Bony avulsion of the supraspinatus origin from the scapular spine

We describe a case of an avulsion of the scapular spine at the origin of the supraspinatus muscle, with successful conservative treatment. An isolated avulsion is rare, as most avulsions occur in combination with other (more severe) injuries such as fractures of the scapula body or neck, coracoid process, glenoid or humerus. These injuries are mostly seen in high-energy trauma cases and need their own specific treatment. One should therefore always rule out concurrent trauma before treating conservatively

From Prototyping to Allotyping. The invention of change of use and the crisis of building types

The chapter analyses the invention and the form of the discourse on building conversion as one particular instance of redefining what a technology is and how it operates. I describe a shift from expert defined closure to lay based openness and tinkering as a shift from prototyping to allotyping: Since the early 1970s, change of use and building conversion have become a central and fashionable discourse among architects and architectural theorists. Before the 1970s, buildings were understood as technologies, as ‘society made durable’. The notion of building type was central to link a building to a given use. A bank was a bank because architects applied existing templates, prototypes, to turn a building into a bank. In the 1970s, suddenly buildings became flexible – discursively, since building conversion always existed: ‘Building type’ no longer was a meaningful link between a building and its use. A bank should not stay a bank, but become a hotel, a theatre or a flat, in short: an allotype. The chapter elucidate this central shift in thinking about buildings and reflects on the special case of allotyping buildings and how it continues to vex thinking about buildings

Blood Biomarkers in Idiopathic Pulmonary Fibrosis.

PURPOSE: Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease of unknown origin whose incidence has been increasing over the latest decade partly as a consequence of population ageing. New anti-fibrotic therapy including pirfenidone and nintedanib have now proven efficacy in slowing down the disease. Nevertheless, diagnosis and follow-up of IPF remain challenging. METHODS: This review examines the recent literature on potentially useful blood molecular and cellular biomarkers in IPF. Most of the proposed biomarkers belong to chemokines (IL-8, CCL18), proteases (MMP-1 and MMP-7), and growth factors (IGBPs) families. Circulating T cells and fibrocytes have also gained recent interest in that respect. Up to now, though several interesting candidates are profiling there has not been a single biomarker, which proved to be specific of the disease and predictive of the evolution (decline of pulmonary function test values, risk of acute exacerbation or mortality). CONCLUSION: Large scale multicentric studies are eagerly needed to confirm the utility of these biomarkers

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease

IL-1/inhibitory kappa B kinase epsilon-induced glycolysis augment epithelial effector function and promote allergic airways disease

BACKGROUND: Emerging studies suggest that enhanced glycolysis accompanies inflammatory responses. Virtually nothing is known about the relevance of glycolysis in patients with allergic asthma. OBJECTIVES: We sought to determine whether glycolysis is altered in patients with allergic asthma and to address its importance in the pathogenesis of allergic asthma. METHODS: We examined alterations in glycolysis in sputum samples from asthmatic patients and primary human nasal cells and used murine models of allergic asthma, as well as primary mouse tracheal epithelial cells, to evaluate the relevance of glycolysis. RESULTS: In a murine model of allergic asthma, glycolysis was induced in the lungs in an IL-1-dependent manner. Furthermore, administration of IL-1beta into the airways stimulated lactate production and expression of glycolytic enzymes, with notable expression of lactate dehydrogenase A occurring in the airway epithelium. Indeed, exposure of mouse tracheal epithelial cells to IL-1beta or IL-1alpha resulted in increased glycolytic flux, glucose use, expression of glycolysis genes, and lactate production. Enhanced glycolysis was required for IL-1beta- or IL-1alpha-mediated proinflammatory responses and the stimulatory effects of IL-1beta on house dust mite (HDM)-induced release of thymic stromal lymphopoietin and GM-CSF from tracheal epithelial cells. Inhibitor of kappaB kinase epsilon was downstream of HDM or IL-1beta and required for HDM-induced glycolysis and pathogenesis of allergic airways disease. Small interfering RNA ablation of lactate dehydrogenase A attenuated HDM-induced increases in lactate levels and attenuated HDM-induced disease. Primary nasal epithelial cells from asthmatic patients intrinsically produced more lactate compared with cells from healthy subjects. Lactate content was significantly higher in sputum supernatants from asthmatic patients, notably those with greater than 61% neutrophils. A positive correlation was observed between sputum lactate and IL-1beta levels, and lactate content correlated negatively with lung function. CONCLUSIONS: Collectively, these findings demonstrate that IL-1beta/inhibitory kappaB kinase epsilon signaling plays an important role in HDM-induced glycolysis and pathogenesis of allergic airways disease