Outer zone radiation belt electrons can undergo gyroresonant interaction with various magnetospheric wave modes including whistler-mode chorus outside the plasmasphere and both whistler-mode hiss and electromagnetic ion cyclotron (EMIC) waves inside the plasmasphere. To evaluate timescales for electron momentum diffusion and pitch angle diffusion, we utilize bounce-averaged quasi-linear diffusion coefficients for field-aligned waves with a Gaussian frequency spectrum in a dipole magnetic field. Timescales for momentum diffusion of MeV electrons due to VLF chorus can be less than a day in the outer radiation belt. Equatorial chorus waves (∣λ W ∣ 15 deg) are also present. Our calculations confirm that chorus diffusion is a viable mechanism for generating relativistic (MeV) electrons in the outer zone during the recovery phase of a storm or during periods of prolonged substorm activity when chorus amplitudes are enhanced. Radiation belt electrons are subject to precipitation loss to the atmosphere due to resonant pitch angle scattering by plasma waves. The electron precipitation loss timescale due to scattering by each of the wave modes, chorus, hiss, and EMIC waves, can be 1 day or less. These wave modes can separately, or in combination, contribute significantly to the depletion of relativistic (MeV) electrons from the outer zone over the course of a magnetic storm. Efficient pitch angle scattering by whistler-mode chorus or hiss typically requires high latitude waves (∣λ W ∣ > 30 deg). Timescales for electron acceleration and loss generally depend on the spectral properties of the waves, as well as the background electron number density and magnetic field. Loss timescales due to EMIC wave scattering also depend on the ion (H+, He+, O+) composition of the plasma. Complete models of radiation belt electron transport, acceleration and loss should include, in addition to radial (cross-L) diffusion, resonant diffusion due to gyroresonance with VLF chorus, plasmaspheric hiss, and EMIC waves. Comprehensive observational data on the spectral properties of these waves are required as a function of spatial location (L, MLT, MLAT) and magnetic activity.
Upon the closing of the merger, C&J and Keane will create a new leading well completion and production services company to be called NexTier Oilfield Solutions C&J Energy Services and Keane shareholders approve merger of equals, announce new combined company name. Photo: courtesy of rawpixel from Pixabay. C&J Energy Services, Inc. (“C&J”) (NYSE: CJ) and Keane Group, Inc. (“Keane”) (NYSE: FRAC) today announced that the shareholders of both companies approved all of the proposals necessary for the closing of the previously announced all-stock merger of equals between Keane and C&J. The merger of equals is anticipated to close on October 31, 2019, following the satisfaction of other customary closing conditions.At the special meeting of C&J shareholders held today in Houston, Texas, C&J shareholders voted to approve the pending transaction with Keane. Approximately 83% of the outstanding shares of C&J common stock voted at the C&J special meeting, with more than 99% of the votes cast in favor of adoption of the merger agreement.At the special meeting of Keane shareholders held today in Houston, Texas, Keane shareholders voted to approve the pending transaction with C&J. Approximately 90% of the outstanding shares of Keane common stock voted at the Keane special meeting, with more than 99% of the votes cast in favor of approving the issuance of Keane common stock to current C&J stockholders pursuant to the merger agreement.Upon the closing of the merger, C&J and Keane will create a new leading well completion and production services company to be called NexTier Oilfield Solutions Inc. NexTier Oilfield Solutions’ common stock will trade on the New York Stock Exchange under the ticker symbol “NEX”.“We are pleased that shareholders voted in favor of this combination, which creates an industry-leading, diversified oilfield services provider,” said Robert Drummond, the designated Chief Executive Officer of NexTier Oilfield Solutions Inc. “Today’s approvals represent a key milestone in completing the transaction and clearly support our view that this merger of equals will provide many strategic and financial benefits, with our increased scale and density across services and geographies and a prominent presence in the most active U.S. basins.”“We appreciate the strong support we have received from shareholders for the transaction,” said Don Gawick, President and Chief Executive Officer of C&J. “In forming a leading U.S. well completions and production services company with Keane, we look forward to continuing our work together to realize the value this combination can bring to our employees, shareholders, customers, suppliers, and the communities in which we operate.”C&J and Keane will each file the final vote results for their respective special meetings on a Form 8-K with the U.S. Securities and Exchange Commission. Source: Company Press Release
