Spectral and spatial observations of microwave spikes and zebra structure in the short radio burst of May 29, 2003

The unusual radio burst of May 29, 2003 connected with the M1.5 flare in AR 10368 has been analyzed. It was observed by the Solar Broadband Radio Spectrometer (SBRS/Huairou station, Beijing) in the 5.2-7.6 GHz range. It proved to be only the third case of a neat zebra structure appearing among all observations at such high frequencies. Despite the short duration of the burst (25 s), it provided a wealth of data for studying the superfine structure with millisecond resolution (5 ms). We localize the site of emission sources in the flare region, estimate plasma parameters in the generation sites, and suggest applicable mechanisms for interpretating spikes and zebra-structure generation. Positions of radio bursts were obtained by the Siberian Solar Radio Telescope (SSRT) (5.7 GHz) and Nobeyama radioheliograph (NoRH) (17 GHz). The sources in intensity gravitated to tops of short loops at 17 GHz, and to long loops at 5.7 GHz. Short pulses at 17 GHz (with a temporal resolution of 100 ms) are registered in the R-polarized source over the N-magnetic polarity (extraordinary mode). Dynamic spectra show that all the emission comprised millisecond pulses (spikes) of 5-10 ms duration in the instantaneous band of 70 to 100 MHz, forming the superfine structure of different bursts, essentially in the form of fast or slow-drift fibers and various zebra-structure stripes. Five scales of zebra structures have been singled out. As the main mechanism for generating spikes (as the initial emission) we suggest the coalescence of plasma waves with whistlers in the pulse regime of interaction between whistlers and ion-sound waves. In this case one can explain the appearance of fibers and sporadic zebra-structure stripes exhibiting the frequency splitting.Comment: 11 pages, 5 figures, in press; A&A 201

Assessment of Potential Augmentation and Management Strategies for Razorback Sucker \u3cem\u3eXyrauchen texanus\u3c/em\u3e in Lake Mead and Grand Canyon: A 2021 Science Panel Summary

Razorback Sucker Xyrauchen texanus is a large-bodied, long-lived species endemic to the Colorado River Basin. This species historically ranged throughout the basin from the Colorado River delta in Mexico to Wyoming and Colorado. Currently, the species persists ,in a small portion of its historical range with the help of intensive management efforts including augmentation. Recruitment to adult life stages is extremely limited in the wild, but is documented consistently in Lake Mead. Research and monitoring efforts in Lake Mead are ongoing since 1996 and have recently expanded to include the Colorado River inflow area and portions of lower Grand Canyon. Despite evidence of recruitment, the current population size in Lake Mead and Grand Canyon is believed to be small (data) and susceptible to stochastic effects. This raised interest in the potential to augment the population to prevent loss of genetic diversity and increase abundance and distribution in general, as well as explore recruitment bottlenecks. To address critical uncertainties surrounding this management option and to brainstorm other potential options, a Planning Committee and Steering Committee made up of representatives of state (Arizona, Nevada), tribal (Hualapai Tribe, Navajo Nation), and federal (Bureau of Reclamation, National Park Service, and U.S. Fish and Wildlife Service) management agencies convened an Expert Science Panel (ESP; 2021), to consider augmentation and management strategies for Razorback Sucker in Lake Mead and Grand Canyon. The purpose of this report is to summarize those findings

Model of the distribution of diastolic left ventricular posterior wall thickness in healthy adults and its impact on the behavior of a string of virtual cardiomyocytes

Correlation of the thickness of the left ventricular posterior wall (LVPWd) with various parameters, including age, gender, weight and height, was investigated in this study using regression models. Multicenter derived database comprised over 4,000 healthy individuals. The developed models were further utilized in the in vitro-in vivo (IVIV) translation of the drug cardiac safety data with use of the mathematical model of human cardiomyocytes operating at the virtual healthy population level. LVPWd was assumed to be equivalent to the length of one-dimensional string of virtual cardiomyocyte cells which was presented, as other physiological factors, to be a parameter influencing the simulated pseudo-ECG (pseudoelectrocardiogram), QTcF and $\Delta$QTcF, both native and modified by exemplar drug (disopyramide) after $I_{Kr}$ current disruption. Simulation results support positive correlation between the LVPWd and QTcF/$\Delta$QTc. Developed models allow more detailed description of the virtual population and thus inter-individual variability influence on the drug cardiac safet

