Man who drowned trying to save teens in Lake Michigan is remembered as a hero – Milwaukee Journal Sentinel

Jesse Brock, 50, is seen in a photo provided by his family. Brock died over the weekend trying to save two drowning teenage boys at McKinley Beach in Milwaukee.(Photo: Courtesy of Jessica Brock)

Jesse Brock was an everyday superhero, always helping people in need.

So when his daughter learned he tried this weekend to save two teenage boys drowning in Lake Michigan, she was not surprised.

"He's always cared more about others than he's worried about himself," Jessica Brock said."If anyone ever needed something, he would give them the shirt off his back. He was just that kind of person."

Brock, 50, died Sunday morning after being swept under the waves at McKinley Beach Saturday evening.

Brock saw twoboys swim out to a deep part of the water where they could not stand, then he saw them go underwater, according to reports released Monday by the Milwaukee County Medical Examiner's Office.

He helped to shore one 14-year-old boy caught in the current, then went back in to try to save the second. But even Brock, standing more than 6 feet tall, was no match for the strong current.

He and the second teen, 14-year-old Tony R. Bishop, were pulled under.

Tony died Saturday night after he was pulled from the water by Milwaukee Fire Department officialsin a rescue boat. They attempted CPR but were unsuccessful. The other boy was hospitalized.

Jesse Brock, 50, is seen in a family photo.(Photo: Courtesy of Jessica Brock)

Jessica Brock was devastated by the loss of her father, who she said was a joyous, constant presence in her life.

"He's always been my superhero, my own personal Superman," she said.

The twosaw each other last week, and Jessica remembers her father laughing and joking. He loved spending time with his three grandchildren, she said.

"We were everything to him," Jessica Brock said.

Brock raised his four children in Illinois and moved to Milwaukee within the last six months, his daughtersaid. He worked as a forklift operator.

His selflessness has been a lifelong trait.

In 1996, Brock saved two women and four young children trapped in a burning home in Ford Heights, Illinois, a Chicago suburb. He helped them jump 15 feet to the grass below, according to a newspaper clipping his family saved.

"They're calling him a hero, but Jesse Brock said his actions were just common sense," the article begins.

Twenty-four years later, Jessica Brock is sure of her father's heroism.

"My dad is now and forever a hero," she said. "He died giving his life to try to help someone else, and I am extremely proud of him.".

The National Weather Service issued a beach hazard warning for Saturday afternoon and evening in Ozaukee and Sheboygan counties because of 3- to 5-foot waves caused by strong winds from the south along the Lake Michigan shore. But the swim risk in Milwaukee County was considered "moderate" by the weather service because waves were smaller in the 2- to 4-foot range.

Saturday's incident was the second drowning at McKinley Beach in less than a month. On July 18,J'Varius Bankhead, 19, drownedwhile trying to save two younger cousins from the water.

Milwaukee County Parks has not staffed lifeguards at McKinley Beach since 2005, according to department spokesman Luke Roman. Lifeguard positions therewere cut due to a tight budget and a lack of lifeguards.

In 2018, Bradford Beach Milwaukee's other major beach was staffed seven days a week, and in 2019 staffing was cut to five days a week.

And even then, lifeguards were only present until 5 p.m. The two teenage boys began struggling around 6:30 p.m. Saturday.

Due to the coronavirus pandemic, the parks department closed deep-well pools for the summer, and it has not staffed lifeguards at any county beach.

Milwaukee County Supervisor Sheldon Wasserman, who chairs the Parks, Energy and Environment Committee, sent a letter Monday to County Executive David Crowley asking for the county to hire lifeguards to staff Bradford and McKinley beaches for the remainder of the summer. He said he was "devastated" by the weekend's drownings.

He also called for larger, better signage at the beaches when they are closed and an emphasis on youth swim lessons next year.

"We have a risk that has been identified and we must be ... able to work out a solution," Wasserman told the Journal Sentinel."And the only solution is to have lifeguards."

Alison Dirr and Meg Jones of the Journal Sentinel staff contributed to this report.

Contact Sophie Carson at (414) 223-5512 or scarson@gannett.com. Follow heron Twitter at @SCarson_News.

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Man who drowned trying to save teens in Lake Michigan is remembered as a hero - Milwaukee Journal Sentinel

Antifa activist submits false ‘terrorist’ report to the FBI, preventing a conservative couple from starting a family in the US – The Post Millennial

By submitting a fake tip to the Federal Bureau of Investigation, an Antifa activist allegedly blocked a British man from living with his wife in the United States, denying the start of their family for four years and counting.

Jack Buckby has spent most of his relationship apart and has yet to step foot on US soil since November 2016. Despite no criminal record, he received suspicious visa denials because of an allegation that falsely claimed he's a terrorist, Buckby told The Post Millennial in an exclusive interview.

"I have spent a very significant sum of money trying to rectify this," Buckby stated. "And lost four years of our life. I just want to be with my wife."

Buckby is a counter-extremism researcher who authored a book, Monster Of Their Own Making: How the Far Left, The Media, And Politicians Are Creating Far Right Extremists, describing his experiences in the British National Party in his youth and how the far- right recruit the young generation.

His wife, Martina Markota, is a victim of Antifa doxxing and cancel culture in her industry. She is a performance artist in New York City who was well-known by her stage persona, "Lady Alchemy." Using her real name, Markota publicly advocated for President Donald Trump during the 2016 primaries, appearing on The Gavin McInnes Show to express her support for Trump and detail how she survived as a conservative in the liberal arts scene.

Following Trump's presidential election, Markota was doxxed by NYC Antifa who published her address, her family's address, and described her as a fascist online. She was then fired from a theatre she had worked at for years, dropped by her agent, and canceled from independent gigs when left-wing performers would contact her clients and call Markota a Nazi.

To this day, Markota is regularly blacklisted from booking rosters.

Then in 2017, Markota was contacted by an FBI agent who told her that they had received a tip, alleging that she was then-engaged to a British man plotting to commit terrorist acts in the U.S. and that their engagement was a fraud for Buckby to obtain a green card.

The FBI informant is named, but Buckby and Markota have asked for her identity to remain anonymous to prevent her social media presence from gaining traction.

That same year, the named informant, also from the NYC arts world, admitted to the tip in her personal blog. In the post, she smears Markota, calling her "Portia" to avoid a defamation lawsuit she knowingly admits she's liable "[f]or legal reasons." Working alongside other burlesque performers who felt Markota had made them "extremely uncomfortable" and "unsafe" with her Republican views, the FBI tipper, a self-described "not so bitter divorcee" with too much time on her hands, sought to take down Markota.

"This was more difficult than you can imagine some days," the blogger wrote as she used her old camcorder and a laptop to capture episodes of The Gavin McInnes Show featuring Markota to show producers proof that the conservative performer was "espousing...anti-LGBTQ and racist views."

"The trickiest part was keeping my cats from meowing too much or walking through the shot," she continued.

She went on to admit that she contacted a local NYC-based Antifa group, switching her focus from Markota to McInnes.

"Portia gave me exactly what my friends wanted," she blogged. "The other performers were happy with what I was giving them but Portia didnt really interest me."

The Antifa group asked for evidence of McInnes inciting violence, but within a couple of months of inactivity, she realized that the organisation wasn't "a good fit."

"I wasnt about to sit through dozens of hours of toxic rants by McInnes for nothing," she wrote.

The blogger moved on to anonymously send a flash drive of footage with a one-page document to the FBI headquarters in NYC.

Then when McInnes was fired from his show on the newly-formed Blaze TV for his association with the far-right Proud Boys, she followed up with roughly 20 padded envelopes of similar contents, using the FBI address as the return address.

"I knew Gavin for many years and was associated with him during the early Proud Boys days. I wasn't happy with the behaviour of the group," Buckby urged.

But Buckby was still looped in with the Proud Boys leak, he alleged.

