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Cartesian Genetic Programming for Memristive Logic Circuits
[chapter]
2012
Lecture Notes in Computer Science
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Usually the important parameters in the design and implementation of combinational logic circuits are the number of gates, transistors, and levels used in the design of a circuit. In this regard, various evolutionary paradigms with different competency have recently been introduced. However, while being advantageous, evolutionary paradigms also have some limitations including a) lack of confidence in reaching the correct answer, b) long convergence time, and c) restriction on the tests
doi:10.1007/978-3-642-29139-5_4
fatcat:mukreo3sbvb4fezmymbjpmfmx4
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... with a higher number of input variables. In this work, we implement a genetic programming approach that given a Boolean function, outputs an equivalent circuit such that the truth table is covered, and the minimum number of gates (and to some extent, transistors and levels) are used. Furthermore, our implementation improves the aforementioned limitations by incorporating a self-repairing feature (improving limitation a); efficient use of the conceivable coding space of the problem, which virtually brings about a kind of parallelism and improves the convergence time (improving limitation b). Moreover, we apply our method to solve the Boolean functions with a higher number of inputs (improving limitation c). These issues are verified through multiple tests, and the results obtained are reported.
On Self-Adaptive Mutation Restarts for Evolutionary Robotics with Real Rotorcraft
[article]
2017
arXiv
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Self-adaptive parameters are increasingly used in the field of Evolutionary Robotics, as they allow key evolutionary rates to vary autonomously in a context-sensitive manner throughout the optimisation process. A significant limitation to self-adaptive mutation is that rates can be set unfavourably, which hinders convergence. Rate restarts are typically employed to remedy this, but thus far have only been applied in Evolutionary Robotics for mutation-only algorithms. This paper focuses on the
arXiv:1703.10754v2
fatcat:j7dynow6nbglfbtezac2mzpcme
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... vel at which evolutionary rate restarts are applied in population-based algorithms with more than 1 evolutionary operator. After testing on a real hexacopter hovering task, we conclude that individual-level restarting results in higher fitness solutions without fitness stagnation, and population restarts provide a more stable rate evolution. Without restarts, experiments can become stuck in suboptimal controller/rate combinations which can be difficult to escape from.
Interventional Fellowship in Structural and Congenital Heart Disease for Adults
2010
JACC: Cardiovascular Interventions
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and Washington, DC Training for structural and adult congenital heart disease interventions remains undeveloped. With the advent of recent percutaneous interventions for the treatment of structural and valvular heart disease, such as transcatheter aortic and pulmonary valve implantation, mitral valve repair, and the expansion of shunt closure procedures, there is a clear need to define the training requirements for this category of procedures. The training needs to be aligned with the goals and
doi:10.1016/j.jcin.2010.08.010
pmid:20850086
fatcat:s6ohjwqflbeabkugo7tdk75ej4
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... priorities of a basic or advanced level and be categorized into acquired and congenital. This document will define the training needs and knowledge base for the developing field of structural heart disease intervention. (J Am Coll Cardiol Intv 2010;3:e1-15)
Stretch-regulated Exocytosis/Endocytosis in Bladder Umbrella Cells
2002
Molecular Biology of the Cell
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The epithelium of the urinary bladder must maintain a highly impermeable barrier despite large variations in urine volume during bladder filling and voiding. To study how the epithelium accommodates these volume changes, we mounted bladder tissue in modified Ussing chambers and subjected the tissue to mechanical stretch. Stretching the tissue for 5 h resulted in a 50% increase in lumenal surface area (from ϳ2900 to 4300 m 2 ), exocytosis of a population of discoidal vesicles located in the
doi:10.1091/mbc.01-09-0435
pmid:11907265
pmcid:PMC99602
fatcat:zgujbngiabhldg5dyiyfs2qbri
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... l cytoplasm of the superficial umbrella cells, and release of secretory proteins. Surprisingly, stretch also induced endocytosis of apical membrane and 100% of biotinlabeled membrane was internalized within 5 min after stretch. The endocytosed membrane was delivered to lysosomes and degraded by a leupeptin-sensitive pathway. Last, we show that the exocytic events were mediated, in part, by a cyclic adenosine monophosphate, protein kinase A-dependent process. Our results indicate that stretch modulates mucosal surface area by coordinating both exocytosis and endocytosis at the apical membrane of umbrella cells and provide insight into the mechanism of how mechanical forces regulate membrane traffic in nonexcitable cells. Article published online ahead of print. Mol. Biol. Cell 10.1091/ mbc.01-09 -0435. Article and publication date are at www.molbiolcell.org/cgi/
