胸腰椎爆裂性骨折短节段伤椎固定三维有限元模型构建及生物力学比较研究

[目的]建立胸腰椎爆裂性骨折后路不同固定方式的尸体标本和三维有限元模型,比较不同固定方式的生物力学特点,优化手术方式选择。[方法]6具20~40岁青壮年胸腰椎(T11~L3)标本,压缩法制作L1椎体爆裂性骨折模型。平均分成3组,分别行后路长节段固定、常规短节段固定和伤椎短节段固定的手术固定方式,三维运动试验机检测标本在10 N·m力矩下前屈、后伸、侧屈和旋转4个方位的运动范围(ROM),材料机评估标本在500 N压力下的轴向压缩刚度。另取1具尸体为正常胸腰椎模型,借助CT扫描和有限元软件,模拟L1节段爆裂性骨折生成三种不同手术固定方式的有限元模型,施加相应载荷,分析各模型的应力分布,比较并进一步验证力学分析结果。[结果]生物力学证明,后路长节段固定、短节段固定和伤椎短节段固定后的胸腰段爆裂性骨折模型的ROM值和轴向压缩刚度组间差异无统计学意义。三维有限元应力分布显示,常规短节段和经伤椎短节段固定在T12平面的应力显著小于后路长节段固定方式。[结论]三种手术固定方式均能达到T11~L3节段的稳定,但后路常规短节段固定和经伤椎短节段固定更易于对伤椎的保护,经伤椎短节段固定具有更高的稳定性。     

Inhibitory effect of interferon-α-2b on expression of cyclooxygenase-2 and vascular endothelial growth factor in human hepatocellular carcinoma inoculated in nude mice

AIM： To evaluate the effects of interferon-α-2b （IFN- α-2b） on expression of cyclooxygenase-2 （COX-2） and vascular endothelial growth factor （VEGF） in human hepatocellular carcinoma （HCC） inoculated in nude mice and to study the underlying mechanism of IFN-α- 2b against HCC growth. METHODS： Thirb/-two nude mice bearing human HCC were randomly divided into four groups （n = 8）. On the 10th day after implantation of HCC cells, the mice in test groups （groups A, B and C） received IFN-α- 2b at a serial dose （10000 IU for group A, 20000 IU for group B, 40000 IU for group C sc daily） for 35 d. The mice in control group received normal saline （NS）. The growth conditions of transplanted tumors were observed. Both genes and proteins of COX-2 and VEGF were detected by RT-PCR and Western blot. Apoptosis of tumor cells in nude mice was detected by TUNEL assay after treatment with IFN-α-2b. RESULTS： Tumors were significantly smaller and had a lower weight in the IFN-α-2b treatment groups than those in the control group （P 〈 0.01）, and the tumor growth inhibition rate in groups A, B and C was 27.78%, 65.22% and 49.64%, respectively. The expression levels of both genes and proteins of COX-2 and VEGF were much lower in the IFN-α-2b treatment groups than in the control group （P 〈 0.01）. The apoptosis index （AI） of tumor cells in the IFN-α-2b treatment groups was markedly higher than that in the control group （P 〈 0.01）. Group B had a higher inhibition rate of tumor growth, a lower expression level of COX-2 and VEGF and a higher AI than groups A and C （P 〈 0.05）, but there was no significant difference between groups A and C. CONCLUSION： The inhibitory effects of IFN-α-2b on implanted tumor growth and apoptosis may be associated with the down-regulation of COX-2 and VEGF expression. There is a dose-effect relationship. The medium dose of IFN-α-2b for inhibiting tumor growth is 20 000 IU/d.     

Gremlin promotes vascular smooth muscle cell proliferation and migration

Recent reports highlight the importance of BMP in the vasculature. We investigated the expression pattern and role of the BMP antagonist gremlin in VSMC. We detected gremlin mRNA constitutive expression in adult and embryonic rat aortic VSMC, and in rat carotids. In vitro analysis demonstrated that angiotensin II, TGF-β1 and PDGF induced significant changes in gremlin mRNA expression. Gremlin stable overexpression in A7r5 cells blocked BMP signaling. BMP-induced reduction in VSMC DNA synthesis was markedly inhibited by gremlin overexpression. In fact, gremlin overexpression increased DNA synthesis and cell counts, and accelerated cell cycle progression of VSMC, through mechanisms that include p27^kip1 down-regulation. Gremlin also led to marked increments in VSMC migration. In addition, gremlin gene silencing promoted a significant blockade on cell proliferation and migration. In vivo studies disclosed increased gremlin protein expression in the neointima of balloon-injured carotid arteries. In summary, the BMP antagonist gremlin is constitutively expressed in the normal vasculature. Gremlin induces VSMC proliferation and migration and is significantly regulated by growth factors and injury. We postulate that gremlin plays a part in the development of pathological phenotypic changes of adult VSMC.     

