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Träfflista för sökning "WFRF:(Swift A) ;mspu:(researchreview)"

Sökning: WFRF:(Swift A) > Forskningsöversikt

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1.
  • Leggio, L, et al. (författare)
  • Role of feeding-related pathways in alcohol dependence: A focus on sweet preference, NPY, and ghrelin.
  • 2011
  • Ingår i: Alcoholism: clinical and experimental research. - : Wiley. - 0145-6008. ; 35:2, s. 194-202
  • Forskningsöversikt (refereegranskat)abstract
    • Converging research evidence suggests that alcohol and food-seeking behaviors share common neural pathways. There is preclinical and clinical evidence linking the consumption of sweets to alcohol intake in both animals and humans. In addition, a growing body of animal and human literature suggests the involvement of "feeding-related" peptides in alcohol-seeking behavior. In particular, both central and peripheral appetitive peptides have shown a possible role in alcohol dependence. The present mini-review will summarize the literature on the link between sweet preference and alcohol dependence, and on the role of feeding-related peptides in alcohol dependence. Specifically, in an attempt to narrow the field, the present mini-review will focus on 2 specific pathways, the central neuropeptide Y and the peripheral gut peptide ghrelin. Although more research is needed, data available suggest that studying feeding-related pathways in alcohol dependence may have theoretic, biologic, diagnostic, and therapeutic implications.
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2.
  • Williams, P., et al. (författare)
  • Quorum sensing and the population-dependent control of virulence
  • 2000
  • Ingår i: Philosophical Transactions of the Royal Society of London. Biological Sciences. - : The Royal Society. - 0962-8436 .- 1471-2970. ; 355:1397, s. 667-680
  • Forskningsöversikt (refereegranskat)abstract
    • One crucial feature of almost all bacterial infections is the need for the invading pathogen to reach a critical cell population density sufficient to overcome host defences and establish the infection. Controlling the expression of virulence determinants in concert with cell population density may therefore confer a significant survival advantage on the pathogen such that the host is overwhelmed before a defence response can be fully initiated. Many different bacterial pathogens are now known to regulate diverse physiological processes including virulence in a cell-density-dependent manner through cell-cell communication. This phenomenon, which relies on the interaction of a diffusible signal molecule (e.g. an N-acylhomoserine lactone) with a sensor or transcriptional activator to couple gene expression with cell population density, has become known as 'quorum sensing'. Although the size of the 'quorum' is likely to be highly variable and influenced by the diffusibility of the signal molecule within infected tissues, nevertheless quorum-sensing signal molecules can be detected in vivo in both experimental animal model and human infections. Furthermore, certain quorum-sensing molecules have been shown to possess pharmacological and immunomodulatory activity such that they may function as virulence determinants per se. As a consequence, quorum sensing constitutes a novel therapeutic target for the design of small molecular antagonists capable of attenuating virulence through the blockade of bacterial cell-cell communication.
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