Increased bone turnover with excessive bone resorption and decreased bone formation is known to impair implant fixation. Strontium ranelate is well known as an effective antiosteoporotic agent by its dual effect of antiresorbing and bone-forming activity. This study was designed to evaluate the effect of systemic strontium ranelate (SR) treatment on fixation of hydroxyapatite (HA)-coated titanium screws in ovariectomized (OVX) rats. Twelve weeks after being OVX (n ¼ 30) or sham (n ¼ 10) operated, 40 female Sprague-Dawley rats received unilateral implants in the proximal tibiae. The OVX rats were randomly divided into the following groups: OVX, OVX þ SR L ('' L '' refers to low SR dose of 500 mg/kg/day), OVX þ SR H ('' H '' refers to high SR dose of 1000 mg/kg/day).Twelve weeks after treatment, bone blocks with implants were evaluated with micro-CT and biomechanical push-out tests. Compared to OVX animals, SR treatment increased the bone volume ratio by 51.5% and 1.1-fold, the percentage osteointegration by 1.0-fold and 1.9-fold in micro-CT evaluation, and the maximal force by 1.9-fold and 3.3-fold in biomechanical push-out test, for the low and high dose of SR, respectively. Significant correlation between micro-CT and biomechanical properties demonstrated that trabecular parameters played an important role in predicting the biomechanical properties of implant fixation. Our findings suggest that SR treatment can dose-dependently improve HA-coated screw fixation in OVX rats and facilitate the stability of the implant in the osteoporotic bone. ß
Synaptic vesicle protein 2A (SV2A) involvement has been reported in the animal models of epilepsy. The aim of this study was to investigate the expression of SV2A in human intractable epilepsy (IE) brain tissue. Using immunohistochemistry, immunofluorescence, and Western blot, we detected SV2A expression in tissue samples from the anterior temporal neocortex of 33 patients who had been surgically treated for IE. We compared these tissues with nine histologically normal anterior temporal lobe samples from controls. SV2A immunoreactive staining was 0.1651+/-0.0564 in patient group and 0.2347+/-0.0187 in the control group (p<0.05) using immunohistochemistry, and this finding was consistently observed with Western blot analysis (0.1727 +/- 0.0471 versus 0.3976+/-0.0983, p<0.05). Immunofluorescence staining showed that SV2A was mainly accumulated in neurons. Our findings demonstrate that down-regulation of SV2A is present in patients with temporal lobe epilepsy.
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