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Träfflista för sökning "WFRF:(Levine D) srt2:(2005-2009)"

Search: WFRF:(Levine D) > (2005-2009)

  • Result 11-15 of 15
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11.
  • Frank, Adrian, et al. (author)
  • Hover, transition, and level flight control design for a single-propeller indoor airplane
  • 2007
  • In: Collection of Technical Papers - AIAA Guidance, Navigation, and Control Conference 2007. - Reston, Virigina : American Institute of Aeronautics and Astronautics. - 1563479044 - 9781563479045 ; , s. 100-117
  • Conference paper (peer-reviewed)abstract
    • This paper presents vehicle models and test flight results for an autonomous fixed-wing aircraft with the capability to take off, hover, transition to and from level-flight, and perch on a vertical landing platform. These maneuvers are all demonstrated in the highly space constrained environment of the Real-time indoor Autonomous Vehicle test ENvironment (RAVEN) at MIT. RAVEN promotes the rapid prototyping of UAV planning and control technologies by allowing the use of unmodified commercially available model aircraft for autonomous flight. Experimental results of several hover tests, transition maneuvers, and perch landings are presented. By enabling a fixed-wing UAV to achieve these feats, we demonstrate that the desirable speed and range performance of an autonomous fixed-wing aircraft in level flight can be complimented by hover capabilities that are typically limited to rotary-wing vehicles. This combination has the potential to significantly ease support and maintenance of operational autonomous vehicles.
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12.
  • Klionsky, Daniel J., et al. (author)
  • Guidelines for the use and interpretation of assays for monitoring autophagy in higher eukaryotes
  • 2008
  • In: Autophagy. - : Landes Bioscience. - 1554-8627 .- 1554-8635. ; 4:2, s. 151-175
  • Research review (peer-reviewed)abstract
    • Research in autophagy continues to accelerate,1 and as a result many new scientists are entering the field. Accordingly, it is important to establish a standard set of criteria for monitoring macroautophagy in different organisms. Recent reviews have described the range of assays that have been used for this purpose.2,3 There are many useful and convenient methods that can be used to monitor macroautophagy in yeast, but relatively few in other model systems, and there is much confusion regarding acceptable methods to measure macroautophagy in higher eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers of autophagosomes versus those that measure flux through the autophagy pathway; thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from fully functional autophagy that includes delivery to, and degradation within, lysosomes (in most higher eukaryotes) or the vacuole (in plants and fungi). Here, we present a set of guidelines for the selection and interpretation of the methods that can be used by investigators who are attempting to examine macroautophagy and related processes, as well as by reviewers who need to provide realistic and reasonable critiques of papers that investigate these processes. This set of guidelines is not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to verify an autophagic response.
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13.
  • Lee, Benjamin H., et al. (author)
  • FLT3 mutations confer enhanced proliferation and survival properties to multipotent progenitors in a murine model of chronic myelomonocytic leukemia
  • 2007
  • In: Cancer Cell. - : Elsevier BV. - 1878-3686 .- 1535-6108. ; 12:4, s. 367-380
  • Journal article (peer-reviewed)abstract
    • Despite their known transforming properties, the effects of leukemogenic FLT3-ITD mutations on hematopoietic stem and multipotent progenitor cells and on hematopoietic differentiation are not well understood. We report a mouse model harboring an ITD in the murine Flt3 locus that develops myeloproliferative disease resembling CMML and further identified FLT3-ITD mutations in a subset of human CMML. These findings correlated with an increase in number, cell cycling, and survival of multipotent stem and progenitor cells in an ITD dose-dependent manner in animals that exhibited alterations within their myeloid progenitor compartments and a block in normal B cell development. This model provides insights into the consequences of constitutive signaling by an oncogenic tyrosine kinase on hematopoietic progenitor quiescence, function, and cell fate.
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14.
  • Packer, M., et al. (author)
  • Clinical effects of endothelin receptor antagonism with bosentan in patients with severe chronic heart failure: results of a pilot study
  • 2005
  • In: Journal of cardiac failure. - : Elsevier BV. - 1071-9164. ; 11:1, s. 12-20
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Endothelin receptor antagonism produces favorable short-term hemodynamic effects in heart failure, but the clinical effects of longer term therapy have not been evaluated. METHODS AND RESULTS: Three hundred and seventy patients with symptoms of heart failure at rest or on minimal exertion and a left ventricular ejection fraction <35% were randomly assigned (double-blind) to placebo (n = 126) or the endothelin receptor antagonist bosentan, titrated slowly (n = 121) or rapidly (n = 123) to a target dose of 500 mg twice daily. Treatment with the study drug was to be maintained for 26 weeks, whereas background medications for heart failure were kept constant. Safety concerns led to early termination of the trial when only 174 patients had had an opportunity to complete 26 weeks of therapy. Bosentan exerted no apparent benefit when all randomized patients were analyzed (P = .709). However, in the first 174 patients who were recruited at least 26 weeks before study termination and who could therefore be followed for the planned duration of the trial, patients in the bosentan groups were more likely to be improved (26% versus 19%) and were less likely to be worse (28% versus 43%), P = .045. When compared with placebo-treated patients, bosentan-treated patients had a increased risk of heart failure during the first month of treatment but a decreased risk of heart failure during the fourth, fifth, and sixth months of therapy. The major noncardiac adverse effects of bosentan included an increase in hepatic transaminases (in 15.6% of patients) and a decrease in hemoglobin (of about 1 g/L). CONCLUSION: Although bosentan exerted no favorable effects in the overall study, our findings suggest that the clinical responses to endothelin antagonism with bosentan in patients with severe chronic heart failure may be dependent on the duration of treatment.
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