Radiation enhancement and "temperature" in the collapse regime of gravitational scattering

We generalize the semiclassical treatment of graviton radiation to gravitational scattering at very large energies $\sqrt{s}\gg m_P$ and finite scattering angles $\Theta_s$, so as to approach the collapse regime of impact parameters $b \simeq b_c \sim R\equiv 2G\sqrt{s}$. Our basic tool is the extension of the recently proposed, unified form of radiation to the ACV reduced-action model and to its resummed-eikonal exchange. By superimposing that radiation all-over eikonal scattering, we are able to derive the corresponding (unitary) coherent-state operator. The resulting graviton spectrum, tuned on the gravitational radius $R$, fully agrees with previous calculations for small angles $\Theta_s\ll 1$ but, for sizeable angles $\Theta_s(b)\leq \Theta_c = O(1)$ acquires an exponential cutoff of the large $\omega R$ region, due to energy conservation, so as to emit a finite fraction of the total energy. In the approach-to-collapse regime of $b\to b_c^+$ we find a radiation enhancement due to large tidal forces, so that the whole energy is radiated off, with a large multiplicity $\langle N \rangle\sim Gs \gg 1$ and a well-defined frequency cutoff of order $R^{-1}$. The latter corresponds to the Hawking temperature for a black hole of mass notably smaller than $\sqrt{s}$.Comment: 5 pages, 2 figures, talk presented at the European Physical Society Conference on High Energy Physics, 5-12 July, Venice, Ital

IFNs Modify the Proteome of <i>Legionella</i>-Containing Vacuoles and Restrict Infection Via IRG1-Derived Itaconic Acid

Macrophages can be niches for bacterial pathogens or antibacterial effector cells depending on the pathogen and signals from the immune system. Here we show that type I and II IFNs are master regulators of gene expression during Legionella pneumophila infection, and activators of an alveolar macrophage-intrinsic immune response that restricts bacterial growth during pneumonia. Quantitative mass spectrometry revealed that both IFNs substantially modify Legionella-containing vacuoles, and comparative analyses reveal distinct subsets of transcriptionally and spatially IFN-regulated proteins. Immune-responsive gene (IRG)1 is induced by IFNs in mitochondria that closely associate with Legionella-containing vacuoles, and mediates production of itaconic acid. This metabolite is bactericidal against intravacuolar L. pneumophila as well as extracellular multidrug-resistant Gram-positive and -negative bacteria. Our study explores the overall role IFNs play in inducing substantial remodeling of bacterial vacuoles and in stimulating production of IRG1-derived itaconic acid which targets intravacuolar pathogens. IRG1 or its product itaconic acid might be therapeutically targetable to fight intracellular and drug-resistant bacteria

Digitale Dingwelten

Der digitale Wandel hat wissenschaftlichen Sammlungen eine Fülle technischer Möglichkeiten an die Hand gegeben, Objekte zu digitalisieren, zu dokumentieren und auf vielfältige Weise nutzbar zu machen. Die sechste Auflage des „Jungen Forums für Sammlungs- und Objektforschung“ widmet sich daher den digitalen Methoden und Werkzeugen, die im Kontext einer forschenden oder auch lehrenden Befassung mit den Sammlungsdingen und ihren digitalen Abbildern zum Einsatz kommen. Dieser Band vereint elf Beiträge von Nachwuchswissenschaftler:innen aus den Bereichen Archäologie, Geschichtsdidaktik, Digital Humanities, Kunstgeschichte, Kunstpädagogik, Kunsttechnologie und Restaurierungswissenschaft, Psychologie sowie der Human- und Veterinärmedizin, die sich mit digitalen Dingwelten auseinandersetzen, indem sie jeweils unterschiedliche Fragestellungen und Methoden heranziehen. Die Reflexion über forschungsleitende methodische Aspekte objektbezogener Forschung bildet einen gemeinsamen Bezugspunkt der Beiträge.Peer Reviewe

St. John's Daily Star, 1920-09-13

The St. John's Daily Star was published daily except Sunday between 17 April 1915 - 23 July 1921

ARTD1-induced poly-ADP-ribose formation enhances PPARγ ligand binding and co-factor exchange

