Education•Flint, Michigan, United States•
About: Kettering University is a(n) education organization based out in Flint, Michigan, United States. It is known for research contribution in the topic(s): RNA & Antigen. The organization has 6842 authors who have published 7689 publication(s) receiving 337503 citation(s). The organization is also known as: GMI Engineering & Management Institute & General Motors Institute.
Topics: RNA, Antigen, DNA, Cancer, Population
Papers published on a yearly basis
01 Mar 2009-Nature Biotechnology
TL;DR: Noggin/SB431542-based neural induction should facilitate the use of hES and hiPS cells in regenerative medicine and disease modeling and obviate the need for protocols based on stromal feeders or embryoid bodies.
Abstract: Current neural induction protocols for human embryonic stem (hES) cells rely on embryoid body formation, stromal feeder co-culture or selective survival conditions. Each strategy has considerable drawbacks, such as poorly defined culture conditions, protracted differentiation and low yield. Here we report that the synergistic action of two inhibitors of SMAD signaling, Noggin and SB431542, is sufficient to induce rapid and complete neural conversion of >80% of hES cells under adherent culture conditions. Temporal fate analysis reveals the appearance of a transient FGF5(+) epiblast-like stage followed by PAX6(+) neural cells competent to form rosettes. Initial cell density determines the ratio of central nervous system and neural crest progeny. Directed differentiation of human induced pluripotent stem (hiPS) cells into midbrain dopamine and spinal motoneurons confirms the robustness and general applicability of the induction protocol. Noggin/SB431542-based neural induction should facilitate the use of hES and hiPS cells in regenerative medicine and disease modeling and obviate the need for protocols based on stromal feeders or embryoid bodies.
TL;DR: Lactic dehydrogenase like serum glutamic oxaloacetic transaminase rises in a characteristic fashion following myocardial infarction, and is associated with a rise in serum lactic dehydrogensase activity.
Abstract: Summary and Conclusions1. Lactic dehydrogenase activity is present in the venous serum of normal human adults. Normal activity ranges from 260 to 850 units per ml with a mean value of470 ± 130 units per ml. 2. Venous whole blood hemolysates of normal adults have a lactic dehydrogenase activity varying between 16,000 to 67,000 units per ml with a mean value of 34,000 ± 12,000 units per ml. 3. Alterations in serum lactic dehydrogenase have been studied in a selected group of disease states. 4. Experimental and clinical myocardial infarction are associated with a rise in serum lactic dehydrogenase activity. 5. Lactic dehydrogenase like serum glutamic oxaloacetic transaminase rises in a characteristic fashion following myocardial infarction.
Anthony Nolan1, University of Oxford2, Biomedical Primate Research Centre3, Kettering University4, Hoffmann-La Roche5, University of Texas MD Anderson Cancer Center6, Fred Hutchinson Cancer Research Center7, University of Washington8, University of California, Los Angeles9, Hallym University10, University of Geneva11, National Marrow Donor Program12, Medical University of Vienna13, Stanford University14, Harvard University15, University of Cambridge16
01 Apr 2010-Tissue Antigens
TL;DR: This report documents the additions and revisions to the nomenclature of HLA specificities following the principles established in previous reports.
Abstract: The WHO Nomenclature Committee for Factors of the HLA System met following the 14th International HLA and Immunogenetics Workshop in Melbourne, Australia in December 2005 and Buzios, Brazil during the 15th International HLA and Immunogenetics Workshop in September 2008. This report documents the additions and revisions to the nomenclature of HLA specificities following the principles established in previous reports (1–18).
05 Oct 2003-Nature Genetics
TL;DR: A role for Dicer, and, by implication, the RNAi machinery, in maintaining the stem cell population during early mouse development is suggested.
Abstract: To address the biological function of RNA interference (RNAi)-related pathways in mammals, we disrupted the gene Dicer1 in mice. Loss of Dicer1 lead to lethality early in development, with Dicer1-null embryos depleted of stem cells. Coupled with our inability to generate viable Dicer1-null embryonic stem (ES) cells, this suggests a role for Dicer, and, by implication, the RNAi machinery, in maintaining the stem cell population during early mouse development.
TL;DR: In this article, BM ablation induces SDF-1, which upregulates MMP-9 expression, and causes shedding of sKitL and recruitment of c-Kit+ stem/progenitors.
Abstract: Stem cells within the bone marrow (BM) exist in a quiescent state or are instructed to differentiate and mobilize to circulation following specific signals. Matrix metalloproteinase-9 (MMP-9), induced in BM cells, releases soluble Kit-ligand (sKitL), permitting the transfer of endothelial and hematopoietic stem cells (HSCs) from the quiescent to proliferative niche. BM ablation induces SDF-1, which upregulates MMP-9 expression, and causes shedding of sKitL and recruitment of c-Kit+ stem/progenitors. In MMP-9−/− mice, release of sKitL and HSC motility are impaired, resulting in failure of hematopoietic recovery and increased mortality, while exogenous sKitL restores hematopoiesis and survival after BM ablation. Release of sKitL by MMP-9 enables BM repopulating cells to translocate to a permissive vascular niche favoring differentiation and reconstitution of the stem/progenitor cell pool.
Showing all 6842 results
|Timothy A. Springer||167||669||122421|
|Murray F. Brennan||161||925||97087|
|Charles M. Rice||154||561||83812|
|Lloyd J. Old||152||775||101377|
|Howard I. Scher||151||944||101737|
|Pier Paolo Pandolfi||146||529||88334|
|Barton F. Haynes||144||911||79014|
|Jedd D. Wolchok||140||713||123336|
|James P. Allison||137||483||83336|
|Harold E. Varmus||137||496||76320|
|Scott W. Lowe||134||396||89376|
|David S. Klimstra||133||564||61682|
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