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moderately crosslinked Gtn-HPA hydrogels (i.e . GH-1.0 and GH-1.2),
# ^$ N4 h. P4 }. I$ D$ Wthese processes contained multiple nuclei along their length and
6 ^+ {% y) J+ t5 t6 E9 j0 v2 }% z2 twere likely to be migratory chains of young neurons ( Fig. 4B eC). On( D, z9 Z n$ y
the other hand, processes in the heavily crosslinked Gtn-HPA4 u% \3 z8 H/ {6 H: ~& O9 P7 v4 x; `
hydrogels (i.e., GH-1.7) did not contain any nucleus and were/ y: y W. w3 P9 J0 z
neurites extending from the neurospheres (Fig. 4D). This was also, `* A, E7 C# E3 e! A4 @+ _$ J
re fl ected in our measurements of process length and particularly,6 S) z2 g3 e( W- c7 m
process width, which gave a strong indication if entire cells were
& M+ D# k- }* ]- F' Hpresent in the process. One-factor ANOVA revealed signi fi cant
! o# p- }+ s/ g. V9 F* \) h% Heffects of crosslinking degree on both process length (p < 0.0 0 01,
6 O' U- V6 ^5 s5 {power ¼ 1) and width ( p < 0.0 01, power ¼ 0.998) (Fig. 4E and F)., Q: L3 `0 m' e5 @' v
Between GH-1.0 and GH-1.2, the increment in crosslinking did not! W" ^$ k, x* f% a
affect the process width but caused a reduction in process length
" F+ k4 e$ H: r8 ?0 V(Fisher’ s post-hoc test, p < 0.05). This agreed with the immuno-staining fi ndings that the increment in crosslinking from GH-1.0 to5 G$ A% P, [# C0 B+ x# ]
GH-1.2 did not prevent chain migration from occurring but did
& M, ^6 P: F g: [impede the extent of migration of the immature neurons along
8 V* a9 f4 I8 i& I8 y; y4 Xthese chains. On the other hand, between GH-1.2 and GH-1.7, both- j+ H. { F# W
process length and width were signifi cantly reduced (Fisher’ s post-hoc test, p < 0.0 01). This was also in line with the immunostaining( l3 ~. Y' [4 i8 O! `/ k
fi ndings that further increment in crosslinking from GH-1.2 to GH-1.7 eliminated chain migration and only permitted the formation of6 p/ C, R9 z+ G( E/ m
neurites.
; D k, B2 l/ a! `% L* X3.5. Influence on |
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