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A central feature of heart disease is a molecular remodeling of signaling pathways in cardiac myocytes. This study focused on novel molecular elements of MAPK-mediated alterations in the pattern of gene expression of the protein phosphatase 2A (PP2A). In an established model of sustained JNK activation, a 70% decrease in expression of the targeting subunit of PP2A, B56c[alpha], was observed in either neonatal or adult cardiomyocytes. This loss in protein abundance was accompanied by a decrease of 69% in B56[alpha] mRNA steady-state levels. Given that the 3'-untranslated region of this transcript contains adenylate-uridylate-rich elements known to regulate mRNA degradation, experiments explored the notion that instability of B56[alpha] mRNA accounts for the response, mRNA time-course analyses with real-time PCR methods showed that B56[alpha] transcript was transformed from a stable (no significant decay over 1 h) to a labile form that rapidly degraded within minutes. These results were supported by complementary experiments that revealed that the RNA-binding protein AUF1, known to destabilize target mRNA, was increased fourfold in JNK-activated cells. A variety of other stress-related stimuli, such as p38 MAPK activation and phorbol ester, upregulated AUF1 expression in cultured cardiac cells as well. In addition, gel mobility shift assays demonstrated that p[37.sup.AUF1] binds with nanomolar affinity to segments of the B56[alpha] 3'-untranslated region. Thus these studies provide new evidence that signaling-induced mRNA instability is an important mechanism that underlies the changes in the pattern of gene expression evoked by stress-activated pathways in cardiac cells. protein phosphatase 2A; mitogen-activated protein kinase; gene expression; AUF1 doi:10.1152/ajpheart.01162.2005

A literature review of harmful substances formed in arc welding of copper and its alloys is presented. Literature data on studying emissions of welding aerosols in welding of copper and copper alloys are considered. It is shown that to create new grades of welding materials that would satisfy not only their welding technology, but also sanitary and hygienic characteristics, it is necessary to continue the study of chemical composition and levels of emissions of welding aerosols using modern standardized international procedures. [ABSTRACT FROM AUTHOR]

The work presents the results of studying harmful substances in the air, released during nonconsumable electrode argon-arc welding of 1201 (Al-Cu-Mn) and 1460 (Al-Cu-Li) aluminium alloys. The objective of this work is performance of sanitary-hygienic assessment of the nature of aerosol and gas evolution from these alloys, in order to ensure favourable sanitary-hygienic working conditions for welders. It is shown that for 1460 alloy with lithium the intensity of welding aerosol formation is 1.5 times higher, and ozone concentration exceeds the maximum admissible concentration 3-4 times in the same welding modes. 13 Ref., 4 Tables, 5 Figures. [ABSTRACT FROM AUTHOR]

Two dimensional mathematical model of loop heat pipe's temperature field is adduced in the paper. The developed mathematical model permits computation of temperature field along the container of loop heat pipe, with allowance for the axial heat transfer through its design elements, when "vapor-liquid" interface is flat and moves within the condensation zone. The above mathematical model can be applied when designing and using complex systems based on the loop heat pipes. [ABSTRACT FROM AUTHOR]

Spontaneous, rhythmic subsarcolemmal local Ca2+ releases driven by cAMP-mediated, protein kinase A (PKA)-dependent phosphorylation are crucial for normal pacemaker function of sinoatrial nodal cells (SANC). Because local Ca2+ releases occur beneath the cell surface membrane, near to where adenylyl cyclases (ACs) reside, we hypothesized that the dual Ca2+ and cAMP/PKA regulatory components of automaticity are coupled via Ca2+ activation of AC activity within membrane microdomains. Here we show by quantitative reverse transcriptase PCR that SANC express Ca2+-activated AC isoforms land 8, in addition to AC type 2, 5, and 6 transcripts. Immunolabeling of cell fractions, isolated by sucrose gradient ultracentrifugation, con- firmed that ACs localize to membrane lipid microdomains. AC activity within these lipid microdomains is activated by Ca2+ over the entire physiological Ca2+ range. In intact SANC, the high basal AC activity produces a high level of cAMP that is further elevated by phosphodiesterase inhibition, cAMP and cAMP-mediated PKA-dependent activation of ion channels and Ca2+ cycling proteins drive sarcoplasmic reticulum Ca2+ releases, which, in turn, activate ACs. This feed forward "fail safe" system, kept in check by a high basal phosphodiesterase activity, is central to the generation of normal rhythmic, spontaneous action potentials by pacemaker cells. [ABSTRACT FROM AUTHOR]