Beam tuning and stabilization using beam phase measurement at GANIL

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A first analysis of the mean motion of CHAMP

The present study consists in studying the mean orbital motion of the CHAMP satellite, through a single long arc on a period of time of 200 days in 2001. We actually investigate the sensibility of its mean motion to its accelerometric data, as measures of the surface forces, over that period. In order to accurately determine the mean motion of CHAMP, we use “observed&quot; mean orbital elements computed, by filtering, from 1-day GPS orbits. On the other hand, we use a semi-analytical model to compute the arc. It consists in numerically integrating the effects of the mean potentials (due to the Earth and the Moon and Sun), and the effects of mean surfaces forces acting on the satellite. These later are, in case of CHAMP, provided by an averaging of the Gauss system of equations. Results of the fit of the long arc give a relative sensibility of about 10^-3, although our gravitational mean model is not well suited to describe very low altitude orbits. This technique, which is purely dynamical, enables us to control the decreasing of the trajectory altitude, as a possibility to validate accelerometric data on a long term basis.<br><br><b>Key words.</b> Mean orbital motion, accelerometric dat

The operation of the GANIL control system

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aPKC regulates apical constriction to prevent tissue rupture in the Drosophila follicular epithelium

Funding: We thank Daniel St Johnston, Juergen Knoblich, Patrick Laprise, Stefano de Renzis, Xiaobo Wang, Yohanns Bellaiche, and the Bloomington and Kyoto Drosophila Stock Centers for reagents. We also thank Yohanns Bellaiche, Ivo Telley, and Romain Levayer for insightful comments on the manuscript. This work is funded by National Funds through FCT—Fundação para a Ciência e a Tecnologia, I.P., under the project PTDC/BIA-CEL/ 1511/2021. E.M.-d.-S.’s salary is funded by the ‘‘FCT Scientific Employment Stimulus’’ program. M.O.,A.B.-C., and A.M.C. were supported by PhD fellowships from FCT. M.O.’s salary was also supported by the Maria de Sousa Award Research in the J.J. lab was supported by Wellcome Trust, the Royal Society, and BBSRC (BB/V001353/1). The authors acknowledge the i3S Scientific Platform ALM, member of the national infrastructure Portuguese Platform of Bioimaging, and the Dundee Imaging Facility for excellent support.Apical-basal polarity is an essential epithelial trait controlled by the evolutionarily conserved PAR-aPKC polarity network. Dysregulation of polarity proteins disrupts tissue organization during development and in disease, but the underlying mechanisms are unclear due to the broad implications of polarity loss. Here, we uncover how Drosophila aPKC maintains epithelial architecture by directly observing tissue disorganization after fast optogenetic inactivation in living adult flies and ovaries cultured ex vivo. We show that fast aPKC perturbation in the proliferative follicular epithelium produces large epithelial gaps that result from increased apical constriction, rather than loss of apical-basal polarity. Accordingly, we can modulate the incidence of epithelial gaps by increasing and decreasing actomyosin-driven contractility. We traced the origin of these large epithelial gaps to tissue rupture next to dividing cells. Live imaging shows that aPKC perturbation induces apical constriction in non-mitotic cells within minutes, producing pulling forces that ultimately detach dividing and neighboring cells. We further demonstrate that epithelial rupture requires a global increase of apical constriction, as it is prevented by the presence of non-constricting cells. Conversely, a global induction of apical tension through light-induced recruitment of RhoGEF2 to the apical side is sufficient to produce tissue rupture. Hence, our work reveals that the roles of aPKC in polarity and actomyosin regulation are separable and provides the first in vivo evidence that excessive tissue stress can break the epithelial barrier during proliferation.proofepub_ahead_of_prin

Transcriptomics-driven lipidomics (TDL) identifies the microbiome-regulated targets of ileal lipid metabolism.

The gut microbiome and lipid metabolism are both recognized as essential components in the maintenance of metabolic health. The mechanisms involved are multifactorial and (especially for microbiome) poorly defined. A strategic approach to investigate the complexity of the microbial influence on lipid metabolism would facilitate determination of relevant molecular mechanisms for microbiome-targeted therapeutics. E. coli is associated with obesity and metabolic syndrome and we used this association in conjunction with gnotobiotic models to investigate the impact of E. coli on lipid metabolism. To address the complexities of the integration of the microbiome and lipid metabolism, we developed transcriptomics-driven lipidomics (TDL) to predict the impact of E. coli colonization on lipid metabolism and established mediators of inflammation and insulin resistance including arachidonic acid metabolism, alterations in bile acids and dietary lipid absorption. A microbiome-related therapeutic approach targeting these mechanisms may therefore provide a therapeutic avenue supporting maintenance of metabolic health

Angiotensin II synergizes with BAFF to promote atheroprotective regulatory B cells.

Angiotensin II (AngII) promotes hypertension, atherogenesis, vascular aneurysm and impairs post-ischemic cardiac remodeling through concerted roles on vascular cells, monocytes and T lymphocytes. However, the role of AngII in B lymphocyte responses is largely unexplored. Here, we show that chronic B cell depletion (Baffr deficiency) significantly reduces atherosclerosis in Apoe -/- mice infused with AngII. While adoptive transfer of B cells in Apoe -/- /Baffr -/- mice reversed atheroprotection in the absence of AngII, infusion of AngII in B cell replenished Apoe -/- /Baffr -/- mice unexpectedly prevented the progression of atherosclerosis. Atheroprotection observed in these mice was associated with a significant increase in regulatory CD1dhiCD5+ B cells, which produced high levels of interleukin (IL)-10 (B10 cells). Replenishment of Apoe -/- /Baffr -/- mice with Il10 -/- B cells reversed AngII-induced B cell-dependent atheroprotection, thus highlighting a protective role of IL-10+ regulatory B cells in this setting. Transfer of AngII type 1A receptor deficient (Agtr1a -/-) B cells into Apoe -/- /Baffr -/- mice substantially reduced the production of IL-10 by B cells and prevented the AngII-dependent atheroprotective B cell phenotype. Consistent with the in vivo data, AngII synergized with BAFF to induce IL-10 production by B cells in vitro via AngII type 1A receptor. Our data demonstrate a previously unknown synergy between AngII and BAFF in inducing IL-10 production by B cells, resulting in atheroprotection