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At least 1,063 records · Page 59Linked to original sources
PubMed2000

Susceptibility to multiple sclerosis: interplay between genes and environment.

Multiple sclerosis is a complex trait of unknown etiology. Epidemiological data have shown that susceptibility to multiple sclerosis is determined by both genetic and environmental factors. It is unknown whether the clinical subcategories of multiple sclerosis are separate diseases with separate etiologies and causes. Recent theories of the pathogenesis of multiple sclerosis and candidate genes are discussed. Other potential nonchromosomal factors involved in multiple sclerosis susceptibility such as mitochondrial DNA and viral factors such as Chlamydia pneumoniae are reviewed.

Environmental Exposure↗
PubMed2004

Psoriasis vulgaris: an interplay of T lymphocytes, dendritic cells, and inflammatory cytokines in pathogenesis.

PURPOSE OF REVIEW: Discuss and update concepts and hypotheses for the pathogenesis of psoriasis based on new research reports (primarily from 2003 and early 2004). RECENT FINDINGS: Increases in newly defined dendritic cell subsets, cytokines, and chemokines have been identified in psoriasis lesions and have modified views of T-cell-mediated pathogenesis. In addition, the psoriasis transcriptome has been defined by large-scale genomic expression studies, and these data suggest distinct molecular mechanisms of type 1 T-cell-mediated inflammation. Somewhat surprisingly, therapeutic clinical trials suggest that tumor necrosis factor is a major pathogenic cytokine in psoriasis, whereas translational studies point to roles of other innate pathways mediated by heat shock proteins, glycolipids, natural killer T cells, or dendritic cells in disease pathogenesis. SUMMARY: An interactive network of inflammatory cytokines, chemokines, dendritic cells, and type 1 T cells or natural killer T cells potentially drives pathogenic inflammation in psoriasis vulgaris. Continued clinical studies with defined immune antagonists provide a critical means to dissect the contribution of different cell subsets and genomic pathways to the pathogenesis of psoriasis vulgaris.

Cytokines↗
PubMed2006

The interplay between haemodynamic load, brain natriuretic peptide and left atrial size in the early stages of essential hypertension.

OBJECTIVE: Left atrial (LA) enlargement is an index of adverse cardiovascular events. We sought to investigate any possible correlation between haemodynamic load, neurohumoral factors and LA size in the early stages of essential hypertension. METHODS: We studied 94 consecutive middle-aged subjects, with newly diagnosed stage I-II essential hypertension without left ventricular (LV) hypertrophy and 34 age and sex-matched normotensive individuals. Ambulatory blood pressure (BP) monitoring, plasma levels of brain natriuretic peptide (BNP), metabolic profile and left atrial volume index (LAVI), an echocardiographic measurement of LA volume indexed for the body surface area, constituted the work-up of all subjects. RESULTS: Hypertensive compared with normotensive subjects had significantly increased office and ambulatory systolic and diastolic BP (P < 0.0001 for all cases) as well as body mass index and waist-to-hip ratio (P < 0.05 for both cases). BNP levels were greater in hypertensive compared with normotensive subjects but were not statistically significant (20.4 versus 17.1 pg/ml, P = NS). Hypertensive compared with normotensive subjects also had significantly increased LV mass index (105 versus 84 g/m, P < 0.0001), LA diameter (39 versus 36 mm, P < 0.0001), and LAVI (22 versus 19 ml/m, P < 0.05). In the hypertensive population, LAVI exhibited significant positive relationships with office systolic BP, ambulatory pulse pressure, LV mass index and BNP. In multiple linear regression analysis only LV mass index and BNP were significantly associated with LAVI (beta = 0.298, P = 0.030 and beta = 0.322, P = 0.009, respectively). CONCLUSIONS: Increased LAVI, closely associated with LV mass index and BNP, was still found in the early stages of essential hypertension. However, the clinical significance of these findings remains to be elucidated in future studies.

Adult↗
PubMed2005

Interplay of platelet polymorphisms, risk factors, and von [corrected] Willebrand factor [corrected] in determining collagen-adenosine diphosphate PFA-100 results in patients with coronary artery disease.

