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Traumatic brain injury (TBI) elicits an inflammatory response in the central nervous system (CNS) that involves both resident and peripheral immune cells. Neuroinflammation can persist for years following a single TBI and may contribute to neurodegeneration. However, administration of anti-inflammatory drugs shortly after injury was not effective in the treatment of TBI patients. Some components of the neuroinf lammatory response seem to play a beneficial role in the acute phase of TBI. Indeed, following CNS injury, early inflammation can set the stage for proper tissue regeneration and recovery, which can, perhaps, explain why general immunosuppression in TBI patients is disadvantageous. Here, we discuss some positive attributes of neuroinflammation and propose that inflammation be therapeutically guided in TBI patients rather than globally suppressed.

\"This book serves as a collectively generated (re)invented sourcebook-a glossary on the edge of extinction, a language for landscapes under threat. This glossary compiles terms (many borrowed, invented, recast) that might help us configure or elaborate our engagements with place. Each entry is a sketch, a notion, an opening\"-- Provided by publisher.

Mild traumatic brain injury (mTBI) can cause meningeal vascular injury and cell death that spreads into the brain parenchyma and triggers local inflammation and recruitment of peripheral immune cells. The factors that dictate meningeal recovery after mTBI are unknown at present. Here we demonstrated that most patients who had experienced mTBI resolved meningeal vascular damage within 2–3 weeks, although injury persisted for months in a subset of patients. To understand the recovery process, we studied a mouse model of mTBI and found extensive meningeal remodeling that was temporally reliant on infiltrating myeloid cells with divergent functions. Inflammatory myelomonocytic cells scavenged dead cells in the lesion core, whereas wound-healing macrophages proliferated along the lesion perimeter and promoted angiogenesis through the clearance of fibrin and production of the matrix metalloproteinase MMP-2. Notably, a secondary injury experienced during the acute inflammatory phase aborted this repair program and enhanced inflammation, but a secondary injury experienced during the wound-healing phase did not. Our findings demonstrate that meningeal vasculature can undergo regeneration after mTBI that is dependent on distinct myeloid cell subsets. Meningeal vascular damage accompanies mild traumatic brain injury, which persists in a fraction of patients. McGavern and colleagues report that distinct myeloid cell subsets are temporally recruited to the wound site during tissue repair; however, re-injury at early time points impairs recovery.

Traumatic brain injury (TBI) and cerebrovascular injury are leading causes of disability and mortality worldwide. Systemic infections often accompany these disorders and can worsen outcomes. Recovery after brain injury depends on innate immunity, but the effect of infections on this process is not well understood. Here, we demonstrate that systemically introduced microorganisms and microbial products interfered with meningeal vascular repair after TBI in a type I interferon (IFN-I)-dependent manner, with sequential infections promoting chronic disrepair. Mechanistically, we discovered that MDA5-dependent detection of an arenavirus encountered after TBI disrupted pro-angiogenic myeloid cell programming via induction of IFN-I signaling. Systemic viral infection similarly blocked restorative angiogenesis in the brain parenchyma after intracranial hemorrhage, leading to chronic IFN-I signaling, blood–brain barrier leakage and a failure to restore cognitive–motor function. Our findings reveal a common immunological mechanism by which systemic infections deviate reparative programming after central nervous system injury and offer a new therapeutic target to improve recovery. Traumatic brain injury and stroke are commonly complicated by systemic infections, which impede recovery and lead to poor clinical outcomes. Using a mouse model, McGavern and colleagues show systemic microbial infections impair central nervous system revascularization and repair by a mechanism involving type I interferon signaling.

The survey and modeling of spatial grid structures is often a challenging task to solve, due to the many bottlenecks present in the reverse modelling process. Geometrical and material complexity, scale variation, shadows effects, low accessibility, mismatch between similar elements, metrical validation, data management are all critical passages. They must be solved to obtain a reliable data able to solve the system maintenance and intervention requirements. In these cases, in particular, when the structure is difficult to be accessed, it is essential to plan an integrated survey approach. This paper shows how the survey and modelling of an impressive structure was carried out using both TLS and RPAS photogrammetry. After being validated, the data is integrated into a single point cloud that completely describes the structure, eliminating shadow areas and hidden parts. In the modeling process, particular attention was paid to verifying the correspondence between as-built and project. Finally, an element of particular interest is represented by the attempt to recognize the individual construction components belonging to specified geometric and dimensional classes, with the advantage of obtaining a complete model that is as faithful as possible to the real situation of the structure.

