Thromboembolic complications of COVID-19

© 2020, American Society of Emergency Radiology. The symptomology of patients afflicted with novel 2019 coronavirus disease (SARS-CoV-2 or COVID-19) has varied greatly, ranging from the asymptomatic state to debilitating hypoxemic respiratory failure caused by severe atypical viral pneumonia. Patients may also develop a hyper-inflammatory state that can lead to multi-organ failure. It has become increasingly apparent that, as part of the hyper-inflammatory state, COVID-19 infection increases susceptibility to systemic thromboembolic complications that can contribute to rapid clinical deterioration or demise. This article aims to review imaging features of various systemic thrombotic complications in six patients with moderate to severe disease. This case series includes examples of pulmonary embolism, stroke, right ventricular thrombosis, renal vein thrombosis, and aortic thrombosis with leg ischemia

Differentiation of Mouse Embryonic Stem Cells into Endoderm without Embryoid Body Formation

Pluripotent embryonic stem cells hold a great promise as an unlimited source of tissue for treatment of chronic diseases such as Type 1 diabetes. Herein, we describe a protocol using all-trans-retinoic acid, basic fibroblast growth factor and dibutyryl cAMP (DBcAMP) in the absence of embryoid body formation, for differentiation of murine embryonic stem cells into definitive endoderm that may serve as pancreatic precursors. The produced cells were analyzed by quantitative PCR, immunohistochemistry and static insulin release assay for markers of trilaminar embryo, and pancreas. Differentiated cells displayed increased Sox17 and Foxa2 expression consistent with definitive endoderm production. There was minimal production of Sox7, an extraembryonic endoderm marker, and Oct4, a marker of pluripotency. There was minimal mesoderm or neuroectoderm formation based on expression levels of the markers brachyury and Sox1, respectively. Various assays revealed that the cell clusters generated by this protocol express markers of the pancreatic lineage including insulin I, insulin II, C-peptide, PDX-1, carboxypeptidase E, pan-cytokeratin, amylase, glucagon, PAX6, Ngn3 and Nkx6.1. This protocol using all-trans-retinoic acid, DBcAMP, in the absence of embryoid bodies, generated cells that have features of definitive endoderm that may serve as pancreatic endocrine precursors

Assessing intraspecific wood density variations of Syzgium sp. in tropical forest of Southwest Sabah

Wood density (WD) is a critical determinant of estimating forest above-ground biomass (AGB) and carbon stock. Thus, heterogeneity in WD on individuals within species trees needs to be scrutinized, and acquisition of fixed WD value is essential to estimate carbon stock with confidence. This study investigated intraspecific variation in WD of Syzgium sp., also known as “Jambu” or “Kelat”. It is the most occurring species in study areas, and is regarded as an economically important species. Firstly, one half-diameter drilling from bark-to-pith measurement was taken per tree using Rinntech Resistograph R650-ED at breast height. Meanwhile, 5.15 mm-diameter core was sampled at 1.30 m above-ground, with DeWalt DCF899HP2 20V impact wrench 950 Nm and Haglöf increment borer. WD was estimated for each core sample using a dimensional method. Drilling resistance (DR) profiles were processed using DECOM 2.38m1 Scientific (c), and several independent variables were extracted from the resistogram. All resistogram-derived variables were positively correlated with field WD (R: 0.2 – 0.70). In addition, variability on WD in Syzgium sp. population is predominantly explained by the Resistograph amplitude, expressed as mean raw scale of adjusted DR (DRadj.RawSC) in a regression model. Given that intraspecific variation in WD is a crucial conjecture in forest AGB estimation, it is recommended to analyze with larger samples, and in-depth exploration on Resistograph-based variables is deemed to improve the accuracy of WD prediction models

Vertical accuracy comparison of multi-source Digital Elevation Model (DEM) with Airborne Light Detection and Ranging (LiDAR)

Digital Elevation Model (DEM) is a digital representation of ground surface topography or terrain. There are many freely available DEM data with a spatial resolution of 30 m to 90 m. Nevertheless, their vertical accuracy may vary, depending on the vegetation cover and terrain characteristics. This study examined the vertical accuracy of open-access global DEMs (ALOS PALSAR, ASTER GDEM3, SRTM, TanDEM-X) and fused DEM (EarthEnvDEM90, MERIT DEM). Their performances were assessed using a Digital Terrain Model (DTM) generated using airborne LiDAR data that had an outstanding absolute vertical accuracy (mean error (ME) = 0.24 m; root mean square error (RMSEz) = 1.20 m). Height differences between the global DEMs and the LiDAR DTM were calculated and examined their performances by forested vs. non-forested, slope, and elevation classes. The results showed the MERIT DEM was superior to other DEMs in most of the testing methods. It outperformed other DEMs with an RMSEz value of 3.02 m in the forested areas, followed by ALOS PALSAR (9.29 m), EarthEnv-DEM90 (9.40 m), SRTM (9.80 m), TanDEM-X (10.41 m), and ASTER GDEM3 (12.57 m). The MERIT DEM also had the best accuracy in the higher elevation areas. Overall, the ASTER GDEM3 had the worst accuracies, with relatively large over-estimations compared to other DEMs. Despite its low spatial resolution, the MERIT DEM was the best for representing terrain elevation for applications over a large area

