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UNLABELLED: On 15 January 2022, Hunga volcano erupted, creating an extensive and high-reaching umbrella cloud over the open ocean, hindering traditional isopach mapping and fallout volume estimation. In MODIS satellite imagery, ocean surface water was discolored around Hunga following the eruption, which we attribute to ash fallout from the umbrella cloud. By relating intensity of ocean discoloration to fall deposit thicknesses in the Kingdom of Tonga, we develop a methodology for estimating airfall volume over the open ocean. Ash thickness measurements from 41 locations are used to fit a linear relationship between ash thickness and ocean reflectance. This produces a minimum airfall volume estimate of 1.8-0.4+0.3 km3. The whole eruption produced > 6.3 km3 of uncompacted pyroclastic material on the seafloor and a caldera volume change of 6 km3 DRE. Our fall estimates are consistent with the interpretation that most of the seafloor deposits were emplaced by gravity currents rather than fall deposits. Our proposed method does not account for the largest grain sizes, so is thus a minimum estimate. However, this new ocean-discoloration method provides an airfall volume estimate consistent with other independent measures of the plume and is thus effective for rapidly estimating fallout volumes in future volcanic eruptions over oceans. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00445-024-01744-6.

Successful pregnancies rely on adaptations within the mother.sup.1, including marked changes within the immune system.sup.2. It has long been known that the thymus, the central lymphoid organ, changes markedly during pregnancy.sup.3. However, the molecular basis and importance of this process remain largely obscure. Here we show that the osteoclast differentiation receptor RANK.sup.4,5 couples female sex hormones to the rewiring of the thymus during pregnancy. Genetic deletion of Rank (also known as Tnfrsf11a) in thymic epithelial cells results in impaired thymic involution and blunted expansion of natural regulatory T (T.sub.reg) cells in pregnant female mice. Sex hormones, in particular progesterone, drive the development of thymic T.sub.reg cells through RANK in a manner that depends on AIRE.sup.+ medullary thymic epithelial cells. The depletion of Rank in the mouse thymic epithelium results in reduced accumulation of natural T.sub.reg cells in the placenta, and an increase in the number of miscarriages. Thymic deletion of Rank also results in impaired accumulation of T.sub.reg cells in visceral adipose tissue, and is associated with enlarged adipocyte size, tissue inflammation, enhanced maternal glucose intolerance, fetal macrosomia, and a long-lasting transgenerational alteration in glucose homeostasis, which are all key hallmarks of gestational diabetes. Transplantation of T.sub.reg cells rescued fetal loss, maternal glucose intolerance and fetal macrosomia. In human pregnancies, we found that gestational diabetes also correlates with a reduced number of T.sub.reg cells in the placenta. Our findings show that RANK promotes the hormone-mediated development of thymic T.sub.reg cells during pregnancy, and expand the functional role of maternal T.sub.reg cells to the development of gestational diabetes and the transgenerational metabolic rewiring of glucose homeostasis. RANK promotes the hormone-mediated development of thymic regulatory T cells during pregnancy; loss of RANK is associated with impaired maturation of maternal regulatory T cells, leading to fetal loss and the development of gestational diabetes., Author(s): Magdalena Paolino [sup.1] [sup.2] [sup.3] , Rubina Koglgruber [sup.1] , Shane J. F. Cronin [sup.1] , Iris Uribesalgo [sup.1] , Esther Rauscher [sup.1] , Jürgen Harreiter [sup.4] , Michael [...]

