The six-month Atlantic Ocean hurricane season begins today (June 1), and the National Oceanic and Atmospheric Administration’s Climate Prediction Center is forecasting a near-normal or below-normal season.Long-range hurricane forecasts are of limited value, because meteorologists can’t predict the intensity or track of any individual storm so far in advance. But forecasters can successfully identify factors that make the development of hurricanes more likely.“The main driver of this year’s outlook is the anticipated development of El Niño this summer,” NOAA writes in its 2014 outlook. “El Niño causes stronger wind shear, which reduces the number and intensity of tropical storms and hurricanes. El Niño can also strengthen the trade winds and increase the atmospheric stability across the tropical Atlantic, making it more difficult for cloud systems coming off of Africa to intensify into tropical storms.”NOAA predicts a 50-percent chance of a below-normal season, a 40-percent chance of a near-normal season and only a 10-percent chance of an above-normal season.For the hurricane season, which ends Nov. 30, NOAA predicts a 70-percent likelihood of eight to 13 named storms (winds of 39 mph or higher), of which three to six could become hurricanes (winds of 74 mph or higher), including one to two major hurricanes (Category 3, 4 or 5; winds of 111 mph or higher).These numbers are near or below the seasonal averages of 12 named storms, six hurricanes and three major hurricanes, based on the average from 1981 to 2010. The Atlantic hurricane region includes the North Atlantic Ocean, Caribbean Sea and Gulf of Mexico.Gerry Bell, Ph.D., lead seasonal hurricane forecaster with NOAA’s Climate Prediction Center, said the Atlantic – which has seen above-normal seasons in 12 of the last 20 years – has been in an era of high activity for hurricanes since 1995.“Atmospheric and oceanic conditions across the tropical Pacific are already taking on some El Niño characteristics. Also, we are currently seeing strong trade winds and wind shear over the tropical Atlantic, and NOAA’s climate models predict these conditions will persist, in part because of El Niño,” Bell said. “The expectation of near-average Atlantic Ocean temperatures this season, rather than the above-average temperatures seen since 1995, also suggests fewer Atlantic hurricanes.”NOAA is rolling out new tools at the National Hurricane Center this year. An experimental mapping tool will be used to show communities their storm surge flood threat. The map will be issued for coastal areas when a hurricane or tropical storm watch is first issued, or approximately 48 hours before the anticipated onset of tropical storm force winds. The map will show land areas where storm surge could occur and how high above ground the water could reach in those areas.NOAA’s seasonal hurricane outlook is not a hurricane landfall forecast; it does not predict how many storms will hit land or where a storm will strike. Forecasts for individual storms and their impacts will be provided throughout the season by NOAA’s National Hurricane Center.— From NOAA National Hurricane Center news release__________Sign up for OCNJ Daily’s free newsletter“Like” us on Facebook
By Ryan GivensExcitement filled the docks on Battersea Road Sunday morning, as kids eagerly to board the boats en route for a fun day on out on the bay. The weather could not have been better for the 25th iteration of Fishing for Kids, a day of charity provided by The Ocean City Marlin and Tuna Club and The Ocean City Yacht Club. This event is a highlight of the year for organizers George Robinson, of OCMTC, And Doug Walter, of OCYC.Year after year nearly 150 kids, family members and camp leaders all member of Big Brothers Big Sisters, the Variety Club, or the Challenger League in the Philadelphia area come to participate in a day out in the water. These camps and clubs center around providing mentoring and fun opportunities to either disadvantaged or disabled children, a mission statement in tune with what had inspired Fishing for Kids a quarter century ago.The families made an early trek to Ocean City to begin boarding around 8:30 in the morning. Filling up on sticky buns from Mallon’s bakery, the soon-to-be boaters began to hop on deck. While many first time boat goers we’re apprehensive rocking on the dock, this quickly changed to thrill as the motors began to go taking them out onto the bay.Casting their lines out for a few hours the lucky few returned fish-in-hand. Bringing back their fresh catches, the fish were filleted on the dock ready for dinner later that night. Those not lucky enough to hook a fish themselves still cherishing the gorgeous day on the water. Members of the Ocean City Police and Fire Departments were on hand to assist everyone on and off their boats. Freshly made lunch was served in the Yacht Club so everyone can refuel from their time in the sun and salty air.Of Course the event is not only a great time for families but the boat owners as well. The members of the Ocean City Marlin and Tuna Club and the Ocean City Yacht Club look forward each year to giving these families a chance to share the boating experience with them. Robinson and Walter when organizing the event note a large portion of the boaters volunteer again the next year, and all noting how rewarding an experience it was. With a long history of happy kids, families, and boaters; Fishing with kids has the recipe for a fun and fulfilling event for years to come.Click here to see all the pictures from this wonderful event.
