Exact soliton solutions of coupled nonlinear Schr\"odinger equations: Shape changing collisions, logic gates and partially coherent solitons

The novel dynamical features underlying soliton interactions in coupled nonlinear Schr{\"o}dinger equations, which model multimode wave propagation under varied physical situations in nonlinear optics, are studied. In this paper, by explicitly constructing multisoliton solutions (upto four-soliton solutions) for two coupled and arbitrary $N$-coupled nonlinear Schr{\"o}dinger equations using the Hirota bilinearization method, we bring out clearly the various features underlying the fascinating shape changing (intensity redistribution) collisions of solitons, including changes in amplitudes, phases and relative separation distances, and the very many possibilities of energy redistributions among the modes of solitons. However in this multisoliton collision process the pair-wise collision nature is shown to be preserved in spite of the changes in the amplitudes and phases of the solitons. Detailed asymptotic analysis also shows that when solitons undergo multiple collisions, there exists the exciting possibility of shape restoration of atleast one soliton during interactions of more than two solitons represented by three and higher order soliton solutions. From application point of view, we have shown from the asymptotic expressions how the amplitude (intensity) redistribution can be written as a generalized linear fractional transformation for the $N$-component case. Also we indicate how the multisolitons can be reinterpreted as various logic gates for suitable choices of the soliton parameters, leading to possible multistate logic. In addition, we point out that the various recently studied partially coherent solitons are just special cases of the bright soliton solutions exhibiting shape changing collisions, thereby explaining their variable profile and shape variation in collision process.Comment: 50 Pages, 13 .jpg figures. To appear in PR

Improving employees' performance through internal marketing and organizational learning: mediating role of organizational innovation in an emerging market

This study identifies a specific relationship between internal marketing and organizational learning as the key drivers of organizational innovation, which build employees performance in the context of the petroleum industry. A model of the antecedents of organizational innovation was examined in a survey conducted among managers and employed specialists working in the oil industry in Iran. Structural equation modelling via Smart PLS was employed to gain insight into the various influences and relationships. We empirically scrutinized relationships between these constructs by validating a conceptual model employing SEM. The results indicate that internal marketing and organizational learning are key drivers of organizational innovation, which they are build employees performance. As well as, the results clarify that it is possible to improve the level of employee performance even through the complementary partial mediating role of organizational innovation. Additionally, this study makes a managerial contribution to the understanding of internal marketing, organizational learning and innovation on employee performance

Periodontal Ehlers-Danlos Syndrome Is Caused by Mutations in C1R and C1S, which Encode Subcomponents C1r and C1s of Complement

Periodontal Ehlers-Danlos syndrome (pEDS) is an autosomal-dominant disorder characterized by early-onset periodontitis leading to premature loss of teeth, joint hypermobility, and mild skin findings. A locus was mapped to an approximately 5.8 Mb region at 12p13.1 but no candidate gene was identified. In an international consortium we recruited 19 independent families comprising 107 individuals with pEDS to identify the locus, characterize the clinical details in those with defined genetic causes, and try to understand the physiological basis of the condition. In 17 of these families, we identified heterozygous missense or in-frame insertion/deletion mutations in C1R (15 families) or C1S (2 families), contiguous genes in the mapped locus that encode subunits C1r and C1s of the first component of the classical complement pathway. These two proteins form a heterotetramer that then combines with six C1q subunits. Pathogenic variants involve the subunit interfaces or inter-domain hinges of C1r and C1s and are associated with intracellular retention and mild endoplasmic reticulum enlargement. Clinical features of affected individuals in these families include rapidly progressing periodontitis with onset in the teens or childhood, a previously unrecognized lack of attached gingiva, pretibial hyperpigmentation, skin and vascular fragility, easy bruising, and variable musculoskeletal symptoms. Our findings open a connection between the inflammatory classical complement pathway and connective tissue homeostasis

Genome-Wide Profile of Pleural Mesothelioma versus Parietal and Visceral Pleura: The Emerging Gene Portrait of the Mesothelioma Phenotype

Malignant pleural mesothelioma is considered an almost incurable tumour with increasing incidence worldwide. It usually develops in the parietal pleura, from mesothelial lining or submesothelial cells, subsequently invading the visceral pleura. Chromosomal and genomic aberrations of mesothelioma are diverse and heterogenous. Genome-wide profiling of mesothelioma versus parietal and visceral normal pleural tissue could thus reveal novel genes and pathways explaining its aggressive phenotype.Well-characterised tissue from five mesothelioma patients and normal parietal and visceral pleural samples from six non-cancer patients were profiled by Affymetrix oligoarray of 38 500 genes. The lists of differentially expressed genes tested for overrepresentation in KEGG PATHWAYS (Kyoto Encyclopedia of Genes and Genomes) and GO (gene ontology) terms revealed large differences of expression between visceral and parietal pleura, and both tissues differed from mesothelioma. Cell growth and intrinsic resistance in tumour versus parietal pleura was reflected in highly overexpressed cell cycle, mitosis, replication, DNA repair and anti-apoptosis genes. Several genes of the “salvage pathway” that recycle nucleobases were overexpressed, among them TYMS, encoding thymidylate synthase, the main target of the antifolate drug pemetrexed that is active in mesothelioma. Circadian rhythm genes were expressed in favour of tumour growth. The local invasive, non-metastatic phenotype of mesothelioma, could partly be due to overexpression of the known metastasis suppressors NME1 and NME2. Down-regulation of several tumour suppressor genes could contribute to mesothelioma progression. Genes involved in cell communication were down-regulated, indicating that mesothelioma may shield itself from the immune system. Similarly, in non-cancer parietal versus visceral pleura signal transduction, soluble transporter and adhesion genes were down-regulated. This could represent a genetical platform of the parietal pleura propensity to develop mesothelioma.Genome-wide microarray approach using complex human tissue samples revealed novel expression patterns, reflecting some important features of mesothelioma biology that should be further explored

The role of the dentate gyrus and adult neurogenesis in hippocampal-basal ganglia associated behaviour

The ability of the brain to continually generate new neurons throughout life is one of the most intensely researched areas of modern neuroscience. While great advancements in understanding the biochemical mechanisms of adult neurogenesis have been made, there remain significant obstacles and gaps in connecting neurogenesis with behavioural and cognitive processes such as learning and memory. The purpose of the thesis was to examine by review and laboratory experimentation the role of the dentate gyrus and of adult neurogenesis within the hippocampus in the performance of cognitive tasks dependent on the hippocampal formation and hippocampal-basal ganglia interactions. Advancement in understanding the role of neurogenesis in these processes may assist in improving treatments for common brain injury and cognitive diseases that affect this region of the brain. Mild chronic stress reduced the acquisition rate of a stimulus-response task (p=0.043), but facilitated the acquisition of a discrimination between a small and a large reward (p=0.027). In locomotor activity assays, chronic stress did not shift the dose-response to methamphetamine. Analysis of 2,5-bromodeoxyuridine incorporation showed that, overall, chronic mild stress did not effect survival of neuronal progenitors . However, learning of the tasks had a positive influence on cell survival in stressed animals (p=0.038). Microinjections of colchicine produced significant lesions of the dentate gyrus and surrounding CA1-CA3 and neocortex. Damage to these regions impaired hippocampal-dependent reference memory (p=0.054) while preserving hippocampal independent simple discrimination learning. In a delay discounting procedure, the lesions did not induce impulsive-like behaviour when delay associated with a large reward was introduced. The experiments uphold a current theory that learning acts as a buffer to mitigate the negative effects of stress on neurogenesis