Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Interplay”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,603 records · Page 89Linked to original sources
PubMed1984

[Interplay of social, intrapsychological and biological factors for the etiopathogenesis of anorexia nervosa].

Intergroup-comparison and hierarchical cluster analyses (method Lance and Williams, x2-test, t-test, p less than 5%) of 170 facts at biological, psychodynamic and social level in 35 patients suffering from anorexia nervosa and 30 patients suffering from postpill-amenorrhea confirm the close relations of these levels for aetiopathogenesis. Postpill-amenorrhea can be taken as hypothalamic dysfunction (overpressing of LH-RH-release after anticonceptives) and therefore as a model for the biological disturbance at anorexia nervosa. Cluster analyses resulted in a division into 3 groups: one group of anorexia nervosa (C) with deep biological disturbances; a main group of anorexia nervosa (B) and the group of postpill-amenorrhea (A). In cluster C are combined early age of onset, rigidity-type in hormonal tests, EEG-changes, psychopathic personality in MMPI and strongest disturbed social interactions. In cluster B are neurotic profile in MMPI combined with severe biological and social difficulties. 13 out of 30 showing anorectic-like behaviour during adolescence are even more disturbed as the other postpill-amenorrhea patient in cluster A. Regressions analyses could not confirm a dependence between loss of weight and some endocrine functions.

Adolescent↗
PubMedDate not supplied

[Systems of H+-K+-exchange in E. coli. Interplay with ATPase complex F1.F0].

A study has been made of the nature of H+-K+-exchanges in the strain E. coli AN 120 with mutation in gene uncA401 (the defect in Mg++-Ca++-ATPase) and in the strain E. coli AN 382 with mutation in gene uncB (F0 is insensitive to N,N1-dicyclohehylcarbodiimide, DCCD). It was shown in E. coli AN 120 that no ATP-dependent and DCCD-sensitive TrkA system operates, exchanging 2H+ from a cell for K+ of the medium and actuating only in the presence of a difference of osmotic pressures between the cell and the medium. At the same time the strain E. coli AN 120 possesses An ATP-independent TrkF system exchanging H+ by K+ with variable stoichiometry and inhibited by DCCD. The TrkA and TrkF systems have lost the sensitivity to DCCD in E. coli AN 382. Moreover the TrkA system in this mutant has turned insensitive to the variation of osmotic pressure in the medium, i. e. DCCD-insensitivity of the TrkA and TrkF systems as well as the osmotic sensitivity of the TrkA system are related to the F0 function. We do not exclude the chance of the ionic channel F0 being a portion of both systems of potassium accumulation.

Adenosine Triphosphatases↗
PubMed1984

Ultrasensitivity in biochemical systems controlled by covalent modification. Interplay between zero-order and multistep effects.

A previous analysis of covalent modification systems (Goldbeter, A., and Koshland, D. E., Jr. (1981) Proc. Natl. Acad. Sci. U. S. A. 78, 6840-6844) showed that steep transitions in the amount of modified protein can occur when the converter enzymes are saturated by their protein substrate. This "zero-order ultrasensitivity" can further be amplified when an effector acts at more than one step in a monocyclic or multicyclic cascade of covalent modification. We analyze the limitations of the latter "multistep ultrasensitivity" and show how it can combine with the zero-order effect to enhance the sensitivity of biochemical systems controlled by covalent modification.

Allosteric Regulation↗
PubMed1982

Aldosterone: a telling case of fruitful interplay between biological and clinical research.

Aldosterone, discovered thirty years ago, has rapidly gained an enviable status among clinicians as well as biologists: this hormone is the main regulator of extracellular fluid volume--essentially through its effect on sodium retention in the distal parts of the nephron. This aspect has been fruitfully approached by means of (amphibian) epithelia carrying out transcellular sodium transport and resembling in this respect the distal renal tubule. Recent results suggest that, at least after prolonged incubation, not only is sodium entry (at the apical border) facilitated by aldosterone, but the latter steroid also somehow improves the handling of the ions by the "pump" located at the basal-lateral border. As a consequence, the target cells exposed to aldosterone are optimally geared for enhanced transcellular sodium transport. Biochemically, both processes depend on the standard pattern of steroid hormone action: after interaction of aldosterone with protein receptors(s) present in the cytoplasm of target cells, and migration of the resulting complex to their nucleus, synthesis of specific messenger ribonucleis acid is stimulated which leads to increased synthesis of proteins eventually responsible for the physiological response. An intriguing aspect of the concerted response to aldosterone documented in amphibian sodium-transporting epithelia, is that both cell borders of target cells are not influenced simultaneously: this is currently investigated [Beauwens et al. 1982b].

Aldosterone↗
PubMed1982

Mucosal barrier mechanisms. Interplay between secretory IgA (SIgA), IgG and mucins on the surface properties and association of salmonellae with intestine and granulocytes.

