Time Resolution of a Few Nanoseconds in Silicon Strip Detectors Using the APV25 Chip

The APV25 front-end chip for the CMS Silicon Tracker has a peaking time of 50 ns, but confines the signal to a single clock period (=bunch crossing) with its internal “deconvolution” filter. This method requires a beam-synchronous clock and thus cannot be applied to a (quasi-) continuous beam. Nevertheless, using the multi-peak mode of the APV25, where 3 (or 6,9,12,...) consecutive shaper output samples are read out, the peak time can be reconstructed externally with high precision. Thus, offtime hits can be discarded which results in significant occupancy reduction. We will describe this method, results from beam tests and the intended implementation in an upgrade of the BELLE Silicon Vertex Detector

Readout and Data Processing Electronics for the Belle-II Silicon Vertex Detector

A prototype readout system has been developed for the future Belle-II Silicon Vertex Detector at the Super-KEK-B factory in Tsukuba, Japan. It will receive raw data from double-sided sensors with a total of approximately 240,000 strips read out by APV25 chips at a trigger rate of up to 30kHz and perform strip reordering, pedestal subtraction, a two-pass common mode correction and zero suppression in FPGA firmware. Moreover, the APV25 will be operated in multi-peak mode, where (typically) six samples along the shaped waveform are used for precise hit-time reconstruction which will also be implemented in FPGAs using look-up tables

Construction and Performance of a Double-Sided Silicon Detector Module Using the Origami Concept

The APV25 front-end chip with short shaping time will be used in the Belle II Silicon Vertex Detector (SVD) in order to achive low occupancy. Since fast amplifiers are more susceptible to noise caused by their capacitive input load, they have to be placed as close to the sensor as possible. On the other hand, material budget inside the active volume has to be kept low in order to constrain multiple scattering. We built a low mass sensor module with double-sided readout, where thinned APV25 chips are placed on a single flexible circuit glued onto one side of the sensor. The interconnection to the other side is done by Kapton fanouts, which are wrapped around the edge of the sensor, hence the name Origami. Since all front-end chips are aligned in a row on the top side of the module, cooling can be done by a single aluminum pipe. The performance of the Origami module was evaluated in a beam test at CERN in August 2009, of which first results are presented here

Interface to high-performance periodic coupled-cluster theory calculations with atom-centered, localized basis functions

Coupled cluster (CC) theory is often considered the gold standard of quantum-chemistry. For solids, however, the available software is scarce. We present CC-aims, which can interface ab initio codes with localized atomic orbitals and the CC for solids (CC4S) code by the group of A. Gr\"uneis. CC4S features a continuously growing selection of wave function-based methods including perturbation and CC theory. The CC-aims interface was developed for the FHI-aims code (https://fhi-aims.org) but is implemented such that other codes may use it as a starting point for corresponding interfaces. As CC4S offers treatment of both molecular and periodic systems, the CC-aims interface is a valuable tool, where DFT is either too inaccurate or too unreliable, in theoretical chemistry and materials science alike

Inhibition of death receptor signals by cellular FLIP.

The widely expressed protein Fas is a member of the tumour necrosis factor receptor family which can trigger apoptosis. However, Fas surface expression does not necessarily render cells susceptible to Fas ligand-induced death signals, indicating that inhibitors of the apoptosis-signalling pathway must exist. Here we report the characterization of an inhibitor of apoptosis, designated FLIP (for FLICE-inhibitory protein), which is predominantly expressed in muscle and lymphoid tissues. The short form, FLIPs, contains two death effector domains and is structurally related to the viral FLIP inhibitors of apoptosis, whereas the long form, FLIP(L), contains in addition a caspase-like domain in which the active-centre cysteine residue is substituted by a tyrosine residue. FLIPs and FLIP(L) interact with the adaptor protein FADD and the protease FLICE, and potently inhibit apoptosis induced by all known human death receptors. FLIP(L) is expressed during the early stage of T-cell activation, but disappears when T cells become susceptible to Fas ligand-mediated apoptosis. High levels of FLIP(L) protein are also detectable in melanoma cell lines and malignant melanoma tumours. Thus FLIP may be implicated in tissue homeostasis as an important regulator of apoptosis

Resolution Studies on Silicon Strip Sensors with fine Pitch

In June 2008 single-sided silicon strip sensors with 50 $\mu$m readout pitch were tested in a highly energetic pion beam at the SPS at CERN. The purpose of the test was to evaluate characteristic detector properties by varying the strip width and the number of intermediate strips. The experimental setup and first results for the spatial resolution are discussed.Comment: proceeding of the International Linear Collider Workshop 2008 (LCWS08); corrected typos, added reference for section

Characterization of the non-functional Fas ligand of gld mice

Mice homozygous for either the gld or lpr mutation develop autoimmune diseases and progressive lymphadenopathy. The lpr mutation is characterized by the absence of functional Fas, whereas gld mice exhibit an inactive FasL due to a point mutation proximal to the extracellular C-terminus. The structural repercussions of this amino acid substitution remain unknown. Here we report that FasL is expressed at similar levels on the surface of activated T lymphocytes from gld and wild-type mice. Using a polyclonal anti-FasL antibody, indistinguishable amounts of a 40 kDa protein are detected in both gld and wild-type splenocytes. The molecular model of FasL, based on the known structure of TNF-alpha, predicts that the Phe --> Leu gld mutation is located at the protomer interface which is close to the FasR interaction site. We conclude that the gld mutation allows normal FasL biosynthesis, surface expression and oligomerization, but induces structural alterations to the Fas binding region leading to the phenotypic changes observed

Maternal Pre-Pregnancy Obesity Is Associated with Altered Placental Transcriptome

Maternal obesity has a major impact on pregnancy outcomes. There is growing evidence that maternal obesity has a negative influence on placental development and function, thereby adversely influencing offspring programming and health outcomes. However, the molecular mechanisms underlying these processes are poorly understood. We analysed ten term placenta's whole transcriptomes in obese (n = 5) and normal weight women (n = 5), using the Affymetrix microarray platform. Analyses of expression data were carried out using non-parametric methods. Hierarchical clustering and principal component analysis showed a clear distinction in placental transcriptome between obese and normal weight women. We identified 72 differentially regulated genes, with most being down-regulated in obesity (n = 61). Functional analyses of the targets using DAVID and IPA confirm the dysregulation of previously identified processes and pathways in the placenta from obese women, including inflammation and immune responses, lipid metabolism, cancer pathways, and angiogenesis. In addition, we detected new molecular aspects of obesity-derived effects on the placenta, involving the glucocorticoid receptor signalling pathway and dysregulation of several genes including CCL2, FSTL3, IGFBP1, MMP12, PRG2, PRL, QSOX1, SERPINE2 and TAC3. Our global gene expression profiling approach demonstrates that maternal obesity creates a unique in utero environment that impairs the placental transcriptome