Ingham paper & Packaging (Ottery St Mary, Devon) supplies paper packaging to bakers. Its siliconised greaseproof paper can be both recycled and composted.Envirocoat non-slip paper pallet liners are used to prevent baked produce slipping in transit. The water-based acrylic coating gives excellent non-slip properties, says the firm, and is grease resistant.
Growing voter apathy has long been a worry for politicians, so what better way to appeal to the disaffected – and to the collective sweet tooth of the US electorate – than to decide the presidential election outcome on the number of cookies people buy?Bakery association Retail Bakers of America (RBA) has organised a poll whereby participating bakers tot up the number of election-themed cookies sold. They can then give a running total as a barometer of how the Republicans and Democrats are faring in the run-up to November’s election.”It reflects people’s concerns right now,” said Rose Wilcox, co-owner of the appropriately named Phatso’s Bakery in Chester, Pennsylvania, commenting on the presidential cookies (possibly overlooking the near meltdown of the American economy).The results in so far from participating bakeries who have sent in their totals show the Democrats way out in front.Unfortunately, cookies are not about to replace the ballot card any time soon (though we’d encourage the RBA to keep on lobbying).
WhatsApp WhatsApp (Tommie Lee/95.3 MNC) The South Shore Line will be busing passengers August 10 through August 14 between Carroll Avenue and the South Bend International Airport.The Line says train service between those stops will be canceled Monday through Friday for upgrades to the track and segments of the overhead wire.Buses will run between those stops, but will not be available to and from the Hudson Lake Station.Trains will run as scheduled between Michigan City and Chicago. Google+ South Shore train service disruption planned Facebook Previous articleNotre Dame updates their residence hall policiesNext articleSouth Bend man sentenced to 16 years in prison Tommie Lee Pinterest By Tommie Lee – August 6, 2020 0 349 Pinterest Twitter Google+ IndianaLocalNewsSouth Bend Market Twitter Facebook
“Closer” At the 16th annual Bayou Rendezvous down in New Orleans this year, George Porter, bassist of the iconic funk band The Meters, gathered a number of his friends in the Crescent City to help the New Orleans Musicians Clinic. With help from keyboard wizard Ivan Neville and guitarist Ian Neville of Dumpstaphunk, drummer Stanton Moore of Galactic, guitarist Eric Krasno of Soulive and Lettuce, legendary drummer Johnny Vidacovich, and guitarist Eric McFadden, the group, dubbed the NOLA All-Stars, offered up ninety minutes of pure soul-filled funk. All these stars have someone in their extended musical circles who have been helped by this wonderful charity, and it was clear that they were on the stage to play from the heart.As is often the case with these super jams, there wasn’t much planning or things like setlists—at best, George called out to his stellar friends on percussion to give him a beat. But the cadre of musical killers he had assembled was more than capable of delivering a stellar show of improvised and repurposed funk classics that had the audience moving and grooving into the wee hours. The guitar fireworks by Kras, Neville, and McFadden were spectacular against the rock-solid pocket provided by Moore and Vidacovich. As always, Porter served as both the heart and the soul of each jam and let his sweet tone and canyon-deep fills do the talking.We’ve put together a pair of exclusive clips for your enjoyment featuring the twenty-plus minutes of the show’s opening and closing jams, which were chock full of the inspiration that comes from playing for a cause. The New Orleans Musicians Clinic provides much needed medical assistance to the players who fill New Orleans’ days and nights with song. After you’ve finished checking out the clips below check out the fine work the Clinic does here and give any help you can. Enjoy!“Opener”
Read Full Story Gregory Curci can look at a piece of cast metal and read the craftsman’s skill like an archeologist brushing away the sand from a long-forgotten artifact. Deep in the lines and imperfections of a piece of solid iron weighing thousands of pounds, he sees the hands of the maker.“You can see what almost look like brush marks, it’s like they dug the mold out of the sand,” said Curci, running his hand across the 1,500-pound yoke of the bell that once hung in the spire of the Memorial Church. “Someone put every one of these brush strokes in this casting. A modern casting would look like it came out of a machine. This looks like someone made it by hand and sculpted it out of clay.”Boston artist Gregory Curci was given the task of restoring and preserving a piece of Harvard history that weighs in at nearly 4 tons and was created in London in 1926, the same year Queen Elizabeth II was born. The bell that once called students to Morning Prayers each morning, to classes, and rang across the yard to mark occasions of celebration and sorrow, is now on display on the west portico of the Memorial Church following an extensive restoration.The bell will be dedicated at a ceremony following Morning Prayers Friday, April 21, as part of a weekend of events celebrating the reopening of the church following an eight-month renovation project.
