Vital capacity evolution in patients treated with the CMCR brace: statistical analysis of 90 scoliotic patients treated with the CMCR brace

<p>Summary</p> <p>Objective</p> <p>To study the evolution of pulmonary capacity during orthopaedic treatment of scoliosis with the CMCR brace.</p> <p>Background</p> <p>Investigating the impact of moderate scoliosis on respiratory capacity and its evolution during CMCR brace treatment with mobile pads.</p> <p>Context</p> <p>Several studies demonstrate the impact of scoliosis on respiratory capacity but few of them focus on the impact of bracing treatment. We studied the evolution of the pulmonary capacity of a cohort of 90 scoliotic patients.</p> <p>Methods</p> <p>This retrospective study included 90 scoliotic patients treated since 1999 with a brace with mobile pads called CMCR (n = 90; mean age: 13 years; 10-16). These patients were diagnosed with an idiopathic scoliosis (mean angulation 20.6°). All patients underwent a radiographic and respiratory evaluation at the beginning, the middle and the end of treatment.</p> <p>Results</p> <p><it>Mean age at treatment start was </it>13. Before treatment, our patients did not have a normal pulmonary capacity: Forced Vital Capacity (FVC) was only 75% of the theoretical value. All curvature types (thoracic, thoraco-lumbar and combined scoliosis) involved this reduced pulmonary capacity, with moderate-angulated scoliosis having a negative impact. At the beginning of brace treatment, the loss of real vital capacity with brace (0.3 litres) was 10% lower than without brace.</p> <p>At CMCR removal, the FVC had increased by 0.4 litre (21% +/- 4.2% compared to the initial value). The theoretical value had increased by 3%. This positive evolution was most important in girls at a low Risser stage (0,1,2), and before 11 years of age.</p> <p>Conclusion</p> <p>These results supported our approach of orthesis conception for adolescent idiopathic scoliosis which uses braces with mobile pads to preserve thorax and spine mobility.</p

Appropriate care at the end of life. Report number 296

Appropriate care at the end of life

Ataxia telangiectasia mutated activation by transcription- and topoisomerase I-induced DNA double-strand breaks

Ataxia telangiectasia mutated (ATM), the deficiency of which causes a severe neurodegenerative disease, is a crucial mediator for the DNA damage response (DDR). As neurons have high rates of transcription that require topoisomerase I (TOP1), we investigated whether TOP1 cleavage complexes (TOP1cc)—which are potent transcription-blocking lesions—also produce transcription-dependent DNA double-strand breaks (DSBs) with ATM activation. We show the induction of DSBs and DDR activation in post-mitotic primary neurons and lymphocytes treated with camptothecin, with the induction of nuclear DDR foci containing activated ATM, γ-H2AX (phosphorylated histone H2AX), activated CHK2 (checkpoint kinase 2), MDC1 (mediator of DNA damage checkpoint 1) and 53BP1 (p53 binding protein 1). The DSB–ATM–DDR pathway was suppressed by inhibiting transcription and γ-H2AX signals were reduced by RNase H1 transfection, which removes transcription-mediated R-loops. Thus, we propose that Top1cc produce transcription arrests with R-loop formation and generate DSBs that activate ATM in post-mitotic cells