Development and characterization of the readout system for POLARBEAR-2

POLARBEAR-2 is a next-generation receiver for precision measurements of the polarization of the cosmic microwave background (Cosmic Microwave Background (CMB)). Scheduled to deploy in early 2015, it will observe alongside the existing POLARBEAR-1 receiver, on a new telescope in the Simons Array on Cerro Toco in the Atacama desert of Chile. For increased sensitivity, it will feature a larger area focal plane, with a total of 7,588 polarization sensitive antenna-coupled Transition Edge Sensor (TES) bolometers, with a design sensitivity of 4.1 uKrt(s). The focal plane will be cooled to 250 milliKelvin, and the bolometers will be read-out with 40x frequency domain multiplexing, with 36 optical bolometers on a single SQUID amplifier, along with 2 dark bolometers and 2 calibration resistors. To increase the multiplexing factor from 8x for POLARBEAR-1 to 40x for POLARBEAR-2 requires additional bandwidth for SQUID readout and well-defined frequency channel spacing. Extending to these higher frequencies requires new components and design for the LC filters which define channel spacing. The LC filters are cold resonant circuits with an inductor and capacitor in series with each bolometer, and stray inductance in the wiring and equivalent series resistance from the capacitors can affect bolometer operation. We present results from characterizing these new readout components. Integration of the readout system is being done first on a small scale, to ensure that the readout system does not affect bolometer sensitivity or stability, and to validate the overall system before expansion into the full receiver. We present the status of readout integration, and the initial results and status of components for the full array.Comment: Presented at SPIE Astronomical Telescopes and Instrumentation 2014: Millimeter, Submillimeter, and Far-Infrared Detectors and Instrumentation for Astronomy VII. Published in Proceedings of SPIE Volume 915

Interrelation between rifting, faulting, sedimentation, and mantle serpentinization during continental margin formation-including examples from the Norwegian Sea

The conditions permitting mantle serpentinization during continental rifting are explored within 2-D thermotectonostratigraphic basin models, which track the rheological evolution of the continental crust, account for sediment blanketing effects, and allow for kinetically controlled mantle serpentinization processes. The basic idea is that the entire extending continental crust has to be brittle for crustal scale faulting and mantle serpentinization to occur. The isostatic and latent heat effects of the reaction are fully coupled to the structural and thermal solutions. A systematic parameter study shows that a critical stretching factor exists for which complete crustal embrittlement and serpentinization occurs. Increased sedimentation rates shift this critical stretching factor to higher values as sediment blanketing effects result in higher crustal temperatures. Sediment supply has therefore, through the temperature-dependence of the viscous flow laws, strong control on crustal strength and mantle serpentinization reactions are only likely when sedimentation rates are low and stretching factors high. In a case study for the Norwegian margin, we test whether the inner lower crustal bodies (LCB) imaged beneath the Møre and Vøring margin could be serpentinized mantle. Multiple 2-D transects have been reconstructed through the 3-D data set by Scheck-Wenderoth and Maystrenko (2011). We find that serpentinization reactions are possible and likely during the Jurassic rift phase. Predicted thicknesses and locations of partially serpentinized mantle rocks fit to information on LCBs from seismic and gravity data. We conclude that some of the inner LCBs beneath the Norwegian margin may be partially serpentinized mantle

High Natality Rates of Endangered Steller Sea Lions in Kenai Fjords, Alaska and Perceptions of Population Status in the Gulf of Alaska

Steller sea lions experienced a dramatic population collapse of more than 80% in the late 1970s through the 1990s across their western range in Alaska. One of several competing hypotheses about the cause holds that reduced female reproductive rates (natality) substantively contributed to the decline and continue to limit recovery in the Gulf of Alaska despite the fact that there have been very few attempts to directly measure natality in this species. We conducted a longitudinal study of natality among individual Steller sea lions (n = 151) at a rookery and nearby haulouts in Kenai Fjords, Gulf of Alaska during 2003–2009. Multi-state models were built and tested in Program MARK to estimate survival, resighting, and state transition probabilities dependent on whether or not a female gave birth in the previous year. The models that most closely fit the data suggested that females which gave birth had a higher probability of surviving and giving birth in the following year compared to females that did not give birth, indicating some females are more fit than others. Natality, estimated at 69%, was similar to natality for Steller sea lions in the Gulf of Alaska prior to their decline (67%) and much greater than the published estimate for the 2000s (43%) which was hypothesized from an inferential population dynamic model. Reasons for the disparity are discussed, and could be resolved by additional longitudinal estimates of natality at this and other rookeries over changing ocean climate regimes. Such estimates would provide an appropriate assessment of a key parameter of population dynamics in this endangered species which has heretofore been lacking. Without support for depressed natality as the explanation for a lack of recovery of Steller sea lions in the Gulf of Alaska, alternative hypotheses must be more seriously considered

