ABSTRACT
Objective To discuss the surgical treatment of spinal injury, and provide insights on key points and related issues for operations. Methods Two hundred and five cases of spinal fracture were treated through posterior surgical treatment. Under C-arm X-ray monitoring, surgeries had been operated on pedicle screws insertion, vertebral canal decompression, over-extending reduction position, and placed the connecting rod, knocked in the bone graft and finally transplanted the paraspinal bone. Results After operations , the height and morphology of vertebral bodies and spinal physiological curvature were basically recovered analyzed by X ray examination. The follow-up results (in the average of 14 to 36 months) indicated that there were 4 cases of delayed infection, 7 cases of loosen screw, 6 cases of broken screw (14 screws)and 1 case of broken stick, with no secondary nerve injury or other syndromes. Conclusion The vertebral pedicle screw internal fixation manipulated easily, which could sufficiently enlarge vertebral canal in order to decompression. In addition, during the operation, together with over-extending reduction position is beneficial to regain the height of fractured vertebral bodies.
ABSTRACT
The inhibitory effect of wortmannin on leukemic cells and the possible mechanisms were examined. K562 cells were treated with wortmannin of various concentrations (3.125-100 nmol/L) for 0-72 h. MTT assay was used to evaluate the inhibitory effect of wortmannin on the growth of K562 cells. Cell apoptosis was detected by both Annexin-V FITC/PI double-labeled cytometry and transmission electron microscopy (TEM). The expression of p-Akt, T-p-Akt, NF-kappaBp65 and IKK-kappaB was determined by Western blotting and reverse transcription-polymerase chain reaction (RT-PCR). Our results showed that wortmannin obviously inhibited growth and induced apoptosis of K562 cells in vitro in a time- and dose-dependent manner. The IC(50) value of wortmannin for 24 h was 25+/-0.14 nmol/L. Moreover, wortmannin induced K562 cells apoptosis in a dose-dependent manner. TEM revealed typical morphological changes of apoptosis in wortmannin-treated K562 cells, such as chromatin condensation, karyopyknosis, karyorhexis and apoptotic bodies. Additionally, several important intracellular protein kinases such as p-Akt, NF-kappaBp65 and IKK-kappaB experienced degradation of various degrees in a dose-dependent manner both at protein level and transcription level when cultured with wortmannin, but the expression of total Akt showed no change. It is concluded that wortmannin can inhibit the proliferation and induce apoptosis of K562 leukemia cells possibly by down-regulating the survival signaling pathways (PI3K/Akt and NF-kappaB channels).