The results of an X-ray structure determination of 1 ',3',1 "',3"'-tetraethylbiferrocenium triiodide, the effects of changing the relative positions of ethyl substituents from 1 ',3',1 "',3"' t o 1 ',2'"''',2'" o n the intramolecular electron-transfer rates of biferrocenium salts in the solid state, and a theoretical explanation of the influence of steric factors o n the electron-transfer rates are reported.

Three cis‐clerodane‐type acids 3‐5 and one methyl ester 9 were identified from the liverwort Schistochila acuminata. The two new acids 3 and 5 were 12E and 12Z geometric isomers and the methyl ester 9 was first reported from nature.

Background: Methamphetamine (METH) is one of the most widely abused illicit substances around the world; unfortunately, its addiction mechanism remains unclear. Increasing evidence indicates that the change in gene expression and the involvement of chromatin modifications might be related to the lasting effects of METH on the brain. In this study, we took advantage of METH-induced behavioral sensitization as an animal model that reflects some aspects of drug addiction and examined the transcription and histone acetylation changes in gene expression in the prefrontal cortex (PFC) of adult rats.Methods: We conducted mRNA microarray and chromatin immunoprecipitation (ChIP) coupled to DNA microarray (ChIP-chip) analysis to test and screen transcriptional changes and histone acetylation modifications. Functional enrichment analysis, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG), was performed to analyze the differentially expressed genes. We then further identified alterations in ANP32A (acidic leucine-rich nuclear phosphoprotein-32A) and POU3F2 (POU domain, class 3, transcription factor 2) by qPCR and ChIP-PCR assays.Results: In the rat model of METH-induced behavioral sensitization, METH challenge caused 275 differentially expressed genes and a number of hyperacetylations (821 genes with H3 acetylation and 10 genes with H4 acetylation). Based on mRNA microarray and GO and KEGG enrichment analysis, 24 genes may be involved in METH-induced behavioral sensitization, and 7 of them were confirmed by qPCR. We further tested the alterations in ANP32A and POU3F2 transcription and histone acetylation at the different periods of METH-induced behavioral sensitization. The results showed that H4 hyperacetylation contributed to the increased mRNA of ANP32A and that H3/H4 hyperacetylation contributed to the increased mRNA of POU3F2 induced by METH challenge-induced behavioral sensitization but not by acute METH exposure.Conclusions: The present results revealed alterations in transcription and histone acetylation in the rat PFC by METH exposure and provided evidence that modifications of histone acetylation contributed to the alteration of gene expression caused by METH-induced behavioral sensitization.

Background: Methamphetamine (METH) is one of the most widely abused illicit substances worldwide; unfortunately, its addiction mechanism remains unclear. Based on accumulating evidence, changes in gene expression and chromatin modifications might be related to the persistent effects of METH on the brain. In the present study, we took advantage of METH-induced behavioral sensitization as an animal model that reflects some aspects of drug addiction and examined the changes in gene expression and histone acetylation in the prefrontal cortex (PFC) of adult rats.Methods: We conducted mRNA microarray and chromatin immunoprecipitation (ChIP) coupled to DNA microarray (ChIP-chip) analyses to screen and identify changes in transcript levels and histone acetylation patterns. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were performed to analyze the differentially expressed genes. We then further identified alterations in ANP32A (acidic leucine-rich nuclear phosphoprotein-32A) and POU3F2 (POU domain, class 3, transcription factor 2) using qPCR and ChIP-PCR assays.Results: In the rat model of METH-induced behavioral sensitization, METH challenge caused 275 differentially expressed genes and a number of hyperacetylated genes (821 genes with H3 acetylation and 10 genes with H4 acetylation). Based on mRNA microarray and GO and KEGG enrichment analyses, 24 genes may be involved in METH-induced behavioral sensitization, and 7 were confirmed using qPCR. We further examined the alterations in the levels of the ANP32A and POU3F2 transcripts and histone acetylation at different periods of METH-induced behavioral sensitization. H4 hyperacetylation contributed to the increased levels of ANP32A mRNA and H3/H4 hyperacetylation contributed to the increased levels of POU3F2 mRNA induced by METH challenge-induced behavioral sensitization, but not by acute METH exposure.Conclusions: The present results revealed alterations in transcription and histone acetylation in the rat PFC by METH exposure and provided evidence that modifications of histone acetylation contributed to the alterations in gene expression caused by METH-induced behavioral sensitization.

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