Calculative practices, social movements and the rise of collective identity: how #istayathome mobilised a nation

Purpose – The Italian government addressed the first wave of its COVID-19 outbreak with a series of social restrictions and calculative practices, all branded with the slogan #istayathome. The hashtag quickly went viral, becoming both a mandate and a mantra and, as the crisis played out, we witnessed the rise of the Italian social movement #istayathome. This study examines how the government’s calculative practices led to #istayathome and the constituents that shaped this social movement. Design/methodology/approach – The authors embrace social movement theory and the collective identity perspective to examine #istayathome as a collective action and social movement. Using passive netnography, text mining and interpretative text analysis enhanced by machine learning, the authors analysed just over 350,000 tweets made during the period March to May 2020, each brandishing the hashtag #istayathome. Findings – The #istayathome movement gained traction as a response to the Italian government’s call for collective action. Thus, people became an active part of mobilising collective responsibility, enhancing the government’s plans. A collective identity on the part of the Italian people sustained the mass mobilisation, driven by cohesion, solidarity and a deep cultural trauma from COVID-19’s dramatic effects. Popular culture and Italy’s long traditions also helped to form the collective identity of #istayathome. This study found that calculative practices acted as a persuasive technology in forming this collective identity and mobilising people’s collective action. Numbers stimulated the cognitive, moral and emotional connections of the social ties shaping collective identity and responsibility. Thus, through collective identity, calculative practices indirectly influenced mass social behaviors and the social movement. Originality/value – This study offers a novel theoretical perspective and empirical knowledge to explain how government power affects people’s culture and everyday life. It unveils the sociological drivers that mobilise collective behaviors and enriches the accounting literature on the effects of calculative practices in managing emergencies. The study contributes to theory by providing an understanding of how calculative practices can influence collective behaviors and can be used to construct informal networks that go beyond the government’s traditional formalities

Surprising autopsy diagnosis in unclear initial situation. A case of intravascular B cell lymphoma

Intravascular large B cell lymphoma (IVLBCL) is a rare extranodal non-Hodgkin lymphoma characterized by proliferation of malignant cells within the lumen of small vessels, with a predilection for the central nervous system and the skin [1]. IVLBCL clinical course is highly aggressive, clinical signs and symptoms are not specific and may consist in neurological deficits, fever of unknown origin, cutaneous lesions, lacking of a typical neuroimaging pattern [1]. For all these reasons the diagnosis is frequently missed and the exitus is frequent, therefore post-mortem evaluation is necessary to clarify the clinical history. We present a case of IVLBCL in a 62-year-old female with unusual symptomatology, mimicking a vascular multinfarctual cerebropathy; post-mortem autopsy was diriment to define the nature of the disease. Immu- nohistochemical analysis for anti-CD20 revealed the ubiquitary presence of malignant lymphoid B-cells into the vessels of all organs analyzed, allowing the definitive diag- nosis. Although the diagnostic procedure for such pathology is still a matter for fur- ther studies, adequate interpretation of neuro-imaging and morphological findings, as well as of systemic symptoms can provide a right diagnostic hypothesis, suggest- ing focused biopsy in vivo

Coccolithophores as proxy of seawater changes at orbital-to-millennial scale during middle Pleistocene Marine Isotope Stages 14-9 in North Atlantic core MD01-2446

midlatitude North Atlantic, to reconstruct climatically induced sea surface water conditions throughout Marine Isotope Stages (MIS) 14–9. The data are compared to new and available paleoenvironmental proxies from the same site as well as other nearby North Atlantic records that support the coccolithophore signature at glacial‐interglacial to millennial climate scale. Total coccolithophore absolute abundance increases during interglacials but abruptly drops during the colder glacial phases and deglaciations. Coccolithophore warm water taxa (wwt) indicate that MIS11c and MIS9e experienced warmer and more stable conditions throughout the whole photic zone compared to MIS13. MIS11 was a long‐lasting warmer and stable interglacial characterized by a climate optimum during MIS11c when a more prominent influence of the subtropical front at the site is inferred. The wwt pattern also suggests distinct interstadial and stadial events lasting about 4–10 kyr. The glacial increases of Gephyrocapsa margereli‐G. muellerae 3–4 µm along with higher values of Corg, additionally supported by the total alkenone abundance at Site U1313, indicate more productive surface waters, likely reflecting the migration of the polar front into the midlatitude North Atlantic. Distinctive peaks of G. margereli‐muellerae (>4 µm), C. pelagicus pelagicus , Neogloboquadrina pachyderma left coiling, and reworked nannofossils, combined with minima in total nannofossil accumulation rate, are tracers of Heinrich‐type events during MIS12 and MIS10. Additional Heinrich‐type events are suggested during MIS12 and MIS14 based on biotic proxies, and we discuss possible iceberg sources at these times. Our results improve the understanding of mid‐Brunhes paleoclimate and the impact on phytoplankton diversity in the midlatitude North Atlantic region.Provided by PTCRIS: 58282, C2007-FCT/319/2006info:eu-repo/semantics/publishedVersio