On the effects of node duplication and connection-oriented constructivism in neural XCSF
2008
Proceedings of the 2008 GECCO conference companion on Genetic and evolutionary computation - GECCO '08
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For artificial entities to achieve high degrees of autonomy they will need to display appropriate adaptability. In this sense adaptability includes representational flexibility guided by the environment at any given time. This paper presents the use of constructivism-inspired mechanisms within a neural learning classifier system which exploits parameter self-adaptation as an approach to realize such behavior. Various network growth/regression mechanisms are implemented and their performances
doi:10.1145/1388969.1389010
dblp:conf/gecco/HowardB08
fatcat:2uhdczusnbcjridambe7fcmgqi
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... pared. The system uses a rule structure in which each is represented by an artificial neural network. It is shown that appropriate internal rule complexity emerges during learning at a rate controlled by the system.
Interventional fellowship in structural and congenital heart disease for adults
2010
Catheterization and cardiovascular interventions
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Training for structural and adult congenital heart disease interventions remains undeveloped. With the advent of recent percutaneous interventions for the treatment of structural and valvular heart disease, such as transcatheter aortic and pulmonary valve implantation, mitral valve repair, and the expansion of shunt closure procedures, there is a clear need to define the training requirements for this category of procedures. The training needs to be aligned with the goals and priorities of a
doi:10.1002/ccd.22702
pmid:20602482
fatcat:6cebvrz2ubf6nd75priqxnjy74
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... ic or advanced level and be categorized into acquired and congenital. This document will define the training needs and knowledge base for the developing field of structural heart disease intervention. V C 2010 Wiley-Liss, Inc.
ORGANIC MEMRISTOR DEVICES FOR LOGIC ELEMENTS WITH MEMORY
2012
International Journal of Bifurcation and Chaos in Applied Sciences and Engineering
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2012 pre-print arXiv:1212.3425v1 fatcat:jrfxzpthsfg3naegqfuuaal3iu
However, the realization of logic elements based on memristors has also been reported , Xia et al.(2009)] , including automated search of potential circuit topologies [Howard et al.(2012) ]. ...
doi:10.1142/s0218127412502835
fatcat:4kufxcj5fnfo3fknah4pz4qd74
Personalized genetic assessment of age associated Alzheimers disease risk
[article]
2016
bioRxiv
pre-print
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Importance: Identifying individuals at risk for developing Alzheimers disease (AD) is of utmost importance. Although genetic studies have identified APOE and other AD associated single nucleotide polymorphisms (SNPs), genetic information has not been integrated into an epidemiological framework for personalized risk prediction. Objective: To develop, replicate and validate a novel polygenic hazard score for predicting age-specific risk for AD. Setting: Multi-center, multi-cohort genetic and
doi:10.1101/074864
fatcat:ig2cwzkq25gdroh7p7k3clg6ia
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... ical data. Participants: We assessed genetic data from 17,008 AD patients and 37,154 controls from the International Genetics of Alzheimers Project (IGAP), and 6,409 AD patients and 9,386 older controls from Phase 1 Alzheimers Disease Genetics Consortium (ADGC). As independent replication and validation cohorts, we also evaluated genetic, neuroimaging, neuropathologic, CSF and clinical data from ADGC Phase 2, National Institute of Aging Alzheimers Disease Center (NIA ADC) and Alzheimers Disease Neuroimaging Initiative (ADNI) (total n = 20,680) Main Outcome(s) and Measure(s): Use the IGAP cohort to first identify AD associated SNPs (at p < 10-5). Next, integrate these AD associated SNPs into a Cox proportional hazards model using ADGC phase 1 genetic data, providing a polygenic hazard score (PHS) for each participant. Combine population based incidence rates, and genotype-derived PHS for each individual to derive estimates of instantaneous risk for developing AD, based on genotype and age. Finally, assess replication and validation of PHS in independent cohorts. Results: Individuals in the highest PHS quantiles developed AD at a considerably lower age and had the highest yearly AD incidence rate. Among APOE 3/3 individuals, PHS modified expected age of AD onset by more than 10 years between the lowest and highest deciles. In independent cohorts, PHS strongly predicted empirical age of AD onset (p = 1.1 x 10-26), longitudinal progression from normal aging to AD (p = 1.54 x 10-10) and associated with markers of AD neurodegeneration. Conclusions: We developed, replicated and validated a clinically usable PHS for quantifying individual differences in age-specific risk of AD. Beyond APOE, polygenic architecture plays an important role in modifying AD risk. Precise quantification of AD genetic risk will be useful for early diagnosis and therapeutic strategies.
