Chiral crossover in QCD at zero and non-zero chemical potentials

We present results for pseudo-critical temperatures of QCD chiral crossovers at zero and non-zero values of baryon ($B$), strangeness ($S$), electric charge ($Q$), and isospin ($I$) chemical potentials $\mu_{X=B,Q,S,I}$. The results were obtained using lattice QCD calculations carried out with two degenerate up and down dynamical quarks and a dynamical strange quark, with quark masses corresponding to physical values of pion and kaon masses in the continuum limit. By parameterizing pseudo-critical temperatures as $T_c(\mu_X) = T_c(0) \left[ 1 -\kappa_2^{X}(\mu_{X}/T_c(0))^2 -\kappa_4^{X}(\mu_{X}/T_c(0))^4 \right]$, we determined $\kappa_2^X$ and $\kappa_4^X$ from Taylor expansions of chiral observables in $\mu_X$. We obtained a precise result for $T_c(0)=(156.5\pm1.5)\;\mathrm{MeV}$. For analogous thermal conditions at the chemical freeze-out of relativistic heavy-ion collisions, i.e., $\mu_{S}(T,\mu_{B})$ and $\mu_{Q}(T,\mu_{B})$ fixed from strangeness-neutrality and isospin-imbalance, we found $\kappa_2^B=0.012(4)$ and $\kappa_4^B=0.000(4)$. For $\mu_{B}\lesssim300\;\mathrm{MeV}$, the chemical freeze-out takes place in the vicinity of the QCD phase boundary, which coincides with the lines of constant energy density of $0.42(6)\;\mathrm{GeV/fm}^3$ and constant entropy density of $3.7(5)\;\mathrm{fm}^{-3}$

Correlation of collagen synthesis and procollagen messenger RNA levels with transformation in rat embryo fibroblasts.

A line of normal rat embryo fibroblasts was transformed with N-methyl-N'-nitro-N-nitrosoguanidine (a chemical carcinogen), SV40 and polyoma virus (two DNA viruses), and Rous sarcoma virus (an RNA tumor virus). In this study, we report a comparison of the levels of collagen synthesis and procollagen messenger RNA (mRNA) in 13 lines selected after transformation with one of these agents. Collagen synthesis and procollagen mRNA levels were compared with the degree of transformation determined from morphology, saturation density, growth in agarose, and tumorigenicity in nude mice. Each class of transformants had a characteristic level of collagen synthesis; this level correlated inversely with the degree of transformation of the rat embryo fibroblasts. In N-methyl-N'-nitro-N-nitrosoguanidine and SV40 transformants which were moderately transformed, collagen synthesis was hardly affected, but, in polyoma virus and Rous sarcoma virus transformants which were more severely transformed, collagen synthesis was 30 to 48% and 12 to 25%, respectively, of control levels. Type I procollagen mRNA activity measured in RNA from nine of the lines by an in vitro translation assay also decreased with increasing severity of transformation. Procollagen mRNA levels were reduced to about one-half of control levels in one SV40 transformant and to 17 to 23% of controls in polyoma virus and Rous sarcoma virus transformants. We conclude that, in this series of rat fibroblast lines, transformation with different agents resulted in characteristic levels of collagen synthesis and that collagen synthesis was most reduced in the cells which were most transformed by other criteria

Skewness and kurtosis of net baryon-number distributions at small values of the baryon chemical potential

We present results for the ratios of mean (MB), variance (σ2B), skewness (SB) and kurtosis (κB) of net baryon-number fluctuations obtained in lattice QCD calculations with physical values of light and strange quark masses. Using next-to-leading order Taylor expansions in baryon chemical potential we find that qualitative features of these ratios closely resemble the corresponding experimentally measured cumulant ratios of net proton-number fluctuations for beam energies down to √sNN≥19.6  GeV. We show that the difference in cumulant ratios for the mean net baryon-number, MB/σ2B=χB1(T,μB)/χB2(T,μB), and the normalized skewness, SBσB=χB3(T,μB)/χB2(T,μB), naturally arises in QCD thermodynamics. Moreover, we establish a close relation between skewness and kurtosis ratios, SBσ3B/MB=χB3(T,μB)/χB1(T,μB) and κBσ2B=χB4(T,μB)/χB2(T,μB), valid at small values of the baryon chemical potential

Bestrophin Gene Mutations Cause Canine Multifocal Retinopathy: A Novel Animal Model for Best Disease

