Predictors of cervical lordosis loss after laminoplasty in patients with cervical spondylotic myelopathy.

PURPOSE: To determine whether radiological, clinical, and demographic findings in patients with cervical spondylotic myelopathy (CSM) were independently associated with loss of cervical lordosis (LCL) after laminoplasty. METHODS: The prospective study included 41 consecutive patients who underwent laminoplasty for CSM. The difference in C2-7 Cobb angle between the postoperative and preoperative films was used to evaluate change in cervical alignment. Age, sex, body mass index (BMI), smoking history, preoperative C2-7 Cobb angle, T1 slope, C2-7 range of motion (C2-7 ROM), C2-7 sagittal vertical axis (C2-7 SVA), and cephalad vertebral level undergoing laminoplasty (CVLL) were assessed. Data were analyzed using Pearson and Spearman correlation test, and univariate and stepwise multivariate linear regression. RESULTS: T1 slope, C2-7 SVA, and CVLL significantly correlated with LCL (P < 0.001), whereas age, BMI, and preoperative C2-7 Cobb angle did not. In multiple linear regression analysis, higher T1 slope (B = 0.351, P = 0.037), greater C2-7 SVA (B = 0.393, P < 0.001), and starting laminoplasty at C4 level (B = - 7.038, P < 0.001) were significantly associated with higher postoperative LCL. CONCLUSIONS: Cervical alignment was compromised after laminoplasty in patients with CSM, and the degree of LCL was associated with preoperative T1 slope, C2-7 SVA, and CVLL.

Do Modic changes affect cervical sagittal alignment and motion in symptomatic patients?

PURPOSE: The cervical segmental instability often occurs simultaneously with Modic changes (MCs). However, it is unknown whether there is a relation between the two diseases. The aim of this study was to evaluate the relationship between MCs and cervical segmental instability, cervical curvature and range of motion (ROM) in the cervical spine. METHODS: A total of 464 patients with neck pain or cervical neurologic symptoms who underwent imaging examination were analyzed retrospectively. Based on MRI imaging cervical MCs were diagnosed, and patients were divided into with or without MCs groups. The cervical curvature and range of motion were measured. We compared the incidence of cervical instability, cervical curvature and ROM between the two group patients and their relationships with MCs were studied. Logistic regression was used to study the risk factors associated with MCs. RESULTS: MCs were observed in 94 of 464 patients and 122 of total 2320 cervical segments and were most frequent at C5-6 segment. The incidence of the cervical instability was significantly higher in patients with MCs than those without MCs at cervical level C3-7. In addition, cervical curvature and ROM in patients with MCs were less than those without MCs. Logistic regression analysis showed that the occurrence of cervical spine instability, less cervical curvature and ROM were risk factors for MCs. CONCLUSIONS: Patients with MCs were prone to have cervical instability at the same cervical level and may have a higher possibility of less cervical curvature and ROM.

Knockdown of SALL4 inhibits the proliferation and reverses the resistance of MCF-7/ADR cells to doxorubicin hydrochloride.

BACKGROUND: Breast cancer is the most frequent malignancy in women and drug resistance is the major obstacle for its successful chemotherapy. In the present study, we analyzed the involvement of an oncofetal gene, sal-like 4 (SALL4), in the tumor proliferation and drug resistance of human breast cancer. RESULTS: Our study showed that SALL4 was up-regulated in the drug resistant breast cancer cell line, MCF-7/ADR, compared to the other five cell lines. We established the lentiviral system expressing short hairpin RNA to knockdown SALL4 in MCF-7/ADR cells. Down-regulation of SALL4 inhibited the proliferation of MCF-7/ADR cells and induced the G1 phase arrest in cell cycle, accompanied by an obvious reduction of the expression of cyclinD1 and CDK4. Besides, down-regulating SALL4 can re-sensitize MCF-7/ADR to doxorubicin hydrochloride (ADMh) and had potent synergy with ADMh in MCF-7/ADR cells. Depletion of SALL4 led to a decrease in IC50 for ADMh and an inhibitory effect on the ability to form colonies in MCF-7/ADR cells. With SALL4 knockdown, ADMh accumulation rate of MCF-7/ADR cells was increased, while the expression of BCRP and c-myc was significantly decreased. Furthermore, silencing SALL4 also suppressed the growth of the xenograft tumors and reversed their resistance to ADMh in vivo. CONCLUSION: SALL4 knockdown inhibits the growth of the drug resistant breast cancer due to cell cycle arrest and reverses tumor chemo-resistance through down-regulating the membrane transporter, BCPR. Thus, SALL4 has potential as a novel target for the treatment of breast cancer.