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1 ry, and chemokine expression, and normalized tissue survival.
2 tration resulted in the greatest decrease in tissue survival.
3 le factor 1alpha stabilization and increased tissue survival.
4 lar networks in vertebrates are essential to tissue survival.
5  pathological TNF-alpha reaction and promote tissue survival.
6 ry progression, suggesting an active role in tissue survival.
7 al activation of these receptors may promote tissue survival.
8  adversely affect microvascular function and tissue survival after an ischemic episode, and previous
9 l mitogenesis, a repair process important to tissue survival after ischemic damage, was not disrupted
10 e results highlight a pathway that preserves tissue survival and muscle function in the setting of is
11 wth, differentiation, homing to their target tissues, survival and activation are all controlled, to
12 al to evaluate implant integration with host tissue, survival, and functionality.
13  playing roles in signaling, cell migration, tissue survival, anti-inflammation, and T-cell-mediated
14 d energy is utilized to ensure that cell and tissue survival are maintained.
15 vity (firing rate and thermosensitivity) and tissue survival as a function of time and slice thicknes
16 ligonucleotide to CD47 or control agents and tissue survival assessed.
17  therapeutic peptide that increases cell and tissue survival by acting as a cofactor to PDGF-BB.
18 to assess endogenous cytokine expression and tissue survival comparable to undelayed TRAM flaps.
19 1%, P<0.005) that resulted in impaired gross tissue survival compared with young mice (2 to 6 months)
20 diated vascular smooth muscle relaxation and tissue survival following ischemic injury in skin flaps
21 cking TSP1-CD47 signaling increases ischemic tissue survival in random cutaneous porcine flaps.
22                                 Furthermore, tissue survival of ischemic injury and acute recovery of
23 tanding of how Hh signaling governs cell and tissue survival remains incomplete.
24 pholino knock down of CD47 greatly increased tissue survival to ischemia.
25 imulated blood flow and growth and composite tissue survival to ischemia.
26             Cerebral blood flow required for tissue survival was higher in the mutants, leading to in
27 myocutaneous flap model for ischemic injury, tissue survival was significantly enhanced in thrombospo
28 rin loss may be incompatible with epithelial tissue survival, whereas partial compensation can result

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