Within days of the FBI tip, Buckby said that he logged online to view his visa waiver status, but his account read "Travel Not Authorized."

Shortly after, Buckby arranged an appointment at the U.S. Embassy in London to obtain a tourist visa. After a long interview, his case was considered Pending Administrative Processing," to be decided after a 60-day background check. Buckby was ordered to leave. For now, his case was considered denied. Two years passed with no contact, decision, or explanation.

Luke Burke, a senior member of the Homeland Security Committee, told Buckby: I have spoken to the FBI and to U.S. Customs and Border Protection and all I can say is that your name is being flagged for something in the [Electronic System for Travel Authorization] application system.

Then in December 2017, Iowa Rep. Steve King asked the U.S. Embassy in London for answers, noting that the "extremely long wait time" was "highly unusual."

King was told: Mr. Buckbys application is subjected to additional, mandatory administrative processingWhile administrative processing usually lasts up to 60 days, in some instances it can take significantly longer.

A year after the tourist visa application, a British member of European Parliament, Janice Atkinson, requested information on Buckby's behalf and received a similar response.

In 2018, Buckby applied for a journalist visa out of frustration to see if that would be accepted. He was denied because the tourist visa was still inexplicably in administrative processing.

Then Buckby decided to file a civil rights lawsuit against Secretary of State Mike Pompeo, former Secretary of Homeland Security Kirstjen Nielsen, and former acting U.S. Attorney General Matthew Whitaker.

"After two years of no response from the Embassy, and no answers to numerous politicians requesting information as to why I was being treated in such a mysterious way, I sued the United States government to compel them to process the visa," Buckby told The Post Millennial.

The suit was withdrawn once Buckby received an answer on his tourist visa, which was successfully processed but denied.

"Again, I meet all the criteria for a visa. I have never broken the law. I am a law-abiding, tax-paying citizen," Buckby emphasized.

Once the lawsuit ended, Buckby applied for a spousal visa, which is still ongoing. And for seven months now, Markota has not visited him in the United Kingdom due to the global COVID-19 shutdown.

Since, Arizona Rep. Paul Gosar has assisted Buckby with his case.

Tom Van Flein, Gosar's chief of staff, wrote that his office has reached out to the Department of Homeland Security and "ultimately had the matter reviewed to clear the Buckbys."

"What happened to them is a clear case of doxxing and bordered on the crime of swatting," Van Flein stated in an email to The Post Millennial.

Gosar's office determined that the false allegation had "harmed [Buckby's] ability to travel."

At no point was there ever any evidence of violence, threats or anything else that would violate U.S. laws that could even remotely warrant a travel ban," he wrote.

Van Flein noted that "[t]here was no reason for the extremely long delay" in reviewing the claim against Buckby "to which the bureaucracy unfortunately failed to vet, verify, confirm or reject."

Meanwhile, Markota's sister was diagnosed with leukemia and hospitalized. Not only was Buckby restricted from visiting his wife's family at a grave time, but Markota, a blacklisted performer, could not financially support her family when they needed it most.

There has been no mainstream media coverage on Buckby's case and "how Antifa worked to destroy our lives," Buckby exclusively told The Post Millennial.

To this day, Buckby is mocked by leftists online.

If Buckby's case is told by left-wing outlets, the FBI informant will be rewarded with the attention she craves and hailed as a hero, Buckby explained.

"She is desperately trying to get credit for hurting us and others, and is really clambering to be relevant," Buckby warned.

"But at the same time, we feel like we need to get this story out there to show how vindictive these people are," he continued.

"[The accuser] and her friends in Antifa and the NYC performing arts scene really believe they are fighting Nazis, but we are just a couple who want to be together and start a family," Buckby concluded.

The Post Millennial reached out the Antifa activist who told us that she did not name Buckby or his wife by name. She went on to say, "As far as Antifa is concerned, I'm a moderate Democrat who is against fascism and that's all you'll get out of me."

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Antifa activist submits false 'terrorist' report to the FBI, preventing a conservative couple from starting a family in the US - The Post Millennial

Inexperienced Lancaster golfers continue to grow and improve – Lancaster Eagle Gazette

Lancaster sophomore Riley Seften puts during an early-season match last week. Seften shot a career-low 82 during the Mount Vernon Invitational at Chapel Hill Golf Course.(Photo: Submitted photo)

LANCASTER With no seniors, the Lancaster boys golf team will be a work in progress, but they have already shown a ton of growth in the early part of the season and will look to continue that trend as the year progresses.

We dont have any seniors in our program, which I guess is a good problem to have because we are building for the next couple of years, but what is exciting is we are going to see a lot of growth this year, Lancaster coach Luke Truex said. Weve already seen that in the first three tournaments weve played in and the boys are battling through some adversities of being in some tough situations. Im really proud of how they fought through some adversity and are battling for each other.

After opening the season last Wednesday, Lancaster followed up its season-opener by lowering its scores in its next two matches.

The Golden Gales began their season at the Pickerington Central Invitational, held at Turnberry Golf Course and finished with a 363-team total. They were led by sophomore Riley Senftens 88 and he was followed by Luke Wildermuth (89), Isaac Reif (91), Harrison Allen (95) and Jagger Snoke (101).

On Thursday, the Gales traveled to Apple Valley Golf Course to compete in the first round of Ohio Capital Conference-Buckeye Division and Lancaster placed third with a 359. Snoke led the way for the Gales with an 87 and he was followed by Senften (89), Reif (91), Allen (93) and Wildermuth (94).

On Friday, Lancaster competed in the Mount Vernon Invitational at Chapel Hill Golf Course and finished with a 353, which was 10 strokes lower than its season-opening score.

The Gales were led by Senften, who shot a career-low 82. He easily could have shot in the 70s but opened with a double bogey and tripled 18. Even though he is a sophomore, Truex sees a lot of potential in Senften.

Riley has taken advantage of some opportunities, Truex said. He fell into a position as a freshman where he moved up to varsity late in the year last year, which has helped him this year. He has really put in some time this off season and he played in some competitive tournaments that has allowed him to grow before our season got going. He has really taken to the game and really wants to get better and that shows with his scores.

Im super proud of his mental toughness and how he has responded when things arent going his way. He got off to a rough start and it easily could have gone the other way at Chapel Hill, but he hung in there. He carries himself well and puts himself in position to score well and thats why he is going to be successful. Because of that, he will continue to grow as a golfer.

Other scores for the Gales during the Mount Vernon Invite were Reif (89), Snoke (90), Allen (92) and Wildermuth (95).

Truex understands there are going to be times when his young squad struggles, mainly because of their inexperience, but Lancaster also faces top-notch competition each time out. As they navigate through season, he feels like they will only get better.

We have to be realistic with ourselves, Truex said. Pickerington Central is the team to beat in our league and right now, we just arent there as a team, but I like where we are headed. After our first tournament we dropped 10 strokes. Because of our inexperience, it is an uphill battle, but the guys arent discouraged, and Im not discouraged.

"We are just trying to compete against ourselves right now and really grow and take one day at a time and thats what you want. You want to make sure you are getting better.

twilson@lancastereaglegazette.com

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Twitter: @twil2323

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It meant the world to us: Porteria, Ott recall Ceres Negros’ 2017 AFC Cup glory | Football News | AFC Cup 2017 – The Official Home of Asian Football

Bacolod: Ceres Negros victory in the 2017 AFC Cup ASEAN Zonal Final, three years ago on Sunday, was a historic moment for football in the Philippines.

A 3-2 aggregate victory over Singapore's Home United ensured the Filipino club became the AFC Cup's first-ever ASEAN Zone champions, with their 2-0 victory in Bacolod on August 9, 2017, sealing their place in the tournament's record books.

To commemorate the achievement, the-AFC.com spoke exclusively to the Ceres goalscorers, OJ Porteria and Manny Ott, to reflect on a magical night at Panaad Park.

