Low temperature relation for the trace of the energy-momentum tensor in QCD with light quarks

It is shown that the temperature derivatives of the anomalous and normal (quark massive term) contributions to the trace of the energy-momentum tensor in QCD are equal to each other in the low temperature region. The physical consequences of this relation are discussed.Comment: RevTeX, 4 pages, no figure

Enhanced effective mass in doped SrTiO3 and related perovskites

The effective mass is one of the main factors determining the Seebeck coefficient and electronic conductivity. Nb-doping increases the effective mass because of two reasons, lattice constants increase and electronic effects. In this ab-initio study the effective mass is estimated from the curvature of electronic bands and it could be clarified that the deformation of SrTiO3 crystals has a significant influence on bandgap and effective DOS and band mass, which are both in excellent agreement to experimental data. However, the electronic effect due to the e2g- band flattening near the Gamma-point due to Nb-doping up to 0.2 at% is the main factor for the increase of effective mass. Doping of La shows a linear decrease of the effective mass; this is explained by the different surrounding of A- and B-site. Substitution of other elements like Ba on the A-site and V on the B-site in SrTiO3 were also found to increase the effective mass.Comment: 10 pages, 11 figures, 3 table

Dynamical symmetry breaking in the Nambu-Jona-Lasino model with external gravitational and constant electric fields

An investigation of the Nambu-Jona-Lasino model with external constant electric and weak gravitational fields is carried out in three- and four- dimensional spacetimes. The effective potential of the composite bifermionic fields is calculated keeping terms linear in the curvature, while the electric field effect is treated exactly by means of the proper- time formalism. A rich dynamical symmetry breaking pattern, accompanied by phase transitions which are ruled, independently, by both the curvature and the electric field strength is found. Numerical simulations of the transitions are presented.Comment: 20 pages, LaTeX, 6 .ps-figures, Final version published in "Classical and Quantum Gravity

Log-transformed plasma level of brain natriuretic peptide during the acute phase of Kawasaki disease is quantitatively associated with myocardial dysfunction

PurposeBrain natriuretic peptide (BNP) has been considered a biochemical marker for myocarditis in Kawasaki disease. We performed this study to determine its quantitative significance.MethodsWe attempted to correlate log-transformed BNP concentrations (log-BNP) and clinical, laboratory, and echocardiographic variables in 81 children with Kawasaki disease. Stepwise multiple linear regression analysis was used to determine the variables independently associated with log-BNP concentration.ResultsSerum C-reactive protein level (P<0.0001), serum alanine aminotransferase concentration (P=0.0032), white blood cell count (P=0.0030), and left ventricular mass index (P=0.0024) were positively related with log-BNP, and hemoglobin level (P<0.0001), serum albumin level (P<0.0001), Na+ concentrations (P<0.0001), left ventricular fractional shortening (P=0.0080), and peak early diastolic tissue velocity of the left ventricular basal lateral segment (P=0.0045) were negatively related to the log-BNP concentration. Multiple regression analysis showed that serum albumin concentration (R2=0.31, P=0.0098) and left ventricular mass index (R2=0.09, P=0.0004) were significantly associated with the log-BNP concentration.ConclusionElevated BNP levels during the acute phase of Kawasaki disease may be attributable to cardiac dysfunction associated with the increase in left ventricular mass, and log-BNP concentration may be a quantitative biochemical marker of myocarditis in Kawasaki disease

Diagnosis of incomplete Kawasaki disease

Several authors suggested that the clinical characteristics of incomplete presentation of Kawasaki disease are similar to those of complete presentation and that the 2 forms of presentation are not separate entities. Based on this suggestion, a diagnosis of incomplete Kawasaki disease in analogy to the findings of complete presentation is reasonable. Currently, the diagnosis of incomplete Kawasaki disease might be made in cases with fewer classical diagnostic criteria and with several compatible clinical, laboratory or echocardiographic findings on the exclusion of other febrile illness. Definition of incomplete presentation in which coronary artery abnormalities are included as a necessary condition, is restrictive and specific. The validity of the diagnostic criteria of incomplete presentation by the American Heart Association should be thoroughly tested in the immediate future

