FlexAuc: Serving Dynamic Demands in a Spectrum Trading Market with Flexible Auction

In secondary spectrum trading markets, auctions are widely used by spectrum holders (SHs) to redistribute their unused channels to secondary wireless service providers (WSPs). As sellers, the SHs design proper auction schemes to stimulate more participants and maximize the revenue from the auction. As buyers, the WSPs determine the bidding strategies in the auction to better serve their end users. In this paper, we consider a three-layered spectrum trading market consisting of the SH, the WSPs and the end users. We jointly study the strategies of the three parties. The SH determines the auction scheme and spectrum supplies to optimize its revenue. The WSPs have flexible bidding strategies in terms of both demands and valuations considering the strategies of the end users. We design FlexAuc, a novel auction mechanism for this market to enable dynamic supplies and demands in the auction. We prove theoretically that FlexAuc not only maximizes the social welfare but also preserves other nice properties such as truthfulness and computational tractability.Comment: 11 pages, 7 figures, Preliminary version accepted in INFOCOM 201

Quantitative proteomic analysis of sphere-forming stem-like oral cancer cells.

IntroductionThe purpose of this study is to identify target proteins that may play important functional roles in oral cancer stem-like cells (CSCs) using mass spectrometry-based quantitative proteomics.MethodsSphere-formation assays were performed on highly invasive UM1 and lowly invasive UM2 oral cancer cell lines, which were derived from the same tongue squamous cell carcinoma, to enrich CSCs. Quantitative proteomic analysis of CSC-like and non-CSC UM1 cells was carried out using tandem mass tagging and two-dimensional liquid chromatography with Orbitrap mass spectrometry.ResultsCSC-like cancer cells were found to be present in the highly invasive UM1 cell line but absent in the lowly invasive UM2 cell line. Stem cell markers SOX2, OCT4, SOX9 and CD44 were up-regulated, whereas HIF-1 alpha and PGK-1 were down-regulated in CSC-like UM1 cells versus non-CSC UM1 cells. Quantitative proteomic analysis indicated that many proteins in cell cycle, metabolism, G protein signal transduction, translational elongation, development, and RNA splicing pathways were differentially expressed between the two cell phenotypes. Both CREB-1-binding protein (CBP) and phosphorylated CREB-1 were found to be significantly over-expressed in CSC-like UM1 cells.ConclusionsCSC-like cells can be enriched from the highly invasive UM1 oral cancer cell line but not from the lowly invasive UM2 oral cancer cell line. There are significant proteomic alterations between CSC-like and non-CSC UM1 cells. In particular, CBP and phosphorylated CREB-1 were significantly up-regulated in CSC-like UM1 cells versus non-CSC UM1 cells, suggesting that the CREB pathway is activated in the CSC-like cells

Normalized solutions for Sobolev critical Schr\"odinger-Bopp-Podolsky systems

We study the Sobolev critical Schr\"odinger-Bopp-Podolsky system \begin{gather*} -\Delta u+\phi u=\lambda u+\mu|u|^{p-2}u+|u|^4u\quad \text{in }\mathbb{R}^3, -\Delta\phi+\Delta^2\phi=4\pi u^2\quad \text{in } \mathbb{R}^3, \end{gather*} under the mass constraint $$\int_{\mathbb{R}^3}u^2\,dx=c$$ for some prescribed $c>0$, where $2<p<8/3$, $\mu>0$ is a parameter, and $\lambda\in\mathbb{R}$ is a Lagrange multiplier. By developing a constraint minimizing approach, we show that the above system admits a local minimizer. Furthermore, we establish the existence of normalized ground state solutions.Comment: 19 page

THE MITOCHONDRIAL GENOME OF THE BLUE CRAB (CALLINECTES SAPIDUS), AN INFORMATIVE GENETIC MARKER FOR THE EVOLUTIONARY BIOLOGY AND POPULATION GENETICS OF THE SPECIES