Hello Manny and OJ. It's three years to the day that Ceres Negros became the AFC Cup's first-ever ASEAN Zonal Champions But before we go into that match, what are your memories from the first leg a week earlier in Singapore?

Ott: It was a very a difficult game. For one, we didnt play at our best that day but also credit to Home United playing very smart and giving us a hard time in Jalan Besar. Of course, the first leg was a disappointing result for us, but we knew that at Panaad Stadium we always show our best side, so that gave us confidence.

Porteria: I didnt start in the first leg at Jalan Besar Stadium. I could see that Home United were a good side playing at home in Singapore, but I knew that we had better quality. Even after playing against them in Singapore I was confident that we would beat them at home.

What do you remember feeling ahead of that decisive second leg?

Ott: We knew we had to win to get what we worked so hard for, but most importantly we wanted to leave it all out on the field, redeeming ourselves for the first leg performance.

Porteria: The feeling I had leading up to the second leg against Home United was excitement. I knew we were going to play in front of home crowd in Bacolod and that would give us an extra push.

The opening goal came just two minutes after the kick-off, scored by OJ, what can you both recall of that moment?

Porteria: I remember Iain Ramsay crossing the ball and the defenders trying to head it out but luckily the ball came to my foot and it went in. And Panaad went electric, I coudnt even hear a thing. It was kind of like a weight lifted off my shoulders, I was just so proud to be a part of everything and to contribute to the teams success.

Ott: It was a super cross from Rambo and OJ's goal definitely lifted our spirits even more. While I actually didn't care who scored that day, I'm happy he was there at the right time to net the first goal of the game.

And then Manny added an important second just before half-time...

Ott: Sometimes after training, we did some shooting and free-kicks, and I was very comfy shooting from that position. So when that free-kick happened, I just had that feeling that it would be mine to take. So I told the guys I would score. And happily I did.

Porteria: Mannys goal was vital for us because it gave us the cushion we needed to secure the win. I remember Panaad being packed and not being able to hear a thing. Every time we won a free-kick, corner or throw-in the crowd would go crazy.

You still had to ride out the second half and just one goal would have brought Home United back on level terms. How was the feeling amongst the team?

Ott: Even when we missed our chances, like Fernando [Rodriguez] missing a penalty in the first half, we never panicked. We just wanted to win that final so badly since we were working towards being ASEAN Zonal champions for the years before.

Porteria: I wasnt too concerned about Fernando missing the penalty because I could feel the energy that the team was giving. Once the game started in Bacolod, I could feel that we were going to win the game.Our momentum was hard to stop in this game and I knew that right after kick off.

What was going through your mind when the referee blew for full-time and you became the first ASEAN Zonal champions?

Porteria: I remember when the whistle blew everybody just stormed the pitch. I remember being in tears, everyone in the team understood what we had to do .All of the guys were just hugging each other, crying, jumping and screaming. It was like a weight had lifted off our shoulders and we did our country proud.

Ott: It was an unbelievable feeling. Everyone was so happy and to achieve our goal was just amazing. I remember everyone just hugging each other, guys were getting all teared up. It was a crazy atmosphere that night, on and off the pitch. That was very special and all of the boys will always remember that moment.

No matter what comes next, Ceres Negros will go down in tournament history as the AFC Cup's first-ever ASEAN Zonal champions. What does that achievement mean to you?

Ott: Everything went right that year and it just felt amazing, it still does thinking back to those days. To have been ASEAN Zonal champions will always be something we will remember, and Im just very proud to have been part of that team.

Porteria: It meant the world to us. A club from the Philippines, a club from Bacolod, to rise up and be the first ASEAN Zonal Final champions was big for the Philippines. We were so proud of everyone involved. We were proud to be a part of Ceres, we were proud to be from Bacolod and we were proud to be Filipinos.

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Karnataka SSLC result: 100% scorers up even as pass percentage dips, board says proud of holding exams – The Indian Express

By: Education Desk | New Delhi | Updated: August 10, 2020 7:14:58 pmPass percentage decline from last year in KSEEB SSLC 2020 result (Representational image)

Even as the number of students clearing the Karnataka SSLC has declined as compared to last year, KSEEB in an official statement said, The board owns the pride of conducting the exams successfully. This is because Karnataka is among the few states to have conducted the board exams despite the pandemic.

This years exam was a challenging job not only for students but also for the government and board. Apart from maintaining the sanctity and confidentiality of exams, winning the confidence of parents and ensuring the health of students was a challenge, Karnataka Board said in an official statement.

Karnataka SSLC 10th Result 2020 LIVE Updates

The pass percentage dipped from 73.70 per cent last year to 71.80 per cent this year, however, the number of students scoring 100 per cent has gone up.

As many as six students got 100 per cent marks with 625 marks out of 625. Last year, only two students could attain the feat. Most students got 100/100 in the third language as many as 21,745 students got full marks in the subject. A total of 43,661 answer scripts across the SSLC exams have got 100 marks across the subjects.

Following the last years trend, girls have outperformed boys. As 77.74 per cent girls who appeared in the exams cleared it while for boys, the pass percentage was recorded at 66.41 per cent.

The best pass percentage was delivered by unaided schools with 82.31 per cent students clearing the exams while the far second is government-run schools with a pass percentage of 72.79 per cent, followed by aided schools with a pass percentage of 70.60 per cent.

Region-wise, students from rural areas continued to have an advantage as the pass percentage obtained by them was 77.18 per cent while 73.41 per cent of students from urban areas cleared the exam. The trend was similar last year too.

The board had also allowed students to change their exam centres and a total of 12,674 students availed of this benefit, as per the official statement. As many as 8,11,050 students attended the exams this year. The evaluation was done from July 12 to 20. In urban and Bangalore rural districts, the evaluation began around July 15, as informed by KSEEB.

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Karnataka SSLC result: 100% scorers up even as pass percentage dips, board says proud of holding exams - The Indian Express

Hinghams Grace Bennis gave it her best shot at the ASFL charity shooting challenge – Wicked Local Hingham

B-R's Shay Bollin shoots her way to the ASFL charity challenge championship.

HANOVER Bridgewater-Raynhams Shay Bollin added to her already ultra-impressive basketball resume on Wednesday at the Starland Sportsplex.

Competing in the A Shot For Life Challenge, a charity basketball competition that raises money for cancer research, Bollin was crowned the best girls shooter in the state. For two hours, Bollin shot free throws, mid-range and 3-point shots at a 80.91 percent clip edging Ashlands Kayla Madden (80.71 percent) by the narrowest of margins.

Its a huge honor to win, said Bollin, a two-time Enterprise All-Scholastic who led the Trojans to a Division 1 South title in the winter. Its such a good cause.

In all, over $40,000 was raised for the Dr. Curry Research Laboratory at Mass. General Hospital that pitted 17 of the top high school girls basketball players against each other. On Tuesday, Scituates Jack Poirier was the runner-up in the boys competition.

Im really proud of the way the ASFL family reacted to everything thrown at us this year, said ASFL founder Mike Slonina. In a time where every event is getting cancelled, ours stood tall and figured out a way to do it safely. Im so extremely proud of our staff to make this happen and of our organization tonight. We had to adjust a ton on the fly. There wasnt much that was not thrown at us this year, but we made it work and Im really proud of that.

Bollin was just one of several locals competing. In fact, her point guard Kenzie Matulonis was also in the event. Hinghams Grace Bennis and Carvers Emma Simmons also competed.

The two hours was definitely more difficult than I expected, said Bollin. It took a lot of mental toughness to continue using the right form and continue making every single shot. When youre shooting for two hours straight, its easy to get mentally lax.

With only 16 available hoops for the 17 competitors, Madden shot from 6-8 p.m. before the other competitors had their turn from 8:15-10:15 p.m.

