阿托伐他汀对自发性高血压大鼠主动脉活性氧、p22phox表达和SOD活性的影响

目的　探讨自发性高血压大鼠(SHR)主动脉活性氧(ROS)和p22phox mRNA表达、超氧化物歧化酶(SOD)活性的变化及相关性,并探讨阿托伐他汀治疗对上述指标的影响。方法　以WKY大鼠为对照,观察给予SHR阿托伐他汀50mg/(kg·d)灌胃30 d后,大鼠血压、血清SOD、一氧化氮(NO)、主动脉ROS含量以及p22phox mRNA表达的变化。结果　阿托伐他汀治疗30 d后,SHR的血压、主动脉ROS含量及p22phox mRNA表达下降,血清SOD、NO水平上升。主动脉ROS含量与p22phox mRNA表达呈正相关,与SOD活性呈负相关。结论　p22phox亚单位表达上调和SOD活性降低是高血压血管ROS增多的重要机制。阿托伐他汀可下调p22phox亚单位表达和增加SOD活性,从而减少ROS。     

富马酸二甲酯对肾草酸钙结石大鼠肾功能和氧化应激的影响及其机制研究

目的 基于p38丝裂原活化蛋白激酶（MAPK）信号通路,探讨富马酸二甲酯对肾草酸钙结石大鼠肾功能及氧化应激的影响及其作用机制。方法 将30只SPF级SD雄性大鼠随机分为对照组、模型组、富马酸二甲酯组,每组10只。其中模型组、富马酸二甲酯组大鼠腹腔注射0.25% L-羟脯氨酸2.5 kg/（kg·d）复制肾草酸钙结石大鼠模型。富马酸二甲酯组大鼠腹腔注射富马酸二甲酯25 mg/（kg·d）,连续28 d,对照组、模型组同时腹腔注射等量生理盐水。采用全自动生化分析仪检测大鼠尿蛋白、尿钙,以及血肌酐水平;HE染色检测大鼠肾组织草酸钙晶体形成情况;试剂盒检测血清超氧化物歧化酶（SOD）活性、丙二醛（MDA）及活性氧簇（ROS）水平;Western bloting检测大鼠肾组织p38 MAPK通路蛋白相对表达量。结果 与对照组比较,模型组和富马酸二甲酯组大鼠肾组织SOD活性降低,草酸钙晶体含量、尿蛋白、尿钙、血肌酐及肾组织MDA、ROS水平,p-JNK、p-p38蛋白相对表达量升高（P <0.05）;但富马酸二甲酯组大鼠SOD活性高于模型组（P <0.05）,肾组织草酸钙晶体含量、尿蛋白、尿钙、血肌酐,肾组织MDA、ROS水平,p-JNK、p-p38蛋白相对表达量低于模型组（P <0.05）。结论 富马酸二甲酯可能通过抑制p38 MAPK通路活化,抑制肾脏组织氧化应激反应,从而抑制肾草酸钙结石形成,进而保护肾功能。     

Chronic intermittent hypoxia aggravates cardiomyocyte apoptosis in rat ovariectomized model

Background  The prevalence of obstructive sleep apnea (OSA) increases after menopause in women, but remains under diagnosed because of social or lifestyle factors. It is important to evaluate the hazards of OSA on cardiovascular disease in menopausal women. We tested the hypothesis that chronic intermittent hypoxia (CIH) may aggravate cardiomyocyte apoptosis in ovariectomized (OVX) Sprague Dawley (SD) rats; the changes of anti-oxidation ability in cardiac muscles may be one of the reasons for cardiomyocyte apoptosis.

Methods  Forty-eight 60-day old female SD rats were randomly divided into a CIH group, OVX group, OVX+CIH (OC) group, and handled control (HC) group, and the rats were exposed either to CIH (nadir O₂ 6%) or handled normoxic controls. The changes of body weight and whole heart weight were measured. Super oxide dismutase (SOD) and malonaldehyde (MDA) were used to evaluate the level of oxidative stress. TdT-mediated dUTP nick end labeling (TUNEL) was used to measure apoptosis in each rat. Western blotting was used to measure apoptosis associated proteins in cardiac muscle samples from each rat.

