Observation of ballistic phonons in silicon crystals induced by α particles

We have observed the ballistic-phonon-focusing pattern along the [100] axis of a 1-mm-thick silicon crystal using α-particle bombardment as the phonon source. These experiments on phonon-mediated particle detection are performed in vacuum at about 400 mK and use titanium-superconducting-transition-edge phonon sensors on the crystal surfaces. The ballistic time of flight is confirmed in one experiment and the focusing patterns are spatially resolved in another. These data indicate that about 1/3 of the phonon energy striking the back face during the first μsec is ballistic

Numerical optimization of integrating cavities for diffraction-limited millimeter-wave bolometer arrays

Far-infrared to millimeter-wave bolometers designed to make astronomical observations are typically encased in integrating cavities at the termination of feedhorns or Winston cones. This photometer combination maximizes absorption of radiation, enables the absorber area to be minimized, and controls the directivity of absorption, thereby reducing susceptibility to stray light. In the next decade, arrays of hundreds of silicon nitride micromesh bolometers with planar architectures will be used in ground-based, suborbital, and orbital platforms for astronomy. The optimization of integrating cavity designs is required for achieving the highest possible sensitivity for these arrays. We report numerical simulations of the electromagnetic fields in integrating cavities with an infinite plane-parallel geometry formed by a solid reflecting backshort and the back surface of a feedhorn array block. Performance of this architecture for the bolometer array camera (Bolocam) for cosmology at a frequency of 214 GHz is investigated. We explore the sensitivity of absorption efficiency to absorber impedance and backshort location and the magnitude of leakage from cavities. The simulations are compared with experimental data from a room-temperature scale model and with the performance of Bolocam at a temperature of 300 mK. The main results of the simulations for Bolocam-type cavities are that (1) monochromatic absorptions as high as 95% are achievable with <1% cross talk between neighboring cavities, (2) the optimum absorber impedances are 400 Ω/sq, but with a broad maximum from ~150 to ~700 Ω/sq, and (3) maximum absorption is achieved with absorber diameters ≥1.5λ. Good general agreement between the simulations and the experiments was found

Lack of interaction between ErbB2 and insulin receptor substrate signaling in breast cancer

Background: ErbB2 Receptor Tyrosine Kinase 2 (ErbB2, HER2/Neu) is amplified in breast cancer and associated with poor prognosis. Growing evidence suggests interplay between ErbB2 and insulin-like growth factor (IGF) signaling. For example, ErbB2 inhibitors can block IGF-induced signaling while, conversely, IGF1R inhibitors can inhibit ErbB2 action. ErbB receptors can bind and phosphorylate insulin receptor substrates (IRS) and this may be critical for ErbBmediated anti-estrogen resistance in breast cancer. Herein, we examined crosstalk between ErbB2 and IRSs using cancer cell lines and transgenic mouse models. Methods: MMTV-ErbB2 and MMTV-IRS2 transgenic mice were crossed to create hemizygous MMTV-ErbB2/MMTVIRS2 bigenic mice. Signaling crosstalk between ErbB2 and IRSs was examined in vitro by knockdown or overexpression followed by western blot analysis for downstream signaling intermediates and growth assays. Results: A cross between MMTV-ErbB2 and MMTV-IRS2 mice demonstrated no enhancement of ErbB2 mediated mammary tumorigenesis or metastasis by elevated IRS2. Substantiating this, overexpression or knockdown of IRS1 or IRS2 in MMTV-ErbB2 mammary cancer cell lines had little effect upon ErbB2 signaling. Similar results were obtained in human mammary epithelial cells (MCF10A) and breast cancer cell lines. Conclusion: Despite previous evidence suggesting that ErbB receptors can bind and activate IRSs, our findings indicate that ErbB2 does not cooperate with the IRS pathway in these models to promote mammary tumorigenesis