Enzyme最新文献_第7页

Heterogenous zonal distribution of lysosomal enzymes in rat liver. 大鼠肝脏溶酶体酶的异质带状分布。

Enzyme Pub Date : 1991-01-01 DOI: 10.1159/000468886

A R Pösö, K E Penttilä, K O Lindros

引用次数: 4

Aldehyde dehydrogenase, aldose reductase, and free radical scavengers in cataract. 白内障中的醛脱氢酶、醛糖还原酶和自由基清除剂。

Enzyme Pub Date : 1991-01-01 DOI: 10.1159/000468888

M J Crabbe, S T Hoe

引用次数: 15

About the presence of a circulating anti-alkaline phosphatase antibody in a trisomy 21 patient's serum. 关于21三体患者血清中循环抗碱性磷酸酶抗体的存在。

Enzyme Pub Date : 1991-01-01 DOI: 10.1159/000468878

A Brissson-Lougarre, H Vergnes, J Grozdea

引用次数: 1

Dexamethasone and glucagon cause synergistic increases of urea cycle enzyme activities in livers of normal but not adrenalectomized rats. 地塞米松和胰高血糖素引起正常而非肾上腺切除大鼠肝脏尿素循环酶活性的协同增加。

Enzyme Pub Date : 1991-01-01 DOI: 10.1159/000468862

P J Snodgrass

引用次数: 6

Sugar chain heterogeneity of bone and liver alkaline phosphatase in serum. 血清骨、肝碱性磷酸酶糖链异质性。

Enzyme Pub Date : 1991-01-01 DOI: 10.1159/000468866

T Kuwana, O Sugita, M Yakata

引用次数: 16

Guanidino compound metabolism in arginine-free diet induced hyperammonemia. 无精氨酸饮食中胍类化合物代谢诱导高氨血症。

Enzyme Pub Date : 1991-01-01 DOI: 10.1159/000468879

D R Deshmukh, K Meert, A P Sarnaik, B Marescau, P P De Deyn

{"title":"Guanidino compound metabolism in arginine-free diet induced hyperammonemia.","authors":"D R Deshmukh, K Meert, A P Sarnaik, B Marescau, P P De Deyn","doi":"10.1159/000468879","DOIUrl":"https://doi.org/10.1159/000468879","url":null,"abstract":"Guanidino compounds, intermediates of arginine metabolism, are altered in many pathological conditions especially those involving the urea cycle. Arginine and creatine play an important role in nitrogen metabolism whereas other guanidino compounds such as guanidinosuccinic acid and N-acetylarginine are toxins. Our objective was to investigate the relationship between guanidino compounds and hyperammonemia. Young and adult ferrets were fed a single meal of either an arginine-containing diet (ACD) or an arginine-free diet (AFD). Guanidino compounds were determined by HPLC in the plasma, liver, kidney and brain 3 h after feeding the specified diet. Only young ferrets fed AFD developed hyperammonemia. Plasma and kidney arginine was decreased whereas guanidinosuccinic acid was increased in young ferrets fed AFD. Hepatic creatine and kidney and brain guanidinoacetic acid were significantly decreased in this group. These results indicate that AFD-induced hyperammonemia produced decreased methylation activity in the liver and transamidination activity in kidney. Elevated guanidinosuccinate levels coupled with deficient hepatic creatine synthesis may play a role in the pathophysiology of hyperammonemia.","PeriodicalId":11933,"journal":{"name":"Enzyme","volume":"45 3","pages":"128-36"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468879","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12977766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Insulin resistance in myotonic dystrophy. 强直性肌营养不良患者的胰岛素抵抗。

