239) Fibroblast growth factors (FGFs) regulate the prolife |
240) le of controlling the release of multiple growth factors (GFs) could potentially pro |
241) Plasma rich in growth factors (PRGF®-Endoret®) is an au |
242) ockage capability of vascular endothelial growth factors (VEGF). |
243) ditions: no treatment; in the presence of growth factors (neuregulin-1, bFGF and for |
244) iloring culture conditions using specific growth factors and biomechanical loading p |
245) d on the increase in the concentration of growth factors and in the secretion of pro |
246) or cells to proliferate in the absence of growth factors and increases their surviva |
247) the gene expression by qRT-PCR regarding growth factors and matrixmetalloproteinase |
248) The application of specific growth factors for osteoinduction without |
249) xpression induced upregulation of various growth factors in GC cells as well as exhi |
250) The influence of chondrogenic growth factors on neosynthesis of ECM prot |
251) Incorporation of the two growth factors onto Hep-Ti was evaluated b |
252) toneal cavity of rohu, without use of any growth factors or feeder cells. |
253) h plasma (PRP) is an autogenous source of growth factors shown to facilitate human b |
254) maturation, and are also known to produce growth factors that regulate the stromal c |
255) olecules can possibly replace recombinant growth factors used in most directed diffe |
256) mmobilized with heparin, and then the two growth factors were coated onto the Hep-Ti |
257) c differentiation without the addition of growth factors. |
258) nt when used in combination with cells or growth factors. |
259) the adhesive properties of plasma rich in growth factors. |
260) using conditioned medium, without adding growth factors. |
261) ing a combination of cells, materials and growth factors. |
262) ollagen-rich matrix containing functional growth factors. |
263) ation of the in vitro culture medium with growth/differentiation factors (GDFs). |
264) Growth inhibition and cell cycle effects w |
265) also showed significant (p > 0.05) growth inhibition as compared to MB14, whe |
266) in MCF-10A cells, and (b) mammary cancer growth inhibition by WA administration is |
267) o DNA damage and results in p53-dependent growth inhibition compared with correspond |
268) crobial activity results in a significant growth inhibition of C. |
269) metric analysis of cells that experienced growth inhibition support apoptotic death |
270) However, dose-dependent cell growth inhibition was found at all the SWC |
271) Dose-dependent cell growth inhibition was observed following h |
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