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)

In view of uncertainties about the best way to estimate mean alveolar gases in patients with ventilation-perfusion inequalities, three different methods were evaluated on 54 patients. 1) O2 and CO2 were recorded by mass spectrometer on an O2 (x)-CO2 (y) diagram. The coordinates at the intersect of the expiratory record with the mixed expired R line (RE) ives the mean alveolar values (PAo2 and PAco2. 2)pa'co2 was calculated with the Bohr equation using a predicted anatomic dead space and PA'o2 was derived with the alveolar equation. 3) End-tidal (ET) P02 were averaged over 1 min at rest in steady state. Mean RET calculated from 3 was identical with RE. Mean values for PAco2, PA'CO2. and PETco2 differed by less that 1 Torr, but the variance was least with the end-tidal method. There was a highly significant correlation between delta aAPco2 using PETco2 and VD/VT, better than with either of the other methods. The end-tidal measurement appears to give the best approximation of mean alveolar gas in pulmonary patients.
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PMID:Mean alveolar gases and alveolar-arterial gradients in pulmonary patients. 43 24

Five cases of radiation myelopathy were found in a total of 10,000 cases given radiotherapy from 1968 to 1977. The clinical presentation and treatment details including the total dose, treatment volume, number of fractionations, overall time, and the RET value at the spinal cord were calculated and compared with other reports on this subject. The total number of fractionations ranged from 20 to 26 with an overall time of 32 days to 37 days. The dose received by four patients ranged from 1030 to 1900 RET, a little higher than the tolerance level of the spinal cord as compared to reported values. Two patients in this series had high blood pressure. The incidence of radiation myelopathy, already acceptably low, could possibly be reduced further by meticulous planning of radiation.
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PMID:Radiation myelopathy. 44 80

A table has been devised to allow rapid determination of the RET and TDF values for five-day a week therapy schemes which might be included in realistic treatment planning. 2. The table allows easy comparison of the RET and TDF values for different fractionation schemes or, conversely, the devising of equivalent fractionations for similar RET and TDF values. 3. Utilizing the decay tables of Orton and Ellis, it is possible to utilize the table for determining rapidly the total TDF for interrupted or split course treatment regimens. 4. In those departments which treat four days, rather than five days, per week, a table devised on the four-day treatment schedule could easily be devised.
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PMID:A table for the rapid determination of RET and TDF values. 121 6

Thirty-one new RFLP systems corresponding to 24 loci have been identified from a chromosome 10-specific cosmid library. Twelve of the markers on the proximal long arm (cen-q11.2) of this chromosome, including four RFLP systems for the RET locus, will be especially useful in efforts to identify the gene responsible for multiple endocrine neoplasia type 2A (MEN2A). The new panel of markers also may contribute to fine-scale mapping of tumor suppressor genes associated with glioblastoma multiforme or renal cell carcinoma, because allelic deletions in these tumors have implied the presence of a tumor suppressor gene(s) on chromosome 10.
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PMID:Thirty-one new RFLP systems detected by twenty-four DNA markers on human chromosome 10. 134 81

Genetic linkage mapping and contig assembly using yeast artificial chromosome (YAC) technology form the basis of our strategy to clone and define the genomic structure of the pericentromeric region of chromosome 10 containing the multiple endocrine neoplasia type 2A gene. Thus far YAC walks have been initiated from five chromosome 10 pericentromeric loci including RBP3, D10S94, RET, D10Z1, and FNRB. Long range pulsed-field gel electrophoresis maps are constructed from the YACs isolated to define clone overlaps and to identify putative CpG islands. Bidirectional YAC walks are continued by rescreening the YAC library with sequence-tagged site assays developed from end-clones. Several new restriction fragment length polymorphisms and simple sequence repeat polymorphism markers have been identified from the YAC clones. In particular, two highly informative (CA)n dinucleotide repeat markers, sTCL-1 from proximal chromosome 10p (16 alleles, PIC = 0.68) and sJRH-1 from the RBP3 locus (18 alleles, PIC = 0.88), provide useful reagents for a polymerase chain reaction-based predictive genetic test that can be performed rapidly from small amounts of DNA.
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PMID:Isolation of YAC clones from the pericentromeric region of chromosome 10 and development of new genetic markers linked to the multiple endocrine neoplasia type 2A gene. 136 7

The in vivo micronucleus test is conventionally performed using mouse bone marrow cells (BM assay). Using phenacetin as a test chemical, an alternative method using reticulocytes (RET assay) was examined to determine if this could be substituted for the BM assay. Single doses of 400, 600, and 800 mg/kg gave negative results 24 h after i.p. administration, but positive results were obtained with 600 and 800 mg/kg after 48 h. Responses were weak at 72 h. Double treatment enhanced the responses; 400 mg/kg gave a positive result. Maximum responses were generally reached 24 h after the second treatment, 48 h if doses were highly toxic. When the BM and RET assays were compared, the BM assay seemed to be slightly more sensitive than the RET assay; double treatment was superior to a single treatment in both BM and RET assays. Both assays can be used routinely but in the RET assay, sequential samples can be obtained from the same individuals without killing them, providing a firm basis to substitute it for the BM assay. Taking advantage of this characteristic of the RET assay, a regimen of double treatments and double sampling at 24 and 48 h is recommended for a wide range of doses. These data were obtained with CD-1 mice; MS/Ae mice gave a higher incidence of micronuclei than did the CD-1 strain.
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PMID:The micronucleus test with peripheral reticulocytes from phenacetin-treated mice. 137 99

