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Biomedical subjects

J Berndt

Publications and source records attributed to J Berndt.

At least 19 recordsLinked to original sources
PubMed2006

Secondary electron emission of carbonaceous dust particles.

In this paper we present measurements of the secondary electron emission yield (gamma) of a carbonaceous dust particle material, which was grown in argon diluted acetylene plasmas. One aim was to reach a better understanding of charging and discharging processes of dust particles in complex plasmas due to secondary electron emission and consequently to try to explain the anomalous behavior of electron density observed in afterglows of pulsed rf plasmas. We compared the results of a simple model and of a Monte Carlo simulation to the previously measured time dependence of the electron density in complex plasma afterglow. It was found that the value of the intrinsic secondary electron yield from the carbonaceous dust material is too low to explain the increase of electron density in the afterglow. It is, however, possible that the electrons charging the particles are weakly attached so that they may be released with high efficiency by ion bombardment due to field induced emission or by other mechanisms.

Journal Article↗
PubMed2002

Water maze training in aged rats: effects on brain metabolic capacity and behavior.

The effects of Morris water maze training on brain metabolism and behavior were compared between aged (20-22 months) and young (2-4 months) Fischer 344 male rats. Each group had yoked controls, which swam the same amount of time as the trained rats but without the platform. This was followed after 9 days by quantitative histochemical mapping of brain cytochrome oxidase, the terminal enzyme for cellular respiration. The aged rats spent a significantly lower percent of time in the correct quadrant and had a longer latency to escape to the hidden platform, relative to the young rats. Metabolic differences between trained aged and young rats were found in regions related to escape under stress: perirhinal cortex, basolateral amygdala and lateral habenula; and vestibular nuclei that guide orientation in three-dimensional space. These differences were not found in the yoked swimming rats. The results suggest that, at the time point investigated, water maze training in aged Fischer 344 rats produces altered oxidative energy metabolism in task-relevant limbic and vestibular regions.

Aging↗
PubMed1999

Malignant myoepithelioma of the vulva resembling a rhabdoid tumour.

AIMS: We report an example of malignant myoepithelioma of the vulva, which has not been hitherto described. We discuss the differential diagnosis and briefly review the literature. METHODS AND RESULTS: The lesion was found in an 81-year-old woman as an indolent 40 mm tumour. The neoplastic cells showed a myoid, spindled, epithelioid and plasmacytoid phenotype. Hyalinization of extracellular material and myxoid changes were present. There was a partly solid and microcystic pattern and a tight cohesiveness of cells was lacking. The circumscribed multinodular tumour somewhat resembled an extrarenal rhabdoid tumour, having large tumour cells with prominent nucleoli and large amounts of acidophilic cytoplasm. Immunohistochemically, the tumour cells were immunoreactive for cytokeratin, vimentin, muscle-specific actin, alpha-smooth muscle actin, and S100 protein, but not for desmin, epithelial membrane antigen, factor VIII-related antigen, CD34 and CD31. CONCLUSIONS: The histological and cytomorphological appearance of the tumour well as the immunohistochemical findings suggest the diagnosis of malignant myoepithelioma, possibly derived from minor vestibulary glands or ectopic breast tissue. Differential diagnoses are, in particular, extrarenal rhabdoid tumour and 'proximal type' epithelioid sarcoma. Differentiation is important, because the tumours show a different behaviour and prognosis.

Aged↗
PubMed1991

Protooncogene expression in rat liver by polychlorinated biphenyls (PCB).

1. The expression of 10 protooncogenes was studied in control rat liver and at various times after exposure to polychlorinated biphenyls (PCB), a known tumour promoter. 2. The expression of protooncogenes in liver is more pronounced in those rats treated with PCB beginning at weaning ('weanlings') than in adult rats. 3. The RNA levels of c-Ha-ras, c-raf, c-yes, c-erbA and c-erbB are elevated after PCB feeding. 4. Nuclear run-on transcription analysis revealed that the altered expression of the protooncogenes is transcriptionally regulated. 5. In one group the prompt rise of the protooncogene transcription rate is followed by a decline (c-Ha-ras, c-raf c-yes). In a second group a further increase in transcription at later feeding times (c-erbA, c-erbB) was observed. 6. A correlation between the altered expression of these protooncogenes and the action of PCB as a tumour promotor remains to be determined.

