Zdzislaw Beksinski’s Paintings of the “Fantastic Period” as an Expression of Early Childhood Experience

This article is an attempt to indicate possibilities for the interpretation of Zdzisław Beksiński’s work, based on selected examples of paintings from the so-called "fantastic period". A grotesque look at art, which would explain the style of the artist's paintings, so compulsively using the language of de formation, attaining alarming degeneration, is a look from the generally inaccessible, cavernous depths of the subconscious. Thanks to psychoanalysis, art can be read as a representation of the inner world of the creator, who unknowingly embeds the story of his childhood into his work. The direction of the foregoing, represents the position of Alice Miller, a Swiss psychotherapist, in whose opinion knowledge stored in the subconscious is not pure fantasy, but rather an explanation referring to the reality of early [email protected] of Fine Arts, Maria Curie Sklodowska University, 2b al. Kraśnicka St., 20-718 Lublin, Poland1115616

Chloroacetaldehyde-induced mutagenesis in Escherichia coli: the role of AlkB protein in repair of 3,N4-ethenocytosine and 3,N4-α-hydroxyethanocytosine

Etheno () adducts are formed in reaction of DNA bases with various environmental carcinogens and endogenously created products of lipid peroxidation. Chloroacetaldehyde (CAA), a metabolite of carcinogen vinyl chloride, is routinely used to generate -adducts. We studied the role of AlkB, along with AlkA and Mug proteins, all engaged in repair of -adducts, in CAA-induced mutagenesis. The test system used involved pIF102 and pIF104 plasmids bearing the lactose operon of CC102 or CC104 origin (C.G. Cupples, J.H. Miller. Proc. Natl. Acad. Sci. U.S.A. 86 (1989) 5345-5349) which allowed to monitor Lac+ revertants, the latter arose by GCAT or GCTA substitutions, respectively, as a result of modification of guanine and cytosine. The plasmids were CAA-damaged in vitro and replicated in E. coli of various genetic backgrounds. To modify the levels of AlkA and AlkB proteins, mutagenesis was studied in E. coli cells induced or not in adaptive response. Formation of C proceeds via a relatively stable intermediate, 3,N4--hydroxyethanocytosine (HEC), which allowed to compare repair of both adducts. The results indicate that all three genes, alkA, alkB and mug, are engaged in alleviation of CAA-induced mutagenesis. The frequency of mutation was higher in AlkA-, AlkB- and Mug-deficient strains in comparison to alkA+, alkB+, and mug+ controls. Considering the levels of CAA-induced Lac+ revertants in strains harboring the pIF plasmids and induced or not in adaptive response, we conclude that AlkB protein is engaged in the repair of C and HEC in vivo. Using the modified TTCTT 5-mers as substrates, we confirmed in vitro that AlkB protein repairs C and HEC although far less efficiently than the reference adduct 3-methylcytosine. The pH optimum for repair of HEC and εC is significantly different from that for 3-methylcytosine. We propose that the protonated form of adduct interact in active site of AlkB protein

An exploratory longitudinal acculturation study with Polish immigrant teenagers in Ireland : parental and children\u27s perspectives

THESIS 10805The objective of this research project was to understand how young immigrants adjust to their new socio-cultural context, and to contribute to the existing understanding of the social phenomena of acculturation, on the example of the Polish immigrant teenagers in Ireland. This included exploration of tlie transnational migration and socio-cultural adjustment from Polish parents and key informants\u27 perspectives. The main aim of the research was to ascertain what it is like to be a Polish immigrant teenager in Ireland. The research was conducted by using the qualitative multi-actor longitudinal design that combined qualitative interviews with standardised measurements in order to examine the acculturation process

The role of AlkB protein in repair of 1,N6-ethenoadenine in Escherichia coli cells

