Post-Pandemic Cities: An Urban Lexicon of Accelerations/Decelerations

COVID-19 has stimulated renewed societal and academic debate about the future of cities and urban life. Future visons have veered from the ‘death of the city’ to visual renderings and limited experiments with 15-minute neighbourhoods. Within this context, we as a diverse group of urban scholars sought to examine the emergent ‘post’-COVID city through the production of an urban lexicon that investigates its socio-material contours. The urban lexicon makes three contributions. First, to explore how the pandemic has accelerated certain processes and agendas while at the same time, other processes, priorities and sites have been decelerated and put on hold. Second, to utilise this framing to examine the impacts of the pandemic on how cities are governed, on how urban geographies are managed and lived, and with how care emerged as a vital urban resource. Third, to tease out what might be temporary intensifications and what may become configurational in a variety of urban domains, including governance, platforming, density, crowds, technosolutionism, dwelling, respatialisation, reconcentration, care, improvisation, and atmosphere. The urban lexicon proposes a vocabulary for delineating, describing, and understanding some of the key aspects of the emergent post-pandemic city

Elevated A20 promotes TNF-induced and RIPK1-dependent intestinal epithelial cell death

Intestinal epithelial cell (IEC) death is a common feature of inflammatory bowel disease (IBD) that triggers inflammation by compromising barrier integrity. In many patients with IBD, epithelial damage and inflammation are TNF-dependent. Elevated TNF production in IBD is accompanied by increased expression of the TNFAIP3 gene, which encodes A20, a negative feedback regulator of NF-κB. A20 in intestinal epithelium from patients with IBD coincided with the presence of cleaved caspase-3, and A20 transgenic (Tg) mice, in which A20 is expressed from an IEC-specific promoter, were highly susceptible to TNF-induced IEC death, intestinal damage, and shock. A20-expressing intestinal organoids were also susceptible to TNF-induced death, demonstrating that enhanced TNF-induced apoptosis was a cell-autonomous property of A20. This effect was dependent on Receptor Interacting Protein Kinase 1 (RIPK1) activity, and A20 was found to associate with the Ripoptosome complex, potentiating its ability to activate caspase-8. A20-potentiated RIPK1-dependent apoptosis did not require the A20 deubiquitinase (DUB) domain and zinc finger 4 (ZnF4), which mediate NF-κB inhibition in fibroblasts, but was strictly dependent on ZnF7 and A20 dimerization. We suggest that A20 dimers bind linear ubiquitin to stabilize the Ripoptosome and potentiate its apoptosis-inducing activity

Constitutive intestinal NF-κB does not trigger destructive inflammation unless accompanied by MAPK activation

Constitutive NF-κB activation in IECs induces inflammatory cytokines and chemokines in the lamina propria, but does not result in overt tissue damage unless acute inflammatory insults are present, causing TNF-dependent destruction and barrier disruption

Acute Inflammatory Arthropathy and Hypercalcemia Leading to a Diagnosis of Primary Hyperparathyroidism in a Patient With Known Sarcoidosis.

Calcium pyrophosphate deposition disease (CPPD) is a crystal-induced arthropathy characterized by calcium pyrophosphate crystal deposition in joints and soft tissues. The diagnosis is suggested by the presence of chondrocalcinosis on x-ray but is most often diagnosed by synovial fluid analysis (SFA). CPPD is associated with aging and metabolic disorders such as hyperparathyroidism. In this case, we present an 87-year-old woman with known sarcoidosis who presented with acute arthropathy, hypercalcemia, and radiographic evidence of CPPD. Her hypercalcemia had been attributed to her sarcoidosis in the past without a full workup. Hypercalcemia in the setting of suspected CPPD led to a full workup for hypercalcemia and ultimately led to a diagnosis of primary hyperparathyroidism. This case highlights the importance of a complete evaluation for hypercalcemia in the setting of CPPD, even when another disease, such as sarcoidosis, could explain hypercalcemia. Ultimately, CPPD aided in diagnosing hyperparathyroidism in our patient with known sarcoidosis