Platelets play a pivotal role in thrombus formation in patients with coronary artery disease (CAD), since the high shear generated in the presence of severe coronary stenoses can increase platelet reactivity (PR) and trigger thrombogenesis. Several reports have suggested a functional effect of human platelet antigen (HPA)-1 and HPA-2 gene polymorphisms on PR. However, the true determinants of high-shear PR in CAD patients taking their usual medications are still incompletely understood. In 104 patients with stable CAD we analyzed the possible clinical, biochemical and genetic factors affecting high-shear PR, measured by the ex vivo platelet function analyzer (PFA-100) collagen-adenosine diphosphate method. In univariate analysis, a lower PR was associated with decreased plasma von Willebrand factor-ristocetin cofactor activity, increased blood levels of triglycerides, female sex, use of thienopyridines, lower platelet count, and HPA-1b carriership. All variables, except HPA-1b, remained associated with lower PR in multivariate analysis. However, the introduction in the model of the HPA-1 and HPA-2 genotypes as interaction terms led to a significant improvement in the prediction of PR, although the quantitative effect was small (about 3% improvement, P=0.046).Thus, in CAD patients, there seems to be only a mild effect of the platelet glycoprotein HPA-1 and HPA-2 polymorphisms on collagen-adenosine diphosphate-stimulated PR after the effect of well-established clinical and biochemical determinants are considered.

Adenosine Diphosphate↗
PubMed2005

The interplay of positive and negative species interactions across an environmental gradient: insights from an individual-based simulation model.

Positive interspecific interactions are commonplace, and in recent years ecologists have begun to realize how important they can be in determining community and ecosystem dynamics. It has been predicted that net positive interactions are likely to occur in environments characterized by high abiotic stress. Although empirical field studies have started to support these predictions, little theoretical work has been carried out on the dynamic nature of these effects and their consequences for community structure. We use a simple patch-occupancy model to simulate the dynamics of a pair of species living on an environmental gradient. Each of the species can exist as either a mutualist or a cheater. The results confirm the prediction: a band of mutualists tends to occur in environmental conditions beyond the limits of the cheaters. The region between mutualists and cheaters is interesting: population density here is low. Mutualists periodically occupy this area, but are displaced by cheaters, who themselves go extinct in the absence of the mutualists. Furthermore, the existence of mutualists extends the area occupied by the cheaters, essentially increasing their realized niche. Our approach has considerable potential for improving our understanding of the balance between positive and negative interspecific interactions and for predicting the probable impacts of habitat loss and climate change on communities dominated by positive interspecific interactions.

Computer Simulation↗
PubMed2007

The interplay between a self-organized process and an environmental template: corpse clustering under the influence of air currents in ants.

Many spatial patterns observed in nature emerge from local processes and their interactions with the local environment. The clustering of objects by social insects represents such a pattern formation process that can be observed at both the individual and the collective level. In this paper, we study the interaction between air currents and clustering behaviour in order to address the coordinating mechanisms at the individual level that underlie the spatial pattern formation process in a heterogeneous environment. We choose the corpse clustering behaviour of the ant Messor sanctus as an experimental paradigm. In a specifically designed experimental set-up with a well-controlled laminar air flow (approx. 1 cm s-1), we first quantify the modulation of the individual corpse aggregation behaviour as a function of corpse density, air flow intensity and the ant's position with respect to corpse piles and air flow direction. We then explore by numerical simulation how the forming corpse piles modify the laminar air flow around them and link this result with the individual behaviour modulation. Finally, we demonstrate on the collective level that this laminar air flow leads to an elongation and a slow displacement of the formed corpse piles in the direction of the air current. Both the individual behaviour modulated by air flow and the air flow modulated by the forming corpse piles can explain the pile patterns observed on the collective level as a stigmergic process. We discuss the generality of this coordinating mechanism to explain the clustering phenomena in heterogeneous environments reported in the literature.

Animals↗
PubMed1990

The interplay of population dynamics and the evolutionary process.

