Topology Control for Maintaining Network Connectivity and Maximizing Network Capacity Under the Physical Model

In this paper we study the issue of topology control under the physical Signal-to-Interference-Noise-Ratio (SINR) model, with the objective of maximizing network capacity. We show that existing graph-model-based topology control captures interference inadequately under the physical SINR model, and as a result, the interference in the topology thus induced is high and the network capacity attained is low. Towards bridging this gap, we propose a centralized approach, called Spatial Reuse Maximizer (MaxSR), that combines a power control algorithm T4P with a topology control algorithm P4T. T4P optimizes the assignment of transmit power given a fixed topology, where by optimality we mean that the transmit power is so assigned that it minimizes the average interference degree (defined as the number of interferencing nodes that may interfere with the on-going transmission on a link) in the topology. P4T, on the other hand, constructs, based on the power assignment made in T4P, a new topology by deriving a spanning tree that gives the minimal interference degree. By alternately invoking the two algorithms, the power assignment quickly converges to an operational point that maximizes the network capacity. We formally prove the convergence of MaxSR. We also show via simulation that the topology induced by MaxSR outperforms that derived from existing topology control algorithms by 50%-110% in terms of maximizing the network capacity

Enhancing Neurogenesis in the Aging Brain through mTOR Pathway Activation

poster abstractThe U.S. population is aging. Age-related cognitive decline is a major public health problem. Developing an approach to treat or delay cognitive decline is critical. Neurogenesis by neural stem/progenitor cells (NSCs) in the hippocampus is related to cognitive function, and is greatly affected by the aging process. The molecular signaling that regulates age-related decline in neurogenesis is still poorly understood. Here we took the advantage of a transgenic mouse, Nestin-GFP, to assess neurogenesis and molecular signaling related to age-related decline in neurogenesis. We found that the total number of NSCs, including quiescent neural progenitors (QNPs) and amplifying neural progenitors (ANPs) decreased as the mice aged, but more importantly, ANPs are more significantly affected than QNPs, leading to further reduction in number and proliferation of ANPs. We further found that the mTOR signaling pathway is impaired in NSCs as mice age. Activating the mTOR signaling pathway through Ketamine injections increased NSC proliferation in aged mice. In contrast, inhibiting the activity of the mTOR signaling pathway by rapamycin is sufficient to reduce ANP proliferation in young mice. These results indicate that NSCs become more quiescent when the activity of mTOR signaling is compromised in aged mice, and stimulating the activity of mTOR signaling can overcome the age-associated decline in NSC proliferation. Following stimulation of the mTOR signaling pathway with Ketamine, we found a significant increase in the number of mature neurons. In order to determine whether or not a further increase in hippocampal neurogenesis is possible, we will next examine the ratio of newborn neuron survival

Remote pipeline assessment and condition monitoring using low-frequency axisymmetric waves: a theoretical study of torsional wave motion

Waves that propagate at low frequencies in buried pipes are of considerable interest in a variety of practical scenarios, for example leak detection, remote pipe detection, and pipeline condition assessment and monitoring. Particularly useful are the n=0, or axisymmetric, modes in which there is no displacement (or pressure) variation over the pipe cross section. Previous work has focused on two of the three axisymmetric wavetypes that can propagate: the s=1, fluid-dominated wave; and the s=2, shell-dominated wave. In this paper, the third axisymmetric wavetype, the s=0 torsional wave, is studied. Whilst there is a large body of research devoted to the study of torsional waves and their use for defect detection in pipes at ultrasonic frequencies, little is known about their behaviour and possible exploitation at lower frequencies. Here, a low-frequency analytical dispersion relationship is derived for the torsional wavenumber for a buried pipe from which both the wavespeed and wave attenuation can be obtained. How the torsional waves subsequently radiate to the ground surface is then investigated, with analytical expressions being presented for the ground surface displacement above the pipe resulting from torsional wave motion within the pipe wall. Example results are presented and, finally, how such waves might be exploited in practice is discussed