Short-term salivary acetaldehyde increase due to direct exposure to alcoholic beverages as an additional cancer risk factor beyond ethanol metabolism

<p>Abstract</p> <p>Background</p> <p>An increasing body of evidence now implicates acetaldehyde as a major underlying factor for the carcinogenicity of alcoholic beverages and especially for oesophageal and oral cancer. Acetaldehyde associated with alcohol consumption is regarded as 'carcinogenic to humans' (IARC Group 1), with sufficient evidence available for the oesophagus, head and neck as sites of carcinogenicity. At present, research into the mechanistic aspects of acetaldehyde-related oral cancer has been focused on salivary acetaldehyde that is formed either from ethanol metabolism in the epithelia or from microbial oxidation of ethanol by the oral microflora. This study was conducted to evaluate the role of the acetaldehyde that is found as a component of alcoholic beverages as an additional factor in the aetiology of oral cancer.</p> <p>Methods</p> <p>Salivary acetaldehyde levels were determined in the context of sensory analysis of different alcoholic beverages (beer, cider, wine, sherry, vodka, calvados, grape marc spirit, tequila, cherry spirit), without swallowing, to exclude systemic ethanol metabolism.</p> <p>Results</p> <p>The rinsing of the mouth for 30 seconds with an alcoholic beverage is able to increase salivary acetaldehyde above levels previously judged to be carcinogenic in vitro, with levels up to 1000 μM in cases of beverages with extreme acetaldehyde content. In general, the highest salivary acetaldehyde concentration was found in all cases in the saliva 30 sec after using the beverages (average 353 μM). The average concentration then decreased at the 2-min (156 μM), 5-min (76 μM) and 10-min (40 μM) sampling points. The salivary acetaldehyde concentration depends primarily on the direct ingestion of acetaldehyde contained in the beverages at the 30-sec sampling, while the influence of the metabolic formation from ethanol becomes the major factor at the 2-min sampling point.</p> <p>Conclusions</p> <p>This study offers a plausible mechanism to explain the increased risk for oral cancer associated with high acetaldehyde concentrations in certain beverages.</p

Highly Efficient Elimination of Colorectal Tumor-Initiating Cells by an EpCAM/CD3-Bispecific Antibody Engaging Human T Cells

With their resistance to genotoxic and anti-proliferative drugs and potential to grow tumors and metastases from very few cells, cancer stem or tumor-initiating cells (TICs) are a severe limitation for the treatment of cancer by conventional therapies. Here, we explored whether human T cells that are redirected via an EpCAM/CD3-bispecific antibody called MT110 can lyse colorectal TICs and prevent tumor growth from TICs. MT110 recognizes EpCAM, a cell adhesion molecule expressed on TICs from diverse human carcinoma, which was recently shown to promote tumor growth through engagement of elements of the wnt pathway. MT110 was highly potent in mediating complete redirected lysis of KRAS-, PI3 kinase- and BRAF-mutated colorectal TICs, as demonstrated in a soft agar assay. In immunodeficient mice, MT110 prevented growth of tumors from a 5,000-fold excess of a minimally tumorigenic TIC dose. T cells engaged by MT110 may provide a potent therapeutic means to eradicate TICs and bulk tumor cells derived thereof

Cellular and complement-dependent cytotoxicity of Ep-CAM-specific monoclonal antibody MT201 against breast cancer cell lines

MT201 is a fully human monoclonal IgG1 antibody with moderate affinity for epithelial cell adhesion molecule (Ep-CAM) being clinically developed for the treatment of carcinomas. Like many other clinically validated IgG1 monoclonal antibodies, MT201 primarily acts by antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC). Here, we analysed ADCC and CDC induced by MT201 and, as reference, trastuzumab against a panel of nine human breast cancer cell lines expressing distinct surface levels of Ep-CAM and human epithelial growth factor receptor type 2 antigen. Maximal cell lysis by ADCC by MT201 and trastuzumab in the presence of peripheral mononuclear cells did not significantly differ when averaged over the nine cell lines, but showed marked differences with respect to individual cell lines. The extent of cell lysis at intermediate surface target density was highly variable, suggesting a dominant influence of other susceptibility factors. Only one breast cancer cell line was eliminated via CDC, but only by MT201. Resistance to CDC appeared to correlate with high expression levels of complement resistance factors. Our present data as well as recent data on the prevalence and prognostic relevance of Ep-CAM expression in metastatic breast cancer suggest that Ep-CAM-specific monoclonal IgG1 antibodies may have a significant therapeutic potential in the treatment of breast cancer