Results  When compared with the HC and CIH groups, the levels of oxidative stress in the OC and OVX groups were significantly higher. The levels of SOD in the HC, CIH, OC, and OVX groups were (47.99±4.89), (53.60±4.47), (20.99±2.72), and (30.64±3.79) mmol/mg protein; significantly increased in the CIH group (P <0.05) and significantly decreased in the OC (P <0.01) and OVX (P <0.05) groups. The levels of MDA in the HC, CIH, OVX, and OC groups were (1.63±0.20), (1.93±0.77), (3.30±0.39), and (1.95±0.20) mmol/mg protein; it significantly increased in the CIH (P <0.05), OC (P <0.01), and OVX (P <0.05) groups compared with the HC group. Bax protein expression was significantly increased and bcl-2 protein expression was significantly reduced after CIH compared with HC rats (P <0.05). The protein expression of bax and bcl-2 in the OC group was not significantly different from the CIH group, but the ratio of bax/bcl-2 was significantly increased in the OC group (P <0.05); this was associated with severe cardiomycyte apoptosis in the OC group. TUNEL confirmed this observation.

Conclusions  This study found that CIH may induce oxidative stress in OVX rats but not in CIH rats, and cause more severe cardiomyocyte apoptosis in OVX rats compared with CIH rats. This means that OVX rats exposed to CIH suffered more severe cardiac injury compared with CIH rats due to reduced antioxidation. These findings may partly explain the reason why OSA has a worse cardiovascular impact on menopausal women, and emphasize the importance of detection and early treatment of OSA in menopausal patients.

     

sRAGE对缺氧/复氧心肌细胞氧化应激的影响

目的观察可溶性晚期糖基化终产物(soluble form of receptor for advanced glycation end products,sRAGE)对缺氧/复氧心肌细胞氧化应激的影响。方法乳鼠心肌细胞原代培养48 h,以低氧3 h、复氧2 h复制缺氧/复氧损伤模型,采用抽签法将乳鼠心肌细胞随机分为4组:常氧对照组(Control,Con)、常氧+sRAGE组(Con-sRAGE)、缺氧/复氧组(Hypoxia/reoxygenation,H/R))、缺氧/复氧+sRAGE组(H/R-sRAGE)。采用四甲基偶氮唑蓝〔3(4,5-dimethyl-thiazol)-2,5-diphenyl-tetrazolium,MTT〕比色法检测心肌细胞活力和培养液中乳酸脱氢酶(lactate dehydrogenase,LDH)浓度,黄嘌呤氧化酶法测定超氧化物歧化酶(superoxide dismutase,SOD)活力,硫代巴比妥酸显色法测定丙二醛(malondialdehyde,MDA)含量,2',7'-二氯荧光黄双乙酸盐(DCFH-DA)荧光探针联合流式细胞仪检测细胞荧光强度-反应活性氧(reactive oxygen species,ROS)水平,硝酸还原酶法测定一氧化氮(nitric oxide,NO)含量。结果与H/R组相比,H/R-sRAGE组可以提高心肌细胞活力,减少LDH漏出量,增加SOD活力,降低MDA、ROS、NO含量(P<0.05)。结论 sRAGE可以直接作用于心肌细胞拮抗缺氧/复氧损伤,其保护性作用与抑制氧化应激有关。     

