Focal epilepsy may be induced acutely in the brain in vivo by measures which reduce inhibition or enhance excitation. Athough the various models involve different mechanisms causing the epilepsy, their epileptiform discharge patterns vary only little. Intracellular analyses in vivo and in vitro reveal that the cellular hallmark of epileptic discharge, the paroxysmal depolarization shift, is followed by a giant hyperpolarization. The latter is comprised of several, overlapping, components with different durations, including calcium dependent potassium currents and GABA dependent inhibitions. Relative reduction of one inhibitory component is compensated by other inhibitory components. In epilepsy caused by reduction of GABAergic inhibition, the absolute duration and amplitude of GABAergic inhibition may even be increased in comparison to the responses following afferent stimulation under control conditions since the excitatory drive of the paroxysmal discharges on the interneurons is strongly increased. In some interictal discharge patterns, the enhanced inhibitions within the focus determine the refractory periods of the focus. The latter is paced by neurons from the perifocal area which show a shorter inibition associated with the interictal epileptic event. The discharge pattern of the focus may switch to other patterns, either spontaneously, or as entrained by external stimulation. Such changes are caused e.g. by progressive potassium accumulations in the extracellular space with critically small intervals of the epileptic events. It is concluded that the epileptiform discharge patterns reflect intrinsic properties of the brain, and do not very well reflect the mechanism of action of the epileptogenic model. The brain is thus equipped with inherent mechanisms which favor rhythmic epileptiform discharges under certain conditions.
Lipase activity of the gypsy moth (Lymantria dispar L.) was studied by the spectrophotometric method using crude homogenate of fifth-instar larval midgut tissues as the enzyme source and p-nitrophenyl caprylate (pNPC) as substrate. A Km value of 0.310mM and a Vmax value of 1.479U/mg prot. were obtained for this substrate. Among various p-nitrophenyl esters tested, maximum activity was obtained for p-nitrophenyl caprylate and p-nitrophenyl caprate. The enzyme was most active at alkaline pH, with maximum at pH 8.2. Decreased activity was detected after preincubation in buffers of pH below 7.0 and above 8.2. The enzyme was unstable at room temperature. The enzyme was Ca2+ independent. Its activity was inhibited by PMSF, Fe2+, Ag+ and Pb2+, while Fe3+ inhibited enzyme activity by about 40%.
Defence-Aggression Reaction including its cardiovascular components may be inhibited during habituation or by stimulation in the restricted area of the prefrontal cortex. During the process of habituation components of the Defence-Aggression Reaction are inhibited on the level of nucleus paragigatocellularis lateralis of the ventral lateral medulla. The prefrontal cortex probably plays an important role in developing inhibition during habituation of the Defence-Aggression Reaction.
In the investigations carried out on anaerobic biodegradation of pesticides, specific sludge activity and toxity of pesticides in batch tests were determined.The specific methanogenic sludge activity was deterined i.e. the amount of acetate as an amount of COD for methane production per gam of sludge VSS (voatile suspended solid) per 1 day. Using the toxity test the magnitude of inhibition caused by presence of Metaxychlor - organochlorine insecticide group of pesticides - was assessed.The laboratory model of UASB was used for sludge cultivtion ((for methanogenic activity tests).Total voume of the reactor was 6.4 l.A portion of digested sludge taken from a Myslenice municipal wastewater treatment plant was used as an inoculum.
Suppressors of cytokine signaling (SOCS) proteins have been identified as important mediators of negative regulatory circuits within cytokine receptor signaling. They are induced upon stimulation by an increasing set of cytokines as well as further immunological stimuli and are capable to inhibit Janus-kinases and signal transducer and activator of transcription signaling. Inhibition is mediated by interfering directly with signal transduction at the receptor as well as targeting of associated molecules for proteosomal degradation. Targeted gene deletion approaches have revealed the importance of SOCS mediated termination of cytokine signaling during normal cellular activation. In addition to their function as classical feedback inhibitors SOCS proteins display a broad panel of inhibitory activity thereby mediating cross-talk modulation between different stimuli. The consequences for regulation of innate and adaptive immune responses are thus obvious. Finally, there are emerging data showing involvement of SOCS proteins in various immune diseases. Modulating SOCS activity could be a promising new approach for molecular therapeutic strategies.
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