Randomized, Controlled Trial: Efficacy of Ultrasound and Exercise in Patients With Ankylosing Spondylitis.

CONTEXT: The aim in treating ankylosing spondylitis (AS) is to reduce patients' symptoms, including pain, stiffness, and fatigue; to correct their posture; and to improve their quality of life. Currently, no definitive therapy is available for treating AS. Previous studies have reported positive results regarding the efficacy of exercise. OBJECTIVE: This study aimed to assess the efficacy of ultrasound, combined with exercise, in patients with AS. DESIGN: The research team designed a randomized, double-blind, 2-arm parallel-group, placebo-controlled trial. SETTING: The study took place at the Affiliated Hongqi Hospital of Mudanjiang Medical University (Mudanjiang, China). PARTICIPANTS: Participants were 62 individuals with AS who were patients at the hospital. INTERVENTION: Participants were randomly assigned to one of 2 groups: (1) the intervention group, who received exercise and ultrasound therapy; or (2) the control group, who received exercise and placebo ultrasound therapy, without an active probe, both for 8 wk. OUTCOME MEASURES: The outcome measures included (1) the numerical rating scale (NRS), (2) the Bath ankylosing spondylitis metrology index (BASMI), (3) the Bath ankylosing spondylitis disease activity index (BASDAI), (4) the Bath ankylosing spondylitis functional index (BASFI), and (5) the ankylosing spondylitis quality of life (ASQoL) questionnaire. All outcomes were measured at baseline and at the end of 4 and 8 wk of treatment. RESULT: Fifty-seven patients fulfilled the requirements of the study. Ultrasound and exercise therapy showed greater efficacy than the placebo ultrasound and exercise in decreasing the scores for the NRS, daily and at night; the BASMI; the BASDAI; the BASFI; and the ASQoL, at the end of both 4 and 8 wk of treatment. No adverse events were noted in either group. CONCLUSIONS: The study demonstrated that 8 wk of ultrasound and exercise therapy was efficacious in patients with AS.

Knockdown of ephrin receptor A7 suppresses the proliferation and metastasis of A549 human lung cancer cells.

Previous studies have demonstrated that ephrin (Eph) family receptor tyrosine kinases and ligands promote cancer growth, invasion and metastasis. In addition, it has been reported that Eph receptor A7 (EphA7) is transcriptionally activated in lung cancer; however, the effects of silencing EphA7 expression on the growth of lung cancer cells, and the underlying molecular mechanisms, have yet to be determined. Therefore, the present study aimed to investigate whether silencing EphA7 with small interfering (si)RNA could induce apoptosis in non­small cell lung cancer (NSCLC) cells. Furthermore, the effects of siEphA7 on cell migration and invasion were evaluated using Transwell assays. The mechanisms underlying the effects of siEphA7 on the tumorigenic properties of A549 cells were also examined. The results of the present study demonstrated that transfection with siEphA7 inhibited the proliferation, migration and invasion of A549 cells. In addition, siEphA7 significantly increased the protein expression levels of B­cell lymphoma 2 (Bcl­2)­associated X protein and caspase­3, and decreased the protein expression levels of Bcl­2, thus suggesting that siEphA7 was able to induce apoptosis via the intrinsic apoptotic pathway. In addition, the expression levels of phosphatase and tensin homolog (PTEN) were significantly upregulated, and the expression levels of total AKT were not altered, whereas the levels of phosphorylated­AKT were reduced. These findings indicated that EphA7 may have an important role in the pathogenesis of NSCLC by regulating PTEN expression via the PTEN/AKT pathway. Silencing EphA7 may provide a novel approach for the treatment of NSCLC.

Wnt/ß-catenin pathway is required for epithelial to mesenchymal transition in CXCL12 over expressed breast cancer cells.

CXCL12 is positively associated with the metastasis and prognosis of various human malignancies. Cancer-associated fibroblasts (CAFs), the main cells secreting CXCL12, are capable of inducing epithelial to mesenchymal transition (EMT) of breast cancer cells. However, it has not been completely understood whether CXCL12 is involved in EMT of breast cancer cells and the underlying mechanisms. The present study aimed to investigate the effects of CXCL12 on the EMT and cancer stem cell (CSC)-like phenotypes formation by transfecting pEGFP-N1-CXCL12 plasmid into MCF-7 cells. Real time-PCR and Western blot analysis demonstrated the successful over expression of CXCL12 in MCF-7 cells. Cell counting kit-8 assay, wound healing assay and Transwell invasion analysis confirmed that over expression of CXCL12 significantly promoted the proliferation, migration and invasion in MCF-7 cells (P<0.05). In addition, ALDH activity was dramatically enhanced compared with parental (P<0.001), accompanied by the notably elevated mRNA and protein levels of OCT-4, Nanog, and SOX2 in CXCL12 overexpressed-MCF-7 cells (P<0.001). Furthermore, we observed the down regulation of E-cadherin and up regulation of vimentin, N-cadherin, and α-SMA in CXCL12 overexpressed-MCF-7 cells (P<0.01). Meanwhile, western blot and immunofluorescence assay showed that over expression of CXCL12 activated Wnt/ß-catenin pathway to induce EMT of MCF-7 cells, as evidenced by the increased expression of E-cadherin after silencing ß-catenin by siRNA interference (P<0.001). Collectively, our findings suggested that over expression of CXCL12 could trigger EMT by activating Wnt/ß-catenin pathway and induce CSC-like phenotypes formation to promote the proliferation and metastasis in MCF-7. Hence, CXCL12 may become a promising candidate for breast cancer therapy.