J-PLUS: The javalambre photometric local universe survey

ABSTRACT: TheJavalambrePhotometric Local UniverseSurvey (J-PLUS )isanongoing 12-band photometricopticalsurvey, observingthousands of squaredegrees of theNorthernHemispherefromthededicated JAST/T80 telescope at the Observatorio Astrofísico de Javalambre (OAJ). The T80Cam is a camera with a field of view of 2 deg2 mountedon a telescopewith a diameter of 83 cm, and isequippedwith a uniquesystem of filtersspanningtheentireopticalrange (3500–10 000 Å). Thisfiltersystemis a combination of broad-, medium-, and narrow-band filters, optimallydesigned to extracttherest-framespectralfeatures (the 3700–4000 Å Balmer break region, Hδ, Ca H+K, the G band, and the Mg b and Ca triplets) that are key to characterizingstellartypes and delivering a low-resolutionphotospectrumforeach pixel of theobservedsky. With a typicaldepth of AB ∼21.25 mag per band, thisfilter set thusallowsforanunbiased and accuratecharacterization of thestellarpopulation in our Galaxy, itprovidesanunprecedented 2D photospectralinformationforall resolved galaxies in the local Universe, as well as accuratephoto-z estimates (at the δ z/(1 + z)∼0.005–0.03 precisionlevel) formoderatelybright (up to r ∼ 20 mag) extragalacticsources. Whilesomenarrow-band filters are designedforthestudy of particular emissionfeatures ([O II]/λ3727, Hα/λ6563) up to z < 0.017, theyalsoprovidewell-definedwindowsfortheanalysis of otheremissionlines at higherredshifts. As a result, J-PLUS has thepotential to contribute to a widerange of fields in Astrophysics, both in thenearbyUniverse (MilkyWaystructure, globular clusters, 2D IFU-likestudies, stellarpopulations of nearby and moderate-redshiftgalaxies, clusters of galaxies) and at highredshifts (emission-line galaxies at z ≈ 0.77, 2.2, and 4.4, quasi-stellarobjects, etc.). Withthispaper, wereleasethefirst∼1000 deg2 of J-PLUS data, containingabout 4.3 millionstars and 3.0 milliongalaxies at r <  21mag. With a goal of 8500 deg2 forthe total J-PLUS footprint, thesenumbers are expected to rise to about 35 millionstars and 24 milliongalaxiesbytheend of thesurvey.Funding for the J-PLUS Project has been provided by the Governments of Spain and Aragón through the Fondo de Inversiones de Teruel, the Spanish Ministry of Economy and Competitiveness (MINECO; under grants AYA2017-86274-P, AYA2016-77846-P, AYA2016-77237-C3-1-P, AYA2015-66211-C2-1-P, AYA2015-66211-C2-2, AYA2012-30789, AGAUR grant SGR-661/2017, and ICTS-2009-14), and European FEDER funding (FCDD10-4E-867, FCDD13-4E-2685

Development and characterisation of a novel 3D in vitro model of obesity-associated breast cancer as a tool for drug testing

Obesity is associated with worse breast cancer outcomes and decreased therapeutic efficacy. However, the mechanisms driving obesity-associated therapy resistance remain unclear; in part due to a lack of suitable models that recapitulate the obese tumour microenvironment. To address this, we developed a 3D in vitro model of obesity-associated breast cancer, to investigate biological mechanisms and to use as a drug testing tool. A penta-culture system was developed by co-culturing adipocyte spheroids with breast tumour cells, myoepithelial cells, macrophages, and fibroblasts in a collagen matrix. Tumour cells and macrophages infiltrated adipocyte spheroids, replicating the inflamed-adipose border typical of obese patients. This model was then assessed as a drug testing platform. Obese cultures exhibited increased sensitivity to metformin and, conversely, resistance to paclitaxel, compared to non-obese cultures. This 3D organotypic model effectively recapitulates key features of the obese adipose tumour microenvironment, providing a useful tool to interrogate mechanisms underpinning obesity-related therapy resistance

Author correction: development and characterisation of a novel 3D in vitro model of obesity-associated breast cancer as a tool for drug testing

Correction to: npj Breast Cancerhttps://doi.org/10.1038/s41523-025-00766-3, published online 30 May 2025 In this article, an incorrect version of Figure 5 was inadvertently uploaded after acceptance. The original article has been corrected.</p

Immunotherapy targeting inhibitory Fc? receptor IIB (CD32b) in the mouse is limited by monoclonal antibody consumption and receptor internalization

