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The mechanism of increased speed and incidence of fusion using growth factors (rhOP-1) is delineated by this comprehensive study of preferential intramembranous ossification.
Without question, direct radiation exposure to the cerebellum dramatically increases the incidence of fusion between BM-derived cells and Purkinje cells [ 12, 46].
However, radiation therapy enhances the incidence of fusion hybrid formation and could result in a more aggressive and invasive tumours (Shabo et al., 2009; Seyfried et al., 2011).
This idea is supported by our observation that there was a significant incidence of fusion failure after vangl2 disruption, an effect that was enhanced in embryos where both vangl2 and ofd1 were downregulated.
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Incidence of fusions were observed through radiography and calculated using a one-way analysis of variance model (GLM procedure, SAS 9.1 software, SAS Institute Inc., USA).
Polykaryons expressing MIEF1-V5 significantlyicantly higher incidence of mitochondrial fusion as compared with control, suggesting that MIEF1 promotes mitochondrial fusion.
The reported incidence of TMPRSS2 ETV1 fusion in these studies (1 2%) was, however, considerably lower than the observed incidence of ETV1 gene overexpression (∼10% in prostate cancer).
Along with a recent increase in the incidence of lumbar fusion surgery, the importance of lumbar lordosis maintenance has been highlighted [ 9, 10].
Experimentally, the incidence of cell fusion in the brain is enhanced with age, radiation exposure, inflammation, chemotherapeutic drugs and even selective damage to the neurons themselves.
This conclusion is further strengthened by the observation that 1mM Ni2+, a non-specific cation channel blocker, also decreased the incidence of post-fusion [Ca2+]c increase to 16.7%.
Pre-incubation of cells with SKF96365 for 15 min at 37°C further decreased the incidence of post-fusion [Ca2+]c increase to 9.5% (n = 21; 11 experiments, 5 cell preparations; Figure 3), suggesting that Ca2+ enters the cytoplasm through channels.
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