OVERCOMING THE AGE-ASSOCIATED DECLINE IN NEURAL STEM CELL PROLIFERATION

poster abstractThe U.S. population is aging. Age-related cognitive decline is a major public health problem. Developing an approach to treat or delay cognitive decline is critical. Neurogenesis by neural stem/progenitor cells (NSCs) in the hippocampus is related to cognitive function, and is greatly affected by the aging process. The molecular signaling that regulates age-related decline in neurogenesis is still poorly understood. Here we took the advantage of a transgenic mouse, Nestin-GFP, to assess neurogenesis and molecular signal-ing related to age-related decline in neurogenesis. We found that the total number of NSCs, including quiescent neural progenitors (QNPs) and amplify-ing neural progenitors (ANPs) decreased as the mice aged, but more im-portantly, ANPs are more significantly affected than QNPs, leading to further reduction in number and proliferation of ANPs. We further found that the mTOR signaling pathway is impaired in NSCs as mice age. Activating the mTOR signaling pathway through Ketamine injections increased NSC prolif-eration in aged mice. In contrast, inhibiting the activity of the mTOR signal-ing pathway by rapamycin is sufficient to reduce ANP proliferation in young mice. These results indicate that NSCs becomes more quiescent when the activity of mTOR signaling is compromised in aged mice, and stimulating the activity of mTOR signaling can overcome the age-associated decline in NSC proliferation. This data suggests that promoting stem cell proliferation to en-hance neurogenesis may be a potential approach for attenuating cognitive decline in the aging brain.This work was supported by funding from the Ralph W. and Grace M. Showalter Research Award, Indiana University Biological Research Grant, NIH grants RR025761 and 1R21NS072631-01A, and Undergraduate Research Opportunities Program (UROP)

The Role of Social Novelty in Risk Seeking and Exploratory Behavior: Implications for Addictions.

Novelty preference or sensation seeking is associated with disorders of addiction and predicts rodent compulsive drug use and adolescent binge drinking in humans. Novelty has also been shown to influence choice in the context of uncertainty and reward processing. Here we introduce a novel or familiar neutral face stimuli and investigate its influence on risk-taking choices in healthy volunteers. We focus on behavioural outcomes and imaging correlates to the prime that might predict risk seeking. We hypothesized that subjects would be more risk seeking following a novel relative to familiar stimulus. We adapted a risk-taking task involving acceptance or rejection of a 50:50 choice of gain or loss that was preceded by a familiar (pre-test familiarization) or novel face prime. Neutral expression faces of males and females were used as primes. Twenty-four subjects were first tested behaviourally and then 18 scanned using a different variant of the same task under functional MRI. We show enhanced risk taking to both gain and loss anticipation following novel relative to familiar images and particularly for the low gain condition. Greater risk taking behaviour and self-reported exploratory behaviours was predicted by greater right ventral putaminal activity to novel versus familiar contexts. Social novelty appears to have a contextually enhancing effect on augmenting risky choices possibly mediated via ventral putaminal dopaminergic activity. Our findings link the observation that novelty preference and sensation seeking are important traits predicting the initiation and maintenance of risky behaviours, including substance and behavioural addictions.VV is a Wellcome Trust Intermediate Fellow in Clinical Neurosciences (093705/Z/10/Z). The study was conducted at, and supported by, the National Institute of Neurological Disorders and Stroke, National Institutes of Health.This is the final version of the article. It first appeared from PLOS via http://dx.doi.org/10.1371/journal.pone.015894

Aging impairs dendrite morphogenesis of newborn neurons and is rescued by 7, 8-dihydroxyflavone

All aging individuals will develop some degree of decline in cognitive capacity as time progresses. The molecular and cellular mechanisms leading to age-related cognitive decline are still not fully understood. Through our previous research, we discovered that active neural progenitor cells selectively become more quiescent in response to aging, thus leading to the decline of neurogenesis in the aged hippocampus. Here, we further find that aging impaired dendrite development of newborn neurons. Currently, no effective approach is available to increase neurogenesis or promote dendrite development of newborn neurons in the aging brain. We found that systemically administration of 7, 8-dihydroxyflavone (DHF), a small molecule imitating brain-derived neurotrophic factor (BDNF), significantly enhanced dendrite length in the newborn neurons, while it did not promote survival of immature neurons, in the hippocampus of 12-month-old mice. DHF-promoted dendrite development of newborn neurons in the hippocampus may enhance their function in the aging animal leading to a possible improvement in cognition

Multi-Omics Analyses Detail Metabolic Reprogramming in Lipids, Carnitines, and Use of Glycolytic Intermediates between Prostate Small Cell Neuroendocrine Carcinoma and Prostate Adenocarcinoma.