Rough Salmonella typhimurium 395 MR 10 bacteria sensitized with SIgA were used to assess the effect of secretory IgA (SIgA) on bacterial association with the intestine of rat and with a column of hog gastric mucin, and on IgG-mediated surface properties and interaction with polymorphonuclear leucocytes. It was found that SIgA increased the affinity for mucus belt of the intestine and for the mucin column, but reduced IgG-enhanced phagocytosis and surface hydrophobicity and charge of the bacteria. It is suggested that the ability of SIgA to render bacteria mucophilic and to modify IgG-mediated reactions serve the purpose of secluding bacteria from contact with mucosal membranes and depress inflammatory reactions at the site of infection.

Animals↗
PubMed1995

Mechanisms of nuclear signalling by vitamin D3. Interplay with retinoid and thyroid hormone signalling.

Hormones that act through nuclear receptors contribute to vertebrate development and homeostasis by serving as biological signals to control cellular growth and differentiation. Their response pathways must meet two requirements, which can be contradictory: they must be highly specific for a given signal, but at the same time they have to be flexible, allowing different responses under different physiological conditions. The current model for nuclear signalling of vitamin D3 (calcitriol), thyroid hormone and retinoic acid seems to be too simple to solve the specificity puzzle. Therefore, an advanced model is proposed that combines recent findings on the structure of hormone response elements, the promiscuous dimerization of the receptors for vitamin D3, thyroid hormone and retinoids and the heterodimer polarity. Special attention is taken on the mechanism of vitamin D3 signalling, where at least 14 different pathways are differentiated.

Animals↗
PubMed1995

Interplay between promoter and structural gene variants control basal serum level of mannan-binding protein.

Mannan-binding protein (MBP) is a serum lectin participating in the innate immune defense by opsonizing various microorganisms for phagocytosis. Opsonization defect due to MBP deficiency and low levels of the protein can partially be explained by the dominant effect of three different mutations in the structural part of the MBP gene. Large interracial differences in the frequencies of these variants have previously been described, but they cannot explain the large interindividual variation in MBP serum concentration. We describe the existence of additional polymorphisms at positions -550 (H/L variants) and -221 (X/Y variants) in the promoter region of the gene. The promoter haplotypes, HY, LY, and LX, show associations with high, medium, and low levels of MBP serum concentrations, respectively. Moreover, this represents a genetic system with additive effect of haplotypes in which a low producing LX haplotype in the homozygous state down-regulates the basal expression of MBP as effectively as a single structural variant. Populations of pure Eskimos, Caucasoids, and black Africans show marked interethnic differences in the frequencies of promoter haplotypes regulating the expression of the normal peptide, with the HY haplotype frequency varying from 0.83 in Eskimos via 0.33 in Caucasoids to 0.08 in Africans. The LY haplotype frequency varies from 0.04 in Eskimos via 0.39 in Caucasoids to 0.23 in Africans. The LX haplotype frequency varies from 0.03 in Eskimos via 0.24 in Caucasoids to 0.23 in Africans. The effect of the promoter variants can explain almost all of the ethnic differences not explainable by the structural variants alone.

Base Sequence↗
PubMed1993

Rewarding and aversive effects of ethanol: interplay of GABA, glutamate and dopamine.

Ethanol (EtOH) administration is considered to elicit its reinforcing properties by stimulating dopaminergic (DA) transmission in the mesolimbic system. Accordingly, (EtOH) activates dopamine neuronal firing in the Ventro-Tegmental Area (VTA) and DA output in the nucleus accumbens. Concomitantly, EtOH reduces the firing rate of Pars Reticulata (PR) neurons which are thought to exert an inhibitory control over DA neurons. Further, chronic ingestion of EtOH produces tolerance to its sedative effects as to the depressant effect on PR neurons but no tolerance to the DA stimulating action. Moreover the NMDA antagonist MK-801, but not SL-820715, stimulates DA firing, suggesting that this effect is not a general characteristic of NMDA receptor antagonists and questioning the possibility that NMDA-receptor blockade may underlie EtOh-induced activation of DA-ergic transmission. The results indicate that activation of the mesolimbic DA tract is essential in the rewarding properties of EtOH and that neither GABA-ergic inhibition nor NMDA-receptor blockade by EtOH, are causally linked to the EtOH-induced activation of DA-ergic transmission.

Alcoholism↗
PubMed1994

Influence of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, lipoic acid and L-deprenyl on the interplay between cellular redox systems.

