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Cells from XP patients with mutations in the XPC DNA repair gene have defective global genome DNA repair and normal transcription coupled repair.
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The authors hypothesized that quantitative three-dimensional analysis would reveal distinct differences among diseased, repaired, and normal mitral valves.
In conclusion, we have shown that A-T post-mitotic neurons display normal electrophysiological activity, defective expression of maturation markers, attenuated response to and repair of DSBs, but normal capacity to repair SSBs and normal BER activities.
Using a GRE T2* approach with the same T2* sequence, Welsch et al. found 2.3 years after MACI a comparable T2 between repair tissue and normal cartilage but a lower T2* in repair tissue.
By directing further research toward factors which contribute to the transcriptome dissimilarities of repair tissue and normal articular cartilage phenotypes, we should advance our understanding of the repair process and improve upon therapeutic strategies directed at restoring the structural and biomechanical integrity of the joint surface.
On the contrary, T2 values were not significantly different between repair cartilage and normal cartilage.
Domayer et al. reported no significant difference between the delta relaxation rates in repair tissue and normal cartilage [ 117].
Holtzman et al. reported that 3 to 6 months and 1 year after OAT T2 values showed no significant difference between repair cartilage and normal cartilage [ 139].
T1-Gd was not significantly different between repair tissue and normal cartilage 9 to 18 years after ACI according to Vasiliadis et al. [ 177].
One previous study has shown that one mutation in the gene associated with mismatch repair efficiency and normal p53 expression [ 33].
Stelzeneder et al. reported that at 1-year followup after arthroscopic autologous collagen-induced chondrogenesis (ACIC) T2* was not significantly different between repair tissue and normal cartilage [ 166].
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