Constraints on the structure and seasonal variations of Triton's atmosphere from the 5 October 2017 stellar occultation and previous observations

Context. A stellar occultation by Neptune's main satellite, Triton, was observed on 5 October 2017 from Europe, North Africa, and the USA. We derived 90 light curves from this event, 42 of which yielded a central flash detection. Aims. We aimed at constraining Triton's atmospheric structure and the seasonal variations of its atmospheric pressure since the Voyager 2 epoch (1989). We also derived the shape of the lower atmosphere from central flash analysis. Methods. We used Abel inversions and direct ray-tracing code to provide the density, pressure, and temperature profiles in the altitude range similar to 8 km to similar to 190 km, corresponding to pressure levels from 9 mu bar down to a few nanobars. Results. (i) A pressure of 1.18 +/- 0.03 mu bar is found at a reference radius of 1400 km (47 km altitude). (ii) A new analysis of the Voyager 2 radio science occultation shows that this is consistent with an extrapolation of pressure down to the surface pressure obtained in 1989. (iii) A survey of occultations obtained between 1989 and 2017 suggests that an enhancement in surface pressure as reported during the 1990s might be real, but debatable, due to very few high S/N light curves and data accessible for reanalysis. The volatile transport model analysed supports a moderate increase in surface pressure, with a maximum value around 2005-2015 no higher than 23 mu bar. The pressures observed in 1995-1997 and 2017 appear mutually inconsistent with the volatile transport model presented here. (iv) The central flash structure does not show evidence of an atmospheric distortion. We find an upper limit of 0.0011 for the apparent oblateness of the atmosphere near the 8 km altitude.J.M.O. acknowledges financial support from the Portuguese Foundation for Science and Technology (FCT) and the European Social Fund (ESF) through the PhD grant SFRH/BD/131700/2017. The work leading to these results has received funding from the European Research Council under the European Community's H2020 2014-2021 ERC grant Agreement nffi 669416 "Lucky Star". We thank S. Para who supported some travels to observe the 5 October 2017 occultation. T.B. was supported for this research by an appointment to the National Aeronautics and Space Administration (NASA) Post-Doctoral Program at the Ames Research Center administered by Universities Space Research Association (USRA) through a contract with NASA. We acknowledge useful exchanges with Mark Gurwell on the ALMA CO observations. This work has made use of data from the European Space Agency (ESA) mission Gaia (https://www.cosmos.esa.int/gaia), processed by the Gaia Data Processing and Analysis Consortium (DPAC, https://www.cosmos.esa.int/web/gaia/dpac/consortium).Funding for the DPAC has been provided by national institutions, in particular the institutions participating in the Gaia Multilateral Agreement. J.L.O., P.S.-S., N.M. and R.D. acknowledge financial support from the State Agency for Research of the Spanish MCIU through the "Center of Excellence Severo Ochoa" award to the Instituto de Astrofisica de Andalucia (SEV-2017-0709), they also acknowledge the financial support by the Spanish grant AYA-2017-84637-R and the Proyecto de Excelencia de la Junta de Andalucia J.A. 2012-FQM1776. The research leading to these results has received funding from the European Union's Horizon 2020 Research and Innovation Programme, under Grant Agreement no. 687378, as part of the project "Small Bodies Near and Far" (SBNAF). P.S.-S. acknowledges financial support by the Spanish grant AYA-RTI2018-098657-J-I00 "LEO-SBNAF". The work was partially based on observations made at the Laboratorio Nacional de Astrofisica (LNA), Itajuba-MG, Brazil. The following authors acknowledge the respective CNPq grants: F.B.-R. 309578/2017-5; R.V.