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Objective To investigate the clinical effect of mouse nerve growth factor (mNGF) and methylcobalamin (MeCbl) for the treatment of lumbar disk herniation (LDH) with foot drop. Methods A total of 46 patients suffering from LDH with foot drop who underwent transforaminal lumbar interbody fusion (TLIF) surgery in our department from January 2015 to December 2017 were retrospectively analyzed. We divided these patients into two groups according to the different postoperative treatment which independently selected by patients after signing informed consent form: one group of 25 patients was treated with MeCbl alone (Group MeCbl), the other group of 21 patients was treated with a combination of mNGF and MeCbl (Group MeCbl+mNGF). Patient demographics, the visual analogue scale (VAS) scores, sensory and muscular strength improvement statistics at 1 week, 4 weeks, 12 weeks, and 12 months postoperatively were recorded. Motor/sensory deficits, sciatica and overall neurological outcome after treatment of MeCbl alone and combination of mNGF and MeCbl were retrospectively analyzed. Results The follow‐up ranged between 12 and 42 months (mean 20.8 months). There were no significant differences between these two groups of patients with respect to sex ratio, age, smoking, diabetes, disease course, section of protruding disc(s), muscular strength of foot dorsiflexion or preoperative visual analogue scale (VAS) score (P > 0.05). The VAS scores of Group MeCbl+mNGF were significantly lower than Group MeCbl at 1 week, 4 weeks, 12 weeks, and 12 months postoperatively (4.32 ± 0.75 vs 5.25 ± 0.79,2.65 ± 0.48 vs 3.42 ± 0.52, 1.72 ± 0.36 vs 2.45 ± 0.39, 1.12 ± 0.22 vs 1.52 ± 0.24, P < 0.05). The effective rates of sensory improvement were significantly higher in Group MeCbl+mNGF compared with Group MeCbl at 12‐week/12‐month follow‐up time point (90.48% vs 52.00%,95.24% vs 68.00%, P, Application of mNGF in combination with MeCbl had clinical effects on promoting the recovery of neurological function in patients suffering from LDH with foot drop.

Night shift workers with disordered rhythmic mechanical loading are more prone to intervertebral disc degeneration (IDD). Our results showed that circadian rhythm (CR) was dampened in degenerated and aged NP cells. Long-term environmental CR disruption promoted IDD in rats. Excessive mechanical strain disrupted the CR and inhibited the expression of core clock proteins. The inhibitory effect of mechanical loading on the expression of extracellular matrix genes could be reversed by BMAL1 overexpression in NP cells. The Rho/ROCK pathway was demonstrated to mediate the effect of mechanical stimulation on CR. Prolonged mechanical loading for 12 months affected intrinsic CR genes and induced IDD in a model of upright posture in a normal environment. Unexpectedly, mechanical loading further accelerated the IDD in an Light-Dark (LD) cycle-disrupted environment. These results indicated that intrinsic CR disruption might be a mechanism involved in overloading-induced IDD and a potential drug target for night shift workers., Lower back pain: Mechanical strain exacerbated by night shift work Working long shifts at times when the body should be at rest can have lasting effects on the intervertebral discs in the back, leading to chronic pain. Night shift workers are susceptible to developing certain health conditions because of chronic disruption to their circadian rhythms. Now, Li-Bo Jiang at Zhongshan Hospitial, Fudan University in Shanghai and co-workers across China have uncovered a link between circadian rhythm disruption and intervertebral disc degeneration. In experiments on human tissue samples and rat models, the team found that oscillation of the expression of clock-related genes and proteins was reduced in severely degenerated disc cells. Cellular clock mechanisms were disrupted in disc cells that had been repeatedly placed under mechanical strain at night. This disruption appears to influence degradation of the extracellular matrix, which the team believe may in turn accelerate disc degeneration.

Lung cancer invading the spine was previously considered unresectable and fatal and, consequently, there are few reports focusing on tumors located in the lower lung lobe and invading the spine. With the development of spinal instrumentation and surgical techniques, and wider acceptance of spondylectomy by surgeons, radical surgical resection has become feasible. Here, we present a case of a male patient with a left lower lung cancer invading thoracic vertebrae who underwent complete resection with sagittal en bloc hemivertebrectomy with video‐assisted thoracoscopy. A 60‐year‐old man complained of left chest pain for 3 months. Chest computed tomography and thoracic vertebrae magnetic resonance image revealed that a tumor in the left lower lung lobe had invaded the seventh and eighth thoracic vertebrae and the eighth rib. As no lymph node or distant metastasis was detected by positron emission tomography‐computed tomography, the patient was diagnosed with left lower lung cancer directly invading the seventh and eighth thoracic vertebrae and the eighth rib (T4N0M0, stage IIIA) instead of metastasizing to the thoracic vertebrae. An en bloc resection of the lung tumor and the involved vertebrae was performed by a thoracic surgeon and orthopaedic surgeon with video‐assisted thoracoscopy. Six months after the operation, there was no evidence of local recurrence, and the patient had recovered well. En Bloc resection with video‐assisted thoracoscopy for lung cancer invading thoracic vertebrae is a safe and feasible surgical method. This method can significantly improve the safety and convenience of this type of surgery.

Zn(2+) is an essential component of metalloproteinases, and is required for their activity in cartilage; however, the effect of Zn(2+) on nucleus pulposus (NP) cells has not been widely investigated. The aim of this paper was to investigate the effect of intracellular Zn(2+) concentration ([Zn(2+)]i) in hypoxia-induced regulation of metalloproteinases (MMPs) and extracellular matrix (ECM) production in NP cells. NP cells from Sprague-Dawley (SD) rats were cultured as monolayers or in alginate beads. [Zn(2+)]i was assayed by FluoZin-3 AM staining. Alcian Blue staining, immunochemistry, 1,9-dimethylmethylene blue (DMMB) assay, and real-time PCR were used to assay collagen II, proteoglycan, and COL2A1, MMP-13, and ADAMTS-5 mRNA expression. ZIP8, a main Zn(2+) transporter in chondrocytes, was assayed by immunochemistry and in Western blotting. Interleukin (IL)-1β- and ZnCl2-induced increases of [Zn(2+)]i were significantly inhibited by hypoxia. Hypoxia did not reverse a decline of ECM expression caused by IL-1β and ZnCl2 in monolayer cultures, but did significantly attenuate the decreases of proteoglycan, glycosaminoglycan (GAG), and COL2A1 mRNA expression following IL-1β and ZnCl2 treatment in alginate bead cultures. However, ZnCl2 inhibited the protective effect of hypoxia. Both an intracellular Zn(2+) chelator and hypoxia prevented the increase in MMP-13 mRNA expression. IL-1β and ZnCl2 treatment increased ZIP8 expression in NP cells, and hypoxia inhibited ZIP8 expression. In conclusion, decrease of Zn(2+) influx mediates the protective role of hypoxia on ECM and MMP-13 expression. Consequently, changes in intracellular Zn(2+) concentration maybe involved in intervertebral disc degeneration.