Aging↗
PubMed1990

Animal research in psychology: declining or thriving?

From Dialog's PsychINFO database the number of studies with 6 species reported in the Psychological Abstracts was calculated for each year from 1967 to 1988. Also, the number of studies with an additional 11 species were calculated for each year from 1973 to 1988. A hand search in the Journal of the Experimental Analysis of Behavior and Learning and Motivation was also conducted to explore trends in studies on 12 species from 1970 to 1987. The numbers of studies on many species (e.g., baboons, bats, chimpanzees, dolphins, gerbils, guinea pigs, gorillas, hamsters, lemurs, mice, pigeons, rats, seals, and snakes) have remained stable. There has, however, been a steady decline in the numbers of studies on selected species (e.g., cats, dogs, and rabbits). Possible reasons for changing trends in studies on selected species include: increased costs, the cognitive emphasis in psychology, and arguably, animal rights activism.

Animal Welfare↗
PubMed1989

Mutation of the proteolipid protein gene PLP in a human X chromosome-linked myelin disorder.

Myelin is a highly specialized membrane unique to the nervous system that ensheaths axons to permit the rapid saltatory conduction of impulses. The elaboration of a compact myelin sheath is disrupted in a diverse spectrum of human disorders, many of which are of unknown etiology. The X chromosome-linked human disorder Pelizaeus-Merzbacher disease is a clinically and pathologically heterogeneous group of disorders that demonstrate a striking failure of oligodendrocyte differentiation. This disease appears pathologically and genetically to be similar to the disorder seen in the dysmyelinating mouse mutant jimpy, which has a point mutation in the gene encoding an abundant myelin protein, proteolipid protein (PLP). We report that the molecular defect in one Pelizaeus-Merzbacher family is likewise a point mutation in the PLP gene. A single T----C transition results in the substitution of a charged amino acid residue, arginine, for tryptophan in one of the four extremely hydrophobic domains of the PLP protein. The identification of a mutation in this Pelizaeus-Merzbacher family should facilitate the molecular classification and diagnosis of these X chromosome-linked human dysmyelinating disorders.

Amino Acid Sequence↗
PubMed1988

Mechanism of inhibition of cyclo-oxygenase in human blood platelets by carbamate insecticides.

Carbamates are a widely used class of insecticides and herbicides. They were tested for their ability to affect human blood platelet aggregation and arachidonic acid metabolism in platelets. (1) The herbicides of the carbamate type have no, or only little, influence up to a concentration of 100 microM; the carbamate insecticides, however, inhibit both aggregation and arachidonic acid metabolism in a dose- and time-dependent manner. (2) Carbaryl, the most effective compound, inhibits platelet aggregation and cyclo-oxygenase activity completely at 10 microM. The liberation of arachidonic acid from phospholipids and the lipoxygenase pathway are not affected, whereas the products of the cyclo-oxygenase pathway are drastically decreased. (3) By using [14C]carbaryl labelled in the carbamyl or in the ring moiety, it could be proved that the carbamyl residue binds covalently to platelet proteins. In contrast with acetylsalicylic acid, which acetylates only one protein, carbaryl carbamylates a multitude of platelet proteins. (4) One of the carbamylated proteins was found to be the platelet cyclo-oxygenase, indicating that carbaryl resembles in this respect acetylsalicylic acid, which is known to inhibit this enzyme specifically by acetylation.

Arachidonic Acid↗
PubMed1988

Modes of action and combination effects of polychlorinated biphenyls and gamma-hexachlorocyclohexane on the regulation of rat liver 3-hydroxy-3-methylglutaryl coenzyme A reductase.