Test Characteristics of Cross-sectional Imaging and Concordance With Endoscopy in Postoperative Crohn’s Disease

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钙激活钾通道增龄变化及其与高血压血管重构的相关性

目的:探讨大电导钙激活钾通道(BKCa)增龄变化及其与高血压血管重构的关系。方法:①选取雄性9、15、21、27、33周龄自发性高血压大鼠(SHR)及正常血压(WKY)大鼠,每周龄大鼠各4只;②测量腹主动脉平均动脉血压;③分离肠系膜小动脉及其血管平滑肌细胞(VSMCs);④利用膜片钳全细胞模式记录肠系膜小动脉VSMCsBKCa电流密度;⑤观察肠系膜小动脉血管内径、中膜厚度、中膜与内径比的变化;⑥探讨BKCa电流密度增龄变化与血管重构的关系。结果:①不同周龄SHR组血压明显高于WKY组,且随增龄渐增高,而WKY组血压始终正常;②SHR肠系膜小动脉VSMCs BKCa电流密度随增龄降低,而WKY随增龄的变化差异无统计学意义(P>0.05);③SHR肠系膜小动脉血管内径增龄减小及中膜厚度、中膜厚度/内径比增龄增大显著(P<0.05),而WKY增龄无明显变化;④SHR肠系膜小动脉VSMCsBKCa电流密度与肠系膜小动脉血管内径、中膜厚度、中膜厚度/内径比均高度相关(r分别为0.8534、-0.8767、-0.8911)。结论:BKCa电流和电流密度随增龄衰减,与高血压血管重构高度相关。     

丙丁酚对氧化型低密度脂蛋白和氧自由基促血管平滑肌细胞增殖的影响

本文用细胞计数和ＭＴＴ快速比色计量法观察到体外培养的半主动脉平滑肌细胞分别与氧化型低密度脂蛋白和黄嘌呤－黄嘌呤氧化酶共厕培养后，前者明显增殖（Ｐ＜０．０１）。抗氧化剂丙丁酚（１００μｍｏｌ·Ｌ－１）能抑制氧化型低密度脂蛋白和黄嘌呤－黄嘌呤氧化酶促平滑肌细胞增殖作用；一氧化氮合成酶抑制剂ＮＧ－硝基－Ｌ－精氨酸对两者促平滑肌细胞增殖的作用无影响，同时也不能阻断丙丁酚的抑制两者促细胞增殖作用．这一结果提示，丙丁酚能抑制氧化型低密度脂蛋白和外源性氧自由基促平滑肌细胞增殖，这一作用可能与血管平滑肌细胞中一氧化氮的合成及释放无关。     

Hypoxia does not activate ATP-sensitive K+ channels in arteriolar muscle cells

OBJECTIVE: To test the hypothesis that hypoxia activates ATP-sensitive K+ (KATP) channels in cremasteric arteriolar muscle cells, resulting in membrane hyperpolarization and inhibition of norepinephrine-induced contraction. METHODS: Arteriolar muscle cells were isolated enzymatically from second- and third-order arterioles that were surgically removed from hamster cremaster muscles. The effects of hypoxia (PO2 = 12-15 mm Hg) were then examined on norepinephrine-induced contraction, membrane currents, and membrane potential in these cells at room temperature. Whole-cell currents and membrane potential were recorded using the perforated patch technique. RESULTS: Hypoxia (12-15 mm Hg PO2) reversibly inhibited norepinephrine-induced contraction to 52 +/- 6% of the response in normoxic solutions (156 mm Hg, n = 12 digests, p < 0.05). These effects of hypoxia could be prevented by superfusion of the cells with either solutions containing the KATP channel antagonist glibenclamide (1 microM) or solutions containing 35 mM K+ to reduce the electrochemical gradient for K+ diffusion. Cromakalim, an activator of KATP channels, also inhibited norepinephrine-induced contraction to a similar extent as hypoxia, and in a glibenclamide and 35 mM K(+)-sensitive manner. These results are consistent with the KATP channel hypothesis. In contrast, hypoxia had no effect on estimated whole-cell membrane conductance between -40 and -90 mV in voltage-clamp experiments; on holding current measured at -60 mV in cells superfused with 143 mM K+ under voltage-clamp conditions; or on membrane potential in current-clamp experiments, despite positive effects of cromakalim in all three protocols. These electrophysiological data lead to rejection of the hypothesis that hypoxia activates KATP channels. CONCLUSIONS: Hypoxia inhibits norepinephrine-induced contraction of cremasteric arteriolar muscle cells by a mechanism that does not involve KATP channels. It is speculated that the inhibitory effects of glibenclamide and 35 mM K+ on the effects of hypoxia on contraction resulted from depolarization induced by these treatments rather than specific inhibition of KATP channels.     

晚期糖基化终末产物对小鼠骨髓干细胞向血管内皮细胞分化的影响

观察晚期糖基化终末产物(AGEs)对骨髓干细胞(BMSC)向内皮细胞分化的影响.结果 发现,20μg/ml AGEs对BMSC分化的影响不明显,100μg/ml AGEs使BMSC分化能力明显下降,血管内皮生长因子受体2阳性细胞计数和百分数均明显降低.     

Estrogen Activation of G-Protein–Coupled Estrogen Receptor 1 Regulates Phosphoinositide 3-Kinase and mTOR Signaling to Promote Liver Growth in Zebrafish and Proliferation of Human Hepatocytes

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