The performance of muon reconstruction, identification, and triggering in CMS has been studied using 40 pb −1 of data collected in pp collisions at √ s = 7 TeV at the LHC in 2010. A few benchmark sets of selection criteria covering a wide range of physics analysis needs have been examined. For all considered selections, the efficiency to reconstruct and identify a muon with a transverse momentum p T larger than a few GeV/c is above 95% over the whole region of pseudorapidity covered by the CMS muon system, |η| < 2.4, while the probability to misidentify a hadron as a muon is well below 1%. The efficiency to trigger on single muons with p T above a few GeV/c is higher than 90% over the full η range, and typically substantially better. The overall momentum scale is measured to a precision of 0.2% with muons from Z decays. The transverse momentum resolution varies from 1% to 6% depending on pseudorapidity for muons with p T below 100 GeV/c and, using cosmic rays, it is shown to be better than 10% in the central region up to p T = 1 TeV/c. Observed distributions of all quantities are well reproduced by the Monte Carlo simulation.

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These results suggest a possibility that metabolic changes of frontal-subcortical and parietal-cerebellar circuit changes may underlie cognitive improvements in patients with OCD.

Hypoxia-inducible factor-1a (HIF-1a) is destabilized via the ubiquitin-proteasome system. Thus HIF-1a expression is robustly upregulated by proteasome inhibition, but paradoxically its activity is reduced. In the present study, we investigated the mechanism underlying the paradoxical response of HIF-1a to proteasome inhibition. In both Hep3B and HEK293 cells, a proteasome inhibitor MG132 noticeably attenuated hypoxic induction of erythropoietin and VEGF mRNAs. MG132 inactivated HIF-1a C-terminal transactivation domain (CAD), independently of factor inhibiting HIF-1 (FIH) and inhibited p300 recruitment by HIF-1a. We next tested the possibility that CITED2 is involved in the HIF-1 inactivation. CITED2 was found to be degraded via the ubiquitin-proteasome system and thus was stabilized by proteasome inhibition. Both the activity and the p300 binding of HIF-1a were inhibited by CITED2 expression and recovered by CITED2 siRNA in the presence of MG132. These results suggest that CITED2 is stabilized by proteasome inhibition and inactivates HIF-1 by interfering with the HIF-1a-p300 interaction. This may be an important mode-of-action for proteasome inhibition-based cancer therapy.

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