Sandwich brand Cranks has chosen the winner of its NPD competition, The Great Cranks Student Sandwich Challenge, launched earlier this year.Gemma Carey, a student at Manchester Metropolitan University was named the winner with her Tzat’s Tasty sandwich, featuring rocket salad, sunblushed tomatoes, olives and crumbly cheese, topped with lashings of tzatziki.Designed to encourage aspiring marketeers, the competition call for students to create the next Cranks sandwich NPD, for the chance to see it happen for real.The winner was awarded £500-worth of vouchers and the chance to see their sandwich on the shelves in 2014. Carey will now be involved in the development process which will take her prototype from paper to the shelves at university alongside Cranks existing range.Individuals and teams from universities across the UK were invited to submit designs for a sandwich, as well as a breakdown of focus group feedback, market theory behind the flavour combinations and a promotional strategy.More than 100 students registered to take part, with five finalists selected through an online vote hosted on Crank’s Facebook page.
In one of the largest efforts to build a comprehensive catalog of genetic vulnerabilities in cancer, researchers from the Broad Institute of MIT and Harvard and Dana-Farber Cancer Institute have identified more than 760 genes upon which multiple types of cancer cells are strongly dependent for their growth and survival.Many of these “dependencies,” the researchers report today in the journal Cell, are specific to certain cancer types. However, about 10 percent of them are common across multiple cancers, suggesting that a relatively small number of therapies targeting these core dependencies might each hold promise for combating several tumors.To generate these findings, the research team conducted genome-wide RNA interference (RNAi) screens on 501 cell lines representing more than 20 types of cancer, silencing more than 17,000 genes individually in each line to identify genetic dependencies unique to cancerous cells.Cancer cells can harbor a broad variety of genetic errors, from small mutations to wholesale swaps of DNA between chromosomes. If an error shuts down a critical gene, a cancerous cell will compensate by adjusting other genes’ activity, frequently developing a dependence on such adaptations in order to persist.Graphic: The Broad Institute of MIT and HarvardIdentifying these dependencies provides opportunities for scientists to gain deeper insight into cancer biology and determine new therapeutic targets.“Much of what has been and continues to be done to characterize cancer has been based on genetics and sequencing. That’s given us the parts list,” said study co-senior author William Hahn, an institute member in the Broad Cancer Program, chief of the Division of Molecular and Cellular Oncology at Dana-Farber, and a leader in the Cancer Dependency Map initiative, a joint effort spanning the Broad Institute and Dana-Farber. “Mapping dependencies ascribes function to the parts and shows you how to reverse-engineer the processes that underlie cancer.”RNAi silences genes using small pieces of RNA called small interfering RNAs (siRNAs). To run a genome-wide RNAi screen, researchers expose cells to pools of siRNAs and track the cells’ behavior.“The simplest thing one can do with perturbed cells is allow them to keep growing over time and see which ones thrive,” explained study co-senior author David Root, an institute scientist and director of the Genetic Perturbation Platform at the Broad. “If cells with a certain gene silenced disappear, for example, it means that gene is essential for proliferation.”The data revealed striking patterns in cancer cells’ dependencies. Many dependencies were cancer-specific, in that silencing each affected only a subset of the cell lines. However, more than 90 percent of the cell lines had a strong dependency on at least one of a set of 76 genes, suggesting that many cancers rely on a relatively few genes and pathways.Using a set of molecular features (e.g., mutations, gene copy numbers, expression patterns) from each cell line, the team also generated biomarker-based models that helped explain the biology behind 426 of the 769 dependencies. Most of those biomarkers fell into four broad categories:Mutation(s) of a gene;Loss of a copy or reduced expression of a gene;Increased expression of a gene;Reliance on a gene functionally or structurally related to another, lost gene (a.k.a., a paralog dependence).Surprisingly, more than 80 percent of the dependencies with biomarkers were associated with changes (up or down) in a gene’s expression. Mutations, often used as the grounds for pursuing a gene as a drug target, accounted for merely 16 percent of biomarker-associated dependencies.Twenty percent of the dependencies the team discovered were associated with genes previously identified as potential drug targets.