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

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated glucose and amino acid metabolism in tumors and other organs using whole body autoradiography with a short-lived positron emitter and a long-lived beta emitter. The radioactive compounds used were 2-deoxy-2-[18F]-fluoro-D-glucose (18F-FDG) with a half life of 109.8 min and L-[methyl-14C]-methionine (14C-MET) with a half life of 5,730 years. A Donryu rat weighing about 150 g was subcutaneously inoculated at the back with experimental tumors of AH109A and AH272. 74 MBq (2 mCi) of 18F-FDG and 740 kBq (20 microCi) of 14C-MET was administered and after 30 min, the rat was sacrificed. Whole body frozen sections were obtained using autocryotome. For the 18F-FDG autoradiogram, the frozen sections were exposed to an X-ray film for 6 h. After seven days, these frozen sections were again exposed to 14C-MET for a week. Cross-contamination was minimized by adjusting the exposure time, the interval of exposures and the administered dose. The accumulation of the tracers was represented as the optical density ratio of the tissue of interest to the muscle. The tumor ratios were 12.5 for 18F-FDG and 8.6 for 14C-MET showing the highest accumulation in the whole body autoradiogram. In contrast the inflammatory tissue ratios were 1.27 for 18F-FDG and 0.77 for 14C-MET showing very low amino acid metabolism. With the present double tracer whole body autoradiogram, 18F-FDG accumulation was seen in the brain and the heart but not to the liver as against 14C-MET accumulation which was seen to the liver but not to the brain and the heart.
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PMID:[Double tracer whole body autoradiography using a short-lived positron emitter and a long-lived beta emitter]. 270 46

The modifications suffered by the colon after massive intestinal resection (RIM) have been barely studied, especially from the ultrastructural point of view. On the basis of optical microscope studies we planned this experimental study to evaluate fundamentally the ultrastructural changes in the colonic mucosa and its cellular elements. A total of 115 Wistar rats weighing 350 to 550 grams were used. Twenty animals constituted group 0 (controls), 30 underwent intestinal section (group I) and 65 were submitted to resection of 90% of the intestine (group II). After weighing, the animals were sacrificed by groups on days 15, 30, 45 and 60 of the operation to obtain histologic samples of the ascendant colon for study by transmission (MET) and scanning (MEB) electron microscopy. All the animals resected showed statistically significant weight loss (p less than 0.001), an expression of short intestine syndrome. Groups 0 (controls) and I (intestinal section) did not evidence important ultrastructural changes. In contrast, although in the initial electron microscopic scan the colonic mucosal surface offered a normal aspect, at 45 days it presented irregularities, without the appearance of villi. Days 60 there were deep folds and the mucosal surface had acquired a foliaceous aspect similar to that of the surface of the small intestine of the rat. The abundance of microorganisms adhered to the surface, constituting clumps of bacteria, was striking. Transmission electron microscopy confirmed the greater number and height of the enterocytes, covered by well-developed apical microvilli with dimensions that increased throughout the experiment. The cellular nuclei are voluminous and occasionally have various nucleoli. The cytoplasm showed changes that affected fundamentally the mitochondria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ultrastructural study of the colon after massive intestinal resection in rats]. 271 Sep 93

The existence of a relationship between cholecystokinin (CCK)-induced satiety and the serotoninergic system was evaluated. The food intake of 3-h-fasted male rats was studied after treatment with the COOH-terminal octapeptide of CCK (CCK-8) alone or in combination with one of two blockers of serotonin (5-HT) receptors, metergoline (MET; 1.0 or 0.06 mg/kg), active in both the periphery and brain, or xylamidine tosylate (XYL; 1.5 mg/kg), active only in the periphery. CCK-8 reduced food intake in the 30 min after food presentation by 37% at 2 micrograms/kg, 68% at 4 micrograms/kg, and 80% at 8 micrograms/kg compared with controls. Both doses of MET attenuated CCK-8-induced satiety, increasing food intake of rats treated with all doses of CCK-8 to control values. Food intake was significantly increased over base line by the 1.0-mg/kg dose of MET alone but unaffected by the 0.06-mg/kg dose of MET alone. XYL had no effect either given alone or in combination with CCK-8. These results indicate that the inhibitory action of CCK-8 on food intake is dependent on intact functioning of the serotoninergic system, probably at central sites.
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PMID:Cholecystokinin-induced anorexia depends on serotoninergic function. 271 55

