Abstract
To achieve the vacuum quality required for the operation of particle accelerators, the surface of the vacuum vessels must be clean from hydrocarbons. This is usually achieved by wet ...chemistry processes, e.g., degreasing chemical baths that, in case of radioactive vessels, must be disposed accordingly. An alternative way exploits the oxygen plasma produced by a downstream RF plasma source. This technique offers the possibility of operating in-situ, which is an advantageous option to avoid the handling of voluminous and/or fragile components and a more sustainable alternative to large volume disposable baths. In this work, we test a commercial plasma source in dedicated vacuum systems equipped with quartz crystal microbalances (QCMs). The evolution of the etching rates of amorphous carbon (a-C) thin films deposited on the QCMs to mimic contamination are studied as function of operating parameters. We present the results of the plasma cleaning process applied to the real case of a hydrocarbons-contaminated large vacuum vessel. The studies are complemented by transport simulations and surface contamination monitoring by X-ray photoelectron spectroscopy (XPS) analysis. The evaluation of the vessel cleanliness, which is performed via residual gas analysis (RGA) measurements, is based on CERN’s outgassing acceptance criteria and agrees with both simulations and XPS results.
We report on the design and characterization of an antiproton deceleration beamline, based on a pulsed drift tube, for the PUMA experiment at the Antimatter Factory at CERN. The design has been ...tailored to high-voltage (100 kV) and ultra-high vacuum (below \(10^{-10}\) mbar) conditions. A first operation achieved decelerating antiprotons from an initial energy of 100 keV down to (\(3898\pm 3\)) eV, marking the initial stage in trapping antiprotons for the PUMA experiment. Employing a high-voltage ramping scheme, the pressure remains below \(2\cdot 10^{-10}\) mbar upstream of the pulsed drift tube for 75% of the cycle time. The beamline reached a transmission of (\(55 \pm 3\))% for antiprotons decelerated to 4 keV. The beam is focused on a position sensitive detector to a spot with horizontal and vertical standard deviations of \({\sigma}_\mathrm{horiz}\) = (\(3.0 \pm 0.1\)) mm and \({\sigma}_\mathrm{vert}\) = (\(3.8 \pm 0.2\)) mm, respectively. This spot size is within the acceptance of the PUMA Penning trap.
Mice deficient in SOCS2 display an excessive growth phenotype characterized by a 30-50% increase in mature body size. Here we show that the SOCS2-/- phenotype is dependent upon the presence of ...endogenous growth hormone (GH) and that treatment with exogenous GH induced excessive growth in mice lacking both endogenous GH and SOCS2. This was reflected in terms of overall body weight, body and bone lengths, and the weight of internal organs and tissues. A heightened response to GH was also measured by examining GH-responsive genes expressed in the liver after exogenous GH administration. To further understand the link between SOCS2 and the GH-signaling cascade, we investigated the nature of these interactions using structure/function and biochemical interaction studies. Analysis of the 3 structural motifs of the SOCS2 molecule revealed that each plays a crucial role in SOCS2 function, with the conserved SOCS-box motif being essential for all inhibitory function. SOCS2 was found to bind 2 phosphorylated tyrosines on the GH receptor, and mutational analysis of these amino acids showed that both were essential for SOCS2 function. Together, the data provide clear evidence that SOCS2 is a negative regulator of GH signaling.
Suppressor of cytokine signaling (SOCS)-2 is a member of a family of intracellular proteins implicated in the negative regulation
of cytokine signaling. The generation of SOCS-2-deficient mice, which ...grow to one and a half times the size of their wild-type
littermates, suggests that SOCS-2 may attenuate growth hormone (GH) signaling. In vitro studies indicate that, while SOCS-2 can inhibit GH action at low concentrations, at higher concentrations it may potentiate
signaling. To determine whether a similar enhancement of signaling is observed in vivo or alternatively whether increased SOCS-2 levels repress growth in vivo , we generated and analyzed transgenic mice that overexpress SOCS-2 from a human ubiquitin C promoter. These mice are not
growth-deficient and are, in fact, significantly larger than wild-type mice. The overexpressed SOCS-2 was found to bind to
endogenous GH receptors in a number of mouse organs, while phosphopeptide binding studies with recombinant SOCS-2 defined
phosphorylated tyrosine 595 on the GH receptor as the site of interaction. Together, the data implicate SOCS-2 as having dual
effects on GH signaling in vivo .
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