Genetic deficiency of the inhibitory Fc receptor, Fc?RIIB (CD32b), has been shown to augment the activity of activatory Fc?R and promote mAb immunotherapy. To investigate whether mAbs capable of blocking Fc?RIIB have similar capacity, we recently generated a panel of specific anti-mouse Fc?RIIB mAbs that do not cross-react with other FcRs, allowing us to study the potential of Fc?RIIB as a therapeutic target. Previous work revealed a number of these mAbs capable of eliciting programmed cell death of targets, and in the present study we demonstrated their ability to promote target cell phagocytosis. However, in a variety of murine tumor models, anti-Fc?RIIB mAbs demonstrated limited therapeutic activity despite optimized treatment regimens. Unexpectedly, we observed that the anti-Fc?RIIB mAbs are rapidly and extensively consumed in vivo, both by the tumor and host cells, including B cells, leading to a precipitous loss from the circulation. Closer analysis revealed that the anti-Fc?RIIB mAbs become extensively internalized from the cell surface within 24 h in vivo, likely explaining their suboptimal efficacy. Subsequent studies revealed that anti-Fc?RIIB mAb immunotherapy was effective when used against Fc?RIIB+ tumors in Fc?RIIB?/? recipients, indicating that consumption of the mAb by nontumor cells is the primary limitation of these reagents. Importantly, similar rates of internalization were not seen on human target cells, at least in vitro. These studies further highlight the need to determine the propensity of mAb therapeutics to internalize target receptors and also identify potential key differences between human and mouse cells in this respect

The contribution of N-rich stars to the Galactic stellar halo using APOGEE red giants

The contribution of dissolved globular clusters (GCs) to the stellar content of the Galactic halo is a key constraint on models for GC formation and destruction, and the mass assembly history of the Milky Way. Earlier results from APOGEE pointed to a large contribution of destroyed GCs to the stellar content of the inner halo, by as much as 25 percent, which is an order of magnitude larger than previous estimates for more distant regions of the halo. We set out to measure the ratio between nitrogen-rich (N-rich) and normal halo field stars, as a function of distance, by performing density modelling of halo field populations in APOGEE DR16. Our results show that at 1.5 kpc from the Galactic Centre, N-rich stars contribute a much higher 16.8+10.0-7.0, percent fraction to the total stellar halo mass budget than the 2.7 +1.0-0.8percent ratio contributed at 10 kpc. Under the assumption that N-rich stars are former GC members that now reside in the stellar halo field, and assuming the ratio between first and second population GC stars being 1:2, we estimate a total contribution from disrupted GC stars of the order of 27.5+15.4-11.5 percent at r = 1.5 kpc and 4.2+1.5-1.3 percent at r = 10 kpc. Furthermore, since our methodology requires fitting a density model to the stellar halo, we integrate such density within a spherical shell from 1.5 to 15 kpc in radius, and find a total stellar mass arising from dissolved and/or evaporated GCs of MGC,total = 9.6+4.0-2.6 × 107 M·. © 2021 2020 The Author(s) Published by Oxford University Press on behalf of Royal Astronomical Society.Immediate accessThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Fc gamma receptor IIb on target B cells promotes rituximab internalization and reduces clinical efficacy

The anti-CD20 mAb rituximab is central to the treatment of B-cell malignancies, but resistance remains a significant problem. We recently reported that resistance could be explained, in part, by internalization of rituximab (type I anti-CD20) from the surface of certain B-cell malignancies, thus limiting engagement of natural effectors and increasing mAb consumption. Internalization of rituximab was most evident in chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL), but the extent of internalization was heterogeneous within each disease. Here, we show that the inhibitory Fc?RIIb on target B cells promotes this process and is largely responsible for the observed heterogeneity across a range of B-cell malignancies. Internalization correlated strongly with Fc?RIIb expression on normal and malignant B cells, and resulted in reduced macrophage phagocytosis of mAb-coated targets. Furthermore, transfection of Fc?RIIb into Fc?RIIb negative Ramos cells increased internalization of rituximab in a dose-dependent manner. Target-cell Fc?RIIb promoted rituximab internalization in a cis fashion and was independent of Fc?RIIb on neighboring cells. It became phosphorylated and internalized along with CD20:anti-CD20 complexes before lysosomal degradation. In MCL patients, high Fc?RIIb expression predicted less durable responses after rituximab-containing regimens. Therefore, target-cell Fc?RIIb provides a potential biomarker of response to type I anti-CD20 mA