How is rape a weapon of war?: feminist international relations, modes of critical explanation and the study of wartime sexual violence

Rape is a weapon of war. Establishing this now common claim has been an achievement of feminist scholarship and activism and reveals wartime sexual violence as a social act marked by gendered power. But the consensus that rape is a weapon of war obscures important, and frequently unacknowledged, differences in ways of understanding and explaining it. This article opens these differences to analysis. Drawing on recent debates regarding the philosophy of social science in IR and social theory, it interprets feminist accounts of wartime sexual violence in terms of modes of critical explanation – expansive styles of reasoning that foreground particular actors, mechanisms, reasons and stories in the formulation of research. The idea of a mode of critical explanation is expanded upon through a discussion of the role of three elements (analytical wagers, narrative scripts and normative orientations) which accomplish the theoretical work of modes. Substantive feminist accounts of wartime sexual violence are then differentiated in terms of three modes – of instrumentality, unreason and mythology – which implicitly structure different understandings of how rape might be a weapon of war. These modes shape political and ethical projects and so impact not only on questions of scholarly content but also on the ways in which we attempt to mitigate and abolish war rape. Thinking in terms of feminist modes of critical explanation consequently encourages further work in an unfolding research agenda. It clarifes the ways in which an apparently commonality of position can conceal meaningful disagreements about human action. Exposing these disagreements opens up new possibilities for the analysis of war rape

Active wetting of epithelial tissues

Development, regeneration and cancer involve drastic transitions in tissue morphology. In analogy with the behavior of inert fluids, some of these transitions have been interpreted as wetting transitions. The validity and scope of this analogy are unclear, however, because the active cellular forces that drive tissue wetting have been neither measured nor theoretically accounted for. Here we show that the transition between 2D epithelial monolayers and 3D spheroidal aggregates can be understood as an active wetting transition whose physics differs fundamentally from that of passive wetting phenomena. By combining an active polar fluid model with measurements of physical forces as a function of tissue size, contractility, cell-cell and cell-substrate adhesion, and substrate stiffness, we show that the wetting transition results from the competition between traction forces and contractile intercellular stresses. This competition defines a new intrinsic lengthscale that gives rise to a critical size for the wetting transition in tissues, a striking feature that has no counterpart in classical wetting. Finally, we show that active shape fluctuations are dynamically amplified during tissue dewetting. Overall, we conclude that tissue spreading constitutes a prominent example of active wetting --- a novel physical scenario that may explain morphological transitions during tissue morphogenesis and tumor progression

Chemotactic smoothing of collective migration

Collective migration-the directed, coordinated motion of many self-propelled agents-is a fascinating emergent behavior exhibited by active matter with functional implications for biological systems. However, how migration can persist when a population is confronted with perturbations is poorly understood. Here, we address this gap in knowledge through studies of bacteria that migrate via directed motion, or chemotaxis, in response to a self-generated nutrient gradient. We find that bacterial populations autonomously smooth out large-scale perturbations in their overall morphology, enabling the cells to continue to migrate together. This smoothing process arises from spatial variations in the ability of cells to sense and respond to the local nutrient gradient-revealing a population-scale consequence of the manner in which individual cells transduce external signals. Altogether, our work provides insights to predict, and potentially control, the collective migration and morphology of cellular populations and diverse other forms of active matter. eLife digest Flocks of birds, schools of fish and herds of animals are all good examples of collective migration, where individuals co-ordinate their behavior to improve survival. This process also happens on a cellular level; for example, when bacteria consume a nutrient in their surroundings, they will collectively move to an area with a higher concentration of food via a process known as chemotaxis. Several studies have examined how disturbing collective migration can cause populations to fall apart. However, little is known about how groups withstand these interferences. To investigate, Bhattacharjee, Amchin, Alert et al. studied bacteria called Escherichia coli as they moved through a gel towards nutrients. The E. coli were injected into the gel using a three-dimensional printer, which deposited the bacteria into a wiggly shape that forces the cells apart, making it harder for them to move as a collective group. However, as the bacteria migrated through the gel, they smoothed out the line and gradually made it straighter so they could continue to travel together over longer distances. Computer simulations revealed that this smoothing process is achieved by differences in how the cells respond to local nutrient levels based on their position. Bacteria towards the front of the group are exposed to more nutrients, causing them to become oversaturated and respond less effectively to the nutrient gradient. As a result, they move more slowly, allowing the cells behind them to eventually catch-up. These findings reveal a general mechanism in which limitations in how individuals sense and respond to an external signal (in this case local nutrient concentrations) allows them to continue migrating together. This mechanism may apply to other systems that migrate via chemotaxis, as well as groups whose movement is directed by different external factors, such as temperature and light intensity