Madden volunteered to shoot early to accommodate all the other girls. Sporting a blue number 10 ASFL jersey and white Nike basketball sneakers, Madden was joined on the court by Ashland girls coach Dave Lyth and Clockers assistant coach Justin Leip.

Oh, and the smooth-shooting Springfield College-bound Madden ended up finishing in second place at 80.71 percent, just .2 percent behind Bollin.

It was definitely different, but Im happy with how I did, Madden said. Shooting before has its pluses and minuses, Id say. It was more of a workout type of feel being in more of an empty gym. But the music was going, I had my rebounders, Slo coming over and giving me time checks. I still felt like I was part of it even though I was shooting before.

Im excited I got to raise more money that goes to a great cause. Its such an honor being welcomed back. Mike asked if I could shoot before, which shows his trust, and Im just thankful to be part of this amazing organization.

Madden was selected to participate last year, but was unable to after tearing her ACL at a tournament in Kentucky.

It was tough for her watching from the bench, making it that much more special that she was able to actually compete this year.

A lot more fun being able to shoot and participate this year, Madden said. I was excited to shoot. Last year was so heartbreaking because I got hurt probably a month before the event. This year, with the pandemic and gyms being closed, there were more obstacles thrown my way. I was excited because this is one of the first basketball things I was able to do.

Also competing from the MetroWest area were recent Natick grad Brenna McDonald, recent Medway grad Lauren Beach, and Franklin rising junior Olivia Quinn.

This is really special, said McDonald, who is headed to Yale University to play. I hadnt been able to get in a gym. Shooting outside is different and Im really fortunate I was able to shoot on a real basket, but also to a part of a special organization that takes something I love - playing basketball - and turns it into helping others.

This is a really big honor, said Quinn, who dazzled for the Panthers this past winter. To wear this jersey and to be here is just such an honor for me, particularly after just finishing my sophomore year. I thought I shot pretty well today, especially with it being my first time. It was a lot of fun and Im really glad Mike was able to make it work with all the circumstances.

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Hinghams Grace Bennis gave it her best shot at the ASFL charity shooting challenge - Wicked Local Hingham

Drive-In Movie Night in Parkland: The Sandlot – Parkland Talk – Parkland Talk

By Jill Fox

Parkland families have a chance to have some fun while keeping a safe distance.

Residents are invited to the recently rescheduled family drive-in movie on Saturday, August 15, at the Equestrian Center.

This time, the featured movie is an older one The Sandlot. The classic 1993 film takes place over a summer in the sixties. Its filled with the adventures of a group of boys who bond over baseball and life lessons.

Gates open at 7:00 p.m., and cars will be parked in pre-measured rows practicing 6-foot physical distancing in a way that makes sure everyone has a great view of the screen. The movie will start at approximately 8:25 p.m.

The City of Parkland is proud to host the drive-in movie free of charge to the community. There is no entry fee or ticket required to attend, but space is limited.

Social distancing requirements are in effect, and movie-goers will need to remain in their vehiclesor on them.

Golf carts and pets are not permitted to attend, and concessions will not be available, so residents should bring their own snacks and drinks.

It is a great way to enjoy a fun family night out in a safe way, said Mayor Christine Hunschofsky.

The special events hotline will be updated if any changes or weather updates occur at 954-757-4215. The Equestrian Center is located at 83560 Ranch Road in Parkland.

Send your news to Parklands #1 News SourceParkland Talk.

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Cyberpunk 2077 details weapons and origin story "life paths" in latest livestream – Eurogamer.net

There're still a few months to go until Cyberpunk 2077 is ready to burst forth from the cocoon of its extended development, but CD Projekt is already hard at work feverishly cranking the handle of its neon-hued hype machine. To that end, it's now offered a closer look at two more Cyberpunk 2077 features - weapons and life paths - as part of its latest livestream.

Life paths are potentially the most exciting of the two (unless you're particularly partial to shooting things), as these determine how your time in Night City will unfold each play through, impacting both your starting point and how your personal adventure will progress.

Cyberpunk 2077 features three distinct life paths - that of Street Kid, Nomad, and Corpo - and each offers a very distinct origin story. Those that opt for Street Kid, for instance, have been raised in Night City, and are more than familiar with the criminal element bubbling away beneath the metropolis' glitzy veneer, providing them with particular avenues and connections that might prove useful as the story unfolds.

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Nomads, meanwhile, are "outcast among outcasts" with a hunger for freedom, who've lived in the desolate desert Badlands beyond the limits of Night City. Those that opt for the Nomad life will begin their story outside the city; having left their clan, they're now trying to get inside to make a new life for themselves. CD Projekt notes that other paths will still be able to explore the Badlands later in their adventure, along as they're prepared for the dangers its holds.

Lastly then, are Corpos; these corporate stooges, members of the Arasaka Corporation, are at home in the boardroom rather than on the streets or out in the desert - but while that might imply a more sheltered, less resilient existence, they're still able to leverage their business know-how and other skills to forge their own distinct path.

CD Projekt says Cyberpunk's "real RPG" focus means that life paths aren't just about beginnings, and will remain important throughout the game, with each opening up different opportunities, dialogue options, and progression routes during missions. Should you wish to know more, there's some introductory scene-setting for each life path in the video below.

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As part of its latest livestream, CD Projekt also took some time to focus on the various weapons players will gain access to throughout Cyberpunk 2077, loosely splint into three categories: melee, ranged, and cyberware - the latter being offensive body modifications, such as the razor-like Mantis Blade, punch-packing Gorilla Arms, and Projective Launch System.

The weapon focus for today's presentation, however, was guns, which also fall into three categories. Power Weapons are described as being the most similar to contemporary weapons (although their bullets can ricochet off surfaces), while Tech Weapons use electromagnetic power to propel metal projectiles at extreme velocity, meaning they can punch through cover. Lastly are the Smart Weapons, capable of tracking targets in real-time, making it possible to hit an enemy while they're hiding behind cover or even running away.

Keen to highlight Cyberpunk 2077's RPG credentials further, CD Projekt stressed that RPG elements will also tie closely to combat, explaining that protagonist V will grow more proficient over time as their rise to Night City legend continues. As such, skilled players can expect to utilise the likes of quicker reloads, more accurate aiming, and speedier movement.

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And outside of personal skill, weapons themselves can also be improved to better suit them to specific combat situations. Not only do they come in different rarities (legendary weapons might only be accessible by wrestling them out of specific NPCs' cold dead hands, potentially making for some tough choices), they can also be upgraded in a variety of ways.

Modifications, for instance, are visible attachments (think scopes and silencers) that offer advantages and more gameplay opportunities. Software Mods, meanwhile, are small chips which have the capacity to change the statistics of a gun - such as its accuracy, damage, fire range, and so on - once equipped. CD Projekt has broken out its weapons chat into a separate video above if you want to know more.

Today's livestream, which also touched a little on Cyberpunk 2077's music, is only the second to release so far, so expect plenty more info-drops to occur between now and the game's Xbox One, PS4, and PC release on 19th November.

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Cyberpunk 2077 details weapons and origin story "life paths" in latest livestream - Eurogamer.net

Humans have had mystery DNA for 300,000 yearsand now we might finally know what it is – SYFY WIRE

Humans getting into interspecies dating? Not on this planet oh wait, that already happened.While there was really no such thing as dating hundreds of thousands of years ago, when it was more of a find your mate and dont get eaten sort of thing, there is evidence that Homo sapiens interbred with other proto-human species in the distant past.

Neanderthals were one of those species (and also the butt of endless caveman jokes). Denisovans were another. Geneticist and computer scientistAdam Siepel developed an algorithm to trace human genetics and recently published a study in PLOS Genetics. He andhis research teamhave now found that these groups gave us more of their DNA than we thought, and thatsome of us have genes from a mysterious ancestral hominid, possibly Homo erectus. There was only one way for that to happen. But why did Homo sapiens end up taking over while Neanderthals and Denisovans eventually vanished?

