Electron (positron) beam polarization by Compton scattering on circularly polarized laser photons

In a number of papers an attractive method of laser polarization of electrons (positrons) at storage rings or linear colliders has been proposed. We show that these suggestions are incorrect and based on errors in simulation of multiple Compton scattering and in calculation of the Compton spin-flip cross sections. We argue that the equilibrium polarization in this method is zero.Comment: 11 pages, LaTeX, talk at 9-th Intern. Workshop on Linear Colliders (LC02), Feb. 4-8, 2002, SLAC, Stanford, US

Development of imaging bolometers for magnetic fusion reactors (invited)

Imaging bolometers utilize an infrared (IR) video camera to measure the change in temperature of a thin foil exposed to the plasma radiation, thereby avoiding the risks of conventional resistive bolometers related to electric cabling and vacuum feedthroughs in a reactor environment. A prototype of the IR imaging video bolometer (IRVB) has been installed and operated on the JT-60U tokamak demonstrating its applicability to a reactor environment and its ability to provide two-dimensional measurements of the radiation emissivity in a poloidal cross section. In this paper we review this development and present the first results of an upgraded version of this IRVB on JT-60U. This upgrade utilizes a state-of-the-art IR camera (FLIR/Indigo Phoenix-InSb) (3?5?μm, 256×360?pixels, 345 Hz, 11 mK) mounted in a neutron/gamma/magnetic shield behind a 3.6 m IR periscope consisting of CaF2 optics and an aluminum mirror. The IRVB foil is 7?cm×9?cm×5?μm tantalum. A noise equivalent power density of 300 ?μW/cm2 is achieved with 40×24 channels and a time response of 10 ms or 23?μW/cm2 for 16×12 channels and a time response of 33 ms, which is 30 times better than the previous version of the IRVB on JT-60U

Protease Allergens Induce the Expression of IL-25 via Erk and p38 MAPK Pathway

Allergic diseases, including asthma, are characterized by T helper type 2 (Th2) cell-mediated inflammations, coupled with tissue infiltration by eosinophils. In this study, we demonstrate that multiple protease allergens, including papain and DerP1, efficiently induce interleukin (IL)-25 and thymic stromal lymphopoietin (TSLP) gene expression, and this phenomenon is dependent on the protease activities of these allergens. The IL-25 cytokine level in bronchial alveolar lavage (BAL) was also profoundly and significantly increased after treatment with papain. Additionally, the levels of Th2 cytokines were significantly increased, as compared to those in the OVA-only treatment group. The various protease allergens triggered the expression of IL-25 and TSLP mRNA in mouse lung epithelial cells (MLE12) and primary mouse lung epithelial cells; these effects were inhibited by the deactivation of the protease activity of papain. The allergen papain activates the ErK and p38 MAP pathways; the inhibition of these pathways, but not the NFκB or PI-3 kinase pathways, impairs the induction of IL-25 and TSLP expression by proteases. In this study, we demonstrate that the protease allergens induce IL-25 and TSLP via the MAP kinase signal pathways, and their protease activities are essential to this pathway

The Prevalence of TNFα-Induced Necrosis over Apoptosis Is Determined by TAK1-RIP1 Interplay

Death receptor-induced programmed necrosis is regarded as a secondary death mechanism dominating only in cells that cannot properly induce caspase-dependent apoptosis. Here, we show that in cells lacking TGFβ-activated Kinase-1 (TAK1) expression, catalytically active Receptor Interacting Protein 1 (RIP1)-dependent programmed necrosis overrides apoptotic processes following Tumor Necrosis Factor-α (TNFα) stimulation and results in rapid cell death. Importantly, the activation of the caspase cascade and caspase-8-mediated RIP1 cleavage in TNFα-stimulated TAK1 deficient cells is not sufficient to prevent RIP1-dependent necrosome formation and subsequent programmed necrosis. Our results demonstrate that TAK1 acts independently of its kinase activity to prevent the premature dissociation of ubiquitinated-RIP1 from TNFα-stimulated TNF-receptor I and also to inhibit the formation of TNFα-induced necrosome complex consisting of RIP1, RIP3, FADD, caspase-8 and cFLIPL. The surprising prevalence of catalytically active RIP1-dependent programmed necrosis over apoptosis despite ongoing caspase activity implicates a complex regulatory mechanism governing the decision between both cell death pathways following death receptor stimulation

Isolated human islets require hyperoxia to maintain islet mass, metabolism, and function