Long-term maintenance of genetic diversity is affected by ecological forces that are driven in turn by current levels of genetic variation. The strength of population regulation and the consequent patterns of population fluctuations determine the likelihood of genetic changes considered pivotal for rapid speciation. However, genetic diversity in the susceptibility to regulatory forces can reduce the magnitude of such fluctuations and minimize the likelihood of genetic revolutions. A group of populations that experiences local extinctions and recolonizations may hold lower levels of genetic diversity than in the absence of such extinctions, but local adaption, which provides enhanced genetic diversity, can reduce the likelihood of local extinctions. Tightly regulated populations experience different selection pressures than poorly regulated populations, although tighter regulation itself can evolve. When genotypic variation affects the outcome of interspecific interactions on a local scale, this effect, coupled with appropriate spatial variation, can enhance the resilience of the interactive system.

Animals↗
PubMed2002

Novel insights into the interplay between peripheral reactions encoded by xyl genes and the chlorocatechol pathway encoded by tfd genes for the degradation of chlorobenzoates by Ralstonia eutropha JMP134.

Many bacteria can grow on chloroaromatic pollutants because they can transform them into chlorocatechols, which are further degraded by enzymes of a specialized ortho-cleavage pathway. Ralstonia eutropha JMP134 is able to grow on 3-chlorobenzoate by using two pJP4-encoded, ortho-cleavage chlorocatechol degradation gene clusters (tfdC(I)D(I)E(I)F(I) and tfdD(II)C(II)E(II)F(II)). Very little is known about the acquisition of new catabolic genes encoding enzymes that lead to the formation of chlorocatechols in R. eutropha JMP134. The effect on the catabolic properties of an R. eutropha JMP134 derivative that received the xylS-xylXYZL gene module, encoding the xylS-regulated expression of the broad-substrate-range toluate 1,2-dioxygenase (xylXYZ) and the 1,2-dihydro-1,2-dihydroxytoluate dehydrogenase (xylL) from pWW0, which allows the transformation of 4-chlorobenzoate into 4-chlorocatechol, was studied. Such a derivative could efficiently grow on 4-chlorobenzoate. Unexpectedly, this derivative also grew on 3,5-dichlorobenzoate, a substrate for XylXYZL but not an inducer of the XylS regulatory protein. The ability to grow on 4-chlorobenzoate or 3,5-dichlorobenzoate was also observed in derivatives of strain JMP134 containing the xyl gene module but lacking xylS, indicating the presence of an xylS-like element in R. eutropha with an inducer profile different from that of the pWW0-encoded regulator. Growth on 4-chlorobenzoate was also observed after introduction of the xyl gene module into strain JMP222, a JMP134 derivative lacking pJP4, but only if multiple copies of tfdC(I)D(I)E(I)F(I) or tfdD(II)C(II)E(II)F(II) were present. However, only the derivative containing multiple copies of tfdD(II)C(II)E(II)F(II) was able to grow on 3,5-dichlorobenzoate. These observations indicate that although the acquisition of new catabolic genes actually enhances the catabolic abilities of R. eutropha JMP134, these new properties are strongly influenced by the dosage of the tfd genes, the presence of a chromosomal xylS-like regulatory element and the different contributions of the tfd gene clusters.

Bacterial Proteins↗
PubMed2005

The interplay of glycogen metabolism and differentiation provides an insight into the developmental biology of Streptomyces coelicolor.

