Slacklining as therapy to address non-specific low back pain in the presence of multifidus arthrogenic muscle inhibition

Low back pain(LBP)represents the most prevalent,problematic and painful of musculoskeletal conditions that affects both the individual and society with health and economic concerns.LBP is a heterogeneous condition with multiple diagnoses and causes.In the absence of consensus definitions,partly because of terminology inconsistency,it is further referred to as non-specific LBP(NSLBP).In NSLBP patients,the lumbar multifidus(MF),a key stabilizing muscle,has a depleted role due to recognized myocellular lipid infiltration and wasting,with the potential primary cause hypothesized as arthrogenic muscle inhibition(AMI).This link between AMI and NSLBP continues to gain increasing recognition.To date there is no‘gold standard’or consensus treatment to alleviate symptoms and disability due to NSLBP,though the advocated interventions are numerous,with marked variations in costs and levels of supportive evidence.However,there is consensus that NSLBP management be cost-effective,self-administered,educational,exercise-based,and use multi-modal and multi-disciplinary approaches.An adjuvant therapy fulfilling these consensus criteria is‘slacklining’,within an overall rehabilitation program.Slacklining,the neuromechanical action of balance retention on a tightened band,induces strategic indirect-involuntary therapeutic muscle activation exercise incorporating spinal motor control.Though several models have been proposed,understanding slacklining’s neuro-motor mechanism of action remains incomplete.Slacklining has demonstrated clinical effects to overcome AMI in peripheral joints,particularly the knee,and is reported in clinical case-studies as showing promising results in reducing NSLBP related to MF deficiency induced through AMI(MF-AMI).Therefore,this paper aims to:rationalize why and how adjuvant,slacklining therapeutic exercise may positively affect patients with NSLBP,due to MF-AMI induced depletion of spinal stabilization;considers current understandings and interventions for NSLBP,including the contributing role of MF-AMI;and details the reasons why slacklining could be considered as a potential adjuvant intervention for NSLBP through its indirect-involuntary action.This action is hypothesized to occur through an over-ride or inhibition of central down-regulatory induced muscle insufficiency,present due to AMI.This subsequently allows neuroplasticity,normal neuro-motor sequencing and muscle re-activation,which facilitates innate advantageous spinal stabilization.This in-turn addresses and reduces NSLBP,its concurrent symptoms and functional disability.This process is hypothesized to occur through four neuro-physiological processing pathways:finite neural delay;movement-control phenotypes;inhibition of action and the innate primordial imperative;and accentuated corticospinal drive.Further research is recommended to investigate these hypotheses and the effect of slacklining as an adjuvant therapy in cohort and control studies of NSLBP populations.

Inhibiting Smooth Muscle Cell Proliferation via Immobilization of Heparin/Fibronectin Complexes on Titanium Surfaces

The aim of this study was to investigate the inhibitory effect of heparin/fibronectin （Hep/Fn） complexes on neointimal hyperplasia following endovascular intervention. Hep/Fn complexes were immobilized onto titanium （Ti） surfaces, with subsequent X-ray photoelectron spectroscopy （XPS）, Toluidine Blue 0 （TBO） and immunohistochemistry methods were used to characterize surface properties. Smooth muscle cell （SMC） cultures were used to evaluate the effect of Hep/Fn complexes on SMC proliferation. Results showed that Hep/Fn complexes successfully immobilized onto Ti surfaces and resulted in an inhibition of SMC proliferation. This study suggests that Hep/Fn surface-immobilized biomaterials develop as a new generation of biomaterials to prevent neointimal hyperplasia, particularly for use in cardiovascular implants.

Inhibition of vascular smooth muscle cell proliferation by in troduction of retinoblastoma gene via a recombinant adenovirus vector

This study was supported in part by grant from National Natural Science Foundation of China (No. 39570775). Objective To investigate the vascular smooth muscle cell (SMC) growth suppression by recombinant adenovirus vector expressing a retinoblastoma (Rb) protein and to explore a gene therapy approach for vascular proliferative disorders including atherosclerosis and artery restenosis. Methods A replication deficient adenovirus vector encoding a wild type Rb and AdCMVRb, was constructed and transfected into cultured rabbit aortic SMC. The efficiency of gene transfection and expression was detected by immunochemical staining and polymerase chain reaction. The role of Rb in regulating vascular SMC proliferation was observed by cell counting, thymidine incorporation, and flow cytometry. Results Wild type Rb gene transfected effectively into the cultured SMC with AdCMVRb can suppress growth factor stimulated cell proliferation through regulation of DNA synthesis and cell cycle progression. Conclusion The results demonstrate the potential of adenovirus mediated Rb gene therapy for atherosclerosis and artery restenosis after balloon angioplasty.