Signal classification through multifractal analysis and complex domain neural networks

This paper describes a system capable of classifying stochastic self-affine nonstationary signals produced by nonlinear systems. The classification and the analysis of these signals are important because these are generated by many real-world processes. The first stage of the signal classification process entails the transformation of the signal into the multifractal dimension domain, through the computation of the variance fractal dimension trajectory (VFDT). Features can then be extracted from the VFDT using a Kohonen self-organizing feature map. The second stage involves the use of a complex domain neural network and a probabilistic neural network to determine the class of a signal based on these extracted features. The results of this paper show that these techniques can be successful in creating a classification system which can obtain correct classification rates of about 87% when performing classification of such signals without knowing the number of classes.     

Branching and pruning: An optimal temporal POCL planner based on constraint programming

A key feature of modern optimal planners such as graphplan and blackbox is their ability to prune large parts of the search space. Previous Partial Order Causal Link (POCL) planners provide an alternative branching scheme but lacking comparable pruning mechanisms do not perform as well. In this paper, a domain-independent formulation of temporal planning based on Constraint Programming is introduced that successfully combines a POCL branching scheme with powerful and sound pruning rules. The key novelty in the formulation is the ability to reason about supports, precedences, and causal links involving actions that are not in the plan. Experiments over a wide range of benchmarks show that the resulting optimal temporal planner is much faster than current ones and is competitive with the best parallel planners in the special case in which actions have all the same duration.¹     

Cortical cholinergic impairment and behavioral deficits produced by kainic acid lesions of rat magnocellular basal forebrain.

The rat magnocellular basal forebrain (MNBF) is homologous to the human nucleus basalis of Meynert, a structure implicated in the cholinergic hypothesis of cognitive impairment in Alzheimer's disease (AD). In the present study, 18 male Sprague-Dawley rats with kainic acid lesions in the MNBF were compared with 6 unoperated controls, 10 sham-operated controls, and 6 controls injected with kainic acid in the cortical area directly above the MNBF. MNBF lesions depleted choline acetyltransferase in cortex but not in striatum or hippocampus. Cortical dopamine levels were unchanged; serotonin levels were unchanged in hippocampus and parietal cortex but decreased in frontal cortex. Compared with controls, MNBF-lesioned Ss were impaired in 24-hr retention, but not acquisition, of a passive avoidance task with escapable footshock. The groups did not differ in mean number of daily avoidances on a barpress active avoidance task, although learning was slower in MNBF-lesioned Ss. In a serial spatial discrimination reversal test, MNBF-lesioned Ss performed significantly worse than controls. This model may be useful for studying the role of the cholinergic system in memory and possibly for developing treatment strategies to alleviate the cognitive dysfunction of AD. (63 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Diverse Fab specific for acetylcholine receptor epitopes from a myasthenia gravis thymus combinatorial library

The muscle weakness in myasthenia gravis (MG) is caused by heterogeneous high-affinity IgG autoantibodies to the nicotinic acetylcholine receptor (AChR), a complex ion channel glycoprotein. These antibodies are clearly responsible for reducing AChR numbers at the neuromuscular junction in myasthenia; however, the origins, diversity, specificity and pathogenicity of individual antibodies have not yet been established. We have cloned and characterized four different AChR-specific Fab from an MG patient's thymus by screening an IgG1/kappa gene combinatorial lambda phage library with soluble human AChR labeled with [125I] alpha-bungarotoxin. Unlike most previously cloned human antibodies, all four Fab immunoprecipitated soluble human muscle AChR. Two Fab strongly inhibited binding of mAb to the main immunogenic region on the alpha subunits and one Fab bound to an epitope on the fetal-specific gamma subunit. In sensitivity and fine specificity, these Fab resembled the anti-AChR antibodies found in many MG patients, including the donor. The closest germline counterparts for their heavy chains were in VH families 1, 3 and 4; however, there were many differences consistent with an antigen-driven response of diverse B cell clones. The combinatorial approach holds promise for further analysis of human autoantibodies.     

