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  • 1
    Online Resource
    Online Resource
    Global Nuclear Energy Partnership. (2009)
    Hauppauge :Nova Science Publishers, Incorporated,
    Details
    Keywords: United States. -- Dept. of Energy -- Rules and practice. ; Reactor fuel reprocessing -- Waste disposal -- United States. ; Radioactive waste disposal -- United States. ; Spent reactor fuels -- Storage -- United States. ; Radioactive waste repositories -- United States. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (61 pages)
    Edition: 1st ed.
    ISBN: 9781613249567
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=3019828
    DDC: 333.7924153
    Language: English
    Note: Intro -- GLOBAL NUCLEAR ENERGYPARTNERSHIP -- GLOBAL NUCLEAR ENERGYPARTNERSHIP -- CONTENTS -- PREFACE -- RESULTS IN BRIEF -- BACKGROUND -- Materials in Spent Nuclear Fuel -- Technologies for Recycling Spent Nuclear Fuel -- DOE'S ORIGINAL ENGINEERING-SCALEAPPROACH WOULD MEET GNEP'SOBJECTIVES IF ADVANCED RECYCLINGTECHNOLOGIES ARE SUCCESSFULLYDEVELOPED -- Successful Development of Advanced RecyclingTechnologies Would Be an Initial Step toward GreatlyExtending the Capacity of a Geologic Repository -- Advanced Recycling Technologies Envisioned underDOE's Original Approach to GNEP Pose LowerProliferation Risks Than Existing Recycling Technologies -- Lack of Industry Participation Could Reduce theProspects for Commercialization and Widespread Use ofAdvanced Recycling Technologies -- DOE's Original Approach to GNEP Included Building aSeparate Engineering-Scale Reprocessing Plant beforeConducting R& -- D that Would Help in Designing the Plant -- The R& -- D Facility and Advanced Reactor Would EnableDOE to Develop the Advanced Recycling TechnologiesEnvisioned under Its Original Approach to GNEP -- DOE'S ACCELERATED APPROACH WOULDLIKELY RELY ON TECHNOLOGIES THAT FALLSHORT OF MEETING GNEP'S OBJECTIVES -- Two Other Industry Consortia Proposed to AddressGNEP's Objectives by Using Technologies That Are NotMature Enough for Commercial Deployment -- The Government Would Likely Bear Substantial Costsfor Commercial-Scale Recycling Facilities -- DOE Officials Recognize the Limitations of AcceleratingDeployment of Commercial-Scale Facilities but CiteOther Benefits -- CONCLUSIONS -- RECOMMENDATIONS FOR EXECUTIVEACTION -- AGENCY COMMENTS AND OUR EVALUATION -- List of Committees -- APPENDIX I.SCOPE AND METHODOLOGY -- APPENDIX II.DOE'S USE OF TECHNOLOGY READINESSLEVELS TO ASSESS THE MATURITY OF SPENTFUEL RECYCLING TECHNOLOGIES -- INDEX.
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    GEOMAR EBL
  • 2
    Electronic Resource
    Electronic Resource
    The program of friend cell erythroid differentiation: Early changes in Na+/K+ ATPase function (1978)
    New York, N.Y. : Wiley-Blackwell
    Journal of Supramolecular Structure 8 (1978), S. 431-438 
    Details
    ISSN: 0091-7419
    Keywords: Friend cells ; Na+/K+ ATPase ; K+ ion levels ; transport changes ; differentiation ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Treatment of Friend erythroleukemia cells with several different chemical agents causes an early decrease in the 86Rb+ influx mediated by Na+/K+ adenosine triphosphatase (ATPase). These agents, which induced Friend cells to differentiate, include dimethylsulfoxide (DMSO), ouabain, hypoxanthine, and actinomycin D. The magnitude of the early decrease in 86Rb+ influx correlates with the proportion of cells in cultures of inducible Friend cell clones which later go on to synthesize hemoglobin. Compounds which do not incude differentiation in these cells, such as xanthine, exogenous hematin, and erythropoietin, do not cause a change in 86Rb+ influx. A change in the intracellular K+ ion concentration does not occur during induction by DMSO because, although there is a decrease in K+ content per cell soon after induction, there is a parallel decrease in cell volume. These results and previous observations from this laboratory are discussed in terms of the posible involvement of the Na+/K+ ATPase in Friend cell differentiation.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jss.400080405
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    Paper (German National Licenses)
    Fulltext
  • 3
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    Brain Transforming Growth Factor-{beta} Resists Hypertension Via Regulating Microglial Activation [Basic Sciences] (2017)
    American Heart Association (AHA)
    In: Stroke
    Details
    Publication Date: 2017-08-29
    Description: Background and Purpose—Hypertension is the major risk factor for stroke. Recent work unveiled that hypertension is associated with chronic neuroinflammation; microglia are the major players in neuroinflammation, and the activated microglia elevate sympathetic nerve activity and blood pressure. This study is to understand how brain homeostasis is kept from hypertensive disturbance and microglial activation at the onset of hypertension.Methods—Hypertension was induced by subcutaneous delivery of angiotensin II, and blood pressure was monitored in conscious animals. Microglial activity was analyzed by flow cytometry and immunohistochemistry. Antibody, pharmacological chemical, and recombinant cytokine were administered to the brain through intracerebroventricular infusion. Microglial depletion was performed by intracerebroventricular delivering diphtheria toxin to CD11b-diphtheria toxin receptor mice. Gene expression profile in sympathetic controlling nucleus was analyzed by customized qRT-PCR array.Results—Transforming growth factor-β (TGF-β) is constitutively expressed in the brains of normotensive mice. Removal of TGF-β or blocking its signaling before hypertension induction accelerated hypertension progression, whereas supplementation of TGF-β1 substantially suppressed neuroinflammation, kidney norepinephrine level, and blood pressure. By means of microglial depletion and adoptive transfer, we showed that the effects of TGF-β on hypertension are mediated through microglia. In contrast to the activated microglia in established hypertension, the resting microglia are immunosuppressive and important in maintaining neural homeostasis at the onset of hypertension. Further, we profiled the signature molecules of neuroinflammation and neuroplasticity associated with hypertension and TGF-β by qRT-PCR array.Conclusions—Our results identify that TGF-β–modulated microglia are critical to keeping brain homeostasis responding to hypertensive disturbance.
    Keywords: Hypertension
    Print ISSN: 0039-2499
    Electronic ISSN: 1524-4628
    Topics: Medicine
    Published by American Heart Association (AHA)
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    PAPER CURRENT
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