“We can’t say we’ve found everything, but we can say that the genes we’re seeing fall into a relatively small number of bins, some of which are familiar, some less so,” Hahn said. “That initial taxonomy is a great starting point for building a full map.”“Our results provide a starting point for therapeutic projects to decide where to focus their efforts,” said study co-first author Francisca Vazquez, a Cancer Dependency Map project leader. She added that while there was still much to do to validate the list, “It’s becoming increasingly easier to triangulate data and generate hypotheses as more genome-scale systematic data sets, like those from the Cancer Cell Line Encyclopedia, Genotype-Tissue Expression, and the Cancer Genome Atlas projects, become available.“Bringing of all the data together will help us generate a truly comprehensive cancer dependency map.”To eliminate false-positive results caused by seed effects — a phenomenon by which siRNAs inadvertently silence irrelevant genes — study co-first author Aviad Tsherniak led the development of a novel computational tool dubbed DEMETER.“People sometimes take a dim view of RNAi because seed effects make the data so noisy,” said Tsherniak, leader of the Broad Cancer Program’s Data Science group. “DEMETER models gene knockdown and seed effects within the data, and computationally subtracts the seed effects. It cleans up the data and helps you find true dependencies.”According to Hahn, the data argue that the time is ripe to pay more attention to the broader landscape of functional aspects of cancer, in addition to focusing on protein-coding gene mutations and variations.“I think we’re close to the end of finding genes that are mutated or focally amplified in cancer,” he said. “To me, that’s a huge opportunity, because it means we have many heretofore untapped avenues for understanding cancer.”Jesse Boehm, associate director of the Broad Cancer Program, and Todd Golub, director of the Cancer Program and chief scientific officer of the Broad Institute, were also co-senior authors on this study.Complete results from the study are available through a dedicated portal.This work was conducted as part of the Slim Initiative in Genomic Medicine for the Americas (SIGMA), a joint U.S.-Mexico project funded by the Carlos Slim Foundation. SIGMA focuses on several key diseases with particular relevance to public health in Mexico and Latin America, including type 2 diabetes and cancer. Additional funding was provided by the National Cancer Institute.
New tool finds compounds that inhibit enzymes, enabling more precise and efficient technologies Pig organs for human patients: A challenge fit for CRISPR Brian Liau didn’t want the standard off-white. He wanted bold, bright, and unexpected.To work out his new lab’s paint scheme, Liau came up with a systematic — or, one could say, scientific — process. He left patches of various paint colors on the walls for days to assess the long-term impression they made. He eliminated options, selected his favorites, and opened the final decision to a lab-wide vote. Now, morning-glory blue blooms in the hallway, sunrise orange enlivens the tissue-culture room, and a soft spa green pops up wherever an accent is needed.But within those sunny walls, Liau, an assistant professor of Chemistry and Chemical Biology, investigates a dark problem: how to beat cancer, in particular acute myeloid leukemia (AML), which the American Cancer Society predicts will kill 11,000 people in the U.S. in 2019.Two out of three AML patients achieve remission with chemotherapy. To help patient No. 3, drug developers are trying a different tack. Since AML starts in the bone marrow when mutated genes fail to prevent blood cells from replicating again and again and growing into tumors, new drugs aim to reverse the mutation’s effects, reclaim hijacked cells, and halt growth. But these drugs don’t always work.Now, in a paper published in Nature Chemical Biology, Liau explains how certain AML drugs work.Using a new technique he calls CRISPR-suppressor scanning, Liau combines CRISPR scanning, a form of gene editing, with small-molecule profiling (a way to screen numerous drug molecules in one go) to investigate how current drugs fit into the nooks and crannies of the malfunctioning genes they target. He and his team systematically identify mutations in LSD1, a critical protein in AML, and in doing so expose details about the relationship between cells and the drugs used on them that may one day lead to faster, more targeted treatments not just for that third patient but for all cancer patients.Designing a drug is far more complicated than designing a new lab space. But, just like blue can be periwinkle, sky, or sapphire, each drug molecule can have many variations. Developers tinker with these to see if slight alterations — a bump on this side, a hole on the other — make their treatments more or less effective.