The regression of this hemangioma subsequent to steroid therapy was accompanied by a significant increase in mast cell density, reduced transcription of several cytokines, and an enhanced expression of the mitochondrial cytochrome b gene.
We estimate the impact of participating in the NZ Marsden Fund on research output trajectories, by comparing the subsequent performance of funded researchers to those who submitted proposals but were not funded. We control for selection bias using the evaluations of the proposals generated by the grant selection process. We carry out the analysis in two data frames. First we consider the researcher teams behind 1263 second-round proposals submitted 2003-2008, and look at the post-proposal publication and citation performance of the team as a whole, as a function of pre-proposal performance, the ranking of the proposal by the panel, and the funding. This estimation does not deal with individual researchers' multiple proposals and funding over time. To disentangle these effects, we consider the 1500 New Zealand researchers who appeared on any of these proposals, and estimate a model predicting annual individual performance as a function of previous performance, recent proposal activity, ranking of any recent proposals, and funding received through recent proposals. Overall, we find that funding is associated with a 6-15% increase in publications and a 22-26% increase in citation-weighted papers for research teams. For individuals, funding is associated with a 3-5% increase in annual publications, and a 5-8% increase in citation-weighted papers for 5 years after grant; however, the lag structure and persistence of this effect post-grant is difficult to pin down. Surprisingly, we find no systematic evidence that the evaluation of proposals by the Marsden system is predictive of subsequent success. We conclude that the Marsden Fund is modestly successful in increasing scientific performance, but that the selection process does not appear to be effective in discriminating among second-round proposals in terms of their likely success.
Hemangioma is a primary tumor of microvasculature. Its development typically exhibits a proliferative phase followed by an involuting phase that continues into the involuted phase. Although apoptosis has been reported, the mechanisms regulating the spontaneous regression of hemangioma are largely unknown. The authors recently demonstrated up-regulation of the mitochondrial cytochrome b gene in hemangioma associated with steroid-induced regression. The present study investigated whether a similar change occurred during spontaneous regression. Biopsy material was obtained from 11 patients with hemangiomas at different phases of development. In one of these patients, a biopsy was taken from the proliferative, involuting, and involuted areas of the hemangioma. In another patient, a biopsy was taken before and 5 weeks after the intralesional administration of steroids. From each tissue specimen, RNA was isolated and subjected to reverse transcriptase-polymerase chain reaction analysis by use of specific primers for the human mitochondrial cytochrome b gene. Semiquantitative reverse transcriptase-polymerase chain reaction analysis revealed that the strongest expression of the mitochondrial cytochrome b transcripts was in specimens taken from hemangiomas in the involuting phase compared with those from the proliferative and involuted phases. The authors concluded that mitochondrial cytochrome b is associated with both the spontaneous and the steroid-induced regression of hemangioma, probably by regulating apoptosis.
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