Meteorology

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Bats of St. Vincent, Lesser Antilles

The chiropteran fauna of the island of Saint Vincent, represented by 12 species, is among the most complex in the Lesser Antilles, being represented by four families including Noctilionidae (1 species), Mormoopidae (1), Phyllostomidae (8), and Molossidae (2). This fauna includes four trophic guilds as represented by Noctilio leporinus (piscivore/insectivore); Glossophaga longirostris and Monophyllus plethodon (nectarivore/pollenivore); Artibeus lituratus, A. schwartzi, Brachyphylla cavernarum, Ardops nichollsi, and Sturnira paulsoni (frugivore); and Pteronotus fuscus, Micronycteris buriri, Molossus molossus, and Tadarida brasiliensis (insectivore). One species—Micronycteris buriri—and two subspecies—Sturnira paulsoni paulsoni and Ardops nichollsi vincentensis—are endemic to the island. Recent advancements in population genomics have led to the discovery of the reticulated evolutionary history of Artibeus schwartzi and it is likely that the formation of the hybrid evolutionary trajectory of this species is linked with classical island biogeography. The bat fauna of St. Vincent is unique in the West Indies, characterized by being a crossroads for species, an outpost for both northern and southern species, the boundary for a multi-island bat fauna as marked by Koopman’s Line, and a site of endemism. Based on our studies, we place the bat fauna of St. Vincent as the southern-most island in the Lesser Antillean Faunal Core

Extracellular Vimentin as a Target Against SARS-CoV-2 Host Cell Invasion

Infection of human cells by pathogens, including SARS-CoV-2, typically proceeds by cell surface binding to a crucial receptor. The primary receptor for SARS-CoV-2 is the angiotensin-converting enzyme 2 (ACE2), yet new studies reveal the importance of additional extracellular co-receptors that mediate binding and host cell invasion by SARS-CoV-2. Vimentin is an intermediate filament protein that is increasingly recognized as being present on the extracellular surface of a subset of cell types, where it can bind to and facilitate pathogens’ cellular uptake. Biophysical and cell infection studies are done to determine whether vimentin might bind SARS-CoV-2 and facilitate its uptake. Dynamic light scattering shows that vimentin binds to pseudovirus coated with the SARS-CoV-2 spike protein, and antibodies against vimentin block in vitro SARS-CoV-2 pseudovirus infection of ACE2-expressing cells. The results are consistent with a model in which extracellular vimentin acts as a co-receptor for SARS-CoV-2 spike protein with a binding affinity less than that of the spike protein with ACE2. Extracellular vimentin may thus serve as a critical component of the SARS-CoV-2 spike protein-ACE2 complex in mediating SARS-CoV-2 cell entry, and vimentin-targeting agents may yield new therapeutic strategies for preventing and slowing SARS-CoV-2 infection

Unique Role of Vimentin Networks in Compression Stiffening of Cells and Protection of Nuclei from Compressive Stress

In this work, we investigate whether stiffening in compression is a feature of single cells and whether the intracellular polymer networks that comprise the cytoskeleton (all of which stiffen with increasing shear strain) stiffen or soften when subjected to compressive strains. We find that individual cells, such as fibroblasts, stiffen at physiologically relevant compressive strains, but genetic ablation of vimentin diminishes this effect. Further, we show that unlike networks of purified F-actin or microtubules, which soften in compression, vimentin intermediate filament networks stiffen in both compression and extension, and we present a theoretical model to explain this response based on the flexibility of vimentin filaments and their surface charge, which resists volume changes of the network under compression. These results provide a new framework by which to understand the mechanical responses of cells and point to a central role of intermediate filaments in response to compression

Extracellular vimentin is sufficient to promote cell attachment, spreading, and motility by a mechanism involving N-acetyl glucosamine-containing structures

Vimentin intermediate !laments form part of the cytoskeleton of mesenchymal cells, but under pathological conditions often associatedwith in ammation, vimentin !laments depolymerize as the result of phosphorylation or citrullination, and vimentin oligomers are secreted or released into the extracellular environment. In the extracellular space, vimentin can bind surfaces of cells and the extracellular matrix, and the interaction between extracellular vimentin and cells can trigger changes in cellular functions, such as activation of !broblasts to a !brotic phenotype. The mechanism by which extracellular vimentin binds external cell membranes and whether vimentin alone can act as an adhesive anchor for cells is largely uncharacterized. Here, we show that various cell types (normal and vimentin null !broblasts, mesenchymal stem cells, and A549 lung carcinoma cells) attach to and spread on polyacrylamide hydrogel substrates covalently linked to vimentin. Using traction force microscopy and spheroid expansion assays, we characterize how different cell types respond to extracellular vimentin. Cell attachment to and spreading on vimentin-coated surfaces is inhibited by hyaluronic acid degrading enzymes, hyaluronic acid synthase inhibitors, soluble heparin or N-acetyl glucosamine, all of which are treatments that have little or no effect on the same cell types binding to collagen-coated hydrogels. These studies highlight the effectiveness of substratebound vimentin as a ligand for cells and suggest that carbohydrate structures, including the glycocalyx and glycosylated cell surface proteins that contain N-acetyl glucosamine, form a novel class of adhesion receptors for extracellular vimentin that can either directly support cell adhesion to a substrate or !ne-tune the glycocalyx adhesive properties

Social interaction, co-worker altruism, and incentives

Social interaction with colleagues is an important job attribute for many workers. To attract and retain workers, managers therefore need to think about how to create and preserve high-quality co-worker relationships. This paper develops a principal-multi-agent model where agents do not only engage in productive activities, but also in social interaction with their colleagues, which in turn creates co-worker altruism. We study how financial incentives for productive activities can improve or damage the work climate. We show that both team incentives and relative incentives can help to create a good work climate