Ohio State redshirt junior forward Makayla Waterman (24) looks to pass to a teammate in the fourth quarter of the Buckeyes’ semifinal game against Rutgers on March 2 at Banker’s Life Fieldhouse in Indianapolis. Ohio State beat Rutgers 82-57. Credit: Alyssia Graves | Assistant Sports DirectorThe Ohio State women’s basketball team starts its regular season with a matchup against No. 22 South Florida on Tuesday in the Schottenstein Center, the first of six preseason ranked Top 25 matchups. The Buckeyes, who come into the season unranked, have a lot to prove after losing over 90 percent of their scoring output from last year with the departures of guard Kelsey Mitchell, forward Stephanie Mavunga and guard Linnae Harper, among others. Finding a new reliable scoring threat will be one of many things the new-look Buckeyes hope to figure out as the season progresses, with Tuesday’s opener as the first official test of a fresh roster. Head coach Kevin McGuff acknowledges there are questions that need answers in regard to the new team, but said he sees it as an opportunity for more players to get involved to help the team win.“We’re still just kind of trying to gel and get things to come together, but we’re going to have to be a really balanced team and we don’t have necessarily that one player that can just go get points,” McGuff said. “We’re going to have to execute well and spread the ball around.” The Buckeyes were able to spread the ball around during their preseason win over IUP Sunday with a 72-50 victory that saw four separate players score double digits: freshman forward Dorka Juhasz, 14, redshirt senior guard Carly Santoro, 14, freshman guard Janai Crooms, 12 and freshman forward Aaliyah Patty, 12. A healthy dose of freshman scoring is a good sign for the young team still trying to find its identity. While Ohio State wasn’t entirely consistent all the way through, the young players made their mark on both sides of the ball, with two big steals and a block from Crooms in the second quarter that began to take the life out of IUP. There was also a mixture of older help with the scoring outbreak from Santoro, who hit three 3-pointers within three minutes in the third quarter to keep the momentum in favor of Ohio State. The most ideal situation, McGuff said, is to get all players contributing to the team and ready to make an impact for the best chance at winning, which he saw glimpses of against IUP.Getting another chance to breed chemistry will do the team some good as the season progresses. Santoro believes the team is beginning to work well together. “I think we’re gelling really well,” Santoro said. “We’re friends outside of basketball, and basketball we all work really well together. We all want the best for each other.” This theory will be put to the test against USF, which found itself making an early exit in the first round of the NCAA Tournament last season to an upset against No. 11 Buffalo. Shortly after the battle against USF, the Buckeyes will face Detroit Mercy Nov. 9 at home, followed by a trip to Storrs, Connecticut, to face off against t No. 2 UConn, which has gone to 11 straight Final Fours and has won six of them, on Nov. 11. The tests of the season begin heavy with two of the first three matchups against highly-ranked opponents, so the fresh-faced Buckeyes will have to learn fast and work together to show what they are made of.
Bayern Munich have announced that Franck Ribery has sustained a hamstring injury at their winter training camp in Doha, QatarThe 35-year-old winger, who will be out of contract at the end of this season, suffered the injury in a practice match at Qatar.Bayern haven’t released any possible timetable for when Ribery may return to action with the club only stating that he’ll be out for the time being.“Franck Ribery is facing a spell on the sidelines after tearing a hamstring in Wednesday evening’s internal friendly match between members of the Bayern squad,” read a statement on the club website.Fiorentina owner: “Ribery played better than Ronaldo!” Andrew Smyth – September 14, 2019 Fiorentina owner Rocco Commisso was left gushing over Franck Ribery’s performance against Juventus, which he rates above that of even Cristiano Ronaldo’s.Ribery has managed five goals and one assist in 22 appearances for Bayern across all competitions this season.Meanwhile, both Arjen Robben (thigh) and Corentin Tolisso (cruciate) remain sidelined from Bayern’s winter preparations.Niko Kovac’s side will return to action away to Hoffenheim on January 19 in the Bundesliga.