“We took advantage of the fact that this system recognizes mutant DNA but not normal DNA and uses a dual recognition system for enhanced precision,” said study first author Bence György, who conducted the work while at Harvard Medical School and is now at the Institute of Molecular and Clinical Ophthalmology in Basel, Switzerland. “This approach resulted in an unprecedented level of specificity in targeting the mutant gene.”In an initial set of experiments in cells with and without the Beethoven mutation, the tool accurately distinguished between mutant DNA and normal DNA in copies of the Tmc1 gene. Further analysis revealed that in Beethoven cells, which contained one defective and one normal copy of the gene, at least 99 percent of the molecular “cuts” occurred exclusively in the defective copy of the gene.Next, researchers injected the gene-editing treatment into the inner ears of mice with and without the Beethoven mutation. DNA analysis showed that editing activity occurred only in the inner ear cells of mice with the Beethoven defect. No editing changes were detected in cells from the inner ears of treated mice that didn’t have the mutation — a finding that confirmed the tool’s precision.To determine whether the gene-editing therapy interfered with normal gene function, the scientists stimulated hearing cells — called hair cells — from the inner ears of treated mice that didn’t carry the Beethoven defect. The cells showed unchanged, normal hearing responses, affirming that the gene-editing therapy had no effect on normal gene function.Silencing BeethovenTo measure whether the therapy worked in animals rather than just in cells, researchers performed the gold-standard test for hearing. They measured the animals’ auditory brainstem responses, which capture how much sound is detected by hair cells in the inner ear and transmitted to the brain.Without treatment, Beethoven mice typically are completely deaf by 6 months of age. By comparison, mice without the defect retain normal hearing throughout life and can detect sounds at around 30 decibels — a level similar to a whisper.Two months after receiving the therapy, Beethoven mice exhibited markedly better hearing than untreated siblings carrying the genetic mutation. The treated animals were capable of detecting sounds at about 45 decibels — the level of a normal conversation — or about 16 times quieter than untreated mice. The Beethoven mouse with the greatest hearing preservation was capable of hearing sounds at 25 to 30 decibels, virtually indistinguishable from its healthy peers.Taken together, the findings demonstrate that the novel gene therapy effectively silenced the defective copy of the gene and salvaged the animals’ hearing from the rapid demise typically seen in the disease.Because the disease is marked by progressive hearing loss, the researchers assessed the effect of therapy on progression over several months. Researchers administered treatment shortly after birth and tested hearing levels in treated and untreated mice with and without the mutation every four weeks for up to six months. In month one, untreated Beethoven mice could hear low-frequency sounds but had notable hearing loss at high frequencies. By month six after birth, untreated Beethoven mice had lost all their hearing. In contrast, treated Beethoven mice retained near-normal hearing at low frequencies, with some showing near-normal hearing even at high frequencies.Notably, treated animals that didn’t carry the genetic defect did not experience any hearing loss as a result of the gene therapy — a finding that demonstrated the safety of the procedure and its ability to selectively target the aberrant copy of the gene. Even more encouragingly, a small subset of treated Beethoven mice that were followed for nearly a year retained stable, near-normal hearing.,Because the Beethoven defect is marked by progressive deterioration and death of hearing cells in the inner ear, the researchers used electron microscopy to visualize the structure of these critical cells. As expected, in the untreated Beethoven mice, the researchers saw gradual loss of hearing cells along with deterioration in their structure. By contrast, treated Beethoven mice and treated healthy mice both retained a normal number of hearing cells with intact or near-intact structure.In a final experiment, the scientists tested the effect of the treatment in a line of human cells carrying the Beethoven mutation. DNA analysis revealed that treatment caused editing exclusively in the mutant copy of the Tmc1 gene and spared the normal one.Because of its ability to target single-point genetic mutations, the approach holds promise for 15 other forms of inherited deafness also caused by a single-letter mutation in the DNA sequence of other hearing genes.Additionally, the team said, the technique could be adapted for use in other dominantly inherited genetic diseases caused by single-point mutations. To determine its hypothetical utility, the scientists scanned the federal ClinVar database, a national repository of all known genetic mutations linked to human diseases. The analysis showed that based on the tool’s specificity, it could correctly identify 3,759 defective gene variants that are collectively responsible for one-fifth of dominant human genetic mutations.