90,060 research outputs found
The genomics of Acinetobacter baumannii: Insights into genome plasticity, antimicrobial resistance and pathogenicity
No full textImperi F, Antunes L, Blom J, et al. The genomics of Acinetobacter baumannii: Insights into genome plasticity, antimicrobial resistance and pathogenicity. IUBMB life. 2011;63(12):1068-1074
A. F. Kamp ex librise
No full texthttp://www.lib.unideb.huDebreceni Egyetem Egyetemi és Nemzeti KönyvtárVakolatlan téglaépítkezésű épületek által határolt szűk tér vagy udvar, szemben faajtóval. A nyomat hátoldalán ceruzával: J. R. van Blom 1930metsze
P.1.04 Expression of histone variants H3.3 and H2a.z in the rat brain: Physiopathological and pharmacological implications
No full textIn the overall context of epigenetic modifications in charge of managing genome plasticity and dynamics [1, 2], the role of nucleosomal loading of histone variants is becoming increasingly captivating. Two replication-independent isoforms of histones H3 and H2A, namely H3.3 and H2A.Z, have caught attention because of their involvement in neuronal plasticity processes, cognitive functions and behavioral outcomes. In fact, their incorporation/eviction in nucleosomes and their turnover in neurons influence chromatin accessibility and therefore transcription. H3.3 enrichment at gene bodies and promoters of genes involved in synaptic plasticity was proved to be positively correlated with their expression, while learning-induced H2A.Z eviction in specific genes promotes gene transcription, intervening in memory consolidation processes. H3.3 is encoded by H3f3a and H3f3b independent genes, generating identical proteins, namely H3.3A and H3.3B. Notably, H3f3b gene, but not H3f3a, was proved responsive to neuronal activating stimuli as well as environmental triggers and stressful procedures [3]. H2A.Z hypervariants H2A.Z.1 and H2A.Z.2, encoded respectively by H2afz and H2afv genes, regulate both basal and stimulus-induced neuronal gene expression of independent gene sets [4]. Starting from this evidence, the purpose of this study was to characterize basal expression levels of all genes encoding for the histones variants above mentioned in rodent hippocampus and prefrontal cortex (PFC), two brain regions closely related to brain plasticity, cognition and behavior. Adult male rats (n=7) were sacrificed, their brains removed and dissected. Total RNA extraction was performed, followed by total RNA reverse transcription and Real Time PCR, where specific forward and reverse primer were used for each gene encoding for H3.3 (H3f3a and H3f3b), H2A.Z (H2afz and H2afv) and endogenous control GAPDH. Statistical analysis was performed by means of one-way ANOVA; p<0.05 was considered as a threshold for statistically significant difference. Molecular analyses revealed that, for both hippocampus and PFC, H3f3a mRNA was more expressed at the steady-state compared to H3f3b (p<0.001), as happens for H2afz mRNA, which displays higher levels than H2afv (p<0.001). Moreover, comparing hippocampal and PFC mRNA levels for each variant, H3f3a and H3f3b expression was increased in the hippocampus with respect to the prefrontal cortex (p<0.001), and a comparable outcome was showed for H2afv (p<0.001) but not for H2afz (p>0.05). Our results suggest that 1) differential basal expression levels of genes encoding for H3.3 and H2A.Z may underlie unique gene responsiveness following different stimuli, as previously hypothesized by others [3,4], and this may be crucial in highly-responsive, pathological- and environment-related tissues like hippocampus and PFC; 2) striking lower steady-state expression of H3f3b and H2afv genes might imply a major sensitivity to neuronal inputs compared to their correspondent counterparts; 3) higher expression levels in the hippocampus with respect to the PFC might underpin brain-region specific expression and function for histone variants and their