Many epidemiological studies demonstrate that treatment with non-steroidal anti-inflammatory drugs （NSAIDs） reduce the incidence and mortality of certain malignancies, especially gastrointestinal cancer. The cycloox...Many epidemiological studies demonstrate that treatment with non-steroidal anti-inflammatory drugs （NSAIDs） reduce the incidence and mortality of certain malignancies, especially gastrointestinal cancer. The cyclooxygenase （COX） enzymes are well-known targets of NSAIDs. However, conventional NSAIDs nonselectively inhibit both the constitutive form COX-1, and the inducible form COX-2. Recent evidence indicates that COX-2 is an important molecular target for anticancer therapies. Its expression is undetectable in most normal tissues, and is highly induced by proinflammatory cytokines, mitogens, tumor promoters and growth factors. It is now well-established that COX-2 is chronically overexpressed in many premalignant, malignant, and metastastic cancers, including hepatocellular carcinoma （HCC）. Overexpression of COX-2 in patients with HCC is generally higher in welldifferentiated HCCs compared with less-differentiated HCCs or histologically normal liver, suggesting that COX-2 may be involved in the early stages of hepatocarcinogenesis, and increased expression of COX-2 in noncancerous liver tissue has been significantly associated with shorter disease-free survival in patients with HCC. In tumors, overexpression of COX-2 leads to an increase in prostaglandin （PG） levels, which affect many mechanisms involved in carcinogenesis, such as angiogenesis, inhibition of apoptosis, stimulation of cell growth as well as the invasiveness and metastatic potential of tumor cells. The availability of novel agents that selectively inhibit COX-2 （COXIB）, has contributed to shedding light on the role of this molecule. Experimental studies on animal models of liver cancer have shown that NSAIDs, including both selective and non-selective COX-2 inhibitors, exert chemopreventive as well as therapeutic effects. However, the key mechanism by which COX-2 inhibitors affect HCC cell growth is as yet not fully understood. Increasing evidence suggests the involvement of molecular targets other than COX-2 in the antiprol展开更多
Viral-mediated gene transfer of thymidine kinase ofherpes simplex virus (HSV-tk) has been used to confercytotoxic sensitivity to ganciclovir (GCV) in a variety oftnmor cells. HSV-tk converts GCV into a phosphorylatedc...Viral-mediated gene transfer of thymidine kinase ofherpes simplex virus (HSV-tk) has been used to confercytotoxic sensitivity to ganciclovir (GCV) in a variety oftnmor cells. HSV-tk converts GCV into a phosphorylatedcompound which is toxic for dividing cells by blockingDNA synthesis. Our previous study has shown展开更多
The Al-9Zn-2.8Mg-2.5Cu-xZr-ySc alloys （x=0, 0.15%, 0.15%; y=0, 0.05%, 0.15%）, produced by low-frequent electromagnetic casting technology, were subjected to homogenization treatment, hot extrusion, solution and agin...The Al-9Zn-2.8Mg-2.5Cu-xZr-ySc alloys （x=0, 0.15%, 0.15%; y=0, 0.05%, 0.15%）, produced by low-frequent electromagnetic casting technology, were subjected to homogenization treatment, hot extrusion, solution and aging treatment. The effects of minor Sc and Zr addition on microstructure, recrystallization and properties of alloys were studied by optical microscopy （OM）, scanning electron microscopy （SEM） and transmission electron microscopy （TEM）. The results show that Sc and Zr addition can refine grains of the as-cast alloy by precipitation of primary Al3（Sc,Zr） particles formed during solidification as heterogeneous nuclei. Secondary Al3（Sc,Zr） precipitates formed during homogenization treatment strongly pin the movement of dislocation and subgrain boundaries, which can effectively inhibit the alloys recrystallization. Compared with the alloy without Sc and Zr addition, the Al-Zn-Mg-Cu-Zr alloy with 0.05%Sc and 0.15%Zr shows the increase in tensile strength and yield strength by 172 MPa and 218 MPa, respectively. Strengthening comes from the contributions of precipitation, substructure and grain refining.展开更多
Ganoderma lucidum polysaccharides have protective effects against apoptosis in neurons exposed to ischemia/reperfusion injury, but the mechanisms are unclear. The goal of this study was to investigate the underlying m...Ganoderma lucidum polysaccharides have protective effects against apoptosis in neurons exposed to ischemia/reperfusion injury, but the mechanisms are unclear. The goal of this study was to investigate the underlying mechanisms of the effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis. Hydrogen peroxide（H_2O_2） was used to induce apoptosis in cultured cerebellar granule cells. In these cells, ganoderma lucidum polysaccharides remarkably suppressed H_2O_2-induced apoptosis, decreased expression of caspase-3, Bax and Bim and increased that of Bcl-2. These findings suggested that ganoderma lucidum polysaccharides regulate expression of apoptosis-associated proteins, inhibit oxidative stress-induced neuronal apoptosis and, therefore, have significant neuroprotective effects.展开更多