An explainable model of host genetic interactions linked to COVID-19 severity

We employed a multifaceted computational strategy to identify the genetic factors contributing to increased risk of severe COVID-19 infection from a Whole Exome Sequencing (WES) dataset of a cohort of 2000 Italian patients. We coupled a stratified k-fold screening, to rank variants more associated with severity, with the training of multiple supervised classifiers, to predict severity based on screened features. Feature importance analysis from tree-based models allowed us to identify 16 variants with the highest support which, together with age and gender covariates, were found to be most predictive of COVID-19 severity. When tested on a follow-up cohort, our ensemble of models predicted severity with high accuracy (ACC = 81.88%; AUCROC = 96%; MCC = 61.55%). Our model recapitulated a vast literature of emerging molecular mechanisms and genetic factors linked to COVID-19 response and extends previous landmark Genome-Wide Association Studies (GWAS). It revealed a network of interplaying genetic signatures converging on established immune system and inflammatory processes linked to viral infection response. It also identified additional processes cross-talking with immune pathways, such as GPCR signaling, which might offer additional opportunities for therapeutic intervention and patient stratification. Publicly available PheWAS datasets revealed that several variants were significantly associated with phenotypic traits such as "Respiratory or thoracic disease", supporting their link with COVID-19 severity outcome.A multifaceted computational strategy identifies 16 genetic variants contributing to increased risk of severe COVID-19 infection from a Whole Exome Sequencing dataset of a cohort of Italian patients

Carriers of ADAMTS13 Rare Variants Are at High Risk of Life-Threatening COVID-19

Thrombosis of small and large vessels is reported as a key player in COVID-19 severity. However, host genetic determinants of this susceptibility are still unclear. Congenital Thrombotic Thrombocytopenic Purpura is a severe autosomal recessive disorder characterized by uncleaved ultra-large vWF and thrombotic microangiopathy, frequently triggered by infections. Carriers are reported to be asymptomatic. Exome analysis of about 3000 SARS-CoV-2 infected subjects of different severities, belonging to the GEN-COVID cohort, revealed the specific role of vWF cleaving enzyme ADAMTS13 (A disintegrin-like and metalloprotease with thrombospondin type 1 motif, 13). We report here that ultra-rare variants in a heterozygous state lead to a rare form of COVID-19 characterized by hyper-inflammation signs, which segregates in families as an autosomal dominant disorder conditioned by SARS-CoV-2 infection, sex, and age. This has clinical relevance due to the availability of drugs such as Caplacizumab, which inhibits vWF-platelet interaction, and Crizanlizumab, which, by inhibiting P-selectin binding to its ligands, prevents leukocyte recruitment and platelet aggregation at the site of vascular damage

Gain- and Loss-of-Function CFTR Alleles Are Associated with COVID-19 Clinical Outcomes

Carriers of single pathogenic variants of the CFTR (cystic fibrosis transmembrane conductance regulator) gene have a higher risk of severe COVID-19 and 14-day death. The machine learning post-Mendelian model pinpointed CFTR as a bidirectional modulator of COVID-19 outcomes. Here, we demonstrate that the rare complex allele [G576V;R668C] is associated with a milder disease via a gain-of-function mechanism. Conversely, CFTR ultra-rare alleles with reduced function are associated with disease severity either alone (dominant disorder) or with another hypomorphic allele in the second chromosome (recessive disorder) with a global residual CFTR activity between 50 to 91%. Furthermore, we characterized novel CFTR complex alleles, including [A238V;F508del], [R74W;D1270N;V201M], [I1027T;F508del], [I506V;D1168G], and simple alleles, including R347C, F1052V, Y625N, I328V, K68E, A309D, A252T, G542*, V562I, R1066H, I506V, I807M, which lead to a reduced CFTR function and thus, to more severe COVID-19. In conclusion, CFTR genetic analysis is an important tool in identifying patients at risk of severe COVID-19

