The intervertebral disc is characterized by a tension-resisting annulus fibrosus and a compression-resisting nucleus pulposus composed largely of proteoglycan. The most important function of the annulus and nucleus is to provide mechanical stability to the disc. Degenerative disc disease in the lumbar spine is a serious health problem. Although the three joint complex model of the degenerative process is widely accepted, the etiological basis of this degeneration is poorly understood. With the recent progress in molecular biology and modern biological techniques, there has been dramatic improvement in the understanding of aging and degenerative changes of the disc. Knowledge of the pathophysiology of the disc degeneration can help in the appropriate choice of treatment and to develop tissue engineering for biological restoration of degenerated discs.

We reviewed 15 patients with femoral nonunion after interlocking intramedullary nailing treated with plate augmentation and bone grafting with the nail in situ. The mean time from primary nailing to plate augmentation and bone grafting was 10 months. At the time of presentation, the patients had undergone an average of 1.6 operations from the time of their original injury. To achieve stability of the fracture, we applied an AO plate on the lateral aspect of the femur. The retained nail maintained alignment of the fracture, and plating did not require an extensive surgical approach. In all patients, there was visible motion at the fracture site; however, the motion disappeared after plate augmentation. All patients achieved radiological solid union at an average of 7.2 months.

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BackgroundWeakness of cervical extensor muscles causes loss of cervical lordosis, which could also cause neck pain. The aim of this study was to investigate the impact of fat infiltration in cervical extensor muscles on cervical lordosis and neck pain.MethodsFifty-six patients who suffered from neck pain were included in this study. Fat infiltration in cervical extensor muscles was measured at each level of C2–3 and C6–7 using axial magnetic resonance imaging. The visual analogue scale (VAS), 12-Item Short Form Health Survey (SF-12), and Neck Disability Index (NDI) were used for clinical assessment.ResultsThe mean fat infiltration was 206.3 mm2 (20.3%) at C2–3 and 240.6 mm2 (19.5%) at C6–7. Fat infiltration in cervical extensor muscles was associated with high VAS scores at both levels (p = 0.047 at C2–3; p = 0.009 at C6–7). At C2–3, there was a negative correlation between fat infiltration of the cervical extensor muscles and cervical lordosis (r = −0.216; p = 0.020). At C6–7, fat infiltration in the cervical extensor muscles was closely related to NDI (p = 0.003) and SF-12 (p > 0.05). However, there was no significant correlation between cervical lordosis and clinical outcomes (VAS, p = 0.112; NDI, p = 0.087; and SF-12, p > 0.05).ConclusionsThese results suggest that fat infiltration in the upper cervical extensor muscles has relevance to the loss of cervical lordosis, whereas fat infiltration in the lower cervical extensor muscles is associated with cervical functional disability.

Study DesignA cross-sectional study.PurposeTo explore the impact of chronic low back pain (CLBP) on individuals' quality of life; to understand current treatment practices and level of satisfaction with treatment in patients with CLBP.Overview of LiteratureAssessing subjective, patient-reported outcomes such as quality of life is essential to health care research.MethodsInfluences of the CLBP were analyzed via a questionnaire, which contained the character of CLBP, effect of pain management, Korean version Oswestry Disability Index (K-ODI) and Korean version of 12-item Short Form Health Survey (SF-12v2).ResultsOf 3,121 subjects who responded, 67.3% had moderate to severe pain; 43.5% presented prolonged CLBP of more than two years; and 32.4% had suffered from sleep disturbance due to pain. 22.8% of the patients were not satisfied with current pain management. The mean K-ODI score was 37.63; and it was positively correlated with the mean pain intensity (r=0.6, p<0.001). The SF-12v2 result was negatively correlated with mean pain intensity (PCS: r=-0.5, p<0.001; MCS: r=-0.4, p<0.001) and also negatively correlated with the K-ODI score (PCS: r=-0.75, p<0.001; MCS: r=-0.5, p<0.001). The conformity between patients and doctors in pain assessment was fair (κ=0.2463).ConclusionsCLBP negatively affects quality of life. Of total 22.8% of the patients were not satisfied with current pain management. Such needs to be taken more seriously by doctors for improvement of satisfaction and quality of life in patients with CLBP.

Stress proteins have been implicated in pathological cardiovascular conditions. We hypothesized that a heat-shock response modulates contractility of vascular smooth muscles. Rat aortic ring preparations were mounted in organ baths, exposed to 42 degrees C for 45 min, and subjected to contractions. Expression of HSP70 and phosphorylation of myosin light chain were examined with immunoblots. Heat shock enhanced contractile response to KCl in parallel with HSP70 expression in rat aortic rings from 8 h but not 1 h after the end of heat shock. Heat shock also augmented vascular contractility to phenylephrine whether endothelium was intact or denuded. Treatment of heat shock-preconditioned aortic rings with Bay K8644, a calcium channel activator, but not treatment with phorbol dibutyrate (1 micromol/l), a protein kinase C activator, enhanced contractions of the rings as compared with those of the control. The levels of phosphorylation of myosin light chains after administration of phenylephrine in heat shock-preconditioned tissues were statistically significantly higher than those in control tissues. Pretreatment with wortmannin (300 nmol/l), an inhibitor of myosin light chain kinase, decreased both contractility and phosphorylation of myosin light chains in parallel. However, heat-shock response did not affect relaxation responses to either acetylcholine in endothelium-intact aortic rings or sodium nitroprusside in endothelium-denuded rings. These results suggest that the heat-shock response is associated with enhanced vascular smooth muscle contractility through a modulation of thick-filament regulation.