Chemotactic smoothing of collective migration

Collective migration -- the directed, coordinated motion of many self-propelled agents -- is a fascinating emergent behavior exhibited by active matter that has key functional implications for biological systems. Extensive studies have elucidated the different ways in which this phenomenon may arise. Nevertheless, how collective migration can persist when a population is confronted with perturbations, which inevitably arise in complex settings, is poorly understood. Here, by combining experiments and simulations, we describe a mechanism by which collectively migrating populations smooth out large-scale perturbations in their overall morphology, enabling their constituents to continue to migrate together. We focus on the canonical example of chemotactic migration of Escherichia coli, in which fronts of cells move via directed motion, or chemotaxis, in response to a self-generated nutrient gradient. We identify two distinct modes in which chemotaxis influences the morphology of the population: cells in different locations along a front migrate at different velocities due to spatial variations in (i) the local nutrient gradient and in (ii) the ability of cells to sense and respond to the local nutrient gradient. While the first mode is destabilizing, the second mode is stabilizing and dominates, ultimately driving smoothing of the overall population and enabling continued collective migration. This process is autonomous, arising without any external intervention; instead, it is a population-scale consequence of the manner in which individual cells transduce external signals. Our findings thus provide insights to predict, and potentially control, the collective migration and morphology of cell populations and diverse other forms of active matter

Emergence and spread of highly pathogenic avian influenza A(H5N8) in Europe in 2016‐2017

Circulation of highly pathogenic avian influenza (HPAI) viruses poses a continuousthreat to animal and public health. After the 2005–2006 H5N1 and the 2014–2015H5N8 epidemics, another H5N8 is currently affecting Europe. Up to August 2017,1,112 outbreaks in domestic and 955 in wild birds in 30 European countries havebeen reported, the largest epidemic by a HPAI virus in the continent. Here, the mainepidemiological findings are described. While some similarities with previous HPAIvirus epidemics were observed, for example in the pattern of emergence, significantdifferences were also patent, in particular the size and extent of the epidemic. Eventhough no human infections have been reported to date, the fact that A/H5N8 hasaffected so far 1,112 domestic holdings, increases the risk of exposure of humansand therefore represents a concern. Understanding the epidemiology of HPAIviruses is essential for the planning future surveillance and control activities.info:eu-repo/semantics/publishedVersio

Neuropathogenesis of a highly pathogenic avian influenza virus (H7N1) in experimentally infected chickens

In order to understand the mechanism of neuroinvasion of a highly pathogenic avian influenza virus (HPAIV) into the central nervous system (CNS) of chickens, specific pathogen free chickens were inoculated with a H7N1 HPAIV. Blood, cerebrospinal fluid (CSF), nasal cavity and brain tissue samples were obtained from 1 to 4 days post-inoculation (dpi) of infected and control chickens. Viral antigen topographical distribution, presence of influenza A virus receptors in the brain, as well as, the role of the olfactory route in virus CNS invasion were studied using different immunohistochemistry techniques. Besides, viral RNA load in CSF and blood was quantified by means of a quantitative real-time reverse transcription-polymerase chain reaction. Viral antigen was observed widely distributed in the CNS, showing bilateral and symmetrical distribution in the nuclei of the diencephalon, mesencephalon and rhombencephalon. Viral RNA was detected in blood and CSF at one dpi, indicating that the virus crosses the blood-CSF-barrier early during infection. This early dissemination is possibly favoured by the presence of Siaα2,3 Gal and Siaα2,6 Gal receptors in brain vascular endothelial cells, and Siaα2,3 Gal receptors in ependymal and choroid plexus cells. No viral antigen was observed in olfactory sensory neurons, while the olfactory bulb showed only weak staining, suggesting that the virus did not use this pathway to enter into the brain. The sequence of virus appearance and the topographical distribution of this H7N1 HPAIV indicate that the viral entry occurs via the haematogenous route, with early and generalized spreading through the CSF

The role of innate immune responses against two strains of PEDV (S INDEL and non-S INDEL) in newborn and weaned piglets inoculated by combined orogastric and intranasal routes

