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)

Distribution within the brain of a 3-fold modified ACTH4-9 analog with a remarkably potentiated behavioral activity, 4-MET (O2), 8-d-Lys, 9-Phe-ACTH4-9, was investigated. The radioactive labeled [7-3H-Phe]ACTH4-9 analog was administered intraventricularly in urethane anesthetized rats in a dose of approximately 170 ng. Total radioactivity in CSF, measured in samples drawn from the cisterna magna, decreased over the period of 0.5-4 h after injection from 51 to 2% of the injected dose. Intraventricular injection of the ACTH4-9 analog resulted in high intact peptide levels in the brain. At 2 h after injection the distribution of radioactivity over 2500 micronm and 300 micronm frontal cut brain slices was rather homogenous. Data from distribution studies over topographically defined gross brain structures indicated that the septal area, which is involved in eliciting behavioral activities of ACTH-like neuropeptides, accumulated most of the injected radioactivity per gram wet weight. The distribution profiles within the brain of the [3H]ACTH4-9 analog and [3H]Phe showed considerable differences. Uptake studies in various brain nuclei after intraventricular administration of the [3H]ACTH4-9 analog demonstrated that the greatest part of the investigated nuclei exhibited relative low or medium uptake of radioactivity. This was also true for hippocampal and thalamic nuclei, which have been suggested as effected sites of action for ACTH peptides. Very high accumulation of radioactivity occurred only in the septal nuclei, particularly the dorsal and fimbrial septal nuclei. The results indicate selective uptake of the ACTH4-9 analog in the septal area, suggesting a possible significance of this area as a site of action of ACTH neuro-peptides.
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PMID:Distribution of a behaviorally highly potent ACTH4-9 analog in rat brain after intraventricular administration. 19 19

Out-of-hospital cardiac arrest was studied in suburban King County, Washington in an attempt to determine the impact of paramedic services on community cardiac mortality. A portion of the study area received paramedic services and the remainder received basic emergency medical technician (EMT) services. A surveillance system identified all prehospital cardiac arrest incidents. The etiology and outcome were determined. Deaths due to primary heart disease (ICDA) codes 410-414) were compared to community cardiac mortality figures for the same period of time and in the paramedic and EMT areas. Between April 1, 1976 and August 31, 1977, 1,449 deaths due to primary heart disease occurred (annual rate of 19.2/10,000 in the EMT area and 13.4/10,000 in the paramedic area). For the same period, 487 patients with out-of-hospital cardiac arrest received emergency resuscitation. The annual incidence of out-of-hospital cardiac arrest was similar in the EMT and paramedic areas (5.6 and 6.0/10,000 respectively). Proportionately more lives of persons with cardiac arrest were saved in the paramedic area than in the MET area. During this 17 month period, the reduction in community cardiac mortality was 8.4 per cent in the paramedic area and 1.3 per cent in the EMT area. These findings suggest that paramedic services have a small but measurable effect on community cardiac mortality.
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PMID:Paramedic programs and out-of-hospital cardiac arrest: II. Impact on community mortality. 42 Mar 54

Published reports indicate that normal rodent cells can grow in medium containing either L-methionine or L-homocysteine, whereas malignant rodent cells have an absolute requirement for L-methionine. Our studies with two normal human cell lines (fetal lung fibroblasts and bladder epithelial cells) exhibit equal growth in media containing either L-methionine or L-homocysteine. The same is true for five malignant human cell lines (carcinoma of the cervix [HeLa], adenocarcinoma of the breast [AlAb], acute lymphoblastic leukemia [MOLT-3], Wilms' tumor [SK-NEP-1], and reticulum cell sarcoma [T-77], whereas four other malignant cell lines (adenocarcinoma of the breast [SK-BR-2-III], the two lymphoblastic leukemias [CCRF-HSB-2 and CCRF-SB], and a neuroblastoma [SK-N-MC]) have absolute requirements for L-methionine. Two malignant cell lines, an adenocarcinoma of the lung (A549) and an adenocarcinoma of the pancreas (Capan-1), showed restricted growth under the experimental conditions used. L-Methionlinase (L-methionine-alpha-deamino-gamma-mercaptomethane-lyase, EC 4.4.1.11) at a concentration of 0.1 unit/ml leads to complete growth inhibition of cell cultures of both the normal human fetal lung fibroblasts (F-136-35-56) and the acute lymphoblastic leukemia (CCRF-HSB-2). L-Homocysteine-thiolactone in medium containing L-methioninase could partly "rescue" the normal but not the malignant cells.
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PMID:Tumor therapy by deprivation of L-methionine: rationale and results. 46 46

Indomethacin inhibits prolactin liberating effects by MET-enkefalin-NH2, a synthetic analogue of MET-enkefalin, both in intact and in ovariectomized, estradiol benzoate treated rats. The introduction of PGE1 increases the intensity of this effect. It is therefore possible to suppose that the PGs are involved as intermediaries of the prolactin relasing effect induced by MET-ENH-NH2.
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PMID:[Inhibitory effects of indomethacin on prolactin liberation induced with peptides with opium-like activity]. 54 65

Racemic and dextro forms of propranolol were equipotent in their anticonvulsant activity in normal rats by the MES test. In an attempt to determine any difference in the anticonvulsant activity of the two forms a variety of adrenergic agents were used, viz. phenoxybenzamine, reserpine, alphamethyl dopa and acetazolamide. There was no difference between the two forms, in the absence or presence of several adrenergic drugs employed. However, racemic but not dextro propranolol reduced MET, in normal as well as in nialamide primed rats.
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PMID:Beta blockade and anticonvulsant activity of propranolol. 72 Dec 51

