Equation of state of hadronic matter with dibaryons in an effective quark model

The equation of state of symmetric nuclear matter with the inclusion of non-strange dibaryons is studied. We pay special attention to the existence of a dibaryon condensate at zero temperature. These calculations have been performed in an extended quark-meson coupling model with density-dependent parameters, which takes into account the finite size of nucleons and dibaryons. A first-order phase-transition to pure dibaryon matter has been found. The corresponding critical density is strongly dependent on the value of the dibaryon mass. The density behavior of the nucleon and dibaryon effective masses and confining volumes have also been discussed.Comment: 9 pages, LaTex, 3 Postscript figures, a misprint correcte

Taichunamides: Prenylated Indole Alkaloids from Aspergillus taichungensis (IBT 19404)

Seven new prenylated indole alkaloids, taichunamides A–G, were isolated from the fungus Aspergillus taichungensis (IBT 19404). Taichunamides A and B contained an azetidine and 4‐pyridone units, respectively, and are likely biosynthesized from notoamide S via (+)‐6‐epi‐stephacidin A. Taichunamides C and D contain endoperoxide and methylsulfonyl units, respectively. This fungus produced indole alkaloids containing an anti‐bicyclo[2.2.2]diazaoctane core, whereas A. protuberus and A. amoenus produced congeners with a syn‐bicyclo[2.2.2]diazaoctane core. Plausible biosynthetic pathways to access these cores within the three species likely arise from an intramolecular hetero Diels–Alder reaction.Sieben neue prenylierte Indolalkaloide wurden aus A. taichungensis isoliert. Dieser Pilz erzeugt Alkaloide mit anti‐Bicyclo[2.2.2]diazaoctan‐Kern, während A. protuberus und A. amoenus syn‐Derivate herstellen. Die Strukturdiversität der von Tryptophan abgeleiteten Sekundärmetaboliten deutet auf stereochemisch und strukturell hoch entwickelte Synthesefunktionen für Sekundärmetaboliten in diesen orthologen Pilzen hin.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/137451/1/ange201509462.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137451/2/ange201509462-sup-0001-misc_information.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/137451/3/ange201509462_am.pd

Equation of state of hadron resonance gas and the phase diagram of strongly interacting matter

The equation of state of hadron resonance gas at finite temperature and baryon density is calculated taking into account finite-size effects within the excluded volume model. Contributions of known hadrons with masses up to 2 GeV are included in the zero-width approximation. Special attention is paid to the role of strange hadrons in the system with zero total strangeness. A density- dependent mean field is added to guarantee that the nuclear matter has a saturation point and a liquid-gas phase transition. The deconfined phase is described by the bag model with lowest order perturbative corrections. The phase transition boundary is found by using the Gibbs conditions with the strangeness neutrality constraint. The sensitivity of the phase diagram to the hadronic excluded volume and to the parametrization of the mean-field is investigated. The possibility of strangeness-antistrangeness separation in the mixed phase is analyzed. It is demonstrated that the peaks in the kaon to pion and lambda to pion multiplicity ratios can be explained by a nonmonotonous behavior of the strangeness fugacity along the chemical freeze-out line.Comment: 40 pages, 31 figure

Acute ECG ST-segment elevation mimicking myocardial infarction in a patient with pulmonary embolism

Pulmonary embolism is a common cardiovascular emergency, but it is still often misdiagnosed due to its unspecific clinical symptoms. Elevated troponin concentrations are associated with greater morbidity and mortality in patients with pulmonary embolism. Right ventricular ischemia due to increased right ventricular afterload is believed to be underlying mechanism of elevated troponin values in acute pulmonary embolism, but a paradoxical coronary artery embolism through opened intra-artrial communication is another possible explanation as shown in our case report

Precise remote-monitoring technique of water volume and temperature of a crater lake in Aso volcano, Japan: implications for a sensitive window of a volcanic hydrothermal system

A high-resolution Digital Surface Model and a commercial digital camera have enabled precise and continuous monitoring of the crater lake at Aso volcano. From July 2006 onwards, infrared (IR) thermometry has been used with this system, enabling more accurate measurements of lake volume and temperature based on simple and intensive observations than has been possible in any other previous studies. The heat discharge remained largely constant at approximately 220 MW, with the exception of an abrupt increase to 280 MW that coincided with a rapid decrease in the water level in August 2007. Simultaneously, an increase in temperature at a shallow depth was suggested by other observations. The crater lake was found to respond to even slight changes in volcanic fluid supply, which can be well quantified by our method. Thus, a crater lake can be monitored more precisely than subaerial fumaroles whose energy estimation is often accompanied by large uncertainties. Our monitoring technique of a crater lake provides information on the subsurface hydrothermal system beneath it, for which any in-situ measurements are practically impossible

NOX2, p22phox and p47phox are targeted to the nuclear pore complex in ischemic cardiomyocytes colocalizing with local reactive oxygen species.

BACKGROUND: NADPH oxidases play an essential role in reactive oxygen species (ROS)-based signaling in the heart. Previously, we have demonstrated that (peri)nuclear expression of the catalytic NADPH oxidase subunit NOX2 in stressed cardiomyocytes, e.g. under ischemia or high concentrations of homocysteine, is an important step in the induction of apoptosis in these cells. Here this ischemia-induced nuclear targeting and activation of NOX2 was specified in cardiomyocytes. METHODS: The effect of ischemia, mimicked by metabolic inhibition, on nuclear localization of NOX2 and the NADPH oxidase subunits p22(phox) and p47(phox), was analyzed in rat neonatal cardiomyoblasts (H9c2 cells) using Western blot, immuno-electron microscopy and digital-imaging microscopy. RESULTS: NOX2 expression significantly increased in nuclear fractions of ischemic H9c2 cells. In addition, in these cells NOX2 was found to colocalize in the nuclear envelope with nuclear pore complexes, p22(phox), p47(phox) and nitrotyrosine residues, a marker for the generation of ROS. Inhibition of NADPH oxidase activity, with apocynin and DPI, significantly reduced (peri)nuclear expression of nitrotyrosine. CONCLUSION: We for the first time show that NOX2, p22(phox) and p47(phox) are targeted to and produce ROS at the nuclear pore complex in ischemic cardiomyocytes

Potent Cardioprotective Effect of the 4-Anilinoquinazoline Derivative PD153035: Involvement of Mitochondrial KATP Channel Activation

Background: The aim of the present study was to evaluate the protective effects of the 4-anilinoquinazoline derivative PD153035 on cardiac ischemia/reperfusion and mitochondrial function. Methodology/Principal Findings: Perfused rat hearts and cardiac HL-1 cells were used to determine cardioprotective effects of PD153035. Isolated rat heart mitochondria were studied to uncover mechanisms of cardioprotection. Nanomolar doses of PD153035 strongly protect against heart and cardiomyocyte damage induced by ischemia/reperfusion and cyanide/aglycemia. PD153035 did not alter oxidative phosphorylation, nor directly prevent Ca(2+) induced mitochondrial membrane permeability transition. The protective effect of PD153035 on HL-1 cells was also independent of AKT phosphorylation state. Interestingly, PD153035 activated K(+) transport in isolated mitochondria, in a manner prevented by ATP and 5-hydroxydecanoate, inhibitors of mitochondrial ATP-sensitive K(+) channels (mitoK(ATP)). 5-Hydroxydecanoate also inhibited the cardioprotective effect of PD153035 in cardiac HL-1 cells, demonstrating that this protection is dependent on mitoK(ATP) activation. Conclusions/Significance: We conclude that PD153035 is a potent cardioprotective compound and acts in a mechanism involving mitoK(ATP) activation