Institution
Saint Francis University
Education•Loretto, Pennsylvania, United States•
About: Saint Francis University is a education organization based out in Loretto, Pennsylvania, United States. It is known for research contribution in the topics: Population & Osteoblast. The organization has 1694 authors who have published 2038 publications receiving 87149 citations.
Topics: Population, Osteoblast, Growth factor, Bone cell, Bone remodeling
Papers published on a yearly basis
Papers
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Houston Methodist Hospital1, Mount Sinai Health System2, Riverside Methodist Hospital3, The Texas Heart Institute4, University of Michigan5, University of Pittsburgh6, Spectrum Health7, University of Kansas8, Saint Francis University9, Duke University10, PinnacleHealth System11, Johns Hopkins University12, Kaiser Permanente13, Mayo Clinic14, Medtronic plc15, Harvard University16
TL;DR: In patients with severe aortic stenosis who are at increased surgical risk, the higher rate of survival with a self-expanding TAVR compared with surgery was sustained at 2 years.
369 citations
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Yale University1, Cedars-Sinai Medical Center2, University of California, Los Angeles3, University of North Carolina at Chapel Hill4, Saint Francis University5, Loma Linda University6, University of California, Irvine7, University of Utah8, University of British Columbia9, Dartmouth College10, Wake Forest University11, Rhode Island Hospital12, Tel Aviv University13, Columbia University14, Boston Children's Hospital15
TL;DR: A high-resolution genetic map of DS phenotypes based on an analysis of 30 subjects carrying rare segmental trisomies of various regions of HSA21 is presented, demonstrating the value of combining advanced genomics with cohorts of rare patients for studying DS, a prototype for the role of copy-number variation in complex disease.
Abstract: Down syndrome (DS), or trisomy 21, is a common disorder associated with several complex clinical phenotypes. Although several hypotheses have been put forward, it is unclear as to whether particular gene loci on chromosome 21 (HSA21) are sufficient to cause DS and its associated features. Here we present a high-resolution genetic map of DS phenotypes based on an analysis of 30 subjects carrying rare segmental trisomies of various regions of HSA21. By using state-of-the-art genomics technologies we mapped segmental trisomies at exon-level resolution and identified discrete regions of 1.8-16.3 Mb likely to be involved in the development of 8 DS phenotypes, 4 of which are congenital malformations, including acute megakaryocytic leukemia, transient myeloproliferative disorder, Hirschsprung disease, duodenal stenosis, imperforate anus, severe mental retardation, DS-Alzheimer Disease, and DS-specific congenital heart disease (DSCHD). Our DS-phenotypic maps located DSCHD to a <2-Mb interval. Furthermore, the map enabled us to present evidence against the necessary involvement of other loci as well as specific hypotheses that have been put forward in relation to the etiology of DS-i.e., the presence of a single DS consensus region and the sufficiency of DSCR1 and DYRK1A, or APP, in causing several severe DS phenotypes. Our study demonstrates the value of combining advanced genomics with cohorts of rare patients for studying DS, a prototype for the role of copy-number variation in complex disease.
356 citations
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TL;DR: Both intracellular and extracellular antagonists are regulated by BMPs, indicating the existence of local feedback mechanisms to modulate BMP cellular activities.
Abstract: Skeletal homeostasis is determined by systemic hormones and local factors. Bone morphogenetic proteins (BMPs) are unique because they induce the commitment of mesenchymal cells toward cells of the osteoblastic lineage and also enhance the differentiated function of the osteoblast. BMP activities in bone are mediated through binding to specific cell surface receptors and through interactions with other growth factors. BMPs are required for skeletal development and maintenance of adult bone homeostasis, and play a role in fracture healing. BMPs signal by activating the mothers against decapentaplegic (Smad) and mitogen activated protein kinase (MAPK) pathways, and their actions are tempered by intracellular and extracellular proteins. The BMP antagonists block BMP signal transduction at multiple levels including pseudoreceptor, inhibitory intracellular binding proteins, and factors that induce BMP ubiquitination. A large number of extracellular proteins that bind BMPs and prevent their binding to signaling receptors have emerged. The extracellular antagonists are differentially expressed in cartilage and bone tissue and exhibit BMP antagonistic as well as additional activities. Both intracellular and extracellular antagonists are regulated by BMPs, indicating the existence of local feedback mechanisms to modulate BMP cellular activities.
