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22 result(s) for "苯丙氨酸"
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松针褐斑病菌毒素处理后湿地松组培苗PAL、PPO、SOD活性变化研究
为研究抗松针褐斑病菌在湿地松子代组培苗体内的苯丙氨酸解氨酶(PAL)、多酚氧化酶(PPO)、超氧化物歧化酶(SOD)的活性变化与其抗病性的关系,以抗病湿地松瓶内组培苗和温室1年生组培苗针叶为材料,测定PAL、PPO、SOD的活性。结果表明:松针褐斑病菌毒素处理后,湿地松PAL和PPO活性与抗病性成一定正相关关系,SOD活性与植株抗病性在48 168 h内表现有一定的负相关性。
柠条幼苗苯丙氨酸解氨酶的纯化
用离子交换层析和分子筛层析分离纯化了真叶期柠条根、速生期柠条叶、茎中的苯丙氨酸解氨酶(PAL),并测定了PAL全酶的分子量。用SDS-PAGE鉴定了全酶的组成,测定了各亚基的分子量。结果表明:柠条叶中存在306KD和222KD两种PAL,前者是由82KD和74KD亚基组成的异聚体,后者是由74KD亚基组成的同聚体;而柠条根和茎中仅存在74KD亚基组成的222KD全酶。该研究为pal基因的克隆及应用奠定了基础。
离体毛竹笋纤维素和木质素含量及POD和PAL活性研究
研究了离体后毛竹笋纤维素、木质素含量以及苯丙氨酸解氨酶(PAL)、过氧化物酶(POD)活性的变化。结果显示:笋体纤维素、木质素含量从笋尖到笋基部逐渐增加;PAL、POD活性笋尖明显高于笋基部。离体后贮藏的竹笋纤维素、木质素含量随贮藏时间的延长而增加,在前5d纤维素的增加速度极快,在后5d增加速度明显趋缓,但木质素含量随贮藏时间的延长基本呈匀速态势增加;POD、PAL活性随贮藏时间的延长,活性均显著增加。对离体竹笋进行低温处理(4℃)可显著降低竹笋的PAL、POD活性,减少木质素和纤维素合成,低温对纤维素的影响高于木质素。
银杏细胞培养中影响黄酮积累量的几个因素
S792.95; 以幼苗茎段为外植体建立了生长黄酮的悬浮细胞培养体系,对细胞生长周期、相应的黄酮积累量变化以及苯丙氨酸解氨酶(PAL)活性进行了研究.结果表明,黄酮的积累在细胞生长对数期内增加,于15 d达最高峰.在黄酮积累的过程中PAL活性也呈增加趋势.当培养细胞转换新鲜培养基时,PAL活性增加了2倍(从0.05到0.15OD).用紫外线处理,培养于暗中细胞的PAL活性增加了11倍(从0.05到0.60OD).
采后竹笋老化生理研究
4月份出笋期挖取毛竹春笋和高节竹笋,测定了笋体从基部向顶部0、5、10、15、20、25cm各位段的苯丙氨酸解氨酶(PAL)和过氧化物酶(PO)活性,以及纤维素和木质素含量。竹笋在25℃放置96h自然老化,测定了24、84、72、96h,5、10、15、20、25cm各位段的苯丙氨酸解氨酶和过氧化物酶活性,以及10cm位段24、48、72、96h纤维素和木质素含量的变化。结果表明:PAL和PO活性以及纤维素和木质素的含量从基部向顶部逐渐降低,呈梯形分布,木质化进程是从基部向顶部推进的;竹笋离体后,PAL和PO活性大幅度增高,纤维素和木质素含量大量增加加速了老化进程。讨论了PAL和PO在竹笋老化过程中的活性变化,及其在竹笋老化过程中的作用。
An integrated metabonomic and proteomic study on Kidney-Yin Deficiency Syndrome patients with diabetes mellitus in China
Aim: To investigate specific changes in metabolites and proteins of Kidney-Yin Deficiency Syndrome (KYDS) patients with diabetes mellitus (DM) in China. Methods: KYDS (n=29) and non-KYDS (n=23) patients with DM were recruited for this study. The KYDS was diagnosed by two senior TCM clinicians separately. The metabonomic and proteomic profiles of the patients were assessed using a metabonomic strategy based on NMR with multivariate analysis and a proteomic strategy based on MALDI-TOF-MS, respectively. Results: Eighteen upregulated peptides and thirty downregulated peptides were observed in the plasma of the KYDS patients. Comparing the proteomic profiles of the KYDS and non-KYDS groups, however, no significantly differentially expressed peptides were found. At the same time, major metabolic alterations were found to distinguish the two groups, including eight significantly changed metabolites (creatinine, citrate, TMAO, phenylalanine, tyrosine, alanine, glycine and taurine). The levels of creatinine, citrate, TMAO, phenylalanine and tyrosine were decreased, whereas the levels of alanine, glycine and taurine were increased in the KYDS patients. These biochemical changes were found to be associated with alterations in amino acid metabolism, energy metabolism and gut microflora. Conclusion: The identification of distinct expression profiles of metabolites and signaling pathways in KYDS patients with DM suggests that there are indeed molecular signatures underlying the principles of 'Syndrome Differentiation' in traditional Chinese medicine.
