An algebraic description of screw dislocations in SC and BCC crystal lattices

We give an algebraic description of screw dislocations in a crystal, especially simple cubic (SC) and body centered cubic (BCC) crystals, using free abelian groups and fibering structures. We also show that the strain energy of a screw dislocation based on the spring model is expressed by the Epstein-Hurwitz zeta function approximately.Comment: 41 pages, 7 figure

EU, NAFTA, and Asian Responses: A Perspective from the Calculus of Participation

This paper assesses the economic conditions for Asian countries to cope with the formation of EU and NAFTA. Is it desirable for them to form their own trading area? And, if desirable, is it better to have a closed one like the EAEC or a more open one like the APEC? Relying on public economics and the calculus of participation combined with the Dixit-Stiglitz-Krugman framework, we find the following: (i) the development of the EAEC by the leadership of Malaysia would be a natural response of Asian countries against two big blocs in the world, EU and NAFTA; (ii) it is natural for the United States to discourage this move because the formation of an economic bloc in Asia will have a negative economic impact on the non- Asian countries; (iii) it is natural for the U.S. to propose an opposing coalition like the APEC to nullify the possible economic impact of the EAEC; but (iv) perhaps the APEC will be a good roundabout way towards international free trade.

MicroRNA-194 inhibits epithelial to mesenchymal transition of endometrial cancer cells by targeting oncogene BMI-1

<p>Abstract</p> <p>Background</p> <p>Epithelial-mesenchymal transition (EMT) is the key process driving cancer metastasis. Oncogene/self renewal factor BMI-1 has been shown to induce EMT in cancer cells. Recent studies have implied that noncoding microRNAs (miRNAs) act as crucial modulators for EMT. The aims of this study was to determine the roles of BMI-1 in inducing EMT of endometrial cancer (EC) cells and the possible role of miRNA in controlling BMI-1 expression.</p> <p>Methods and results</p> <p>We evaluated the expression of BMI-1 gene in a panel of EC cell lines, and detected a strong association with invasive capability. Stable silencing of BMI-1 in invasive mesenchymal-type EC cells up-regulated the epithelial marker E-cadherin, down-regulated mesenchymal marker Vimentin, and significantly reduced cell invasion <it>in vitro</it>. Furthermore, we discovered that the expression of BMI-1 was suppressed by miR-194 via direct binding to the BMI-1 3'-untranslated region 3'-UTR). Ectopic expression of miR-194 in EC cells induced a mesenchymal to epithelial transition (MET) by restoring E-cadherin, reducing Vimentin expression, and inhibiting cell invasion <it>in vitro</it>. Moreover, BMI-1 knockdown inhibited <it>in vitro </it>EC cell proliferation and clone growth, correlated with either increased p16 expression or decreased expression of stem cell and chemoresistance markers (SOX-2, KLF4 and MRP-1).</p> <p>Conclusion</p> <p>These findings demonstrate the novel mechanism for BMI-1 in contributing to EC cell invasion and that repression of BMI-1 by miR-194 could have a therapeutic potential to suppress EC metastasis.</p

Induction of Tissue Factor Expression in Endothelial Cells by Basic Fibroblast Growth Factor and its Modulation by Fenofibric acid

BACKGROUND: Tissue factor (TF), expressed in endothelial cells (ECs) and enriched in human atherosclerotic lesions, acts as a critical initiator of blood coagulation in acute coronary syndrome. Basic fibroblast growth factor (bFGF) induces the proliferation and migration of ECs and plays a role in angiogenesis and restoration of endothelial integrity. As TF is implicated in angiogenesis, we studied the effect of bFGF on TF gene and protein expression. Methods: Human umbilical vein ECs (HUVECs) were exposed to bFGF. TF mRNA was assessed by Northern blot and TF protein was assessed by Western blot. TF promoter activity was assessed by transient transfection assay and transcription factor was identified by electro mobility shift assay. RESULTS: bFGF increased TF mRNA and protein expression in HUVECs. Increased TF mRNA was attenuated by inhibition of extracellular signal-regulated kinase kinase in human ECV304 cells. Transient transfection assays of the human TF promoter-luciferase construct (-786/+121 bp) demonstrated that bFGF induced transcription was dependent on the elements within the -197 to -176 bp relative to the transcription start site of the human TF gene. This region contains NF-κB like binding site. Electro mobility shift assay showed that bFGF increased nuclear translocation or DNA binding of NF-κB transcription factor to TF promoter. Nucleotide substitution to disrupt NF-κB like site reduced bFGF stimulated promoter activity. Fenofibric acid, an agonist ligand for the peroxisome proliferator activated receptor-α, reduced basal and bFGF stimulated TF expression. CONCLUSIONS: These results indicate that bFGF may increase TF production in ECs through activation of transcription at NF-κB binding site, and control coagulation in vessel walls. Fibrate can inhibit TF expression and therefore reduce the thrombogenecity of human atherosclerotic lesions

Communication-Efficient Inner Product Private Join and Compute with Cardinality

Private join and compute (PJC) is a paradigm where two parties owing their private database securely join their databases and compute a function over the combined database. Inner product PJC, introduced by Lepoint et al. (Asiacrypt\u2721), is a class of PJC that has a wide range of applications such as secure analysis of advertising campaigns. In this computation, two parties, each of which has a set of identifier-value pairs, compute the inner product of the values after the (inner) join of their databases with respect to the identifiers. They proposed inner product PJC protocols that are specialized for the unbalanced setting where the input sizes of both parties are significantly different and not suitable for the balanced setting where the sizes of two inputs are relatively close. We propose an inner product PJC protocol that is much more efficient than that by Lepoint et al. for balanced inputs in the setting where both parties are allowed to learn the intersection size additionally. Our protocol can be seen as an extension of the private intersection-sum protocol based on the decisional Diffie-Hellman assumption by Ion et al. (EuroS&P\u2720) and is especially communication-efficient as the private intersection-sum protocol. In the case where both input sizes are $2^{16}$, the communication cost of our inner-product PJC protocol is $46\times$ less than that of the inner product PJC protocol by Lepoint et al

Secure Statistical Analysis on Multiple Datasets: Join and Group-By

We implement a secure platform for statistical analysis over multiple organizations and multiple datasets. We provide a suite of protocols for different variants of JOIN and GROUP-BY operations. JOIN allows combining data from multiple datasets based on a common column. GROUP-BY allows aggregating rows that have the same values in a column or a set of columns, and then apply some aggregation summary on the rows (such as sum, count, median, etc.). Both operations are fundamental tools for relational databases. One example use case of our platform is in data marketing in which an analyst would join purchase histories and membership information, and then obtain statistics, such as Which products were bought by people earning this much per annum? Both JOIN and GROUP-BY involve many variants, and we design protocols for several common procedures. In particular, we propose a novel group-by-median protocol that has not been known so far. Our protocols rely on sorting protocols, and work in the honest majority setting and against malicious adversaries. To the best of our knowledge, this is the first implementation of JOIN and GROUP-BY protocols secure against a malicious adversary