Hydrothermal eruptions are the most violent and hazardous phenomena within geothermal fields. The largest of these may produce kilometer-sized craters and breccia deposits that are tens of meters thick. The geological and hydrothermal priming that leads to these types of eruptions is poorly understood. To understand large hydrothermal eruptions, we investigated a series of prehistoric events at the Rotokawa geothermal field in New Zealand. By revising the stratigraphy and distribution of hydrothermal breccia deposits and correlating these with componentry, crater morphology, and subsurface geological structure, we estimated the frequency, priming processes, triggers, and dynamics of multiple eruptions. Seventeen large hydrothermal eruptions occurred centuries to millennia apart in the period from ca. 22 cal ka B.P. to ca. 3.4 cal ka B.P. Of six hydrothermal eruptions since ca. 7 ka, four produced oval-shaped craters up to 2 km in diameter, creating a broad, shallow depression within the geothermal field. The two youngest eruptions occurred northeast of earlier eruption centers and have narrower and elongated vents. We infer that in the central depression, newly formed craters rimmed by breccia deposits and high-relief country rock hosted temporary lakes tens of meters deep. Crater-lake breakout(s) and/or seismic events caused sudden pressure reduction above the hydrothermal aquifer, triggering hydrothermal eruptions. Northeast of the basin, hydrothermal alteration produced caprocks above intensively fractured areas. In this case, earthquakes are the most likely trigger for cap-rupture and eruption. All eruptions excavated shallow and large craters mostly within partially altered Oruanui Formation and pre-fragmented breccias. The size and localization of the eruptions was likely due to a combination of (1) availability of undisturbed porous ignimbrite hosting large thermal aquifers, (2) efficient crater excavation within or alongside pre-fragmented breccia, and (3) the location of fracture and fault zones that channeled deep fluid upflow, favoring priming processes. This study highlights how an interplay of tectonic, magmatic, and hydrologic processes is responsible for the timing, dynamics, and ultimate size of hydrothermal eruptions in geothermal fields. Some events may be very large and destructive depending on the right priming and geological conditions. [ABSTRACT FROM AUTHOR]

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive, malignant, and lethal cancers, displaying strong resistance to immunotherapy. In this issue of Cell Metabolism , a study by Liu et al. identifies tetrahydrobiopterin metabolic dysregulation as a key driver for the immunosuppressive PDAC environment in mouse and human. [ABSTRACT FROM AUTHOR]

Genetic regulators and environmental stimuli modulate T cell activation in autoimmunity and cancer. The enzyme co-factor tetrahydrobiopterin (BH4) is involved in the production of monoamine neurotransmitters, the generation of nitric oxide, and pain.sup.1,2. Here we uncover a link between these processes, identifying a fundamental role for BH4 in T cell biology. We find that genetic inactivation of GTP cyclohydrolase 1 (GCH1, the rate-limiting enzyme in the synthesis of BH4) and inhibition of sepiapterin reductase (the terminal enzyme in the synthetic pathway for BH4) severely impair the proliferation of mature mouse and human T cells. BH4 production in activated T cells is linked to alterations in iron metabolism and mitochondrial bioenergetics. In vivo blockade of BH4 synthesis abrogates T-cell-mediated autoimmunity and allergic inflammation, and enhancing BH4 levels through GCH1 overexpression augments responses by CD4- and CD8-expressing T cells, increasing their antitumour activity in vivo. Administration of BH4 to mice markedly reduces tumour growth and expands the population of intratumoral effector T cells. Kynurenine--a tryptophan metabolite that blocks antitumour immunity--inhibits T cell proliferation in a manner that can be rescued by BH4. Finally, we report the development of a potent SPR antagonist for possible clinical use. Our data uncover GCH1, SPR and their downstream metabolite BH4 as critical regulators of T cell biology that can be readily manipulated to either block autoimmunity or enhance anticancer immunity. Tetrahydrobiopterin (BH4) is an enzyme co-factor that is involved in the nervous system; it is shown here to also function in T cell activation and proliferation, with roles in autoimmunity, allergic inflammation and cancer., Author(s): Shane J. F. Cronin [sup.1] [sup.2] [sup.3] , Corey Seehus [sup.2] [sup.3] , Adelheid Weidinger [sup.4] , Sebastien Talbot [sup.2] [sup.3] [sup.5] , Sonja Reissig [sup.6] , Markus Seifert [...]