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Objective: Our objective was to investigate whether people who use internal cues of satiation when eating a meal are likely to weigh less than people who instead rely on external cues. In addition to exploring the role that internal and external cues play in meal cessation, this study raises an overlooked explanation of the French paradox. Research Methods and Procedures: A demographically‐matched student sample of 133 Parisians and 145 Chicagoans completed a brief survey on meal cessation that asked the extent to which they agreed with statements associated with internal cessation cues and statements with external cessation cues. Their answers to these were compared across BMI levels and across countries. Results: Normal‐weight people indicated that they were more likely to be influenced by internal cues of meal cessation (p = 0.043), while overweight people indicated that they were more influenced by external cues (p = 0.005). Similarly, while the French were influenced by internal cues of meal cessation (p < 0.001), Americans were more influenced by external cues (p < 0.001). Discussion: This research revisits Schachter's externality hypothesis and suggests that one's over‐reliance on external cues may prove useful in offering a partial explanation of why BMI might vary across people and potentially across cultures. Relying on internal cues for meal cessation, rather than on external cues, may improve eating patterns over the long term. 相似文献
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Albert DG de Roos 《Biology direct》2007,2(1):7-17
Background
The timing of the origin of introns is of crucial importance for an understanding of early genome architecture. The Exon theory of genes proposed a role for introns in the formation of multi-exon proteins by exon shuffling and predicts the presence of conserved splice sites in ancient genes. In this study, large-scale analysis of potential conserved splice sites was performed using an intron-exon database (ExInt) derived from GenBank. 相似文献4.
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Cuppen E van Ham M Wansink DG de Leeuw A Wieringa B Hendriks W 《European journal of cell biology》2000,79(4):283-293
The small adaptor protein RIL consists of two segments, the C-terminal LIM and the N-terminal PDZ domain, which mediate multiple protein-protein interactions. The RIL LIM domain can interact with PDZ domains in the protein tyrosine phosphatase PTP-BL and with the PDZ domain of RIL itself. Here, we describe and characterise the interaction of the RIL PDZ domain with the zyxin-related protein TRIP6, a protein containing three C-terminal LIM domains. The second LIM domain in TRIP6 is sufficient for a strong interaction with RIL. A weaker interaction with the third LIM domain in TRIP6, including the proper C-terminus, is also evident. TRIP6 also interacts with the second out of five PDZ motifs in PTP-BL. For this interaction to occur both the third LIM domain and the proper C-terminus are necessary. RNA expression analysis revealed overlapping patterns of expression for TRIP6, RIL and PTP-BL, most notably in tissues of epithelial origin. Furthermore, in transfected epithelial cells TRIP6 can be co-precipitated with RIL and PTP-BL PDZ polypeptides, and a co-localisation of TRIP6 and RIL with Factin structures is evident. Taken together, PTP-BL, RIL and TRIP6 may function as components of multi-protein complexes at actin-based sub-cellular structures. 相似文献
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Background
Trinucleotide instability is a hallmark of degenerative neurological diseases like Huntington's disease, some forms of spinocerebellar ataxia and myotonic dystrophy type 1 (DM1). To investigate the effect of cell type and cell state on the behavior of the DM1 CTG•CAG repeat, we studied a knock-in mouse model for DM1 at different time points during ageing and followed how repeat fate in cells from liver and pancreas is associated with polyploidization and changes in nuclearity after the onset of terminal differentiation. 相似文献7.
Sergey M Zuev Stephen F Kingsmore Damian DG Gessler 《Theoretical biology & medical modelling》2006,3(1):8-15
Background
Sepsis (bloodstream infection) is the leading cause of death in non-surgical intensive care units. It is diagnosed in 750,000 US patients per annum, and has high mortality. Current understanding of sepsis is predominately observational and correlational, with only a partial and incomplete understanding of the physiological dynamics underlying the syndrome. There exists a need for dynamical models of sepsis progression, based upon basic physiologic principles, which could eventually guide hourly treatment decisions. 相似文献8.
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Ralph J. A. Oude Ophuis Mietske Wijers Miranda B. Bennink Fons A. J. van de Loo Jack A. M. Fransen Bé Wieringa Derick G. Wansink 《PloS one》2009,4(11)
Background
Studies on the myotonic dystrophy protein kinase (DMPK) gene and gene products have thus far mainly concentrated on the fate of length mutation in the (CTG)n repeat at the DNA level and consequences of repeat expansion at the RNA level in DM1 patients and disease models. Surprisingly little is known about the function of DMPK protein products.Methodology/Principal Findings
We demonstrate here that transient expression of one major protein product of the human gene, the hDMPK A isoform with a long tail anchor, results in mitochondrial fragmentation and clustering in the perinuclear region. Clustering occurred in a variety of cell types and was enhanced by an intact tubulin cytoskeleton. In addition to morphomechanical changes, hDMPK A expression induces physiological changes like loss of mitochondrial membrane potential, increased autophagy activity, and leakage of cytochrome c from the mitochondrial intermembrane space accompanied by apoptosis. Truncation analysis using YFP-hDMPK A fusion constructs revealed that the protein''s tail domain was necessary and sufficient to evoke mitochondrial clustering behavior.Conclusion/Significance
Our data suggest that the expression level of the DMPK A isoform needs to be tightly controlled in cells where the hDMPK gene is expressed. We speculate that aberrant splice isoform expression might be a codetermining factor in manifestation of specific DM1 features in patients. 相似文献10.
Johannes A Hofberger Beifei Zhou Haibao Tang Jonathan DG Jones M Eric Schranz 《BMC genomics》2014,15(1)