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  • 1
    Publication Date: 2019
    Description: 〈p〉Hypercholesterolemia, the driving force of atherosclerosis, accelerates the expansion and mobilization of hematopoietic stem and progenitor cells (HSPCs). The molecular determinants connecting hypercholesterolemia with hematopoiesis are unclear. Here, we report that a somite-derived prohematopoietic cue, AIBP, orchestrates HSPC emergence from the hemogenic endothelium, a type of specialized endothelium manifesting hematopoietic potential. Mechanistically, AIBP-mediated cholesterol efflux activates endothelial Srebp2, the master transcription factor for cholesterol biosynthesis, which in turn transactivates Notch and promotes HSPC emergence. Srebp2 inhibition impairs hypercholesterolemia-induced HSPC expansion. Srebp2 activation and Notch up-regulation are associated with HSPC expansion in hypercholesterolemic human subjects. Genome-wide chromatin immunoprecipitation followed by sequencing (ChIP-seq), RNA sequencing (RNA-seq), and assay for transposase-accessible chromatin using sequencing (ATAC-seq) indicate that Srebp2 transregulates Notch pathway genes required for hematopoiesis. Our studies outline an AIBP-regulated Srebp2-dependent paradigm for HSPC emergence in development and HPSC expansion in atherosclerotic cardiovascular disease.〈/p〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2019
    Description: 〈p〉Hypercholesterolemia, the driving force of atherosclerosis, accelerates the expansion and mobilization of hematopoietic stem and progenitor cells (HSPCs). The molecular determinants connecting hypercholesterolemia with hematopoiesis are unclear. Here we report that a somite-derived pro-hematopoietic cue, AIBP, orchestrates HSPC emergence from the hemogenic endothelium, a type of specialized endothelium manifesting hematopoietic potential. Mechanistically, AIBP-mediated cholesterol efflux activates endothelial Srebp2, the master transcription factor for cholesterol biosynthesis, which in turn transactivates Notch and promotes HSPC emergence. Srebp2 inhibition impairs hypercholesterolemia-induced HSPC expansion. Srebp2 activation and Notch upregulation are associated with HSPC expansion in hypercholesterolemic human subjects. Genome-wide ChIP-seq, RNA-seq, and ATAC-seq indicate that Srebp2 trans-regulates Notch pathway genes required for hematopoiesis. Our studies outline an AIBP-regulated Srebp2-dependent paradigm for HSPC emergence in development and HPSC expansion in atherosclerotic cardiovascular disease.〈/p〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Natural Sciences in General
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  • 3
    Publication Date: 1999-02-26
    Description: A processing approach has been identified and reduced to practice in which a residual stress profile can be designed such that cracks in a brittle material are arrested or grow in a stable manner. In the approach, cracks in the body encounter an increase in the magnitude of residual compression as the crack propagates. If correctly designed, the process increases strength and significantly decreases strength variability. This approach was demonstrated for a silicate glass, and multiple cracking was observed as a forewarning of the final failure. Normally, such glasses would fail catastrophically with the propagation of a dominant crack.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green -- Tandon -- Sglavo -- New York, N.Y. -- Science. 1999 Feb 26;283(5406):1295-1297.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Materials Science and Engineering, Pennsylvania State University, University Park, PA 16802, USA. Caterpillar Inc. Technical Center, Peoria, IL 61656, USA. Dipartimento di Ingegneria dei Materiali, Universita di Trento, I-38050 Trento, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10037593" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 1989-03-17
    Description: Infections with the human malaria parasite Plasmodium falciparum are characterized by sequestration of erythrocytes infected with mature forms of the parasite. Sequestration of infected erythrocytes appears to be critical for survival of the parasite and to mediate immunopathological abnormalities in severe malaria. A leukocyte differentiation antigen (CD36) was previously suggested to have a role in sequestration of malaria-infected erythrocytes. CD36 was purified from platelets, where it is known as GPIV, and was shown to be a receptor for binding of infected erythrocytes. Infected erythrocytes adhered to CD36 immobilized on plastic; purified CD36 exhibited saturable, specific binding to infected erythrocytes; and purified CD36 or antibodies to CD36 inhibited and reversed binding of infected erythrocytes to cultured endothelial cells and melanoma cells in vitro. The portion of the CD36 molecule that reverses cytoadherence may be useful therapeutically for rapid reversal of sequestration in cerebral malaria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ockenhouse, C F -- Tandon, N N -- Magowan, C -- Jamieson, G A -- Chulay, J D -- New York, N.Y. -- Science. 1989 Mar 17;243(4897):1469-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Walter Reed Army Institute of Research, Washington, DC 20307.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2467377" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/immunology ; Antigens, CD36 ; Antigens, Differentiation/*metabolism ; Aotus trivirgatus ; Blood Platelets/*physiology ; Cell Adhesion ; Erythrocytes/*parasitology ; Humans ; In Vitro Techniques ; Plasmodium falciparum ; Platelet Membrane Glycoproteins/*physiology ; Receptors, Cell Surface/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2008-04-26
