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At least 307 records · Page 17Linked to original sources
PubMed1983

[Pathogenic properties of Yersinia pseudotuberculosis in different biological models].

The study of the action of Y. pseudotuberculosis introduced into the cavity of the ligated intestinal loop of a rabbit, into the stomach of 2- to 4-day-old suckling mice or injected intradermally has made it possible to establish the importance of the invasive and toxic activity of this microbe in the pathogenesis of pseudotuberculosis infection. The lesion of the small intestine develops due to the penetration of the bacteria into the mucous membrane and the combined action of the microbial cells inhabiting the stroma, and secreting into the environment of cytotoxins, toxic substances with an enterotropic action or enterotoxins and factors increasing the permeability of the vessels. Y. pseudotuberculosis strains with high and low invasiveness have been isolated.

Animals↗
PubMed1981

[Transport of cytidinediphosphocholine in different biological models. II - Transport of (5 3H, Met 14C) cytidinediphosphocholine in isolated and perfused rat liver].

The uptake of double labeled CDP-choline by isolated and perfused rat liver has been investigated. The time course of CDP-choline uptake is different for 3H and 14C, showing the existence of the degradation process of the molecule. The identification and characterization of CDP-choline and its metabolites, in the perfusate and in the hepatic extract are performed by high pressure liquid chromatography.

Animals↗
PubMed1993

[A comparison of the antioxidative activity of carnosine by using chemical and biological models].

The difference in the efficiency of carnosine as an antioxidant was found to be explained both by the source of carnosine and the specificity of models used to achieve visualization. Commercial carnosine samples were contaminated with compound (s) absorbing at 255-332 nm. At the same time they possessed better antioxidant activity in the models with Fe2-induced peroxidation process. In the case of chemical models for generation of active forms of oxygen (several modifications of the Fenton reaction) or during burst of superoxide generation by leucocytes, the antioxidant effect of carnosine did not depend of the source of the compound under study.

Animals↗
PubMed1995

[Biological models of depression: effect of antidepressants on sleep].

The relationship between insomnia and depression cannot be summarized as a symptom/disease relationship. It is well admitted now that sleep deprivation has an antidepressant effect on depressed patients. The effect is immediate, global but transient : the relapse occurs after subsequent sleep, diurnal nap or recovery night. On an other hand, sleep architecture is impaired in depressed patients, some of these alterations, especially in REM sleep, might have been considered specific of depressive disease. Antidepressant drugs exert an effect on sleep architecture which is different. This effect varies over time and generally tend to correct sleep impairment. This has led some authors to propose the hypothesis that sleep himself might be involved in the causal process of depression. Three main hypotheses will be considered, excluding those involving circadian rhythm impairment, according to their strong and weak points. For G. Vogel, an excess of REM sleep is the causal process in depression. As a matter of fact, he did show that selective REM sleep deprivation exerts an antidepressant effect following the same temporal profile as antidepressant drugs. An other argument is that the shortening of REM latency and the increased amount of REM sleep in the first half of the night are evidences of the excess of REM sleep and at last, most antidepressant drugs are REM suppressors and may act through REM sleep suppression. The second hypothesis is the process S deficiency proposed by Alexander Borbely, according to his two process model of sleep homeostasis. The impairment of process S, which is reflected by slow wave activity, is responsible for depression. This explain disruptions and shortening of sleep in depressed patients, REM sleep abnormalities being only secondary to the slow wave sleep reduction. More recently, D. Beersma and R. van den Hoofdakker proposed that non REM sleep might be depressogenic after an experiment of selective REM sleep deprivation in normals which showed that non REM sleep deprivation was also largely reduced. REM suppression effects might therefore also be attributed to non REM suppression. All these hypothesis must explain the effect of antidepressant drugs on sleep. There is a large heterogeneity of effects on slow wave, non REM and even REM sleep, hardly compatible with a causal role of sleep, REM or non REM.

Antidepressive Agents↗
PubMed1997

Behavior of tetrahydrolipstatin in biological model membranes and emulsions.