Phenylalanine Hydroxylase Deficiency and Citrin Deficiency in a Chinese Infant
To the Editor: Tandem mass spectrometry (MS/MS)-based expanded newborn screening was first introduced in Pediatric Endocrinology/ Genetics of Xin Hua Hospital in 2003. The screening is expected to detect genetic disorders leading to a secondary increase in blood phenylalanine (Phe) in newborns. We reported a rare case in a Chinese infant with hyperphenylalaninemia (HPA) caused by phenylalanine hydroxylase (PAH) deficiency and neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD). This constellation of two different metabolic pathway defects in one patient has not been reported previously.
Field Efficacy of Agricultural Antibiotic 702 against Rice Leaf Blast and Panicle Blast
The control effects of agricultural antibiotic 702 ( ag-antibiotic 702) on rice leaf blast and panicle blast were evaluated in field trials. With ag-antibiotic 702 and the two-line early hybrid rice 287 as test materials, different concentrations of ag-antibiotic 702 liquids were sprayed at tiUering stage and full heading stage of rice. In leaf blast test, the disease indexes of leaf blast at tillering stage were surveyed at 1 d prior to the first spraying and at 15 d post spraying, respectively. The disease indexes (DI) and the rice yield in panicle blast test was investigated at milky stage. Meanwhile, enzyme activities, including peroxidase ( POD), catalase (CAT), superoxide dismutase (SOD), phenylalanine ammonia-lyase (PAL), and polyphanol oxidase (PPO), were measured. Kasugamycin (45 μg/mL) and deionized water were designed as positive and negative controls. When the concentrations of ag-antibiotie 702 were 15, 30 and 45 μg/mL, the control effects against leaf blast were 72.14%, 80.32% and 85.22%, respectively; the control effects on panicle blast were 74.08%, 84.87% and 86.58%, respectively; and the yield increase rates were 17.28%, 21.40% and 22.57%, respectively. So, ag-antibiotic 702, as a new agricultural antibiotic fungicide, could effectively cantrel rice blast by inducing defensive enzymes, and increase rice yield. The results will contribute to further development of ag-antibiotic 702 and its application in rice blast control.
CFTR: a missing link between exocrine and endocrine pancreas
Cystic fibrosis (CF), a life-shortening hereditary disease mainly afflicting people of Caucasian origins, is caused by loss-of-function mutations in the CFTR (Cystic Fibrosis Transmembrane conductance Regulator) gene, which encodes a phosphorylation-activated, but ATP-gated anion channel expressed primarily in epithelial cells. To date, nearly 2000 mutations have been identified as pathogenic, but the deletion of a single amino acid phenylalanine at position 508 (i.e., deltaF508) accounts for -70% of all disease-associated mutations and thus is present in at least one allele of -90% of patients with CF, This mutation not only decreases the number of functional CFTR molecules in the plasma membrane due to defective folding of the deltaF508-CFTR protein, but also disrupts ATP-dependent opening and closing (or gating) of the CFTR channel for the minor fraction of deltaF508-CFTR channels that do reach and stay in the cell membrane. While currently there is no cure for this debilitating disease, in the past decades, tremendous efforts have been committed to developing rea- gents that may help CFTR folding (i.e., correctors) or gating (i.e., potentiators). Recent successes in the discovery of an effective CFTR potentiator VX-770 (or Ivacaftor) and in its subsequent clinical trials not only establish an important precedent for realizing personalized medicine but also may serve as a stepping-stone for attaining the eventual goal of curing CF.