    Description: McGillicuddy et al. (Reports, 18 May 2007, p. 1021) proposed that eddy/wind interactions enhance the vertical nutrient flux in mode-water eddies, thus feeding large mid-ocean plankton blooms. We argue that the supply of nutrients to ocean eddies is most likely affected by submesoscale processes that act along the periphery of eddies and can induce vertical velocities several times larger than those due to eddy/wind interactions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mahadevan, Amala -- Thomas, Leif N -- Tandon, Amit -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):448; author reply 448. doi: 10.1126/science.1152111.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Earth Sciences, Boston University, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436758" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Oceans and Seas ; Phytoplankton/*growth & development ; Plankton/growth & development ; *Seawater ; *Water Movements ; *Wind
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2012-09-01
    Description: We present a DNA library preparation method that has allowed us to reconstruct a high-coverage (30x) genome sequence of a Denisovan, an extinct relative of Neandertals. The quality of this genome allows a direct estimation of Denisovan heterozygosity indicating that genetic diversity in these archaic hominins was extremely low. It also allows tentative dating of the specimen on the basis of "missing evolution" in its genome, detailed measurements of Denisovan and Neandertal admixture into present-day human populations, and the generation of a near-complete catalog of genetic changes that swept to high frequency in modern humans since their divergence from Denisovans.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617501/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617501/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Meyer, Matthias -- Kircher, Martin -- Gansauge, Marie-Theres -- Li, Heng -- Racimo, Fernando -- Mallick, Swapan -- Schraiber, Joshua G -- Jay, Flora -- Prufer, Kay -- de Filippo, Cesare -- Sudmant, Peter H -- Alkan, Can -- Fu, Qiaomei -- Do, Ron -- Rohland, Nadin -- Tandon, Arti -- Siebauer, Michael -- Green, Richard E -- Bryc, Katarzyna -- Briggs, Adrian W -- Stenzel, Udo -- Dabney, Jesse -- Shendure, Jay -- Kitzman, Jacob -- Hammer, Michael F -- Shunkov, Michael V -- Derevianko, Anatoli P -- Patterson, Nick -- Andres, Aida M -- Eichler, Evan E -- Slatkin, Montgomery -- Reich, David -- Kelso, Janet -- Paabo, Svante -- GM100233/GM/NIGMS NIH HHS/ -- R01 GM040282/GM/NIGMS NIH HHS/ -- R01 GM100233/GM/NIGMS NIH HHS/ -- R01-GM40282/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Oct 12;338(6104):222-6. doi: 10.1126/science.1224344. Epub 2012 Aug 30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Evolutionary Genetics, Max Planck Institute for Evolutionary Anthropology, D-04103 Leipzig, Germany. mmeyer@eva.mpg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936568" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Animals ; Base Sequence ; Fossils ; Gene Flow ; Gene Library ; *Genetic Variation ; Genome, Human/*genetics ; *Heterozygote ; Humans ; Molecular Sequence Data ; Neanderthals/*genetics ; Sequence Analysis, DNA
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  • 7
    Publication Date: 1981-06-19
    Description: In soybean root nodules, which export recently fixed nitrogen mainly as the ureides allantoin and allantoic acid, cells uninfected by rhizobia undergo a pronounced ultrastructural differentiation not shown by the infected cells, including enlargement of the microbodies and proliferation of smooth endoplasmic reticulum. Since some of the enzymes contributing to ureide synthesis occur in these subcellular components in root nodule preparations, the uninfected cells may participate in ureide synthesis and thus play an essential role in the symbiosis between host and bacterium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newcomb, E H -- Tandon, S R -- New York, N.Y. -- Science. 1981 Jun 19;212(4501):1394-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17746261" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2018-04-20
    Description: The genetic basis of autism spectrum disorder (ASD) is known to consist of contributions from de novo mutations in variant-intolerant genes. We hypothesize that rare inherited structural variants in cis-regulatory elements (CRE-SVs) of these genes also contribute to ASD. We investigated this by assessing the evidence for natural selection and transmission distortion of CRE-SVs in whole genomes of 9274 subjects from 2600 families affected by ASD. In a discovery cohort of 829 families, structural variants were depleted within promoters and untranslated regions, and paternally inherited CRE-SVs were preferentially transmitted to affected offspring and not to their unaffected siblings. The association of paternal CRE-SVs was replicated in an independent sample of 1771 families. Our results suggest that rare inherited noncoding variants predispose children to ASD, with differing contributions from each parent.
    Keywords: Genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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