Examining New Preoperative Assessment Tools
2016
Journal of The American Geriatrics Society
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Fibronectin Fragments and the Cleaving Enzyme ADAM-8 in the Degenerative Human Intervertebral Disc
2014
Spine
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Study Design-The presence fibronectin fragments (FN-fs) and the cleaving enzyme, A disintegrin and metalloproteinase domain-containing protein (ADAM)-8 were examined in human intervertebral disc (IVD) tissue in vitro. Objective-To investigate the presence and pathophysiological concentration of FN-fs and their cleaving enzyme, ADAM-8, in the human IVD tissue. Summary of Background Data- The 29kDa FN-f has been shown to result in extracellular matrix loss in rabbit IVDs. However, the
doi:10.1097/brs.0000000000000397
pmid:25010013
pmcid:PMC4229950
fatcat:3ifh76vgqncwjflw4x3ne4h5gq
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... n of this biologically active fragment in the degenerative human IVD tissue has previously not been determined. Further, it is critical to identify the enzyme(s) responsible for FN cleavage in the IVD. Methods-Human degenerative IVD tissues were removed during spinal surgery. A normal appearing young adult and an infant human cadaveric sample were obtained as controls. Soluble proteins were extracted, and analyzed by Western blotting utilizing antibodies specific for the human FN neoepitope VRAA 271 . A purified 29 kDa FN-f was used to allow estimation of the
Exploring concordance and discordance for return of incidental findings from clinical sequencing
2012
Genetics in Medicine
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Special article Purpose: The aim of this study was to explore specific conditions and types of genetic variants that specialists in genetics recommend should be returned as incidental findings in clinical sequencing. methods: Sixteen specialists in clinical genetics and/or molecular medicine selected variants in 99 common conditions to return to the ordering physician if discovered incidentally through whole-genome sequencing. For most conditions, the specialists independently considered three
doi:10.1038/gim.2012.21
pmid:22422049
pmcid:PMC3763716
fatcat:juropz5dnfdlthux3hduisw5uu
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... olecular scenarios for both adults and minor children: a known pathogenic mutation, a truncating variant presumed pathogenic (where other truncating variants are known to be pathogenic), and a missense variant predicted in silico to be pathogenic. Results: On average, for adults and children, respectively, each specialist selected 83.5 and 79.0 conditions or genes of 99 in the known pathogenic mutation categories, 57.0 and 53.5 of 72 in the truncating variant categories, and 33.4 and 29.7 of 72 in the missense variant categories. Concordance in favor of disclosure within the adult/ known pathogenic mutation category was 100% for 21 conditions or genes and 80% or higher for 64 conditions or genes. conclusion: Specialists were highly concordant for the return of findings for 64 conditions or genes if discovered incidentally during whole-exome sequencing or whole-genome sequencing. Genet Med 2012:14(4):405-410
Lipid associated polygenic enrichment in Alzheimer's disease
[article]
2018
bioRxiv
pre-print
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Cardiovascular (CV) and lifestyle associated risk factors (RFs) are increasingly recognized as important for Alzheimer's disease (AD) pathogenesis. Beyond the ε4 allele of apolipoprotein E (APOE), comparatively little is known about whether CV associated genes also increase risk for AD (genetic pleiotropy). Using large genome-wide association studies (GWASs) (total n > 500,000 cases and controls) and validated tools to quantify genetic pleiotropy, we systematically identified single nucleotide
doi:10.1101/383844
fatcat:g4sf3v7kyzcj3fmqdbp6wg5jcu
