[Congenital esophago-bronchial fistulas in adults].
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Adult↗
Biomedical subjects
M Isobe
Publications and source records attributed to M Isobe.
Prediction of pulmonary arterial pressure in adults by pulsed Doppler echocardiography.
Doppler echocardiography was used to estimate pulmonary artery (PA) pressure in 45 adult patients with various kinds of heart disease and the patterns were compared with those of 32 normal control subjects. Doppler signals obtained in the right ventricular (RV) outflow tract just proximal to the pulmonary valve and electrocardiogram were recorded simultaneously. Doppler velocity time intervals were measured as follows: RV preejection period, acceleration time from the onset of the RV ejection flow velocity to the peak, and RV ejection time. Thirty patients had PA hypertension and 16 patients had a low cardiac index. The best correlation with PA pressure was achieved by the RV preejection period/acceleration time index (r = 0.89 vs mean pressure). Sensitivity and specificity for predicting PA hypertension were 93% and 97%, respectively. Acceleration time correlated best with the logarithm of PA mean pressure (r = 0.88). Patients were separated into 2 groups according to cardiac index. In those patients with a cardiac index of less than 2.5 liters/min/m2, both RV preejection period/acceleration time and acceleration time were significantly correlated with PA mean pressure (r = 0.87) and log (PA mean pressure) (r = -0.87), respectively. However, the slope of the regression line for acceleration time and log (PA mean pressure) was significantly steeper than that for patients with a cardiac index of greater than or equal to 2.5 liters/min/m2 (p less than 0.05), whereas the relation between RV preejection period/acceleration time and PA mean pressure in the 2 groups could not be differentiated statistically from each other. Other intervals and ratios were less quantitative because of late systolic turbulent flow and individual variability.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Transmitral reversed blood flow during mid- and end diastole in constrictive pericarditis.
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Adult↗
Actively transcribed genes in the raf oncogene group, located on the X chromosome in mouse and human.
Murine and human cDNAs, related to but distinct from c-raf-1, have been isolated and designated mA-raf and hA-raf, respectively. The mA-raf and hA-raf cDNAs detect the same murine and human fragments in Southern blots of restriction enzyme-cleaved murine and human cellular DNA. The murine restriction enzyme fragments homologous to mA-raf cDNA cosegregate with mouse chromosome X in a panel of Chinese hamster-mouse hybrid cells, thus localizing the mA-raf locus to mouse chromosome X. Two independently segregating loci, detected by the hA-raf cDNA (or mA-raf cDNA), hA-raf-1 and hA-raf-2, are located on human chromosomes X and 7, respectively. The mA-raf locus and the hA-raf-1 locus are actively transcribed in several mouse and human cell lines.
Animals↗
The gene encoding the T-cell surface protein T4 is located on human chromosome 12.
The surface glycoproteins T4 and T8 define functionally distinct populations of T lymphocytes. We have obtained cDNA and genomic clones encoding the T4 molecule and used these as probes to determine the chromosomal location of this gene. Genomic blotting experiments, along with in situ hybridization analyses, indicate that the T4 gene resides on the short arm of human chromosome 12, at region p12-pter. Thus, the T4 gene is not linked to any known member of the immunoglobulin gene family, including its counterpart gene, T8, which resides on human chromosome 2 immediately distal to the immunoglobulin kappa locus.
Antigens, Differentiation, T-Lymphocyte↗
The nerve growth factor receptor gene is at human chromosome region 17q12-17q22, distal to the chromosome 17 breakpoint in acute leukemias.
Genomic and cDNA clones for the human nerve growth factor receptor have been used in conjunction with somatic cell hybrid analysis and in situ hybridization to localize the nerve growth factor receptor locus to human chromosome region 17q12-q22. Additionally, part, if not all, of the nerve growth factor receptor locus is present on the translocated portion of 17q (17q21-qter) from a poorly differentiated acute leukemia in which the chromosome 17 breakpoint was indistinguishable cytogenetically from the 17 breakpoint observed in the t(15;17)(q22;q21) translocation associated with acute promyelocytic leukemia. Thus the nerve growth factor receptor locus may be closely distal to the acute promyelocytic leukemia-associated chromosome 17 breakpoint at 17q21.
Chromosome Mapping↗
Changes in CoA pools in hepatic peroxisomes of the rat under various conditions.
Changes in peroxisomal CoA pools in the liver of fasted, diabetic, high-fat diet-fed and clofibrate-treated rats were studied. Total-CoA increased slightly in the fasted group and markedly in the diabetic, high-fat and clofibrate-treated groups. Fractionation studies showed that changes in free CoA levels were much greater in peroxisomes than in mitochondria. The concentrations of CoAs were calculated from the contents of CoAs in organelles and the changes in volume of organelles under these conditions; the concentration of total CoA in peroxisomes was higher than that in cytosol, but lower than that in mitochondria. These changes were accompanied by an increase in the activity of peroxisomal beta-oxidation. The results obtained from these experiments indicate that the peroxisomal beta-oxidation system is controlled not only at the enzyme level but also at the substrate or co-factor level.
