Quadratic optimal functional quantization of stochastic processes and numerical applications

In this paper, we present an overview of the recent developments of functional quantization of stochastic processes, with an emphasis on the quadratic case. Functional quantization is a way to approximate a process, viewed as a Hilbert-valued random variable, using a nearest neighbour projection on a finite codebook. A special emphasis is made on the computational aspects and the numerical applications, in particular the pricing of some path-dependent European options.Comment: 41 page

Modulatory effects of Tabebuia impetiginosa (Lamiales, Bignoniaceae) on doxorubicin-induced somatic mutation and recombination in Drosophila melanogaster

The wing Somatic Mutation and Recombination Test (SMART) in D. melanogaster was used to study genotoxicity of the medicinal plant Tabebuia impetiginosa. Lapachol (naphthoquinone) and β-lapachone (quinone) are the two main chemical constituents of T. impetiginosa. These compounds have several biological properties. They induce apoptosis by generating oxygen-reactive species, thereby inhibiting topoisomerases (I and II) or inducing other enzymes dependent on NAD(P)H:quinone oxidoreductase 1, thus affecting cell cycle checkpoints. The SMART was used in the standard (ST) version, which has normal levels of cytochrome P450 (CYP) enzymes, to check the direct action of this compound, and in the high bioactivation (HB) version, which has a high constitutive level of CYP enzymes, to check for indirect action in three different T. impetiginosa concentrations (10%, 20% or 40% w/w). It was observed that T. impetiginosa alone did not modify the spontaneous frequencies of mutant spots in either cross. The negative results observed prompted us to study this phytotherapeuticum in association with the reference mutagen doxorubicin (DXR). In co-treated series, T. impetiginosa was toxic in both crosses at higher concentration, whereas in the HB cross, it induced a considerable potentiating effect (from ~24.0 to ~95.0%) on DXR genotoxity. Therefore, further research is needed to determine the possible risks associated with the exposure of living organisms to this complex mixture

A pivotal role for starch in the reconfiguration of 14C-partitioning and allocation in Arabidopsis thaliana under short-term abiotic stress.

Plant carbon status is optimized for normal growth but is affected by abiotic stress. Here, we used 14C-labeling to provide the first holistic picture of carbon use changes during short-term osmotic, salinity, and cold stress in Arabidopsis thaliana. This could inform on the early mechanisms plants use to survive adverse environment, which is important for efficient agricultural production. We found that carbon allocation from source to sinks, and partitioning into major metabolite pools in the source leaf, sink leaves and roots showed both conserved and divergent responses to the stresses examined. Carbohydrates changed under all abiotic stresses applied; plants re-partitioned 14C to maintain sugar levels under stress, primarily by reducing 14C into the storage compounds in the source leaf, and decreasing 14C into the pools used for growth processes in the roots. Salinity and cold increased 14C-flux into protein, but as the stress progressed, protein degradation increased to produce amino acids, presumably for osmoprotection. Our work also emphasized that stress regulated the carbon channeled into starch, and its metabolic turnover. These stress-induced changes in starch metabolism and sugar export in the source were partly accompanied by transcriptional alteration in the T6P/SnRK1 regulatory pathway that are normally activated by carbon starvation

Controls on gut phosphatisation : the trilobites from the Weeks Formation Lagerstätte (Cambrian; Utah)