Etheno () DNA adducts, including 1,N6-ethenoadenine (A), are formed by various bifunctional agents of exogenous and endogenous origin. The AT→TA transversion, the most frequent mutation provoked by the presence of A in DNA, is very common in critical codons of the TP53 and RAS genes in tumors induced by exposure to carcinogenic vinyl compounds. Here, using a method that allows examination of the mutagenic potency of a metabolite of vinyl chloride, chloroacetaldehyde (CAA), but eliminates its cytotoxicity, we studied the participation of alkA, alkB and mug gene products in the repair of A in E. coli cells. The test system used comprised the pIF105 plasmid bearing the lactose operon of CC105 origin which allowed monitoring of Lac+ revertants that arose by ATTA substitutions due to the modification of adenine by CAA. The plasmid was CAA-modified in vitro and replicated in E. coli of various genetic backgrounds (wt, alkA, alkB, mug, alkAalkB, alkAmug and alkBmug). To modify the levels of the AlkA and AlkB proteins, mutagenesis was studied in E. coli cells induced or not in adaptive response to alkylating agents. Considering the levels of CAA-induced Lac+ revertants in strains harboring the CAA-modified pIF105 plasmid and induced or not in adaptive response, we conclude that the AlkB dioxygenase plays a major role in decreasing the level of ATTA mutations, thus in the repair of A in E. coli cells. The observed differences of mutation frequencies in the various mutant strains assayed indicate that Mug glycosylase is also engaged in the repair of A, whereas the role the AlkA glycosylase in this repair is negligible

A new role of AMP-activated protein kinase in regulating proliferation of mesenchymal stem cells

Purpose: Natriuretic peptides (NPs) administered during early reperfusion are protective in models of myocardial infarction. A previous study examining the endogenous components of B-type natriuretic peptide (BNP) protection of reperfused myocardium, implicated both sarcolemmal (s) KATP and mitochondrial (m) KATP channels. The indirect evidence characterising the relationship between BNP signalling and KATP was obtained using sulphonylurea receptor inhibitors in a rat isolated heart model of ischaemia-reperfusion injury. Here we seek to further examine the relationship between NPs and sKATP openings using single channel electrophysiology. Given our previous findings and the overarching consensus that cardioprotective autacoids open KATP channels, it was hypothesised that NPs elicit sKATP opening. Methods: Cardiomyocyte isolation. Left ventricular cardiomyocytes were isolated from male Sprague-Dawley rat hearts subjected to enzymatic digestion with Liberase Blendzyme DL. Cardiomyocytes were cultured overnight in Medium 199, prior to patch clamp. Single channel patch clamp. Single channel recordings at room temperature (22°C) were made from cell attached patches bathed in Na+ Locke, pH 7.2. The recording pipette contained high KCl (140 mM), pH 7.2. Recordings (45 sec) were made over a range of patch potentials (0, -30, -60, -90, -120 mV), in the absence (control) and in the presence of bath applied BNP (10, 100 nM and 1 µM), pinacidil (200 µM) or pinacidil vehicle (DMSO, 0.25%). Recordings were also made with BNP and pinacidil applied concomitantly. Data are mean ± S.E.M. Results: The current voltage relationship of sKATP under control conditions was linear at –ve patch potentials, the mean conductance being 52.9 ± 1.8 pS (n = 18 hearts, n = 35 cells). Pinacidil caused a four fold increase in sKATP open probability compared to control. Mean channel conductance in the presence of pinacidil was 59.9 ± 1.9 pS (n = 16 hearts, n = 44 cells). Interestingly BNP at all concentrations had negligible effects on sKATP open probability and unitary conductance. However, BNP at all concentrations and patch potentials inhibited pinacidil induced sKATP openings, restoring channel open probability to baseline. Conclusion: These data illustrate the inhibitory effect of NP signalling on sKATP function in the cardiomyocyte under normoxia. They are concordant with the inhibitory effect of atrial NP on KATP in the pancreatic beta cell, but are in apparent conflict with the current cardioprotection paradigm. However, differential effects on sKATP and mKATP and the effects of hypoxia-reoxygenation require further exploration