Acetyl Coenzyme A↗
A case of Takayasu's disease with ruptured carotid aneurysm.
Recently, a number of cases of Takayasu's disease having dilatative or aneurysmal lesions have been reported. Such lesions have come to be considered important manifestations of Takayasu's disease. A case, whose right common carotid artery perforated spontaneously and became a pseudoaneurysm, without any other stenotic lesion is presented with a review of the literature. Surgical treatment was performed successfully.
Adult↗
Chromosomal localization of a human band 3-like gene to region 7q35----7q36.
Band 3, the major transmembrane protein of erythrocytes, mediates the exchange of anions across the membrane and anchors the erythroid membrane skeleton. Proteins immunologically related to Band 3 have been detected in a variety of nonerythroid cells. We have isolated a human cDNA clone that encodes a protein related to but distinct from the erythroid form of Band 3, based on the comparison of the amino acid sequence for the two proteins. The presence of the gene for the Band 3-like protein in a panel of mouse-human somatic cell hybrids containing subsets of human chromosomes correlated with the presence of human chromosome 7. In situ hybridization analysis using the c-DNA for this nonerythroid Band 3 gene further localized the gene to region 7q35----7q36 of human metaphase chromosomes.
Animals↗
Localization of the gene encoding human erythroid-potentiating activity to chromosome region Xp11.1----Xp11.4.
We have localized the human gene for erythroid potentiating activity (EPA) to the X chromosome by analysis of its segregation pattern in mouse-human somatic cell hybrids. The EPA gene has been further localized to human chromosome region Xp11.1----Xp11.4 by in situ hybridization of a molecularly cloned EPA genomic fragment to metaphase chromosomes.
Animals↗
[Biochemical assessment of the effects of coronary thrombolysis by serum cardiac myosin light chain levels].
To establish the method of biochemical assessment of effects of intracoronary thrombolysis after acute myocardial infarction (MI), the relationships between plasma creatine kinase (CK) or serum cardiac myosin light chain (LC) I levels and changes in left ventricular (LV) wall motion were evaluated. Twenty-seven cases with acute MI without previous infarction were included in this study. Intracoronary thrombolysis was successful within seven hours after onset of MI in 13 patients (reperfusion group), and 14 patients were treated in a conventional manner (control group). Peak levels of CK reached earlier in the reperfusion group (11.3 +/- 2.9 hours) than in the control group (20.9 +/- 5.3 hours). The peak appearance time of CK in the reperfusion group was significantly related to the time between the onset of MI and achievement of coronary reperfusion (r = 0.76). The relationship between total CK release and LV ejection fraction determined by cineangiography one month after onset was not good (r = -0.42). Peak levels of CK were not related to LV ejection fraction. Peak levels of LC appeared about four days after onset in both groups. Peak levels of LC were closely related to LV ejection fraction (r = -0.72). Twenty-four-hour and four-day levels of LC were also related to LV ejection fraction (r = -0.62 and -0.73, respectively). Peak levels of LC were related to asynergic area determined by biplane cineangiography.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[Nursing action and peaceful death at home--professional conference at the hospital and home nursing].
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Adult↗
Change in concentrations of myogenic components of serum during 93 h of strenuous physical exercise.
Effects of 93 h of long, strenuous ranger training on activities of creatine kinase (CK) and lactate dehydrogenase (LD), along with their isoenzymes, and on concentration of myosin light chain were examined in sera of young soldiers. Total CK activity in serum was measured before, during, and after the training. Throughout, total CK activity in serum increased steadily. At the end of the training, activity of CK-MB was increased but its activity ratio to total CK remained unchanged; the activity ratio of LD1/LD2 also was not increased, although total LD activity was increased. Myosin light chain was increased by about fourfold at the end of the training and remained high for three days thereafter. However, its concentration was much lower than in myopathies such as polymyositis and Duchenne muscle dystrophy. The increased activities in serum of total CK and CK-MB isoenzyme on strenuous physical exercise evidently were of noncardiac origin. Although CK activity was comparable with that seen in myopathies accompanied by disintegration of skeletal muscle, the relatively low concentration of myosin light chain in serum suggests minimal skeletal muscle damage.
Adult↗
The human gene encoding GM-CSF is at 5q21-q32, the chromosome region deleted in the 5q- anomaly.
Human granulocyte-macrophage colony-stimulating factor (GM-CSF) is a 22,000-dalton glycoprotein that stimulates the growth of myeloid progenitor cells and acts directly on mature neutrophils. A full-length complementary DNA clone encoding human GM-CSF was used as a probe to screen a human genomic library and isolate the gene encoding human GM-CSF. The human GM-CSF gene is approximately 2.5 kilobase pairs in length with at least three intervening sequences. The GM-CSF gene was localized by somatic cell hybrid analysis and in situ hybridization to human chromosome region 5q21-5q32, which is involved in interstitial deletions in the 5q- syndrome and acute myelogenous leukemia. An established, human promyelocytic leukemia cell line, HL60, contains a rearranged, partially deleted GM-CSF allele and a candidate 5q- marker chromosome, indicating that the truncated GM-CSF allele may reside at the rejoining point for the interstitial deletion on the HL60 marker chromosome.