"That is a great matter of speculation among both archaelogists and geneticistscould be disease, conquest, out-competition for scarce resources, or perhaps the modern humans simply absorbed them.There is little hard evidence,"Siepeltold SYFY WIRE."But the one thing that we can see, as geneticists, is that these Neanderthal and Denisovan populations had relatively low levels of genetic diversity, suggesting they may have been prone to genetic diseases and/or particularly susceptible to infectious diseases."

Hybridization of a species results in introgression, or the genetic exchange which occurs in interbreeding species. Humans migrated out of Africa to Eurasia about 50,000 years ago and interbred with the Neanderthal population there. This is the migration and subsequent genetic merging that is the most recognized example of such a phenomenon. What Siepel found, using an updated ancestral recombination graph (ARG) algorithm called ARGweaver-D, is that they were already headed elsewhere much earlier, around 200,000-300,000 years ago. The algorithm also revealed interbreeding between mystery super-archaic ancestors with both Neanderthals and Denisovans before either of those species interbred with ancient Homo sapiens.

Homo erectus is the most likely ancient relative of humans to be that ancestor. Now extinct except for fragments of DNA that show up in some modern human samples, these proto-humans were the first Homo sapiensrelatives that showed body proportions similar to what you see when you look in the mirror. Unlike earlier hominids, the arms and legs of Homo erectus had evolved to be shorter than its torso. They were also the first hominids believed to have migrated out of Africa. This strengthens the case for interbreeding with Denisovans and Neanderthals, especially Denisovans.

That has to make you wonder. If you've ever taken a commercial DNA test and your results came back with a small percentage labeled "unknown", could that be a connection to the mystery ancestor?

"Some of the commercial tests specifically look for Neanderthal ancestry, but yes, it is possible that superarchaic ancestry, or ancestry from a highly divergent branch of Neanderthals or Denisovans, would be labeled 'unknown'by a commercial test," Siepel said.

The most common genetic transfers happened between Neanderthals and Denisovans, Neanderthals and ancient Homo sapiens, super-archaic ancestors and ancient Homo sapiens who stayed in Africa, and super-archaic ancestors and Denisovans. Alleles, or alternate versions of genes, shared by Denisovans and the mystery ancestor support super-archaic DNA making its way into the modern gene pool when that species interbred with Denisovans. Unfortunately, so did mutations.

"It appears that Neanderthals and Denisovansintroduced deleterious mutations into modern human populations when they interbred with them," Siepel explained."Many of these mutations gradually fadedover time, but some undoubtedly persist.Interestingly, however, we could not find clear evidence of the reverse effectof modern humans introducing deleterious mutations into Neanderthals through this interbreeding.It is possible, though, that we do not yet have enough sensitivity to detect this phenomenon."

Even with an advanced algorithm, it still proved more difficult to identify when and where super-archaic human ancestors interbred with Denisovans than it was to find the same information about Neanderthal or Denisovan interbreeding with Homo sapiens. This is probably because no sequence exists for the genes of the super-archaic ancestor yet, and also because they have been broken over and over again by recombining with the genes of ancient humans and the other two hominid groups so many times. Will we ever really know who the super-archaic ghosts of our ancestors were?

"That is the big question we are all wondering about," said Siepel."It is conceivable that it could be done, at least in principle,if very well-preserved remains were recovered from permafrost or from a cave that is well protected from the environment. But I do not know of any promising leads at present."

So dont be offended if someone calls you a Neanderthal. Just tell them science says you probably are to some extent, and so are they.

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Humans have had mystery DNA for 300,000 yearsand now we might finally know what it is - SYFY WIRE

The Secret to a Long, Healthy Life Is in the Genes of the Oldest Humans Alive – Singularity Hub

The first time I heard nematode worms can teach us something about human longevity, I balked at the idea. How the hell can a worm with an average lifespan of only 15 days have much in common with a human who lives decades?

The answer is in their genesespecially those that encode for basic life functions, such as metabolism. Thanks to the lowly C. elegans worm, weve uncovered genes and molecular pathways, such as insulin-like growth factor 1 (IGF-1) signaling that extends healthy longevity in yeast, flies, and mice (and maybe us). Too nerdy? Those pathways also inspired massive scientific and popular interest in metformin, hormones, intermittent fasting, and even the ketogenic diet. To restate: worms have inspired the search for our own fountain of youth.

Still, thats just one success story. How relevant, exactly, are those genes for humans? Were rather a freak of nature. Our aging process extends for years, during which we experience a slew of age-related disorders. Diabetes. Heart disease. Dementia. Surprisingly, many of these dont ever occur in worms and other animals. Something is obviously amiss.

In this months Nature Metabolism, a global team of scientists argued that its high time we turn from worm to human. The key to human longevity, they say, lies in the genes of centenarians. These individuals not only live over 100 years, they also rarely suffer from common age-related diseases. That is, theyre healthy up to their last minute. If evolution was a scientist, then centenarians, and the rest of us, are two experimental groups in action.

Nature has already given us a genetic blueprint for healthy longevity. We just need to decode it.

Long-lived individuals, through their very existence, have established the physiological feasibility of living beyond the ninth decade in relatively good health and ending life without a period of protracted illness, the authors wrote. From this rare but valuable population, we can gain insight into the physiology of healthy aging and the development of new therapies to extend the human healthspan.

While it may seem obvious now, whether genes played a role in longevity was disputed for over a century. After all, rather than genes, wouldnt access to health care, socioeconomic status, diet, smoking, drinking, exercise, or many other environmental and lifestyle factors play a much larger role? Similar to height or intelligence (however the latter is assessed), the genetics of longevity is an enormously complicated and sensitive issue for unbiased studying.

Yet after only a few genetic studies of longevity, a trend quickly emerged.

The natural lifespan in humans, even under optimal conditions in modern societies, varies considerably, the authors said. One study, for example, found that centenarians lived much longer than people born around the same time in the same environment. The offspring of centenarians also have lower chances of age-related diseases and exhibit a more youthful profile of metabolism and age-related inflammation than others of the same age and gender.

Together, about 25 to 35 percent of the variability in how long people live is determined by their genesregardless of environment. In other words, rather than looking at nematode worm genes, we have a discrete population of humans whove already won the genetic lottery when it comes to aging. We just need to parse what winning means in terms of biology. Genes in hand, we could perhaps tap those biological phonelines and cut the wires leading to aging.

Identification of the genetic factors that underlie extreme human lifespan should provide insights into the mechanisms of human longevity and disease resistance, the authors said.

Once scientists discovered that genes play a large role in aging, the next question was which ones are they?

They turned to genome-wide association studies, or GWAS. This big data approach scans existing genomic databases for variations in DNA coding that could lead to differences in some outcomefor example, long versus short life. The differences dont even have to be in so-called coding genes (that is, genes that make proteins). They can be anywhere in the genome.

Its a powerful approach, but not that specific. Think of GWAS as rudimentary debugging software for biological code: it only looks for differences between different DNA letter variants, but doesnt care which specific DNA letter swap most likely impacts the final biological program (aging, in this case).

Thats a huge problem. For one, GWAS often finds dozens of single DNA letter changes, none powerful enough to change the trajectory of aging by itself. The technique highlights a village of DNA variants, that together may have an effect on aging by controlling the cells course over a lifetime, without indicating which are most important. Its also hard to say that a DNA letter change causally leads to (or protects against) aging. Finally, GWAS studies are generally performed on populations of European ancestry, which leaves out a huge chunk of humansfor example, the Japanese, who tend to produce an outsized percentage of centenarians.

So what needs to change?

Rather than focusing on the general population, the key is to home in on centenarians of different cultures, socioeconomic status, and upbringing. If GWAS are like fishing for a rare species in several large oceans, then the authors point is to focus on pondsdistributed across the worldwhich are small, but packed with those rare species.