脂联素通过激活p38MAPK信号通路调节大鼠肝星状细胞MMP-13及TIMP-1表达

目的观察外源性脂联素对体外培养的大鼠肝星状细胞系(HSC-T6)细胞脂联素受体1(AdipoR1)表达的调节作用及对细胞内p38MAPK信号通路的影响,并观察该通路是否参与调节脂联素对HSC细胞基质金属蛋白酶-13(MMP-13)、基质金属蛋白酶抑制因子-1(TIMP-1)表达的影响。方法 MTT法观察不同浓度脂联素对HSC生长的影响。荧光定量PCR法检测脂联素作用下HSC-T6细胞AdipoR1、MMP-13、TIMP-1的mRNA表达情况。Western blotting方法检测脂联素作用下HSC-T6细胞信号蛋白p38MAPK的活化及活性和AdipoR1、MMP-13、TIMP-1的蛋白表达情况。结果 0.5μg/mL～2.0μg/mL脂联素处理HSC细胞,各组细胞增生无明显变化。0.5μg/mL、1.0μg/mL、1.5μg/mL脂联素作用下AdipoR1mRNA和蛋白表达增加。1.0μg/mL脂联素处理HSC后,p38MAPK激酶磷酸化水平随时间增加而增高,在120min达最大值,之后又开始下降。不同浓度脂联素处理HSC120min后,p38MAPK激酶磷酸化水平均增加,并具有浓度依赖性。p38MAPK抑制剂SB203580可抑制p38MAPK激酶的磷酸化及活性。脂联素处理组HSC细胞MMP-13mRNA及蛋白表达均较对照组明显增加,而TIMP-1mRNA及蛋白表达较对照组降低,而SB203580可以抑制这种效应。结论脂联素可上调活化肝星状细胞AdipoR1的表达,通过激活p38MAPK信号通路,调节HSC细胞MMP-13及TIMP-1的表达。     

IGFBP-4对A549细胞免疫原性细胞死亡的作用及其机制

目的：探讨IGFBP-4对A549细胞免疫原性细胞死亡（ICD）的作用及其分子机制。方法：体外培养A549细胞,将细胞分为对照组、IGFBP-4组、IGFBP-4+NAC组和IGFBP4+si-p38组。经培养48 h后,用MTT法检测细胞存活率,流式细胞技术检测细胞内ROS、钙网蛋白（CRT）含量,ELISA法检测培养基中高迁移率族蛋白1（HMGB1）含量和细胞内SOD、MDA含量,Western blot法检测p-p38和p38表达。结果：与对照组相比,IGFBP-4组细胞内ROS、CRT、HMGB1、MDA含量、p-p38和p38表达升高,细胞存活率、SOD2含量下降（P＜0.05）;与IGFBP-4组相比,IGFBP-4+NAC组和IGFBP-4+si-p38细胞内ROS、CRT、HMGB1和MDA含量下降,细胞存活率、SOD2含量增高（P＜0.05）。结论：IGFBP-4通过激活p38 MAPK通路,诱发细胞内氧化应激促使A549细胞发生免疫原性细胞死亡。     

螺内酯对高糖诱导的肾小球系膜细胞氧化应激的影响

目的:观察螺内酯对高糖诱导的肾小球系膜细胞氧化应激的影响,并且探讨该作用是否与MAPKs家族信号通路相关?方法:采用高糖和(或)螺内酯处理人肾小球系膜细胞株(HMC)后,DHE荧光染色检测细胞内活性氧(ROS)水平,NBT试剂盒法检测细胞内超氧化物歧化酶(SOD)活性,Western blot法检测MAPKs家族ERK?JNK?p38MAPK的磷酸化及总蛋白水平?结果:DHE染色结果显示,高糖可明显增加HMC内ROS含量,而给予螺内酯干预处理后,细胞内ROS水平明显降低,与高糖刺激组相比,螺内酯干预组细胞内SOD活性明显增加(P < 0.05);Western blot结果表明,高糖可明显增加HMC细胞内ERK及p38MAPK的磷酸化水平,给予螺内酯处理后可逆转高糖的上述作用(P < 0.05),而各组之间磷酸化JNK及总ERK?p38MAPK?JNK蛋白水平无明显变化?结论:螺内酯可能通过下调MAPK家族信号蛋白的磷酸化水平,降低细胞内ROS含量,增加SOD活性,拮抗由高糖所引起的氧化应激,从而起到保护肾小球系膜细胞,延缓肾小球硬化的作用?     