UV resonance Raman spectroscopy of size-selected linear sp-carbon chains unveils vibrational overtones and combinations up to the fifth order. Thanks to the tunability of the synchrotron source, we excited each H-terminated polyyne (HC n H with n  = 8,10,12) to the maxima of its vibronic absorption spectrum allowing us to precisely determine the electronic and vibrational structure of the ground and excited states for the main observed vibrational mode. Selected transitions are shown to enhance specific overtone orders in the Raman spectrum in a specific way that can be explained by a simple analytical model based on Albrecht’s theory of resonance Raman scattering. The determined Huang–Rhys factors indicate a strong and size-dependent electron-phonon coupling increasing with the sp-carbon chain length. H-capped polyynes are the simplest system to observe finite-length effects in carbyne. Here, the authors exploit synchrotron-based UV resonance Raman spectroscopy to explain a peculiar intensity behavior of multiple phonons scattering and show a size-dependent electron-phonon coupling.

Infiltrating monocyte-derived macrophages (MDMs) and resident microglia dominate central nervous system (CNS) injury sites. Differential roles for these cell populations after injury are beginning to be uncovered. Here, we show evidence that MDMs and microglia directly communicate with one another and differentially modulate each other's functions. Importantly, microglia-mediated phagocytosis and inflammation are suppressed by infiltrating macrophages. In the context of spinal cord injury (SCI), preventing such communication increases microglial activation and worsens functional recovery. We suggest that macrophages entering the CNS provide a regulatory mechanism that controls acute and long-term microglia-mediated inflammation, which may drive damage in a variety of CNS conditions.

Oncogenic FGFR3–TACC3 gene fusions signal through phosphorylated PIN4 to trigger biogenesis of peroxisomes and synthesis of new proteins, enabling mitochondrial respiration and tumour growth. Fusion gene stimulates tumour metabolism FGFR3 - TACC3 gene fusions are oncogenic and have been found in many cancer types, but how they drive tumour growth is unknown. Antonio Iavarone and colleagues show that the fusion protein activates mitochondrial metabolism, which promotes protein synthesis and thereby stimulates tumour growth. The team suggest that this reliance on mitochondrial respiration could open up a new therapeutic route for treating tumours that carry the FGFR3 - TACC3 fusion gene. Chromosomal translocations that generate in-frame oncogenic gene fusions are notable examples of the success of targeted cancer therapies 1 , 2 , 3 . We have previously described gene fusions of FGFR3 - TACC3 (F3–T3) in 3% of human glioblastoma cases 4 . Subsequent studies have reported similar frequencies of F3–T3 in many other cancers, indicating that F3–T3 is a commonly occuring fusion across all tumour types 5 , 6 . F3–T3 fusions are potent oncogenes that confer sensitivity to FGFR inhibitors, but the downstream oncogenic signalling pathways remain unknown 2 , 4 , 5 , 6 . Here we show that human tumours with F3–T3 fusions cluster within transcriptional subgroups that are characterized by the activation of mitochondrial functions. F3–T3 activates oxidative phosphorylation and mitochondrial biogenesis and induces sensitivity to inhibitors of oxidative metabolism. Phosphorylation of the phosphopeptide PIN4 is an intermediate step in the signalling pathway of the activation of mitochondrial metabolism. The F3–T3–PIN4 axis triggers the biogenesis of peroxisomes and the synthesis of new proteins. The anabolic response converges on the PGC1α coactivator through the production of intracellular reactive oxygen species, which enables mitochondrial respiration and tumour growth. These data illustrate the oncogenic circuit engaged by F3–T3 and show that F3–T3-positive tumours rely on mitochondrial respiration, highlighting this pathway as a therapeutic opportunity for the treatment of tumours with F3–T3 fusions. We also provide insights into the genetic alterations that initiate the chain of metabolic responses that drive mitochondrial metabolism in cancer.

The paper describes an ongoing research project granted by the University of Naples Federico II (2017–2020) concerning masonry domes considered as visual poles in the historic urban landscape and as a constructively vulnerable built heritage. Studies focus on Renaissance domes in Campania region (Naples included) and combine established strategies with innovative ones for the knowledge of visible/invisible parts. Verticals and curved structures are investigated with a unitary approach, together with the pre-reinforcements placed during the construction phases or for later strengthening. These topics deal with issues crucial for the domes’ study: firstly, the overlapping of inner and outer surfaces that hide structural elements and do not enable their comprehension. In addition, we must consider the recurring difficult inspection or inaccessibility due to the big dimensions and heights from the ground. All these factors, together with the fact that decorated surfaces are a limit for the traditional diagnosis, require new investigation strategies – remote and by non-destructive methods – so as to document the invisible both for emerging and for underground parts. A model for knowledge characterized by the interlacement of ‘humanistic’ interpretation and bottom-up/bottom-down surveys is discussed. The understanding of what is invisible to direct inspection is considered a stimulating frontier for proposing innovative dissemination tools for the comprehension of cultural heritage, able to reach new communicative horizons related to the construction of complex forms of architecture. The transposition of the research outcomes into digital “accessible” data aims at having impacts for sharing a broader cultural awareness of the built heritage historical constructive significance.