Breast Neoplasms ; therapy ; Humans ; Medicine, Chinese Traditional ; Yin Deficiency

Vitreous liquefaction is an age-related degenerative change,which will further alter the physicochemical properties of the vitreous and its surrounding tissues,resulting in various related eye diseases.The principal pathologic changes of that are the gradual depletion of hyaluronic acid and the collapse of collagen fibrillar network,with a series of biomechanical changes in vitreous body.This article reviews biomechanical properties of normal vitreous,the current measurements of these properties,formation mechanism and changes of biomechanics properties of vitreous liquefaction and correlation between synchesis and related ocular diseases,which provide insight into the ideas for the effective reduction and treatment of vitreous liquefaction.

Objective: To construct the extracellular region of PCP-2(PCP-2EC) and the immunoglobin IgG Fc fusi on protein expression vector,and then express and purify the soluble PCP-2EC/Fc fusion protein for the study of its function in neuronal adhesion. Methods: PCP-2 extracellular region was amplified and cloned into an expression vector pIGplus containing human IgG Fc; PCP-2EC/Fc fusion protein was expressed by COS-7 and 293 cells transfected by the constructed plasmid and purified by protein A. The purified fusion protein was used as substrate to study its function in neuronal adhesion. Results: PCP2 extracellular region was cloned into IgG Fc expression vector successfully; PCP 2EC/Fc fusion protein was expressed and purified in mammal cells; and the purified fusion protein promoted neuronal adhesion. Conclusion:PCP 2EC/Fc fusion protein expression system is successfully constructed and the purified fusion protein can promote neuronal adhesion. These results lay a foundation for the research on the PCP-2 function in neuronal adhesion and the further functional study in the nervous system and other fields.

Objective To observe the effect of intravenous injection of different doses of propofol on the ceil apoptosis and NF-kB p65 in the acute lung injury(ALl)induced by LPS in rats.Method Sixty SD rats were randomly(random number)divided into five groups,namely,control(NS)group,Au model group and propofol intervention groups(P1,P2,P3 groups).The lung injury was evaluated by using microscopy with hematoxylin and eosin(HE)staining and arterial blood gas,and Western blotting Was applied to evaluating the nuclear translocation of NF-KB P65 in lung tissues.The apoptosis rate of lung tissue Was determined by flow cytometric analysis.Results Lung injury in model group reached the pathologic criteria of acute lung injury,and it was attenuated apparently in propofol intervention groups(P1,P2,P3 groups)in dose-dependent manner.Western blotting results showed that the nuclear translocation of NF-KB P65 and the apoptosis rate increased significantly in ALI model group compared with control group(P<0.05),and decreased in propofol intervention groups compared with ALl model group(P<0.05).Conclusions Propofol Can attenuate acute lung injury induced by LPS in rats,and significantly inhibit the nuclear translocation of NF-KB P65 and the cell apoptosis in lung tissues.The effect of propofol attenuating acute lung injury induced by LPS in rats may be attributed to the inhibition of nuclear translocation of NF-KB P65and ceil apoptosis in lung tissues.

Objective To investigate the effects of propofol on activation of NF-κB in polymorphonuclear neutrophils (PMNs) in rats with LPS-induced acute lung injury (ALI). Methods Sixty healthy SD rats of both sexes, aged 3 months, weighing 250-350 g, were randomly divided into 5 groups (n = 12 each):control group (group C), ALI group and 3 different dose of propofol groups (group P1, P2, P3). The animals were anesthetized with intraperitaneal 3% pentobarbital sodium 40 mg/kg. LPS 5 mg/kg was injected via femoral vein in group ALI.Propofol 5, 10 and 15 mg· kg- 1· h- 1 was infused intravenously over 2 h immeliately after injection of LPS 5 ng/kg through femoral vein in group P1, P2 and P3 respectivey. In group C normal saline 10 ml was injected via femoral vein instead. All rats were killed by exsanguination at the end of infusion of propofol. The right lung was removed for microscopic examination. The morphologic changes were scored 0-3 (0 = normal, 3 = severe morphologic changes). Blood samples were collected from carotid artery for determination of the expression of total NF-κB and activated NF-κB in PMNs by Western blot. Results Compared with group C, morphologic change scores and activated NF-κB expression in PMNs were significantly increased in group ALI, P1 and P2, and morphologic change scores increased in group P3. Morphologic change scores in group P1 and P2 and activated NF-κB expression in PMNs in group P1, P2 and P3 were significantly decreased compared with those in group ALl. Morphologic change scores and activated NF-κB expression in PMNs were decreased gradually in group P1, P2 and P3 . There was no significant difference in total NF-κB expression in PMNs among all groups. Conclusion Propofol can attenuate ALI induced by LPS through inhibition of the activation of NF-κB in PMNs in rats.