补心软脉颗粒含药血清对AngⅡ诱导的HUVEC细胞抗氧化作用

目的?观察补心软脉颗粒含药血清对AngⅡ诱导HUVEC细胞所致氧化损伤的相关指标SOD、NADPH、MDA、p40phox、p47phox、p67phox的影响。方法?大鼠被随机分为正常组、缬沙坦组、补心软脉颗粒组,每组10只,灌胃6周,取动脉血制备药物血清。建立10-6mol/L AngⅡ诱导的HUVEC细胞凋亡损伤模型,并予各药物血清干预,采用黄嘌呤氧化酶法检测细胞上清液中总SOD活力,ELISA法检测NADPH氧化酶,TBA法检测MDA含量,Bradford法p40phox、p47phox、p67phox蛋白定量;Western blot法分别检测细胞膜与细胞质p40phox、p47phox、p67phox蛋白表达。结果?AngⅡ诱导HUVEC细胞损伤,模型组SOD活力下降,NADPH、MDA升高,p40phox、p47phox、p67phox向细胞膜转移,出现氧化损伤;补心软脉颗粒组SOD活力上升,MDA、NADPH下降,抑制p40phox、p47phox、p67phox向细胞膜转移,减轻氧化损伤。结论?补心软脉含药血清对AngⅡ诱导体外培养的HUVEC损伤有抑制氧化作用,防止动脉硬化。      

Effects of lead exposure on placental cellular apoptosis and endoplasmic reticulum stress in rats

Background Lead exposure during pregnancy contributes to fetal abortion and/or teratogenesis.Endoplasmic reticulum （ER） apoptosis can be induced by various pathological conditions when ER function is disturbed.However,it is unclear whether ER stress and apoptosis play a role in the etiology of lead-exposed disease status.We aimed to investigate whether lead induced placental apoptosis and subsequent toxicity is initiated by ER apoptosis via caspase-12.Methods Sixty-three female Wistar rats were exposed to lead in drinking water during various gestational periods.Blood lead level was determined by atomic absorption spectrophotometry.Placental cytoplasmic organelles were examined by electronic microscopy.Placental caspase-12 mRNA expression was evaluated by qRT-PCR.TUNEL assay was used to determine the placental apoptosis.Results Lead exposure significant induced ER apoptosis compared to that of the controls （P ＜0.05）,accompanied with increased caspase-12 mRNA expression.Significant differences of caspase-12 mRNA expression levels were observed among the four groups （F=13.78,P ＜0.05）.Apoptotic index （AI） was significantly increased in experimental groups compared to that of the controls （F=96.15,P ＜0.05）.In lead-exposed groups,trophoblast cells underwent degeneration and fibrin deposition; Mitochondria were swollen and decreased in number; ER swelling,expansion,and vacuolization were observed.Conclusion Lead exposure contributes to placental apoptosis,as well as increased caspase-12 mRNA expression,which in turn promoted ER stress.     

Effects of phlorizin on vascular complications in diabetes db/db mice

Background  Diabetic macrovascular complications are important causes of cardiovascular and cerebrovascular diseases and also one of the major causes of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Phlorizin has been reported to be effective in reducing the blood glucose level in diabetic mellitus, while little is known about its effects on vascular complications. This study aimed to observe the effects of phlorizin on the aorta of diabetes db/db mice and explore its mechanism.

Methods  Diabetic db/db mice (n=16) and age-matched db/m mice (n=8) were divided into three groups: normal control group (CC group, db/m mice, n=8), untreated diabetic group (DM group, db/db mice, n=8) and diabetic group treated by phlorizin (DMT group, db/db mice, n=8). Phlorizin (20 mg/kg body weight) was given in normal saline solution intragastrically for 10 weeks. Animals were weighed weekly. At the 10th weekend, all mice were fasted overnight and then sacrificed. Fasting blood was collected, and the aortas were dissected. The blood samples were analyzed for fasting blood glucose (FBG), serum advanced glycation end products (AGEs), malondialdehyde (MDA) and superoxide dismutase (SOD) activity, the aortic ultrastructure was studied.

Results  The weight and serum concentration of FBG, AGEs, and MDA in the DM group were higher than that in the CC group (P <0.01), and they were significantly lower in the DMT group (P <0.05). Serum SOD activity was lower than that in the CC group (P <0.01), and it is significantly higher in the DMT group (P <0.05). The severity of aorta damage in the DMT group was less than that in the DM group.

Conclusions  Phlorizin protected the db/db mice from diabetic macrovascular complications, attributed to the decreasing of blood glucose and AGEs level, and its antioxidant potential. This study may provide a new natural medicine for treating diabetic macrovascular complications.

