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The red double headed arrow indicates the width of the cleft.
Differences between centers could not be explained by the randomization criteria birth weight and cleft width of the cleft at trial entrance and corresponding treatment protocols until the age of 1.5 years these.
It is based on the palatal index description for cleft palate deformity (proportion between the width of the cleft (cleft's severity) and the summary of the width of the two palatal segments (tissue deficiency)) measured at the level of the hard and soft palates junction [ 43]: mild index: less than 0.2 (score: 1), moderate index: 0.2 to 0.4 (score: 2), severe index: greater than 0.4 (score: 4).
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We measured the postsynaptic area and the width of the synaptic cleft in surgery and MV groups.
The synapse number, the width of the synaptic cleft and the thickness of PSD were measured using ImageJ (NIH) software, as described previously [ 16].
All gold particles located within the postsynaptic spine and the presynaptic terminal were recorded; the width of the synaptic cleft was also measured.
The width of the synaptic cleft was 16.28 ± 0.27 nm for the lateral and 16.75 ± 0.40 nm for the central region at P2, 16.97 ± 0.58 nm for the lateral and 17.12 ± 1.41 nm for the central region at P30 with no significant change between both ages (see Table 1).
In the CA1 asymmetric synapses of sut mice, there were no apparent changes in the synapse number, the width of synaptic cleft and the thickness of PSD compared with WT mice, excluding the possibility that the reduced LTP in sut mice is caused by abnormal synaptic structures.
The PSD areas and the widths of the synaptic cleft in surgical mice treated with MV were not significantly different from those of surgical mice (P >0.05).
Recently, preoperative orthopedics, such as the NAM procedure, was reported to contribute to the narrowing of the cleft width and therefore reducing the rate of oronasal fistula developed following primary palatal surgery [ 10, 17, 18].
As reported previously (Wu et al., 2012a), Ctnnb1 mutation in muscles did not alter the number of terminals per NMJ and the width of synaptic clefts.
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