Effect of Pentoxifyiline on necrosis rate and hemorrheology of free flap

Objective To investigate effect of Pentoxifylline on free flap. Methods Forty Wistar rats were chosen as experimental models and free flaps were harvested from the back of rats,which as pect ratio was 3: 1. Then they were divided into two groups randomly. Group A was as the experimental group,receiving drug treatment.

Influence of neoadjuvant chemotherapy on proliferation, apoptosis and multi-drug resistance in osteosarcoma cells

Objective: To study the influence of neoadjuvant chemotherapy on the expression of cyclin D1, Bcl-2, PCNA and P- gp in osteosarcoma cells and the relationship between the expression and tumor cell necrosis rate (TCNR) after chemotherapy. Methods: By using immunohistochemistry, the expression of cyclin D1, Bcl-2, PCNA and P-gp was detected in 23 cases of osteosarcoma and TCNR were calculated. Results: The pre-chemotherapy positive expression rate of cyclin D1, Bcl-2, PCNA and P-gp was 73.9%, 69.6%, 91.3% and 21.7%, respectively, and that post-chemotherapy positive expression rate was 52.1%, 34.8%, 43.5% and 56.5%, respectively. The positive expression rate of Bcl-2 and PCNA after chemotherapy was much lower than that before chemotherapy (P=0.039, 0.034). After chemotherapy, the expression rate of P-gp was higher (P=0.021) and the expression of cyclin D1 had no statistically significant difference (P=0.180) comparing with that before chemotherapy. No correla- tion existed between the expression of cyclin D1, Bcl-2, PCNA, P-gp and TCNR before chemotherapy (P=0.155, 0.371, 1.000 and 0.640). There was a negative correlation between the expression of Bcl-2, PCNA, P-gp and TCNR (P=0.009, 0.012 and 0.015), but no relationship existed between the cyclin D1 and TCNR (P=0.100) after chemotherapy. Conclusion: Chemotherapy could inhibit proliferation and induce apoptosis of osteosarcoma cells. At the same time, due to the overexpression of the P-gp, the drug resistance of the osteosarcoma cells was increased. The detection of cyclin D1, Bcl-2, PCNA and P-gp in osteosarcoma samples before chemotherapy might not be used to predict the curative effect of the chemotherapy.

The Inhibitory Effect of Endostatin and Doxycycline Administration on B16 Melanoma Angiogenesis and Cellular Proliferation

OBJECTIVE To investigate the effect of endostatin and doxycycline on melanoma cellular proliferation and tumor angiogenesis.METHODS The effects of endostatin and doxycycline were studied in mice transplanted with B16 melanoma cells. The mice were divided into 4 groups that were treated as follows： endostatin treatment （E group）, doxycycline treatment （D group）, endostatin plus doxycycline trearment （DE group）, controls （C group） received no treatment. Following 9 days of treatment the tumor tissue was removed to compare the differences in the tumor necrotic rate and micro-vessel density （MVD） among the different groups. Immunohistochemical staining was conducted to detect the expression of proliferating cell nuclear antigen （PCNA） in the different groups.RESULTS The MVD of the 3 experimental groups was significantly less than the control group, （F = 10.888, P 〈 0.05）, indicating that doxycycline and endostatin can inhibit tumor angiogenesis by decreasing the tumor blood supply. This effect results in inhibition of tumor cellular proliferation and promotion of tumor cell necrosis. The tumor cell necrotic rate of the 3 experimental groups were all significantly higher than the C group （F = 7.229, P 〈 0.05） and the difference between the DE and C groups also was statistically significant. PCNA expression in all 3 experimental groups was statistically less than the C group （F = 17.729, P 〈 0.05）.CONCLUSION The combined use of endostatin and doxycycline in vivo can influence PCNA expression and angiogenesis in melanoma, and significantly inhibit melanoma cellular proliferation.

NHL患者血清TNF-α、LDH水平及与血沉的相关性研究

目的探讨非霍奇金淋巴瘤(NHL)患者血清TNF-αs、TNFRI、LDH、球蛋白、白蛋白水平及血沉的变化和意义。方法严格选取25例初诊NHL患者和26例正常人为研究对象,采用ELISA法测定血清TNF-α及sTNFRI水平,采用OLYMPUS 600血生化仪测定血清LDH、球蛋白及白蛋白水平,采用魏氏法测定血沉。结果NHL患者血清TNF-αs、TNFRI、LDH、球蛋白水平及血沉值均高于对照组,且血清TNF-αs、TNFRI、LDH、球蛋白水平与血沉值均具有相关性;两组血清白蛋白水平差异无显著性,NHL患者血清白蛋白水平血沉值成负相关。结论NHL患者TNF-α、sTN-FRI、LDH、球蛋白、白蛋白改变与血沉增快均有关系,其中TNF-α、白蛋白及LDH作用较大。

肿瘤坏死因子-α与血沉的相关性研究

目的探讨恶性肿瘤及糖尿病患者血清肿瘤坏死因子-α(TNF-α)与血沉(ESR)的关系。方法选取25例恶性肿瘤患者和32例糖尿病患者,采用酶联免疫吸附法(ELISA)分别测定血清TNF-α及可溶性肿瘤坏死因子受体-Ⅰ(sTNFRⅠ)水平。同时采用魏氏法测定血沉值。结果肿瘤患者和糖尿病患者的血清TNF-αs、TNFRⅠ水平及ESR值均显著高于正常对照组(所有P<0.05),且血清TNF-α、sTNFRⅠ水平与ESR值之间均有相关关系(rT=0.645,PT<0.01;rs=0.638,Ps<0.01);ESR值愈大,血清TNF-α、sTNFRⅠ水平愈高。结论在恶性肿瘤及糖尿病疾病中随着ESR值增大,血清TNF-α、sTNFRⅠ水平增高,血清TNF-αs、TNFRⅠ水平与ESR间存在相关关系,TNF-α及sTNFRⅠ可能是导致ESR增快的原因之一。