A genome-wide association study for survival from a multi-centre European study identified variants associated with COVID-19 risk of death

: The clinical manifestations of SARS-CoV-2 infection vary widely among patients, from asymptomatic to life-threatening. Host genetics is one of the factors that contributes to this variability as previously reported by the COVID-19 Host Genetics Initiative (HGI), which identified sixteen loci associated with COVID-19 severity. Herein, we investigated the genetic determinants of COVID-19 mortality, by performing a case-only genome-wide survival analysis, 60 days after infection, of 3904 COVID-19 patients from the GEN-COVID and other European series (EGAS00001005304 study of the COVID-19 HGI). Using imputed genotype data, we carried out a survival analysis using the Cox model adjusted for age, age2, sex, series, time of infection, and the first ten principal components. We observed a genome-wide significant (P-value < 5.0 × 10-8) association of the rs117011822 variant, on chromosome 11, of rs7208524 on chromosome 17, approaching the genome-wide threshold (P-value = 5.19 × 10-8). A total of 113 variants were associated with survival at P-value < 1.0 × 10-5 and most of them regulated the expression of genes involved in immune response (e.g., CD300 and KLR genes), or in lung repair and function (e.g., FGF19 and CDH13). Overall, our results suggest that germline variants may modulate COVID-19 risk of death, possibly through the regulation of gene expression in immune response and lung function pathways

The polymorphism L412F in TLR3 inhibits autophagy and is a marker of severe COVID-19 in males

The polymorphism L412F in TLR3 has been associated with several infectious diseases. However, the mechanism underlying this association is still unexplored. Here, we show that the L412F polymorphism in TLR3 is a marker of severity in COVID-19. This association increases in the sub-cohort of males. Impaired macroautophagy/autophagy and reduced TNF/TNFα production was demonstrated in HEK293 cells transfected with TLR3L412F-encoding plasmid and stimulated with specific agonist poly(I:C). A statistically significant reduced survival at 28 days was shown in L412F COVID-19 patients treated with the autophagy-inhibitor hydroxychloroquine (p = 0.038). An increased frequency of autoimmune disorders such as co-morbidity was found in L412F COVID-19 males with specific class II HLA haplotypes prone to autoantigen presentation. Our analyses indicate that L412F polymorphism makes males at risk of severe COVID-19 and provides a rationale for reinterpreting clinical trials considering autophagy pathways. Abbreviations: AP: autophagosome; AUC: area under the curve; BafA1: bafilomycin A1; COVID-19: coronavirus disease-2019; HCQ: hydroxychloroquine; RAP: rapamycin; ROC: receiver operating characteristic; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; TLR: toll like receptor; TNF/TNF-α: tumor necrosis factor

SARS-CoV-2 susceptibility and COVID-19 disease severity are associated with genetic variants affecting gene expression in a variety of tissues

Variability in SARS-CoV-2 susceptibility and COVID-19 disease severity between individuals is partly due to genetic factors. Here, we identify 4 genomic loci with suggestive associations for SARS-CoV-2 susceptibility and 19 for COVID-19 disease severity. Four of these 23 loci likely have an ethnicity-specific component. Genome-wide association study (GWAS) signals in 11 loci colocalize with expression quantitative trait loci (eQTLs) associated with the expression of 20 genes in 62 tissues/cell types (range: 1:43 tissues/gene), including lung, brain, heart, muscle, and skin as well as the digestive system and immune system. We perform genetic fine mapping to compute 99% credible SNP sets, which identify 10 GWAS loci that have eight or fewer SNPs in the credible set, including three loci with one single likely causal SNP. Our study suggests that the diverse symptoms and disease severity of COVID-19 observed between individuals is associated with variants across the genome, affecting gene expression levels in a wide variety of tissue types

Calibration of the CMS hadron calorimeters using proton-proton collision data at root s=13 TeV

Methods are presented for calibrating the hadron calorimeter system of theCMSetector at the LHC. The hadron calorimeters of the CMS experiment are sampling calorimeters of brass and scintillator, and are in the form of one central detector and two endcaps. These calorimeters cover pseudorapidities vertical bar eta vertical bar ee data. The energy scale of the outer calorimeters has been determined with test beam data and is confirmed through data with high transverse momentum jets. In this paper, we present the details of the calibration methods and accuracy.Peer reviewe