-M. 304544/2017-5, 401903/2016-8; J.I.B.C. 308150/2016-3 and 305917/2019-6; M.A. 427700/20183, 310683/2017-3, 473002/2013-2. This study was financed in part by the Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior -Brasil (CAPES) -Finance Code 001 and the National Institute of Science and Technology of the e-Universe project (INCT do e-Universo, CNPq grant 465376/2014-2). G.B.R. acknowledges CAPES-FAPERJ/PAPDRJ grant E26/203.173/2016 and CAPES-PRINT/UNESP grant 88887.571156/2020-00, M.A. FAPERJ grant E26/111.488/2013 and A.R.G.Jr. FAPESP grant 2018/11239-8. B.E.M. thanks CNPq 150612/2020-6 and CAPES/Cofecub-394/2016-05 grants. Part of the photometric data used in this study were collected in the frame of the photometric observations with the robotic and remotely controlled telescope at the University of Athens Observatory (UOAO; Gazeas 2016). The 2.3 m Aristarchos telescope is operated on Helmos Observatory by the Institute for Astronomy, Astrophysics, Space Applications and Remote Sensing of the National Observatory of Athens. Observations with the 2.3 m Aristarchos telescope were carried out under OPTICON programme. This project has received funding from the European Union's Horizon 2020 research and innovation programme under grant agreement No 730890. This material reflects only the authors views and the Commission is not liable for any use that may be made of the information contained therein. The 1. 2m Kryoneri telescope is operated by the Institute for Astronomy, Astrophysics, Space Applications and Remote Sensing of the National Observatory of Athens. The Astronomical Observatory of the Autonomous Region of the Aosta Valley (OAVdA) is managed by the Fondazione Clement Fillietroz-ONLUS, which is supported by the Regional Government of the Aosta Valley, the Town Municipality of Nus and the "Unite des Communes valdotaines Mont-Emilius". The 0.81 m Main Telescope at the OAVdA was upgraded thanks to a Shoemaker NEO Grant 2013 from The Planetary Society. D.C. and J.M.C. acknowledge funds from a 2017 'Research and Education' grant from Fondazione CRT-Cassa di Risparmio di Torino. P.M. acknowledges support from the Portuguese Fundacao para a Ciencia e a Tecnologia ref. PTDC/FISAST/29942/2017 through national funds and by FEDER through COMPETE 2020 (ref. POCI010145 FEDER007672). F.J. acknowledges Jean Luc Plouvier for his help. S.J.F. and C.A. would like to thank the UCL student support observers: Helen Dai, Elise Darragh-Ford, Ross Dobson, Max Hipperson, Edward Kerr-Dineen, Isaac Langley, Emese Meder, Roman Gerasimov, Javier Sanjuan, and Manasvee Saraf. We are grateful to the CAHA, OSN and La Hita Observatory staffs. This research is partially based on observations collected at Centro Astronomico HispanoAleman (CAHA) at Calar Alto, operated jointly by Junta de Andalucia and Consejo Superior de Investigaciones Cientificas (IAA-CSIC). This research was also partially based on observation carried out at the Observatorio de Sierra Nevada (OSN) operated by Instituto de Astrofisica de Andalucia (CSIC). This article is also based on observations made with the Liverpool Telescope operated on the island of La Palma by Liverpool John Moores University in the Spanish Observatorio del Roque de los Muchachos of the Instituto de Astrofisica de Canarias with financial support from the UK Science and Technology Facilities Council. Partially based on observations made with the Tx40 and Excalibur telescopes at the Observatorio Astrofisico de Javalambre in Teruel, a Spanish Infraestructura Cientifico-Tecnica Singular (ICTS) owned, managed and operated by the Centro de Estudios de Fisica del Cosmos de Aragon (CEFCA). Tx40 and Excalibur are funded with the Fondos de Inversiones de Teruel (FITE). A.R.R. would like to thank Gustavo Roman for the mechanical adaptation of the camera to the telescope to allow for the observation to be recorded. R.H., J.F.R., S.P.H. and A.S.L. have been supported by the Spanish projects AYA2015-65041P and PID2019-109467GB-100 (MINECO/FEDER, UE) and Grupos Gobierno Vasco IT1366-19. Our great thanks to Omar Hila and their collaborators in Atlas Golf Marrakech Observatory for providing access to the T60cm telescope. TRAPPIST is a project funded by the Belgian Fonds (National) de la Recherche Scientifique (F.R.S.-FNRS) under grant PDR T.0120.21. TRAPPIST-North is a project funded by the University of Liege, and performed in collaboration with Cadi Ayyad University of Marrakesh. E.J. is a FNRS Senior Research Associate

