We compute the next-to-leading order O(g) correction to the thermal photon production rate in a QCD plasma. The NLO contributions can be expressed in terms of gauge invariant condensates on the light cone, which are amenable to novel sum rules and Euclidean techniques. We expect these technologies to be generalizable to other NLO calculations. For the phenomenologically interesting value of α s = 0.3, the NLO correction represents a 20% increase and has a functional form similar to the LO result.

This paper summarizes the newly developed immersed finite element method (IFEM) and its applications to the modeling of biological systems. This work was inspired by the pioneering work of Professor T.J.R. Hughes in solving fluid-structure interaction problems. In IFEM, a Lagrangian solid mesh moves on top of a background Eulerian fluid mesh which spans the entire computational domain. Hence, mesh generation is greatly simplified. Moreover, both fluid and solid domains are modeled with the finite element method and the continuity between the fluid and solid subdomains is enforced via the interpolation of the velocities and the distribution of the forces with the reproducing Kernel particle method (RKPM) delta function. The proposed method is used to study the fluid-structure interaction problems encountered in human cardiovascular systems. Currently, the heart modeling is being constructed and the deployment process of an angioplasty stent has been simulated. Some preliminary results on monocyte and platelet deposition are presented. Blood rheology, in particular, the shear-rate dependent de-aggregation of red blood cell (RBC) clusters and the transport of deformable cells, are modeled. Furthermore, IFEM is combined with electrokinetics to study the mechanisms of nano/bio filament assembly for the understanding of cell motility.

We compute the spectral densities of T µν and J µ in high temperature QCD plasmas at small frequency and momentum, ω, k ∼ g 4 T . The leading log Boltzmann equation is reformulated as a Fokker Planck equation with non-trivial boundary conditions, and the resulting partial differential equation is solved numerically in momentum space. The spectral densities of the current, shear, sound, and bulk channels exhibit a smooth transition from free streaming quasi-particles to ideal hydrodynamics. This transition is analyzed with conformal and non-conformal second order hydrodynamics, and a second order diffusion equation. We determine all of the second order transport coefficients which characterize the linear response in the hydrodynamic regime.

IntroductionHigh-fat diets (HFDs) are known to cause obesity and are associated with breast cancer progression and metastasis. Because obesity is associated with breast cancer progression, it is important to determine whether dietary fat per se stimulates breast cancer progression in the absence of obesity. This study investigated whether an HFD increases breast cancer growth and metastasis, as well as mortality, in obesity-resistant BALB/c mice.MethodsThe 4-week-old, female BALB/c mice were fed HFD (60% kcal fat) or control diet (CD, 10% kcal fat) for 16 weeks. Subsequently, 4T1 mammary carcinoma cells were injected into the inguinal mammary fat pads of mice fed continuously on their respective diets. Cell-cycle progression, angiogenesis, and immune cells in tumor tissues, proteases and adhesion molecules in the lungs, and serum cytokine levels were analyzed with immunohistochemistry, Western blotting, and enzyme-linked immunosorbent assay (ELISA). In vitro studies were also conducted to evaluate the effects of cytokines on 4T1 cell viability, migration, and adhesion.ResultsSpleen and gonadal fat-pad weights, tumor weight, the number and volume of tumor nodules in the lung and liver, and tumor-associated mortality were increased in the HFD group, with only slight increases in energy intake and body weight. HF feeding increased macrophage infiltration into adipose tissues, the number of lipid vacuoles and the expression of cyclin-dependent kinase (CDK)2, cyclin D1, cyclin A, Ki67, CD31, CD45, and CD68 in the tumor tissues, and elevated serum levels of complement fragment 5a (C5a), interleukin (IL)-16, macrophage colony-stimulating factor (M-CSF), soluble intercellular adhesion molecule (sICAM)-1, tissue inhibitors of metalloproteinase (TIMP)-1, leptin, and triggering receptor expressed on myeloid cells (TREM)-1. Protein levels of the urokinase-type plasminogen activator, ICAM-1, and vascular cell adhesion molecule-1 were increased, but plasminogen activator inhibitor-1 levels were decreased in the lungs of the HFD group. In vitro assays using 4T1 cells showed that sICAM-1 increased viability; TREM-1, TIMP-1, M-CSF, and sICAM-1 increased migration; and C5a, sICAM-1, IL-16, M-CSF, TIMP-1, and TREM-1 increased adhesion.ConclusionsDietary fat increases mammary tumor growth and metastasis, thereby increasing mortality in obesity-resistant mice.

PurposePatient-derived tumor xenografts (PDXs) can provide more reliable information about tumor biology than cell line models. We developed PDXs for epithelial ovarian cancer (EOC) that have histopathologic and genetic similarities to the primary patient tissues and evaluated their potential for use as a platform for translational EOC research.Materials and MethodsWe successfully established PDXs by subrenal capsule implantation of primary EOC tissues into female BALB/C-nude mice. The rate of successful PDX engraftment was 48.8% (22/45 cases). Hematoxylin and eosin staining and short tandem repeat analysis showed histopathological and genetic similarity between the PDX and primary patient tissues.ResultsPatients whose tumors were successfully engrafted in mice had significantly inferior overall survival when compared with those whose tumors failed to engraft (p=0.040). In preclinical tests of this model, we found that paclitaxel-carboplatin combination chemotherapy significantly deceased tumor weight in PDXs compared with the control treatment (p=0.013). Moreover, erlotinib treatment significantly decreased tumor weight in epidermal growth factor receptor–overexpressing PDX with clear cell histology (p=0.023).ConclusionPDXs for EOC with histopathological and genetic stability can be efficiently developed by subrenal capsule implantation and have the potential to provide a promising platform for future translational research and precision medicine for EOC.