Perspective:Societally connected multimedia across cultures

The advance of the Internet in the past decade has radically changed the way people communicate and col- laborate with each other. Physical distance is no more a barrier in online social networks, but cultural differences (at the individual, community, as well as societal levels) still govern human-human interactions and must be con- sidered and leveraged in the online world. The rapid de-ployment of high-speed Internet allows humans to interact using a rich set of multimedia data such as texts, pictures, and videos. This position paper proposes to define a new research area called ’connected multimedia’, which is the study of a collection of research issues of the super-area social media that receive little attention in the literature. By connected multimedia, we mean the study of the social and technical interactions among users, multimedia data, and devices across cultures and explicitly exploiting the cultural differences. We justify why it is necessary to bring attention to this new research area and what benefits of this new research area may bring to the broader scientific research community and the humanity.     

The effects of withholding feed and water on carcass shrinkage and meat quality in beef cattle

Eighty beef crossbred steers with an average weight of 493 kg (4·66 kg SD) were allocated at random to one of five treatments to assess the effects of withholding feed and water on carcass shrinkage and meat quality. The five treatments were: slaughter from the feedlot (T1); and 12, 24, 36 and 48 h periods without feed and water prior to slaughter (T2-5).Weights were taken of the live animal and the carcass to monitor shrinkage along with relevant meat quality measurements. There were no treatment differences (P > 0·05) in initial farm weight, but plant weight shrinkage increased from 31gkg(-1) for T1 to 106 g kg(-1) for T5. Warm carcass weight decreased (P < 0·05) from 278·8 kg for T1, to 270·7 kg for T3 and 261·9 kg for T5. Liver, alimentary tract components, hide and head decreased as a proportion of farm weight as time without feed and water increased. Muscle pH at 6 days post mortem was increased (P < 0·05) in T3-5 compared to T1, with the result that muscle colour became darker, and steaks had less drip loss. Shear values increased (P < 0·05) from 6·3 kg in T1 to 7·7 kg in T4 and T5 indicating an increase in muscle toughness as time without feed and water increased. It was concluded that steers lose live weight rapidly within the first 24 h without feed and water, and that these relatively short periods of time (24 h) can have detrimental effects on carcass shrinkage and muscle quality.     

Nuclear Receptor Nur77 Controls Cardiac Fibrosis through Distinct Actions on Fibroblasts and Cardiomyocytes

Fibrosis is a hallmark of adverse cardiac remodeling, which promotes heart failure, but it is also an essential repair mechanism to prevent cardiac rupture, signifying the importance of appropriate regulation of this process. In the remodeling heart, cardiac fibroblasts (CFs) differentiate into myofibroblasts (MyoFB), which are the key mediators of the fibrotic response. Additionally, cardiomyocytes are involved by providing pro-fibrotic cues. Nuclear receptor Nur77 is known to reduce cardiac hypertrophy and associated fibrosis; however, the exact function of Nur77 in the fibrotic response is yet unknown. Here, we show that Nur77-deficient mice exhibit severe myocardial wall thinning, rupture and reduced collagen fiber density after myocardial infarction and chronic isoproterenol (ISO) infusion. Upon Nur77 knockdown in cultured rat CFs, expression of MyoFB markers and extracellular matrix proteins is reduced after stimulation with ISO or transforming growth factor–β (TGF-β). Accordingly, Nur77-depleted CFs produce less collagen and exhibit diminished proliferation and wound closure capacity. Interestingly, Nur77 knockdown in neonatal rat cardiomyocytes results in increased paracrine induction of MyoFB differentiation, which was blocked by TGF-β receptor antagonism. Taken together, Nur77-mediated regulation involves CF-intrinsic promotion of CF-to-MyoFB transition and inhibition of cardiomyocyte-driven paracrine TGF-β-mediated MyoFB differentiation. As such, Nur77 provides distinct, cell-specific regulation of cardiac fibrosis.