The effect of polychlorinated biphenyls, gamma-hexachlorocyclohexane and the effect of a combination of these substances on the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase were investigated. As known from previous investigations polychlorinated biphenyls interfere with the regulation of 3-hydroxy-3-methylglutaryl coenzyme A reductase activity in rat liver via enzyme-lipid interaction and at the pretranslational level. In contrast to polychlorinated biphenyls, gamma-hexachlorocyclohexane did not alter the lipid status of the microsomal membrane. Thus the location of the 3-hydroxy-3-methylglutaryl coenzyme A reductase, and consequently the catalytic activity of the enzyme was not changed. As with polychlorinated biphenyls, gamma-hexachlorocyclohexane interacted with enzyme regulation at the pretranslational level. Northern dot hybridization experiments showed a decrease in the level of m-RNA coding for 3-hydroxy-3-methylglutaryl coenzyme A reductase. The effect of combination of gamma-hexachlorocyclohexane and polychlorinated biphenyls was not additive. The gamma-hexachlorocyclohexane effect appeared to play a more important role than that of the polychlorinated biphenyls. The results indicate that the combination effects are as important as the effects of the single compounds when making risk assessments for xenobiotics.

Animals↗
PubMed1987

Uptake of persistent environmental chemicals by cultured human cells.

Uptake of the persistent environmental chemicals 2,2',4,4',5,5'-hexachlorobiphenyl and 1,1,1-trichloro-2,2-di-(4-chlorophenyl)ethane (the insecticide DDT) by Chang liver cells, an established human cell line, has been investigated. Monolayer cells were incubated with culture medium to which the lipophilic model compounds had been added. The time course of uptake of either compound was biphasic, reaching equilibrium after about 5 hr of incubation. The ratio of DDT:hexachlorobiphenyl uptake was dependent on the presence of serum proteins. Increasing concentrations of serum proteins in the culture medium progressively inhibited uptake. Efflux from the cells was not entirely reversible: 10-20% of the chemicals were not released. Uptake was a linear function of the external concentration of the compounds. Absorptive binding to the outer cell plasma membrane could be determined by removing bound chemicals with fetal calf serum ("back exchange"). With this method, temperature-dependent translocation through the cell plasma membrane could directly be demonstrated. The effect of low temperature as well as the influence of metabolic inhibitors point out the contribution of energy-driven uptake pathways. Demonstration of LDL receptor-like binding protein on Chang liver cells facilitated estimation of the role of receptor-mediated uptake. This route of uptake proved to be of minor importance only, as was transport of the protein-bound chemicals via fluid pinocytosis. The results demonstrate that cellular endocytosis of plasma membrane-bound chemicals constitutes a major uptake pathway for lipophilic chemicals.

Absorption↗
PubMed1987

Stimulation of arachidonic acid metabolism via phospholipase A2 by triethyl lead.

Human blood platelet aggregation and the formation of icosanoids were studied in response to triethyl lead chloride (Et3PbCl). Concentrations higher than 75 microM stimulate platelets to aggregate, whereas low concentrations (less than or equal to 20 microM) caused platelet hypersensitivity to aggregating agents such as collagen or arachidonic acid. Incubation of suspensions of washed platelets with Et3PbCl resulted in a stimulated liberation and subsequent metabolism of arachidonic acid. This response was dependent on the concentration of Et3PbCl and the incubation time. Using low concentrations of Et3PbCl and up to 3 h of incubation, the lipoxygenase product 12-hydroxy-5,8,10,14-icosatetraenoic acid was the major metabolite. Under normal conditions, however, stimulation of platelets with collagen, thrombin, or arachidonic acid leads to higher amounts of the cyclooxygenase products 12-hydroxy-5,8,10-heptadecatrienoic acid and thromboxane B2. The aggregation of human platelets induced by Et3PbCl was inhibited by three different drugs: acetylsalicylic acid, forskolin and quinacrine; but only quinacrine could prevent the liberation of arachidonic acid and the appearance of its metabolites. These specific effects of the inhibitors on Et3PbCl-stimulated platelets as well as the differences in the pattern of arachidonic acid metabolites and phosphatidic acid suggest a direct stimulatory action of Et3PbCl on platelet phospholipase A2.

Arachidonic Acid↗
PubMed1987

Two mechanisms of CCl4-induced fatty liver: lipid peroxidation or covalent binding studied in cultured rat hepatocytes.

