Low temperature thermodynamics of charged bosons in a random potential and the specific heat of La_{2-x}Sr_{x}CuO_{4} below Tc

We propose a simple analytical form of the partition function for charged bosons localised in a random potential and derive the consequent thermodynamics below the superfluid transition temperature. In the low temperature limit, the specific heat, C, depends on the localisation length exponent nu: C is linear for nu1 we find C proportional to T^{1/nu}. This unusual sub-linear temperature dependence of the specific heat has recently been observed in La_{2-x}Sr_{x}CuO_{4} below Tc.Comment: Revtex, 6 pages, 4 postscript figure

Infinite-range Ising ferromagnet in a time-dependent transverse field: quench and ac dynamics near the quantum critical point

We study an infinite range ferromagnetic Ising model in the presence of a transverse magnetic field which exhibits a quantum paramagnetic-ferromagnetic phase transition at a critical value of the transverse field. In the thermodynamic limit, the low-temperature properties of this model are dominated by the behavior of a single large classical spin governed by an anisotropic Hamiltonian. Using this property, we study the quench and AC dynamics of the model both numerically and analytically, and develop a correspondence between the classical phase space dynamics of a single spin and the quantum dynamics of the infinite-range ferromagnetic Ising model. In particular, we compare the behavior of the equal-time order parameter correlation function both near to and away from the quantum critical point in the presence of a quench or AC transverse field. We explicitly demonstrate that a clear signature of the quantum critical point can be obtained by studying the AC dynamics of the system even in the classical limit. We discuss possible realizations of our model in experimental systems.Comment: Revtex4, 10 pages including 10 figures; corrected a sign error in Eq. 32; this is the final published versio

GeNN: a code generation framework for accelerated brain simulations

Large-scale numerical simulations of detailed brain circuit models are important for identifying hypotheses on brain functions and testing their consistency and plausibility. An ongoing challenge for simulating realistic models is, however, computational speed. In this paper, we present the GeNN (GPU-enhanced Neuronal Networks) framework, which aims to facilitate the use of graphics accelerators for computational models of large-scale neuronal networks to address this challenge. GeNN is an open source library that generates code to accelerate the execution of network simulations on NVIDIA GPUs, through a flexible and extensible interface, which does not require in-depth technical knowledge from the users. We present performance benchmarks showing that 200-fold speedup compared to a single core of a CPU can be achieved for a network of one million conductance based Hodgkin-Huxley neurons but that for other models the speedup can differ. GeNN is available for Linux, Mac OS X and Windows platforms. The source code, user manual, tutorials, Wiki, in-depth example projects and all other related information can be found on the project website http://genn-team.github.io/genn/

Using the DPSIR framework for transdisciplinary training and knowledge elicitation in the Gulf of Thailand

No abstract available

NAMPT-mediated NAD+ biosynthesis is indispensable for adipose tissue plasticity and development of obesity

Objective: The ability of adipose tissue to expand and contract in response to fluctuations in nutrient availability is essential for the maintenance of whole-body metabolic homeostasis. Given the nutrient scarcity that mammals faced for millions of years, programs involved in this adipose plasticity were likely evolved to be highly efficient in promoting lipid storage. Ironically, this previously advantageous feature may now represent a metabolic liability given the caloric excess of modern society. We speculate that nicotinamide adenine dinucleotide (NAD+) biosynthesis exemplifies this concept. Indeed NAD+/NADH metabolism in fat tissue has been previously linked with obesity, yet whether it plays a causal role in diet-induced adiposity is unknown. Here we investigated how the NAD+ biosynthetic enzyme nicotinamide phosphoribosyltransferase (NAMPT) supports adipose plasticity and the pathological progression to obesity. Methods: We utilized a newly generated Nampt loss-of-function model to investigate the tissue-specific and systemic metabolic consequences of adipose NAD+ deficiency. Energy expenditure, glycemic control, tissue structure, and gene expression were assessed in the contexts of a high dietary fat burden as well as the transition back to normal chow diet. Results: Fat-specific Nampt knockout (FANKO) mice were completely resistant to high fat diet (HFD)-induced obesity. This was driven in part by reduced food intake. Furthermore, HFD-fed FANKO mice were unable to undergo healthy expansion of adipose tissue mass, and adipose depots were rendered fibrotic with markedly reduced mitochondrial respiratory capacity. Yet, surprisingly, HFD-fed FANKO mice exhibited improved glucose tolerance compared to control littermates. Removing the HFD burden largely reversed adipose fibrosis and dysfunction in FANKO animals whereas the improved glucose tolerance persisted. Conclusions: These findings indicate that adipose NAMPT plays an essential role in handling dietary lipid to modulate fat tissue plasticity, food intake, and systemic glucose homeostasis. Keywords: Adipose metabolism, Obesity, NAMPT, NAD+ synthesis, Energy homeostasis, Adipose plasticity, Glucose homeostasi

Extreme Food-Plant Specialisation in Megabombus Bumblebees as a Product of Long Tongues Combined with Short Nesting Seasons

© 2015 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. http://creativecommons.org/licenses/by/4.0/ The attached file is the published version of the article

Effect of the altitudinal variation of the gravitational acceleration on the thermosphere simulation

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/95479/1/jgra19341.pd

Disentangling astroglial physiology with a realistic cell model in silico

Electrically non-excitable astroglia take up neurotransmitters, buffer extracellular K+ and generate Ca2+ signals that release molecular regulators of neural circuitry. The underlying machinery remains enigmatic, mainly because the sponge-like astrocyte morphology has been difficult to access experimentally or explore theoretically. Here, we systematically incorporate multi-scale, tri-dimensional astroglial architecture into a realistic multi-compartmental cell model, which we constrain by empirical tests and integrate into the NEURON computational biophysical environment. This approach is implemented as a flexible astrocyte-model builder ASTRO. As a proof-of-concept, we explore an in silico astrocyte to evaluate basic cell physiology features inaccessible experimentally. Our simulations suggest that currents generated by glutamate transporters or K+ channels have negligible distant effects on membrane voltage and that individual astrocytes can successfully handle extracellular K+ hotspots. We show how intracellular Ca2+ buffers affect Ca2+ waves and why the classical Ca2+ sparks-and-puffs mechanism is theoretically compatible with common readouts of astroglial Ca2+ imaging