Tetrahydrolipstatin (orlistat) (S)-1-[(2S,3S)-3-hexyl-4-oxooxetan-2-yl]methyl]dodecyl N-formyl-L-leucinate, a potent inhibitor of pancreatic lipase, is hydrophobic, amphipathic, and water-insoluble. It binds irreversibly to pancreatic lipases and inhibits fat absorption. The focus of this investigation is on the distribution of orlistat in emulsified fat and vesicular membranes such as might be present in the intestine during fat absorption. The models used were unilamellar vesicles and microemulsion particles. [13C]orlistat was synthesized containing 99% 13C in the leucine carbonyl. Spectrawere collected on a Bruker DMX 500 Spectrometer. The chemical shift of the [13C]leucinate carbon was recorded in solvents with increasing hydrogen bonding capacity. The chemical shift moved downfield as H-bonding increased. [13C]orlistat was incorporated into triolein in the presence or absence of water, into sonocated unilamellar egg yolk phosphotidylcholine (EYPC) vesicles, and into microemulsions approximately 300 A in diameter containing triolein and phospholipid in roughly equal molar proportions. [13C] orlistat was soluble in triolein and had a chemical shift at 20 degrees C of 171.46 ppm. When a small amount of water was added, the chemical shift moved down field to 171.69 ppm. When [13C]orlistat was incorporated into EYPC unilamellar vesicles, the chemical shift increased to approximately 172.0 ppm at 25 degrees C, indicating an orientation of [13C]leucinate in orlistat closer to the aqueous interface of vesicles, i.e., more surface oriented. In all systems there was a modest downfield increase in chemical shift as the temperature was raised from 5 degrees to 46 degrees C. When small amounts of [13C]orlistat (1% relative to the emulsion mass) were incorporated into microemulsions, the chemical shift was identical to that in the unilamellar vesicles indicating a surface-like orientation of [13C]orlistat. However, when 3% was incorporated, two peaks appeared, one related to the surface at about 172 ppm, and one related to the core at about 171.65 ppm. Thus, orlistat first partitions into the surface and then when the surface is saturated, it moves into the more hydrophobic core. The fact that the two pools can be resolved using 13C NMR spectroscopy indicates a modestly slow exchange between the core and surface pools. Thus, the potent lipase inhibitor orlistat is ideally situated in the surface layer of emulsion particles and membranes for interaction with enzymes that superficially bind to such surfaces.

Emulsions↗
PubMed2002

The systemic paradigm and its relevance to the modelling of biological functions.

If we are to make advances in the design of information systems for the processing of functional genomic data, we must carefully examine the concepts of gene and function. Therefore, we must consider the biological models that are used to acquire these data from an epistemological point of view. This article introduces three elements of this view: (i) we reviewed the major concepts and the axioms of the systemic paradigm; (ii) we considered their relevance for the modelling of the biological functions within the framework of an intracellular signalling process; (iii) we present an operational input founded on this methodological viewpoint to illustrate the coherence of a theoretical framework and the use of its formalism for the description and the representation of biological activities. This formalism will guide the modelling and the interpretation of molecular interactions in terms of organisational operations producing and transforming the genetic information; thus, providing a better understanding of the complex relationship between the generation, the circulation and the computation of information when biological systems are set up.

Animals↗
PubMed2005

A new journal - "Theoretical Biology and Medical Modelling".

Biology has a conceptual basis that allows one to build models and theorize across many life sciences, including medicine and medically-related disciplines. A dearth of good venues for publication has been perceived during a period when bioinformatics, systems analysis and biomathematics are burgeoning. Steps have been taken to provide the sort of journal with a quick turnaround time for manuscripts which is online and freely accessible to all readers, whatever their persuasion or discipline. We have now been running for some time a journal which has had many good papers presented pre-launch, and a steady stream of papers thereafter. The value of this journal as a new venue has already been vindicated. Within a short space of time, we have founded a state-of-the-art electronic journal freely accessible to all in a much sort-after interdisciplinary field that will be of benefit to the thinking life scientist, which must include medically qualified doctors as well as scientists who prefer to build their new hypotheses on basic principles and sound concepts underpinning biology. At the same time, these principles are not sacrosanct and require critical analysis. The journal http://www.tbiomed.com promises to deliver many exciting ideas in the future.

Computational Biology↗
PubMed1994

[Surfactant interactions in model and biological membranes. IX. Theoretical model of biological activity in relation to the length of hydrocarbon chains].

A theoretical model is proposed according to which the quasi-parabolic dependence of the biological activity of amphiphilic compounds on their hydrophobic substituent chain length (the "cut-off" effect) is caused by a combination of partition equilibria and geometrical parameters of these compounds interacting with the bilayer of phospholipid membranes. The most important parameter seems to be a change in the thickness of the phospholipid bilayer. The model is quantified for the case of normal alcohols.

Cell Membrane↗