Reserpine lowered the MET and this lowering of MET was antagonized by chloridaze-poxide but not by acetazoleamide and phenytoin. With increasing doses of reserpine the extension time in an MES test was increased and this was antagonized by all anticonvulsants tested namely acetazolamide, chlordiazepoxide, phenytoin and propranolol. High doses of reserpine abolished flexion component and this was restored by propranolol, phenytoin, atropine, chlordiazepoxide and acetazolamide.
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PMID:Interactions between reserpine and anticonvulsants on convulsion parameters. 75 Apr 90

The purpose of this investigation was to compare the results from four commonly used maximal treadmill stress tests: Balke, Bruce, Ellestad, and a continuous multistage running protocol. The results compared serial and maximal heart rate, metabolic demands, and ECG determinations. Fifty-one healthy men, 35 to 55 years of age, volunteered for this study and were dichotomized into trained and untrained subjects. Regression analyses showed all the tests to correlate highly. No significant differences were found between tests at maximum for V02, heart rate, and blood pressure, except for V02 for the Balke as compared to the running protocol (39 vs. 41 ml./Kg-min). The Balke protocol showed lower values at maximum in VE and RP than the other three tests as well as the most gradual rate of progression in MET cost (0.5 METS per minute). The increase for the Bruce and Ellestad tests was from 1 to 1.5 METS per minute, and a rapid initial increase (9 METS in the first 3 minutes) made the running test undesirable as a screening method. Although serial plots of heart rate and MET costs were similar to those previously reported for different population samples, the present data further refined these values. Finally, a nomograph comparing treadmill time and V02, max. for the Balke, Bruce, and Ellestad tests was developed from these data.
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PMID:A comparative analysis of four protocols for maximal treadmill stress testing. 96 76

Skin tumour development was studied in groups of mice painted once with 125 mug of 3-methylcholanthrene (MCA) either at 12:00 or at 24:00 MET. Eight animals were kept in each box. The animals were observed weekly for 20 months and all tumours were registered. There was no difference between the two groups of mice as regards tumour induction time or number of papilloma-bearing mice. In the groups of mice treated at 24:00 the number of skin tumours to develop was 9 per cent higher than in groups of mice treated at 12:00. This difference in papilloma yields is not statistically significant. Among female mice painted at 24:00 carcinoma-bearing animals were significantly more numerous (50 per cent) than among those painted at 12:00, whereas there was no difference between the groups of male mice. Considering the groups collectively (males + females), the intergroup difference (17 per cent) in advantage of painting at 24:00 was barely significant (0.5 less than p less than 0.10). There was no difference between the groups as regards the total number of carcinomas to occur. When the tumour yields in individual boxes were found to vary greatly. The slight increase in tumour yield after night painting correlates with the circadian variation in proliferative activity of the epidermidis. Previous reports in the literature have shown similar differences. Further investigations and better methods seem necessary before a definite conclusion can be drawn concerning a possible diurnal variation in the susceptibility of mouse skin to chemical carcinogenesis. It is also emphasized that it is necessary to exercise great caution when the results of classical epidermal chemical carcinogenesis experiments are to be interpreted. It seems necessary to observe animals for at least 15 months before any conclusion can be drawn.
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PMID:Is there a diurnal variation in the susceptibility of mouse skin to the tumorigenic action of methylcholanthrene? A study of tumour yield with special reference to the variation between cages. 98 89

In rats, propranolol potentiated alcohol and pentobarbitone hypnosis, but not barbital sleeping time, indicating enzyme inhibition as a possible mechanism of potentiation. Propranolol showed anticonvulsant effect on normal and reserpine treated rats by MES test, but showed dose related lowering of MET. Probable mechanisms are discussed.
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PMID:Central nervous system pharmacology of propranolol. 120 59

Hepatocyte growth factor (HGF), a heparin-binding polypeptide mitogen, stimulates DNA synthesis in adult rat and human hepatocytes and in several other cells of epithelial origin. Recently, it was determined that scatter factor (SF), a protein that has been shown to cause the dispersion and migration of epithelial cells in culture, is identical to HGF. Moreover, the receptor for HGF was identified as the product of the proto-oncogene, c-MET, a tyrosine kinase-containing transmembrane protein. c-MET expression has been reported in a variety of adult and embryonic mouse tissues. Similarly, we and others have demonstrated that HGF is expressed in various adult rat and human tissues. In the present study, the tissue distribution of HGF during rat development was determined by immunohistochemistry using an HGF-specific polyclonal antiserum. Between day 12 and day 19, immunoreactivity for HGF was present in various locations such as hematopoietic cells, somites, squamous epithelium of the esophagus and skin, periventricular germinal matrix of the brain, bronchial epithelium, renal collecting tubules and chondrocytes. After day 19, HGF immunoreactivity was also present in the pancreas, submaxillary glands and neural tissues. In addition to immunolocalizing HGF in tissue sections, bioreactive and immunoreactive HGF was extracted and purified from rat fetuses. Other studies demonstrated the presence of HGF and c-MET mRNA in total fetal rat, and in fetal and neonatal rat liver. Addition of purified HGF to fetal and neonatal rat liver cultures enriched for hepatocytes stimulated DNA synthesis up to six-fold over controls. These findings strongly suggest a pivotal role for this potent regulator of growth and development.
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PMID:The presence of hepatocyte growth factor in the developing rat. 128 14


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