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The earliest Cambrian Meishucunian phosphoritic succession in eastern Yunnan,China,contains well−preserved molluscan shells that offer insights into the early evolution of skeletonization. Phosphate internal moulds,phosphate replaced originally carbonate shells,and phosphate coatings show lamello−fibrillar structure,prismatic structure,and regularly foliated structure. The lamello−fibrillar structure appears earlier in the fossil record than laminar structures such as nacreous or foliated structures. It has been identified in fossil mollusks,which occur in China as early as the lower phosphate layer of the Zhongyicun Member of the Meishucunian. Therefore,the lamello−fibrillar structure appears to be primitive in mollusks. The lamello−fibrillar and prismatic aragonite is the most common shell material of molluscan skeletons in the Early Cambrian Meishucunian and equivalents around the world. Although the early molluscan microstructure is not so diverse as that of extant mollusks,it may be of use in high rank taxonomic classification as shown by the early conchiferan mollusks discussed here. These mollusks are characterized by the horizontal fibrillae that are layered and parallel,and thereby differ from hyoliths,in which the horizontal fibrillae appear to be in the form of the bundles of fibres that can branch or anastomose.
Background: Hypoxia plays a critical role in many cancers. Hypoxia inducible factor-1α (HIF-1α) is an important mediator of the hypoxia response. It regulates the expression of various chemokines involved in tumor growth, angiogenesis and metastasis but the associated pathway needs further investigation. Methods: The expression level of HIF-1α was determined in hepatocellular carcinoma (HCC) cells. The correlation of interleukin-8 (IL-8) and HIF-1α was assessed by knocking down HIF-1α. These cells were also used to assess its influence on HCC cell migration and invasion was checked. Pyrrolidinedithiocarbamate (PDTC), an inhibitor of NF-κB, was used to confirm the associated signaling pathway. Results: HIF-1α was significantly expressed in HCC cells and found to promote HCC cell migration and invasion in an IL-8-dependent manner. NF-κB was confirmed to be involved in the process. Conclusions: HIF-1α promotes HCC cell migration and invasion by modulating IL-8 via the NF-κB pathway.
Background: Hepatocellular carcinoma (HCC) is the fifth most common cancer and the third most common cause of cancer-related death worldwide. The 5-year survival rate remains low despite considerable research into treatments of HCC, including surgery, radiotherapy and chemotherapy. Many mechanisms within HCC still require investigation, including the influence of hypoxia, which has a crucial role in many cancers and is associated with metastasis. Hypoxia inducible factor-1α (HIF-1α) is known to regulate the expression of many chemokines, including interleukin-8 (IL-8), which is associated with tumor metastasis. Although many studies have reported that HIF-1α is associated with HCC migration and invasion, the underlying mechanisms remain unknown. Methods: The expression level of HIF-1α was determined in HCC cells. The correlation of IL-8 and HIF-1α expressions was assessed via knockdown of HIF-1α. HCC cells were also used to assess the influence of HIF-1α on HCC cell migration and invasion. LY294002, an inhibitor of the Akt pathway, was used to confirm the associated signaling pathways. Results: We observed a significant attenuation of cell migration and invasion after silencing of HIF-1α. Exogenously expressing IL-8 restored migration and invasion. Akt was found to be involved in this process. Conclusion: Hypoxia promotes HCC cell migration and invasion through the HIF-1α–IL8–Akt axis.
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