10Kin1day: A Bottom-Up Neuroimaging Initiative.

We organized 10Kin1day, a pop-up scientific event with the goal to bring together neuroimaging groups from around the world to jointly analyze 10,000+ existing MRI connectivity datasets during a 3-day workshop. In this report, we describe the motivation and principles of 10Kin1day, together with a public release of 8,000+ MRI connectome maps of the human brain

LPA Induces Colon Cancer Cell Proliferation through a Cooperation between the ROCK and STAT-3 Pathways

<div><p>Lysophosphatidic acid (LPA) plays a critical role in the proliferation and migration of colon cancer cells; however, the downstream signaling events underlying these processes remain poorly characterized. The aim of this study was to investigate the signaling pathways triggered by LPA to regulate the mechanisms involved in the progression of colorectal cancer (CRC). We have used three cell line models of CRC, and initially analyzed the expression profile of LPA receptors (LPAR). Then, we treated the cells with LPA and events related to their tumorigenic potential, such as migration, invasion, anchorage-independent growth, proliferation as well as apoptosis and cell cycle were evaluated. We used the Chip array technique to analyze the global gene expression profiling that occurs after LPA treatment, and we identified cell signaling pathways related to the cell cycle. The inhibition of these pathways verified the conclusions of the transcriptomic analysis. We found that the cell lines expressed LPAR1, -2 and -3 in a differential manner and that 10 μM LPA did not affect cell migration, invasion and anchorage-independent growth, but it did induce proliferation and cell cycle progression in HCT-116 cells. Although LPA in this concentration did not induce transcriptional activity of β-catenin, it promoted the activation of Rho and STAT-3. Moreover, ROCK and STAT-3 inhibitors prevented LPA-induced proliferation, but ROCK inhibition did not prevent STAT-3 activation. Finally, we observed that LPA regulates the expression of genes related to the cell cycle and that the combined inhibition of ROCK and STAT-3 prevented cell cycle progression and increased the LPA-induced expression of cyclins E1, A2 and B1 to a greater degree than either inhibitor alone. Overall, these results demonstrate that LPA increases the proliferative potential of colon adenocarcinoma HCT-116 cells through a mechanism involving cooperation between the Rho-ROCK and STAT3 pathways involved in cell cycle control.</p></div

Upregulated genes related to cell cycle of LPA-treated cells.

<p>* Fold changes of LPA-treated cells vs. control groups.</p><p>** Genes validated by Western blotting.</p><p>Upregulated genes related to cell cycle of LPA-treated cells.</p

LPA regulates cyclin E1, A2 and B1 expression through Rho-ROCK and STAT-3 signaling.

<p>a) HCT-116 cells were treated with LPA at the indicated times, and the total lysates were obtained and prepared for western blotting. LPA increased cyclin E1, A2 and B1 expression. The numbers represent the ratio of the optical density of LPA-treated to untreated cells normalized by GAPDH. b) HCT-116 cells were pre-treated for 1 h with the respective chemical inhibitors prior to LPA treatment at the indicated times. The immunoblotting analysis indicated that either ROCK or STAT-3 inhibition significantly decreased cyclin A2 LPA-mediated expression; however, the concomitant inhibition of these proteins reduced LPA-induced cyclin E1, A2 and B1 expression. The bar graphs are normalized as the percentage of protein expression in which the control group is 1, and the GAPDH protein was used as a loading control. Statistical analyses were performed using <i>one-way</i> ANOVA (*** p<0.001, ** p<0.01, * p<0.05, vs. control; ### p<0.001, ## p<0.01, # p<0.05, vs. LPA; ♦♦ p<0.01 vs. LPA+Y-27632; ★ p<0.05 vs.LPA+STA21). O.D., optical density. Average scores± SEM for three independent experiments are shown.</p

LPA mediates cell proliferation through RhoA-ROCK activation.

<p>Subconfluent cell monolayers were FBS depleted for 24 h and treated with LPA at the indicated times. a) Crystal violet staining of HCT-116 showed that the ROCK inhibitor Y-27632 (10 μM) prevented an LPA-mediated increase in the relative cell number after 48 h of treatment. Statistical analyses were performed using <i>two-way</i> ANOVA with <i>post-hoc</i> Bonferroni test. *** p<0.001, vs control; ### p<0.001, vs LPA. Average scores± SEM. for three independent experiments are shown. b) The FACS analysis via PI staining showed that ROCK inhibition with Y-27632 prevented the LPA-induced increase in the proportion of cells in the S-G2/M phase. The statistical analyses were performed using <i>one-way</i> ANOVA with <i>post-hoc</i> Bonferroni test. Data are presented as mean ± SEM. (*** p<0.001, vs control; ## p<0.01, vs LPA).</p

RhoA-ROCK and STAT-3 signaling pathways cooperate to control LPA-mediated cell proliferation.

