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A North Florida high school student has quite a decision to make on his college education.Craig McFarland,a student at Stanton College Preparatory School in Jacksonville, recently learned that he has been accepted to all eight Ivy League schools.The teen, who has a 4.98 grade point average and and has never gotten a “B” on his high school report card, is unsure which university he will ultimately attend.“With coronavirus, I can’t do that, so the only metric that I have is based on experiences of current students and their virtual campus tours,” McFarland says.CONGRATULATIONS! Craig McFarland, senior at Stanton College Preparatory School, is the newest member of a very exclusive club: The “I Was Accepted into Every Ivy League University In The Country Club.” #TeamDuval #WeHaveThatFull Story: https://t.co/ep0gwfw1g8— DCPS (@DuvalSchools) April 21, 2020 He heard from Yale first, and then received acceptance letters from Harvard, Princeton, Columbia, University of Pennsylvania, Brown, Dartmouth, and Cornell.“With each school, I was more and more in shock,” adds McFarland, who says he plans to study medicine or law.According to Craig’s mother, Donabel Santiago, he has always demonstrated strong initiative.The single mom explains, “I’m very proud of him. I have three kids and I told them I don’t accept a ‘B’ as a grade because I know that they can bring me A’s.”
Playing in what turned out to be a wintery vortex at the McClimon Soccer Complex Saturday night, fourth-seeded Wisconsin women’s soccer topped the previously undefeated DePaul Blue Demons in a memorable 2-0 match to advance to the second round of the NCAA tournament.With players on both sides slipping left and right, forwards found open space more often than usual, leading to a combined 14 shots in the first half. Leading the charge early for DePaul in the first half was sophomore forward Abby Reed, who had three breakaway shots on-target in the first 45 minutes.Despite Reed beating the Badgers (19-2-2) back line and earning one-on-one opportunities on those occasions, Wisconsin’s senior goalkeeper Genevieve Richard recorded a series of miraculous saves to keep the Badgers in it.Richard noted the importance of making a statement with an early lead, and a big part of that is keeping the shutout intact to support the offense.“I think it helps the team a lot to keep a clean sheet, and it gives us the opportunity to score first and that’s always good,” Richard said. “It just leads to a good momentum, so I’m just glad I did my job.”While DePaul (16-1-4) had trouble finishing their chances in the opening minutes, the Badgers certainly did not. Just 12 minutes into the game, junior midfielder Kinley McNicoll found an open lane into the box, crossing it through the defense to senior forward Cara Walls. Walls then promptly redirected the pass with a header that bounced into the left corner of the goal for the 1-0 lead.The assist was the team-leading 27th point scored by McNicoll, while the goal was number 12 for Walls, also tops on the Badgers.A little while later in the 20th minute, the Badgers got some insurance, upping their lead to 2-0 after redshirt senior forward Kodee Williams found Walls over the middle for a sliding goal through the increasingly snowy field.Looking back at her early goals and the conditions on the field, Walls said the snow really only hindered her ability to fire shots.“I honestly thought the conditions weren’t as bad,” Walls said. “I felt that I was able to pass the ball fine and I don’t think the conditions played as big of a role in the chances of opportunities we created.”For a team that averaged less than one goal allowed per game all season, the Blue Demons found themselves in an early hole, but with plenty of time left to respond. Perhaps due to the snowy field, the Badgers defense appeared more vulnerable than usual, giving up a few costly turnovers in the first half. On one occasion in the closing minutes of the first half, an errant pass back over the middle intended for Richard was intercepted by Reed, who had an open look but barely missed the net wide right.The near miss for Reed epitomized the frustrating night for DePaul’s offense, which finished the night with five shots on-target compared to the Wisconsin’s seven.After a fast-paced first half, the second half showcased far fewer scoring opportunities as the field got increasingly slick and players lost their footing. While the refs appeared to be relatively lenient with calling fouls, there were still plenty to go around, with Wisconsin committing 14 of the 20 total.The big difference maker was Wisconsin’s back line finding some rhythm after a spotty first half. After giving the defense fits in the opening segment, Reed had no on target attempts in the final 45 minutes and was essentially taken out of the game by the Badgers defense, led by senior Alexandra Heller and junior Brianna Stelzer.The Badgers offense successfully maintained control of the ball in the attacking third for the majority of the second half, but couldn’t capitalize. Looking for a dagger in the 84th minute, a sneaky pass to McNicoll in the box looked promising, but DePaul junior goalkeeper Alejandria Godinez stole the ball away before a finishing touch could be made.Sensing the fate of their season in the balance, DePaul began to play desperately in the closing moments. The Blue Demon offense tried several shots from long range, likely hoping for Richard to succumb to the slick field and miss a save. The efforts, however, were too little too late, as the final 2-0 score line punched the Badgers’ ticket to Tallahassee for the second round.After spending two hours in ice and snow, head coach Paula Wilkins said the idea of heading down south for the second round was more than welcoming for her team. That being said, Wilkins emphasized the trip will be business as usual.“I think the players are excited to be in a little bit warmer climate,” Wilkins said. “But, it’s definitely not going to be a vacation for us. They are going to be focused and they have some goals in mind. It will be very exciting.”The Badgers will be on the pitch next against UCF Nov. 21 at the Florida State campus, starting at 3:30 p.m. CT.