Expected Performance of the ATLAS Experiment - Detector, Trigger and Physics

A detailed study is presented of the expected performance of the ATLAS detector. The reconstruction of tracks, leptons, photons, missing energy and jets is investigated, together with the performance of b-tagging and the trigger. The physics potential for a variety of interesting physics processes, within the Standard Model and beyond, is examined. The study comprises a series of notes based on simulations of the detector and physics processes, with particular emphasis given to the data expected from the first years of operation of the LHC at CERN

Search for direct stau production in events with two hadronic tau-leptons in root s=13 TeV pp collisions with the ATLAS detector

A search for the direct production of the supersymmetric partners ofτ-leptons (staus) in final stateswith two hadronically decayingτ-leptons is presented. The analysis uses a dataset of pp collisions corresponding to an integrated luminosity of139fb−1, recorded with the ATLAS detector at the LargeHadron Collider at a center-of-mass energy of 13 TeV. No significant deviation from the expected StandardModel background is observed. Limits are derived in scenarios of direct production of stau pairs with eachstau decaying into the stable lightest neutralino and oneτ-lepton in simplified models where the two staumass eigenstates are degenerate. Stau masses from 120 GeV to 390 GeV are excluded at 95% confidencelevel for a massless lightest neutralino

B7-H4 Treatment of T Cells Inhibits ERK, JNK, p38, and AKT Activation

B7-H4 is a newly identified B7 homolog that plays an important role in maintaining T-cell homeostasis by inhibiting T-cell proliferation and lymphokine-secretion. In this study, we investigated the signal transduction pathways inhibited by B7-H4 engagement in mouse T cells. We found that treatment of CD3+ T cells with a B7-H4.Ig fusion protein inhibits anti-CD3 elicited T-cell receptor (TCR)/CD28 signaling events, including phosphorylation of the MAP kinases, ERK, p38, and JNK. B7-H4.Ig treatment also inhibited the phosphorylation of AKT kinase and impaired its kinase activity as assessed by the phosphorylation of its endogenous substrate GSK-3. Expression of IL-2 is also reduced by B7-H4. In contrast, the phosphorylation state of the TCR proximal tyrosine kinases ZAP70 and lymphocyte-specific protein tyrosine kinase (LCK) are not affected by B7-H4 ligation. These results indicate that B7-H4 inhibits T-cell proliferation and IL-2 production through interfering with activation of ERK, JNK, and AKT, but not of ZAP70 or LCK

Publisher Correction: Toxoplasma Modulates Signature Pathways of Human Epilepsy, Neurodegeneration & Cancer.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper

Pten (phosphatase and tensin homologue gene) haploinsufficiency promotes insulin hypersensitivity

AIMS/HYPOTHESIS: Insulin controls glucose metabolism via multiple signalling pathways, including the phosphatidylinositol 3-kinase (PI3K) pathway in muscle and adipose tissue. The protein/lipid phosphatase Pten (phosphatase and tensin homologue deleted on chromosome 10) attenuates PI3K signalling by dephosphorylating the phosphatidylinositol 3,4,5-trisphosphate generated by PI3K. The current study was aimed at investigating the effect of haploinsufficiency for Pten on insulin-stimulated glucose uptake. MATERIALS AND METHODS: Insulin sensitivity in Pten heterozygous (Pten(+/−)) mice was investigated in i.p. insulin challenge and glucose tolerance tests. Glucose uptake was monitored in vitro in primary cultures of myocytes from Pten(+/−) mice, and in vivo by positron emission tomography. The phosphorylation status of protein kinase B (PKB/Akt), a downstream signalling protein in the PI3K pathway, and glycogen synthase kinase 3β (GSK3β), a substrate of PKB/Akt, was determined by western immunoblotting. RESULTS: Following i.p. insulin challenge, blood glucose levels in Pten(+/−) mice remained depressed for up to 120 min, whereas glucose levels in wild-type mice began to recover after approximately 30 min. After glucose challenge, blood glucose returned to normal about twice as rapidly in Pten(+/−) mice. Enhanced glucose uptake was observed both in Pten(+/−) myocytes and in skeletal muscle of Pten(+/−) mice by PET. PKB and GSK3β phosphorylation was enhanced and prolonged in Pten(+/−) myocytes. CONCLUSIONS/INTERPRETATION: Pten is a key negative regulator of insulin-stimulated glucose uptake in vitro and in vivo. The partial reduction of Pten due to Pten haploinsufficiency is enough to elicit enhanced insulin sensitivity and glucose tolerance in Pten(+/−) mice