The modulation of liver growth control by the tumor promoter, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), was investigated in primary hepatocytes of adult rats. Under defined conditions in serum-free cultures, the interaction of TCDD with growth-related hormones was studied. TCDD-treatment of the cultured hepatocytes for two days caused a transient stimulation of both DNA synthesis and mitotic activity. This effect was maximal at the very low nontoxic concentration of 10(-12) M TCDD, i.e., two orders of magnitude below the optimal concentrations for induction of drug metabolizing enzymes. Growth stimulation by TCDD was dependent on the presence of growth-related hormones; in primary rat hepatocytes, TCDD acted synergistically with insulin and epidermal growth factor (EGF) and antagonized the growth inhibition by dexamethasone. Under culture conditions allowing high rates of DNA synthesis, e.g., at low concentrations of dexamethasone, in the presence of EGF plus alpha 1-adrenergic agonists or rat serum, no significant effect of TCDD on cellular growth was observed. Furthermore, TCDD failed to stimulate DNA synthesis in a rat hepatoma cell line, H4IIE, which is less sensitive to growth controlling factors than normal hepatocytes. Therefore, the results suggest that the growth modulation of primary rat hepatocytes by TCDD is the most sensitive parameter of the agent thus far observed. This effect may involve both a release from the growth inhibition caused, for instance, by glucocorticoids, as well as a direct growth-stimulating effect, synergistic to the one induced by insulin.

Adrenergic alpha-Agonists↗

PubMedDate not supplied

Certification of a long-term sampling system for PCDFs and PCDDs in the flue gas from industrial facilities.

AMESA (adsorption method for sampling of dioxins) is a fully automatic system for long term monitoring of dioxin emissions from industrial processes based on the adsorption method. The system has been tested and undergoing a certification procedure according to the German guidelines for certification of systems for continuous monitoring of special substances. The certification covered parameters such as disposability of the system, reproducibility of the results and comparability of the sampling method with German and European standard methods. Furthermore break through, blanks and sample storability were investigated. The results prove that AMESA is a state of the art sampling system for continuous monitoring of dioxin/furan emissions.

Adsorption↗

PubMedDate not supplied

[Guidelines for the sociomedical assessment of performance in patients suffering from coronary heart disease (CHD)].

The following guidelines were developed for the medical assessment services of the German Federal Insurance Institute for Salaried Employees (BfA). Starting from day-to-day practice criteria and attributes to guide decisions for a systemisation of the sociomedical assessment of performance in coronary heart disease (CHD) were compiled. The guidelines aim at standardising the sociomedical assessment of performance and help to make the decision-making process more transparent - e.g. for the assessment of applications for decreased earning capacity benefits. The guidelines summarise typical manifestations of CHD and describe the necessary medical information for the sociomedical assessment of performance. Relevant assessment criteria for the medical history, clinical examination and for diagnostic tests - especially of myocardial functioning - are illustrated. The assessment of the individual's capacity is outlined, taking occupational factors into account. Following the determination of dysfunctions the remaining abilities and disabilities, respectively, are deduced and compared with occupational demands. Finally inferences are drawn regarding the occupational capacity of the individual.

Coronary Disease↗

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[Acute chorea following heart surgery with hypothermia and total bypass].

We report a 6 year old girl who developed acute chorea following cardiac surgery using hypothermia and total cardiopulmonary bypass. Rheumatic disease, cerebral embolism or hemorrhage were excluded. Cerebral hypoperfusion during surgery is the most probable cause for this neurologic event. Treatment with Tiaprid (Tiapridex) resulted in a rapid resolution of symptoms.

Brain Ischemia↗

PubMedDate not supplied

Comprehensive team care.

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Adaptation, Psychological↗

PubMedDate not supplied

Pathogenesis of carbon tetrachloride-induced hepatocyte injury bioactivation of CCI4 by cytochrome P450 and effects on lipid homeostasis.

The CCl4-induced development of liver damage was studied in monolayer cultures of primary rat hepatocytes: (1) CCl4 caused accumulation of triglycerides in hepatocytes following cytochrome P450 induction with beta-naphthoflavone or metyrapone. Ethanol or a high dose of insulin plus triiodothyronine had the same effect. (2) CCl4 increased the synthesis of fatty acids and triglycerides and the rate of lipid esterification. Cholesterol and phospholipid synthesis from acetate was also increased. (3) CCl4 reduced beta-oxidation of fatty acids as assessed by CO2-release and ketone body formation. Hydrolysis of triglycerides was also reduced. (4) The content of unsaturated fatty acids in microsomal lipids was decreased by almost 50% after incubation with CCl4, while saturated fatty acids increased slightly. (5) CCl4 exerted a pronounced inhibitory effect on the exocytosis of macromolecules (albumin), but did not affect secretion of bile acids from hepatocytes.