<p>HCT-116 cells were pre-treated with the ROCK inhibitor Y-27632 for 1 h and then treated with LPA as indicated. a) Western blotting against the phosphorylated form of STAT-3 at tyrosine 705 showed that ROCK inhibition did not prevent STAT-3 phosphorylation mediated by LPA. O.D., optical density. Data are presented as mean ± SEM. b) Confocal images indicating that ROCK inhibition did not prevent the LPA induction of pSTAT3 (green) translocation to the nucleus (blue). The STAT-3 inhibitor, STA 21, was used as a positive control. Cont: control. Scale bar, 20 μm. c) Cell cycle analyses through PI staining indicated that the dual inhibition of STAT-3 and ROCK using both STA 21 and Y-27632 significantly reduced the number of cells in the S-G2/M phase after LPA treatment. Statistical analyses were performed using <i>one-way</i> ANOVA. Average scores ± SEM. for three independent experiments are shown (*** p<0.001, vs. control; ### p<0.001; ## p<0.01, vs. LPA; * p<0.05, LPA+Y-27632+STA21 vs. LPA + Y-27632).</p

LPA increased proliferation in HCT-116 cells but did not induce cell death.

<p>Colon cancer cells were FBS starved for 24 h and then treated with LPA (10 μM) for 24, 48 or 72 h. The relative cell number was evaluated through crystal violet staining (a), and apoptosis was followed by the Annexin-V/PI double staining method (b). a) LPA increased the relative number of HCT-116 cells, but not Caco-2 or HT-29 cells. Statistical analyses were performed using <i>two-way</i> ANOVA with <i>post-hoc</i> Bonferroni test. ** p< 0.01; *** p<0.001. Average scores± SEM. for three independent experiments are shown. b) FACs analysis via Annexin V-FITC/PI staining showed that LPA did not reduce cell death in HCT-116 cells. Four different cell populations were detected after the Annexin V/PI staining of HCT-116 cells. Alive cells are grouped in the lower left part of the panel, early apoptotic cells are grouped in the lower right part of the panel, late apoptotic cells are grouped in the higher right part of the panel and necrotic cells are grouped in the higher left part of the panel. FL1-H, Annexin V; FL2-H, PI. c) Data obtained from the flow cytometric analyses are plotted in a graph. There was no increased percentage of LPA-mediated apoptosis.</p

A model for the regulation of the LPA-induced cell cycle.

<p>LPA, through its G protein-coupled receptors, induces both Rho-ROCK and STAT-3 signaling pathways to mediate cyclin E1, A2 and B1 expression and to regulate the HCT-116 cell cycle.</p

LPA mediates cell proliferation through STAT-3 activation.

<p>Subconfluent monolayers of HCT-116 cells were FBS depleted overnight and treated with LPA at the indicated times. a) Total lysates were obtained and prepared for western blotting using a specific antibody against the phosphorylated form of STAT-3 at tyrosine 705 (p-STAT3). The band images were quantified by optical density, and the score was calculated using the ratio between p-STAT3, STAT3 and α-tubulin. LPA increased STAT-3 phosphorylation after 5–15 min of treatment. b) Immunofluorescence of HCT-116 cells corroborated the increase in pSTAT-3 after LPA treatment (green, arrows) and displayed its nuclear location (nucleus, blue). Scale bar, 20 μm. c) The relative cell number of LPA-treated HCT-116 cells was evaluated using crystal violet staining. STAT-3 inhibition using STA 21 prevented the increase in cell numbers after 48 h of LPA treatment. Statistical analyses were performed using <i>two-way</i> ANOVA with <i>post-hoc</i> Bonferroni test (*** p<0.001, vs control; ### p<0.001, vs. LPA). d) Cell cycle analyses through PI staining indicated that STAT-3 inhibition reduced the number of cells at the S-G2/M phase after LPA treatment. Statistical analyses were performed using <i>one-way</i> ANOVA (*** p<0.001, vs. control; ### p<0.001, vs. LPA). Data are presented as mean ± SEM.</p