Enroll Now for Free This hands-on workshop will give you the tools to authentically connect with an increasingly skeptical online audience. This story originally appeared on Fortune Magazine 3 min read Free Workshop | August 28: Get Better Engagement and Build Trust With Customers Now Today’s automobiles now come loaded with software and sensors that can help drivers navigate the roads more safely and even do away with the need to have human drivers at all.However, this world of connected vehicles involving on board computers collecting and transmitting data about location, speed, and engine performance also leads to a much more insecure automobile landscape.This is why the Alliance of Automobile Manufacturers (AAM)—an alliance of twelve automakers including Ford, General Motors, and Mercedes-Benz—said Tuesday that it is creating an information sharing and analysis center (ISAC). This center will let participating companies swap cyber security data and keep each other abreast of the latest hacking threats targeting vehicles.The organization said that the new center will be up and running later on this year, and that it will be distributing cyber threat information to the automakers involved with the hub. The goal is to “further enhance the industry’s ongoing efforts to safeguard vehicle electronic systems and networks,” explained Robert Strassburger, vice president for vehicle safety at the AAM, in a statement.As the threat-sharing hub matures, the AAM expects that other companies related to vehicle manufactures—such as auto part suppliers, telecommunication providers, and even tech companies—will join the hub.Google has been busy developing its own self-driving car, so one would imagine the hub would like to tap into any security related information the tech giant might have that could help car companies.Consulting firm Booz Allen Hamilton was selected to help the AAM develop the center. The auto organization is also asking the government to help out by including “legal protections that facilitate cyber security information sharing,” explained Strassburger.President Obama has recently called for companies and government agencies to swap security related informationto help prevent cyber attacks. Additionally, a couple of cyber security bills were recently created to encourage the private and public sector to exchange security data. Both bills support the idea of a government-sanctioned threat-exchange hub and would offer some sort of legal protection for companies willing to swap data in case any privacy-related lawsuits emerge.Considering how regulated auto manufacturers are, it’s probable a given that they expect the government to get involved with their new threat-sharing hub somehow.Whether tech companies like Google, Facebook, or Apple choose to participate remains to be seen. The tech industry has made it clear that it doesn’t want the government to participate in any data-swapping initiative they may be involved with.Additionally, carmakers have made it clear that they want to limit the amount of data like engine and braking information they share with tech companies like Google and Apple so only they can be the ones holding valuable data that could improve their bottom line. July 15, 2015
State Rep. Jason Wentworth has been named to the bipartisan House Community, Access, Resources, Education and Safety (C.A.R.E.S.) task force to explore ways to enable Michigan veterans facing mental health challenges to live happier and healthier lives, Speaker Tom Leonard announced today.The task force aims to enhance coordination of veteran services to decrease veterans’ vulnerability to incarceration for behavior driven by post-service mental health disorders.“I am honored and humbled to be asked to represent the interests of veterans on this panel,” said Wentworth, chair of the House Military and Veterans Committee.The task force will hold public meetings during July and August to receive input from individuals and professionals from around the state. Additionally, the task force will tour facilities to gain a better understanding of programs available and brainstorm ideas to address the current issues.“Holding meetings and visiting facilities all across Michigan will allow us to gather feedback on a wide variety of topics related to veterans’ mental health care,” said Wentworth, of Clare. “As a former Regional Coordinator for Michigan Veterans Affairs Agency, I am well aware of many of the issues veterans suffer from.”Information gathered from hearings and visits will help the Legislature draft legislation reforms that will result in better mental health services for veterans, and improvements to substance abuse programs and veteran treatment courts.“Veteran treatment courts have been very successful in my district,” Wentworth said. “Many veterans with minor offenses have received the care they need rather than incarceration. I look forward to take the success of the courts in my district and implement similar programs across the state to enhance the coordination of veteran services and prevent more veterans from getting into trouble due to health disorders.”Dates and locations of task force meetings will be announced shortly.### Categories: Wentworth News 17Jul Rep. Wentworth appointed to House C.A.R.E.S. panel to address veterans’ mental health
“Today we are learning the language in which God created life.” That’s a quote from US President Bill Clinton on June 26, 2000 when a rough draft of the human genome was announced to widespread, international fanfare. Clinton was certainly not the only one to make big claims about the Human Genome Project (HGP). Journalists and politicians throughout the developed world heralded that the results would lead to “the end of disease.” Of course, things are never that simple. Little did the community know at the time that the project would only uncover a small portion of what’s really going on in our genes. They were only scratching the surface. What the architects of that project once dismissed literally as junk surrounding our genes is proving far more vital than anyone ever expected—in fact, it may hold the very keys to understanding evolution itself. When scientists began the HGP, they were expecting to find approximately 100,000 protein-coding genes to account for the complexity of our species. What they found instead was that humans only have about 25,000, about the same number as fish and