CLICK TO PLAYMoya Brennan is the latest edition to the growing list of ambassadors for the Donegal Gathering. “I am really pleased to be part of the Gathering; I am not shy when talking about Donegal when I am on stage. The sound that Clannad has created has come from the mountains and the valleys and the Glens in Donegal.”Moya performed at the launch of Donegal Gathering which was streamed live across the globe and directly connected our Diaspora with their friends and family at home.That seminal moment was a classic example of contemporary modernity and traditional culture reaching out, hand in glove, to our people across the world. Moya has always been an exemplary ambassador for Donegal and has never forgotten her roots regardless of where her fame has taken her on tour. Indeed, we say on tour because her home has always remained in Donegal.On that memorable night, Moya stressed how we must all be ambassadors when abroad. And now, we are proud to announce Moya as our newest ambassador.Why not click on to www.donegalgathering.com to watch her speak of her pride in Donegal and how her music has always been inspired by her native county, as she joins our continuing list of renowned Donegal ambassadors.So, like Moya, let’s all play our part in making 2013 a record year for visitor numbers to Donegal by letting friends and family know about the exciting times ahead. DDTV – MOYA BRENNAN SINGS THE PRAISES OF THE GATHERING was last modified: October 15th, 2012 by StephenShare this:Click to share on Facebook (Opens in new window)Click to share on Twitter (Opens in new window)Click to share on LinkedIn (Opens in new window)Click to share on Reddit (Opens in new window)Click to share on Pocket (Opens in new window)Click to share on Telegram (Opens in new window)Click to share on WhatsApp (Opens in new window)Click to share on Skype (Opens in new window)Click to print (Opens in new window) Tags:Moya BrennanThe Gathering
Share Facebook Twitter Google + LinkedIn Pinterest American Agri-Women, the nation’s largest coalition of farm, ranch and agri-business women, is celebrating 40 years of advocating for agriculture with its “Drive Across America,” a five-month educational and advocacy tour. Ohio Corn & Wheat, a market development, education and political advocacy group for the state’s grain farmers, is a sponsor of the Drive.Ohio Corn & Wheat works to create opportunities for long-term Ohio corn and small grain grower profitability through two checkoff based organizations and one legislative entity, Ohio Corn & Wheat Growers Association. The Ohio Corn Checkoff and Ohio Small Grains Checkoff work to develop and expand markets, fund research, and provide education about corn and wheat, respectively. Working with its national counterparts, the National Corn Growers Assn. and the National Assn. of Wheat Growers, the state group works to advocate for supportive public policy and engage with consumer audiences at a grassroots level to ensure a climate for grower success.“Grassroots advocacy is among the best ways to influence change because it focuses on personal connections and shared experiences. We appreciate the work of Ohio Corn & Wheat in influencing policies that promote the future of agriculture. We are so pleased to have them as a sponsor of our Drive Across America,” says AAW President Sue McCrum.“Ohio Corn & Wheat is proud to support the American Agri-Women as they continue to advocate for agriculture and help lead our nation’s agricultural industry,” said John Hoffman, chairman of the Ohio Small Grains Checkoff. “We congratulate them on their 40th anniversary and look forward to their visit to Ohio for this weekend’s Preble County Pork Festival.”McCrum and other AAW leaders and members are driving in a specially wrapped pick-up truck, participating in educational, network and advocacy events hosted by AAW’s more than 50 affiliates. The Drive will finish at the 2015 annual convention in Portland, Maine.