Peroxisome Proliferator-Activated Receptor-Gamma Agonists Suppress Tissue Factor Overexpression in Rat Balloon Injury Model with Paclitaxel Infusion

The role and underlying mechanisms of rosiglitazone, a peroxisome proliferator-activated receptor-gamma (PPAR-γ) agonist, on myocardial infarction are poorly understood. We investigated the effects of this PPAR-γ agonist on the expression of tissue factor (TF), a primary molecule for thrombosis, and elucidated its underlying mechanisms. The PPAR-γ agonist inhibited TF expression in response to TNF-α in human umbilical vein endothelial cells, human monocytic leukemia cell line, and human umbilical arterial smooth muscle cells. The overexpression of TF was mediated by increased phosphorylation of mitogen-activated protein kinase (MAPK), which was blocked by the PPAR-γ agonist. The effective MAPK differed depending on each cell type. Luciferase and ChIP assays showed that transcription factor, activator protein-1 (AP-1), was a pivotal target of the PPAR-γ agonist to lower TF transcription. Intriguingly, two main drugs for drug-eluting stent, paclitaxel or rapamycin, significantly exaggerated thrombin-induced TF expression, which was also effectively blocked by the PPAR-γ agonist in all cell types. This PPAR-γ agonist did not impair TF pathway inhibitor (TFPI) in three cell types. In rat balloon injury model (Sprague-Dawley rats, n = 10/group) with continuous paclitaxel infusion, the PPAR-γ agonist attenuated TF expression by 70±5% (n = 4; P<0.0001) in injured vasculature. Taken together, rosiglitazone reduced TF expression in three critical cell types involved in vascular thrombus formation via MAPK and AP-1 inhibitions. Also, this PPAR-γ agonist reversed the paclitaxel-induced aggravation of TF expression, which suggests a possibility that the benefits might outweigh its risks in a group of patients with paclitaxel-eluting stent implanted

DMSO inhibits human platelet activation through cyclooxygenase-1 inhibition. A novel agent for drug eluting stents?

Background: DMSO is routinely infused together with hematopoietic cells in patients undergoing myeloablative therapy and was recently found to inhibit smooth muscle cells proliferation and arterial thrombus formation in the mouse by preventing tissue factor (TF), a key activator of the coagulation cascade. This study was designed to investigate whether DMSO prevents platelet activation and thus, whether it may represent an interesting agent to be used on drug eluting stents. Methods and results: Human venous blood from healthy volunteers was collected in citrated tubes and platelet activation was studied by cone and platelet analyzer (CPA) and rapid-platelet-function-assay (RPFA). CPA analysis showed that DMSO-treated platelets exhibit a lower adherence in response to shear stress (-15.54+/-0.9427%, n=5, P<0.0001 versus control). Additionally, aggregometry studies revealed that DMSO-treated, arachidonate-stimulated platelets had an increased lag phase (18.0%+/-4.031, n=9, P=0.0004 versus control) as well as a decreased maximal aggregation (-6.388+/-2.212%, n=6, P=0.0162 versus control). Inhibitory action of DMSO could be rescued by exogenous thromboxane A2 and was mediated, at least in part, by COX-1 inhibition. Conclusions: Clinically relevant concentrations of DMSO impair platelet activation by a thromboxane A2-dependent, COX-1-mediated effect. This finding may be crucial for the previously reported anti-thrombotic property displayed by DMSO. Our findings support a role for DMSO as a novel drug to prevent not only proliferation, but also thrombotic complications of drug eluting stents