Mycelial colonies of the developmentally complex actinomycete Streptomyces coelicolor growing on solid medium contain glycogen in two distinct locations. Phase I deposits are found in a substrate mycelium region bordering the developing aerial mycelium. Their production involves GlgBI, one of two glycogen branching enzyme isoforms. Phase II deposits occur in the upper regions of aerial hyphae, in long tip cells that are dividing, or have just divided, into unigenomic prespore compartments. Their formation involves a second branching enzyme isoform, GlgBII. To find out if the gene for the second isoform, glgBII, is regulated by any of the well-studied whiA, B, G, H or I genes needed for sporulation septation, glgBI or glgBII was disrupted in a set of whi mutants, and the glycogen phenotypes examined by transmission electron microscopy. In the whiG mutants, deposits were found throughout the aerial mycelium and the adjacent region of the substrate mycelium, but the morphology of all the deposits, i.e. whether they were in the form of granules of branched glycogen or large blobs of unbranched glycan, depended solely on GlgBI. In contrast, the whiA, B, H and I mutations had no obvious effect on the pattern of glycogen deposition, or on the spatial specificity of the branching enzyme isoforms (though phase II glycogen deposits were reduced in size and abundance in the whiA and B mutants, and increased in the whiH mutant). These results indicate that glgBII is regulated (directly or indirectly) by whiG, and not by any of the other whi genes tested, and that the aerial hyphae of a whiG mutant are atypical in being physiologically similar to the substrate hyphae from which they emerge. A new role for aerial hyphae is proposed.

Bacterial Proteins↗
PubMed2006

Interplay between Ino80 and Swr1 chromatin remodeling enzymes regulates cell cycle checkpoint adaptation in response to DNA damage.

Ino80 and Swr1 are ATP-dependent chromatin remodeling enzymes that have been implicated in DNA repair. Here we show that Ino80 is required for cell cycle checkpoint adaptation in response to a persistent DNA double-strand break (DSB). The failure of cells lacking Ino80 to escape checkpoint arrest correlates with an inability to maintain high levels of histone H2AX phosphorylation and an increased incorporation of the Htz1p histone variant into chromatin surrounding the DSB. Inactivation of Swr1 eliminates this DNA damage-induced Htz1p incorporation and restores H2AX phosphorylation and checkpoint adaptation. We propose that Ino80 and Swr1 function antagonistically at chromatin surrounding a DSB, and that they regulate the incorporation of different histone H2A variants that can either promote or block cell cycle checkpoint adaptation.

Adaptation, Physiological↗
PubMed2006

Crystal structure of SV40 large T-antigen bound to p53: interplay between a viral oncoprotein and a cellular tumor suppressor.

The transformation potential of Simian Virus 40 depends on the activities of large T-antigen (LTag), which interacts with several cellular tumor suppressors including the important "guardian" of the genome, p53. Inhibition of p53 function by LTag is necessary for both efficient viral replication and cellular transformation. We determined the crystal structure of LTag in complex with p53. The structure reveals an unexpected hexameric complex of LTag binding six p53 monomers. Structure-guided mutagenesis of LTag and p53 residues supported the p53-LTag interface defined by the complex structure. The structure also shows that LTag binding induces dramatic conformational changes at the DNA-binding area of p53, which is achieved partially through an unusual "methionine switch" within p53. In the complex structure, LTag occupies the whole p53 DNA-binding surface and likely interferes with formation of a functional p53 tetramer. In addition, we showed that p53 inhibited LTag helicase function through direct complex formation.

Antigens, Polyomavirus Transforming↗
PubMed1993

The interplay between multiple enhancer and silencer elements defines the pattern of decapentaplegic expression.

The product of the zygotically active decapentaplegic (dpp) gene appears to function as a morphogen that specifies positional information in the dorsal half of the Drosophila embryo. The dorsal-specific transcription of dpp is the key step in establishing a morphogen gradient. We demonstrate here that multiple regions within the second intron of the gene cooperate with one another to generate the wild-type level and pattern of dpp transcription. These regions contain both generalized enhancer elements as well as ventral-specific repressor elements. Placed within the context of heterologous promoters, the intron retains its ability to direct general activation and ventral repression. The ventral specific repression of dpp transcription is directly mediated by binding sites for the dorsal (dl) morphogen in the repressor elements. In contrast with the zerknüllt (zen) ventral repressor element, which contains a few high-affinity dl-binding sites, dpp contains multiple relatively low-affinity sites that function together to bring about complete ventral repression. Because dpp and zen have nearly coincident early expression domains, these results indicate that the same boundary of repression can be specified by dl-binding sites of different affinity. We discuss the possibility that unknown factors interact with dl protein to determine the domain of dl-mediated repression.

Animals↗