“To be sure, this is the first step in a long journey,” Holt said. “But what we have here is proof of principle that demonstrates this highly specific, highly targeted treatment could be developed to selectively silence genes that carry single-point mutations and potentially treat many other forms of human disease.”Co-investigators in addition to Kleinstiver and Joung included Carl Nist-Lund, Bifeng Pan, Yukako Asai, K. Domenica Karavitaki, Sara Garcia, Mikolaj Zaborowski, Paola Solanes, Sofia Spataro, Bernard Schneider, and Gwenaëlle Géléoc.The work was funded by the Jeff and Kimberly Barber Fund, NIH grants R01-DC013521, R01-DC05439, R01-DC000304, R01-DC016932, DC008853, K99-CA218870, by the Charles A. King Trust, a Banting Postdoctoral Fellowship, the Richard Floor Biorepository Fund, the Kosciuszko Foundation, and the Bertarelli Foundation. Additional support came from a Desmond and Ann Heathwood MGH Research Scholar award and Edward R. and Anne G. Lefler Postdoctoral Fellowship. Scientists at Harvard Medical School and Boston Children’s Hospital have used a novel gene-editing approach to salvage the hearing of mice with genetic hearing loss, and have succeeded in doing so without any apparent off-target effects as a result of the treatment.The animals — known as Beethoven mice — were treated for the same genetic mutation that causes progressive hearing loss in humans, culminating in profound deafness by the mid-20s.The new approach, described online July 3 in Nature Medicine, involves an optimized, more precise version of the classic CRISPR-Cas9 gene-editing system that is better at recognizing the disease-causing mutation seen in Beethoven mice. The refined tool allowed scientists to selectively disable the defective copy of a hearing gene called Tmc1, while sparing the healthy copy.Notably, the researchers report, their system managed to recognize a single incorrect DNA letter in the defective copy among 3 billion letters in the mouse genome.Much more work remains to be done before even a highly precise gene-editing therapy like this one could be used in humans, the researchers cautioned. However, they said, the work represents a milestone because it greatly improves the efficacy and safety of standard gene-editing techniques.“Our results demonstrate that this more-refined, better-targeted version of the now-classic CRISPR/Cas9 editing tool achieves an unprecedented level of identification and accuracy,” said study co-senior investigator David Corey, the Bertarelli Professor of Translational Medical Science in the Blavatnik Institute at Harvard Medical School.Furthermore, the team said, the results set the stage for using the same precision approach to treat other dominantly inherited genetic diseases that arise from a single defective copy of a gene.Everyone inherits two copies of the same gene, one from each parent. In many cases, one normal gene is sufficient to ensure normal function that spares the individual from disease. By contrast, in so-called dominantly inherited genetic disorders, one defective copy can cause illness.“We believe our work opens the door toward a hyper-targeted way to treat an array of genetic disorders that arise from one defective copy of a gene,” said study co-senior investigator Jeffrey Holt, Harvard Medical School professor of otolaryngology and neurology at Boston Children’s Hospital, who is also affiliated with the F.M. Kirby Neurobiology Center at Boston Children’s. “This truly is precision medicine.”The mice carrying the faulty Tmc1 gene are known as Beethoven mice because the course of their disease mimics the progressive hearing loss experienced by the famed composer. The cause of Ludwig van Beethoven’s deafness, however, remains a matter of speculation.In mice, the Beethoven defect is marked by one incorrect letter in the DNA sequence of the Tmc1 gene — an A instead of a T — a single error that spells the difference between normal hearing and deafness.Disabling, or silencing, the mutant copy of the Tmc1 gene would be sufficient to preserve the animal’s hearing, but how could it be done without inadvertently disabling the healthy gene as well?Two keys are better than oneClassic CRISPR-Cas9 gene editing systems work by using a guiding