基金Supported by a grant from the Associazione Italiana per la Ricerca sul Cancro and from the Italian Ministero dell'Universitàedella Ricerca Scientifica (ex 60%, year 2003)
文摘Many epidemiological studies demonstrate that treatment with non-steroidal anti-inflammatory drugs （NSAIDs） reduce the incidence and mortality of certain malignancies, especially gastrointestinal cancer. The cyclooxygenase （COX） enzymes are well-known targets of NSAIDs. However, conventional NSAIDs nonselectively inhibit both the constitutive form COX-1, and the inducible form COX-2. Recent evidence indicates that COX-2 is an important molecular target for anticancer therapies. Its expression is undetectable in most normal tissues, and is highly induced by proinflammatory cytokines, mitogens, tumor promoters and growth factors. It is now well-established that COX-2 is chronically overexpressed in many premalignant, malignant, and metastastic cancers, including hepatocellular carcinoma （HCC）. Overexpression of COX-2 in patients with HCC is generally higher in welldifferentiated HCCs compared with less-differentiated HCCs or histologically normal liver, suggesting that COX-2 may be involved in the early stages of hepatocarcinogenesis, and increased expression of COX-2 in noncancerous liver tissue has been significantly associated with shorter disease-free survival in patients with HCC. In tumors, overexpression of COX-2 leads to an increase in prostaglandin （PG） levels, which affect many mechanisms involved in carcinogenesis, such as angiogenesis, inhibition of apoptosis, stimulation of cell growth as well as the invasiveness and metastatic potential of tumor cells. The availability of novel agents that selectively inhibit COX-2 （COXIB）, has contributed to shedding light on the role of this molecule. Experimental studies on animal models of liver cancer have shown that NSAIDs, including both selective and non-selective COX-2 inhibitors, exert chemopreventive as well as therapeutic effects. However, the key mechanism by which COX-2 inhibitors affect HCC cell growth is as yet not fully understood. Increasing evidence suggests the involvement of molecular targets other than COX-2 in the antiprol
文摘Viral-mediated gene transfer of thymidine kinase ofherpes simplex virus (HSV-tk) has been used to confercytotoxic sensitivity to ganciclovir (GCV) in a variety oftnmor cells. HSV-tk converts GCV into a phosphorylatedcompound which is toxic for dividing cells by blockingDNA synthesis. Our previous study has shown
基金Project(0211002605132)supported by Institute of Multipurpose Utilization of Mineral Resources,Chinese Academy of Geological Sciences,ChinaProject(0211005303101)supported by the Fundamental Research Funds for the Central Universities,China+1 种基金Project(2010BB4074)supported by Natural Science Foundation Project of CQ CSTC,ChinaProject(2010ZD-02)supported by State Key Laboratory for Advanced Metals and Materials,China
文摘The Al-9Zn-2.8Mg-2.5Cu-xZr-ySc alloys （x=0, 0.15%, 0.15%; y=0, 0.05%, 0.15%）, produced by low-frequent electromagnetic casting technology, were subjected to homogenization treatment, hot extrusion, solution and aging treatment. The effects of minor Sc and Zr addition on microstructure, recrystallization and properties of alloys were studied by optical microscopy （OM）, scanning electron microscopy （SEM） and transmission electron microscopy （TEM）. The results show that Sc and Zr addition can refine grains of the as-cast alloy by precipitation of primary Al3（Sc,Zr） particles formed during solidification as heterogeneous nuclei. Secondary Al3（Sc,Zr） precipitates formed during homogenization treatment strongly pin the movement of dislocation and subgrain boundaries, which can effectively inhibit the alloys recrystallization. Compared with the alloy without Sc and Zr addition, the Al-Zn-Mg-Cu-Zr alloy with 0.05%Sc and 0.15%Zr shows the increase in tensile strength and yield strength by 172 MPa and 218 MPa, respectively. Strengthening comes from the contributions of precipitation, substructure and grain refining.
文摘Ganoderma lucidum polysaccharides have protective effects against apoptosis in neurons exposed to ischemia/reperfusion injury, but the mechanisms are unclear. The goal of this study was to investigate the underlying mechanisms of the effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis. Hydrogen peroxide（H_2O_2） was used to induce apoptosis in cultured cerebellar granule cells. In these cells, ganoderma lucidum polysaccharides remarkably suppressed H_2O_2-induced apoptosis, decreased expression of caspase-3, Bax and Bim and increased that of Bcl-2. These findings suggested that ganoderma lucidum polysaccharides regulate expression of apoptosis-associated proteins, inhibit oxidative stress-induced neuronal apoptosis and, therefore, have significant neuroprotective effects.