As the most common cancer in men, prostate cancer is molecularly heterogeneous. Contributing to this heterogeneity are the poorly understood metabolic adaptations of the two main types of prostate cancer, i.e., adenocarcinoma and small cell neuroendocrine carcinoma (SCNC), the latter being more aggressive and lethal. Using transcriptomics, untargeted metabolomics and lipidomics profiling on LASCPC-01 (prostate SCNC) and LNCAP (prostate adenocarcinoma) cell lines, we found significant differences in the cellular phenotypes of the two cell lines. Gene set enrichment analysis on the transcriptomics data showed 62 gene sets were upregulated in LASCPC-01, while 112 gene sets were upregulated in LNCAP. ChemRICH analysis on metabolomics and lipidomics data revealed a total of 25 metabolite clusters were significantly different. LASCPC-01 exhibited a higher glycolytic activity and lower levels of triglycerides, while the LNCAP cell line showed increases in one-carbon metabolism as an exit route of glycolytic intermediates and a decrease in carnitine, a mitochondrial lipid transporter. Our findings pinpoint differences in prostate neuroendocrine carcinoma versus prostate adenocarcinoma that could lead to new therapeutic targets in each type

The E3 ubiquitin ligase IDOL regulates synaptic ApoER2 levels and is important for plasticity and learning.

Neuronal ApoE receptors are linked to learning and memory, but the pathways governing their abundance, and the mechanisms by which they affect the function of neural circuits are incompletely understood. Here we demonstrate that the E3 ubiquitin ligase IDOL determines synaptic ApoER2 protein levels in response to neuronal activation and regulates dendritic spine morphogenesis and plasticity. IDOL-dependent changes in ApoER2 abundance modulate dendritic filopodia initiation and synapse maturation. Loss of IDOL in neurons results in constitutive overexpression of ApoER2 and is associated with impaired activity-dependent structural remodeling of spines and defective LTP in primary neuron cultures and hippocampal slices. IDOL-deficient mice show profound impairment in experience-dependent reorganization of synaptic circuits in the barrel cortex, as well as diminished spatial and associative learning. These results identify control of lipoprotein receptor abundance by IDOL as a post-transcriptional mechanism underlying the structural and functional plasticity of synapses and neural circuits

Gain-of-function mutations in the UNC-2/CaV2α channel lead to excitation-dominant synaptic transmission in C. elegans

Mutations in pre-synaptic voltage gated calcium channels can lead to familial hemiplegic migraine type 1 (FHM1). While mammalian studies indicate that the migraine brain is hyperexcitable due to enhanced excitation or reduced inhibition, the molecular and cellular mechanisms underlying this excitatory/inhibitory (E/I) imbalance are poorly understood. We identified a gain-of-function (gf) mutation in the Caenorhabditis elegans CaV2 channel α1 subunit, UNC-2, which leads to increased calcium currents. unc-2(zf35gf) mutants exhibit hyperactivity and seizure-like motor behaviors. Expression of the unc-2 gene with FHM1 substitutions R192Q and S218L leads to hyperactivity similar to that of unc-2(zf35gf) mutants. unc-2(zf35gf) mutants display increased cholinergic-and decreased GABAergic-transmission. Moreover, increased cholinergic transmission in unc-2(zf35gf) mutants leads to an increase of cholinergic synapses and a TAX-6/calcineurin dependent reduction of GABA synapses. Our studies reveal mechanisms through which CaV2 gain-of-function mutations disrupt excitation-inhibition balance in the nervous system.Fil: Huang, Yung Chi. University of Massachussets; Estados UnidosFil: Pirri, Jennifer K.. University of Massachussets; Estados UnidosFil: Rayes, Diego Hernán. University of Massachussets; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Bahía Blanca. Instituto de Investigaciones Bioquímicas de Bahía Blanca. Universidad Nacional del Sur. Instituto de Investigaciones Bioquímicas de Bahía Blanca; Argentina. Universidad Nacional del Sur. Departamento de Biología, Bioquímica y Farmacia; ArgentinaFil: Gao, Shangbang. Mount Sinai Hospital; Estados UnidosFil: Mulcahy, Ben. Mount Sinai Hospital; Estados UnidosFil: Grant, Jeff. University of Massachussets; Estados UnidosFil: Saheki, Yasunori. The Rockefeller University; Estados UnidosFil: Francis, Michael M.. University of Massachussets; Estados UnidosFil: Zhen, Mei. University of Toronto; Canadá. Mount Sinai Hospital; Estados UnidosFil: Alkema, Mark J.. University of Massachussets; Estados Unido