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... olymorphisms (SNPs) jointly associated with AD and one or more CV RFs, namely body mass index (BMI), type 2 diabetes (T2D), coronary artery disease (CAD), waist hip ratio (WHR), total cholesterol (TC), low-density (LDL) and high-density lipoprotein (HDL). In fold enrichment plots, we observed robust genetic enrichment in AD as a function of plasma lipids (TC, LDL, and HDL); we found minimal AD genetic enrichment conditional on BMI, T2D, CAD, and WHR. Beyond APOE, at conjunction FDR < 0.05 we identified 57 SNPs on 19 different chromosomes that were jointly associated with AD and CV outcomes including APOA4, ABCA1, ABCG5, LIPG, and MTCH2/SPI1. We found that common genetic variants influencing AD are associated with multiple CV RFs, at times with a different directionality of effect. Expression of these AD/CV pleiotropic genes was enriched for lipid metabolism processes, over-represented within astrocytes and vascular structures, highly co-expressed, and differentially altered within AD brains. Beyond APOE, we show that the polygenic component of AD is enriched for lipid associated RFs. Rather than a single causal link between genetic loci, RF and the outcome, we found that common genetic variants influencing AD are associated with multiple CV RFs. Our collective findings suggest that a network of genes involved in lipid biology also influence Alzheimer's risk.
A platform for discovery: The University of Pennsylvania Integrated Neurodegenerative Disease Biobank
2014
Alzheimer's & Dementia
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Neurodegenerative diseases (NDs) are defined by the accumulation of abnormal protein deposits in the central nervous system (CNS), and only neuropathological examination enables a definitive diagnosis. Brain banks and their associated scientific programs have shaped the actual knowledge of NDs, identifying and characterizing the CNS deposits that define new diseases, formulating staging schemes, and establishing correlations between neuropathological changes and clinical features. However,
doi:10.1016/j.jalz.2013.06.003
pmid:23978324
pmcid:PMC3933464
fatcat:twfsxkfnprgefnn75ukjsu3vru
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... banks have evolved to accommodate the banking of biofluids as well as DNA and RNA samples. Moreover, the value of biobanks is greatly enhanced if they link all the multidimensional clinical and laboratory information of each case, which is accomplished, optimally, using systematic and standardized operating procedures, and in the framework of multidisciplinary teams with the support of a flexible and user-friendly database system that facilitates the sharing of information of all the teams in the network. We describe a biobanking system that is a platform for discovery research at
β-amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity
1995
Cell
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Genetic assessment of age-associated Alzheimer disease risk: Development and validation of a polygenic hazard score
2017
PLoS Medicine
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Genetic variants can be integrated within an epidemiology framework to derive a polygenic score that can quantify individual differences in age-specific genetic risk for AD, beyond APOE. • Quantification of inherited genetic variation may prove useful for AD risk stratification and for therapeutic trials. Polygenic hazard score for Alzheimer disease PLOS Medicine | Fig 2. Kaplan-Meier estimates and Cox proportional hazard model fits among APOE ε3/3 individuals in the ADGC Phase 1 dataset,
doi:10.1371/journal.pmed.1002258
pmid:28323831
pmcid:PMC5360219
fatcat:wjq6syjohnf75mipp32gca3dgy
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... ing NIA ADC and ADNI samples. The solid lines represent the Cox fit, whereas the dashed lines and shaded regions represent the Kaplan-Meier estimations with 95% confidence intervals.
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