Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.6.1.1 (
aspartate aminotransferase
)
21,665
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Kadazans, the largest indigenous group in Sabah, northern Borneo, were surveyed for glyoxalase I, phosphoglucomutase I, red cell acid phosphatase, esterase D, adenosine deaminase, soluble glutamate pyruvate transaminase, soluble
glutamate oxaloacetate transaminase
, 6-phosphogluconate dehydrogenase, uridine monophosphate kinase, adenylate kinase, peptidase B and D, superoxide dismutase, C5, group specific component, haptoglobin and transferrin. Kadazans were found to be polymorphic for GLO I, PGM I, RCAP, esterase D,
ADA
, s-Gpt, 6PGD, UMPK, Gc, C5, haptoglobin and peptidase B. Rare variants were found for transferrin and peptidase D. No variant was found for s-Got, SOD and AK.
...
PMID:Biochemical genetic markers in the Kadazans of Sabah, Malaysia. 28 26
A random sample of 586 Basque individuals from the province of Gipuzkoa was studied for 16 genetic systems: A1A2B0, Rh, MNSs, P, Lewis, Duffy, Kell, GC, TF,
AAT
, ACP, AK,
ADA
, ESD, HP and PGM1. The results of this study indicate that the Basque population of Gipuzkoa presents certain differential values with respect to other Basque series, such as maximum values for RH*cde, AK*2 and PGM1*2+ and minimum for PGM1*1-, while the remaining alleles are located within the range of values found in the Basque population to date. It is suggested that there is intraprovincial heterogeneity, as described for Bizkaia by Aguirre et al. in 1991, and the existence of heterogeneity within the Basque population on an inter-provincial level, backing up previous studies in this respect (by Aguirre et al. in 1989 and Manzano et al. 1993).
...
PMID:Genetic polymorphisms of the Basques from Gipuzkoa: genetic heterogeneity of the Basque population. 883 Sep 16
Although IPC (ischaemic preconditioning) is considered as a protective strategy in HI/R (hepatic ischaemia/reperfusion), the mechanisms for this effect have not been fully elucidated. In the present study we investigate whether PPC (pharmacological preconditioning) by transient activation of A(1)R (adenosine A(1) receptor) protects against long-term HI/R and whether the protective effects of IPC depend on A(1)R activation and whether both preconditionings affect remote organs. Wistar rats underwent IPC and long-term HI/R. Another set of animals were pharmacologically preconditioned with the A(1)R-agonist CCPA [2-chloro-N(6)-cyclopentyladenosine; 0.1 mg/kg of body weight, i.p. (intraperitoneally)] 24 h before HI/R. In other groups, rats received an A(1)R-antagonist, DPCPX (1,3-dipropyl-8-cyclopentylxanthine; 0.1 mg/kg of body weight, i.p.) 24 h before HI/R. Hepatic damage was evaluated by transaminase [
AST
(
aspartate transaminase
), ALT (alanine transaminase)] release; inflammation was assessed by hepatic MPO (myeloperoxidase) and serum TNFalpha (tumour necrosis factor alpha) and NO; oxidative stress was estimated by MDA (malondialdehyde) and 4-HDA (4-hydroxyalkenals), SOD (superoxide dismutase) activity, GSH and
ADA
(adenosine deaminase) as adenosine metabolism. Both preconditionings protected liver and lung against HI/R as indicated by the reduction in transaminases, MPO, MDA+4-HDA, NO, TNFalpha and
ADA
activity as compared with HI/R (P<0.05). However, pre-treatment with DPCPX abolished the protective effects of IPC and PPC. Preconditionings induced a significant increase in hepatic MnSOD (manganese SOD) activity and NO generation compared with the sham group, and this activity was abolished by DPCPX pre-treatment. A(1)R activation induced hepatic delayed preconditioning and blockade of A(1)R abolished hepatic IPC. IPC, as well as PPC, were able to prevent lung damage. These protective effects are associated with a reduction in oxidative stress, inflammation and endogenous antioxidant preservation.
