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The proposed model describes in a quality way the process of tumor-imaging radiopharmaceutical 99mTc-MIBI distribution with taking into account radiopharmaceutical accumulation, elimination, and radioactive decay. The dependencies of concentration versus the time are analyzed. The model can be easily tested by the concentration data of the radioactive pharmaceuticals in the blood measured at early time point and late time point of the scanning, and the obtained data can be used for determination of the washout rate coefficient which is one of the existing oncology diagnostics methods.

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Absence seizures are common in the stargazer mutant mouse. The mutation underlying the epileptic phenotype in stargazers is a defect in the gene encoding the normal expression of the protein stargazin. Stargazin is involved in the membrane trafficking and synaptic targeting of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) at excitatory glutamatergic synapses. Thus, the genetic defect in the stargazer results in a loss of AMPARs and consequently, excitation at glutamatergic synapses. Absence seizures are known to arise in thalamocortical networks. In the present study we show for the first time, using Western blot analysis and quantitative immunogold cytochemistry, that in the epileptic stargazer mouse, there is a global loss of AMPAR protein in nucleus reticularis (RTN) and a selective loss of AMPARs at corticothalamic synapses in inhibitory neurons of the RTN thalamus. In contrast, there is no significant loss of AMPARs at corticothalamic synapses in excitatory relay neurons in the thalamic ventral posterior (VP) region. The findings of this study thus provide cellular and molecular evidence for a selective regional loss of synaptic AMPAR within the RTN that could account for the loss of function at these inhibitory neuron synapses, which has previously been reported from electrophysiological studies. The specific loss of AMPARs at RTN but not relay synapses in the thalamus of the stargazer, could contribute to the absence epilepsy phenotype by altering thalamocortical network oscillations. This is supported by recent evidence that loss of glutamate receptor subunit 4 (GluA4) (the predominant AMPAR-subtype in the thalamus), also leads to a specific reduction in strength in the cortico-RTN pathway and enhanced thalamocortical oscillations, in the Gria4(-/-) model of absence epilepsy. Thus further study of thalamic changes in these models could be important for future development of drugs targeted to absence epilepsy.

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L-type calcium channels play an essential role in synaptic activity-dependent gene expression and are implicated in long-term alterations in synaptic efficacy underlying learning and memory in the hippocampus. The two principal pore-forming subunits of L-type Ca2+ channels expressed in neurons are the Ca(v)1.2 (alpha(1C)) or Ca(v)1.3 (alpha(1D)) subtypes. Experimental evidence suggests that calcium entry through Ca(v)1.2 and Ca(v)1.3 Ca2+ channels occurs in close proximity to key signalling molecules responsible for triggering signalling pathways leading to transcriptional responses. Determining the subcellular distribution of Ca(v)1.2 and Ca(v)1.3 L-type channels in neurons is clearly important for unravelling the molecular mechanisms underlying long-term alterations in neuronal function. In this study, we used immunogold-labelling techniques and electron-microscopy (EM) to analyse the subcellular distribution and density of both Ca(v)1.2 and Ca(v)1.3 Ca2+ channels in rat hippocampal CA1 pyramidal cells in vivo. We confirm that both Ca(v)1.2 and Ca(v)1.3 channel subtypes are predominantly but not exclusively located in postsynaptic dendritic processes and somata. Both Ca(v)1.2 and Ca(v)1.3 are distributed throughout the dendritic tree. However, the smallest (distal) dendritic processes and spines have proportionally more calcium channels inserted into their plasma membrane than located within cytoplasmic compartments indicating the potential targeting of calcium channels to microdomains within neurons. Ca(v)1.2 and Ca(v)1.3 Ca2+ channels are located at the postsynaptic density and also at extra-synaptic sites. The location of L-type Ca(v)1.2 and Ca(v)1.3 channels in distal dendrites and spines would thus place them at appropriate sites where they could initiate synapse to nucleus signalling.

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Lipid peroxidation was intensified by tetrachloromethane in liver. Concentration of lipid peroxidation products was decreased after chitosan injections. It was shown that application of chitosan had a positive effect on the liver of mice intoxicated by tetrachloromethane.

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The efficiency of some polysaccharides was investigated in mice with an experimental toxic hepatitis. Hepatitis was induced by the oral administration of 10% solution CCl4 in olive oil at a dosage of 3 ml/kg body weight every day during 7 days. After that tested substances were administrated every day 30-40 min before a feeding at a dosage of 150 mg/kg body weight during 14-21 days. Results showed that a calcium alginate, two low-methoxyl pectins (one with the degree of esterification about 50% and other with the degree of esterification less 5%), fucoidan, and chitozan, but not lambda-carrageenan and kappa-carrageenan, have beneficial affects on liver total lipid, glycogen, malondialdehyde, and diene conjugates as well as on blood total lipid and alanine aminotransferase activity in animals with experimental toxic hepatitis.

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Plasmapheresis, ultraviolet exposure of the blood, combination of these two methods, and plasmapheresis with removal of the upper layer of cells (partial cytapheresis) were added to routine treatment of 204 coronary patients. The above methods brought about good results, their efficacy being determined by the degree of myocardial involvement. A clear-cut effect of plasmapheresis on DIC, typical of such patients, is worthy of note.

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