Although digoxin is often the drug of choice to control the ventricular response in chronic atrial fibrillation, it fails to control exercise-induced increase in heart rate. The efficacy of diltiazem to control ventricular response and to improve cardiovascular performance during maximal exercise was investigated in 13 digitalized patients with chronic atrial fibrillation. A placebo controlled prospective randomized double-blind study, was preceded by open titration phase. During the diltiazem treatment phase, mean ventricular response diminished at rest (85 +/- 12 versus 107 +/- 19 during digoxin therapy and versus 101 +/- 18 during digoxin and placebo therapy; p less than 0.001), as well as during maximal exercise (142 +/- 13 versus 159 +/- 17 during digoxin treatment and versus 160 +/- 14 during digoxin plus placebo treatment; p less than 0.001). During exercise (50 W), in a subgroup of 7 patients, mean ventricular rate dropped: 109 +/- 19 versus 142 +/- 21 during digoxin treatment and versus 143 +/- 17 during digoxin plus placebo treatment; p less than 0.001). In all patients, the mean rate at rest decreased about 19.3 +/- 6.9% and at maximal exercise about 10.3 +/- 4.9%. In the subgroup of the 7 patients ventricular mean rate at a load of 50 W decreased about 23.6 +/- 7.9%. In all the patients, maximal exercise capacity improved: the MET mean value increased from 3.59 +/- 1.3 to 4.52 +/- 1.18 (p less than 0.001); the mean value of the maximum exercise (MEC), according to the Redfords formula, increased from 65 +/- 48 to 132 +/- 70 (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effectiveness of diltiazem in controlling ventricular response and improving exercise capacity in chronic atrial fibrillation. Double-blind, cross-over study]. 272 Jul 16

The aim of this study was to investigate the effects of estradiol and tamoxifen (TAM) on the growth of human endometrial carcinomas in athymic mice. Tissues from primary tumors were implanted into estradiol-treated mice. In passage 2, animals were treated with (a) placebo, (b) estradiol, (c) estradiol plus TAM, and (d) TAM alone. The size of the tumors was measured weekly. Estrogen receptors (ER) were determined with the dextran-coated charcoal method and/or ER enzyme-linked immunoassay. Progesterone receptors were measured with the dextran-coated charcoal technique. Of 16 primary tumors, 2 grew in the athymic mice and were studied further. Tumor EL was positive for ER (145 fmol/mg protein) and progesterone receptors (993 fmol/mg protein). Tumor EL in passage 2 was not significantly stimulated by estradiol, but was stimulated by a combination of estradiol and TAM. Treatments (estradiol, estradiol plus TAM, or TAM) all increased tumor growth in passage 3. Tumor BR and a metastasis BR-MET were ER and progesterone receptor negative, applying dextran-coated charcoal, ER enzyme-linked immunoassay, and immunocytochemistry. The BR and BR-MET cells contain the complete ER gene but do not express any measurable amounts of ER mRNA as quantitated by Northern blot analysis, using a complete ER complementary DNA probe. In all animal passages the growth rate was significantly higher in estradiol-treated mice compared with the control. TAM alone had some growth stimulatory effect, but much smaller than observed in the estradiol group. TAM inhibited estradiol-stimulated growth. These results suggest that estradiol and possibly TAM are capable of stimulating tumor growth in the athymic mice independently from ER, potentially through a host-mediated mechanism.
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PMID:Enhanced growth of an estrogen receptor-negative endometrial adenocarcinoma by estradiol in athymic mice. 275 9

The objective of this study was to predict the prognosis of patients who become symptomatic after having undergone coronary artery bypass grafting (CABG) using clinical and exercise test responses. A retrospective analysis was performed of all veterans referred for clinical indications to a Veterans Administration Medical Center for a treadmill test after having undergone CABG. Of 2,044 patients who were exercise tested from April 1984 to May 1987, 296 had previously undergone CABG. Clinical data considered included age, sex, medication and symptom status, history of myocardial infarction, type of myocardial infarction and time from CABG. The exercise test responses considered were MET level, maximal heart rate, maximal systolic blood pressure, chest pain pattern and ST-segment response. During a 2-year follow-up after exercise testing, there were 15 deaths, 11 nonfatal myocardial infarctions, 6 repeat CABGs and 3 percutaneous transluminal coronary angioplasties. Although MET level and maximal heart rate were significantly related to prognosis and no patient who exceeded 8 METs died, the predictive power of these exercise test responses was low and ST-segment depression was not predictive at all. The inability of the exercise electrocardiogram to predict cardiac events in patients after CABG requires the use of other methods of testing to identify those who need invasive studies and intervention.
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PMID:Use of the exercise test to predict prognosis after coronary artery bypass grafting. 278 26