SharePrint RelatedWie man einen Geocache verstecktSeptember 3, 2019In “Deutsch”Jetzt schlägt die Stunde der Geocache-Owner!April 13, 2015In “Deutsch”8 Tipps zum Schreiben eines guten Logs (von Cache-Ownern)August 13, 2019In “Deutsch” Sieh Dir das neue Video an und nimm an der Umfrage für Geocache-Owner teil.Einen Geocache zu verstecken, ist eine wichtige und zeitintensive Angelegenheit bei diesem Hobby. Die Planung, der Einsatz, die Konstruktion und die Pflege, die dafür nötig sind, sind wirklich nichts, was man unterschätzen sollte. Aber wenn dann erstmal die Smileys, schönen Logeinträge und Favoritenpunkte eintrudeln, weiß man, dass es den ganzen Aufwand wert war!Wenn du schon einen Geocache versteckt hast, schau dir das neue Video an und hole dir ein paar Ideen um deinen Geocache weiter zu verbessern.Video anschauenHast du das Zeug dazu den nächsten großartigen Geocache zu verstecken? Versuch dich an unserem neuen Quiz für Verstecker und prüfe wie gut du dich mit den Listing-Anforderungen und den Guidelines auskennst.Share with your Friends:More
West Ham boss Pellegrini pleased with Rice progressby Paul Vegasa month agoSend to a friendShare the loveWest Ham boss Manuel Pellegrini is pleased with the progress of Declan Rice.Rice came in for some criticism for his defensive error which contributed to Kosovo’s second goal against England in Tuesday’s European Qualifier at St Mary’s.Hammers manager Pellegrini is confident Rice has the mentality to take everything in his stride and flourish for the national side.”Declan is a very young player, he is improving in every game he plays,” said Pellegrini.”He is only 20 years old and I think with his age it is important he plays for England and it is important for him the way he can demonstrate how he works.”You can expect these mistakes for any kind of player. He is improving and for the moment he is doing well in that position.”If you are 20 years old you always want to play, but we will see if he has any muscle problem. For the moment Declan must continue playing.” About the authorPaul VegasShare the loveHave your say
Source:https://sph.umd.edu/news-item/exercise-may-improve-cognition-reducing-brain-blood-flow-older-adults Reviewed by Alina Shrourou, B.Sc. (Editor)Jan 31 2019Exercise can impact biomarkers of brain function in a way that might prevent or postpone the onset of dementiaExercise training alters brain blood flow and improves cognitive performance in older adults, though not in the way you might think. A new study published by University of Maryland School of Public Health researchers in the Journal of Alzheimer’s Disease showed that exercise was associated with improved brain function in a group of adults diagnosed with mild cognitive impairment (MCI) and a decrease in the blood flow in key brain regions.”A reduction in blood flow may seem a little contrary to what you would assume happens after going on an exercise program,” explained Dr. J. Carson Smith, associate professor in the Department of Kinesiology. “But after 12-weeks of exercise, adults with MCI experienced decreases in cerebral blood flow. They simultaneously improved significantly in their scores on cognitive tests.”Dr. Smith explains that for those beginning to experience subtle memory loss, the brain is in “crisis mode” and may try to compensate for the inability to function optimally by increasing cerebral blood flow. While elevated cerebral blood flow is usually considered beneficial to brain function, there is evidence to suggest it may actually be a harbinger of further memory loss in those diagnosed with MCI. The results of the study by Dr. Smith and his team suggest exercise may have the potential to reduce this compensatory blood flow and improve cognitive efficiency in those in the very early stages of Alzheimer’s Disease.A control group of cognitively healthy older adults without mild cognitive impairment also underwent the exercise training program, consisting of four 30-minute sessions of moderate-intensity treadmill walking per week. But the program yielded different responses from each group.Related StoriesLiver fat biomarker levels linked with metabolic health benefits of exercise, study findsImplanted device uses microcurrent to exercise heart muscle in cardiomyopathy patientsExtremely strenuous exercise can overload the heart without increasing cardiac riskUnlike the group with MCI, whose exercise training decreased