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论齐鲁文化的道德传统 被引量:3
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作者 陈玉华 王世涛 《山东省青年管理干部学院学报(青年工作论坛)》 2010年第1期15-17,共3页
齐鲁文化的道德传统在当今既有积极的一面,也有诸多不适应甚至制约现代经济、社会和人的发展的一面。它体现着浓郁的酒性特征,内含着较多的民粹主义思想因素,阻滞着山东各方面制度的现代化,强化着山东传统的生产方式和生活方式。齐鲁文... 齐鲁文化的道德传统在当今既有积极的一面,也有诸多不适应甚至制约现代经济、社会和人的发展的一面。它体现着浓郁的酒性特征,内含着较多的民粹主义思想因素,阻滞着山东各方面制度的现代化,强化着山东传统的生产方式和生活方式。齐鲁文化精神传统的现代提升和创新发展,需要正视和反思这些消极因素。 展开更多
关键词 齐鲁文化 道德传统 酒性特征 民粹主义 制度现代化
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A Simplified Method for Purifying Osteoclasts from Human Giant Cell Tumor of Bone
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作者 王运林 向光大 夏秦 《The Chinese-German Journal of Clinical Oncology》 CAS 2005年第1期61-63,69,共4页
Objective: To purify and identify the osteoclasts from the tissue of humangiant cell tumor of bone. Methods: We have developed a new method that allows the purification oflarge numbers of authentic osteoclasts (OCs). ... Objective: To purify and identify the osteoclasts from the tissue of humangiant cell tumor of bone. Methods: We have developed a new method that allows the purification oflarge numbers of authentic osteoclasts (OCs). The OCs were isolated from tissue of human giant celltumor of bone by 0.25% trypsin and collagenase. We characterized OCs in terms of the expression ofdifferent phenotypic markers of OCs. The phenotypic markers of OC included Tartrate-resistant acidphosphatase staining (TRAP). The expression of calcitonin receptor (CTR), cathepsin K and receptoractivator of necrosis factor κB (RANK) mRNA were examined by RT-PCR. Results: The OC cell purifiedby above method functioned normally in vitro. The purity was about 79.7%. They showed the normalosteoclast phenotypes markers of OC. Conclusion: The method provides a system for performingbiochemical and molecular studies of OCs. The study indicates that the method of purifying theosteoclasts from human GCT cell can be used for research of bone metabolism. 展开更多
关键词 OSTEOCLASTS TRAP CTR cathepsin K RANK
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Role of alcohol in the regulation of iron metabolism 被引量:10
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作者 Duygu Dee Harrison-Findik 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第37期4924-4930,共7页
Patients with alcoholic liver disease frequently exhibit increased body iron stores, as reflected by elevated serum iron indices (transferrin saturation, ferritin) and hepatic iron concentration. Even mild to moderate... Patients with alcoholic liver disease frequently exhibit increased body iron stores, as reflected by elevated serum iron indices (transferrin saturation, ferritin) and hepatic iron concentration. Even mild to moderate alcohol consumption has been shown to increase the prevalence of iron overload. Moreover, increased hepatic iron content is associated with greater mortality from alcoholic cirrhosis, suggesting a pathogenic role for iron in alcoholic liver disease. Alcohol increases the severity of disease in patients with genetic hemochromatosis, an iron overload disorder common in the Caucasian population. Both iron and alcohol individually cause oxidative stress and lipid peroxidation, which culminates in liver injury. Despite these observations, the underlying mechanisms of iron accumulation and the source of the excess iron observed in alcoholic liver disease remain unclear. Over the last decade, several novel iron-regulatory proteins have been identified and these have greatly enhanced our understanding of iron metabolism. For example, hepcidin, a circulatory antimicrobial peptide synthesized by the hepatocytes of the liver is now known to play a central role in the regulation of iron homeostasis. This review attempts to describe the interaction of alcohol and iron-regulatory molecules. Understanding these molecular mechanisms is of considerable clinical importance because both alcoholic liver disease and genetic hemochromatosis are common diseases, in which alcohol and iron appear to act synergistically to cause liver injury. 展开更多
关键词 Alcoholic liver disease C/EBP alpha Divalentmetal transporter 1 FERROPORTIN HEPCIDIN
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Signaling mechanisms in alcoholic liver injury: Role of transcription factors, kinases and heat shock proteins 被引量:3
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作者 Pranoti Mandrekar 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第37期4979-4985,共7页
Alcoholic liver injury comprises of interactions of various intracellular signaling events in the liver. Innate immune responses in the resident Kupffer cells of the liver, oxidative stress-induced activation of hepat... Alcoholic liver injury comprises of interactions of various intracellular signaling events in the liver. Innate immune responses in the resident Kupffer cells of the liver, oxidative stress-induced activation of hepatocytes, fibrotic events in liver stellate cells and activation of liver sinusoidal endothelial cells all contribute to alcoholic liver injury. The signaling mechanisms associated with alcoholic liver injury vary based on the cell type involved and the extent of alcohol consumption. In this review we will elucidate the oxidative stress and signaling pathways affected by alcohol in hepatocytes and Kupffer cells in the liver by alcohol. The toll-like receptors and their down-stream signaling events that play an important role in alcohol-induced inflammation will be discussed. Alcohol-induced alterations of various intracellular transcription factors such as NFKB, PPARs and AP-1, as well as MAPK kinases in hepatocytes and macrophages leading to induction of target genes that contribute to liver injury will be reviewed. Finally, we will discuss the significance of heat shock proteins as chaperones and their functional regulation in the liver that could provide new mechanistic insights into the contributions of stress-induced signaling mechanisms in alcoholic liver injury. 展开更多
关键词 TNFΑ Toll-like receptors NFKB Heat shockproteins Mitogen-activated protein kinases
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Role of transmethylation reactions in alcoholic liver disease 被引量:3
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作者 Kusum K Kharbanda 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第37期4947-4954,共8页
Alcoholic liver disease is a major health care problem worldwide. Findings from many laboratories, including ours, have demonstrated that ethanol feeding impairs several of the many steps involved in methionine metabo... Alcoholic liver disease is a major health care problem worldwide. Findings from many laboratories, including ours, have demonstrated that ethanol feeding impairs several of the many steps involved in methionine metabolism. Ethanol consumption predominantly results in a decrease in the hepatocyte level of S-adenosylmethionine and the increases in two toxic metabolites, homocysteine and S-adenosylhomocysteine. These changes, in turn, result in serious functional consequences which include decreases in essential methylation reactions v/a inhibition of various methyltransferases. Of particular interest to our laboratory is the inhibition of three important enzymes, phosphatidylethanolamine methyltransferase, isoprenylcysteine carboxyl methyltransferase and protein L-isoaspartate methyltransferase. Decreased activity of these enzymes results in increased fat deposition, increased apoptosis and increased accumulation of damaged proteins- all of which are hallmark features of alcoholic liver injury. Of all the therapeutic modalities available, betaine has been shown to be the safest, least expensive and most effective in attenuating ethanol-induced liver injury. Betaine, by virtue of aiding in the remethylation of homocysteine, removes both toxic metabolites (homocysteine and S-adenosylhomocysteine), restores S-adenosylmethionine level, and reverses steatosis, apoptosis and damaged proteins accumulation. In conclusion, betaine appears to be a promising therapeutic agent in relieving the methylation and other defects associated with alcoholic abuse. 展开更多
关键词 TRANSMETHYLATION S-ADENOSYLHOMOCYSTEINE ALCOHOL BETAINE Liver STEATOSIS Apoptosis METHYLTRANSFERASES
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