The findings demonstrate that mutations in PITX1 can cause a broad spectrum of isolated lower-limb malformations including clubfoot, deficiency of long bones, and mirror-image polydactyly.
The findings demonstrate that mutations in PITX1 can cause a broad spectrum of isolated lower-limb malformations including clubfoot, deficiency of long bones, and mirror-image polydactyly.
Although no SNPs in THBS2 were associated with LSS, haplotypes (HAP4 and HAP5) were significantly associated with progression of LSS in the Korean population, whereas another haplotype (HAP1) may play a protective role against LSS development.
Although no SNPs in COL9A2 were associated with LSS, a COL9A2 haplotype (HAP2) was significantly associated with LSS in the Korean population, whereas another haplotype (HAP4) may play a protective role against LSS development.
Following the data collection on demographic and Health-related quality of life (HRQOL) by ODI and SRS-22, radiologic measurement by EOS system and MRI examination including lumbar spinal stenosis (LSS), facet angle, and segmental instability defined by facet opening were performed.
Exploration on PLIF on LSS and HBL has been reported before while the comparison on total blood loss (TBL), especially HBL of PLIF or PLF on LSS between patients with RA and without RA has not been studied.
The genotypic distribution for the TNF-α promoter -308 G/A position was observed to be nonsignificant and mildly associated during MIP (OR = 1.4) and in WWM (OR = 1.2).
The expression levels of miR‑29a in plasma and intervertebral disc tissue of patients with LSS were significantly lower in patients with LSS compared with in patients with LDH, as well as healthy controls.
Conversely, the protein expression levels of MMP9 and ADAMTS5 were significantly higher in patients with LSS compared with patients with LDH, as well as healthy controls.
First, the IGF-1, phosphorylation of IGF-1 receptor (pIGF-1R), phosphorylation of AKT (pAKT), phosphorylation of S6(pS6), collagen I and collagen III expression levels were examined via immunohistochemistry and Western blotting in LF tissues from patients with LSS or Non-LSS.