148 research outputs found

    Uber den Einfluss einiger aktiven Substanzen auf spezifische und unspezifische Cholinesterase

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    Es wurde ein Unterschied in der Wirkung von Atropin und von d-Tubocurarin auf die Hydrolyse von ACh und BCh durch die Serum-ChE festgestellt. Atropin inhibiert die Hydrolyse von ACh in allen Konzentrationen, die grosser als 1Q-4,5M sind, wahrend die Hydrolyse von BCh durch dieselbe Substanz im Konzentrationsbereiche von 10 - 4, 5 M bis 10- 2,5 M aktiviert wird. Durch d-Tubocurarin werden beide Hydrolysen zurilckgedrangt, doch die Hydrolyse von BCh weniger. Beide Aktivsubstanzen inhibieren viel weniger die ChE der Menschenerythrocyten als die Serum ChE

    Diagnostics of fruit trees phytoplasmas – the importance of latent infections

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    In the period 2000-2008 more than 1300 fruit trees from different regions of Slovenia were tested for the quarantine phytoplasmas Apple proliferation (AP), Pear decline (PD), and European stone fruit yellows (ESFY). The majority of samples were collected within systematic official surveys, which was conducted for assessing the presence of these phytoplasma in Slovenia in production and mother plant orchards. Samples were taken from trees with and without expressed symptoms. DNA was extracted from the symptomatic shoots. In addition some roots from asymptomatic trees were sampled for the evaluation of latent infections. The presence of phytoplasmas was analyzed with a nested PCR, RFLP and a real time PCR (Hren et al., 2007). AP, PD and ESFY were confirmed as being present in several areas in Slovenia where fruit trees are cultivated. AP was found not only in apple, but also in stone fruit trees such as cherry, apricot and plum (Mehle et al., 2007). By using highly sensitive diagnostic methods, such as real time PCR, some latent infections were detected and they were confirmed next year also by less sensitive methods.Keywords: Phytoplasma, AP, PD, ESFY, latent infection, fruit tree

    Abstracts of presentations on plant protection issues at the xth international congress of virology: August 11-16,1996 Binyanei haOoma, Jerusalem, Israel Part 2 Plenary Lectures

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    Transcriptome Analysis of the Hippocampal CA1 Pyramidal Cell Region after Kainic Acid-Induced Status Epilepticus in Juvenile Rats

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    Molecular mechanisms involved in epileptogenesis in the developing brain remain poorly understood. The gene array approach could reveal some of the factors involved by allowing the identification of a broad scale of genes altered by seizures. In this study we used microarray analysis to reveal the gene expression profile of the laser microdissected hippocampal CA1 subregion one week after kainic acid (KA)-induced status epilepticus (SE) in 21-day-old rats, which are developmentally roughly comparable to juvenile children. The gene expression analysis with the Chipster software generated a total of 1592 differently expressed genes in the CA1 subregion of KA-treated rats compared to control rats. The KEGG database revealed that the identified genes were involved in pathways such as oxidative phosporylation (26 genes changed), and long-term potentiation (LTP; 18 genes changed). Also genes involved in Ca2+ homeostasis, gliosis, inflammation, and GABAergic transmission were altered. To validate the microarray results we further examined the protein expression for a subset of selected genes, glial fibrillary protein (GFAP), apolipoprotein E (apo E), cannabinoid type 1 receptor (CB1), Purkinje cell protein 4 (PEP-19), and interleukin 8 receptor (CXCR1), with immunohistochemistry, which confirmed the transcriptome results. Our results showed that SE resulted in no obvious CA1 neuronal loss, and alterations in the expression pattern of several genes during the early epileptogenic phase were comparable to previous gene expression studies of the adult hippocampus of both experimental epileptic animals and patients with temporal lobe epilepsy (TLE). However, some changes seem to occur after SE specifically in the juvenile rat hippocampus. Insight of the SE-induced alterations in gene expression and their related pathways could give us hints for the development of new target-specific antiepileptic drugs that interfere with the progression of the disease in the juvenile age group
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