...
PMID:Ischaemic and pharmacological preconditionings protect liver via adenosine and redox status following hepatic ischaemia/reperfusion in rats. 1830 14
The purpose of this study was to determine serum
ADA
activity in cattle naturally infected with Theileria annulata. In this study, a total of 37 cross-bred cattle which 27 of it showing clinical signs of theileriosis constituted infected group and 10 healthy cattle as control group were used as animal materials. Infected group divided into three groups according to their PCV values. Cattle with PCV > or = 25 were put on group I (n = 9), those with PCV 13-24 were put on group II (n = 11) and those with PCV < or = 12 were put on group III (n = 7). Microscopical diagnosis of the disease was also made. Hematological parameters, serum enzyme activities (
ADA
,
AST
, ALT and ALP) were determined in all cattle. Hematological results revealed that significant progressive decreases in HGB, PLT, PBML counts and ratios from group I onwards to group III, whereas the WBC, PBPL counts and ratios showed an increase from group I onwards to group III. The serum
ADA
,
AST
, ALT and ALP activity increased significantly in all infected groups compared to control group. However, these parameters were also observed to decrease progressively from group I to group III. Furthermore, the highest increase in enzyme activities observed in the infected group I. But, these enzyme's activities started to decrease in infected group II and III in parallel with PBML and PLT counts. Eventhough, this decrease did not reach to the values obtained from control group. On the contrary, PBPL counts and ratios increased in infected group II and III in contrast to decrease in PCV. As a result, increased serum
ADA
activity in tropical theileriosis may reflect the involvement of the cellular immune responses.
...
PMID:Determination of adenosine deaminase activity in cattle naturally infected with Theileria annulata. 1857 73
Due to the irregular of diet and overfeeding greasy and surfeit flavor closely associated with hyperuricemia disease, the lipid emulsion containing high cholesterol was used to model. To obtain a more stable and sustained animal model for the efficacy evaluation of traditional Chinese herbs, we observed the influence on the serum uric acid of rat induced by the lipid emulsion compared with high purine diet. 36 SD male rats were randomized to the normal control group, high purine diet group and lipid emulsion group respectively. The general behavior, body weight and daily food intake of rats were observed. The orbital blood was taken to separate into the serum and 24 hours urine was collected. The serum indexes such as UA, BUN, Cr, ALT,
AST
, TC, TG, LDL-c were determined every 2 weeks, and XOD,
ADA
enzyme activity were determined at the 4th week. The urine indexes such as UA, Cr and Cua/Ccr were determined at the 4th week. After stopping modeling, the serum UA were determined two weeks and four weeks later respectively. At the 2nd week, the body weight and daily food intake of rats in the lipid emulsion group reduced significantly, and the level of serum UA, BUN, Cr, TC, LDL-c, ATL,
AST
raised significantly meanwhile TG reduced. At the 4th week, the serum UA in high purine diet group did not raise, and the serum XOD raised obviously while
ADA
did not; the serum UA in lipid emulsion group was higher significantly, and the serum XOD and
ADA
raised while Cua/Ccr reduced obviously. At the 6th weeks, the serum UA in both the high purine diet group and lipid emulsion group raised obviously. After stopping modeling, the serum UA in lipid emulsion group still maintained a high level at the 2nd week and back to the normal level at the 4th week. Compared with high purine diet, the hyperuricemia model induced by lipid emulsion forms earlierand more stable. It maybe has great value to study the pharmacodynamics of traditional Chinese medicine treatment to hyperuricemia disease. Its mechanism may be related to increasing XOD and
ADA
enzyme activity which can promote uric acid synthesis, meanwhile inhibiting of uric acid excretion.
...
PMID:[Rats hyperuricemia model established by lipid emulsion simulating irregular of diet]. 2639 Jun 65