[Objective] The induced disease resistance of Antarctic bacteria B-3 extracellular oligosaccharide on cucumber was studied.[Method] Taking the cucumber seedlings as experimental materials,the molecular weight,monosacc...[Objective] The induced disease resistance of Antarctic bacteria B-3 extracellular oligosaccharide on cucumber was studied.[Method] Taking the cucumber seedlings as experimental materials,the molecular weight,monosaccharide composition of Antarctic bacteria B-3 extracellular oligosaccharide were studied,its induced effect on the defense enzyme in cucumber leaves and the induced resistance against powdery mildew were also investigated.[Result] Through gel permeation chromatography,the molecular weight of B-3 oligosaccharides was determined to be 2 112 Da;B-3 oligosaccharides was composed by two monosaccharides including of mannose and glucose.The activities of chinitase,β-1,3-glucanse,phenylanine,ammonialyse（PAL）,superoxide dismutase（SOD）,and peroxidase（POD）in cucumber seedlings all increased compared with control when 0.3%,0.5% and 0.8% B-3 extracellular oligosaccharide were sprayed on the seedlings of cucumber for different times,respectively,which had the similar induction effect with 0.5% chitosan;at the same time,0.5% oligosaccharides could significantly reduce the disease index of cucumber powdery mildew,the control effect reached 24.49%.[Conclusion] B-3 oligosaccharides is expected to be developed as a new type of resistance elicitor.展开更多
Inhibition and induction of drug-metabolizing enzymes are the most frequent and dangerous drugdrug interactions. They are an important cause of serious adverse events that have often resulted in early termination of d...Inhibition and induction of drug-metabolizing enzymes are the most frequent and dangerous drugdrug interactions. They are an important cause of serious adverse events that have often resulted in early termination of drug development or withdrawal of drugs from the market. Management of such interactions by dose adjustment in clinical practice is extremely difficult because of the wide interindividual variability in their magnitude. This review examines the genetic, physiological, and environmental factors responsible for this variability, focusing on an important but so far neglected cause of variability, liver functional status. Clinical studies have shown that liver disease causes a reduction in the magnitude of interactions due to enzyme inhibition, which is proportional to the degree of liver function impairment. The effect of liver dysfunction varies quantitatively according to the nature, reversible or irreversible, of the inhibitory interaction. The magnitude of reversible inhibition is more drastically reduced and virtually vanishes in patients with advanced hepatocellular insufficiency. Two mechanisms, in order of importance, are responsible for this reduction: decreased hepatic uptake of the inhibitory drug and reduced enzyme expression. The extent of irreversible inhibitory interactions is only partially reduced, as it is only influenced by the decreased expression of the inhibited enzyme. Thus, for appropriate clinical management of inhibitory drug interactions, both the liver functional status and the mechanism of inhibition must be taken into consideration. Although the inducibility of drugmetabolizing enzymes in liver disease has long been studied, very conflicting results have been obtained, mainly because of methodological differences. Taken together, the results of early animal and human studies indicated that enzyme induction is substantially preserved in compensated liver cirrhosis, whereas no definitive conclusion as to whether it is significantly reduced in the decompensated state of cirrhos展开更多
基金Supported by National"863"Technology Plan Key Projects-Key Techniques for Utilization of Polar Microbial Resources(2007AA091905)~~
文摘[Objective] The induced disease resistance of Antarctic bacteria B-3 extracellular oligosaccharide on cucumber was studied.[Method] Taking the cucumber seedlings as experimental materials,the molecular weight,monosaccharide composition of Antarctic bacteria B-3 extracellular oligosaccharide were studied,its induced effect on the defense enzyme in cucumber leaves and the induced resistance against powdery mildew were also investigated.[Result] Through gel permeation chromatography,the molecular weight of B-3 oligosaccharides was determined to be 2 112 Da;B-3 oligosaccharides was composed by two monosaccharides including of mannose and glucose.The activities of chinitase,β-1,3-glucanse,phenylanine,ammonialyse（PAL）,superoxide dismutase（SOD）,and peroxidase（POD）in cucumber seedlings all increased compared with control when 0.3%,0.5% and 0.8% B-3 extracellular oligosaccharide were sprayed on the seedlings of cucumber for different times,respectively,which had the similar induction effect with 0.5% chitosan;at the same time,0.5% oligosaccharides could significantly reduce the disease index of cucumber powdery mildew,the control effect reached 24.49%.[Conclusion] B-3 oligosaccharides is expected to be developed as a new type of resistance elicitor.
文摘Inhibition and induction of drug-metabolizing enzymes are the most frequent and dangerous drugdrug interactions. They are an important cause of serious adverse events that have often resulted in early termination of drug development or withdrawal of drugs from the market. Management of such interactions by dose adjustment in clinical practice is extremely difficult because of the wide interindividual variability in their magnitude. This review examines the genetic, physiological, and environmental factors responsible for this variability, focusing on an important but so far neglected cause of variability, liver functional status. Clinical studies have shown that liver disease causes a reduction in the magnitude of interactions due to enzyme inhibition, which is proportional to the degree of liver function impairment. The effect of liver dysfunction varies quantitatively according to the nature, reversible or irreversible, of the inhibitory interaction. The magnitude of reversible inhibition is more drastically reduced and virtually vanishes in patients with advanced hepatocellular insufficiency. Two mechanisms, in order of importance, are responsible for this reduction: decreased hepatic uptake of the inhibitory drug and reduced enzyme expression. The extent of irreversible inhibitory interactions is only partially reduced, as it is only influenced by the decreased expression of the inhibited enzyme. Thus, for appropriate clinical management of inhibitory drug interactions, both the liver functional status and the mechanism of inhibition must be taken into consideration. Although the inducibility of drugmetabolizing enzymes in liver disease has long been studied, very conflicting results have been obtained, mainly because of methodological differences. Taken together, the results of early animal and human studies indicated that enzyme induction is substantially preserved in compensated liver cirrhosis, whereas no definitive conclusion as to whether it is significantly reduced in the decompensated state of cirrhos
