Intraspecific interactions and their effect on habitat utilisation by the praying mantid <Emphasis Type="Italic">Ciulfina biseriata</Emphasis> (Mantodea: Liturgusidae)

Tree trunks are spatially separated habitat patches for the tree-running mantid Ciulfina biseriata (Mantodea: Liturgusidae). This paper investigates how intraspecific interactions may affect spacing patterns in C. biseriata. Many mantid species inhabit tree trunk surfaces, but little is known about how they interact with this type of habitat. Behavioural observations and choice tests investigated the effect of a conspecific on habitat utilisation. Field surveys were used to investigate patterns of movement in the field. The decision to inhabit a tree trunk may be affected by the presence of a conspecific. Whereas adult males seek out females when selecting habitat, females will actively avoid males. Habitat choice decisions are primarily based on aspects of their mating system rather than on competition for space or food resources. The behavioural interactions of C. biseriata are described, including novel observations of same-sex mating behaviour in adult males.     

Regulation of the Oxidative Processes in the Organs of Mice under the Effects of Chemical and Physical Factors at Low Doses

Biophysics - The effects of the separate and combined action of lead nitrate in a wide range of doses, uranyl nitrate, and chronic low-dose gamma irradiation on the formation of oxidative stress in...     

The Gut–Brain Axis and Peroxisome Proliferator-Activated Receptors in the Regulation of Epileptogenesis

Journal of Evolutionary Biochemistry and Physiology - A large proportion of patients with epilepsy suffer from pharmacoresistant forms of the disease, and this makes the search for new treatments...     

Effect of TNF-α, IL-2, IL-5 and IL-6 on Rat Tracheal and Bronchial Smooth Muscle Contractions

Journal of Evolutionary Biochemistry and Physiology - The article addresses the role of TNF-α, IL-2, IL-5 and IL-6 in the contractile activity of rat tracheal and bronchial smooth muscle...     

Linoleic acid hydroperoxide favours hypochlorite- and myeloperoxidase-induced lipid peroxidation

Liposomes composed of soybean phosphatidylcholine were peroxidized using the reagent sodium hypochlorite or the myeloperoxidase-hydrogen peroxide-Cl^- system. Linoleic acid hydroperoxide previously prepared from linoleic acid by means of lipoxidase was incorporated into liposomes. The yield of thiobarbituric acid reactive substances (TBARS) continuously increased with higher amounts of hydroperoxide groups after the initiation of lipid peroxidation by hypochlorous acid producing systems. The accumulation of TBARS was inhibited by scavengers of free radicals such as butylated hydroxytoluene and by the scavengers of hypochlorous acid, taurine and methionine. Lipid peroxidation was also prevented by sodium azide or chloride free medium in the myeloperoxidase-hydrogen peroxide-Cl^- system. Here we show for the first time that the reaction of hypochlorous acid with a biologically relevant hydroperoxide yields free radicals able to cause further oxidation of lipid molecules.     

Steady-state kinetics of F1-ATPase. Mechanism of anion activation

The kinetic behaviour of the ATPase activity of beef heart F1 depends largely on the exposure of the enzyme to some anionic ligands such as sulphate and/or EDTA. F1 prepared in the presence of such anions exhibited a triphasic kinetic pattern whereas F1 from which those anions were removed by dialysis exhibited only two Km values for ATP. Conversely to what has been previously reported, bicarbonate did not linearize F1-ATPase kinetics. Moreover, anion activation cannot be simply explained by promotion of ADP release but mainly by an increase in affinity of the third catalytic site for ATP.     

The synthesis of 15N- and deuterium-substituted, spin-labeled analogues of NAD+ and their use in EPR studies of dehydrogenases

Calcium efflux and EGTA-induced calcium release from an internal platelet membrane fraction have been studied after the oxalate-supported calcium uptake had reached steady state. Increasing external calcium concentrations stimulate the calcium efflux velocity, with an apparent half-maximal stimulation at about 5 microM outside calcium concentration and a maximal velocity of calcium efflux of 4.66 +/- 2.32 nmol X min-1 X mg-1. Moreover, the ratio of the liberated calcium on the loaded calcium seems to be independent of the increasing external calcium concentration. Increasing the calculated internal calcium concentration by varying the oxalate potassium concentration from 10 mM to 1 mM results in an increase of the liberated calcium from the membrane vesicles from 7.4% to 63%, respectively, without changing the calcium efflux velocity. Similar conclusions can be drawn from the observation of results from the calcium efflux and EGTA-induced calcium release methods. Moreover, calcium pump reversal does not seem to be responsible for the calcium efflux or calcium release. All these different points added to the previously described regulation of calcium efflux by the catalytic subunit of cAMP protein kinase suggest us that the mechanism of calcium liberation by the platelet membranes is different from the calcium uptake.