Objective To investigate the protective effects of isovolemic hemodilution with 6% hetastarch (HAES) and ligustrazine on myocardium against ischemia/reperfusion injury. Methods Thirty-two healthy male rabbits were anesthetized with 3% pentobarbital 30 mg?kg-1 , tracheotomized and mechanically ventilated. Left femoral artery and vein were cannulated for direct BP monitoring, blood collection and fluid infusion. Chest was opened and myocardial ischemia was produced by temporary ligation of the anterior descending branch of left coronary artery. Myocardial ischemia was confirmed by elevation or depression of S-T segment and /or high T-wave. The animals were randomly divided into 4 equal groups with 8 animals in each group: Ⅰ control group was subjected to 45 min myocardial ischemia followed by 180 min reperfusion without any treatment; Ⅱ hemodilution group in which 9 ml Ⅲ kg-1 blood was removed and blood volume was maintained by simultaneous infusion of equal volume of 6% HAES at 20 min after myocardial ischemia was started; Ⅳ ligustrazine group received ligustrazine injectio 20 mg?kg-1 iv 20 min before and 40 min after myocardial ischemia was started; Ⅱ hemodilution + ligustrazine group in which hemodilution was performed as in group Ⅲ and ligustrazine injectio was given iv as in group Ⅲ . BP and HR were recorded before during and at the end of myocardial ischemia, and at 30, 60, 120, 180 min of reperfusion. Hct was measured before and after hemodilution. Blood samples were taken for determination of plasma CPK and LDH activities before ischemia (T0), at the end of 45 min ischemia (T1) and at the end of 180 min reperfusion (T2 ) . At the end of the experiment, myocardial tissue 0.2 g was obtained from ischemic and non-ischemic area for determination of myocardial CPK and LDH activities and election microscopic examination. Results (1) In all four groups plasma CPK and LDH activities were significantly increased after ischemia (T1 ) and were increased further after reperfusion (T2) (P

Aged ; Ear, Middle ; Eustachian Tube ; Female ; Foreign Bodies ; Humans

Objective:To study the mechanism of anti-proliferative effect of lupeol on highly metastatic human hepatocellular car-cinoma HCCLM3 cells. Methods:CCK-8 assay was performed to evaluate the effects of lupeol at different concentration on cell viability in 12-48 h. Caspase inhibitors were used to identify the subtypes of caspases activated during lupeol-induced cell death. The effects of lupeol on the mRNA expression of caspase family and Bcl-2 related genes were detected by real-time PCR. The effects of lupeol on HC-CLM3 cell phase distribution were investigated by flow cytometry. Results:Compared with the control group, lupeol could inhibit HC-CLM3 cell proliferation in a concentration-dependent manner with IC50 of 93 μmol·L-1 in 24h. The number of HCCLM3 cells in the period of G2/M was increased by 1-fold when the lupeol concentration was within 60-100 μmol·L-1 . Lupeol could activate the path-way of caspase, and the mRNA expression of caspase-3 was elevated by 50%-150% when compared with that in the control group. Mo-reover, the mRNA expression of p53 and Bax were increased above 1-fold by lupeol at 100 μmol·L-1 , and the Bcl-2 and PARP ex-pression were significantly suppressed by lupeol at 60-100 μmol·L-1(P<0. 05 or P<0. 01). Conclusion:The results indicate that lupeol has anti-proliferative effect on the liver cancer cells, which is beneficial to the prevention and treatment of liver cancer.

Objective: To construct the extracellular region of PCP-2(PCP-2EC) and the immunoglobin IgG Fc fusi on protein expression vector,and then express and purify the soluble PCP-2EC/Fc fusion protein for the study of its function in neuronal adhesion.Methods: PCP-2 extracellular region was amplified and cloned into an expression vector pIGplus containing human IgG Fc; PCP-2EC/Fc fusion protein was expressed by COS-7 and 293 cells transfected by the constructed plasmid and purified by protein A.The purified fusion protein was used as substrate to study its function in neuronal adhesion.Results:PCP-2 extracellular region was cloned into IgG Fc expression vector successfully; PCP-2EC/Fc fusion protein was expressed and purified in mammal cells; and the purified fusion protein promoted neuronal adhesion.Conclusion:PCP-2EC/Fc fusion protein expression system is successfully constructed and the purified fusion protein can promote neuronal adhesion.These results lay a foundation for the research on the PCP-2 function in neuronal adhesion and the further functional study in the nervous system and other fields.

恶性肿瘤居中国各类疾病死因之首，发病率与病死率呈逐年上升趋势。近几年来靶向治疗已广泛应用于临床，显示 出良好的抗肿瘤效果，新靶点的探索和鉴定在靶向药物研发过程中起着重要作用。E3泛素连接酶斑点型锌指结构蛋白（speckletype POZ protein，SPOP）作为治疗选择的潜在靶点，能特异性识别底物，使底物发生泛素化降解，广泛参与机体内多种生理、病理 过程。研究发现SPOP基因突变或表达水平改变，通过调控AR/ERG、Akt-mTORC1、Hedgehog/Gli2等多种信号通路影响恶性肿 瘤的发生发展，并与前列腺癌、肾癌、结直肠癌等多种恶性肿瘤细胞增殖及远处转移密切相关。目前，SPOP影响恶性肿瘤发生发 展的相关研究为靶向治疗恶性肿瘤奠定了基础，综述SPOP在恶性肿瘤的最新进展对抗肿瘤研究具有重要的意义。