The blue crab (Callinectes sapidus) is a widely distributed decapod which ranges from Nova Scotia to the northern Argentina coasts. It is one of the most abundant estuarine invertebrates, supporting both commercial and recreational fisheries along the Atlantic and Gulf coasts. This thesis presents data clearly establishing the unprecedented hyper-variability in the mitochondrial genome of C. sapidus. This variation extended to multiple regions, including the cox1, nad2, and nad4 protein coding loci as well as ribosomal 12s RNA molecule. The haplotype diversity of the nad2 gene approached 1, with a nucleotide diversity approaching 1%. This hyper-variability in the mtDNA allows using a single mtDNA gene (nad2) to distinguish hatchery-produced crabs from wild crabs after release to the wild. I found no dominant mtDNA haplotypes in wild populations but instead a distribution of a few low-frequency recurrent haplotypes with a large number of singletons. Because of this high diversity and extensive population mixing, the geographic structure in wild populations exhibits panmixia from the Atlantic to Gulf of Mexico. Some of the high genetic diversity found seems to stem from the heteroplasmic nature of the blue crab mtDNA. By cloning high fidelity PCR products, I confirmed single individual crab and megalopa harbored dozens of copies of mitochondrial haplotypes. A copy number analysis indicates discovery of unique haplotypes was probably not saturated with the possibility of inadequate sampling. The heteroplasmy in the blue crab appears to be under maternal inheritance without paternal contribution. While minor haplotypes are represented in wild populations, other minor haplotypes contained stop codons and/or non-synonymous substitutions which may influence the viability of the mitochondria. Given the blue crab inhabits a broad variety of environments and that the mtDNA genome appears to be under selective pressure, the potential for mtDNA functional correlates with this genetic diversity maybe at the basis for the robust physiological capability of the species

Quantitative proteomic analysis of sphere-forming stem-like oral cancer cells

INTRODUCTION: The purpose of this study is to identify target proteins that may play important functional roles in oral cancer stem-like cells (CSCs) using mass spectrometry-based quantitative proteomics. METHODS: Sphere-formation assays were performed on highly invasive UM1 and lowly invasive UM2 oral cancer cell lines, which were derived from the same tongue squamous cell carcinoma, to enrich CSCs. Quantitative proteomic analysis of CSC-like and non-CSC UM1 cells was carried out using tandem mass tagging and two-dimensional liquid chromatography with Orbitrap mass spectrometry. RESULTS: CSC-like cancer cells were found to be present in the highly invasive UM1 cell line but absent in the lowly invasive UM2 cell line. Stem cell markers SOX2, OCT4, SOX9 and CD44 were up-regulated, whereas HIF-1 alpha and PGK-1 were down-regulated in CSC-like UM1 cells versus non-CSC UM1 cells. Quantitative proteomic analysis indicated that many proteins in cell cycle, metabolism, G protein signal transduction, translational elongation, development, and RNA splicing pathways were differentially expressed between the two cell phenotypes. Both CREB-1-binding protein (CBP) and phosphorylated CREB-1 were found to be significantly over-expressed in CSC-like UM1 cells. CONCLUSIONS: CSC-like cells can be enriched from the highly invasive UM1 oral cancer cell line but not from the lowly invasive UM2 oral cancer cell line. There are significant proteomic alterations between CSC-like and non-CSC UM1 cells. In particular, CBP and phosphorylated CREB-1 were significantly up-regulated in CSC-like UM1 cells versus non-CSC UM1 cells, suggesting that the CREB pathway is activated in the CSC-like cells

Oral cancer cells may rewire alternative metabolic pathways to survive from siRNA silencing of metabolic enzymes.

BackgroundCancer cells may undergo metabolic adaptations that support their growth as well as drug resistance properties. The purpose of this study is to test if oral cancer cells can overcome the metabolic defects introduced by using small interfering RNA (siRNA) to knock down their expression of important metabolic enzymes.MethodsUM1 and UM2 oral cancer cells were transfected with siRNA to transketolase (TKT) or siRNA to adenylate kinase (AK2), and Western blotting was used to confirm the knockdown. Cellular uptake of glucose and glutamine and production of lactate were compared between the cancer cells with either TKT or AK2 knockdown and those transfected with control siRNA. Statistical analysis was performed with student T-test.ResultsDespite the defect in the pentose phosphate pathway caused by siRNA knockdown of TKT, the survived UM1 or UM2 cells utilized more glucose and glutamine and secreted a significantly higher amount of lactate than the cells transferred with control siRNA. We also demonstrated that siRNA knockdown of AK2 constrained the proliferation of UM1 and UM2 cells but similarly led to an increased uptake of glucose/glutamine and production of lactate by the UM1 or UM2 cells survived from siRNA silencing of AK2.ConclusionsOur results indicate that the metabolic defects introduced by siRNA silencing of metabolic enzymes TKT or AK2 may be compensated by alternative feedback metabolic mechanisms, suggesting that cancer cells may overcome single defective pathways through secondary metabolic network adaptations. The highly robust nature of oral cancer cell metabolism implies that a systematic medical approach targeting multiple metabolic pathways may be needed to accomplish the continued improvement of cancer treatment