Despite being internal organs, digestive structures are frequently preserved in Cambrian Lagerstätten. However, the reasons for their fossilisation and their biological implications remain to be thoroughly explored. This is particularly true with arthropods--typically the most diverse fossilised organisms in Cambrian ecosystems--where digestive structures represent an as-yet underexploited alternative to appendage morphology for inferences on their biology. Here we describe the phosphatised digestive structures of three trilobite species from the Cambrian Weeks Formation Lagerstätte (Utah). Their exquisite, three-dimensional preservation reveals unique details on trilobite internal anatomy, such as the position of the mouth and the absence of a differentiated crop. In addition, the presence of paired pygidial organs of an unknown function is reported for the first time. This exceptional material enables exploration of the relationships between gut phosphatisation and the biology of organisms. Indeed, soft-tissue preservation is unusual in these fossils as it is restricted to the digestive structures, which indicates that the gut played a central role in its own phosphatisation. We hypothesize that the gut provided a microenvironment where special conditions could develop and harboured a source of phosphorus. The fact that gut phosphatization has almost exclusively been observed in arthropods could be explained by their uncommon ability to store ions (including phosphorous) in their digestive tissues. However, in some specimens from the Weeks Formation, the phosphatisation extends to the entire digestive system, suggesting that trilobites might have had some biological particularities not observed in modern arthropods. We speculate that one of them might have been an increased capacity for ion storage in the gut tissues, related to the moulting of their heavily-mineralised carapace

Reassessing the role of mitochondrial DNA mutations in autism spectrum disorder

<p>Abstract</p> <p>Background</p> <p>There is increasing evidence that impairment of mitochondrial energy metabolism plays an important role in the pathophysiology of autism spectrum disorders (ASD; OMIM number: 209850). A significant proportion of ASD cases display biochemical alterations suggestive of mitochondrial dysfunction and several studies have reported that mutations in the mitochondrial DNA (mtDNA) molecule could be involved in the disease phenotype.</p> <p>Methods</p> <p>We analysed a cohort of 148 patients with idiopathic ASD for a number of mutations proposed in the literature as pathogenic in ASD. We also carried out a case control association study for the most common European haplogroups (hgs) and their diagnostic single nucleotide polymorphisms (SNPs) by comparing cases with 753 healthy and ethnically matched controls.</p> <p>Results</p> <p>We did not find statistical support for an association between mtDNA mutations or polymorphisms and ASD.</p> <p>Conclusions</p> <p>Our results are compatible with the idea that mtDNA mutations are not a relevant cause of ASD and the frequent observation of concomitant mitochondrial dysfunction and ASD could be due to nuclear factors influencing mitochondrion functions or to a more complex interplay between the nucleus and the mitochondrion/mtDNA.</p

Partial “targeted” embolisation of brain arteriovenous malformations

The treatment of pial arteriovenous brain malformations is controversial. Little is yet known about their natural history, their pathomechanisms and the efficacy and risks of respective proposed treatments. It is known that only complete occlusion of the AVM can exclude future risk of haemorrhage and that the rates of curative embolisation of AVMs with an acceptable periprocedural risk are around 20 to 50%. As outlined in the present article, however, partial, targeted embolisation also plays a role. In acutely ruptured AVMs where the source of bleeding can be identified, targeted embolisation of this compartment may be able to secure the AVM prior to definitive treatment. In unruptured symptomatic AVMs targeted treatment may be employed if a defined pathomechanism can be identified that is related to the clinical symptoms and that can be cured with an acceptable risk via an endovascular approach depending on the individual AVM angioarchitecture. This review article gives examples of pathomechanisms and angioarchitectures that are amenable to this kind of treatment strategy

Multifunctional semi-interpenetrating polymer network-nanoencapsulated cathode materials for high-performance lithium-ion batteries

As a promising power source to boost up advent of next-generation ubiquitous era, high-energy density lithium-ion batteries with reliable electrochemical properties are urgently requested. Development of the advanced lithium ion-batteries, however, is staggering with thorny problems of performance deterioration and safety failures. This formidable challenge is highly concerned with electrochemical/thermal instability at electrode material-liquid electrolyte interface, in addition to structural/chemical deficiency of major cell components. Herein, as a new concept of surface engineering to address the abovementioned interfacial issue, multifunctional conformal nanoencapsulating layer based on semi-interpenetrating polymer network (semi-IPN) is presented. This unusual semi-IPN nanoencapsulating layer is composed of thermally-cured polyimide (PI) and polyvinyl pyrrolidone (PVP) bearing Lewis basic site. Owing to the combined effects of morphological uniqueness and chemical functionality (scavenging hydrofluoric acid that poses as a critical threat to trigger unwanted side reactions), the PI/PVP semi-IPN nanoencapsulated-cathode materials enable significant improvement in electrochemical performance and thermal stability of lithium-ion batteries.open