With cultured hepatocytes it was studied whether CCl4-induced inhibition of secretion of VLDL and HDL from liver cells is a consequence of covalent binding of CCl4 metabolites (i.e. CCl3; CCl3OO.) to cell constituents or of membrane damage by lipid peroxidation. Comparing the kinetics of inhibition of lipoprotein secretion with that of CCl4-bioactivation it was found, that covalent binding of (14C)-CCl4 occurred at early time points (5 min) after CCl4 administration and inhibited the lipoprotein secretion. At 100 microM CCl4 it was depressed by 53% within 60 min. Incubations of CCl4-treated cells with increasing concentrations of vitamin E blocked lipid peroxidation, but lipoprotein secretion was still inhibited. Piperonyl butoxid, a radical scavenger, protected against CCl4-induced inhibition of lipoprotein section, lipid peroxidation and covalent binding. These results show that during the early phases of CCl4 poisoning fat accumulation is the consequence of covalent binding of CCl4 metabolites to cell structures.

Animals↗
PubMed1985

Inhibition by pesticides of prostaglandin formation in blood platelets.

Aggregation of human platelets was investigated after pre-incubation of platelet rich plasma with various pesticides of the carbamate type. Whereas N-methyl-carbamates (insecticides) inhibited the arachidonic acid induced aggregation, N-phenyl-carbamates (herbicides) had no effect. The influence of the different carbamates on aggregation coincided with their inhibition of thromboxane B2-formation. - DDE, a metabolite of the insecticide DDT, affected aggregation to a similar extent as N-methyl-carbamates. DDT, however, had no inhibitory activity.

Blood Platelets↗
PubMed1983

Interaction of the insecticide 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane with the beta-receptor adenylate cyclase system in Chang liver cell membranes.

Interaction of the insecticide 1,1,1-trichloro-2,2-bis-(p-chlorophenyl)-ethane (DDT) with beta-receptor binding and adenylate cyclase activity of biological membranes has been studied. Following exposure of cultured Chang liver cells to DDT, maximal binding of the catecholamine antagonist [125I]-iodohydroxybenzylpindolol (HYP) to isolated cell membranes was decreased by 30% whereas the dissociation constant remained unchanged. Both basal activity and maximal isoproterenol-stimulated activity of adenylate cyclase were not altered. The isoproterenol concentration required for half-maximal stimulation of the enzyme was increased about 2-fold as was the agonist concentration required for half-maximal displacement of the antagonist HYP at the beta-receptor binding site. Thus, coupling efficiency of hormone-stimulated adenylate cyclase activity was not influenced by the presence of DDT in these membranes. The data show that interaction of DDT with the beta-receptor adenylate cyclase complex is restricted to the receptor component. Enzyme activity is directly linked to changes of agonist binding at the beta-receptor. Interference of DDT with signal transduction via 'fluidization' of membrane lipids has not been detected.

Adenylyl Cyclases↗
PubMed1983

Effect of alterations in vitro and in vivo of the cholesterol content in rat liver microsomes on the activity of 3-hydroxy-3-methylglutaryl-CoA reductase.

3-Hydroxy-3-methylglutaryl-CoA reductase, the regulatory enzyme of cholesterol synthesis in liver, is bound to the microsomal fraction. Lipoprotein-bound cholesterol (from human serum) in vitro inhibits the microsomal bound 3-hydroxy-3-methylglutaryl-CoA reductase. The solubilized enzyme, however, is not inhibited. Immunotitration of the microsomal enzyme with a monospecific antibody reveals that the loss in enzyme activity caused by cholesterol corresponds well with the lowering of the equivalence points. In contrast, the equivalence points of the solubilized enzyme remain unchanged. This indicates that the inhibitory effect of cholesterol is restricted to the microsomal bound enzyme. In vivo different physiological conditions lead to relatively small changes in the cholesterol content in the microsomes while drastic changes in the activity of 3-hydroxy-3-methylglutaryl-CoA reductase are observed. When microsomes from these rats are incubated with exogenous cholesterol, the activity of the enzyme is always found to be decreased to the same extent independent of the physiological condition of the animals. The findings suggest that 3-hydroxy-3-methylglutaryl-CoA reductase may be "masked" by a cholesterol-mediated modification of the microsomal membrane.

Animals↗