isoforms. Together, these data clear the way for further studies meant at investigating stimulus-dependent regulation of H3.3 and H2A.Z gene isoforms expression and their putative involvement in the physiopathology of brain and its diseases [5]. References [1] Rigillo, G., Vilella, A., Benatti, C., Schaeffer, L., Brunello, N., Blom, J.M.C., Zoli, M., Tascedda, F., 2018. LPS-induced histone H3 phospho(Ser10)-acetylation(Lys14) regulates neuronal and microglial neuroinflammatory response. Brain Behav Immun. https://doi.org/10.1016/j.bbi.2018.09.019. [2] Ottaviani, E., Accorsi, A., Rigillo, G., Malagoli, D., Blom, J.M., Tascedda, F., 2013. Epigenetic modification in neurons of the mollusc Pomacea canaliculata after immune challenge. Brain Res. 1537, 18–26. [3] Maze, I., Wenderski, W., Noh, K.M., Bagot, R.C., Tzavaras, N., Purushothaman, I., Elsässer, S.J., Guo, Y., Ionete, C., Hurd, Y.L., Tamminga, C.A., Halene, T., Farrelly, L., Soshnev, A.A., Wen, D., Rafii, S., Birtwistle, M.R., Akbarian, S., Buchholz, B.A., Blitzer, R.D., Nestler, E.J., Yuan, Z.F., Garcia, B.A., Shen, L., Molina, H,. Allis, C.D., 2015. Critical Role of Histone Turnover in Neuronal Transcription and Plasticity. Neuron, 87(1), 77-94. [4] Dunn, C. J., Sarkar, P., Bailey, E. R., Farris, S., Zhao, M., Ward, J. M., Dudek, S.M., Saha, R. N., 2017. Histone Hypervariants H2A.Z.1 and H2A.Z.2 Play Independent and Context-Specific Roles in Neuronal Activity-Induced Transcription of Arc/Arg3.1 and Other Immediate Early Genes. eNeuro, 4(4), ENEURO.0040–17.2017. http://doi.org/10.1523/ENEURO.0040-17.2017. [5] Benatti, C., Blom, J.M., Rigillo, G., Alboni, S., Zizzi, F., Torta, R., Brunello, N., Tascedda, F., 2016. Disease-Induced Neuroinflammation and Depression. CNS Neurol. Disord. Drug Targets 15, 414–433
INFRARED BAND CONTOUR ANALYSIS AND MOLECULAR-CONSTANTS OF SPF3 AND NSF3
No full textKONIGER F, BLOM CE, Müller A. INFRARED BAND CONTOUR ANALYSIS AND MOLECULAR-CONSTANTS OF SPF3 AND NSF3. JOURNAL OF MOLECULAR SPECTROSCOPY. 1979;77(1):76-84
Building in Stones and Words: Strategies of Self Presentation in Huygens’ Volumes of Collected Poetry
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ontwikkelingen in zelfgerapporteerde daders, door de politie aangehouden verdachten en strafrechtelijke daders op basis van de Monitor Jeugdcriminaliteit
No full textWhat developments occured in the proportion, nature, and settlement of juvenile delinquency in the period of 1996-2010?In deze rapportage worden diverse ontwikkelingen in de aantallen jeugdige verdachten en daders in de leeftijd 12 tot en met 24 jaar, in samenhang gepresenteerd. Teven wordt ingegaan op delinquent gedrag van twaalfminners (10- en 11-jarigen). Het onderzoek is primair gericht op ontwikkelingen in indicatoren van het aantal jeugdige daders van delinquent gedrag en afdoeningen. De centrale vraag is uitgesplitst in de volgende deelvragen:Welke ontwikkelingen zijn er in zelfgerapporteerd daderschap van jeugdcriminaliteit in de periode 1996-2010?Welke ontwikkelingen zijn er in het aantal jeugdige verdachten van een misdrijf in de periode 1999-2008?Welke ontwikkelingen zijn er in het aantal jeugdige veelplegers in de periode 2003-2008?Welke ontwikkelingen zijn er in het aantal jeugdige strafrechtelijke daders in de periode 1997-2008?Welke ontwikkelingen zijn er in het aantal afdoeningen opgelegd door het OM of de ZM in de periode 1997-2008?Welke ontwikkelingen zijn er in de recidive onder jeugdigen in de periode 1997-2007? INHOUD: 1. Inleiding - A. van der Laan en M. Blom 2. Zelfgerapporteerde daders - A. van der Laan, M. Blom en I. Verburg (medew.) 3. Aangehouden verdachten - F. Huls 4. Verdachten naar pleegcarrière en strafrechtelijke daders - A. van der Laan, M. Blom en N. Tollenaar 5. Afdoeningen tegen jeugdige verdachten - A. van der Laan, M. Blom en F. Huls 6. Slot - A. van der Laan en M. Blo
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