7-Alkoxycoumarin O-Dealkylase↗

PubMedDate not supplied

Hepatocyte damage induced by carbon tetrachloride: inhibited lipoprotein secretion and changed lipoprotein composition.

Changes of lipoprotein secretion and composition in response to CCl4 treatment were studied in monolayer cultures of rat primary hepatocytes. (1) CCl4 decreased secretion of very low density lipoproteins (VLDL) by about 85%, while high density lipoprotein (HDL) secretion was less affected (about 40%). The effect was concentration-dependent. (2) CCl4 significantly inhibited secretion of VLDL- and HDL-associated triglycerides and cholesterol esters. VLDL- and HDL-associated cholesterol was not affected, while secretion of phospholipids was increased. (3) Hepatocytes secreted the apolipoproteins B48, B100, E, C, and A-I. CCl4 reduced secretion of apoproteins associated with VLDL by almost 20%, and by about 75% when associated with HDL. The de novo synthesis of apolipoproteins was attenuated by CCl4. (4) CCl4 caused variations in the apolipoprotein composition in VLDL and HDL. CCl4 intoxication of the liver affected the morphology and/or function of the lipoproteins, which drastically impaired their ability to act as transport vehicles for lipids from the liver to the circulation.

Animals↗

PubMedDate not supplied

Mechanism of carbon tetrachloride-induced hepatotoxicity. Hepatocellular damage by reactive carbon tetrachloride metabolites.

CCl4-induced liver damage was modeled in monolayer cultures of rat primary hepatocytes with a focus on involvement of covalent binding of CCl4 metabolites to cell components and/or peroxidative damage as the cause of injury. (1) Covalent binding of 14C-labeled metabolites was detected in hepatocytes immediately after exposure to CCl4. (2) Low oxygen partial pressure increased the reductive metabolism of CCl4 and thus covalent binding. (3) [14C]-CCl4 was bound to lipids and to proteins throughout subcellular fractions. Binding occurred preferentially to triacylglycerols and phospholipids, with phosphatidylcholine containing the highest amount of label. (4) The lipid peroxidation potency of CCl4 revealed subtle differences compared to other peroxidative substances, viz., ADP-Fe3+ and cumol hydroperoxide, respectively. (5) CCl4, but not the other peroxidative substances, decreased the rate of triacylglycerol secretion as very low density lipoproteins. (6) The anti-oxidant vitamin E (alpha-tocopherol) blocked lipid peroxidation, but not covalent binding, and secretion of lipoproteins remained inhibited. (7) The radical scavenger piperonyl butoxide prevented CCl4-induced lipid peroxidation as well as covalent binding of CCl4 metabolites to cell components, and also restored lipoprotein metabolism. The results confirm that covalent binding of the CCl3* radical to cell components initiates the inhibition of lipoprotein secretion and thus steatosis, whereas reaction with oxygen, to form CCl3-OO*, initiates lipid peroxidation. The two processes are independent of each other, and the extent to which either process occurs depends on partial oxygen pressure. The former process may result in adduct formation and, ultimately, cancer initiation, whereas the latter results in loss of calcium homeostasis and, ultimately, apoptosis and cell death.

Animals↗

PubMedDate not supplied

Severe behavioural disturbance in families of patients with prolonged coma.

This paper describes the psychological dynamics among family members of patients with prolonged coma. We discuss the conflicts these families meet and how they affect their interpersonal relationships. Special focus is placed on overt and covert aggression towards the attending staff, an issue that has not received much attention. The unconscious motives underlying these overt aggressive behaviours are described, with an emphasis on how projective mechanisms come into play. We suggest a partial solution to be implemented in units treating these kinds of patients.

Adult↗

PubMedDate not supplied

[Complete congenital heart block. Its natural history and evolution].

This study describes the natural history and evolution of 67 patients with congenital auriculoventricular heart block admitted in the Instituto Nacional de Cardiología "Ignacio Chávez", Mexico, D.F. from 1944 to 1998. There were 35 (52%) females and 32 (47%) males, with mean follow up period of 93.7 +/- 104 months. Most of the patients were without structural cardiovascular disease (90%). The most frequent symptoms were dyspnea and syncope. Electrocardiograms showed a ventricular heart rate of 42.2 +/- 9 beats/minute. 85.7% of patients had a supra-Hisian complete heart block. In 31% of patients a pacemaker was implanted because syncope. Overall mortality was 4.4% and malignant ventricular arrhythmias were the principal contributors. Risk factors for mortality identified in this study were junctional escape rhythm lower than 50 beats/minute, inappropriate chronotropic response during exercise, R-R interval prolongation at night, enlargement of cardiac chambers, depressed left ventricular ejection fraction and prolonged QT interval. In all of these conditions we recommend permanent pacemaker implantation.

Adolescent↗