Spectrum of quenched twisted mass lattice QCD at maximal twist

Hadron masses are computed from quenched twisted mass lattice QCD for a degenerate doublet of up and down quarks with the twist angle set to pi/2, since this maximally twisted theory is expected to be free of linear discretization errors. Two separate definitions of the twist angle are used, and the hadron masses for these two cases are compared. The flavor breaking, that can arise due to twisting, is discussed in the context of mass splittings within the Delta(1232) multiplet.Comment: 23 pages, 16 figures, added discussion of pion decay constan

Strange quarks in quenched twisted mass lattice QCD

Two twisted doublets, one containing the up and down quarks and the other containing the strange quark with an SU(2)-flavor partner, are used for studies in the meson sector. The relevant chiral perturbation theory is presented, and quenched QCD simulations (where the partner of the strange quark is not active) are performed. Pseudoscalar meson masses and decay constants are computed; the vector and scalar mesons are also discussed. A comparison is made to the case of an untwisted strange quark, and some effects due to quenching, discretization, and the definition of maximal twist are explored.Comment: 37 pages, 12 figures, accepted for publicatio

Parton Distribution Functions with Twisted Mass Fermions

We present a first Wilson twisted mass fermion calculation of the matrix element between pion states of the twist-2 operator, which is related to the the lowest moment of the valence quark parton distribution function in a pion. Using Wilson twisted mass fermions in the quenched approximation we demonstrate that can be computed at small pseudoscalar meson masses down to values of order 250 MeV. We investigate the scaling behaviour of this physically important quantity by applying two definitions of the critical mass and observe a scaling compatible with the expected O(a^2) behaviour in both cases. A combined continuum extrapolation allows to obtain reliable results for at very small pseudoscalar meson masses, which previously could not be explored by lattice QCD simulations.Comment: 15 pages, 3 figure

Inhibitive action of Cystine on the corrosion of low alloy steel ASTM A213 grade T22 in sulfamic acid solutions

AbstractThe effect of Cystine on the corrosion behavior of low alloy steel ASTM A213 grade T22 in 0.5M sulfamic acid solutions have been investigated by various electrochemical techniques. The study was performed using electrochemical impedance spectroscopy (EIS) and the recent technique electrochemical frequency modulation (EFM). The results of the investigation show that the inhibition efficiency increased with increasing inhibitor concentration, but decreased with increasing the solution temperature and stirring velocity. All the collected results from the two techniques are in good agreements, which confirm the ability of EFM technique for monitoring the corrosion inhibition under the studied conditions

Lattice QCD with a twisted mass term and a strange quark

There are three quarks with masses at or below the characteristic scale of QCD dynamics: up, down and strange. However, twisted mass lattice QCD relies on quark doublets. Various options for including three quark flavors within the twisted mass approach are explored by studying the kaon masses, both analytically (through chiral Lagrangians) and numerically (through lattice simulations). Advantages and disadvantages are revealed for each ``strange and twisted'' option

Tissue p53-induced glycolysis and apoptosis regulator (TIGAR) is associated with oxidative stress in benign and malignant colorectal lesions

Background: Colorectal cancer (CRC) is the fourth leading cause of cancer-mortality worldwide. Tissue p53-induced glycolysis and apoptosis regulator gene (TIGAR) has an important role in cellular glycolysis and acts as an oncogene.Objectives: We aimed to investigate the diagnostic utility of TIGAR in both CRC and benign bowel deceases.Methods: One-hundred-eighty tissue samples were recruited and classified into 3 groups: group (1) 60 CRC samples from the tumor mass of colorectal cancer patients, group (2), 60 non-neoplastic colorectal tissue samples and group (3), 60 benign bowel lesions samples (ulcerative-colitis, Chron’s disease, adenoma, and familial adenomatous polyposis). The expressions of tissue mRNA and protein levels of TIGAR were determined. Levels of malondialdehyde and reduced glutathione were also measured.Results: Our results showed upregulated expressions of TIGAR gene and protein levels in CRC tissues and benign colonic lesions compared to non-tumor tissues (p < 0.0001). Their levels were higher in inflammatory bowel diseases compared to non-inflammatory benign lesions. There were significant relations among TIGAR expression, protein levels, TNM staging, and the presence of metastasis (p<0.0001). ROC curve analysis showed that TIGAR mRNA expression and its protein can discriminate between CRC and benign lesions and between benign bowel disease and controls.Conclusions: To the best of our knowledge this is the first study to assess the level of TIGAR in different benign bowel diseases. TIGAR might be involved in the pathogenesis of benign and malignant bowel diseases and could be a potential biomarker for diagnosis

Control of replication stress and mitosis in colorectal cancer stem cells through the interplay of PARP1, MRE11 and RAD51

Cancer stem cells (CSCs) are tumor subpopulations driving disease development, progression, relapse and therapy resistance, and their targeting ensures tumor eradication. CSCs display heterogeneous replication stress (RS), but the functionality/relevance of the RS response (RSR) centered on the ATR-CHK1 axis is debated. Here, we show that the RSR is efficient in primary CSCs from colorectal cancer (CRC-SCs), and describe unique roles for PARP1 and MRE11/RAD51. First, we demonstrated that PARP1 is upregulated in CRC-SCs resistant to several replication poisons and RSR inhibitors (RSRi). In these cells, PARP1 modulates replication fork speed resulting in low constitutive RS. Second, we showed that MRE11 and RAD51 cooperate in the genoprotection and mitosis execution of PARP1-upregulated CRC-SCs. These roles represent therapeutic vulnerabilities for CSCs. Indeed, PARP1i sensitized CRC-SCs to ATRi/CHK1i, inducing replication catastrophe, and prevented the development of resistance to CHK1i. Also, MRE11i + RAD51i selectively killed PARP1-upregulated CRC-SCs via mitotic catastrophe. These results provide the rationale for biomarker-driven clinical trials in CRC using distinct RSRi combinations