412 research outputs found

    Utah Fertilizer Guide

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    Fock space relativistic coupled-Cluster calculations of Two-Valence Atoms

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    We have developed an all particle Fock-space relativistic coupled-cluster method for two-valence atomic systems. We then describe a scheme to employ the coupled-cluster wave function to calculate atomic properties. Based on these developments we calculate the excitation energies, magnetic hyperfine constants and electric dipole matrix elements of Sr, Ba and Yb. Further more, we calculate the electric quadrupole HFS constants and the electric dipole matrix elements of Sr+^+, Ba+^+ and Yb+^+. For these we use the one-valence coupled-cluster wave functions obtained as an intermediate in the two-valence calculations. We also calculate the magnetic dipole hyperfine constants of Yb+^+.Comment: 23 pages, 12 figures, 10 tables typos are corrected and some minor modifications in some of the section

    The MAD-Related Protein Smad7 Associates with the TGFβ Receptor and Functions as an Antagonist of TGFβ Signaling

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    AbstractTGFβ signaling is initiated when the type I receptor phosphorylates the MAD-related protein, Smad2, on C-terminal serine residues. This leads to Smad2 association with Smad4, translocation to the nucleus, and regulation of transcriptional responses. Here we demonstrate that Smad7 is an inhibitor of TGFβ signaling. Smad7 prevents TGFβ-dependent formation of Smad2/Smad4 complexes and inhibits the nuclear accumulation of Smad2. Smad7 interacts stably with the activated TGFβ type I receptor, thereby blocking the association, phosphorylation, and activation of Smad2. Furthermore, mutations in Smad7 that interfere with receptor binding disrupt its inhibitory activity. These studies thus define a novel function for MAD-related proteins as intracellular antagonists of the type I kinase domain of TGFβ family receptors

    Arterial inflammation in mice lacking the interleukin 1 receptor antagonist gene

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    Branch points and flexures in the high pressure arterial system have long been recognized as sites of unusually high turbulence and consequent stress in humans are foci for atherosclerotic lesions. We show that mice that are homozygous for a null mutation in the gene encoding an endogenous antiinflammatory cytokine, interleukin 1 receptor antagonist (IL-1ra), develop lethal arterial inflammation involving branch points and flexures of the aorta and its primary and secondary branches. We observe massive transmural infiltration of neutrophils, macrophages, and CD4(+) T cells. Animals appear to die from vessel wall collapse, stenosis, and organ infarction or from hemorrhage from ruptured aneurysms. Heterozygotes do not die from arteritis within a year of birth but do develop small lesions, which suggests that a reduced level of IL-1ra is insufficient to fully control inflammation in arteries. Our results demonstrate a surprisingly specific role for IL-1ra in the control of spontaneous inflammation in constitutively stressed artery walls, suggesting that expression of IL-1 is likely to have a significant role in signaling artery wall damage

    host extracellular to systemic effects of SARS-CoV-2 infection

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    Funding Information: The opinions expressed in this article are those of the authors and do not reflect the view of the National Institutes of Health, the Department of Health and Human Services, the National Science Foundation, or the United States government. APK’s research is supported by the Department of Defense and Swezey & Jewell, Moore and MacKenzie Research Fund. Funding Information: The opinions expressed in this article are those of the authors and do not reflect the view of the National Institutes of Health, the Department of Health and Human Services, the National Science Foundation, or the United States government. APK’s research is supported by the Department of Defense and Swezey & Jewell, Moore and MacKenzie Research Fund. Funding Information: This work was supported by supplemental funds for COVID-19 research from Translational Research Institute of Space Health through NASA Cooperative Agreement NNX16AO69A (T-0404) to AB, and by a NASA Space Biology Postdoctoral Fellowship (80NSSC19K0426) and Human Research Program Augmentation Award (80NSSC19K1322) to SAN. Publisher Copyright: © 2023, The Author(s).COVID-19, the disease caused by SARS-CoV-2, has caused significant morbidity and mortality worldwide. The betacoronavirus continues to evolve with global health implications as we race to learn more to curb its transmission, evolution, and sequelae. The focus of this review, the second of a three-part series, is on the biological effects of the SARS-CoV-2 virus on post-acute disease in the context of tissue and organ adaptations and damage. We highlight the current knowledge and describe how virological, animal, and clinical studies have shed light on the mechanisms driving the varied clinical diagnoses and observations of COVID-19 patients. Moreover, we describe how investigations into SARS-CoV-2 effects have informed the understanding of viral pathogenesis and provide innovative pathways for future research on the mechanisms of viral diseases.publishersversionpublishe
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