cerebral blood flow, the exercise training increased cerebral blood flow in the frontal cortex in the healthy group after 12 weeks. Their performance on the cognitive tests also significantly improved, as was observed the MCI group.For this study, changes in cerebral blood flow were measured in specific brain regions that are known to be involved in the pathogenesis of Alzheimer’s disease, including the insula (involved in perception, motor control, self-awareness, cognitive functioning), the anterior cingulate cortex (involved in decision making , anticipation, impulse control and emotion) and the inferior frontal gyrus (involved in language processing and speech).Specifically, among those with MCI, the decreased cerebral blood flow in the left insula and in the left anterior cingulate cortex were strongly correlated with improved performance on a word association test used to measure memory and cognitive health.A previous publication from this study led by Dr. Smith focused on how the exercise intervention influenced changes in the brain’s neural networks known to be associated with memory loss and amyloid accumulation, which are both signs of MCI and Alzheimer’s.”Our findings provide evidence that exercise can improve brain function in people who already have cognitive decline,” Dr. Smith said optimistically. “We have an interest in targeting people who are at increased risk for developing Alzheimer’s earlier in the disease process. We are seeing that exercise can impact biomarkers of brain function in a way that might protect people by preventing or postponing the onset of dementia.”
Source:University of Houston The release of catecholamines is a normal and acute occurrence if you’re needing to run a marathon or escape an attack, for instance, but in heart failure it is no longer acute, it becomes a chronic response. Every day for the rest of your life those hormones will be elevated above normal levels. Once this happens, this elevated response desensitizes receptors on the cells of the heart.”Bradley K. McConnell, Associate Professor of Pharmacology Reviewed by James Ives, M.Psych. (Editor)May 23 2019A University of Houston College of Pharmacy researcher is characterizing a potential therapeutic target to increase heart function following a heart attack, helping alleviate the symptoms of heart failure.The National Heart, Lung, and Blood Institute awarded $459,000 to associate professor of pharmacology Bradley K. McConnell to do the work which involves the actions of adrenaline/noradrenaline. They are also known as catecholamines, the “fight-or-flight” response hormones on the heart. Related StoriesSmoking triples the risk of death from cardiovascular diseaseCutting around 300 calories a day protects the heart even in svelte adultsImplanted device uses microcurrent to exercise heart muscle in cardiomyopathy patientsCatecholamines are released and bind to the β-adrenergic receptor (β-AR) located on the cells of the heart. β-AR signaling is the primary mechanism to increase the ability of the heart to contract or pump blood. However, chronic β-AR stimulation, which occurs in heart failure, results in reduced contractility due to desensitization of these receptors and thus the heart is no longer able to respond to the demands of the body.The receptors, once able to bind to the hormones, respond to the overstimulation of the continual adrenaline rush on them by desensitizing, or retracting into the cell itself. If the receptor is no longer there it cannot help respond to the heart’s demands.”I want to try to identify how to get those receptors to stay on the membrane longer so that even during heart failure we can get those receptors to increase heart function,” said McConnell. He said the key is a protein called gravin, or AKAP12, an A-kinase anchoring protein that fine-tunes cellular responses and interacts with the β-AR subtype, β2-AR, to regulate the expression of this receptor on the cells of the heart, allowing it to bind and respond to the catecholamine’s actions.”We are working to identify the role of gravin on regulating the expression of receptors on membranes,” said McConnell. “We have primitive data that without gravin we see a much larger increase of the receptor on the membrane, and the overexpression brings the opposite effect.”McConnell’s co principal investigator on this project is Preethi Gunaratne, professor of biology and biochemistry.