351 citations
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TL;DR: Reteplase, when given as a double bolus of 10 plus 10 megaunits to patients with acute myocardial infarction, achieves significantly higher rates of early reperfusion of the infarct-related coronary artery and requires significantly fewer acute coronary interventions than front-loaded alteplase without an apparent increased risk of complications.
Abstract: Background The therapeutic benefit of thrombolytic therapy has been shown to correlate directly with completeness (TIMI grade 3 flow) and speed of reperfusion of the infarct-related coronary artery. The purpose of the RAPID II study was to determine whether a double-bolus regimen of reteplase, a recently developed deletion mutant of wild-type tissue plasminogen activator, could improve 90-minute coronary artery patency rates achieved with the most successful standard regimen, an “accelerated” front-loaded infusion of alteplase. Methods and Results Three hundred twenty-four patients with acute myocardial infarction were randomized to receive (along with intravenous heparin and aspirin) either a 10 plus 10 megaunits double bolus of reteplase or front-loaded alteplase. The primary end point of “patency at 90 minutes, graded according to the TIMI classification” was centrally assessed in a blinded fashion. Infarct-related coronary artery patency (TIMI grade 2 or 3) and complete patency (TIMI grade 3) at 90 mi...
348 citations
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TL;DR: It is concluded that BMPs induce noggin transcription in Ob cells, a probable mechanism to limit BMP action in osteoblasts.
Abstract: Bone morphogenetic proteins (BMPs) induce the differentiation of cells of the osteoblastic lineage and enhance the function of the osteoblast. Growth factors are regulated by binding proteins, but there is no information about binding proteins for BMPs in skeletal cells. Noggin specifically binds BMPs, but its expression by cells of the osteoblastic lineage has not been reported. We tested for the expression of noggin and its induction by BMP-2 in cultures of osteoblast-enriched cells from 22-d-old fetal rat calvariae (Ob cells). BMP-2 caused a time- and dose-dependent increase in noggin mRNA and polypeptide levels, as determined by Northern and Western blot analyses. The effects of BMP-2 on noggin transcripts were dependent on protein, but independent of DNA synthesis. BMP-2 increased the rates of noggin transcription as determined by nuclear run-on assays. BMP-4, BMP-6, and TGF-beta1 increased noggin mRNA in Ob cells, but basic fibroblast growth factor, platelet- derived growth factor BB, and IGF-I did not. Noggin decreased the stimulatory effects of BMPs on DNA and collagen synthesis and alkaline phosphatase activity in Ob cells. In conclusion, BMPs induce noggin transcription in Ob cells, a probable mechanism to limit BMP action in osteoblasts.
344 citations
Authors
Showing all 1697 results
Name | H-index | Papers | Citations |
---|---|---|---|
Steven M. Greenberg | 105 | 488 | 44587 |
Linus Pauling | 100 | 536 | 63412 |
Ernesto Canalis | 98 | 331 | 30085 |
John S. Gottdiener | 94 | 316 | 49248 |
Dalane W. Kitzman | 93 | 474 | 36501 |
Joseph F. Polak | 91 | 406 | 38083 |
Charles A. Boucher | 90 | 549 | 31769 |
Lawrence G. Raisz | 82 | 315 | 26147 |
Julius M. Gardin | 76 | 253 | 38063 |
Jeffrey S. Hyams | 72 | 357 | 22166 |
James J. Vredenburgh | 65 | 280 | 18037 |
Michael Centrella | 62 | 120 | 11936 |
Nathaniel Reichek | 62 | 248 | 22847 |
Gerard P. Aurigemma | 59 | 212 | 17127 |
Thomas L. McCarthy | 57 | 107 | 10167 |