For several years there is controversy concerning the toxic potency of reaction products catalyzed by monoamine oxidase in neurodegenerative processes. There is uncertainty whether products of catecholamine oxidation are pathogenetically relevant factors for neuronal cell death in Parkinson's disease. To date products responsible for impairment of biochemical functions essential for cell viability are not yet identified, and the primary site of damage within the cell is unknown. Ammonia, aldehydes and hydrogen peroxide are formed via monoamine oxidase catalyzed oxidations of primary amines. But which of them, if any, is damaging to the cell? We discuss some aspects of the oxidative stress theory of cell degeneration in relation to toxicity of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and to monoamine oxidation. Furthermore, we consider possible functional relationships of mitochondrial electron transfer reactions, toxicity of MPTP and MAO activity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1994

Interplay between estrogens, progestins, retinoic acid and AP-1 on a single regulatory site in the progesterone receptor gene.

Transcriptional regulation of the progesterone receptor gene involves induction by estrogens and down-regulation by progestins, retinoic acid, and AP-1 proteins. We have previously identified an intragenic (+698/+723) estrogen-responsive element present in the progesterone receptor gene, which binds the estradiol receptor and mediates estrogen and 4-OH tamoxifen induction. Progesterone receptor gene expression was equally stimulated by estradiol and 4-OH tamoxifen in the presence of a NH2 terminally deleted estrogen receptor mutant lacking activation function 1, suggesting that activation function 2 was the predominant activation domain. This was confirmed by the lack of activity of an estrogen receptor mutant deleted of activation function 2. Repression by progestins, retinoic acid, and AP-1 was mediated by the same estrogen responsive element although retinoic and progesterone receptors as well as AP-1 proteins did not bind to this element. Repression by these proteins appears to involve different transactivating regions of the estrogen receptor. Repression by retinoic receptors involved only activation function 2 whereas repression by progesterone receptor and AP-1 necessitated both functional domains. Since these proteins act without directly contacting the DNA, it seems likely that repression may be achieved by protein-protein interactions among different domains of the estrogen receptor and/or the transcriptional machinery.

Animals↗
PubMed1993

Functional CD4 T cell subset interplay in an intact immune system.

Immunization with human collagen IV has been shown to lead to the selective activation of Th-1 and Th-2-like cells in vivo depending on the I-A genotype of the mice. Mice expressing I-As generate Th-1 cells, and mice expressing I-Ab generate Th-2 cells after immunization. We examined the response of (bxs)F1 hybrid mice to determine the types of CD4 T cell activated. We found that Th-1-like responses dominated, in that CD4 T cells from human collagen IV-primed mice displayed good proliferative responses and little ability to induce antibody formation, and secreted IFN-gamma and not IL-5. Most of the Th-1-like activity of F1 hybrid T cells was I-As restricted. Inhibition of Th-1 cell priming using anti-I-As antibody administered with the priming Ag in vivo revealed Th-2-like activity, in that the CD4 T cells now secreted IL-5 and not IFN-gamma and induced antibody formation. Additional studies indicated that anti-IFN-gamma treatment in vivo also revealed Th-2 cells, suggesting that I-As-restricted CD4 T cells producing or controlling the production of IFN-gamma suppress Th-2 priming.

Animals↗
PubMed1994

Interplay of heterogeneous transcriptional start sites and translational selection of AUGs dictate the production of mitochondrial and cytosolic/nuclear tRNA nucleotidyltransferase from the same gene in yeast.

ATP (CTP):tRNA nucleotidyltransferase catalyzes the addition of the CCA end to tRNAs. In yeast, nucleotidyltransferase is encoded by the CCA1 gene and is localized to three cellular compartments: mitochondria, nucleus, and cytosol. There are three in-frame ATGs near the 5' end of the CCA1 open reading frame. Primer extension experiments show multiple transcription initiation sites upstream of ATG1 and between ATG1 and ATG2. Fractionation of cells carrying a CCA1-COXIV fusion gene demonstrates that all three in-frame AUGs are used as sites of initiation of translation. Therefore, both transcription of CCA1 mRNA with heterogeneous 5' ends and translation from downstream AUGs in CCA1 mRNAs play a role in the synthesis of three nucleotidyltransferase isozymes. Protein initiating from AUG1 is required for mitochondrial protein synthesis and, like many other proteins targeted to mitochondria, it is processed at the amino terminus upon import into the organelle. The shorter proteins arising from AUG2 and AUG3 provide nuclear/cytosol activity.

Amino Acid Sequence↗
PubMed1993

Interplay between differentiation and cell cycle arrest at G1 in phorbol diester-treated human myelocytic leukemia cells.

The cell cycle arrest at G1 of myelocytic leukemia cells by incubation with phorbol diesters was examined in HL-60 cells and more mature THP-1 cells. We found: (1) induction of phenotypic parameters of differentiation prior to G1 arrest; (2) a long induction period in HL-60 cells compared to zero in THP-1 cells; and (3) strong inhibition of G1 arrest with a protein kinase C inhibitor in THP-1 cells. We conclude, from these lines of evidence and some additional information, that differentiation induces G1 arrest. At present, the most plausible causative molecule is Mac-1.

Cell Differentiation↗