molecule — gRNA — to identify the target mutant DNA sequence. Once the target DNA is pinpointed, the cutting enzyme — Cas9 — snips it.So far, these gene editors have shown less-than-perfect accuracy. This is because the guide RNA that leads the Cas9 enzyme to the target site and the Cas9 enzyme that cuts the target DNA are not entirely precise, and could end up cutting the wrong DNA.To circumvent these challenges, researchers adapted a tool originally developed by Keith Joung, HMS professor of pathology, and Ben Kleinstiver, HMS assistant professor of pathology, both at Massachusetts General Hospital. The adapted tool uses a modified Cas9 enzyme derived from Staphylococcus aureus instead of the standard Cas9 that is derived from the bacterium Streptococcus pyogenes.To achieve enhanced accuracy of the detection and disruption, the new, optimized system combines two levels of recognition — gRNA to locate the target gene, and a modified form of Cas9 that can pinpoint the specific DNA mutation in Beethoven mice. Using two forms of identification ensures precise and selective cutting of the aberrant copy — and only the aberrant copy — of that gene. The Beethoven defect is marked by one incorrect letter in the DNA sequence of the Tmc1 gene — an A instead of a T — a single error that spells the difference between normal hearing and deafness.
The Broadway League has confirmed that all Broadway shows apart from Aladdin and The Lion King will perform evening performances. Tuesday January 27 View Comments If you’ve bought a ticket for the below shows through Broadway.com you can exchange or return your ticket in advance of the performance. A Delicate Balance Book of Mormon Chicago Curious Incident Disgraced Hedwig Kinky Boots It’s Only a Play Jersey Boys Les Miserables Matilda Mamma Mia! The Elephant Man The Phantom of the Opera You Can’t Take It With You Wednesday January 28 If you’ve bought a ticket for the below show’s matinee performance through Broadway.com you can exchange your ticket in advance of the performance. If you’ve bought a ticket for the below shows’ matinee or evening performances through Broadway.com you can exchange your ticket in advance of the performance. Here is all you need to about the current status of shows on the very Great White Way as a result of Winter Storm Juno. Check back for updates throughout the day. If you’ve bought your tickets through Broadway.com, call 1-800-BROADWAY for information about refunds or exchanges. A Gentleman’s Guide A Delicate Balance Aladdin Beautiful Cabaret (up to two hours prior) Chicago Disgraced Hedwig It’s Only Play Jersey Boys Kinky Boots Les Miserables Matilda Mamma Mia! The Book of Mormon The Curious Incident The Elephant Man The Lion King The Phantom of the Opera You Can’t Take it With You All Broadway shows were canceled on Monday January 26. The River
In addition to Shelton, Trump nominated St. Louis Fed official Christopher Waller to the Fed board. It is not clear if that vote will happen a the same time as Shelton’s. Democratic senators grilled her over her past support of the gold standard and questions over whether the Fed should operate without political pressure. It is the latter issue of Fed independence that Alexander cited, saying Shelton does not back the concept “as much as I believe the Board of Governors should.”“I don’t want to turn over management of the money supply to a Congress and a President who can’t balance the federal budget,” Alexander added.In a somewhat surprising development last week, Senate Majority Leader Mitch McConnell said he was bringing the Shelton vote to the full floor this week, though no date has been set for the vote. It would be unusual for McConnell to do so unless he believed Shelton had enough votes to get through, and the move came after GOP Sen. Lisa Murkowski of Alaska said she would back the nomination.- Advertisement – Efforts to get Judy Shelton confirmed to the Federal Reserve just got a little tougher as one prominent Republican announced his opposition Monday.Sen. Lamar Alexander (R-Tenn.) said in a statement that he will oppose President Donald Trump’s nomination of Shelton as a Fed governor, CNBC’s Ylan Mui reported.- Advertisement – That brings to three the total of GOP senators against the pick, putting the chamber in a likely 50-50 deadlock. Sens. Mitt Romney of Utah and Susan Collins of Maine are the others.Under a stalemate scenario, Vice President Mike Pence could step in and cast the tiebreaking vote. The White House said Monday that Shelton still has the full backing of the administration and her confirmation is expected, according to Reuters.Shelton’s nomination has been controversial from the beginning.- Advertisement – – Advertisement –
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