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To achieve super high luminosity, high current beams with very short bunch length are needed, which carry high intensity EM fields. For ILC, two bunch trains with bunch length of 300 {micro}m and bunch charge of 3.2nC are needed to collide at the IR to achieve the ILC luminosity goals. When the 300 {micro}m bunches pass through the IR chamber, wakefields will be excited, which will cause HOM power flowing through the IR chamber beam pipe to the final doublets due to the high frequency characteristic of the induced wakefields. Since superconducting technology is adopted for the final doublets of ILC BDS, whose operation stability might be affected by the HOM power produced at the IR chamber, quench might happen. In this paper, we did some analytical estimation and numerical simulation on the wakefield effects in ILC IR chamber.

Results of the collimation studies for the ILC positron source beam line are presented. The calculations of primary positron beam loss are done using the ELEGANT code. The secondary positron and electron beam loss, the synchrotron radiation along the beam line and the bremsstrahlung radiation in the collimators are simulated using the STRUCT code. The first part of the collimation system, located right after the positron source target (0.125 GeV), is used for protection of the RF Linac sections from heating and radiation. The second part of the system is used for final collimation before the beam injection into the Damping Ring at 5 GeV. The calculated power loss in the collimation region is within 100 W/m, with the loss in the collimators of 0.2-5 kW. The beam transfer efficiency from the target to the Damping Ring is 13.5%.

The authors report the first observation of e{sup +}e{sup -} {yields} {rho}{sup +}{rho}{sup -}, in a data sample of 379 fb{sup -1} collected with the BABAR detector at the PEP-II e{sup +}e{sup -} storage ring at center-of-mass energies near {radical}s = 10.58 GeV. The authors measure a cross section of {sigma}(e{sup +}e{sup -} {yields} {rho}{sup +}{rho}{sup -}) = 19.5 {+-} 1.6(stat) {+-} 3.2(syst) fb. Assuming production through single-photon annihilation, there are three independent helicity amplitudes. They measure the ratios of their squared moduli to be |F{sub 00}|{sup 2} : |F{sub 10}|{sup 2} : |F{sub 11}|{sup 2} = 0.51 {+-} 0.14(stat) {+-} 0.07(syst) : 0.10 {+-} 0.04(stat) {+-} 0.01(syst) : 0.04 {+-} 0.03(stat) {+-} 0.01(syst). The |F{sub 00}|{sup 2} result is inconsistent with the prediction of 1.0 made by QCD models with a significance of 3.1 standard deviations including systematic uncertainties.

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The complexities of bubble formation in liquids increase as the system size increases, and a photographic study is presented here to provide some insight into the dynamics of bubble formation for large systems. Air was injected at the bottom of a 28 feet tall by 30 inch diameter column. Different fluids were subjected to different air flow rates at different fluid depths. The fluids were water and non-Newtonian, Bingham plastic fluids, which have yield stresses requiring an applied force to initiate movement, or shearing, of the fluid. Tests showed that bubble formation was significantly different in the two types of fluids. In water, a field of bubbles was formed, which consisted of numerous, distributed, 1/4 to 3/8 inch diameter bubbles. In the Bingham fluid, large bubbles of 6 to 12 inches in diameter were formed, which depended on the air flow rate. This paper provides comprehensive photographic results related to bubble formation in these fluids.

Cell morphology dictates response to a wide variety of stimuli, controlling cell metabolism, differentiation, proliferation, and death. Epithelial-mesenchymal transition (EMT) is a developmental process in which epithelial cells acquire migratory characteristics, and in the process convert from a 'cuboidal' epithelial structure into an elongated mesenchymal shape. We had shown previously that matrix metalloproteinase-3 (MMP3) can stimulate EMT of cultured mouse mammary epithelial cells through a process that involves increased expression of Rac1b, a protein that stimulates alterations in cytoskeletal structure. We show here that cells treated with MMP-3 or induced to express Rac1b spread to cover a larger surface, and that this induction of cell spreading is a requirement of MMP-3/Rac1b-induced EMT. We find that limiting cell spreading, either by increasing cell density or by culturing cells on precisely defined micropatterned substrata, blocks expression of characteristic markers of EMT in cells treated with MMP-3. These effects are not caused by general disruptions in cell signaling pathways, as TGF-{beta}-induced EMT is not affected by similar limitations on cell spreading. Our data reveal a previously unanticipated cell shape-dependent mechanism that controls this key phenotypic alteration and provide insight into the distinct mechanisms activated by different EMT-inducing agents.

The normal mammary gland and invasive breast cancer are both complex 'organs' composed of multiple cell types as well as extracellular matrix (ECM) in three-dimensional (3D) space. Conventionally, both normal and malignant breast cells are studied in vitro as two-dimensional (2D) monolayers of epithelial cells, which results in the loss of structure and tissue function. Many laboratories are now investigating regulation of signaling function in normal mammary gland using 3D cultures. However, it is important also to assay malignant breast cells ex vivo in a physiologically relevant environment to more closely mimic tumor architecture, signal transduction regulation and tumor behavior in vivo. Here we present the potential of these 3D models for drug testing, target validation and guidance of patient selection for clinical trials. We argue also that in order to get full insight into the biology of the normal and malignant breast, and to create in vivo-like models for therapeutic approaches in humans, we need to continue to create more complex heterotypic models to approach the full context the cells encounter in the human body.

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