Significant correlations between atmospherics and the in vivo incorporation of 3H-thymidine into the nuclear DNA of liver cells.
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Biomedical subjects
Publications and source records attributed to G Ruhenstroth-Bauer.
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In primary cultures of rat hepatocytes the induction of 3H-thymidine uptake into DNA of liver cells by the liver cell proliferation factor hepatopoietin demonstrates that this factor is active not only in vivo but also in vitro. Addition of the mushroom toxins alpha-amanitin or phalloidin to liver cell culture decreased the uptake of 3H-thymidine into hepatocytes (in the absence or presence of hepatopoietin) as well as the attachment of the hepatocyte cultures. Mushroom toxins also inhibited the production of plasma proteins in hepatocyte cultures. The inhibition, observed at toxin concentrations from 10(-5) to 10(-7) M, was dose-dependent. At low concentrations of phalloidin the inhibition appears to be selective for certain proteins.
After partial hepatectomy the normal low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormone, the so-called hepatopoietin. This glycoprotein is organ-specific but not species-specific, i.e. an extract from rats is also active in mice. In order to examine the influence of selenium on liver cell proliferation, male albino NMRI mice were fed a selenium-deficient diet containing less than 10 ppb Se for at least 2 months (Se-). In the plasma protein profile and in the basic DNA synthesis rate of Se(-)-animals, no significant changes were observed compared to controls. However, liver cell proliferation induced by hepatopoietin or by partial hepatectomy was increased about 3-fold in Se-deficient mice. We assume a compensated metabolic Se-deficiency state in mice under these nutritional conditions, which leads to expression of enhanced metabolic capacity when induced by stress.
In a previous clinical study it was found that patients with coronary heart disease and diabetics with peripheral artery disease often have an elevated erythrocyte aggregation value (AW) and that there is a positive correlation between AW and the number of risk factors found in a subject. In the present investigation we studied the relationship between AW and the serum concentration of high density lipoprotein cholesterol (HDL-C), which is known to be inversely associated with coronary heart disease (CHD) incidence. We found highly significant negative correlations between AW and HDL-C both in a subsample of the study population of a cross-sectional epidemiologic study on CHD risk factors (First Survey of the MONICA Project Augsburg) and in male patients with angiographically confirmed CHD. Correlation coefficients were -0.233 for normal men (P less than 0.01, n = 136), -0.261 for normal women (P less than 0.01, n = 117), and -0.745 for CHD patients (P less than 0.01, n = 14). The results support the concept that the erythrocyte aggregation value as an indicator of cardiovascular risk is consistent with established risk factor associations.
Release of leukotriene B4 (LTB4) and leukotriene C4 (LTC4) from neutrophils and platelet-neutrophil suspensions in response to ionophore A23187 was measured in 12 multiple sclerosis (MS) patients and 8 healthy volunteers. LTC4 release from neutrophils, as well as from platelet-neutrophil suspensions, was significantly decreased in MS patients compared with the controls. There was no significant difference in the release of LTB4 between MS patients and controls. The findings suggest that permanent stimulation of platelets and neutrophils e.g., by encephalitogenic peptide leads to continuous LTC4 release with subsequent depletion of intracellular substrates serving as precursors for the formation of 5-lipoxygenase products. Since the target of microvascular actions of LTC4 are postcapillary venules, the release of this sulfidopeptide leukotriene might play a pathogenetic role in the formation of MS lesions.
In recent years it has been shown that atmospherics of different frequencies correlate with the onset of epileptic fits and myocardial infarctions. In the present retrospective study (1984) on more than 500 patients with acute hearing loss residing in the Munich area, a statistically significant correlation to atmospherics was also established.
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The date of occurrence of a heart infarct was tabulated for 162 patients admitted to four Munich clinics with cardiology departments from January 1 to July 31, 1981. This occurrence calendar was correlated with the daily average density of 28 KHz and 10 KHz atmospheric (atm) impulses and several classic weather parameters. The occurrence of heart infarcts has a certain positive correlation with the increased appearance of "pure" 28 KHz impulses, the correlation with 10 KHz impulses is very slight. Among the classic weather parameters, the average daily humidity has the highest negative correlation coefficient.
The erythrocyte aggregation value (AW) has been determined in groups of patients with and without coronary heart disease (CHD) and in a group of apparently normal subjects, using the Metricell apparatus as described by Kachel et al. The following results were obtained: There was a close correlation between the AW and the existence of CHD or arteriosclerosis of peripheral arteries. The precision of the retrospective prediction of CHD by this noninvasive test in male subjects aged over 45 years (total CHD prevalence = 0.494) was: sensitivity = 0.571, specificity = 0.767. The predictive value of positive tests (PVpos) was 0.706, of negative test (PVneg) 0.647. The discriminatory ability of the AW test was superior to that of serum cholesterol determinations or measurement of other CHD risk factors made in the same population. The AW rises exponentially with the total score for risk factors for CHD hazard for the subject. It appears, however, from the insignificant correlations observed that there is no direct connection between the AW and any single risk factor.
The uptake of macromolecules by erythrocytes can be achieved with the electrical breakdown technique [2, 4]. In this technique the erythrocyte membranes are subjected to a high external electrical field pulse for a short period. Local, reversible breakdowns of the cell membrane occur above a critical field strength which lead to a time-dependent increase in the permeability of the membrane. By this means, human erythrocyte membranes can be made permeable to DNA, pharmaceutical compounds, and latex particles following an electrical field pulse [1, 3, 5]. Larger particles should also be taken up by erythrocytes using this method. Vienken et al. [5] demonstrated the entrapment of latex particles with a diameter of 0.091 micron in human erythrocyte ghosts, although this was shown with only a single electron micrograph which does not prove that the ghost membrane was intact. In our experiments in order to entrap latex particles with a diameter of 0.26 micron rat erythrocytes were subjected to an electrical field pulse of 12 kV/cm with a decay time of 60 microseconds. Experiments using the electron microscope show that after such an electrical field pulse the uptake of latex particles by rat erythrocytes follows the stomatocytotic pathway. We show further that using electron microscopic techniques, a single section cannot demonstrate the completed uptake of a latex particle by the erythrocyte.
After partial hepatectomy the low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormon, the so-called hepatopoietin. The hormon originates from the Peyer's patches: after their resection, the liver cell proliferation after partial hepatectomy decreases by about 80%. Hepatopoietin effects organ specific but species nonspecific.
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The aim of the present study is to investigate the capacity of damaged rat liver cells to respond to a second inflammation by a change in plasma protein profile, while the first inflammatory process is in progress. Quantitation of these effects would be useful, especially in situations where patients are suffering from complications due to emergence of a new pathological factor. We therefore studied the effect of phalloidin on rat livers already made necrotic by oral intubation of CCl4. Our data showed that a decrease in acute-phase response does not necessarily always imply healing, but may also be indicative of a second pathological complication.
As a result of traumata, cancer or chemical poisoning the level of acute-phase proteins released by the liver undergoes a significant change which can be measured by two-dimensional immunoelectrophoresis. To investigate whether inflammatory reactions following chemical poisoning, tissue necrosis or other treatments result in an uniform change of the plasma protein profile, we examined quantitatively the change in plasma protein profile in the following model situations: 1) alloxan-induced diabetes in rats, 2) thioacetamide-induced liver cirrhosis and 3) ixoten-induced blocking of DNA synthesis in rat liver. Even though the three agents used in the present study or their metabolites directly interacted with liver cells, they did not evoke a uniform change of the plasma protein profile.
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