Anemia↗
The obligatory intermediacy of 16,17 alpha- and 16,17 beta-epoxides in the biotransformation of androsta-5,16-dien-3 beta-ol to androst-5-ene-3 beta, 16 alpha, 17 beta- and -3 beta, 16 beta, 17 alpha-triols by male rat liver microsomes.
The C16-double bond of the biolefinic steroid, androsta-5,16-dien-3 beta-ol (delta 16-ANDO), was regioselectively oxidized by male rat liver microsomes in the presence of NADPH and EDTA to 16 alpha, 17 alpha-epoxyandrost-5-en-3 beta-ol (delta 16-ANDO 16,17 alpha-epoxide), 16 beta,-17 beta-epoxyandrost-5-en-3 beta-ol (delta 16-ANDO 16,17 beta-epoxide), androst-5-ene-3 beta, 16 alpha, 17 beta-triol (delta 16-ANDO 16 alpha, 17 beta-glycol), and androst-5-ene-3 beta, 16 beta, 17 alpha-triol (delta 16-ANDO 16 beta, 17 alpha-glycol). The microsomes hydrolyzed delta 16-ANDO 16,17 alpha-epoxide specifically to the 16 beta, 17 alpha-glycol and delta 16-ANDO 16,17 beta-epoxide to the 16 beta, 17 alpha-glycol and the 16 alpha, 17 beta-glycol in an equal ratio. delta 16-ANDO 16,17 alpha-epoxide was much more susceptible to microsomal hydrolysis than the 16,17 beta-epoxide. The xenobiotic epoxide hydrolase inhibitor, 3,3,3-trichloropropene 1,2-oxide, potently inhibited microsomal hydrolysis of delta 16-ANDO 16,17-epoxides as well as of benzo[a]pyrene 4,5-epoxide and styrene 7,8-epoxide. Addition of 3,3,3-trichloropropene 1,2-oxide accumulated the 16,17-epoxides formed from delta 16-ANDO in the reaction medium with concomitant decrease in the amounts of the 16,17-glycols formed, leading to a conclusion that the 16,17-epoxides played a role as obligatory intermediates in the microsomal delta 16-oxidation of delta 16-ANDO to the 16,17-glycols. Epoxidation of delta 16-ANDO was stereoselectively mediated by a cytochrome P-450 with quite unique properties to form the 16,17 alpha-epoxide as the major oxidation product and the 16,17 beta-epoxide as the minor. The epoxidation was strongly inhibited with CO, activated with 2-diethylaminoethyl 2,2-diphenylvalerate hydrochloride more than twice as much, and little affected with metyrapone and 7,8-benzoflavone. A pretreatment of the animals with 3-methylcholanthrene induced the delta 16-ANDO-epoxidizing activity of their microsomes 1.5 times higher than those from the control animals. However, a pretreatment with phenobarbital reduced the enzyme activity to one-half of the control microsomes. Under the same conditions, microsomal activities of hydroxylation of benzo[a]pyrene and N-demethylation of benzphetamine were significantly induced by the pretreatments with 3-methylcholanthrene and phenobarbital, respectively.
Androstenols↗
Location of gene for beta subunit of human T-cell receptor at band 7q35, a region prone to rearrangements in T cells.
The T-cell receptor is formed by two chains, alpha and beta, for which specific clones were recently obtained. In this report the gene for the beta chain of the human T-cell receptor was located on the long arm of chromosome 7, band q35, by means of in situ hybridization. This chromosome region in T cells is unusually prone to develop breaks in vivo, perhaps reflecting instability generated by somatic rearrangement of T-cell receptor genes during normal differentiation in this cell lineage.
Adult↗
Gene for alpha-chain of human T-cell receptor: location on chromosome 14 region involved in T-cell neoplasms.
A human complementary DNA clone specific for the alpha-chain of the T-cell receptor and a panel of rodent X human somatic cell hybrids were used to map the alpha-chain gene to human chromosome 14 in a region proximal to the immunoglobulin heavy chain locus. Analysis by means of in situ hybridization of human metaphase chromosomes served to further localize the alpha-chain gene to region 14q11q12, which is consistently involved in translocations and inversions detectable in human T-cell leukemias and lymphomas. Thus, the locus for the alpha-chain T-cell receptor may participate in oncogene activation in T-cell tumors.
Animals↗
Gene for the human T cell differentiation antigen Leu-2/T8 is closely linked to the kappa light chain locus on chromosome 2.
We have mapped the gene encoding the T cell differentiation antigen Leu-2/T8 to human chromosome 2 by hybridization of a Leu-2/T8 complementary DNA clone to DNA from a panel of mouse-human cell hybrids. In situ hybridization further localizes the gene to the 2p1 region in close proximity to the Ig kappa light chain gene. The Leu-2/T8 gene translocates with C kappa to chromosome 8 in a Burkitt lymphoma line carrying a t(2;8) translocation. These data support the hypothesis that Leu-2/T8 is the human homologue of the mouse Lyt-2,3 antigen.
Animals↗