The Gemini Multi-conjugate Adaptive Optics System -GeMS, a facility instrument mounted on the Gemini South telescope, delivers a uniform, near diffraction limited images at near infrared wavelengths (0.95 µm -2.5 µm) over a field of view of 120 . GeMS is the first sodium layer based multi laser guide star adaptive optics system used in astronomy. It uses five laser guide stars distributed on a 60 square constellation to measure for atmospheric distortions and two deformable mirrors to compensate for it. In this paper, the second devoted to describe the GeMS project, we present the commissioning, overall performance and operational scheme of GeMS. Performance of each sub-system is derived from the commissioning results. The typical image quality, expressed in full with half maximum, Strehl ratios and variations over the field delivered by the system are then described. A discussion of the main contributor to performance limitation is carried-out. Finally, overheads and future system upgrades are described.

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GeMS, the Gemini Laser Guide Star Multi-Conjugate Adaptive Optics facility system, has seen first light in December 2011, and has already produced images with H band Strehl ratio in excess of 35% over fields of view of 85x85 arcsec, fulfilling the MCAO promise. In this paper, we report on these early results, analyze trends in performance, and concentrate on key or novel aspects of the system, like centroid gain estimation, on-sky noncommon path aberration estimation. We also present the first astrometric analysis, showing very encouraging results.

With two to three deformable mirrors, three Natural Guide Stars (NGS) and five sodium Laser Guide Stars (LGS), the Gemini Multi-Conjugate Adaptive Optics System (Gemini MCAO a.k.a. GeMS) will be the first facility-class MCAO capability to be offered for regular science observations starting in 2013A. The engineering and science commissioning phase of the project was kicked off in January 2011 when the Gemini South Laser Guide Star Facility (GS LGSF) propagated its 50W laser above the summit of Cerro Pachón, Chile. GeMS commissioning has proceeded throughout 2011 and the first half of 2012 at a pace of one 6-to 10-night run per month with a 5-month pause during the 2011 Chilean winter. This paper focuses on the LGSF-side of the project and provides an overview of the LGSF system and subsystems, their top-level specifications, design, integration with the telescope, and performance throughout commissioning and beyond. Subsystems of the GS LGSF include: (i) a diode-pumped solid-state 1.06+1.32 micron sum-frequency laser capable of producing over 50W of output power at the sodium wavelength (589nm); (ii) Beam Transfer Optics (BTO) that transport the 50W beam up the telescope, split the beam five-ways and configure the five 10W beams for projection by the Laser Launch Telescope (LLT) located behind the Gemini South 8m telescope secondary mirror; and (iii) a variety of safety systems to ensure safe laser operations for observatory personnel and equipment, neighbor observatories, as well as passing aircrafts and satellites.

The cardiac L-type calcium channel is a multi-subunit complex that requires co-assembling of the pore-forming subunit CaV1.2 with auxiliary subunits CaVα2δ and CaVβ. Its traffic has been shown to be controlled by these subunits and by the activation of various G-protein coupled receptors (GPCR). Here, we explore the consequences of the prolonged activation of angiotensin receptor type 1 (AT1R) over CaV1.2 channel trafficking. Bioluminescence Resonance Energy Transfer (BRET) assay between β-arrestin and L-type channels in angiotensin II-stimulated cells was used to assess the functional consequence of AT1R activation, while immunofluorescence of adult rat cardiomyocytes revealed the effects of GPCR activation on CaV1.2 trafficking. Angiotensin II exposure results in β-arrestin1 recruitment to the channel complex and an apparent loss of CaV1.2 immunostaining at the T-tubules. Accordingly, angiotensin II stimulation causes a decrease in L-type current, Ca2+ transients and myocyte contractility, together with a faster repolarization phase of action potentials. Our results demonstrate that prolonged AT1R activation induces β-arrestin1 recruitment and the subsequent internalization of CaV1.2 channels with a half-dose of AngII on the order of 100 nM, suggesting that this effect depends on local renin-angiotensin system. This novel AT1R-dependent CaV1.2-trafficking modulation likely contributes to angiotensin II-mediated cardiac remodeling.