Structural sensitivity of chaotic dynamics in Hastings-Powell's model

The classical Hastings-Powell model is well known to exhibit chaotic dynamics in a three-species food chain. Chaotic dynamics appear through period-doubling bifurcation of stable coexistence limit cycle around an unstable interior equilibrium point. A specific choice of parameter value leads to a situation where the chaotic attractor disappears through a collision with an unstable limit cycle. As a result, the top predator goes to extinction. Here we explore the structural sensitivity of this phenomenon by replacing the Holling type II functional responses with Ivlev functional responses. Here we prove the existence of two Hopf-bifurcation thresholds and numerically detect the existence of an unstable limit cycle. The model with Ivlev functional responses does not indicate any possibility of extinction of the top predator. Further, the choice of functional responses depicts a significantly different picture of the coexistence of the three species involved with the model

Vanadium : A Possible Role in the Protection of Host Cells Bearing Transplantable Murine Lymphoma

The effect of oral administration of an optimum dose of ammonium monovanadate was studied in hosts bearing a transplantable ascitic lymphoma. This was supported by the biochemical indices relating to markers like reduced glutathione (GSH), extent of lipid peroxidation and activities of glutathione per-oxidase (GPx) in hepatic tissues of the experimental animals. These biochemi-cal parameters showed substantial alterations during the period of tumor progres-sion in the experimental group treated with a low dose of vanadium (0.005 ,μ-M) suggesting a possible correlation between the observed variation in these markers and the survival rates in the animals receiving vanadium treatment

Case–Control Studies of Gene–Environment Interaction: Bayesian Design and Analysis

With increasing frequency, epidemiologic studies are addressing hypotheses regarding gene-environment interaction. In many well-studied candidate genes and for standard dietary and behavioral epidemiologic exposures, there is often substantial  prior  information available that may be used to analyze current data as well as for designing a new study. In this article, first, we propose a proper full Bayesian approach for analyzing studies of gene–environment interaction. The Bayesian approach provides a natural way to incorporate uncertainties around the assumption of gene–environment independence, often used in such an analysis. We then consider Bayesian sample size determination criteria for both estimation and hypothesis testing regarding the multiplicative gene–environment interaction parameter. We illustrate our proposed methods using data from a large ongoing case–control study of colorectal cancer investigating the interaction of N-acetyl transferase type 2 (NAT2) with smoking and red meat consumption. We use the existing data to elicit a design prior and show how to use this information in allocating cases and controls in planning a future study that investigates the same interaction parameters. The Bayesian design and analysis strategies are compared with their corresponding frequentist counterparts.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78584/1/j.1541-0420.2009.01357.x.pd

Elevated Lipid Peroxidation, Decreased Glutathione Levels and Changes in Glutathione-Related Enzymes in Rats Treated with Human PIacental Extract

The in vivo effects of human placental extract (1-4 ml/kg) on hepatic lipid peroxidation, blood and liver glutathione (GSH) levels and several enzymes associated with the antioxidant defence mechanism; i.e., catalase, glutathione peroxidase, glutathione reductase and glutathione S-transferase, together with some blood biochemical responses were investigated in rats. At an optimal dose level (4 ml/kg), a single acute intraperitoneal administration of the extract caused a significant enhancement (49.9%; p &#60; 0.001) of lipid peroxidation with a decline in GSH level both in blood (45.1%; p &#60; 0.001) and liver (61.0%; p &#60; 0.001) in comparison to control animals. Activities of catalase, glutathione peroxidase and glutathione reductase were inhibited in a dose-responsive way by the treatment with the extract which also increased the activity of glutathione S-transferase in a dose-dependent manner. The extract was found to be hepatotoxic in terms of elevation of serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, serum lactate dehydrogenase and blood methemoglobin concentration. Results of this study suggest the adverse consequences of the administration of the extract due to its substantial ability to alter normal cellular processes.</p

Proton-Induced X-ray Emission (PIXE) Analysis and DNA-chain Break study in rat hepatocarcinogenesis: A possible chemopreventive role by combined supplementation of vanadium and beta-carotene

Combined effect of vanadium and beta-carotene on rat liver DNA-chain break and Proton induced X-ray emission (PIXE) analysis was studied during a necrogenic dose (200 mg/kg of body weight) of Diethyl Nitrosamine (DENA) induced rat liver carcinogenesis. Morphological and histopathological changes were observed as an end point biomarker. Supplementation of vanadium (0.5 ppm ad libitum) in drinking water and beta-carotene in the basal diet (120 mg/Kg of body weight) were performed four weeks before DENA treatment and continued till the end of the experiment (16 weeks). PIXE analysis revealed the restoration of near normal value of zinc, copper, and iron, which were substantially altered when compared to carcinogen treated groups. Supplementation of both vanadium and beta-carotene four weeks before DENA injection was found to offer significant (64.73%, P < 0.001) protection against generation of single-strand breaks when compared with the carcinogen control counter parts. A significant stabilization of hepatic architecture of the cells was observed as compared to carcinogen control in vanadium plus beta-carotene treated group. This study thus suggests that vanadium, a prooxidant but potential therapeutic agent yield safe and effective pharmacological formulation with beta-carotene, an antioxidant, in the inhibition of experimental rat hepatocarcinogenesis

Primitive Sca-1 Positive Bone Marrow HSC in Mouse Model of Aplastic Anemia: A Comparative Study through Flowcytometric Analysis and Scanning Electron Microscopy

