Low Q 2 boundary conditions for DGLAP equations dictated by quantum statistical mechanics

We discuss the role of quantum statistical mechanics in the description of the parton distribution functions in the proton. It provides the low Q 2 boundary conditions for DGLAP equations in terms of Fermi–Dirac and Bose–Einstein functions of the fractional momentum variable x. The successful comparison with experimental data on both the unpolarised and polarised deep inelastic structure functions is reviewed. We argue that the statistical approach for the nucleon parton distributions functions has the nice feature that the free model parameters are fixed from data with high statistics and small systematic uncertainties, providing a strong constraint on the information not supplied by the experiments

The Tumor Suppressor Gene, RASSF1A, Is Essential for Protection against Inflammation -Induced Injury

10.1371/journal.pone.0075483PLoS ONE810-POLN

Effect of plasma density profile inhomogeneity on the self-generated magnetic field

The photon orbital and/or spin angular-momentum absorption in absorbing plasma medium causes the circular motion of electrons and generate the azimuthal component of current density. The axial magnetic field generation due to the azimuthal component of generated current density is known as inverse Faraday effect. In this paper, the axial magnetic field generation in an absorbing plasma with ramped density by the propagation of linear polarized Laguerre-Gaussian beam is taken into consideration. It is shown that the positive slope of the initial electron density causes a considerable enhancement of self-generated axial magnetic field. The magnetic field enhancement depends on the twisted light vortex charge number. The rotation angle of the linearly polarized light which can be employed for measurement of the generated magnetic field, is calculated

Relation between serum ghrelin concentration and blood glucose levels in type-2 diabetic obese males

Background and Objective: Ghrelin is an acylated 28-amino-acid peptide that is the most recently identified adipocytokines, but its role in diabetes is poorly clarified. The objective of this study was to determine the relation between serum ghrelin and blood glucose levels in type 2 diabetic obese males. Materials and Methods: This descriptive study was done on 45 adult obese males with type-2 diabetes in Saveh city, Iran during 2010. Fasting blood glucose, insulin and ghrelin concentrations and Glycosylated hemoglobin HbA1C were measured after overnight fasting. Multiple regression was used for determine ghrelin in relation to glucose, insulin and HbA1C. Results: The multiple regression analyses revealed that HbA1C is not correlated with serum ghrelin levels, while, fasting blood glucose level had positive corrolation with serum ghrelin concentration (P<0.05). Serum ghrelin level had high negative correlation with insulin (P<0.05). Conclusion: This study indicated that elevated endogenous ghrelin led to hyperglycemia. Therefore, serum ghrelin is a precise index of blood glucose level in obese male patients with type-2 diabetes

'MCC' protein interacts with E-cadherin and β-catenin strengthening cell-cell adhesion of HCT116 colon cancer cells.

E-cadherin and β-catenin are key proteins that are essential in the formation of the epithelial cell layer in the colon but their regulatory pathways that are disrupted in cancer metastasis are not completely understood. Mutated in colorectal cancer (MCC) is a tumour suppressor gene that is silenced by promoter methylation in colorectal cancer and particularly in patients with increased lymph node metastasis. Here, we show that MCC methylation is found in 45% of colon and 24% of rectal cancers and is associated with proximal colon, poorly differentiated, circumferential and mucinous tumours as well as increasing T stage and larger tumour size. Knockdown of MCC in HCT116 colon cancer cells caused a reduction in E-cadherin protein level, which is a hallmark of epithelial-mesenchymal transition in cancer, and consequently diminished the E-cadherin/β-catenin complex. MCC knockdown disrupted cell-cell adhesive strength and integrity in the dispase and transepithelial electrical resistance assays, enhanced hepatocyte growth factor-induced cell scatter and increased tumour cell invasiveness in an organotypic assay. The Src/Abl inhibitor dasatinib, a candidate anti-invasive drug, abrogated the invasive properties induced by MCC deficiency. Mechanistically, we establish that MCC interacts with the E-cadherin/β-catenin complex. These data provide a significant advance in the current understanding of cell-cell adhesion in colon cancer cells

JRK is a positive regulator of β-catenin transcriptional activity commonly overexpressed in colon, breast and ovarian cancer.

The loss of β-catenin inhibitory components is a well-established mechanism of carcinogenesis but β-catenin hyperactivity can also be enhanced through its coactivators. Here we first interrogated a highly validated genomic screen and the largest repository of cancer genomics data and identified JRK as a potential new oncogene and therapeutic target of the β-catenin pathway. We proceeded to validate the oncogenic role of JRK in colon cancer cells and primary tumors. Consistent with a β-catenin activator function, depletion of JRK in several cancer cell lines repressed β-catenin transcriptional activity and reduced cell proliferation. Importantly, JRK expression was aberrantly elevated in 21% of colorectal cancers, 15% of breast and ovarian cancers and was associated with increased expression of β-catenin target genes and increased cell proliferation. This study shows that JRK is required for β-catenin hyperactivity regardless of the adenomatous polyposis coli/β-catenin mutation status and targeting JRK presents new opportunities for therapeutic intervention in cancer

JRK is a positive regulator of β-catenin transcriptional activity commonly overexpressed in colon, breast and ovarian cancer

The loss of β-catenin inhibitory components is a well-established mechanism of carcinogenesis but β-catenin hyperactivity can also be enhanced through its coactivators. Here we first interrogated a highly validated genomic screen and the largest repository of cancer genomics data and identified JRK as a potential new oncogene and therapeutic target of the β-catenin pathway. We proceeded to validate the oncogenic role of JRK in colon cancer cells and primary tumors. Consistent with a β-catenin activator function, depletion of JRK in several cancer cell lines repressed β-catenin transcriptional activity and reduced cell proliferation. Importantly, JRK expression was aberrantly elevated in 21% of colorectal cancers, 15% of breast and ovarian cancers and was associated with increased expression of β-catenin target genes and increased cell proliferation. This study shows that JRK is required for β-catenin hyperactivity regardless of the adenomatous polyposis coli/β-catenin mutation status and targeting JRK presents new opportunities for therapeutic intervention in cancer