIE reviews, with 72% of them coming from overseas. Case studies involving groundfish data and stock assessments, and marine-mammal abundance, are described, including the scientific issues, CIE operations, requirements for the reviews, conclusions of the reviewers, and the agency's responses. Impacts of the CIE on the agency's science include improvements to regional stock assessment processes and to stock-assessment and field-survey methods, and reductions in contentious challenges to the agency's science.Keywords: Experts, Peer Review, Fishery Managemen

Visible-light Phase Curves from the Second Year of the TESS Primary Mission

We carried out a systematic study of full-orbit phase curves for known transiting systems in the northern ecliptic sky that were observed during Year 2 of the TESS primary mission. We applied the same methodology for target selection, data processing, and light-curve fitting as we did in our Year 1 study. Out of the 15 transiting systems selected for analysis, seven—HAT-P-7, KELT-1, KELT-9, KELT-16, KELT-20, Kepler-13A, and WASP-12—show statistically significant secondary eclipses and day–night atmospheric brightness modulations. Small eastward dayside hot-spot offsets were measured for KELT-9b and WASP-12b. KELT-1, Kepler-13A, and WASP-12 show additional phase-curve variability attributed to the tidal distortion of the host star; the amplitudes of these signals are consistent with theoretical predictions. We combined occultation measurements from TESS and Spitzer to compute dayside brightness temperatures, TESS-band geometric albedos, Bond albedos, and phase integrals for several systems. The new albedo values solidify the previously reported trend between dayside temperature and geometric albedo for planets with 1500 K < Tday < 3000 K. For Kepler-13Ab, we carried out an atmospheric retrieval of the full secondary eclipse spectrum, which revealed a noninverted temperature–pressure profile, significant H2O and K absorption in the near-infrared, evidence for strong optical atmospheric opacity due to sodium, and a confirmation of the high geometric albedo inferred from our simpler analysis. We explore the implications of the phase integrals (ratios of Bond to geometric albedos) for understanding exoplanet clouds. We also report updated transit ephemerides for all of the systems studied in this work

The Revised TESS Input Catalog and Candidate Target List

We describe the catalogs assembled and the algorithms used to populate the revised TESS Input Catalog (TIC), based on the incorporation of the Gaia second data release. We also describe a revised ranking system for prioritizing stars for 2-minute cadence observations, and assemble a revised Candidate Target List (CTL) using that ranking. The TIC is available on the Mikulski Archive for Space Telescopes (MAST) server, and an enhanced CTL is available through the Filtergraph data visualization portal system at the URL http://filtergraph.vanderbilt.edu/tess_ctl.Comment: 30 pages, 16 figures, submitted to AAS Journals; provided to the community in advance of publication in conjunction with public release of the TIC/CTL on 28 May 201

High expression of HMGA2 independently predicts poor clinical outcomes in acute myeloid leukemia

In acute myeloid leukemia (AML), risk stratification based on cytogenetics and mutation profiling is essential but remains insufficient to select the optimal therapy. Accurate biomarkers are needed to improve prognostic assessment. We analyzed RNA sequencing and survival data of 430 AML patients and identified HMGA2 as a novel prognostic marker. We validated a quantitative PCR test to study the association of HMGA2 expression with clinical outcomes in 358 AML samples. In this training cohort, HMGA2 was highly expressed in 22.3% of AML, mostly in patients with intermediate or adverse cytogenetics. High expression levels of HMGA2 (H + ) were associated with a lower frequency of complete remission (58.8% vs 83.4%, P < 0.001), worse 3-year overall survival (OS, 13.2% vs 43.5%, P < 0.001) and relapse-free survival (RFS, 10.8% vs 44.2%, P < 0.001). A positive HMGA2 test also identified a subgroup of patients unresponsive to standard treatments. Multivariable analyses showed that H + was independently associated with significantly worse OS and RFS, including in the intermediate cytogenetic risk category. These associations were confirmed in a validation cohort of 260 patient samples from the UK NCRI AML17 trial. The HMGA2 test could be implemented in clinical trials developing novel therapeutic strategies for high-risk AML

Mechanisms of neurodegeneration in a preclinical autosomal dominant retinitis pigmentosa knock-in model with a RhoD190N mutation

D190N, a missense mutation in rhodopsin, causes photoreceptor degeneration in patients with autosomal dominant retinitis pigmentosa (adRP). Two competing hypotheses have been developed to explain why D190N rod photoreceptors degenerate: (a) defective rhodopsin trafficking prevents proteins from correctly exiting the endoplasmic reticulum, leading to their accumulation, with deleterious effects or (b) elevated mutant rhodopsin expression and unabated signaling causes excitotoxicity. A knock-in D190N mouse model was engineered to delineate the mechanism of pathogenesis. Wild type (wt) and mutant rhodopsin appeared correctly localized in rod outer segments of D190N heterozygotes. Moreover, the rhodopsin glycosylation state in the mutants appeared similar to that in wt mice. Thus, it seems plausible that the injurious effect of the heterozygous mutation is not related to mistrafficking of the protein, but rather from constitutive rhodopsin activity and a greater propensity for chromophore isomerization even in the absence of light.We greatly appreciate the assistance of the members of the Bernard & Shirlee Brown Glaucoma laboratory, especially to Chun-Wei Hsu for technical support. SHT is a Burroughs-Wellcome Program in Biomedical Sciences Fellow, and is also supported by the Charles E. Culpeper-Partnership for Cures 07-CS3, Crowley Research Fund, Schneeweiss Stem Cell Fund, New York State N09G-302, Foundation Fighting Blindness [TA-NMT-0116-0692- COLU] (Owings Mills, MD), TS080017 from US Department of Defense, NIH Grants [P30EY019007, R01EY018213, R01EY024698, R01EY026682, R21AG050437], Research to Prevent Blindness (New York, NY), and Joel Hoffmann Scholarship. CSL is the Homer McK. Rees Scholar. JSP is a BEST2016 awardee (BEST/ 2016/030, Conselleria de Educación, Investigación, Cultura y Deporte; Generalitat Valenciana) and his research is supported by a Prometeo Grant (PROMETEO/2016/094; Conselleria de Educación, Investigación, Cultura y Deporte; Generalitat Valenciana) and by internal funds from Universidad Católica de Valencia San Vicente Mártir (2018-128-001). VBM is supported by NIH Grants K08EY020530, R01EY016822, The Doris Duke Charitable Foundation Grant #2013103, and Research to Prevent Blindness (New York, NY); GV is supported by NIH Grants [F30EYE027986 and T32GM007337].Author manuscriptMedicin