     

Sodium Tanshinone ⅡA Sulfonate Ameliorates Microcirculatory Disturbance of Small Intestine by Attenuating the Production of Reactive Oxygen Species in Rats with Sepsis

Objective: To examine whether sodium tanshinone ⅡA sulfonate(STS), the main effective component of Salvia miltiorrhiza is effective in relieving the microcirculatory disturbance of small intestine by suppressing the production of reactive oxygen species(ROS) in rats with sepsis. Methods: A rat model of sepsis was induced by cecal ligation and puncture(CLP). Rats(n=40) were randomly divided into 4 groups: sham-operated group(sham, n=10), sepsis group(CLP, n=10), STS treatment group(STS, n=10) and ROS scavenger dimethylthiourea(DMTU, n=10) group. Animals in the STS group were injected with STS(1 mg/kg) for 10 min through the right external jugular vein after the CLP operation, and animals in the CLP group were given the same volume of normal saline after the CLP operation. Animals in the DMTU group were intraperitoneally injected with 5 m L/kg of 20% DMTU 1 h before CLP. The histopathologic changes in the intestinal tissues and changes of mesenteric microcirculation were observed. The levels of ROS in intestinal tissues from each group were qualitatively evaluated using a fluorescent microscope. The expressions of apoptosis signal-regulating kinase(ASK1), phosphorylated ASK1(phospho-ASK1), p38 mitogen-activated protein kinases(p38 MAPK), phosphorylated p38 MAPK(phospho-p38 MAPK) and tissue factor(TF) were determined by Western blotting. Results: It was shown that there were obvious microcirculatory disturbance(P0.05) and tissue injuries in intestinal tissues after CLP operation. The levels of ROS production, phospho-ASK1, phospho-p38 MAPK and TF were increased. Both STS and DMTU suppressed ROS, phospho-ASK1, phospho-p38 MAPK and TF production, and ameliorated the microcirculatory disturbance and tissues injury(P0.01). Conclusion: STS can ameliorate the microcirculatory disturbance of the small intestine by attenuating the production of ROS in rats with sepsis.     

Myelin protein zero and its antibody in serum as biomarkers of n-hexane-induced peripheral neuropathy and neurotoxicity effects

Background Chronic exposure to n-hexane can lead to peripheral neuropathy that no effective treatment regimen could be applied presently. This study investigated whether myelin protein zero （P0） protein and its antibody could be used to distinguish n-hexane intoxication and protect workers from peripheral neuropathy. Methods We compared P0 protein and its antibody among three levels of n-hexane-exposed groups, which included 18 patients with n-hexane-induced peripheral neuropathy as case group, 120 n-hexane-exposed workers as n-hexane- exposed control group, and 147 non-hexane-exposed participants used as control group. ELISA method was applied to detect P0 protein and its antibody. Results P0 protein in serum was significantly higher in the case group and n-hexane-exposed control group in comparison with the control group （P〈0.01）. Compared with the n-hexane-exposed control group, the case group also had significant increase of P0 protein （P〈0.01）. After 6 months therapy, P0 protein was observed to decrease significantly in the case group （P〈0.01）. The P0 antibody in serum was significantly higher in the n-hexane-exposed control group than in the control group （P〈0.01）, but not significantly different between cases and controls. Conclusions P0 antibodies in serum may be a short-term effect biomarker for n-hexane exposure. P0 protein in serum may be an early effective biomarker for peripheral nerve neuropathy and its biological limit value needs investigation in the future study.     

Association between improved trunk stability and walking capacity using ankle-foot orthosis in hemiparetic patients with stroke: evidence from three-dimensional gait analysis

Background Restoration of both normal movement of the pelvis and centre of mass is a primary goal of walking rehabilitation in post-stroke patients because these movements are essential components of effective gait. The aim of this study is to quantitatively analyze the effect of ankle-foot orthosis on walking ability, and to investigate the correlation between improvements in trunk motion and walking capacity.     