PPARγ-dependent gene expression during adipogenesis is facilitated by ADP-ribosyltransferase D-type 1 (ARTD1; PARP1)-catalyzed poly-ADP-ribose (PAR) formation. Adipogenesis is accompanied by a dynamic modulation of the chromatin landscape at PPARγ target genes by ligand-dependent co-factor exchange. However, how endogenous PPARγ ligands, which have a low affinity for the receptor and are present at low levels in the cell, can induce sufficient co-factor exchange is unknown. Moreover, the significance of PAR formation in PPARγ-regulated adipose tissue function is also unknown. Here, we show that inhibition of PAR formation in mice on a high-fat diet reduces weight gain and cell size of adipocytes, as well as PPARγ target gene expression in white adipose tissue. Mechanistically, topoisomerase II activity induces ARTD1 recruitment to PPARγ target genes, and ARTD1 automodification enhances ligand binding to PPARγ, thus promoting sufficient transcriptional co-factor exchange in adipocytes. Thus, ARTD1-mediated PAR formation during adipogenesis is necessary to adequately convey the low signal of endogenous PPARγ ligand to effective gene expression. These results uncover a new regulatory mechanism of ARTD1-induced ADP-ribosylation and highlight its importance for nuclear factor-regulated gene expression

Severe Acute Respiratory Syndrome Coronavirus 2 Outbreak Related to a Nightclub, Germany, 2020

We report an outbreak of coronavirus disease with 74 cases related to a nightclub in Germany in March 2020. Staff members were particularly affected (attack rate 56%) and likely caused sustained viral transmission after an event at the club. This outbreak illustrates the potential for superspreader events and corroborates current club closures.Peer Reviewe

ARTD1 in myeloid cells controls the IL-12/18–IFN-γ axis in a model of sterile sepsis, chronic bacterial infection, and cancer

Mice deficient for ADP-ribosyltransferase diphteria toxin-like 1 (ARTD1) are protected against microbially induced inflammation. To address the contribution of ARTD1 to inflammation specifically in myeloid cells, we generated an Artd1ΔMyel mouse strain with conditional ARTD1 deficiency in myeloid lineages and examined the strain in three disease models. We found that ARTD1, but not its enzymatic activity, enhanced the transcriptional activation of distinct LPS-induced genes that included IL-12, TNF-α, and IL-6 in primary bone marrow-derived macrophages and LPS-induced IL-12/18-IFN-γ signaling in Artd1ΔMyel mice. The loss of Artd1 in myeloid cells also reduced the TH1 response to Helicobacter pylori and impaired immune control of the bacteria. Furthermore, Artd1ΔMyel mice failed to control tumor growth in a s.c. MC-38 model of colon cancer, which could be attributed to reduced TH1 and CD8 responses. Together, these data provide strong evidence for a cell-intrinsic role of ARTD1 in myeloid cells that is independent of its enzymatic activity and promotes type I immunity by promoting IL-12/18 expression

Kunstpflege in Bibliotheken – Kür oder Pflicht? : Wege zur Sichtbarmachung forschungsrelevanter Druckgrafik an der Staats- und Universitätsbibliothek Hamburg

Selten wird das Sammeln von Grafik in Bibliotheken genauer betrachtet, obwohl dies noch im 19. Jahrhundert intensiv gepflegt wurde, gerade in der aktiven bürgerlichen Kultur Hamburgs. Einmal mehr zeigt sich, dass Handel und Kunstsinn durchaus in der Hansestadt zusammengingen. Die Beschäftigung mit den Kupferstichen der Staats- und Universitätsbibliothek Hamburg hat vielfältige Spuren zutage gefördert, die auf die Provenienzen der ursprünglichen Besitzer und auf den bibliothekarischen Umgang mit ihnen hindeuten. Sie wurden von einer Gruppe Studierender der Kunstgeschichte eingehend und mit engagierter Recherchearbeit untersucht und in diesem Buch wissenschaftlich fundiert mit neuen Perspektiven dargelegt. Neben der verzweigten Sammlungsgeschichte möchte das Buch auch auf die Werke selbst aufmerksam machen, die nun digital erfasst und damit zugänglich sind. Die Publikation vereint sowohl historisch-kritische Bibliotheks- und Sammlungsgeschichte als auch die Auseinandersetzung mit modernen Instrumenten ihrer Verfügbarmachung