Enzyme Pub Date : 1991-01-01 DOI: 10.1159/000468860

M G Piccardo, G Pacini, M Rosa, R Vichi

{"title":"Insulin resistance in myotonic dystrophy.","authors":"M G Piccardo, G Pacini, M Rosa, R Vichi","doi":"10.1159/000468860","DOIUrl":"https://doi.org/10.1159/000468860","url":null,"abstract":"The aim of the present study was to obtain a comprehensive picture of the rate of insulin secretion and of tissue sensitivity to the endogenous hormone in myotonic dystrophy patients (MyD). The minimal model approach was utilized for the analysis of frequently sampled intravenous glucose tolerance test data (FSIGT). This method provided the characteristic parameters: SI, insulin sensitivity index; SG fractional glucose disappearance independent of dynamic insulin; n, fractional insulin clearance; phi 1 and phi 2 first and second phase insulin delivery sensitivities to glucose stimulation. In MyD patients SI was reduced (p less than 0.01) by 71% to 1.4 +/- 0.3 x 10(-4) min-1/(microU/ml), whereas in controls it was 4.85 +/- 0.77; SG was within the normal range: 0.044 +/- 0.012 min-1 in MyD patients and 0.036 +/- 0.017 min-1 in controls; phi 1 increased in MyD patients (7.4 +/- 1.3 min (microU/ml)/(mg/dl) versus 4.1 +/- 1.2 in controls); phi 2 increased in MyD patients (126 +/- 47 x 10(4) min-2/(microU/ml)/(mg/dl) versus 17 +/- 6 in controls; p less than 0.05). MyD patients showed a normal tolerance with the glucose disappearance constant, KG within the normal range: 2.75 versus 2.62% min-1 in controls. In MyD patients insulin resistance was associated with a higher than normal insulin delivery for both secretory phases, although the second phase was responsible for releasing a greater amount of hormone. In conclusion MyD patients try to compensate for overall insulin resistance by a more marked pancreatic response.","PeriodicalId":11933,"journal":{"name":"Enzyme","volume":"45 1-2","pages":"14-22"},"PeriodicalIF":0.0,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468860","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"12968213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 11

Serum immunoreactive pancreatic phospholipase A2 in patients with various malignant tumors. 各种恶性肿瘤患者血清免疫反应性胰磷脂酶A2的变化。

Enzyme Pub Date : 1990-01-01 DOI: 10.1159/000468710

Y Oka, M Ogawa, Y Matsuda, A Murata, J Nishijima, K Miyauchi, K Uda, T Yasuda, T Mori

引用次数: 17

Int-2: a member of the fibroblast growth factor family has different subcellular fates depending on the choice of initiation codon. Int-2:成纤维细胞生长因子家族的一员，根据起始密码子的选择有不同的亚细胞命运。

Enzyme Pub Date : 1990-01-01 DOI: 10.1159/000468760

C Dickson, P Acland

{"title":"Int-2: a member of the fibroblast growth factor family has different subcellular fates depending on the choice of initiation codon.","authors":"C Dickson, P Acland","doi":"10.1159/000468760","DOIUrl":"https://doi.org/10.1159/000468760","url":null,"abstract":"The int-2 gene, which encodes a member of the fibroblast growth factor family, was discovered as a protooncogene transcriptionally activated following proviral insertion into adjacent chromosomal DNA. Analyses of the synthesis and processing of the int-2 protein, using an SV40-based vector to express cloned cDNA, showed four major products in the size range 27.5-31.5 kd that were associated with the secretory pathway. Further experiments using a cell-free translation system programmed with int-2 cRNA revealed a larger N-terminally extended protein. Site-directed mutagenesis of possible initiation codons confirmed that the first in-frame AUG codon would specify the start of a protein that includes a signal peptide for transport into the endoplasmic reticulum. However, protein synthesis also initiates at an upstream CUG codon to yield a polypeptide extended at the N-terminus by 29 amino acids. Immunofluorescent staining showed that a substantial proportion of the CUG-initiated protein resides in the cell nucleus, while a truncated int-2, lacking both the N-terminal extension and the signal peptide, was exclusively nuclear. These observations suggest that a nuclear localisation signal occurs in the body of the int-2 molecule, but is only accessible to the nuclear transport system if entry to the secretory pathway is compromised. Thus, the choice of initiation codon changes the subcellular fate of the int-2 protein and provides the potential for a duality of function through alternative transport pathways.","PeriodicalId":11933,"journal":{"name":"Enzyme","volume":"44 1-4","pages":"225-34"},"PeriodicalIF":0.0,"publicationDate":"1990-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000468760","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13126166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Temporal translational regulation of the protamine 1 gene during mouse spermatogenesis. 精蛋白1基因在小鼠精子发生过程中的时间翻译调控。

Enzyme Pub Date : 1990-01-01 DOI: 10.1159/000468752

R E Braun

引用次数: 53