A combined cytogenetic and molecular analysis was performed on 11 cases of papillary thyroid carcinoma. A simple karyotypic abnormality was detected in five tumors, whereas six had no apparent chromosome change. In four of five rearranged cases the presence of a specific chromosomal abnormality involving chromosome 10 (cases 1 and 2) and chromosome 1 (cases 3 and 4) was associated with the rearrangement of two protooncogenes: RET and NTRKI (formerly trk), respectively, with different donor genes. Moreover, the chromosomal localization of the involved genes and the type of chromosomal change observed suggested that RET and NTRKI activation occurred by intrachromosomal rearrangements. The six cases with normal karyotype did not show RET or NTRKI activation. These findings suggest that a combined cytogenetic and molecular approach would be useful in understanding the pathogenesis of thyroid neoplasia.
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PMID:Cytogenetic and molecular genetic characterization of papillary thyroid carcinomas. 138 73

In papillary thyroid carcinomas, we have identified two tumor-specific rearrangements of the RET proto-oncogene leading to the formation of different transforming fusion products sharing the tyrosine kinase (tk) domain of the proto-oncogene and designated ptc-1 and ptc-2. We have analysed ptc-1 and ptc-2 products by immunoprecipitation with specific anti-RET antibodies followed by immunoblotting with the same reagent or with antibodies specific for phosphotyrosine (P-tyr) residues. The anti-RET antibodies were reactive with 64-kDa (p64ptc-1) and 81-kDa (p81ptc-2) proteins from lysates of ptc-1 and ptc-2 transformed cells, respectively, and identified two proteins of 140 kDa and 160 kDa from extracts of SK-N-SH, a neuroblastoma cell line previously shown to express two differently glycosylated forms of the normal RET product. The anti P-tyr antibodies, while detecting the same p64ptc-1 and p81ptc-2 proteins from ptc-1 and ptc-2 extracts, did not show any specific band in the neuroblastoma lysates. An additional set of experiments led us to conclude that, whereas the normal product of the RET proto-oncogene is a membrane-associated receptor-like molecule not intrinsically phosphorylated on tyrosine, both oncogenic forms of RET, ptc-1 and ptc-2, are constitutively phosphorylated on tyrosine, display an 'in vitro' autophosphorylation activity, are translocated from the membrane to the cytoplasm and are apparently unaffected by protein kinase C modulation.
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PMID:Identification of the product of two oncogenic rearranged forms of the RET proto-oncogene in papillary thyroid carcinomas. 143 45

RET/PTC is a transforming sequence created by the fusion of the tyrosine kinase domain of the RET protooncogene with the 5' end of the locus D10S170 designated by probe H4 and is frequently found activated in human papillary thyroid carcinomas. RET and D10S170 have been mapped to contiguous regions of the long arm of chromosome 10: q11.2 and q21, respectively. To identify the mechanism leading to the generation of the oncogenic sequence RET/PTC, a combined cytogenetic and molecular analysis of several cases of papillary thyroid carcinomas was done. In four cases the results indicated that these tumors had RET/PTC activation and a paracentric inversion of the long arm of chromosome 10, inv(10)(q11.2q21), with breakpoints coincident with the regions where RET and D10S170 are located. Therefore, a chromosome 10q inversion provides the structural basis for the D10S170-RET fusion that forms the hybrid transforming sequence RET/PTC.
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PMID:Characterization of an inversion on the long arm of chromosome 10 juxtaposing D10S170 and RET and creating the oncogenic sequence RET/PTC. 154 52

In order to compare the efficacy in preventing recurrencies of symptomatic atrial fibrillation of amiodarone (A.) and slow release disopyramide (D.RET.), 76 consecutive patients with recent onset atrial fibrillation (1 to 24 hrs.) were enrolled. In 20 (26%) conversion to sinus rhythm was obtained by electrical cardioversion, and in 56 (74%) by oral quinidine loading. Forty-one patients (group A) were assigned at random to treatment with D.RET. (250 mg twice daily) and 35 patients (group B) to amiodarone treatment (1200 mg daily for 10 days, and subsequently 200 mg daily). The two groups were similar as to age, sex and cardiac pathology. Patients were followed as to clinical condition, standard and dynamic ECG after one and three months and every three months subsequently for an average of 13.2 months (group A) and 14.1 months (group B). Six group A patients (14%) were excluded from follow-up on account of side effects which arose during the first week of treatment. Crises of symptomatic atrial fibrillation occurred in 20 patients of group A (57%) and in 11 (32%) group patients; this difference is statistically significant (p less than 0.05). Four (10%) group A patients stopped taking the drug due to side effects of an anticholinergic type, and three (8.5%) patients developed hyperthyroidism during follow-up. The authors therefore come to the conclusion that amiodarone is more effective than slow-release disopyramide in preventing recurrencies of atrial fibrillation; besides untoward side effects are less frequent with amiodarone.
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PMID:[A comparison between amiodarone and disopyramide in a delayed-release formulation in the prevention of recurrences of symptomatic atrial fibrillation]. 155 21


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