Extremely long-lived individuals, such as centenarians, compose only a tiny proportion (~0.01 percent to 0.02 percent) of the United States population, but their genes contain a biological blueprint for healthy aging and longevity, the authors said. Theyre spared from usual age-related diseases, and this extreme and extremely rare phenotype is ideal for the study of genetic variants that regulate healthspan and lifespan.

Its an idea that would usually make geneticists flinch. Its generally thought that the larger the study population, the better the result. Here, the recommendation is to narrow our focus.

And thats the point, the authors argue.

Whatever comes out of these studies will likely have a much larger impact on aging than a GWAS fishing experiment. Smaller (genomic) pond; larger (pro-youth) fish. Whats more, a pro-youth gene identified in one European-based long-living population can be verified in another group of centenarianssay, Japaneseensuring that the gene candidates reflect something fundamental about human aging, regardless of race, culture, upbringing, and wealth.

A genomic screen of centenarians can easily be done these days on the cheap. But thats only the first step.

The next step is to validate promising anti-aging genetic differences, similar to how scientists validated such differences in nematode worms during classic longevity studies. For example, a promising pro-youth gene variant can be genetically edited into mice using CRISPR or some other tool. Scientists can then examine how the mice grow up and grow old, compared to their non-edited peers. Does the gene make these mice more resilient to dementia? What about muscle wasting? Or heart troubles? Or hair greying and obesity?

From these observations, scientists can then use an enormous selection of molecular tools to further dissect the molecular pathways underlying these pro-youth genetic changes.

The final step? Guided by centenarian genes and validated by animal models of aging, we can design powerful drugs that sever the connection between the genes and proteins that drive aging and its associated diseases. Metformin is an experimental pill that came out of aging studies in nematode wormsimagine what studies in human centenarians will yield.

Despite enormous improvements in human health over the past century, we remain far from a situation in which living to 100 years of age in fairly good health is the norm, the authors said.

But as centenarians obviously prove, this is possible. By digging into their genes, scientists may find a path towards healthy longevitynot just for the genetically fortunate, but for all of us.

Image credit:Cristian Newman / Unsplash

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LogicBio Therapeutics Reports Second Quarter 2020 Financial Results and Provides Business UpdatesFDA Clears IND Application for LB-001 for the…

LEXINGTON, Mass., Aug. 10, 2020 (GLOBE NEWSWIRE) -- LogicBio Therapeutics, Inc. (Nasdaq:LOGC) (LogicBio or the Company), a company dedicated to extending the reach of genetic medicine with pioneering targeted delivery platforms, today reported financial results for the quarter ended June 30, 2020, provided a business update and announced the U.S. Food and Drug Administration (FDA) has cleared the Companys Investigational New Drug (IND) application for LB-001 for the treatment of methylmalonic acidemia in pediatric patients. LogicBio released a separate press release this morning providing further details on the planned Phase 1/2 clinical design for LB-001.

We are thrilled to have received clearance to move forward with this first-in-human clinical trial with our lead product candidate, LB-001, for the treatment of methylmalonic acidemia, a life-threatening congenital genetic disease with no current therapeutic treatment options. This represents a significant milestone in our goal of bringing a treatment to MMA patients as well as for our GeneRide platform. We have maintained continuous dialogue with the centers of excellence that are planned to participate in the Phase 1/2 clinical trial, and we look forward to activating these sites as quickly as possible, said Fred Chereau, CEO of LogicBio. We have instituted systems attempting to mitigate COVID-19 dynamics on our study start-up process and, based on our best estimates, we plan to enroll our first patient in early 2021.

Commenting on the Next Generation Capsid Program, Mr. Chereau said, We are very excited about the recent advances in our novel capsid program, which has generated liver-tropic capsids intended for use in gene editing technologies such as GeneRide and other gene therapy approaches. We are focused on executing across all of our programs and look forward to sharing further details on our novel capsids in early 2021.

Appointment of Daniel Gruskin, M.D. to SVP, Head of Clinical Development

Daniel Gruskin, M.D. was appointed as SVP, head of clinical development in August 2020. Dr. Gruskin has served as interim head of clinical development of LogicBio since June 2020. In April 2020, Dr. Gruskin started consulting with the Company as a special advisor. Previously, Dr. Gruskin served in roles of increasing responsibility at Sanofi Genzyme, most recently as vice president, head of global medical affairs, rare disease, in which capacity he oversaw medical affairs, life cycle management, scientific affairs and other medical and development activities related to metabolic, rare and/or genetic diseases. Prior to his role at Sanofi Genzyme, Dr. Gruskin served as assistant professor, human genetics and pediatrics at Emory University School of Medicine, where he was also the chief of the genetics section at Childrens Healthcare of Atlanta.

Daniel has been instrumental in leading LB-001 clinical development efforts including getting the IND cleared. His deep experience in genetic medicines and metabolic diseases will serve LogicBio well as we look to execute on our goals for both the GeneRide and Next Generation Capsid platforms in search of transformative medicines, said Mr. Chereau.

Anticipated Milestones for 2020 and 2021:

Second Quarter 2020 Financial Results

Three Months Ended June 30, 2020 and 2019

About LogicBio Therapeutics

LogicBio Therapeuticsis dedicated to extending the reach of genetic medicine with pioneering targeted delivery platforms.

LogicBios proprietary genome editing technology platform, GeneRide, enables the site-specific integration of a therapeutic transgene without nucleases or exogenous promoters by harnessing the native process of homologous recombination. LogicBio has received FDA clearance for the first-in-human clinical trial of LB-001, a wholly owned genome editing program leveraging GeneRide for the treatment of methylmalonic acidemia. Patient enrollment is expected to begin in early 2021. In addition, LogicBio has a collaboration with Takeda to research and develop LB-301, an investigational therapy leveraging GeneRide for the treatment of the rare pediatric disease Crigler-Najjar syndrome.

LogicBio is also developing a Next Generation Capsid platform for use in gene editing and gene therapies. Data presented have shown that the capsids deliver highly efficient functional transduction of human hepatocytes with improved manufacturability with low levels of pre-existing neutralizing antibodies in human samples. Top-tier capsid candidates from this effort demonstrated significant improvements over benchmark AAVs currently in clinical development. LogicBio is developing these highly potent vectors for internal development candidates and potentially for business development collaborations.

LogicBio is headquartered inLexington, Mass. For more information, please visitwww.logicbio.com.

Forward Looking Statements

This press release contains forward-looking statements within the meaning of the federal securities laws, including those related to the Companys plans to initiate, advance and complete its planned SUNRISE Phase 1/2 clinical trial of LB-001 in MMA; the timing, progress and results of the Companys research and development activities, including those related to the GeneRide technology platform and Next Generation Capsid Program; its plans for LB-301 in Crigler-Najjar; and the sufficiency of its cash and cash equivalents to fund operating expenses and capital expenditure requirements. These are not statements of historical facts and are based on managements beliefs and assumptions and on information currently available. They are subject to risks and uncertainties that could cause the actual results and the implementation of the Companys plans to vary materially, including the risks associated with the initiation, cost, timing, progress and results of the Companys current and future research and development activities and preclinical studies and potential future clinical trials. In particular, the impact of the COVID-19 pandemic on the Companys ability to progress with its research, development, manufacturing and regulatory efforts, including the Companys plans to initiate, advance and complete its Phase 1/2 clinical trial for LB-001 in MMA, and the value of and market for the Companys common stock, will depend on future developments that are highly uncertain and cannot be predicted with confidence at this time, such as the ultimate duration of the pandemic, travel restrictions, quarantines, social distancing and business closure requirements in the United States and in other countries, and the effectiveness of actions taken globally to contain and treat the disease. These risks are discussed in the Companys filings with the U.S. Securities and Exchange Commission (SEC), including, without limitation, the Companys Annual Report on Form 10-K filed on March 16, 2020 with the SEC, the Companys Quarterly Report on Form 10-Q filed on May 11, 2020, and the Companys subsequent Quarterly Reports on Form 10-Q and other filings with the SEC. Except as required by law, the Company assumes no obligation to update these forward-looking statements publicly, even if new information becomes available in the future.

