ABSTRACT
BACKGROUND: Patients with anterior cervical discectomy and fusion have a high incidence of dysphagia, which may be associated with a variety of factors. The specific mechanism remains unclear. OBJECTIVE: To explore the related factors of dysphagia after single-level anterior cervical discectomy and fusion. METHODS: We retrospectively analyzed patients with cervical degenerative disc disease receiving single-level anterior cervical discectomy and fusion in First Affiliated Hospital of Soochow University from January 2011 to January 2015. During hospitalization, basic patient data and surgery-related data were recorded, including operation time, intraoperative blood loss, surgical segment, internal fixation device and the use of recombinant human bone morphogenetic protein-2. The cervical alignment and prevertebral soft tissue swelling were measured preoperatively and 3 days postoperatively. At 1, 3, 6, 12, and 24 months postoperatively, the Bazaz swallowing function scoring system was used to assess the swallowing of the patients. RESULTS AND CONCLUSION: A total of 262 patients undergoing single-level anterior cervical discectomy and fusion were involved. The incidence of dysphagia at 1, 3, 6, 12, and 24 months postoperatively was 35.9%, 22.9%, 15.6%, 11.5% and 9.2% respectively. Univariate analysis showed that gender, operation time and course length were associated with postoperative dysphagia. Logistic multivariate regression analysis showed that the duration of operation (≥ 3 hours), female and course length (≥ 8 months) were risk factors for dysphagia after anterior cervical descectomy and fusion. Operation time and female may be associated with early and middle dysphagia postoperatively, and the course length may be associated with chronic dysphagia. Prevertebral soft tissue swelling and other factors are not related to dysphagia after single-level anterior cervical discectomy and fusion. Risk factors for dysphagia after multi-level fusion should be further studied.
ABSTRACT
Objective To establish a method to determine the contents of total flavonoids and shikimic acid in pine needles of Pinus massoniana Lamb.in Wudang Area.Methods Rutin was used as reference standard,and the content of total flavonoids in pine needles of Pinus massoniana Lamb. was determined by UV spectrometry at wavelength of 500 nm. The content of shikimic acid was determined by HPLC-DAD. The Fortis Xi C8 column (5 μm, 250 mm × 4.6 mm) was adopted with acetonitrile - 0.4% phosphoric acid solution (8:92, V/V) as mobile phase at the flow rate of 0.9 mL/min. The detection wavelength was 213 nm; the column temperature was 30 ℃; the injection volume was 20 μL. Results The linear range was 8.26-49.54 μg for rutin (r=0.999 4) with an average recovery of 99.2%, RSD=1.94%. The linear range was 10.26-61.56 μg for shikimic acid (r=0.999 4) with an average recovery of 99.5%,RSD=1.93%.The contents of total flavonoids in pine needles of Pinus massoniana Lamb.was 28.33 mg/g, and shikimic acid was 15.25 mg/g, respectively. Conclusion The method is simple, rapid, accurate and reproducible. It can be used for the content determination of total flavonoids and shikimic acid in pine needles of Pinus massoniana Lamb. in Wudang Area.
ABSTRACT
<p><b>BACKGROUND</b>The cannabinoid receptor-2 (CB2) is important for bone remodeling. In this study, we investigated the effects of CB2 selective antagonist (AM630) on receptor activator of nuclear factor kappa B (RANK) ligand (RANKL) induced osteoclast differentiation and the underlying signaling pathway using a monocyte-macrophage cell line-RAW264.7.</p><p><b>METHODS</b>RAW264.7 was cultured with RANKL for 6 days and then treated with AM630 for 24 hours. Mature osteoclasts were measured by tartrate-resistant acid phosphatase (TRAP) staining using a commercial kit. Total ribonucleic acid (RNA) was isolated and real-time reverse transcriptase-polymerase chain reaction (RT-PCR) was done to examine the expression of RANK, cathepsin K (CPK) and nuclear factor kappa B (NF-κB). The extracellular signal-regulated kinase (ERK), phosphorylation of ERK (P-ERK) and NF-κB production were tested by Western blotting. The effect of AM630 on RAW264.7 viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide (MTT) assay.</p><p><b>RESULTS</b>AM630 did not affect the viability of RAW264.7. However, this CB2 selective antagonist markedly inhibited osteoclast formation and the inhibition rate was dose-dependent. The dose of ≥ 100 nmol/L could reduce TRAP positive cells to the levels that were significantly lower than the control. AM630 suppressed the expression of genes associated with osteoclast differentiation and activation, such as RANK and CPK. An analysis of a signaling pathway showed that AM630 inhibited the RANKL-induced activation of ERK, but not NF-κB.</p><p><b>CONCLUSION</b>AM630 could inhibit the osteoclastogenesis from RAW264.7 induced with RANKL.</p>