Patients typically live to 20 or 30 years of age. There have been important improvements in respiratory care, which used to be what a majority of patients would succumb to. Now, in their 20s and 30s, they’re often succumbing to cardiomyopathy. The heart is functioning with a major component of the cell membrane missing. Over time, it wears out.”Lead author Michelle Parvatiyar, an assistant professor in the Department of Nutrition, Food and Exercise Sciences in FSU’s College of Human Sciences The study was part of continued efforts by UCLA biologist Rachelle H. Crosbie, the study’s corresponding author, who previously identified sarcospan as a protein that could improve mechanical support in skeletal cell membranes lacking dystrophin. Her finding buoyed DMD researchers and affirmed sarcospan’s potential as an effective tool in the fight against the condition.”But nobody had really looked at how increasing the levels of this protein might affect the heart,” Parvatiyar said.Using a unique mouse model with a dearth of dystrophin, Parvatiyar and her collaborators did just that.In their study, the team found that while it’s is not a like-for-like replacement for dystrophin, an overexpression of sarcospan in cardiac cells seems to do the job of stabilizing cell membranes. Even under stress, researchers found, sarcospan overexpression was able to improve the membrane defect in dystrophin-deficient cells.”Sarcospan doesn’t quite do the job of dystrophin, but it acts as a glue to stabilize the membrane and hold protein complexes together when dystrophin is lacking,” said Parvatiyar, explaining a concept developed by Crosbie.Related StoriesWhy Mattresses Could be a Health Threat to Sleeping ChildrenNew network for children and youth with special health care needs seeks to improve systems of careResearchers identify gene mutations linked to leukemia in children with Down’s syndromeCardiac measurements confirmed that sarcospan does protect the cell membrane even when the heart is placed under stress. Study co-author and FSU College of Medicine Associate Professor Jose Pinto performed the measurements, along with FSU graduate student Karissa Dieseldorff Jones and University of Miami Miller School of Medicine research assistant Rosemeire Takeuchi Kanashiro.In addition to serving as a kind of stabilizing glue, researchers said sarcospan could also act as a scaffold that supports other essential proteins at the cell membrane. That function could allow sarcospan to carry mini versions of dystrophin -; which, in its normal state, has a long and unwieldy genetic code -; to the edges of cardiac cells, where they could buttress the fragile membranes.”The idea is that you could administer the sarcospan and the dystrophin at the same time, and the sarcospan could facilitate mini dystrophin localizing to the cell membrane and help hold those complexes in place,” Parvatiyar said.Sarcospan’s two possible functions could augment existing DMD treatments, Parvatiyar said, or they could give rise to novel therapies that fortify weakened cardiac cell membranes and improve the quality of life for people with DMD.In her previous position at UCLA, Parvatiyar had frequent interactions with DMD patients and their families. She said these interactions, and the unshakeable hope she’s witnessed in those suffering from DMD, continue to drive her and her colleagues in the search for new ways to combat this debilitating condition.”Those were the first times in my life I’d ever had someone come up to me and thank me for my work,” she said. “Sometimes you can feel removed from it in the laboratory day after day. You see incremental progress. But to see people who are really yearning for help is motivating. Their positivity is incredibly inspiring.”Source:Florida State UniversityJournal reference:Parvatiyar, M.S. et al. (2019) Stabilization of the cardiac sarcolemma by sarcospan rescues DMD-associated cardiomyopathy. JCI Insight. doi.org/10.1172/jci.insight.123855. Reviewed by James Ives, M.Psych. (Editor)Jun 16 2019A new multi-institution study spearheaded by researchers at Florida State University and the University of California, Los Angeles suggests a tiny protein could play a major role in combating heart failure related to Duchenne muscular dystrophy (DMD), the most common lethal genetic disorder among children.In collaboration with scientists from across the nation, FSU researchers found that increased levels of the protein sarcospan improve cardiac function by reinforcing cardiac cell membranes, which become feeble in patients with DMD.Their findings were published in the journal JCI Insight.The condition, which typically afflicts young boys, is caused by a mutation that prevents the body from producing dystrophin, a protein crucial to the health of skeletal, respiratory and cardiac muscles. Advances in treatment for certain types of DMD-related muscle degradation have helped to prolong patients’ lifespans. However, as DMD patients age, their heart function declines dramatically.