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Aberrant choroid plexus formation drives the development of treatment-related brain toxicity
No full textBrain tumors are commonly treated with radiotherapy, but the efficacy of the treatment is limited by its toxicity to the normal tissue including post-irradiation contrast enhanced lesions often linked to necrosis. The poorly understood mechanisms behind such brain lesions were studied using cerebral organoids. Here we show that irradiation of such organoids leads to dose-dependent growth retardation and formation of liquid-filled cavities but is not correlated with necrosis. Instead, the radiation-induced changes comprise of an enhancement of cortical hem markers, altered neuroepithelial stem cell differentiation, and an increase of ZO1+/AQP1+/CLDN3+-choroid plexus (CP)-like structures accompanied by an upregulation of IGF2 mRNA, known to be expressed in CP and cerebrospinal fluid. The altered differentiation is attributed to changes in the WNT/BMP signaling pathways. We conclude that aberrant CP formation can be involved in radiation-induced brain lesions providing additional strategies for possible countermeasures
Measurement of charge-changing cross section of neutron-rich nitrogen isotopes for determining their proton radii
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First Measurement of the Neutron-Emission Probability with a Surrogate Reaction in Inverse Kinematics at a Heavy-Ion Storage Ring
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Induction of Cytoplasmic dsDNA and cGAS-STING Immune Signaling After Exposure of Breast Cancer Cells to X-ray or High-Energetic Carbon Ions
No full textRadiation therapy can trigger activation of the cyclic GMP-AMP synthase (cGAS)- Stimulator of interferon genes (STING) axis via cytoplasmic dsDNA fragment induction. The activation of cGAS-STING initiates innate immune signaling mediated by interferon type I that can contribute to eradicate the malignancy. The effect was shown to depend on the fractionation scheme employed. We hypothesized that the innate immune response can also depend on radiation quality because densely ionizing radiation, such as carbon ions, have different effects on DNA lesion quality.We exposed an in vitro 4T1 breast cancer model to either photons or carbon ions and measured the clonogenic survival of cells with the colony-forming assay. The occurrence of cytosolic dsDNA fragments was assessed via immunofluorescence, whereas the expression and release of interferon-β by quantitative reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay. Bulk RNA sequencing was used to investigate global radiation-induced changes in gene expression.We show here that carbon ions induced a significantly higher yield of cytosolic dsDNA fragments per unit dose as compared to photons. The higher efficiency also translated in expression and release of interferon-β by the tumor cells. The rate of cytoplasmic dsDNA foci as well as interferon-β release increased with doses up to 20 Gy and no differences for a fractionation scheme (3 × 8 Gy) were found as compared to the single high doses (20 or 24 Gy) of photons.In conclusion, we found that the release of interferon-β after radiation increases with the radiation dose up to 20 Gy and that carbon ions have the potential to elicit a strong innate immune signaling
mCBM@SIS18 2021/22
No full textThis beam time application submitted in June 2020 is a continuation request by the CBM Collaboration, following the proposal on the CBM full-system test-setup at the SIS18 facility under the name mCBM@SIS18 (short “mCBM”), which was fully granted in September 2017. The primary aim of the mCBM setup is to commission and optimize the complex interplay of the different detector systems with the triggerless-streaming data acquisition and the fast online event reconstruction and selection. In particular, it allows testing of the detector and electronics components developed for the CBM experiment as well as the corresponding online/offline software packages under realistic experiment conditions up to the top CBM interaction rates of 10 MHz