Pancreatic islet transplantation has been recognized as an effective treatment for Type 1 diabetes; however, there is still plenty of room to improve transplantation efficiency. Because islets are metabolically active they require high oxygen to survive; thus hypoxia after transplant is one of the major causes of graft failure. Knowing the optimal oxygen tension for isolated islets would allow a transplant team to provide the best oxygen environment during pre- and post-transplant periods. To address this issue and begin to establish empirically determined guidelines for islet maintenance, we exposed in vitro cultured islets to different partial oxygen pressures (pO_2) and assessed changes in islet volume, viability, metabolism, and function. Human islets were cultured for 7 days in different pO_2 media corresponding to hypoxia (90 mmHg), normoxia (160 mmHg), and hyerpoxia (270 or 350 mmHg). Compared to normoxia and hypoxia, hyperoxia alleviated the loss of islet volume, maintaining higher islet viability and metabolism as measured by oxygen consumption and glucose-stimulated insulin secretion responses. We predict that maintaining pre- and post-transplanted islets in a hyperoxic environment will alleviate islet volume loss and maintain islet quality thereby improving transplant outcomes

Alloying and the micromechanics of Co-Al-W-X quaternary alloys

The lattice misfit and diffraction elastic constants in hot rolled polycrystalline Co-7Al-5W-2Ta and Co-6Al-6W-2Ti (at.%) are measured using neutron and synchrotron X-ray diffraction. The misfit in the two alloys was found to be +0.67 and +0.59%, using neutron diffraction at HRPD. The misfit was found to increase with temperature, as in Ni superalloys. This implies that the amount of coherency strengthening increases with temperature. The diffraction elastic constants measured show that the γ ' phase is less stiff than the γ matrix in all orientations, which means that load shedding will occur to the γ phase

MAPping out distribution routes for kinesin couriers

In the crowded environment of eukaryotic cells, diffusion is an inefficient distribution mechanism for cellular components. Long-distance active transport is required and is performed by molecular motors including kinesins. Furthermore, in highly polarized, compartmentalized and plastic cells such as neurons, regulatory mechanisms are required to ensure appropriate spatio-temporal delivery of neuronal components. The kinesin machinery has diversified into a large number of kinesin motor proteins as well as adaptor proteins that are associated with subsets of cargo. However, many mechanisms contribute to the correct delivery of these cargos to their target domains. One mechanism is through motor recognition of subdomain-specific microtubule (MT) tracks, sign-posted by different tubulin isoforms, tubulin post-translational modifications (PTMs), tubulin GTPase activity and MT associated proteins (MAPs). With neurons as a model system, a critical review of these regulatory mechanisms is presented here, with particular focus on the emerging contribution of compartmentalised MAPs. Overall, we conclude that – especially for axonal cargo – alterations to the MT track can influence transport, although in vivo, it is likely that multiple track-based effects act synergistically to ensure accurate cargo distribution

The effect of a clinical pharmacist discharge service on medication discrepancies in patients with heart failure

Objective: Heart failure patients are regularly admitted to hospital and frequently use multiple medication. Besides intentional changes in pharmacotherapy, unintentional changes may occur during hospitalisation. The aim of this study was to investigate the effect of a clinical pharmacist discharge service on medication discrepancies and prescription errors in patients with heart failure. Setting: A general teaching hospital in Tilburg, the Netherlands. Method: An open randomized intervention study was performed comparing an intervention group, with a control group receiving regular care by doctors and nurses. The clinical pharmacist discharge service consisted of review of discharge medication, communicating prescribing errors with the cardiologist, giving patients information, preparation of a written overview of the discharge medication and communication to both the community pharmacist and the general practitioner about this medication. Within 6 weeks after discharge all patients were routinely scheduled to visit the outpatient clinic and medication discrepancies were measured. Main outcome measure: The primary endpoint was the frequency of prescription errors in the discharge medication and medication discrepancies after discharge combined. Results: Forty-four patients were included in the control group and 41 in the intervention group. Sixty-eight percent of patients in the control group had at least one discrepancy or prescription error against 39% in the intervention group (RR 0.57 (95% CI 0.37-0.88)). The percentage of medications with a discrepancy or prescription error in the control group was 14.6% and in the intervention group it was 6.1% (RR 0.42 (95% CI 0.27-0.66)). Conclusion: This clinical pharmacist discharge service significantly reduces the risk of discrepancies and prescription errors in medication of patients with heart failure in the 1st month after discharge

Snail Destabilizes Cell Surface Crumbs3a

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/92424/1/tra1376.pd