Diquark condensation effects on hot quark star configurations

The equation of state for quark matter is derived for a nonlocal, chiral quark model within the mean field approximation.We investigate the effects of a variation of the formfactors of the interaction on the phase diagram of quark matter. Special emphasis is on the occurrence of a diquark condensate which signals a phase transition to color superconductivity and its effects on the equation of state under the condition of beta- equilibrium and charge neutrality. We calculate the quark star configurations by solving the Tolman- Oppenheimer- Volkoff equations and obtain for the transition from a hot, normal quark matter core of a protoneutron star to a cool diquark condensed one a release of binding energy of the order of Delta M c^2 ~ 10^{53} erg. We find that this energy could not serve as an engine for explosive phenomena since the phase transition is not first order. Contrary to naive expectations the mass defect increases when for a given temperature we neglect the possibility of diquark condensation.Comment: 24 pages, 2 tables, 8 figures, references added, figures and text improve

Estimation of redshifts from early galaxies

Dating early galaxies is a current technical, empirical and theoretical problem. Progress has been made recently calculating these dates using the observed redshift, z, alone. While this relaxes the need for simultaneous determination of luminosity distances with redshifts; accurate redshift determination beyond z ≥ 3 is difficult. We have shown that light emissions tend toward blue with increasing emission age and this is supported by recent data. Here we combine calculations of cosmological times from redshifts alone with the emission frequency model for lookback times. This allows a better gauge between recombination and the first galaxies and may provide additional 50-200 M years between these events.Validerad; 2007; 20100917 (andbra)</p

Ameliorative effects of the sesquiterpenoid valerenic acid on oxidative stress induced in hepg2 cells after exposure to the fungicide benomyl

Valerenic acid (VA) is a sesquiterpenoid and a phytoconstituent of the plant valerian used for sleeping disorders and anxiety. The frequency of using herbal components as therapeutic nutritional agents has increased lately. Their ability to improve redox homeostasis makes them a valuable approach against harmful xenobiotics. The purpose of this study was to evaluate the putative beneficial role of VA against the redox-perturbating role of the fungicide benomyl in HepG2 human liver cells in terms of oxidative stress in the cellular environment and in endoplasmic reticulum (ER). Benomyl increased cell total oxidant status and reactive oxygen species production and decreased total antioxidant status. The expression of genes coding for antioxidant molecules, namely, heme oxygenase-1, alpha glutathione s-transferase, NF-kB, and liver fatty acid binding protein, were decreased due to benomyl. VA ameliorated these effects. Benomyl also increased ER-stress-related molecules such as endoplasmic reticulum to nucleus signaling 1 protein, glucose-regulated protein 78, and caspase-12 levels, and VA acted also as a preventive agent. These results indicate that VA exerts ameliorative effects after benomyl-induced oxidative stress. VA, a widely used nutritional supplement, is a compound with potent antioxidant properties, which are valuable for the protection of cells against xenobiotic-induced oxidative damage. © 2021 by the authors. Licensee MDPI, Basel, Switzerland

The sesquiterpenoid valerenic acid protects neuronal cells from the detrimental effects of the fungicide benomyl on apoptosis and DNA oxidation

Background: Valerenic acid (VA), a sesquiterpenoid of the plant Valeriana officinalis, has attracted attention of the research community due to its potential positive role against neurodegenerative diseases induced by chemicals. However, the relevant evidence in the literature is scarce. Therefore, this study aimed to examine the putative protective role of VA on the toxic effects of the fungicide benomyl on SH-SY5Y neural cells. Methods: Cell viability was determined via the MTT and NRU assays, DNA damage was assessed via comet assay and apoptosis was evaluated through the expression of relevant genes. Results: According to the results, exposure of the cells to benomyl enhanced viability inhibition and promoted DNA damage and apoptosis since the expression levels of the genes coding for MAPK8, NF-kB, Bax, Caspase-9 and Caspase-3 were increased. Treatment of the cells with VA ameliorated these effects in a concentration dependent manner. Conclusion: It is concluded that the molecular mechanism through which benomyl exerts its toxic action appears to depend on DNA oxidation and apoptosis induction. Furthermore, VA, a plant-derived compound is a protective antioxidant against pesticide-induced toxicity. Therefore, herbs, extracts and compounds of plant origin could be used as nutritional supplements that back up the beneficial role of medicine in neurodegenerative diseases. © The Author(s) 2022