“As chemists, we have the ability to make nearly anything,” Liau said. “Now, we have the unprecedented ability to systematically change protein structure directly in cells.”Epigenetic changes occur when genes are switched on or off by environmental factors — often things like diet, exercise, and chemical exposure. But in the subtype of AML Liau and his colleagues looked at, mutated genes trigger epigenetic shifts, reprogramming blood cells to grow out of control. Enzymes often regulate the conversation between genes and the cells they supervise, but in this case these proteins malfunction.,Drug developers try to stop the excess growth this causes by impeding the malfunctioning proteins. But most researchers manipulate only one side — the attacking drug. Liau manipulated both drug and protein. LSD1 was his first target.Proteins are like bicycles: They have both essential and nonessential parts, or domains. Without handlebars, for example, the machine can still move; but without wheels, it stops. So, Liau and his team searched for LSD1’s “wheels,” hoping to dismantle them, halting the protein malfunction and the disease.The gene-editing tool CRISPR can make precise cuts in genetic code (DNA). Liau and his group used the tool to execute systematic but random slices across the LSD1 gene.When the cell steps in to repair the cut, tiny scars can form in the genome. These scars produce various kinds of mutant genes, which then produce mutant proteins. One mutant loses handlebars, another pedals, and eventually, one loses its wheels. Even though the first two proteins lost some parts, their cancerous cells live on. But the last is immobilized, and growth shuts down.With their systematic approach, the Liau team can classify which LSD1 weaknesses drug developers can exploit.Still, some mutations can backfire and make proteins less susceptible to drugs. So, the Liau group also examines how each drug interacts with each mutant. Once again, some mutants die while others persist in malignant growth.“Maybe I add something on the drug, like make it bigger or add a bump,” Liau says. “Or maybe I add something to the protein, like a hole. If the bump-hole complement each other, we can tease this information apart with this method.”Liau’s group explored how bumps and holes affect how AML drugs target the mutated LSD1 protein, and they discovered something unexpected: One reason the drugs don’t always work is because they don’t work the way people originally thought. Researchers ID molecules that rein in CRISPR systems Related Through a new license, Harvard lab’s innovations in genome engineering might help to solve the shortage of organs for transplant Drugs that target LSD1 shut down the protein’s enzymatic function. But they also cut off communication between the protein and the transcription factor GFI1B, an important player that helps control the epigenome, or the epigenetic state of the cells. Even though the drugs sometimes work because they sometimes disrupt both actions, the Liau group’s new technique showed that the LSD1-GFI1B relationship is most critical for AML survival. Armed with this new information, pharmaceutical companies can focus their work, hasten drug development, and produce more targeted treatment.Next, Liau and his team plan to investigate more bumps and holes on LSD1, the protein’s darkest corners, and other cancer-relevant proteins. Before, according to Liau, “It wasn’t completely appreciated or understood why certain cancers were sensitive to LSD1 inhibitors.” Now, his technique could reveal new and more potent sensitivities, leading to more effective and efficient treatments for cancer.
Smoke Stack and the Foothill Fury Smokestack & The Foothill Fury, given name Jarod Yerkes, is a vagabond minstrel, a one-man band, traveling the country with his self-styled punk-country-blues. He summons in equal parts the spirits of Son House and Joe Strummer, belting his raspy baritone over a furious slide guitar and a snare/bass drum rhythm section that he plays with his feet. His debut is a 15-track, 45-minute blues explosion that is absolutely, unapologetically balls to the wall—sonic bursts of backwoods bravado.
