40 research outputs found

    Molecular analyses reveal consistent food web structure with elevation in rainforest Drosophila – parasitoid communities

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    The analysis of interaction networks across spatial environmental gradients is a powerful approach to investigate the responses of communities to global change. Using a combination of DNA metabarcoding and traditional molecular methods we built bipartite Drosophila-parasitoid food webs from six Australian rainforest sites across gradients spanning 850 m in elevation and 5° Celsius in mean temperature. Our cost-effective hierarchical approach to network reconstruction separated the determination of host frequencies from the detection and quantification of interactions. The food webs comprised 5-9 host and 5-11 parasitoid species at each site, and showed a lower incidence of parasitism at high elevation. Despite considerable turnover in the relative abundance of host Drosophila species, and contrary to some previous results, we did not detect significant changes to fundamental metrics of network structure including nestedness and specialisation with elevation. Advances in community ecology depend on data from a combination of methodological approaches. It is therefore especially valuable to develop model study systems for sets of closely-interacting species that are diverse enough to be representative, yet still amenable to field and laboratory experiments

    Molecular analyses reveal consistent food web structure with elevation in rainforest Drosophila – parasitoid communities

    Get PDF
    The analysis of interaction networks across spatial environmental gradients is a powerful approach to investigate the responses of communities to global change. Using a combination of DNA metabarcoding and traditional molecular methods we built bipartite Drosophila – parasitoid food webs from six Australian rainforest sites across gradients spanning 850 m in elevation and 5°C in mean temperature. Our cost-effective hierarchical approach to network reconstruction separated the determination of host frequencies from the detection and quantification of interactions. The food webs comprised 5–9 host and 5–11 parasitoid species at each site, and showed a lower incidence of parasitism at high elevation. Despite considerable turnover in the relative abundance of host Drosophila species, and contrary to some previous results, we did not detect significant changes to fundamental metrics of network structure including nestedness and specialisation with elevation. Advances in community ecology depend on data from a combination of methodological approaches. It is therefore especially valuable to develop model study systems for sets of closely-interacting species that are diverse enough to be representative, yet still amenable to field and laboratory experiments

    Polymorphic variants of SCN1A and EPHX1 influence plasma carbamazepine concentration, metabolism and pharmacoresistance in a population of Kosovar Albanian epileptic patients

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    Aim The present study aimed to evaluate the effects of gene variants in key genes influencing pharmacokinetic and pharmacodynamic of carbamazepine (CBZ) on the response in patients with epilepsy. Materials & Methods Five SNPs in two candidate genes influencing CBZ transport and metabolism, namely ABCB1 or EPHX1, and CBZ response SCN1A (sodium channel) were genotyped in 145 epileptic patients treated with CBZ as monotherapy and 100 age and sex matched healthy controls. Plasma concentrations of CBZ, carbamazepine-10,11-epoxide (CBZE) and carbamazepine-10,11-trans dihydrodiol (CBZD) were determined by HPLC-UV-DAD and adjusted for CBZ dosage/kg of body weight. Results The presence of the SCN1A IVS5-91G>A variant allele is associated with increased epilepsy susceptibility. Furthermore, carriers of the SCN1A IVS5-91G>A variant or of EPHX1 c.337T>C variant presented significantly lower levels of plasma CBZ compared to carriers of the common alleles (0.71±0.28 vs 1.11±0.69 μg/mL per mg/Kg for SCN1A IVS5-91 AA vs GG and 0.76±0.16 vs 0.94±0.49 μg/mL per mg/Kg for EPHX1 c.337 CC vs TT; PG showed a reduced microsomal epoxide hydrolase activity as reflected by a significantly decreased ratio of CBZD to CBZ (0.13±0.08 to 0.26±0.17, pT SNP and SCN1A 3148A>G variants were not associated with significant changes in CBZ pharmacokinetic. Patients resistant to CBZ treatment showed increased dosage of CBZ (657±285 vs 489±231 mg/day; P<0.001) but also increased plasma levels of CBZ (9.84±4.37 vs 7.41±3.43 μg/mL; P<0.001) compared to patients responsive to CBZ treatment. CBZ resistance was not related to any of the SNPs investigated. Conclusions The SCN1A IVS5-91G>A SNP is associated with susceptibility to epilepsy. SNPs in EPHX1 gene are influencing CBZ metabolism and disposition. CBZ plasma levels are not an indicator of resistance to the therapy

    Kainic Acid and Nitrergic Neurons Kainic Acid and Nitrergic Neurons in Immature Hippocampus

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    Jandová K.; Riljak V.; Pokorný J.; Langmeier M. Abstract: Using histochemical analysis the effect of intraperitoneal administration of kainic acid on hippocampal neurons was studied. 18-day-old male rats of the Wistar strain received kainic acid (10mg/kg) in one dose. Two days later, the 20-day-old animals were transcardially perfused with 4% paraformaldehyde under deep thiopental anaesthesia. Cryostat sections were stained to identify NADPH-diaphorase positive neurons that were then quantified in the CA1 and CA3 areas of the hippocampus, in the dorsal and ventral blades of the dentate gyrus and in the hilus of the dentate gyrus. Combination of the Fluoro-Jade B and bis-benzimide (Hoechst 33342) was used in the same areas, to identify possible neurodegeneration. After the kainic acid administration the number of NADPH-d positive neurons was lower in CA1 and CA3 areas of the hippocampus and in the hilus of the dentate gyrus, compared to the control group which we consider as baseline. Fluoro-Jade B staining detected a moderate density of neurodegeneration after KA administration in CA3 and CA1 areas of the hippocampus and the hilus of the dentate gyrus

    Effects of Magnetic Field 0.1 and 0.05 mT on Leukocyte Adherence Inhibition

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    Keywords Biological effects of magnetic field; Cell-mediated immunity; Effect of cancer on cell-mediated immunity

    Mitochondrial Metabolism – Neglected Link of Cancer Transformation and Treatment

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    Physical processes in living cells were not taken into consideration among the essentials of biological activity, regardless of the fact that they establish a state far from thermodynamic equilibrium. In biological system chemical energy is transformed into the work of physical forces for various biological functions. The energy transformation pathway is very likely connected with generation of the endogenous electrodynamic field as suggested by experimentally proved electrodynamic activity of biological systems connected with mitochondrial and microtubule functions. Besides production of ATP and GTP (adenosine and guanosine triphosphate) mitochondria form a proton space charge layer, strong static electric field, and water ordering around them in cytosol – that are necessary conditions for generation of coherent electrodynamic field by microtubules. Electrodynamic forces are of a long-range nature in comparison with bond and cohesive forces. Mitochondrial dysfunction leads to disturbances of the electromagnetic field; its power and coherence may be diminished, and frequency spectrum altered. Consequently, defective electrodynamic interaction forces between cancer and healthy cells may result in local invasion of cancer cells. Further deformation of interaction forces connected with experimentally disclosed spatial disarrangement of the cytoskeleton and disordered electrodynamic field condition metastatic process. Cancer therapeutic strategy targeting mitochondria may restore normal physiological functions of mitochondria and open the apoptotic pathway. Apoptosis of too much damaged cancer cells was observed. Considerable experience with DCA (dichloroacetate) cancer treatment in humans was accumulated. Clinical trials should assess DCA therapeutic potential and collect data for development of novel more effective drugs for mitochondrial restoration of various cancers
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