Erikssonsilva3505
On the 23 March 2020, a country-wide COVID-19 lockdown was imposed on the UK. The following 100 days saw anthropogenic movements quickly halt, before slowly easing back to a "new" normality. In this short communication, we use data from official UK air-quality sensors (DEFRA AURN) and the UK Met Office stations to show how lockdown measures affected air quality in the UK. We compare the 100 days post-lockdown (23 March to 30 June 2020) with the same period from the previous 7 years. We find, as shown in numerous studies of other countries, the nitrogen oxides levels across the country dropped substantially (∼ 50%). However, we also find the ozone levels increased (∼ 10%), and the levels of sulphur dioxide more than doubled across the country. These changes, driven by a complex balance in the air chemistry near the surface, may reflect the influence of low humidity as suggested by Met Office data, and potentially, the reduction of nitrogen oxides and their interactions with multiple pollutants.It is often assumed that people with high ability in a domain will be excellent raters of quality within that same domain. This assumption is an underlying principle of using raters for creativity tasks, as in the Consensual Assessment Technique. While several prior studies have examined expert-novice differences in ratings, none have examined whether experts' ability to identify the quality of a creative product is being driven more by their ability to identify high quality work, low quality work, or both. To address this question, a sample of 142 participants completed individual difference measures and rated the quality of several sets of creative captions. Unbeknownst to the participants, the captions had been identified a prior by expert raters as being of particularly high or low quality. Hierarchical regression analyses revealed that after controlling for participants' background and personality, those who scored significantly higher on any of three external measures of creativity also rated low-quality captions significantly lower than their peers; however, they did not rate the high-quality captions significantly higher. These findings support research in other domains suggesting that ratings of quality may be driven more by the lower end of the quality spectrum than the high end.
Pathological flows in patients with severe aortic stenosis are associated with acquired von Willebrand syndrome. This syndrome is characterized by excessive cleavage of von Willebrand factor by its main protease, A Disintegrin and Metalloproteinase with a Thrombospondin Type 1 Motif, Member 13 (ADAMTS13) leading to decreased VWF function and mucocutaneous bleeding. Aortic valve replacement and correction of the flow behavior to physiological levels reverses the syndrome, supporting the association between pathological flow and acquired von Willebrand syndrome. We investigated the effects of shear and elongational rates on von Willebrand factor cleavage in the presence of ADAMTS13.
We identified acquired von Willebrand syndrome in five patients with severe aortic stenosis. Doppler echography values from these patients were used to develop three computational fluid dynamic (CFD) aortic valve models (normal, mild and severe stenosis). Shear, elongational rates and exposure times identified in the CFD simulations were used as parameters for the design of microfluidic devices to test the effects of pathologic shear and elongational rates on the structure and function of von Willebrand factor.
The shear rates (0-10,000s
), elongational rates (0-1000 s
) and exposure times (1-180 ms) tested in our microfluidic designs mimicked the flow features identified in patients with aortic stenosis. The shear and elongational rates tested
did not lead to excessive cleavage or decreased function of von Willebrand factor in the presence of the protease.
High shear and elongational rates in the presence of ADAMTS13 are not sufficient for excessive cleavage of von Willebrand Factor.
High shear and elongational rates in the presence of ADAMTS13 are not sufficient for excessive cleavage of von Willebrand Factor.
Induced pluripotent stem cell (iPSC)-derived endothelial cells (ECs) have the potential for therapeutic application in several cardiovascular diseases. Mechanical strain is known to regulate EC behavior and stem cell differentiation and may play a role in directing EC differentiation of iPSCs.
, a long non-coding RNA (lncRNA), is known to affect ECs in several mechanically relevant pathologies and may play a role in this process as well. click here Therefore, we investigated expression changes of
resulting from mechanical stimulation during EC differentiation, as well as functional effects on EC tube formation.
iPSCs were subjected to 5% cyclic mechanical strain during EC differentiation. RT-PCR and flow cytometry were used to assess changes in mesoderm differentiation and gene expression in the final ECs as a result of strain. Functional outcomes of mechanically differentiated ECs were assessed with a tube formation assay and changes in
.
was also overexpressed in human umbilical vein endothelial cells (HUVECs) to assess its role in non-
-expressing ECs.
Mechanical strain promoted mesoderm differentiation, marked by increased expression of brachyury 24 h after initiation of differentiation. Strain also increased expression of
,
, VE-cadherin, and
in differentiated ECs. Strain-differentiated ECs formed tube networks with higher junction and endpoint density than statically-differentiated ECs. Overexpression of
in HUVECs resulted in similar patterns of tube formation.
expression is increased by mechanical strain and promotes tube branching in iPSC-derived ECs.
H19 expression is increased by mechanical strain and promotes tube branching in iPSC-derived ECs.
NETosis is an innate immune response elicited by activated neutrophils to fight microbial infections. Activated neutrophils release DNA fibers decorated with anti-microbial proteins called neutrophil extracellular traps (NETs) into the extracellular space to trap and kill surrounding microbes.
Here, we show that tumor-derived IL-8 released by cancer cells also activates the release of NETs. Until now, there have been no existing technologies that leverage NETs as an anti-tumor drug delivery vehicle. In this study, we demonstrate the re-engineering of neutrophils to express an apoptosis-inducing chimeric protein, supercharged eGFP-TRAIL, on NETs that can ensnare and kill tumor cells while retaining their anti-microbial capabilities.
We observed significant TRAIL-induced apoptosis in tumor cells captured by TRAIL-decorated NETs.
This work demonstrates NETs as a promising technology to deliver protein in response to local cytokine signals.
This work demonstrates NETs as a promising technology to deliver protein in response to local cytokine signals.
