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Biomedical subjects

J Hradec

Publications and source records attributed to J Hradec.

At least 73 records · Page 4Linked to original sources
PubMed1988

The nature of cardiac hypertrophy in acromegaly: an echocardiographic study.

M-mode echocardiography was used to study cardiac involvement in 78 patients with acromegaly. Proportionate concentric or eccentric left ventricular hypertrophy (LVH) was a common finding. Calculated left ventricular mass (LVM) was increased significantly in a hormonally active disease group compared to an inactive disease group or a control group (153 +/- 7 vs. 96 +/- 8 and 89 +/- 3 g/m2 resp.; p less than 0.001 for both). The increase of LVM in hormonally active disease is due to predominantly LV dilatation, whereas associated hypertension, if present, aggravates the LVH exclusively due to thickening of the LV wall. Hypocorticalism, if present, does not influence the degree of LVH. Asymmetric septal hypertrophy was not found to be specific for acromegaly and was seen in only 7.7% of patients. There was no correlation between LVM and both the plasma levels of growth hormone and duration of disease. On the basis of a retrospective analysis of LVM in successfully treated patients the authors conclude that specific heart muscle disease in acromegaly, manifesting itself as LVH, is slowly reversible after cessation of the growth hormone hyperproduction.

Acromegaly↗
PubMed1986

Comparison of M-mode echocardiography and angiography in the evaluation of left ventricular hypertrophy.

The authors analysed in a group of 82 patients with a symmetric left ventricle and a homogeneous ventricular wall thickness the reliability of M-mode echocardiography in recognizing left ventricular hypertrophy. In concentric hypertrophies, a sufficient diagnostic criterion is ventricular wall thickness. Measurement of the interventricular septum offers a better correlation with angiographic values (r = 0.609, p less than 0.001) than measurement of the posterior wall (r = 0.358, p less than 0.01); a correct diagnosis can be determined in 84%. In excentric hypertrophies, the hypertrophy must be assessed on the basis of calculating the left ventricular mass. The most accurate of echocardiographic methods proved to be the calculation according to the authors' own formula (r = 0.760, p less than 0.001), which recognizes left ventricular hypertrophy correctly in 85%. The diagnostic correctness of Teichholz' formula is 80% and of the cubic formula 74%. Fortuin's equations proved to be of no value for documenting ventricular hypertrophy. In a group of 13 patients with hypertrophic cardiomyopathy, the correlation between angiographic and echocardiographic values of the left ventricular mass was very low (r = 0.534, p = 0.05).

Angiography↗
PubMed1986

A critical appraisal of M-mode echocardiography in mitral stenosis.

The reliability of M-mode echocardiography in confirming mitral stenosis and in assessing its severity was tested in 39 patients with mitral stenosis. None of the conventional echocardiographic signs of mitral stenosis is absolutely reliable. Unless at least 2 signs are combined, the diagnosis is not conclusive (sensitivity = 0.97, specificity = 1.00). Of a number of echocardiographic parameters and equations recommended (as tools) to determine the severity of mitral stenosis, the early diastolic velocity of anterior leaflet opening (EF) is the only one with a statistically significant relationship to the mitral valve area (MVA) calculated by Gorlin (r = 0.712, p less than 0.001), and this only in uncomplicated unoperated mitral stenoses, but not in mitral restenoses and combined mitral defects. Even the recently published Seitz's equation for calculating MVA from echocardiographic data is not reliable. M-mode echocardiography is an excellent technique for the primary diagnosis of mitral stenosis. However, it is not suitable to even an approximate assessment of its haemodynamic severity.

Calcinosis↗
PubMed1985

The role of cholesteryl 14-methylhexadecanoate in the function of eukaryotic peptide elongation factor 1.

The binding of [3H]cholesteryl 14-methylhexadecanoate by a highly purified peptide elongation factor 1 from rabbit reticulocytes is significantly enhanced by GTP and CTP, much less by guanosine 5'-[beta, gamma-methylene]-triphosphate and not at all by ATP or UTP. Removal of endogenous cholesteryl 14-methylhexadecanoate present in the molecule of the factor [Hradec, J. et al. (1971) Biochem. J. 123, 959-966] by digestion with immobilized cholesterol esterase resulted in an almost complete loss of GTPase activity and this could be restored to nearly normal values by the addition of the ester. The same holds true for the GTP-dependent autophosphorylation of the protein-synthesis factor. Cholesteryl 14-methylhexadecanoate was bound only by the beta subunit of the factor. Addition of the alpha subunit, which was inactive on its own, stimulated the binding of the ester to the beta subunit in a sigmoid dependence. The binding of the ester was significantly stimulated by aminoacyl-tRNA but this effect was fully abolished by sodium fluoride, indicating a relation of cholesteryl 14-methylhexadecanoate to the dephosphorylation of the peptide elongation factor. Treatment of the factor with cholesterol esterase decreased its activity in the poly(U)-dependent binding of phenylalanyl-tRNA to ribosome and this activity was again restored by the addition of cholesteryl 14-methylhexadecanoate. The ester thus interacts with the GTP-dependent autophosphorylation of peptide elongation factor 1 and in this way modulates the activity of the factor. A putative scheme is presented explaining the mode of action of cholesteryl 14-methylhexadecanoate.