Sign up for our COVID-19 newsletter to stay up-to-date on the latest coronavirus news throughout New York The emails of New York officials will no longer be automatically deleted after 90 days, aides to Gov. Andrew Cuomo announced last week in response to political pressure over the purge policy.It’s been a slow burn leading to the policy shift. The purge policy was first reported by the Albany Times Union back in mid-2013, but didn’t stir much protest until more recently, following coverage by ProPublica and Capital New York.At a public meeting Friday, aides to the governor said they had reviewed the policies of other states and, going forward, any email deletion would be manual. That means more government communications should be retained and be accessible in response to public records requests or in the case of investigations of wrongdoing.Good government groups welcomed the move, writing in an open letter that it “shows the power the governor has to lead by example to increase transparency” — rare praise for Cuomo, whose administration has generally been marked by secrecy.Since the purge policy has been in effect for about two years in some state agencies, it’s probable that some public records have been lost.“The purged emails are not coming back,” said John Kaehny, head of the pro-transparency group Reinvent Albany, in an email. “There is no Freedom of Information Law or archive ‘police’ to ensure that email records are actually being saved.”Kaehny also noted that government officials sometimes use their non-government emails for work-related correspondence, another way to avoid public disclosure. We’ve previously reported on aides to Cuomo using private email accounts to conduct public business.The deletion of emails and the use of private accounts has become a recurring issue for politicians across the country, from Hillary Clinton’s controversial use of her own email server when she was secretary of state to aides to New Jersey Gov. Chris Christie using private accounts to communicate during what later became known as the Bridgegate scandal.Earlier this month, the email issue emerged in Kansas, where the Wichita Eagle reported that Gov. Sam Brownback uses a private account, potentially putting his communications outside the bounds of the state’s freedom of information law.ProPublica is a Pulitzer Prize-winning investigative newsroom. Sign up for their newsletter.
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I just received word that Larry Sintz of Brookville will be inducted into the Indiana Refereeing Hall of Fame this summer. Larry has been a referee for most of his adult life. His tourney resume for both boys and girls numbers over 100 tourney games officiated. Larry was one of those referees who was always on an even keel. His laid back style worked well for both players and coaches. In recent years Larry spent a lot of time refereeing volleyball.I not only know Larry as a referee but also as a former sports writer and friend. He worked for the Brookville Democrat as the sports editor until his retirement. While I was actively coaching, Larry wrote a lot of articles about my coaching results here at Batesville. He was always very positive and very fair in all of his reporting. Congratulations, Larry! It is a well-deserved honor!
Ludovico Nitoglia had two tries while Mat Berquist kept the points flowing from his boot as Munster missed out on the chance to become the first side ever to begin a league season with maximum points from their opening three games. Keith Earls and Stephen Archer both crossed Munster, but ill discipline cost them as Berquist amassed 19 points, scoring five penalties, while three different Munster players endured spells in the sin bin. Press Association Things began well for Munster as they bossed the opening stages with Earls opening the scoring with a seventh-minute try. But Ian Keatley, having already missed a penalty, was off target with the conversion, and two Berquist penalties soon saw the momentum swing the other way. Munster regained the lead with a penalty try when Treviso’s scrum collapsed after a gutsy call from captain Peter O’Mahony, Keatley finding his aim this time to make it 12-6. Another Berquist penalty cut the deficit before half-time but when Archer crossed early in the second half, Keatley’s conversion pushed Munster’s advantage into double figures and all looked well for the Irish. That feeling lasted only a couple of minutes before Nitoglia notched his first try, and Berquist’s penalty on the hour mark had the teams tied once more. Nitoglia then dove over from close range for his second score and Berquist sealed it with Munster again down in numbers as Cathal Sheridan took his turn in the sin bin. ends Munster were knocked off the top of the RaboDirect PRO12 table as they were upset 29-19 by Benetton Treviso in Italy.