Wafer-level packaged RF-MEMS switches fabricated in a CMOS fab

Reports on wafer-level packaged RF-MEMS switches fabricated in a commercial CMOS fab. Switch fabrication is based on a metal surface micromachining process. A novel wafer-level packaging scheme is developed, whereby the switches are housed in on-chip sealed cavities using benzocyclobutene (BCB) as the bonding and sealing material. Measurements show that the influence of the wafer-level package on the RF performance can be made very small.\ud \u

Low-loss singlemode PECVD silicon nitride photonic wire waveguides for 532-900 nm wavelength window fabricated within a CMOS pilot line

PECVD silicon nitride photonic wire waveguides have been fabricated in a CMOS pilot line. Both clad and unclad single mode wire waveguides were measured at lambda = 532, 780, and 900 nm, respectively. The dependence of loss on wire width, wavelength, and cladding is discussed in detail. Cladded multimode and singlemode waveguides show a loss well below 1 dB/cm in the 532-900 nm wavelength range. For singlemode unclad waveguides, losses < 1 dB/cm were achieved at lambda = 900 nm, whereas losses were measured in the range of 1-3 dB/cm for lambda = 780 and 532 nm, respectively

Characterization of PECVD Silicon Nitride Photonic Components at 532 and 900 nm Wavelength

Low temperature PECVD silicon nitride photonic waveguides have been fabricated by both electron beam lithography and 200 mm DUV lithography. Propagation losses and bend losses were both measured at 532 and 900 nm wavelength, revealing sub 1dB/cm propagation losses for cladded waveguides at both wavelengths for single mode operation. Without cladding, propagation losses were measured to be in the 1-3 dB range for 532 nm and remain below 1 dB/cm for 900 nm for single mode waveguides. Bend losses were measured for 532 nm and were well below 0.1 dB per 90 degree bend for radii larger than 10 mu m

Universal cloning of continuous quantum variables

The cloning of quantum variables with continuous spectra is analyzed. A universal - or Gaussian - quantum cloning machine is exhibited that copies equally well the states of two conjugate variables such as position and momentum. It also duplicates all coherent states with a fidelity of 2/3. More generally, the copies are shown to obey a no-cloning Heisenberg-like uncertainty relation.Comment: 4 pages, RevTex. Minor revisions, added explicit cloning transformation, added reference

It's all in the details: methods in breast development and cancer

The inaugural European Network for Breast Development and Cancer (ENBDC) meeting on 'Methods in Mammary Gland Development and Cancer' was held in Weggis, Switzerland last April. The goal was to discuss the details of techniques used to study mammary gland biology and tumourigenesis. Highlights of this meeting included the use of four-colour fluorescence for protein co-localisation in tissue microarrays, genome analysis at single cell resolution, technical issues in the isolation of normal and tumour stem cells, and the use of mouse models and mammary gland transplantations to elucidate gene function in mammary development and to study drug resistance in breast cancer

Preclinical mouse models for BRCA1-associated breast cancer

A substantial part of all hereditary breast cancer cases is caused by BRCA1 germline mutations. In this review, we will discuss the insights into BRCA1 functions that we obtained from mouse models with conventional and conditional mutations in Brca1. The most advanced models closely resemble human BRCA1-related breast cancer and may therefore be useful for addressing clinically relevant questions

IL-17A Synergizes with IFN-γ to Upregulate iNOS and NO Production and Inhibit Chlamydial Growth

IFN-γ-mediated inducible nitric oxide synthase (iNOS) expression is critical for controlling chlamydial infection through microbicidal nitric oxide (NO) production. Interleukin-17A (IL-17A), as a new proinflammatory cytokine, has been shown to play a protective role in host defense against Chlamydia muridarum (Cm) infection. To define the related mechanism, we investigated, in the present study, the effect of IL-17A on IFN-γ induced iNOS expression and NO production during Cm infection in vitro and in vivo. Our data showed that IL-17A significantly enhanced IFN-γ-induced iNOS expression and NO production and inhibited Cm growth in Cm-infected murine lung epithelial (TC-1) cells. The synergistic effect of IL-17A and IFN-γ on Chlamydia clearance from TC-1 cells correlated with iNOS induction. Since one of the main antimicrobial mechanisms of activated macrophages is the release of NO, we also examined the inhibitory effect of IL-17A and IFN-γ on Cm growth in peritoneal macrophages. IL-17A (10 ng/ml) synergizes with IFN-γ (200 U/ml) in macrophages to inhibit Cm growth. This effect was largely reversed by aminoguanidine (AG), an iNOS inhibitor. Finally, neutralization of IL-17A in Cm infected mice resulted in reduced iNOS expression in the lung and higher Cm growth. Taken together, the results indicate that IL-17A and IFN-γ play a synergistic role in inhibiting chlamydial lung infection, at least partially through enhancing iNOS expression and NO production in epithelial cells and macrophages

Interleukin-13 Promotes Susceptibility to Chlamydial Infection of the Respiratory and Genital Tracts

Chlamydiae are intracellular bacteria that commonly cause infections of the respiratory and genital tracts, which are major clinical problems. Infections are also linked to the aetiology of diseases such as asthma, emphysema and heart disease. The clinical management of infection is problematic and antibiotic resistance is emerging. Increased understanding of immune processes that are involved in both clearance and immunopathology of chlamydial infection is critical for the development of improved treatment strategies. Here, we show that IL-13 was produced in the lungs of mice rapidly after Chlamydia muridarum (Cmu) infection and promoted susceptibility to infection. Wild-type (WT) mice had increased disease severity, bacterial load and associated inflammation compared to IL-13 deficient (−/−) mice as early as 3 days post infection (p.i.). Intratracheal instillation of IL-13 enhanced bacterial load in IL-13−/− mice. There were no differences in early IFN-g and IL-10 expression between WT and IL-13−/− mice and depletion of CD4+ T cells did not affect infection in IL-13−/− mice. Collectively, these data demonstrate a lack of CD4+ T cell involvement and a novel role for IL-13 in innate responses to infection. We also showed that IL-13 deficiency increased macrophage uptake of Cmu in vitro and in vivo. Moreover, the depletion of IL-13 during infection of lung epithelial cells in vitro decreased the percentage of infected cells and reduced bacterial growth. Our results suggest that enhanced IL-13 responses in the airways, such as that found in asthmatics, may promote susceptibility to chlamydial lung infection. Importantly the role of IL-13 in regulating infection was not limited to the lung as we showed that IL-13 also promoted susceptibility to Cmu genital tract infection. Collectively our findings demonstrate that innate IL-13 release promotes infection that results in enhanced inflammation and have broad implications for the treatment of chlamydial infections and IL-13-associated diseases

BRCA1-deficient mammary tumor cells are dependent on EZH2 expression and sensitive to Polycomb Repressive Complex 2-inhibitor 3-deazaneplanocin A

10.1186/bcr2354Breast Cancer Research114R6