熊果酸(UA)对大鼠活化型肝星状细胞(HSC)的NADPH氧化酶(NOX)亚基及PI3K/Akt、P38MAPK信号通路活化的影响

 目的  观察熊果酸(ursolic acid,UA)对大鼠活化型肝星状细胞-6 (hepatic stellate cell T6,HSC-T6) NADPH氧化酶(NAPDH oxidase,NOX)亚基及其调控的磷脂酰肌醇-3-羟激酶/蛋白激酶(phosphatidyl inositol 3-kinase/Akt,PI3K/Akt)、P38丝裂原活化蛋白激酶(P38 mitogen activated protein kinase,P38MAPK)信号通路及其对基质金属蛋白酶组织抑制剂-1 (tissue inhibitor of metalloproteinase-1,TIMP-1)、基质金属蛋白酶-1(metal matrix proteinase -1,MMP-1)蛋白表达的影响,并探讨其机制。方法  取对数生长期的HSC-T6细胞,随机分成6组:空白对照组、瘦素组(100 ng/mL)、UA干预组(UA 50 μmol/L+瘦素)、NOX抑制剂DPI干预组(DPI 20 μmol/L+瘦素)、P38MAPK抑制剂SB203580干预组(SB203580 10 μmol/L+瘦素)及PI3K抑制剂LY294002干预组(LY294002 10 μmol/L+瘦素)。采用Western blot法分别检测NOX亚基gp91phox、p22phox、p67phox、Rac1蛋白表达;信号通路PI3K、Akt、P38MAPK的活化及TIMP 1、MMP 1蛋白表达。结果  UA能显著抑制瘦素诱导的gp91phox、 p22phox、p67phox、Rac1蛋白表达(P均<0.01),但UA对gp91phox、p67phox蛋白表达的抑制作用不及DPI和LY294002。UA能抑制瘦素诱导的PI3K蛋白表达及Akt、P38MAPK蛋白磷酸化(P均<0.01),与DPI及LY294002作用的差异无统计学意义。UA能抑制瘦素诱导的TIMP-1蛋白表达,同时促进MMP-1蛋白表达(P均<0.01)。结论  UA能抑制瘦素诱导的大鼠HSC T6细胞NOX亚基gp91phox、p22phox、p67phox、Rac1表达及PI3K/Akt、P38MAPK信号通路的活化;其下调TIMP-1蛋白及上调MMP-1蛋白表达的机制可能与UA抑制NOX调控的PI3K/Akt及P38MAPK信号通路有关。     

吡格列酮对2型糖尿病患者氧化应激的影响

目的 探讨吡格列酮对2型糖尿病患者氧化应激的影响.方法 收集于本院就诊的2型糖尿病患者130例,随机分成对照组和吡格列酮组,每组65例.对照组给予门冬胰岛素30和二甲双胍控制血糖;吡格列酮组使用门冬胰岛素30、二甲双胍和吡格列酮(15 mg/d)降糖治疗,均治疗3个月.治疗前后检测并比较两组患者血清氧化应激指标:超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA).结果 治疗后吡格列酮组患者血清SOD、GSH-Px活性[(54±18)U/ml和(82±18)U/ml]较治疗前[(39±16)U/ml和(71±22)U/ml]显著升高,MDA水平[(2.6±1.7)nmol/ml]较治疗前[(3.8±2.3)nmol/ml]显著降低,差异有统计学意义(P＜0.05),且治疗后吡格列酮组上述3种指标与对照组[(42±18)U/ml、(73±19)U/ml和(3.5±1.8)nmol/ml]比较,差异有统计学意义(P＜0.01).结论 吡格列酮能提高2型糖尿病患者血清SOD和GSH-Px活性,降低MDA水平,而且吡格列酮的这种作用不依赖于降糖作用.     

Kyphoplasty versus vertebroplasty for the treatment of malignant vertebral compression fractures caused by metastases: a retrospective study

Background There are few comparative studies regarding kyphoplasty (KP) and vertebroplasty (VP) for the treatment of painful vertebral compression fractures (VCF) in patients with cancer. The purpose of this study is to retrospectively compare KP with VP in pain improvement, cement leakage incidence, and the cost of treatment of malignant VCF.

Methods We performed a retrospective study of clinical data for 80 patients with multiple spinal metastases, treated with KP in 42 cases and VP in 38. Visual analog scale (VAS) scores were collected pre-operatively, post-operatively, at 1 month, 6 months, and 1 year after treatment. Cement leakage was identified using fluoroscopy and CT scan. Total cost per patient was also collected.