Recipes and mechanisms of cellular reprogramming: a case study on budding yeast Saccharomyces cerevisiae

<p>Abstract</p> <p>Background</p> <p>Generation of induced pluripotent stem cells (iPSCs) and converting one cell type to another (transdifferentiation) by manipulating the expression of a small number of genes highlight the progress of cellular reprogramming, which holds great promise for regenerative medicine. A key challenge is to find the recipes of perturbing genes to achieve successful reprogramming such that the reprogrammed cells function in the same way as the natural cells.</p> <p>Results</p> <p>We present here a systems biology approach that allows systematic search for effective reprogramming recipes and monitoring the reprogramming progress to uncover the underlying mechanisms. Using budding yeast as a model system, we have curated a genetic network regulating cell cycle and sporulation. Phenotypic consequences of perturbations can be predicted from the network without any prior knowledge, which makes it possible to computationally reprogram cell fate. As the heterogeneity of natural cells is important in many biological processes, we find that the extent of this heterogeneity restored by the reprogrammed cells varies significantly upon reprogramming recipes. The heterogeneity difference between the reprogrammed and natural cells may have functional consequences.</p> <p>Conclusions</p> <p>Our study reveals that cellular reprogramming can be achieved by many different perturbations and the reprogrammability of a cell depends on the heterogeneity of the original cell state. We provide a general framework that can help discover new recipes for cellular reprogramming in human.</p

Comparison of glucose tolerance in renal transplant recipients and hemodialysis patients

BACKGROUND: Impaired glucose tolerance is a risk factor for atherosclerosis in hemodialysis patients and renal transplant recipients. METHODS: To check the relationship of impaired glucose tolerance with the other atherosclerotic risk factors, fasting blood sugar and the standard two hour glucose tolerance test, serum tryglyceride, serum cholesterol, cyclosporine through level (in renal tranpslant recipients) and hemoglobin A1C were measured in 55 stable renal transplant recipients, 55 hemodialysis patients and 55 healthy controls with similar demographic characteristics. Patients with diabetes mellitus and propranolol consumers were excluded. The mean age and female to male ratio were 39 +/- 7 years and 23/22, respectively. RESULTS: Four of the renal transplant recipients and twelve of the hemodialysis patients had impaired glucose tolerance. Significant linear correlation was observed with body mass index and IGT only in hemodialysis patients (r = 0.4, p = 0.05). Glucose tolerance also had a significant correlation with triglyceride levels (217.2 +/- 55 mg/dl in hemodialysis patients vs. 214.3 +/- 13 mg/dl in renal transplant recipients and 100.2 +/- 18 mg/dl in control groups, p = 0.001). The glucose tolerance had significant relationship with higher serum cholesterol levels only in the renal transplant recipients (269.7 +/- 54 in renal transplant recipients vs. 199.2 +/- 36.6 mg/dl in hemodialysis and 190.5 +/- 34 mg/dl in control groups, p = 0.0001). In the renal transplant recipients, a linear correlation was observed with glucose tolerance and both the serum cyclosporine level (r = 0.9, p = 0.001) and the hemoglobin A1C concentration (6.2 +/- 0.9 g/dl). The later correlation was also observed in the hemodialysis patients (6.4 +/- 0.7 g/dl; r = 67, p = 0.001). CONCLUSIONS: We conclude that although fasting blood sugar is normal in non-diabetic renal transplant and hemodialysis patients, impaired glucose tolerance could be associated with the other atherosclerotic risk factors