Background: Posterior pedicle screw fixation had been applied to maintain spinal stability and avoid further nerve damage in thoracolumbar fracture. This study aimed to evaluate the efficacy of short-segment posterior fixation with monoaxial pedicle screws versus polyaxial pedicle screws in treating thoracolumbar fracture.Methods: A total of 75 patients with thoracolumbar fracture who underwent short-segment posterior fixation with monoaxial pedicle screw (group A) or polyaxial pedicle screw (group B) were retrospectively enrolled. The patient demographic and radiological data were analyzed between the two groups.Results: A total of 63 patients with an average age of 44.7±11.5 years were finally recruited in this study.There were no significant differences in age, gender, fracture level, thoracolumbar injury classification and severity scale (TLISS) score, American Spinal Injury Association (ASIA) score, Arbeitsgemeinschaft für Osteosynthesefragen (AO) classification, and hospital stay between the two groups (P>0.05). At the last follow-up, the prevertebral height ratio and normal-to-injured vertebral height ratio were significantly decreased in group A compared to group B (P=0.027 and P=0.007, respectively).Conclusions: Short-segment posterior fixation with monoaxial or polyaxial pedicle screw for fractured thoracolumbar vertebra can restore injured vertebral height. Compared with polyaxial pedicle screw, monoaxial pedicle screw endows stronger leverage which is more beneficial for restoring injured vertebral height and recovery of the damaged endplate in thoracolumbar short-segment posterior fixation.
ABT-737 is a BH-3 mimetic that inhibits Bcl-2 and induces apoptosis of cancer cells, which has potential for anticancer therapies. Studies have shown that Bcl-2 expression in human osteosarcoma (OS) cells plays a significant role in tumor progression; however, its effects on OS cell apoptosis are still unknown. Therefore, we examined whether ABT-737 was effective in eliminating human U-2OS cells, either alone or in combination with the chemotherapy drug cisplatin [cis-diamminedichloroplatinum (II); DDP]. Furthermore, we studied the molecular mechanisms of ABT-737 in combination with DDP to induce apoptosis. To analyze the role of ABT-737 and/or DDP on osteosarcoma progression, CCK-8 viability assay, flow cytometry, Hoechst 33258 staining, and western blots were performed. Combined use of ABT-737 and DDP synergistically suppressed cell viability and induced apoptosis in human U-2OS cells when compared with either compound treated alone at low doses. We found that the combination of ABT-737 and DDP upregulated the expression of the pro-apoptotic protein Bax and downregulated the expression of the pro-survival protein Bcl-2, resulting in a change in the Bax/Bcl-2 ratio, release of cytochrome c, and activation of the mitochondrial apoptotic pathway, which resulted in caspase-9 and caspase-3 activation and PARP cleavage. Our results demonstrated that ABT-737 alone has a nominal influence on human U-2OS cells when treated within the clinically administered range, but when combined with DDP, it can inhibit the proliferation of human U-2OS cells by inducing apoptosis via the mitochondrial apoptotic pathway.
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