Microtopographic drivers of vegetation patterning in blanket peatlands recovering from erosion

Blanket peatlands are globally rare, and many have been severely eroded. Natural recovery and revegetation (‘self-restoration’) of bare peat surfaces are often observed but are poorly understood, thus hampering the ability to reliably predict how these ecosystems may respond to climatic change. We hypothesised that morphometric/topographic-related microclimatic variables may be key controls on successional pathways and vegetation patterning in self-restoring blanket peatlands. We predicted the occurrence probability of four common peatland plant species (Calluna vulgaris, Eriophorum vaginatum, Eriophorum angustifolium, and Sphagnum spp.) using a digital surface model (DSM) generated from drone imagery at a pixel size of 20 cm, a suite of variables derived from the DSM, and an ensemble learning method (random forests). All four species models provided accurate fine-scale predictions of habitat suitability (accuracy > 90%, area under curve (AUC) > 0.9, recall and precision > 0.8). Mean elevation (within a 1 m radius) was often the most influential variable. Topographic position, wind exposure, and the heterogeneity or ruggedness of the surrounding surface were also important for all models, whilst light-related variables and a wetness index were important in the Sphagnum model. Our approach can be used to improve prediction of future responses and sensitivities of peatland recovery to climatic changes and as a tool to identify areas of blanket peatlands that may self-restore successfully without management intervention

Chasing a rarity: a retrospective single-center evaluation of prognostic factors in primary gliosarcoma

Background and purpose!#!Primary gliosarcoma (GS) is a rare variant of IDH-wildtype glioblastoma multiforme. We performed a single-center analysis to identify prognostic factors.!##!Patients and methods!#!We analyzed the records of 26 patients newly diagnosed with primary WHO grade IV GS. Factors of interest were clinical and treatment data, as well as molecular markers, time to recurrence, and time to death.!##!Results!#!Median follow-up was 9 months (range 5-21 months). Gross total resection did not lead to improved survival, most likely due to the relatively small sample size. Low symptom burden at the time of diagnosis was associated with longer PFS (P = 0.023) and OS (P = 0.018). Median OS in the entire cohort was 12 months. Neither MGMT promoter hypermethylation nor adjuvant temozolomide therapy influenced survival, consistent with some previous reports.!##!Conclusion!#!In this retrospective study, patients exhibiting low symptom burden at diagnosis showed improved survival. None of the other factors analyzed were associated with an altered outcome

Opposing Roles of Dendritic Cell Subsets in Experimental GN.

Dendritic cells (DCs) are thought to form a dendritic network across barrier surfaces and throughout organs, including the kidney, to perform an important sentinel function. However, previous studies of DC function used markers, such as CD11c or CX3CR1, that are not unique to DCs. Here, we evaluated the role of DCs in renal inflammation using a CD11c reporter mouse line and two mouse lines with DC-specific reporters

Monocyte-derived macrophages aggravate pulmonary vasculitis via cGAS/STING/IFN-mediated nucleic acid sensing

Autoimmune vasculitis is a group of life-threatening diseases, whose underlying pathogenic mechanisms are incompletely understood, hampering development of targeted therapies. Here, we demonstrate that patients suffering from anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) showed increased levels of cGAMP and enhanced IFN-I signature. To identify disease mechanisms and potential therapeutic targets, we developed a mouse model for pulmonary AAV that mimics severe disease in patients. Immunogenic DNA accumulated during disease onset, triggering cGAS/STING/IRF3-dependent IFN-I release that promoted endothelial damage, pulmonary hemorrhages, and lung dysfunction. Macrophage subsets played dichotomic roles in disease. While recruited monocyte-derived macrophages were major disease drivers by producing most IFN-β, resident alveolar macrophages contributed to tissue homeostasis by clearing red blood cells and limiting infiltration of IFN-β-producing macrophages. Moreover, pharmacological inhibition of STING, IFNAR-I, or its downstream JAK/STAT signaling reduced disease severity and accelerated recovery. Our study unveils the importance of STING/IFN-I axis in promoting pulmonary AAV progression and identifies cellular and molecular targets to ameliorate disease outcomes