IntroductionPorcine epidemic diarrhea (PED) is a severe gastrointestinal disease in swine caused by PED virus (PEDV), leading to significant economic losses worldwide. Newborn piglets are especially vulnerable, with nearly 100% mortality, unlike older pigs. Disease severity also varies depending on the PEDV strain, with non-S INDEL strains being more virulent than S INDEL ones.MethodsThis study examined early pathogenesis and innate immunity in 5-day-old suckling and 5-week-old weaned piglets (n=8 per age group, 4 per strain) inoculated with S INDEL or non-S INDEL PEDV strains via combined orogastric and intranasal route. Age matched negative controls (n=3 per age group) were included. Body weight, temperature, and clinical signs were monitored for 48 hours post-inoculation (hpi). PEDV RNA levels were assessed in rectal swabs (RS) at 0 and 48 hpi, while pathological analyses and viral RNA loads were measured in jejunal content and intestinal mucosa. Gene expression of 75 selected antiviral and inflammatory genes were determined in laser capture microdissection (LCM)–derived jejunal samples using microfluidic qPCR at 48 hpi.ResultsSuckling piglets showed severe clinical signs, while weaned piglets were mostly asymptomatic at 48 hpi. In general, clinical signs and lesions in suckling piglets were similar, regardless of the PEDV strain. Both viral strains produced comparable viral RNA loads in the small intestine and feces, as well as consistent villous atrophy and fusion across age groups. In LCM-derived jejunal samples, weaned piglets had higher expression of antiviral genes (type I/III interferons, ISGs) and Th1/Th17 pro-inflammatory genes, particularly with the non-S INDEL strain. Conversely, the anti-inflammatory cytokine IL-10 was overexpressed in suckling compared to weaned piglets for both strains.DiscussionOverall, PEDV-induced intestinal damage, viral replication, and excretion were similar in studied groups regardless of viral strain or piglet age. The reduced clinical severity in weaned piglets may result from their stronger intestinal antiviral and pro-inflammatory response

Previous SARS-CoV-2 Infection Increases B.1.1.7 Cross-Neutralization by Vaccinated Individuals

With the spread of new variants of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there is a need to assess the protection conferred by both previous infections and current vaccination. Here we tested the neutralizing activity of infected and/or vaccinated individuals against pseudoviruses expressing the spike of the original SARS-CoV-2 isolate Wuhan-Hu-1 (WH1), the D614G mutant and the B.1.1.7 variant. Our data show that parameters of natural infection (time from infection and nature of the infecting variant) determined cross-neutralization. Uninfected vaccinees showed a small reduction in neutralization against the B.1.1.7 variant compared to both the WH1 strain and the D614G mutant. Interestingly, upon vaccination, previously infected individuals developed more robust neutralizing responses against B.1.1.7, suggesting that vaccines can boost the neutralization breadth conferred by natural infection

Detection of volcanic ash clouds from Nimbus 7/total ozone mapping spectrometer

Measured radiances from the Version 7 reprocessing of the Nimbus 7/total ozone mapping spectrometer (TOMS) 340- and 380-nm channels are used to detect absorbing particulates injected into the atmosphere after the El Chichon eruption on April 4, 1982. It is shown that while the single-channel reflectivity determined from the 380-nm channel is able to detect clouds and haze composed of nonabsorbing aerosols, the spectral contrast between the 340- and 380-nm channels is sensitive to absorbing particulates such as volcanic ash, desert dust, or smoke from biomass burning. In this paper the spectral contrast between these two channels is used to detect the volcanic ash injection into the atmosphere and to track its evolution for several days. The movement of the ash clouds is shown to be consistent with the motions expected from the National Centers for Environmental Prediction (NCEP)-derived balanced wind fields in the troposphere and lower stratosphere. The movement of the volcanic SO2 cloud detected from TOMS data was also in agreement with the NCEP wind at higher altitudes of up to 100–10 mbar. The vertical wind shear in the neighborhood of the eruption site resulted in a clear separation of the ash and SO2 clouds. The location and movement of the ash cloud are consistent with information obtained by the advanced very high resolution radiometer (AVHRR) instrument on board the NOAA 7 satellite and to ground reports of ash fall

Heterogeneous Infectivity and Pathogenesis of SARS-CoV-2 Variants Beta, Delta and Omicron in Transgenic K18-hACE2 and Wildtype Mice

The emerging SARS-CoV-2 variants of concern (VOCs) may display enhanced transmissibility, more severity and/or immune evasion; however, the pathogenesis of these new VOCs in experimental SARS-CoV-2 models or the potential infection of other animal species is not completely understood. Here we infected K18-hACE2 transgenic mice with B.1, B.1.351/Beta, B.1.617.2/Delta and BA.1.1/Omicron isolates and demonstrated heterogeneous infectivity and pathogenesis. B.1.351/Beta variant was the most pathogenic, while BA.1.1/Omicron led to lower viral RNA in the absence of major visible clinical signs. In parallel, we infected wildtype (WT) mice and confirmed that, contrary to B.1 and B.1.617.2/Delta, B.1.351/Beta and BA.1.1/Omicron can infect them. Infection in WT mice coursed without major clinical signs and viral RNA was transient and undetectable in the lungs by day 7 post-infection. In silico modeling supported these findings by predicting B.1.351/Beta receptor binding domain (RBD) mutations result in an increased affinity for both human and murine ACE2 receptors, while BA.1/Omicron RBD mutations only show increased affinity for murine ACE2