Global gene expression analysis of human erythroid progenitors

This article is available open access through the publisher’s website. Copyright @ 2011 American Society of Hematology. This article has an erratum: http://bloodjournal.hematologylibrary.org/content/118/26/6993.3.Understanding the pattern of gene expression during erythropoiesis is crucial for a synthesis of erythroid developmental biology. Here, we isolated 4 distinct populations at successive erythropoietin-dependent stages of erythropoiesis, including the terminal, pyknotic stage. The transcriptome was determined using Affymetrix arrays. First, we demonstrated the importance of using defined cell populations to identify lineage and temporally specific patterns of gene expression. Cells sorted by surface expression profile not only express significantly fewer genes than unsorted cells but also demonstrate significantly greater differences in the expression levels of particular genes between stages than unsorted cells. Second, using standard software, we identified more than 1000 transcripts not previously observed to be differentially expressed during erythroid maturation, 13 of which are highly significantly terminally regulated, including RFXAP and SMARCA4. Third, using matched filtering, we identified 12 transcripts not previously reported to be continuously up-regulated in maturing human primary erythroblasts. Finally, using transcription factor binding site analysis, we identified potential transcription factors that may regulate gene expression during terminal erythropoiesis. Our stringent lists of differentially regulated and continuously expressed transcripts containing many genes with undiscovered functions in erythroblasts are a resource for future functional studies of erythropoiesis. Our Human Erythroid Maturation database is available at https://cellline.molbiol.ox.ac.uk/eryth/index.html.National Health Service Blood and Transplant, National Institute for Health Research Biomedical Research Center Program, and National Institute for Health Research

JNK pathway plays a critical role for expansion of human colorectal cancer in the context of BRG1 suppression

Tumor stem cells (TSCs), capable of self-renewal and continuous production of progeny cells, could be potential therapeutic targets. We have recently reported that chromatin remodeling regulator Brg1 is required for maintenance of murine intestinal TSCs and stemness feature of human colorectal cancer (CRC) cells by inhibiting apoptosis. However, it is still unclear how BRG1 suppression changes the underlying intracellular mechanisms of human CRC cells. We found that Brg1 suppression resulted in upregulation of the JNK signaling pathway in human CRC cells and murine intestinal TSCs. Simultaneous suppression of BRG1 and the JNK pathway, either by pharmacological inhibition or silencing of c-JUN, resulted in even stronger inhibition of the expansion of human CRC cells compared to Brg1 suppression alone. Consistently, high c-JUN expression correlated with worse prognosis for survival in human CRC patients with low BRG1 expression. Therefore, the JNK pathway plays a critical role for expansion and stemness of human CRC cells in the context of BRG1 suppression, and thus a combined blockade of BRG1 and the JNK pathway could be a novel therapeutic approach against human CRC

Near-threshold boson pair production in the model of smeared-mass unstable particles

Near-threshold production of boson pairs is considered within the framework of the model of unstable particles with smeared mass. We describe the principal aspects of the model and consider the strategy of calculations including the radiative corrections. The results of calculations are in good agreement with LEP II data and Monte-Carlo simulations. Suggested approach significantly simplifies calculations with respect to the standard perturbative one.Comment: 15 pages, 6 figures, minor corrections, references adde

Pancreatic RECK inactivation promotes cancer formation, epithelial-mesenchymal transition, and metastasis

膵癌悪性化の分子機構解明 --RECK発現の低下が膵癌の浸潤・転移を引き起こす--. 京都大学プレスリリース. 2023-09-19.RECK is downregulated in various human cancers; however, how RECK inactivation affects carcinogenesis remains unclear. We addressed this issue in a pancreatic ductal adenocarcinoma (PDAC) mouse model and found that pancreatic Reck deletion dramatically augmented the spontaneous development of PDAC with a mesenchymal phenotype, which was accompanied by increased liver metastases and decreased survival. Lineage tracing revealed that pancreatic Reck deletion induced epithelial-mesenchymal transition (EMT) in PDAC cells, giving rise to inflammatory cancer-associated fibroblast–like cells in mice. Splenic transplantation of Reck-null PDAC cells resulted in numerous liver metastases with a mesenchymal phenotype, whereas reexpression of RECK markedly reduced metastases and changed the PDAC tumor phenotype into an epithelial one. Consistently, low RECK expression correlated with low E-cadherin expression, poor differentiation, metastasis, and poor prognosis in human PDAC. RECK reexpression in the PDAC cells was found to downregulate MMP2 and MMP3, with a concomitant increase in E-cadherin and decrease in EMT-promoting transcription factors. An MMP inhibitor recapitulated the effects of RECK on the expression of E-cadherin and EMT-promoting transcription factors and invasive activity. These results establish the authenticity of RECK as a pancreatic tumor suppressor, provide insights into its underlying mechanisms, and support the idea that RECK could be an important therapeutic effector against human PDAC