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Xiang Li,1,2 Guangsheng Li,1,3 Keith Dip-Kei Luk,1 Yong Hu1–3 1Department of Orthopaedics and Traumatology, The University of Hong Kong, Pokfulam, Hong Kong, 2Shenzhen Key Laboratory for Innovative Technology in Orthopaedic Trauma, The University of Hong Kong-Shenzhen Hospital, Shenzhen, 3Spinal Division, Department of Orthopaedics, Affiliated Hospital of Guangdong Medical University, Guangdong, People’s Republic of China Background: Cervical spondylotic myelopathy (CSM) is a chronic compression injury of the spinal cord, with potentially reversible conditions after surgical decompression, and a unique model of incomplete spinal cord injury. Several animal studies showed pathological changes of demyelination, axon loss and neuron apoptosis in rats with chronic spinal cord compression. However, there is a limited understanding of the neurological change in the spinal cord after surgical decompression. The aim of this study was to validate the neurorestoratology of myelopathic lesions in the spinal cord in a rat model. Materials and methods: A total of 16 adult Sprague-Dawley rats were divided into four groups: sham control (group 1); CSM model with 4-week chronic compression (group 2), 2 weeks (group 3) and 4 weeks (group 4) after surgical decompression of CSM model. The compression and decompression were verified by magnetic resonance imaging (MRI) test. Neurological function was evaluated by Basso, Beattie, and Bresnahan (BBB) locomotor rating scale, ladder rung walking test and somatosensory-evoked potentials (SEPs). Neuropathological change was evaluated by histological examinations. Results: MRI confirmed the compression of the cervical spinal cord as well as the reshaping of cord morphology after decompression. After decompression, significant changes of neurological function were observed in BBB scores (p < 0.01, F = 10.52), ladder rung walking test (p < 0.05, F = 14.21) and latencies (p < 0.05, F = 5.76) and amplitudes (p < 0.05, F = 3.8) of SEP. Neuronal degeneration was obvious in the ventral horn with gradual restoration. After decompression, the motor neuron number in the ventral horn did not show significant changes (p > 0.05). However, increasing trend of myelin area and staining intensity were observed in all columns of the white matter (p < 0.05) after decompression, especially in the compressed lateral column. Conclusion: The established rat model is able to simulate histopathological characteristics of cervical myelopathy in human beings. The neuropathological change demonstrated that neurorestoratology in the myelopathic spinal cord would probably attribute to axonal remyelination of the white matter, but there would be an incapability of neuronal regeneration. Keywords: neurorestoratology, surgical decompression, chronic spinal cord injury, animal model, cervical spondylotic myelopathy

Jianwen Qin, Guangsheng Li, Jingmin Zhou Department of Respiratory and Critical Care Medicine, Tianjin Chest Hospital, Tianjin, People’s Republic of China Objective: To investigate the clinical features, diagnosis, and treatment status of elderly patients with chronic obstructive pulmonary disease (COPD) complicated with lung cancer.Patients and methods: This was a retrospective study of 206 patients aged >60 years with COPD and newly diagnosed lung cancer at the Tianjin Chest Hospital Respiratory Centre between September 2008 and September 2013. Lung function, radiology, and clinical data were retrieved.Results: Among all patients, 57% (117/206) were hospitalized due to acute COPD aggravation, 47% (96/206) had COPD grade III or IV, 95% (195/206), showed diffusion dysfunction in pulmonary function examination, 90% (185/206) had a history of smoking, and 26% (54/206) were treated with inhaled corticosteroids for COPD treatment. Ninety-eight patients suffered from squamous carcinoma, 73 from adenocarcinoma, and 35 from small-cell carcinoma. Clinical staging was I in 36 patients, II in 47 patients, III in 78 patients, and IV in 45 patients. Initial treatments were surgery in 59 patients, chemotherapy in 30 patients, and no treatment in 117 patients. Multivariate analysis showed that age (P

Hao Lin,1,* Bo Wei,1,* Guangsheng Li,1 Jinchang Zheng,1 Jiecong Sun,1 Jiaqi Chu,2 Rong Zeng,1 Yanru Niu21Department of Spinal Surgery, Affiliated Hospital of Guangdong Medical College, Zhanjiang, People’s Republic of China; 2Laboratory Institute of Minimally Invasive Orthopedic Surgery, Affiliated Hospital of Guangdong Medical College, Zhanjiang, People’s Republic of China *These authors contributed equally to this work Abstract: Apoptosis of osteoblasts triggered by high-dose glucocorticoids (GCs) has been identified as a major cause of osteoporosis. However, the underlying molecular mechanisms accounting for this action remain elusive, which has impeded the prevention and cure of this side effect. Sulforaphane (SFP) is a naturally occurring isothiocyanate that has huge health benefits for humans. In this study, by using osteoblastic MC3T3-E1 cells as a model, we demonstrate the protective effects of SFP against dexamethasone (Dex)-induced apoptosis and elucidate the underlying molecular mechanisms. The results show that SFP could effectively inhibit the Dex-induced growth inhibition and release of lactate dehydrogenase in MC3T3-E1 cells. Treatment with Dex induced caspase-dependent apoptosis in MC3T3-E1 cells, as evidenced by an increase in the Sub-G1 phase, chromatin condensation, and deoxyribonucleic acid fragmentation, which were significantly suppressed by coincubation with SFP. Mitochondria-mediated apoptosis pathway contributed importantly to Dex-induced apoptosis, as revealed by the activation of caspase-3/-9 and subsequent cleavage of poly adenosine diphosphate ribose polymerase, which was also effectively blocked by SFP. Moreover, treatments of Dex strongly induced overproduction of reactive oxygen species and inhibited the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and the downstream effectors HO1 and NQO1. However, cotreatment with SFP effectively reversed this action of Dex. Furthermore, silencing of Nrf2 by small interfering ribonucleic acid significantly blocked the cytoprotective effects of SFP against Dex-induced apoptosis, which suggest the important role of Nrf2 signaling pathway and cell apoptosis induced by Dex. Taken together, this study provides a novel strategy for molecular intervention against Dex-induced osteoporosis using phytochemicals. Keywords: osteoporosis, glucocorticoid, apoptosis, sulforaphane, Nrf2 pathway

The benefits of physical activity (PA) on health are well documented. However, inactivity among university students is prevalent. This study examined whether emotional intelligence (EI) was one of the possible underlying psychological mechanisms responsible for behavior change that may be associated with the low levels of effectiveness of PA interventions. The purposes of this study were: (1) to compare EI, health-related physical fitness (HRPF), and health-related quality of life (HRQL) for the different levels of PA in Taiwan college students; (2) to explore the predictability of PA levels, HRQL, and HRPF towards EI. A total of 599 Taiwan college students were assessed utilizing HRPF measurement, and two questionnaires including the Bar-On Emotional Quotient Inventory (EQ-I) and the Medical Outcomes Study 36-item Short-Form Health Survey (MOS SF-36). College participants who reported a recommended level of PA scored significantly higher than their insufficient and inactive counterparts in EI, and some measures of HRQL and HRPF. The variables of 'physical activity', 'mental health', 'gender', 'social function', and 'flexibility' were found to be the best linear combination to significantly (p < 0.05) predict the EI of Taiwan college students. It was concluded that participation in PA might be an effective way to improve the physical, psychological, as well as emotional health of college students. Thus, the importance of increasing exercise participation at the college level should be reinforced and implemented. The findings provide a basis for research aimed at determining the causal relationship between EI and PA. [ABSTRACT FROM AUTHOR]