PURPOSE. Canine multifocal retinopathy (cmr) is an autosomal recessive disorder of multiple dog breeds. The disease shares a number of clinical and pathologic similarities with Best macular dystrophy (BMD), and cmr is proposed as a new large animal model for Best disease. METHODS. cmr was characterized by ophthalmoscopy and histopathology and compared with BMD-affected patients. BEST1 (alias VMD2), the bestrophin gene causally associated with BMD, was evaluated in the dog. Canine ortholog cDNA sequence was cloned and verified using RPE/choroid 5′- and 3′-RACE. Expression of the canine gene transcripts and protein was analyzed by Northern and Western blotting and immunocytochemistry. All exons and the flanking splice junctions were screened by direct sequencing. RESULTS. The clinical phenotype and pathology of cmr closely resemble lesions of BMD. Canine VMD2 spans 13.7 kb of genomic DNA on CFA18 and shows a high level of conservation among eukaryotes. The transcript is predominantly expressed in RPE/choroid and encodes bestrophin, a 580-amino acid protein of 66 kDa. Immunocytochemistry of normal canine retina demonstrated specific localization of protein to the RPE basolateral plasma membranes. Two disease-specific sequence alterations were identified in the canine VMD2 gene: a C73T stop mutation in cmr1 and a G482A missense mutation in cmr2. CONCLUSIONS. The authors propose these two spontaneous mutations in the canine VMD2 gene, which cause cmr, as the first naturally occurring animal model of BMD. Further development of the cmr models will permit elucidation of the complex molecular mechanism of these retinopathies and the development of potential therapies

Meson screening masses in (2+1)-flavor QCD

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Chiral crossover in QCD at zero and non-zero chemical potentials

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Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

The completion of the human genome sequence has made possible genome-wide studies of retroviral DNA integration. Here we report an analysis of 3,127 integration site sequences from human cells. We compared retroviral vectors derived from human immunodeficiency virus (HIV), avian sarcoma-leukosis virus (ASLV), and murine leukemia virus (MLV). Effects of gene activity on integration targeting were assessed by transcriptional profiling of infected cells. Integration by HIV vectors, analyzed in two primary cell types and several cell lines, strongly favored active genes. An analysis of the effects of tissue-specific transcription showed that it resulted in tissue-specific integration targeting by HIV, though the effect was quantitatively modest. Chromosomal regions rich in expressed genes were favored for HIV integration, but these regions were found to be interleaved with unfavorable regions at CpG islands. MLV vectors showed a strong bias in favor of integration near transcription start sites, as reported previously. ASLV vectors showed only a weak preference for active genes and no preference for transcription start regions. Thus, each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection

A mitochondrial mutator plasmid that causes senescence under dietary restricted conditions

BACKGROUND: Calorie or dietary restriction extends life span in a wide range of organisms including the filamentous fungus Podospora anserina. Under dietary restricted conditions, P. anserina isolates are several-fold longer lived. This is however not the case in isolates that carry one of the pAL2-1 homologous mitochondrial plasmids. RESULTS: We show that the pAL2-1 homologues act as 'insertional mutators' of the mitochondrial genome, which may explain their negative effect on life span extension. Sequencing revealed at least fourteen unique plasmid integration sites, of which twelve were located within the mitochondrial genome and two within copies of the plasmid itself. The plasmids were able to integrate in their entirety, via a non-homologous mode of recombination. Some of the integrated plasmid copies were truncated, which probably resulted from secondary, post-integrative, recombination processes. Integration sites were predominantly located within and surrounding the region containing the mitochondrial rDNA loci. CONCLUSION: We propose a model for the mechanism of integration, based on innate modes of mtDNA recombination, and discuss its possible link with the plasmid's negative effect on dietary restriction mediated life span extension

QCD equation of state to O(μB6) from lattice QCD

We calculated the QCD equation of state using Taylor expansions that include contributions from up to sixth order in the baryon, strangeness and electric charge chemical potentials. Calculations have been performed with the Highly Improved Staggered Quark action in the temperature range T∈[135  MeV,330  MeV] using up to four different sets of lattice cutoffs corresponding to lattices of size N3σ×Nτ with aspect ratio Nσ/Nτ=4 and Nτ=6−16. The strange quark mass is tuned to its physical value, and we use two strange to light quark mass ratios ms/ml=20 and 27, which in the continuum limit correspond to a pion mass of about 160 and 140 MeV, respectively. Sixth-order results for Taylor expansion coefficients are used to estimate truncation errors of the fourth-order expansion. We show that truncation errors are small for baryon chemical potentials less then twice the temperature (μB≤2T). The fourth-order equation of state thus is suitable for the modeling of dense matter created in heavy ion collisions with center-of-mass energies down to √sNN∼12  GeV. We provide a parametrization of basic thermodynamic quantities that can be readily used in hydrodynamic simulation codes. The results on up to sixth-order expansion coefficients of bulk thermodynamics are used for the calculation of lines of constant pressure, energy and entropy densities in the T−μB plane and are compared with the crossover line for the QCD chiral transition as well as with experimental results on freeze-out parameters in heavy ion collisions. These coefficients also provide estimates for the location of a possible critical point. We argue that results on sixth-order expansion coefficients disfavor the existence of a critical point in the QCD phase diagram for μB/T≤2 and T/Tc(μB=0)>0.9