A Cadaveric Pilot Study

This study investigates the adhesion capacity of a polyglycolic acid- (PGA-) hyaluronan scaffold with a structural modification based on a planar polymer (PM) surface in a cadaver cartilage defect model. Two cadaver specimens were used to serially test multiple chondral matrices. In a cadaver hip model, cell free polymer-based cartilage implants with a planar bioinspired PM surface (PGA-PM-scaffolds) were implanted arthroscopically on 10 mm × 15 mm full- thickness femoral hip cartilage lesions. Unprocessed cartilage implants without a bioinspired PM surface were used as control group. The cartilage implants were fixed without and with the use of fibrin glue on femoral hip cartilage defects. After 50 movement cycles and removal of the distraction, a rearthroscopy was performed to assess the outline attachment and integrity of the scaffold. The fixation techniques without and with fibrin fixation showed marginal differences for outline attachment, area coverage, scaffold integrity, and endpoint fixation after 50 cycles. The PGA-PM-scaffolds with fibrin fixation achieved a higher score in terms of the attachment, integrity, and endpoint fixation than the PGA-scaffold on the cartilage defect. Relating to the outline attachment, area coverage, scaffold integrity, and endpoint fixation, the fixation with PGA-PM-scaffolds accomplished significantly better results compared to the PGA-scaffolds . PGA-PM-scaffolds demonstrate increased observed initial fixation strength in cadaver femoral head defects relative to PGA-scaffold, particularly when fibrin glue is used for fixation

Arthroscopic Fixation of Cell Free Polymer-Based Cartilage Implants with a Bioinspired Polymer Surface on the Hip Joint: A Cadaveric Pilot Study

This study investigates the adhesion capacity of a polyglycolic acid-(PGA-) hyaluronan scaffold with a structural modification based on a planar polymer (PM) surface in a cadaver cartilage defect model. Two cadaver specimens were used to serially test multiple chondral matrices. In a cadaver hip model, cell free polymer-based cartilage implants with a planar bioinspired PM surface (PGA-PM-scaffolds) were implanted arthroscopically on 10 mm x 15 mm full-thickness femoral hip cartilage lesions. Unprocessed cartilage implants without a bioinspired PM surface were used as control group. The cartilage implants were fixed without and with the use of fibrin glue on femoral hip cartilage defects. After 50 movement cycles and removal of the distraction, a rearthroscopy was performed to assess the outline attachment and integrity of the scaffold. The fixation techniques without and with fibrin fixation showed marginal differences for outline attachment, area coverage, scaffold integrity, and endpoint fixation after 50 cycles. The PGA-PM-scaffolds with fibrin fixation achieved a higher score in terms of the attachment, integrity, and endpoint fixation than the PGA-scaffold on the cartilage defect. Relating to the outline attachment, area coverage, scaffold integrity, and endpoint fixation, the fixation with PGA-PM-scaffolds accomplished significantly better results compared to the PGA-scaffolds (P = 0.03752, P = 0.03078, P = 0.00512, P = 0.00512). PGA-PM-scaffolds demonstrate increased observed initial fixation strength in cadaver femoral head defects relative to PGA-scaffold, particularly when fibrin glue is used for fixation

La Vigie marocaine

12 mai 19371937/05/12 (A28,N9288)-1937/05/12

Additional file 7: of HOTAIR and its surrogate DNA methylation signature indicate carboplatin resistance in ovarian cancer

Ten-fold internal cross-validations to identify an optimal DNAme signature. Upper panel shows the total misclassification error (y-axis) as a function of the shrinkage threshold (x-axis) used. Lower panel shows the misclassification error for each phenotype (1 = low HOTAIR expression, 2 = high HOTAIR expression) as a function of the same shrinkage threshold. The optimal minimal classifier was found at a threshold of approximately 1.47, corresponding to a 67-CpG signature at an estimated false discovery rate (FDR) of approximately 0.17 (not shown). The FDR was estimated using a permutation scheme as implemented in the pamr R-package, and the relatively low FDR (only about 17 % of the 67 CpGs are expected to be false positives) demonstrates the presence of a genuine DNAme signal associated with HOTAIR expression. (PDF 13 kb

Additional file 3: of HOTAIR and its surrogate DNA methylation signature indicate carboplatin resistance in ovarian cancer

Normalised beta-value DNAme data matrix that was used to identify the 67 HOTAIR -associated CpGs. This data matrix has dimensions 5000 CpGs (the 5000 most variable positions) by 134 samples; samples are annotated according to whether they are HOTAIRâ +â ve/-ve and type of chemotherapy received. (XLSX 9331 kb

HOTAIR and its surrogate DNA methylation signature indicate carboplatin resistance in ovarian cancer

BACKGROUND: Understanding carboplatin resistance in ovarian cancer is critical for the improvement of patients' lives. Multipotent mesenchymal stem cells or an aggravated epithelial to mesenchymal transition phenotype of a cancer are integrally involved in pathways conferring chemo-resistance. Long non-coding RNA HOTAIR (HOX transcript antisense intergenic RNA) is involved in mesenchymal stem cell fate and cancer biology. METHODS: We analyzed HOTAIR expression and associated surrogate DNA methylation (DNAme) in 134 primary ovarian cancer cases (63 received carboplatin, 55 received cisplatin and 16 no chemotherapy). We validated our findings by HOTAIR expression and DNAme analysis in a multicentre setting of five additional sets, encompassing 946 ovarian cancers. Chemo-sensitivity has been assessed in cell culture experiments. RESULTS: HOTAIR expression was significantly associated with poor survival in carboplatin-treated patients with adjusted hazard ratios for death of 3.64 (95 % confidence interval [CI] 1.78-7.42; P < 0.001) in the discovery and 1.63 (95 % CI 1.04-2.56; P = 0.032) in the validation set. This effect was not seen in patients who did not receive carboplatin (0.97 [95 % CI 0.52-1.80; P = 0.932]). HOTAIR expression or its surrogate DNAme signature predicted poor outcome in all additional sets of carboplatin-treated ovarian cancer patients while HOTAIR expressors responded preferentially to cisplatin (multivariate interaction P = 0.008). CONCLUSIONS: Non-coding RNA HOTAIR or its more stable DNAme surrogate may indicate the presence of a subset of cells which confer resistance to carboplatin and can serve as (1) a marker to personalise treatment and (2) a novel target to overcome carboplatin resistance