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J Tsuji

Publications and source records attributed to J Tsuji.

41 records · Page 3Linked to original sources
PubMed1982

Double antibody enzyme immunoassay for the quantitation of adenosine 3', 5' -cyclic monophosphate (cyclic AMP) and guanosine 3', 5'-cyclic monophosphate (cyclic GMP) in tissue and plasma.

A sensitive double antibody enzyme immunoassay for the quantitation of cyclic AMP and cyclic GMP is presented. Specific antisera to each nucleotide were raised in rabbits by immunization with succinyl cyclic nucleotide-human serum albumin conjugates. For competitive reaction, antibodies were incubated with a mixture of succinyl cyclic nucleotide labelled with beta-D-galactosidase and unlabelled succinylated standard or sample cyclic nucleotides. The antibody-bound enzyme-hapten was separated from free hapten by anti-rabbit IgG immobilized to a polystyrene ball. Activity of the enzyme on the solid phase was fluorometrically determined. The assay system made it possible to ascertain values as low as 5 fmole of cyclic AMP or cyclic GMP. Cyclic nucleotides in plasma could be accurately determined by this method without requiring a deproteinizing reagent as the first step of assay.

Animals↗
PubMed1981

Enzyme immunoassay of cyclic adenosine 5', 5' - monophosphate (AMP) using beta-D-galactosidase as label.

Succinyl cyclic adenosine monophosphate (AMP) was synthesized and coupled to beta-D-galactosidase using 1-ethyl-3-(3-dimethylaminopropyl)carbodimide. An antiserum to cyclic AMP was raised in rabbits by immunization with a succinyl cyclic AMP-human serum albumin conjugate. An enzyme immunoassay of cyclic AMP was successfully performed via the competitive binding procedure using the succinyl cyclic AMP-enzyme conjugate and the antiserum to cyclic AMP. The sensitivity of this assay has been increased several hundredfold by prior 2'-O-succinylation of cyclic AMP as already described by Cailla et al. in the radioimmunoassay of cyclic nucleotides. The assay system makes it possible to ascertain values as low as 6 fmol of cyclic AMP/tube. Human plasma cyclic AMP could be accurately determined by this method without requiring a deproteinizing reagent as the first step of assay. The concentration of TCA-extracted cyclic AMP from various tissues of mice was determined by both enzyme immunoassay and radioimmunoassay. There was a good correlation between the values for cyclic AMP determined by the two methods (Y = 1.01X - 0.15, r = 0.996, n = 39). Succinylated nucleotides and nucleosides such as cyclic GMP, ATP, ADP, and AMP, adenosine, adenine, GTP, GDP, GMP, guanosine, and guanine had no effect on the immunoassay of cyclic AMP.

Animals↗
PubMed1978

Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy.

Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 +/- 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a,a') derived from P-V and normalized P-V relations, respectively, for end-diastolic myocardial elastic stiffness (ES or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (KS or KE) of the circumferential stress-strain relation. Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 +/- 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV,dP/dV/V,ES and EE and a tendency for increase in the chamber stiffness constants (a,a') and myocardial stiffness constants (KS, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid- and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.

Adult↗
PubMed1978

Evaluation of chamber and myocardial compliance in pressure overload hypertrophy.

The effect of pressure overload hypertrophy on isolated myocardial muscle preparations remains controversial. Moreover, the ultimate effect on the diastolic function of the left ventricle in the pressure overload states of man and the relative changes in chamber and myocardial stiffness remain incompletely studied. We review here the methods as well as results of dynamic diastolic stiffness analysis in 18 patients with valvular aortic stenosis and 5 normal subjects based upon the pressure-volume and circumferential stress-strain relations obtained by simultaneous left ventricular micromanometry and high-speed cineangiography. In addition, complementary analysis of dynamic diastolic stiffness findings in chronically instrumented animals, before and after the induction of hypertrophy, are reviewed. Increased diastolic intracavitary pressures during concentric hypertrophy were found to be attributable to both increased muscle mass as well as enhanced myocardial stiffness. However, both chamber and myocardial stiffness changes during hypertrophy were quite variable with some patients (and 2 of 6 dogs) showing no enhancement of stiffness parameters. In the chronically instrumented animals where dynamic, instantaneous stiffness changes and strain rates are more readily studied than in man, viscous (velocity dependent) effects were noted to be enhanced during hypertrophy. It is postulated that variable increases in diastolic stiffness during concentric hypertrophy in the intact heart results from varying degrees of myofiber architectural distortion and/or inconstant collagen content, and further correlative studies of morphology and mechanical function are needed.

Animals↗