Objective To discuss diagnosis and anterior surgical treatment of hyperextensian cervical spine injury combined with intervertebral disk injury. Methods A retrospective study was done on clinical data of 27 patients who suffered from hyperextension cervical spine injury combined with intervertebral disk injury to analyze their age distribution, clinical symptomes, X-ray and MRi manifesta-tions and perioperative intervertebral disk injury. All patients were treated with discectomy, strut bone grafting within vertebral bodies and internal fixation with titanium plate. The clinical outcomes were evalu-ated by using Frankel scale and ASIA motor score (AMS). Results Both MRI and X-ray detected following abnormal pathological changes in all patients: rupture of anterior longitudinal ligament, horizon-tal tear of disk, intervertebral disk hernia, compression and edema of spinal cord. The follow-up lasted for 9-32 months (average 17.5 months), which showed that all patients got improvement for 1-3 scales except that one patient with Frankel A had no improvement in neurological function. Compared with AMS on admission, both AMS at two months after surgery and at final follow-up was increased significantly, with recovery rate of AMS for 44.9% and 68.1%, respectively. There found no hardware related compli-cations such as implant loosening, defluxion or breakage. Bone fusion was found in all fixation segments. Conclusions MRI and X-ray are important examination means for hyperextension cervical spine injury combined with intervertebral disk injury. On a specified diagnosis, anterior surgical treatment should be done early and can get satisfactory recovery of spinal cord function.

Obeticholic acid (OCA), the first FXR-targeting drug, has been claimed effective in the therapy of liver fibrosis. However, recent clinical trials indicated that OCA might not be effective against liver fibrosis, possibly due to the lower dosage to reduce the incidence of the side-effect of pruritus. Here we propose a combinatory therapeutic strategy of OCA and apoptosis inhibitor for combating against liver fibrosis. CCl-injured mice, d-galactosamine/LPS (GalN/LPS)-treated mice and cycloheximide/TNF (CHX/TNF)-treated HepG2 cells were employed to assess the effects of OCA, or together with IDN-6556, an apoptosis inhibitor. OCA treatment significantly inhibited hepatic stellate cell (HSC) activation/proliferation and prevented fibrosis. Elevated bile acid (BA) levels and hepatocyte apoptosis triggered the activation and proliferation of HSCs. OCA treatment reduced BA levels but could not inhibit hepatocellular apoptosis. An enhanced anti-fibrotic effect was observed when OCA was co-administrated with IDN-6556. Our study demonstrated that OCA inhibits HSCs activation/proliferation partially by regulating BA homeostasis and thereby inhibiting activation of HSCs. The findings in this study suggest that combined use of apoptosis inhibitor and OCA at lower dosage represents a novel therapeutic strategy for liver fibrosis.