Oxidation of DL-2-hydroxy 4-methylthiobutanoic acid (DL-HMB), DL-methionine (DL-MET) and L-methionine (L-MET) in chicken tissue homogenates was compared using 1-14C-labelled tracers. The pattern of oxidation of the substrates was similar at both low (0.7 mM) and high (20 mM) concentrations. The rate of conversion to 2-keto 4-methylthiobutanoic acid (KMB) was highest for DL-MET and lowest for L-MET in kidney, liver and intestinal mucosa. In breast muscle, rates for DL-MET and L-MET were similar at 0.7 mM, but DL-HMB showed the highest rate at 20 mM. Kidney contained the highest specific activity for oxidation of all three substrates. Raising the pH of liver and kidney homogenates from 7.5 to 8.6 increased the oxidation of DL-MET, exclusively. Experiments with inhibitors of D-2-hydroxy acid dehydrogenase (EC 1.1.99.6) and L-2-hydroxy acid oxidase (EC 1.1.3.15) suggested that D- and L-HMB were stereospecifically oxidized by the enzymes. KMB stimulated L-MET oxidation in kidney yet inhibited L-MET oxidation in liver homogenates. The effect of KMB on DL-MET and DL-HMB oxidation also varied between tissues. Amino-oxyacetate inhibited L-MET oxidation completely and DL-MET and DL-HMB oxidation almost completely in both kidney and liver. L-Cycloserine was less potent than amino-oxyacetate and decreased L-MET oxidation more in kidney than in liver. It can be calculated from the results that, at low substrate concentrations, the liver contributes principally to the whole body oxidation of both DL-HMB and DL-MET. At high (greater than physiological) concentrations, DL-HMB would be oxidized principally in skeletal muscle. At all concentrations, L-MET would be converted to KMB mainly in the muscle.
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PMID:Oxidation of methionine and 2-hydroxy 4-methylthiobutanoic acid stereoisomers in chicken tissues. 278 90

Abnormalities of chromosome 7 are among the most frequent cytogenetic aberrations found in MDS, including de novo cases and cases secondary to chemo- and/or radiotherapy. Since MET is located on 7q and as Cooper et al (1984) showed that MET proto-oncogene could be activated by a chemical carcinogen, we tried to evaluate whether it could be implicated in some cases of MDS. With specific probes for MET we analysed the DNA of 88 MDS patients (81 de novo and seven secondary cases). In 17 of them the RNA was also studied. We found no rearrangement or aberrant expression of MET in any samples studied. Our results, however, do not rule out point mutations or rearrangement of other regions of MET or adjacent DNA regions.
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PMID:Absence of rearrangement of proto-oncogene MET in 88 cases of myelodysplastic syndromes (MDS). 280 76

We isolated overlapping cDNA clones corresponding to the major MET protooncogene transcript. The cDNA nucleotide sequence contained an open reading frame of 1408 amino acids with features characteristic of the tyrosine kinase family of growth factor receptors. These features include a putative 24-amino acid signal peptide and a candidate, hybrophobic, membrane-spanning segment of 23 amino acids, which defines an extracellular domain of 926 amino acids that could serve as a ligand-binding domain. A putative intracellular domain 435 amino acids long shows high homology with the SRC family of tyrosine kinases and within the kinase domain is most homologous with the human insulin receptor (44%) and v-abl (41%). Despite these similarities, however, we found no apparent sequence homology to other growth factor receptors in the putative ligand-binding domain. We conclude from these results that the MET protooncogene is a cell-surface receptor for an as-yet-unknown ligand.
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PMID:Sequence of MET protooncogene cDNA has features characteristic of the tyrosine kinase family of growth-factor receptors. 281 73

We reported earlier complete linkage between cystic fibrosis and an RFLP of the met proto-oncogene revealed by the probe pmetH. Another clone, pmetD, detects another polymorphism with the TaqI restriction enzyme. Further linkage studies, now involving 22 families, have confirmed the tight linkage of cystic fibrosis to the MET and D7S8 loci. Significant allelic association was found between CF and allelic series defined by the pmetH probe.
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PMID:Further linkage data on cystic fibrosis: the Utah Study. 287 38


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