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Biomedical subjects

B Nagy

Publications and source records attributed to B Nagy.

At least 181 records · Page 10Linked to original sources

Organic compounds in lunar samples: pyrolysis products, hydrocarbons, amino acids.

Lunar fines and a chip from inside a rock pyrolyzed in helium at 700 degrees C gave methane, other gases, and aromatic hydrocarbons. Benzene/methanol extracts of fines yielded traces of high molecular weight alkanes and sulfur. Traces of glycine, alanine, ethanolamine, and urea were found in aqueous extracts. Biological controls and a terrestrial rock, dunite, subjected to exhaust from the lunar module descent engine showed a different amino acid distribution. Interpretation of the origin of the carbon compounds requires extreme care, because of possible contamination acquired during initial sample processing.

Amino Acids↗

Saturated hydrocarbons in bovine liver.

A homologous series of n-alkanes (C(14)-C(33)) and two isoprenoid hydrocarbons, 2,6,10,14-tetramethylhexadecane (phytane) and 2,6,10,14-tetramethylpentadecane (pristane) have been identified in bovine liver. Another branched but non-isoprenoid alkane and three isomers of molecular formula C(20)H(40) were partially identified. Phytane and the C(18)-C(22) and C(29)-C(33)n-alkanes were found to be the major components in liver, suggesting that at least the main hydrocarbon components were derived from various plants in the diet. The hydrocarbons were separated and identified by a series of steps involving solvent extraction, saponification, elution chromatography on alumina and silica gel columns, molecular sieving and by infrared and ultraviolet spectroscopy, followed by combined capillary gas chromatography-mass spectrometry.

Alkanes↗

Distribution of apolipoprotein(a) isoforms in normotensive and severe preeclamptic women.

OBJECTIVE: Preeclampsia is a pregnancy-related disorder constituting one of the primary causes of worldwide maternal and fetal mortality, but despite intensive research its pathogenesis remains unclear. Lipids have been implicated in the development of preeclampsia, although this possible association remains controversial and not yet fully investigated. This study set out to examine the potential association between lipoprotein(a) and the development of severe preeclampsia. The focus of this study was to investigate the potential utility of apolipoprotein(a) isoforms as possible diagnostic markers for identifying women at risk for developing preeclampsia. METHODS: Study participants included a control group of nonpregnant female volunteers (n = 59), a group of healthy pregnant (normotensive) female volunteers (n = 51), and a group of severe preeclamptic female volunteers (n = 59). Serum lipoprotein(a) concentrations were measured using double-antibody ELISA methods and were found to be 17.0+/-23.6 mg/dl among nonpregnant controls (n = 51), 15.9+/-15.8 mg/dl among healthy pregnant normotensives (n = 51), and 16.2+/-16.7 mg/dl in the preeclamptic group (n = 59). In addition, apolipoprotein (a) isoforms were identified using high-resolution SDS-agarose electrophoresis followed by immunoblotting. RESULTS: We detected no significant differences between the groups studied in the distribution of isoforms (Chi-square = 1.21, df = 4, P = 0.89); however, in a 1-week interval we detected a 42.2% rise in Lp(a) levels as well as a 67.1% rise in C-reactive protein concentrations among 10 volunteers in the preeclamptic group (median = 9.6; P < 0.05). CONCLUSIONS: Although the exact mechanism of pathogenesis continues to elude investigators, our results suggest that lipoprotein(a) may act as an acute-phase reactant during preeclampsia. Although our results are preliminary, they are consistent with growing evidence implicating lipids as among those factors involved in the etiology of preeclampsia. Changes in apolipoprotein(a) may be among those important biochemical markers that are found to be useful in the early identification of high-risk women and warrant further study.

Adult↗

Analysis of maternal circulation and renal function in physiologic pregnancies; parallel examinations of the changes in the cardiac output and the glomerular filtration rate.

OBJECTIVE: The aim of the study was to examine the temporal relations between the parameters of the maternal hemodynamics and homeostasis in different phases of pregnancy and the postpartum period. METHODS: Eleven healthy pregnant women were involved in the study. The value of the peripheric vasodilatation was measured by the ratio I/A of the maternal sphygmogram (I: incisure point, A: amplitude of the carotid pressure curve). The change of the cardiac output was determined by the ejection angle composed from maternal carotid sphygmogram and its first electrical derivate (dP/dT). The glomerular filtration rate (GFR) was measured with the in vitro radiofluorescent method. RESULTS: The primary peripheral vasodilatation and GFR increase occur early in the first trimester of a normal pregnancy, start to decrease at the end of the third trimester, and return to the normal value in the postpartum period. The increase of GFR precedes the increase of cardiac output. The cardiac output increases progressively from the first trimester and starts to decrease in the third trimester of a normal pregnancy. The extracellular volume increases at the beginning of first trimester progressively until the end of pregnancy and returns to the normal value in the postpartum period. DISCUSSION: The increase of GFR and the cardiac output during pregnancy are contributed to volume-establishment and to the cessation of the special "underfilled" condition of the maternal circulation in the normal pregnancy. We suppose that the maximal increase of GFR precedes the maximal increase of the cardiac output because the GFR increase is caused by maximal renal vasodilatation. The increase of cardiac output is caused in the first trimester by the shunt effect of the enhanced renal blood flow of maternal kidneys, and in the second and third trimester by the shunt effect of the feto-placental unit and the shunt effect of the maternal kidneys.

Adolescent↗

Plasminogen activator activity in clonogenic cell populations separated from a murine fibrosarcoma.

Tumor cells from a murine fibrosarcoma (FSa) produce plasminogen activator (PA), a protease that converts the zymogen plasminogen into the trypsin-like enzyme plasmin. Several studies indicate that tumor cell invasion is accompanied by proteolysis and that PA, generated by highly malignant cells, is by far the most ubiquitous protease associated with malignant transformation. Subpopulations of FSa cells were isolated by using density gradient centrifugation and the ability of these populations to form lung colonies was compared with their associated levels of PA production. Five populations of cells from a murine fibrosarcoma were separated in continuous gradients of Renografin in the density range 1.05-1.18 g/cm2. The PA activities of an unseparated control cell lysate and cell lysates of the five separated populations were determined by using [125I]fibrin as a substrate in a reaction between cell lysate and plasminogen. The assay was based on the release of digested [125I]fibrin from the surface of Petri dishes into the supernatant solution, and the results were expressed as a percentage of the total radioactivity. The cell populations collected at densities of 1.05 and 1.09 (B1, B2) were the more clonogenic with relative clonogenic efficiencies of 2.6 and 3.3 times that of the unseparated tumor population, respectively. Analysis for PA demonstrated that enzyme formation was restricted mostly to these two populations. Cells from populations 4 and 5 did not secrete increased amounts of PA and had reduced clonogenic efficiencies compared with the unseparated FSa control population. These results are consistent with the hypothesis that PA activity is correlated with the clonogenicity of tumor subpopulations isolated from a heterogeneous and complex tumor system such as the FSa.

Animals↗

Application of aspartic acid racemization to forensic odontology: post mortem designation of age at death.

The extent of racemization of aspartic acid in the dentin of healthy, carious and impacted teeth was used to define the ages of individuals at the time of their death. These determinations were performed with an error of +/- 4 years. This method holds the promise of simplifying procedures in, and extending the application of forensic odontology. The current error range of this method may be reduced by analyzing teeth of the same positional types from deceased individuals of known age. Using this method, it appears that post mortem preservation of up to 10 years has a negligible effect on the values determined for the age of individuals at death.

Adolescent↗