Regularity of weak solutions to rate-independent systems in one-dimension

We show that under some appropriate assumptions, every weak solution (e.g. energetic solution) to a given rate-independent system is of class SBV, or has fi�nite jumps, or is even piecewise C1. Our assumption is essentially imposed on the energy functional, but not convexity is required

Self-gravitating Newtonian disks revisited

Recent analytic results concerning stationary, self-gravitating fluids in Newtonian theory are discussed. We give a theorem that forbids infinitely extended fluids, depending on the assumed equation of state and the rotation law. This part extends previous results that have been obtained for static configurations. The second part discusses a Sobolev bound on the mass of the fluid and a rigorous Jeans-type inequality that is valid in the stationary case.Comment: A talk given at the Spanish Relativity Meeting in Portugal 2012. To appear in Progress in Mathematical Relativity, Gravitation and Cosmology, Proceedings of the Spanish Relativity Meeting ERE2012, University of Minho, Guimaraes, Portugal, 3-7 September 2012, Springer Proceedings in Mathematics & Statistics, Vol. 6

Another construction of BV solutions to rate-independent systems

We study one kind of weak solutions to rate-independent systems, which is constructed by using the local minimality in a small neighborhood of order ε and then taking the limit ε → 0. We show that the resulting solution satisfies both the weak local stability and the new energy-dissipation balance, similarly to the BV solutions constructed by vanishing viscosity introduced recently by Mielke, Rossi and Savare

BV solutions constructed by epsilon-neighborhood method

We study a certain class of weak solutions to rate-independent systems, which is constructed by using the local minimality in a small neighborhood of order $\varepsilon$ and then taking the limit $\varepsilon \to 0$. We show that the resulting solution satisfies both the weak local stability and the new energy-dissipation balance, similarly to the BV solutions constructed by vanishing viscosity introduced recently by Mielke, Rossi and Savar\'e

Federal Employees Health Benefits Program (FEHBP): Available Health Insurance Options

FEHBP is generally available to employees, annuitants, and their dependents. Eligible individuals may elect coverage in an approved health benefits plan for either individual or family coverage. For the 2013 plan year, there are about 230 different plan choices, including all regionally available options. As a practical matter, an individual’s choice of plans is often limited to 10 to 15 different plans, depending on where the individual resides. While enrollees have a range of choices, they typically decide which options best match their needs, the amount of their wages they will contribute to health insurance, and how risk-averse they are to potential out-of-pocket costs. While most federal employees or annuitants reaching age 65 are automatically entitled to Medicare Part A, Medicare-eligible employees may also voluntarily choose to enroll in Medicare Part B and Part D. For individuals covered under a FEHBP plan as an annuitant, Medicare is the primary payer and FEHBP is the secondary payer. As a secondary payer, FEHBP could cover a share of Medicare deductibles and coinsurance for any services that are covered by both plans, and FEHBP would continue to reimburse for its covered services that are not covered by Medicare. FEHBP is administered by the Office of Personnel Management (OPM), which is statutorily given the authority to contract with qualified carriers offering plans and to prescribe regulations necessary to carry out the statute, among other duties. Some of OPM’s additional duties include coordinating the administration of FEHBP with employing offices, managing contingency reserve funds for the plans, and applying sanctions to health care providers according to the prescribed regulations

PPAR-alpha: a novel target in pancreatic cancer

Background: Current targeted therapies in pancreatic cancer have been ineffective. The tumor stroma, including intra- and peri-tumoral inflammation and fibrosis, is increasingly implicated in pancreatic cancer. Pancreatic cancer is characterized by a highly fibrotic tumor environment resulting in stromal resistance to chemotherapy. Peroxisome proliferator-activated receptor-alpha (PPARα), a ligand-activated nuclear receptor/transcription factor, is a negative regulator of inflammation. In PPARα deficient mice, stromal processes inhibit tumor growth, resulting in dormant tumors. The presence of PPARα in the tumor cells as well as in the host is necessary for unabated tumor growth. Objective: We hypothesized that blocking the PPARα pathway with a small molecule PPARα antagonist (NXT) may prevent pancreatic cancer progression by targeting tumor cells as well as non-neoplastic cells in the tumor microenvironment. Methods: Growth inhibitory activity of the PPARα antagonist was assessed in murine as well as human pancreatic tumor cell lines (Panc0H7 and BxPC3) and in a murine macrophage cell line (RAW 264.7). Cell viability was determined by trypan blue exclusion assay. AKT, P-AKT, PCNA, BAX, and p27 levels were analyzed by western blot analysis. Cell cycle changes were detected by flow cytometry. Cellular senescence was determined by senescence-associated β-gal (SA-β-gal) staining. Results: The PPARα antagonist inhibited cell growth in macrophages and in pancreatic tumor cells as confirmed by reduced protein level expression of PCNA and activated AKT. Treatment of the PPARα antagonist was non-cytotoxic to tumor cells. Inhibition of PPARα induced cell cycle arrest at G0/G1 in tumor cells and macrophages. The induction of cellular senescence was observed in pancreatic cancer cells. Interestingly, we observed a reduction in protein level expression of BAX, a marker for apoptosis, and p27, an inhibitor of the cell cycle. Conclusion: We now demonstrate that a PPARα antagonist exerts its anti-growth activity by inducing G0/G1 cell cycle arrest, thereby inducing cellular senescence without cell death. These findings provide a mechanism for the anti-tumorigenic activity of PPARα inhibition, and the rationale to use PPARα antagonists as a novel therapeutic approach to pancreatic cancer.2016-11-03T00:00:00