Contacts:

Investors:Brian LuqueAssociate Director, Investor Relationsbluque@logicbio.com951-206-1200

Media:Stephanie SimonTen Bridge CommunicationsStephanie@tenbridgecommunications.com617-581-9333

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LogicBio Therapeutics Reports Second Quarter 2020 Financial Results and Provides Business UpdatesFDA Clears IND Application for LB-001 for the...

Research on Tasmanian devil offers new insights into tackling human cancer – National Science Foundation

Findings offer hope for the Tasmanian devil, at the brink of extinction

This Tasmanian devil's future hangs in the balance, and with it, perhaps human health discoveries.

August 10, 2020

A rare, transmissible tumor has brought the iconic Tasmanian devil to the brink of extinction, but new research by scientists at Washington State University and the Fred Hutchinson Cancer Research Center in Seattle shows hope for the animals' survival -- and possible new treatments for human cancers.

The U.S. National Science Foundation-funded study, published in Genetics, found a single genetic mutation that leads to reduced growth of a transmissible cancer in Tasmanian devils in the wild.

"This gene is also implicated in human prostate and colon cancers," said biologist Andrew Storfer. "The findings hold the promise of helping save the world's few remaining Tasmanian devils, and could also translate to human health."

The research team studied the genomes of cases of devil facial tumor disease that regressed spontaneously -- that is, the cancer began disappearing on its own.

The scientists were surprised to find that the mutation contributing to tumor regression doesn't change the gene function but instead turns on a gene that slows cell growth in the tumor. At least, it behaves that way in the lab.

While infections cause up to 20% of all human cancers -- such as gastric cancer from Helicobacter pylori and cervical cancer from human papillomavirus -- for Tasmanian devils, the cancer is the infection.

The devil facial tumor disease spreads between the animals when they bite each other during common social behaviors. Since the mid-1990s, the disease has decimated the population of these carnivorous marsupials, which are now found only on the island state of Tasmania, off the southeastern coast of Australia.

"Although this disease is largely fatal, we're seeing tumors disappear from an increasing number of individual animals," Storfer said. "We hope to learn something that could be applied to understanding and possibly treating a number of human cancers in the future."

Added Sam Scheiner, a program director in NSF's Division of Environmental Biology, "These results show that basic research can produce totally unexpected results that are important for a completely different problem."

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Research on Tasmanian devil offers new insights into tackling human cancer - National Science Foundation

Human Genetics Market 2020 Size by Product Analysis, Application, End-Users, Regional Outlook, Competitive Strategies and Forecast to 2027 – Owned

New Jersey, United States,- Market Research Intellect aggregates the latest research on Human Genetics Market to provide a concise overview of market valuation, industry size, SWOT analysis, revenue approximation, and regional outlook for this business vertical. The report accurately addresses the major opportunities and challenges faced by competitors in this industry and presents the existing competitive landscape and corporate strategies implemented by the Human Genetics market players.

The Human Genetics market report gathers together the key trends influencing the growth of the industry with respect to competitive scenarios and regions in which the business has been successful. In addition, the study analyzes the various limitations of the industry and uncovers opportunities to establish a growth process. In addition, the report also includes a comprehensive research on industry changes caused by the COVID-19 pandemic, helping investors and other stakeholders make informed decisions.

Key highlights from COVID-19 impact analysis:

Unveiling a brief about the Human Genetics market competitive scope:

The report includes pivotal details about the manufactured products, and in-depth company profile, remuneration, and other production patterns.

The research study encompasses information pertaining to the market share that every company holds, in tandem with the price pattern graph and the gross margins.

Human Genetics Market, By Type

Human Genetics Market, By Application

Other important inclusions in the Human Genetics market report:

A brief overview of the regional landscape:

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Market Research Intellect provides syndicated and customized research reports to clients from various industries and organizations with the aim of delivering functional expertise. We provide reports for all industries including Energy, Technology, Manufacturing and Construction, Chemicals and Materials, Food and Beverage, and more. These reports deliver an in-depth study of the market with industry analysis, the market value for regions and countries, and trends that are pertinent to the industry.

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University of Texas researchers find mutation that led to 2015-2016 Zika outbreak – Homeland Preparedness News

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A team from The University of Texas Medical Branch at Galveston has found a Zika virus mutation that may be responsible for the outbreak that occurred in 2015 and 2016.

Mosquitoes primarily transmit the Zika virus. Because it circulates between mosquitoes and animals/humans, they are prone to genetic mutations, making them highly capable of emerging and causing epidemics.

The UTMB team has identified a mutation in the Zika envelope protein that can enhance mother-to-baby transmission in pregnant mice, increase neurological disease and lethality in newborn mice and elevate virus levels in the blood of infected non-human primates.

Our study demonstrates that the Zika envelope mutation V473M, which just occurred before the 2015 epidemic in the Americas, enhances Zika virus particle assembly in infected cells. The enhanced virus assembly leads to increased human disease and maternal transmission, Pei-Yong Shi, I.H. Kempner professor of Human Genetics at UTMB, said. The viral genetic change reported here, combined with the nave herd immunity, may have accounted for the Zika epidemic and severe diseases in 2015 and 2016.

The UTMB team has received grants from the National Institutes of Health and philanthropic support from the Sealy & Smith Foundation; Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation; John S. Dunn Foundation; Amon G. Carter Foundation; Gillson Longenbaugh Foundation; Summerfield G. Roberts Foundation.

RNA viruses are the pathogens most often responsible for outbreaks and epidemics, including Ebola virus and SARS-CoV-2, the virus causing COVID-19, Shi said. Understanding the mechanisms of viral emergence and transmission is essential to detect and respond to future outbreaks. Although the world is currently focusing on COVID-19, I am certain that COVID-19 will not be the last emerging virus we face. Moving forward, building public health capacity and countermeasure technology are the only effective means to overcome these threats.

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University of Texas researchers find mutation that led to 2015-2016 Zika outbreak - Homeland Preparedness News

Blood lipid levels may be altered in some autistic people – Spectrum

Blood biomarker: Levels of lipids, such as cholesterol and triglycerides, may be altered in a subgroup of people with autism.

Sebastian Kaulitzki / Science Photo Library / Getty Images

Nearly 7 percent of autistic people in the United States have abnormal blood levels of fatty compounds called lipids, according to a study published today in Nature Medicine1. The studys approach, drawing on multiple datasets, could help researchers parse autism into subtypes, the researchers say.

Past studies have shown a link between this metabolic condition, called dyslipidemia, and autism in people with rare genetic conditions2.But this is the first in-depth, multidimensional analysis to establish a robust association with autism more broadly, says Yuan Luo, study investigator and associate professor of preventive medicine at Northwestern University in Chicago, Illinois.

The study used a comprehensive approach integrating large datasets, including healthcare claims, electronic health records, familial gene sequences and an atlas of developmental gene-expression patterns.

Just as combining geographical data from various maps can help navigation tools create a more comprehensive view of the world, integrating datasets about various facets of autism can help us better understand the condition, says lead investigator Isaac Kohane, professor of biomedical informatics at Harvard University.

Using one modality gives you only one perspective, whereas using multiple modalities gives you a holistic perspective, he says.

Autism is a highly varied condition, with multiple genetic and environmental influences. Analyzing large and diverse datasets can help researchers parse the condition into smaller subgroups with shared phenotypes and devise bespoke treatments, Kohane says.