Results There was a significant difference between the pre- and post-operative VAS scores (7.4±2.0 to 3.8±1.6, P <0.001 in the KP group; 6.7±2.4 to 3.7±1.4, P <0.001 in the VP group), and was maintained at 1-year follow-up (3.2±1.4 in the KP group, 3.1±1.3 in the VP group). However, the difference in VAS score between these two groups was insignificant at baseline and every follow-up assessment post-operatively (P >0.05). The incidence of cement leakage in the KP group was lower than that of the VP group (16.9% (14/83) vs 30.3% (23/76), P <0.05). However, none of the patients developed any symptoms. The length of postoperative hospital stay in the VP group was shorter than that of the KP group ((2.4±1.3) vs (5.3±1.9) days, P <0.05). Total hospital cost in the KP group was much higher than that of the VP group (RMB Yuan 8 492±3 332 vs RMB Yuan 3 173±1 341, P <0.01).

Conclusions VP and KP are both effective in providing pain relief for patients with cancer-related VCF. KP provides no greater degree of pain improvement. KP is associated with a lower rate of cement leakage compared with VP. VP is associated with lower cost and shorter postoperative hospital stay in China.

     

Comparison of two and three dimensional quantitative coronary angiography to intravascular ultrasound in the assessment of left main coronary artery bifurcation lesions

Background Angiographic evaluation of left main coronary artery （LMCA） bifurcation lesions is often limited, twodimensional （2D） quantitative coronary angiography （QCA） with segmental analysis provides accuracy for quantificationof the degree of stenosis in the main vessel and side branch ostium but can be affected by foreshortening and variablemagnification. The accuracy of three dimensional （3D） QCA has recently developed to overcome 2D QCA limitations,however, accuracy and precision of 3D bifurcation QCA measurements in LMCA bifurcation lesions has not beenestablished.Methods We investigated whether such 3D and 2D bifurcation QCA measurements differ in their accuracy in assessingsignificant LMCA bifurcation lesions defined by intravascular ultrasound （IVUS） as a minimum luminal area （MLA） 〈6 mm2of LMCA and MLA 〈4 mm2 of proximal left anterior descending （LAD） and/or proximal left circumflex （LCX）Results LMCA bifurcation lesions were assessed in 44 patients undergoing elective percutaneous coronary intervention.From 2D QCA measurements, MLA correlated moderately with threshold intravascular ultrasound MLA for LMCA （r=0.81,P 〈0.000 1）, LAD 0=0.54, P=0.000 1） and LCX （r=0.58, P 〈0.000 1）. Severity of lesion as MLA by derived 3D QCA,correlated moderately with threshold intravascular ultrasound MLA for LMCA （t=0.84, P 〈0.000 1）, LAD （t=0.53, P=0.000 2）;LCX （r=0.66, P 〈0.000 1）. Overall, the C statistics tended to be slightly higher for 3D QCA and 2D QCA measurementsin LMCA segment compared with proximal LAD and LCX segments, and there were no significant predictive power ofpercent diameter stenosis and percent area stenosis on 3D QCA for LCX IVUS MLA 〈4 mm2 （percent diameter stenosis：area under curve 0.55, cutoff 23%, sensitivity 88%, specificity 37%, P=0.618 6; percent arer stenosis： area under curve0.56, cutoff 41%, sensitivity 83%, specificity 38%, P=0.518 4, respectively）.Conclusions The accuracy of 3D bifurcation QCA in detecting significant LMCA bifurcation lesions is limited, especiallythe proximal LCX ostium. When IVUS is not available or contraindicated, 3D QCA may assist in the evaluation ofintermediate LMCA lesions with MLA.     

Clinical results and intramedullary signal changes of posterior decompression with transforaminal interbody fusion for thoracic myelopathy caused by combined ossification of the posterior longitudinal ligament and ligamentum flavum

Background Surgical treatment of thoracic myelopathy caused by ossification of the posterior longitudinal ligament （OPLL） and ossification of the ligamentum flavum （OLF） is technically demanding, and the results tend to be unfavorable. Various operative approaches and treatment strategies have been attempted, and posterior decompression with transforaminal thoracic interbody fusion （PTTIF） may be the optimal method with which the anterior-posterior compression was removed in one step. It is comparatively less traumatic with fewer serious complications.