Self-renewing Hematopoietic Stem Cells (HSCs) are responsible for reconstitution of all blood cell lineages. Sca-1 is the “stem cell antigen” marker used to identify the primitive murine HSC population, the expression of which decreases upon differentiation to other mature cell types. Sca-1+ HSCs maintain the bone marrow stem cell pool throughout the life. Aplastic anemia is a disease considered to involve primary stem cell deficiency and is characterized by severe pancytopenia and a decline in healthy blood cell generation system. Studies conducted in our laboratory revealed that the primitive Sca-1+ BM-HSCs (bone marrow hematopoietic stem cell) are significantly affected in experimental Aplastic animals pretreated with chemotherapeutic drugs (Busulfan and Cyclophosphamide) and there is increased Caspase-3 activity with consecutive high Annexin-V positivity leading to premature apoptosis in the bone marrow hematopoietic stem cell population in Aplastic condition. The Sca-1bright, that is, “more primitive” BM-HSC population was more affected than the “less primitive” BM-HSC Sca-1dim  population. The decreased cell population and the receptor expression were directly associated with an empty and deranged marrow microenvironment, which is evident from scanning electron microscopy (SEM). The above experimental evidences hint toward the manipulation of receptor expression for the benefit of cytotherapy by primitive stem cell population in Aplastic anemia cases

Alteration in Marrow Stromal Microenvironment and Apoptosis Mechanisms Involved in Aplastic Anemia: An Animal Model to Study the Possible Disease Pathology

Aplastic anemia (AA) is a heterogeneous disorder of bone marrow failure syndrome. Suggested mechanisms include a primary stem cell deficiency or defect, a secondary stem cell defect due to abnormal regulation between cell death and differentiation, or a deficient microenvironment. In this study, we have tried to investigate the alterations in hematopoietic microenvironment and underlying mechanisms involved in such alterations in an animal model of drug induced AA. We presented the results of studying long term marrow culture, marrow ultra-structure, marrow adherent and hematopoietic progenitor cell colony formation, flowcytometric analysis of marrow stem and stromal progenitor populations and apoptosis mechanism involved in aplastic anemia. The AA marrow showed impairment in cellular proliferation and maturation and failed to generate a functional stromal microenvironment even after 19 days of culture. Ultra-structural analysis showed a degenerated and deformed marrow cellular association in AA. Colony forming units (CFUs) were also severely reduced in AA. Significantly decreased marrow stem and stromal progenitor population with subsequently increased expression levels of both the extracellular and intracellular apoptosis inducer markers in the AA marrow cells essentially pointed towards the defective hematopoiesis; moreover, a deficient and apoptotic microenvironment and the microenvironmental components might have played the important role in the possible pathogenesis of AA

Barreras naturales para las horquillas de replicación DNA en Schizosaccharomyces pombe

106 p.-35 fig.En la naturaleza, el crecimiento vegetativo de S. pombe es normalmente haploide. Sólo bajo condiciones ambientales adversas, como en condiciones de ayuno de fuentes nitrógeno, dos células de tipos de apareamiento contrarios, P (plus) y M (minus), conjugan y forman un cigoto diploide (Egel, 1989; Dalgaard y Klar, 2001). Para cada tipo de apareamiento, existen células denominadas switchable (s) y células unswitchable (u). Cada célula de S. pombe que acaba de adquirir un tipo de apareamiento concreto, da lugar a otra del tipo de apareamiento contrario tras dos divisiones mitóticas. Cuando una célula u se divide da lugar a dos células del mismo tipo de apareamiento que la célula parental, una de ellas s y la otra u. Cuando se divida, la célula s dará lugar a una célula u de tipo de apareamiento contrario a la parental y a otra célula s del mismo tipo de apareamiento que la parental (Miyata y Miyata, 1981; Egel y Eie, 1987; Klar, 1987, 1990). Aunque el mecanismo molecular responsable del cambio del tipo de apareamiento en S. pombe no se conoce aún en detalle, algunas de las claves han sido ya descifradas (ver Dalgaard y Klar, 2001 y apartado 1.4.2.). Una vez que producida la conjugación, los núcleos se fusionan y el cigoto diploide resultante sufre meiosis inmediatamente. El cigoto se convierte en una estructura de resistencia denominada asca, que contiene cuatro esporas haploides. Este proceso representa un ejemplo de diferenciación celular. Cuando las condiciones ambientales vuelven a ser favorables, las esporas son liberadas y pueden germinar, cerrándose de este modo el ciclo. Las poblaciones naturales de S. pombe, son homotálicas, es decir, están compuestas por células de los dos tipos de apareamiento y entran en diferenciación sexual bajo condiciones de estrés ambiental. En el laboratorio, a menudo se emplean estirpes heterotálicas, las cuales necesitan otra estirpe del tipo de apareamiento contrario para aparear. En el laboratorio se puede promover la entrada de los cigotos a la división mitótica y seleccionarlos usando mutaciones auxotróficas complementarias en el proceso de conjugación, obteniendo así estirpes diploides que, eventualmente, pueden inducirse a entrar en ciclo mitótico colocándolas en unas condiciones de cultivo adecuadas.Financiación del Proyecto SAF2001-1740; de la Beca del CSIC de Postgrado para la Formación y Especialización en Líneas de Investigación para el Sector Industrial con REF.: I3P-BPG2004 y del Proyecto BFU2004-00125/BMC.Peer reviewe