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Fast radio bursts are mysterious millisecond-duration transients prevalent in the radio sky. Rapid accumulation of data in recent years has facilitated an understanding of the underlying physical mechanisms of these events. Knowledge gained from the neighbouring fields of gamma-ray bursts and radio pulsars has also offered insights. Here I review developments in this fast-moving field. Two generic categories of radiation model invoking either magnetospheres of compact objects (neutron stars or black holes) or relativistic shocks launched from such objects have been much debated. selleckchem The recent detection of a Galactic fast radio burst in association with a soft gamma-ray repeater suggests that magnetar engines can produce at least some, and probably all, fast radio bursts. Other engines that could produce fast radio bursts are not required, but are also not impossible.The growing importance of applications based on machine learning is driving the need to develop dedicated, energy-efficient electronic hardware. Compared with von Neumann architectures, which have separate processing and storage units, brain-inspired in-memory computing uses the same basic device structure for logic operations and data storage1-3, thus promising to reduce the energy cost of data-centred computing substantially4. Although there is ample research focused on exploring new device architectures, the engineering of material platforms suitable for such device designs remains a challenge. Two-dimensional materials5,6 such as semiconducting molybdenum disulphide, MoS2, could be promising candidates for such platforms thanks to their exceptional electrical and mechanical properties7-9. Here we report our exploration of large-area MoS2 as an active channel material for developing logic-in-memory devices and circuits based on floating-gate field-effect transistors (FGFETs). The conductance of our FGFETs can be precisely and continuously tuned, allowing us to use them as building blocks for reconfigurable logic circuits in which logic operations can be directly performed using the memory elements. After demonstrating a programmable NOR gate, we show that this design can be simply extended to implement more complex programmable logic and a functionally complete set of operations. Our findings highlight the potential of atomically thin semiconductors for the development of next-generation low-power electronics.Since their discovery in 20071, much effort has been devoted to uncovering the sources of the extragalactic, millisecond-duration fast radio bursts (FRBs)2. A class of neutron stars known as magnetars is a leading candidate source of FRBs3,4. Magnetars have surface magnetic fields in excess of 1014 gauss, the decay of which powers a range of high-energy phenomena5. Here we report observations of a millisecond-duration radio burst from the Galactic magnetar SGR 1935+2154, with a fluence of 1.5 ± 0.3 megajansky milliseconds. This event, FRB 200428 (ST 200428A), was detected on 28 April 2020 by the STARE2 radio array6 in the 1,281-1,468 megahertz band. The isotropic-equivalent energy released in FRB 200428 is 4 × 103 times greater than that of any radio pulse from the Crab pulsar-previously the source of the brightest Galactic radio bursts observed on similar timescales7. FRB 200428 is just 30 times less energetic than the weakest extragalactic FRB observed so far8, and is drawn from the same population as the observed FRB sample. The coincidence of FRB 200428 with an X-ray burst9-11 favours emission models that describe synchrotron masers or electromagnetic pulses powered by magnetar bursts and giant flares3,4,12,13. The discovery of FRB 200428 implies that active magnetars such as SGR 1935+2154 can produce FRBs at extragalactic distances.An amendment to this paper has been published and can be accessed via a link at the top of the paper.Glucocorticoids (GCs) are small lipid hormones produced by the adrenals that maintain organismal homeostasis. Circadian and stress-induced changes in systemic GC levels regulate metabolism, cardiovascular and neural function, reproduction and immune activity. Our understanding of GC effects on immunity comes largely from administration of exogenous GCs to treat immune or inflammatory disorders. However, it is increasingly clear that endogenous GCs both promote and suppress T cell immunity. Examples include selecting an appropriate repertoire of T cell receptor (TCR) self-affinities in the thymus, regulating T cell trafficking between anatomical compartments, suppressing type 1 T helper (TH1) cell responses while permitting TH2 cell and, especially, IL-17-producing T helper cell responses, and promoting memory T cell differentiation and maintenance. Furthermore, in addition to functioning at a distance, extra-adrenal (local) production allows GCs to act as paracrine signals, specifically targeting activated T cells in various contexts in the thymus, mucosa and tumours. These pleiotropic effects on different T cell populations during development and immune responses provide a nuanced understanding of how GCs shape immunity.Paxillin (PXN), a key component of the focal adhesion complex, has been associated with cancer progression, but the underlying mechanisms are poorly understood. The purpose of this study was to elucidate mechanisms by which PXN affects cancer growth and progression, which we addressed using cancer patient data, cell lines, and orthotopic mouse models. We demonstrated a previously unrecognized mechanism whereby nuclear PXN enhances angiogenesis by transcriptionally regulating SRC expression. SRC, in turn, increases PLAT expression through NF-ĸB activation; PLAT promotes angiogenesis via LRP1 in endothelial cells. PXN silencing in ovarian cancer mouse models reduced angiogenesis, tumor growth, and metastasis. These findings provide a new understanding of the role of PXN in regulating tumor angiogenesis and growth.Oncolytic viruses selectively replicate and destroy cancer cells while sparing normal cells, prompting their recognition as promising antitumor agents. Herpes simplex virus (HSV) is suitable as an anticancer agent, given its considerable therapeutic gene capacity and excellent safety profile in clinical trials. Interleukin (IL)-12 induces a Th1-type immune response that mediates interferon (IFN)-γ release from natural killer (NK), CD4+ and CD8+ T cells. Granulocyte-macrophage colony-stimulating factor (GM-CSF) induces the generation of antigen-presenting cells and promotes dendritic cell differentiation. We established a novel oncolytic HSV-1 (∆6/GM/IL12) co-expressing IL-12 and GM-CSF and tested its effects against a B16-F10 murine melanoma model. ∆6/GM/IL12 administration diminished tumor growth and prolonged survival compared to treatment with ∆6/GM or ∆6/IL12 expressing each individual cytokine. Flow cytometry and histological analysis showed increased activation of CD4+ and CD8+ T cells in ∆6/GM/IL12-treated mice.

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