11,551 research outputs found

    Informational drives for sensor evolution

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    © 2012 Massachusetts Institute of Technology Published under a Creative Commons Attribution 4.0 International (CC BY 4.0) licenseIt has been hypothesized that the evolution of sensors is a pivotal driver for the evolution of organisms, and especially, as a crucial part of the perception-action loop, a driver for cognitive development. The questions of why and how this is the case are important: what are the principles that push the evolution of sensorimotor systems? An interesting aspect of this problem is the co-option of sensors for functions other than those originally driving their development (e.g. the auditive sense of bats being employed as a 'visual' modality). Even more striking is the phenomenon found in nature of sensors being driven to the limits of precision, while starting from much simpler beginnings. While a large potential for diversification and exaptation is visible in the observed phenotypes, gaining a deeper understanding of why and how this can be achieved is a significant problem. In this present paper, we will introduce a formal and generic information-theoretic model for understanding potential drives of sensor evolution, both in terms of improving sensory ability and in terms of extending and/or shifting sensory function

    Hyperbolic Structures and Root Systems

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    We discuss the construction of a one parameter family of complex hyperbolic structures on the complement of a toric mirror arrangement associated with a simply laced root system. Subsequently we find conditions for which parameter values this leads to ball quotients

    Low-carbohydrate diets affect energy balance and fuel homeostasis differentially in lean and obese rats

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    In parallel with increased prevalence of overweight people in affluent societies are individuals trying to lose weight, often using low-carbohydrate diets. Nevertheless, long-term metabolic consequences of those diets, usually high in (saturated) fat, remain unclear. Therefore, we investigated long-term effects of high-fat diets with different carbohydrate/protein ratios on energy balance and fuel homeostasis in obese (fa/fa) Zucker and lean Wistar rats. Animals were fed high-carbohydrate (HC), high-fat (HsF), or low-carbohydrate, high-fat, high-protein (LC-HsF-HP) diets for 60 days. Both lines fed the LC-HsF-HP diet displayed reduced energy intake compared with those fed the HsF diet (Zucker, -3.7%) or the HC diet (Wistar rats, -12.4%). This was not associated with lower weight gain relative to HC fed rats, because of increased food efficiencies in each line fed HsF and particularly LC-HsF-HP food. Zucker rats were less glucose tolerant than Wistar rats. Lowest glucose tolerances were found in HsF and particularly in LC-HsF-HP-fed animals irrespective of line, but this paralleled reduced plasma adiponectin levels, elevated plasma resistin levels, higher retroperitoneal fat masses, and reduced insulin sensitivity (indexed by insulin-induced hypoglycemia) only in Wistar rats. In Zucker rats, however, improved insulin responses during glucose tolerance testing and tendency toward increased insulin sensitivities were observed with HsF or LC-HsF-HP feeding relative to HC feeding. Thus, despite adverse consequences of LC-HsF diets on blood glucose homeostasis, principal differences exist in the underlying hormonal regulatory mechanisms, which could have benefits for B-cell functioning and insulin action in the obese state but not in the lean state.

    The role of leptin in the regulation of energy balance and adiposity

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    Since its discovery, leptin (a 167-amino acid product of the OB gene) has quickly moved to the forefront as an important hormone for regulation of energy balance. It closes a feedback loop from adipose tissue to hypothalamic neuropeptide-containing neural circuitry involved in regulation of food intake and neuroendocrine/autonomic outflow. While increased central leptin signalling reduces adiposity via a reduction in food intake, it also has remarkable metabolic effects that promote leanness, independent of food intake. These include: (i) increased energy expenditure, (ii) in-place degradation of fat, and (iii) increased thermogenesis. Hypothalamic neurones that synthesize corticotropin releasing hormone and melanocortins (i.e. alpha -melanocyte-stimulating hormone and agouti-related protein) are likely effector pathways that mediate the anorexigenic and metabolic effects of leptin. Activation of sympathetic outflow (via neuropeptidergic effector pathways of central leptin) to a number of tissues that store fat might be an important mechanism through which these peripheral metabolic effects are elicited. It is proposed that these peripheral metabolic effects contribute to the satiating properties of leptin.</p
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