mice. In fact, according to biologist Dr. Michael Skinner, “the human genome is probably not as complex and doesn’t have as many genes as plants do.” That’s sort of a problem, because if we humans are supposed to be the complex species we hold ourselves out to be, then why don’t we have as many genes as an oak tree? Maybe because genes are only part of the story. Clinical geneticist Marcus Pembrey thought so… and long before the genome was ever mapped. Back in the early 1980s, Pembrey headed the clinical genetics department at Great Ormond Street Hospital for Children in London, where he treated families with unusual genetic conditions. According to Pembrey, “We were constantly coming across families which didn’t fit the rules and didn’t fit any of the patterns that genetics were supposed to fit.” The most tantalizing example was the paradox shown by two incredibly rare and separate genetic disorders: Angelman syndrome, and Prader-Willi syndrome. These two completely different diseases were eventually chased down to their genetic roots. Astonishingly, they were both caused by the same genetic defect, a certain sequence of DNA that was deleted from chromosome 15. How could this be? How could the same deletion, the same genetic abnormality, cause two completely different diseases? When Pembrey dug into the inheritance pattern for the conditions, he came across something remarkable. It was the origin of the mutation, not the change alone, that determined which disease would manifest itself. We all receive a set of chromosomes from each of our parents. If the deletion was on the chromosome 15 that the child inherited from the father, then he or she would be born with Prader-Willi syndrome. If, however, the deletion was on the chromosome 15 that the child inherited from the mother, he or she would be born with Angelman syndrome. It’s as if the chromosome 15 knows where it came from. This might not sound profound. But what Pembrey stumbled upon showed for the first time in humans that there is more to inheritance than simply the coded sequence of DNA, and that something other than genes was being passed between generations. Discoveries like Pembrey’s helped spawn a budding area of science—epigenetics—that aims to answer just how much of “us” comes from outside our genes. Epigenetics could help explain how a complex human, capable of language and mathematics and philosophy, can be created with only 25,000 genes. It could help us better understand what causes disease and provide us with a wealth of new opportunities for drug discovery and development in areas such as cancer, diabetes, and neurodegenerative disorders. The best way to begin to explain epigenetics, which literally means “on or above genetics, is with an analogy. Think of your genome—your DNA—as like the hardware of a computer. Your epigenome is much like the software, which tells the hardware what to do. It’s the epigenome that tells our cells what sort of cells they should be – a skin cell, a heart cell, etc. All these cells have the same genes, but your epigenome decides how much or whether some genes are expressed in different cells in your body. Here’s a very simplified explanation of how this works: The human body contains billions (if not trillions) of cells. Each of these cells (apart from red blood cells and reproductive cells) contains your DNA, the blueprint of your genetic code. But just because the cells have the DNA doesn’t mean that they know what to do with it. So they receive outside instructions from organic compounds called methyl groups. The methyl groups bind to the DNA in different ways and tell it things like “don’t express this gene” or “do express this gene.” They also bind differently to a skin cell versus a heart cell, for example; that’s one of the ways that a skin cell knows it’s a skin cell and a heart cell knows it’s a heart cell. In addition to methyl groups, epigenetics is also controlled by histones, proteins that function basically like spools that the DNA wraps itself around. These histones can change how tightly or loosely the DNA is wound around them. The more tightly wound, the less the gene can express, and vice versa. In other words, methyl groups act like gene switches, turning them on and off, while the histones are more like a dial that controls the volume (i.e., the degree to which the gene is expressed). Distinct methylation and histone patterns exist in every cell to tell it what to do, which constitutes a sort of second genome that we call the epigenome. What’s particularly interesting about the epigenome is that, unlike the genome, it’s dynamic. While epigenetic instructions do pass on as cells divide, they can change throughout your life based on environmental factors, what we eat, and how we live—and these changes can apparently (though not conclusively proven yet) be passed on to our children and our children’s children. Since these epigenetic tags decide what genes get expressed and to what degree, the implications of a dynamic epigenome are profound. As geneticist Randy Jirtle puts it: “We’ve got to get people thinking more about what they do. They have a responsibility for their epigenome. Their genome they inherit. But their epigenome, they potentially can alter, and particularly that of their children. And that brings in responsibility, but it also brings in hope. You’re not necessarily stuck with this. You can alter this.” At the end of the day, epigenetics might sound like sort of a buzzkill because if the current thinking is right, it would make it tough to ever enjoy another guilt-free French fry, cocktail, or fine cigar. But with the bad comes the good. For example, mounting evidence suggests that certain types of cancer and other diseases are caused by misplaced or missing epigenetic tags; scientists are hard at work developing drugs to silence some of those “bad” genes that were supposed to be turned off in the first place. We’re already seeing the archaic days of genetic modification give way to much more subtle and precise forms of genetic medicine, like the temporary genetic suppression available in the first generation of RNAi therapies just now coming to market—a trend we have followed to great profitability in Casey Extraordinary Technology. Now, we can only hope that epigenetics follows the same amazing curve of advancement that the HGP unleashed for genetics. If it does, the possibilities are extraordinary.