Osteoblast apoptosis increased in the tibias of apoE −/− mice fed with a high-fat diet, decreasing bone formation. The expression of p53 mRNA in marrow adherent cells increased. LDL or oxidized LDL increased apoptosis in the calvarial cells of apoE −/− mice. The increase in p53-mediated apoptosis is apparently related to a high-fat diet-induced osteopenia in apoE −/− mice.
Introduction:The effects of high-fat loading and the apolipoprotein E (apoE) gene on bones have not been elucidated. We hypothesized that apoE gene deficiency (apoE
a b s t r a c tCellular perturbations such as stress to the endoplasmic reticulum induce an integrated stress response, which activates phosphorylation of eIF2a and leads to alleviation of cellular injury or apoptosis. This study investigated the role of mechanical stimulation in the regulation of eIF2a and cell death. Mechanical stimulation was applied to mouse ulnae, MC3T3 cells, and mesenchymal stem cells. The results demonstrate that mechanical stimulation reduces phosphorylation of eIF2a through inactivation of Perk. Furthermore, flow pre-treatment reduces thapsigargin-induced cell mortality through suppression of phosphorylation of Perk. However, H 2 O 2 -driven cell mortality, which is not mediated by Perk, is not suppressed by mechanical stimulation. Taken together, our observations suggest a pro-survival role of mechanical stimulation in Perk-mediated stress responses.
We report a case of ulnar nerve palsy following forearm fracture in a 13-year-old girl. Significant anterior angulation and displacement of the ulna were noted. Operation was performed 3 months after the injury, when no recovery of numbness and claw hand deformity were demonstrated. Intra-operatively the ulnar nerve was found to be embedded between fragments of the fractured ulna, which showed lack of callus formation on the preoperative radiograph. The patient achieved complete recovery of sensory and motor functions 4 months after the surgery.
ABSTRACT:Introduction: NO is synthesized by three different NO synthase (NOS) isoforms, including neuronal (nNOS), inducible (iNOS) and endothelial NOS (eNOS). The roles of NO in bone metabolism have been extensively investigated in pharmacological studies and in studies with NOS isoform-deficient mice. However, because of the nonspecificity of agents and compensation among the NOS isoforms, the ultimate roles of endogenous NO are still poorly understood. To address this point, we successfully generated mice in which all three NOS genes are completely disrupted. In this study, we examined whether bone metabolism is abnormal in those mice. Materials and Methods: Experiments were performed in 12-wk-old male wildtype, singly nNOS
We hypothesised that using a palmaris longus tendon ball (PLTB) with bone core (w bc) after excisional arthroplasty for Kienböck disease would maintain post-operative carpal height compared to a PLTB without bone core (w/o bc). Seventeen hands of 16 consecutive patients with Kienböck disease at Lichtman stage IIIA or IIIB were treated by replacement of the lunate with a PLTB w bc or w/o bc. We evaluated the clinical and radiological outcomes at one, three and 12 months after surgery. According to Dornan and Lichtman criteria respectively, there were no significant differences between the two groups. In the w bc group, the post-operative values of the carpal height ratio (CHR) were maintained at the same level as pre-operative values for one year, while the post-operative CHR values in the w/o bc group were significantly lower than those in the w bc group. Our results indicate that in Kienböck disease, arthroplasty using a PLTB w bc can maintain CHR at one year after surgery compared to arthroplasty using a PLTB w/o bc.
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