Animals↗
PubMed1985

Regulation of the activity of eukaryotic peptide elongation factor 1 by autocatalytic phosphorylation.

Highly purified peptide elongation factor 1 from rabbit reticulocytes liberates the terminal phosphate from [gamma-32P]GTP and incorporates it into its own protein. Approximately one phosphate residue becomes bound by one molecule of the factor. Only the eEF-1 alpha subunit of the factor (Mr 53 000) becomes phosphorylated as revealed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate followed by autoradiography and by the incubation of [gamma-32P]GTP with individual subunits of the elongation factor separated by chromatofocusing in the presence of 5 M urea. The phosphorylation also takes place, though to a lesser extent, if the factor is incubated with Na2H32PO4, probably due to the presence of endogenous GTP bound in the molecule of the factor. The content of endogenous GTP in various factor preparations was 0.21-0.43 mol/mol factor. Phosphorylation of the peptide elongation factor is ribosome-independent, acid-labile and apparently autocatalytic since no other proteins are required for this reaction. Preincubation of the factor with GTP or with inorganic phosphate results in the phosphorylation of the factor and is followed by an enhanced binding of phenylalanyl-tRNA to 80S ribosomes in the presence of poly(U). This is accompanied by a dephosphorylation of the factor protein and thus the reversible autophosphorylation of the factor apparently activates its binding site for aminoacyl-tRNA. This is supported by the observation that sodium fluoride, which inhibits the dephosphorylation of the factor, blocks the factor-catalyzed binding of aminoacyl-tRNA to ribosomes. The incorporation of phosphate into factor protein also inhibits the formation of an eEF-1 X GDP complex, which is inactive in protein synthesis. Thus GDP liberated by the GTPase activity of the factor cannot affect its binding site for aminoacyl-tRNA. This may be the other reason for the enhanced activity of the phosphorylated factor. The autocatalytic GTP-dependent phosphorylation of the peptide elongation factor 1 apparently modifies its function and may thus play a regulatory role in protein synthesis.

Animals↗
PubMed1985

Septal aneurysm with associated anomalies.

A 15-year-old boy had a history of a functional systolic murmur with systolic and diastolic murmurs and radiological evidence of left ventricular hypertrophy. The angiocardiogram demonstrated an aneurysm of the membranous septum, bicuspid aortic valve, dilatation of the left subclavian artery and left common carotid artery. Echocardiography showed a holosystolic prolapse of the mitral valve with mitral insufficiency and a bicuspid aortic valve with insignificant incompetence of the aortic valve. Classical TM mode echocardiography did not show an aneurysm of the membranous septum.

Adolescent↗
PubMed1985

Microsome-mediated alkylation of rat liver initiator tRNA by 3,3-dimethyl-1-phenyltriazene and its ring-chlorinated derivatives.

3,3-[3H]Dimethyl-1-phenyltriazene, 1-(4-chlorophenyl)-3,3-[3H]dimethyltriazene and 3,3-[3H]dimethyl-1-(2,4,6-trichlorophenyl)-triazene methylate initiator tRNA in vitro only after pre-incubation with microsomal enzymes and NADPH. The finding confirms that procarcinogenic dialkyl aryltriazenes must be enzymatically converted into reactive metabolites, presumably into the corresponding monoalkyltriazenes, which ultimately react with tRNA. The methylation at 37 degrees C requires 40-60 min and individual triazenes showed differential alkylating capacity if tRNA was the limiting factor. Enzymatic hydrolysis of the modified initiator tRNA, followed by separation of nucleosides on Sephadex G10 or Dowex 50 columns, revealed that 7-methylguanosine was the principal labelled product. The methylated tRNA showed a significantly increased acceptance for L-methionine. It appears that methylation of initiator tRNA at N7 of guanine affected the conformation of initiator tRNA and rendered the nucleic acid more accessible for cognate aminoacyl-tRNA synthetase.

Alkylation↗
PubMed1985

Cardiac involvement in progressive polyarthritis--an echocardiographic study.

Echocardiographic, electrocardiographic and roentgenologic examinations were performed in 50 patients with progressive polyarthritis without clinical signs of pericardial affection. At the same time, laboratory signs of the activity of the disease were evaluated. Using one-dimensional echocardiography, pericardial effusion was detected in 27 patients (54%). Neither valvular involvement nor specific changes in the myocardium were found. In the serum of patients with pericardial effusion the presence of the rheumatoid factor was statistically significantly more frequent than in patients without effusion. Patients with steroid therapy of the primary disease and a statistically significantly lower incidence of effusions than patients who were subjected to other forms of treatment. Echocardiography again proved to be the only sensitive non-invasive method capable of detecting small and medium-sized effusions.

Adrenal Cortex Hormones↗