The new work may also help clinicians identify biological markers for screening autistic children early in development, rather than relying on behavioral traits.

This is important because currently autism diagnosis is only based on symptoms. But when you actually see these symptoms, its already too late, Luo says. [These findings] could be of immediate clinical utility, and we plan to directly test those by future studies, including clinical trials.

First the team mapped out how genes work in concert during prenatal human brain development, a critical time window for autism. They used the BrainSpan online atlas to obtain data on the expression patterns of exons the parts of genes that code for proteins in 26 brain regions. They then narrowed in on clusters of exons that are expressed differently between boys and girls, given sex differences seen in autism.

Next, the researchers identified autism-related mutations found in the exons of autistic people. To do so, they searched a database of genetic sequences for 3,531 people from 50 families with two to five autistic children, looking for mutations shared by all autistic siblings within each family, as well as 1,704 families with autistic and unaffected sibling pairs, focusing on the mutations found only in the children with autism.

They then looked for overlaps between the exon clusters identified via the atlas and those with autism mutations, identifying 33 in common. Some contain the exons of genes involved in lipid protein regulation; mutations in them could lead to low levels of lipoproteins, cholesterol and triglycerides in the blood. The findings point to a possible association between autism and dyslipidemia, the researchers say.

To test this theory, the team analyzed medical records of 2.75 million people at Boston Childrens Hospital in Massachusetts, 25,514 of whom are children with autism. As a group, autistic children show significant alterations in blood lipid profiles compared with age-matched controls. For example, children with autism have higher triglyceride levels, regardless of age, medication, sex or metabolic conditions, such as obesity or diabetes.

The team examined healthcare claims for more than 34 million people across the United States, including 80,714 autistic people. They found that 6.6 percent of people with autism have dyslipidemia.

The study also found that parents with a history of dyslipidemia have up to 16 percent greater odds of having autistic children a result the researchers hope to investigate further in future studies, Luo says.

The findings jibe with previous research showing that dyslipidemia-associated genes are involved with several mechanisms key to neuronal function, such as controlled cell death.

However, its still unclear how lipids may affect the human brain, says Michael Snyder, professor of genetics at Stanford University in Palo Alto, California, who was not involved in the study. More research manipulating lipid levels by either knocking out dyslipidemia-associated genes in mice or using medication may offer a clearer understanding of this association.

In particular, researchers should try using lipid-lowering drugs, such as statins, in autistic people with dyslipidemia to determine whether the treatment improves their lipid levels and eases autism traits, Snyder says.

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NIH taps Dr. Lindsey Criswell as director of the National Institute of Arthritis and Musculoskeletal and Skin Diseases – National Institutes of Health

News Release

Thursday, August 6, 2020

National Institutes of Health Director Francis S. Collins, M.D., Ph.D., has selected Lindsey A. Criswell, M.D., M.P.H., D.Sc., as director of NIHs National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS). A rheumatologist, Dr. Criswell is currently the vice chancellor of research at the University of California, San Francisco (UCSF). She is a professor of rheumatology in UCSFs Department of Medicine, as well as a professor of orofacial sciences in its School of Dentistry. She is expected to begin her new role as the NIAMS director in early 2021. She will succeed long-time directorStephen I. Katz, M.D., Ph.D., who passed away suddenly in December 2018.

Dr. Criswell has rich experience as a clinician, researcher and administrator. Her ability to oversee the research program of one of the countrys top research-intensive medical schools, and her expertise in autoimmune diseases, including rheumatoid arthritis and lupus, make her well-positioned to direct NIAMS, said Dr. Collins. I look forward to having her join the NIH leadership team early next year. I also want to thank Robert H. Carter, M.D., for his exemplary work as the acting director of NIAMS since December 2018.

As NIAMS director, Dr. Criswell will oversee the institutes annual budget of nearly $625 million, which supports research into the causes, treatment and prevention of arthritis and musculoskeletal and skin diseases. The institute advances health through biomedical and behavioral research, research training and dissemination of information on research progress in these diseases.

The NIAMS Division of Extramural Research supports scientific studies and research training and career development throughout the country through grants and contracts to research organizations in fields that include rheumatology, muscle biology, orthopaedics, bone and mineral metabolism and dermatology. NIAMS-supported research addresses some of the most common and disabling chronic diseases that affect almost every household in America.

Dr. Criswell has been a principal investigator on multiple NIH grants since 1994 and has published more than 200 peer-reviewed journal papers. Her research focuses on the genetics and epidemiology of human autoimmune disease, particularly rheumatoid arthritis and systemic lupus erythematosus. Using genome-wide association and other genetic studies, her research team contributed to the identification of more than 30 genes linked to these disorders.

Dr. Criswells many honors include the Kenneth H. Fye, M.D., endowed chair in rheumatology and the Jean S. Engleman Distinguished Professorship in Rheumatology at UCSF, and the Henry Kunkel Young Investigator Award from the American College of Rheumatology. She also received UCSFs 2014 Resident Clinical and Translational Research Mentor of the Year. During her career, she has mentored some four dozen students (high school through medical/graduate school), medical residents, postdoctoral fellowsand junior faculty.

Dr. Criswell earned a bachelors degree in genetics and a masters degree in public health from the University of California, Berkeley; a D.Sc. in genetic epidemiology from the Netherlands Institute of Environmental Health Sciences, Rotterdam; and an M.D. from UCSF. In addition to completing a residency in internal medicine and a fellowship in rheumatology, she is certified as a first responder in wilderness medicine.

The mission of the NIAMS, a part of the U.S. Department of Health and Human Services' National Institutes of Health (NIH), is to support research into the causes, treatment and prevention of arthritis and musculoskeletal and skin diseases; the training of basic and clinical scientists to carry out this research; and the dissemination of information on research progress in these diseases. For more information about the NIAMS, call the information clearinghouse at (301) 495-4484 or (877) 22-NIAMS (free call) or visit the NIAMS website at https://niams.nih.gov.

About the National Institutes of Health (NIH):NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

NIHTurning Discovery Into Health

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NIH taps Dr. Lindsey Criswell as director of the National Institute of Arthritis and Musculoskeletal and Skin Diseases - National Institutes of Health

‘Hyper urban’ coyote genomes are growing apart from their city and rural cousins – Massive Science

Imagine a coyote, rangy and resilient. Is she ambling through a canyon dotted with sagebrush or loping in an urban alley lined with dumpsters? In recent decades, the latter has become a more common sight. As cities expand, coyotes move right in. Rather than shrinking from the big-city lights, they rummage for opportunities.

But even as individual coyotes thrive, cities' built features are shaping their genomesacross generations, according to a recent study in the Journal of Urban Ecology. A widening genetic gulf separates city coyotes and their country cousins. And as urban space sprawls, coyotes genetic diversity declines. This finding suggests that humans built environment has consequences even for creatures that seem to thrive in our midst.

Scientists already know city coyotes tend to differ from their country counterpartsin behavior: theyre bolder and more exploratory, more likely to eat human-sourced foods and occupy a smaller territory. But the picture of what genetic differences if any might exist between coyotes has been more murky.

About 30 years ago, fewgeneticdifferences existed between coyotes across North America suggesting coyotes moved freely, and so did their genes. Historically, coyotes ranged only across the arid West and Great Plains. Since 1900, they have beenpushing out of their home turf, and today they prowl the continent from coast to coast. Scientists assumed that mobile, adaptable coyotes weren't impeded much by urban sprawl. More recent studies have found coyotes clustering genetically by range or region, but few have honed in on specific urban areas.

Urban coyote

National Park Service

By narrowing their focus to the greater Los Angeles area, scientists from Pepperdine University uncovered a more complex picture lurking in urban coyotes genes. Pulling DNA from 125 samples of muscle, liver, and skin, they examined coyotes living in mountains, farmland, suburbs, and the city. The team mapped coyotes genetic structure alongside the surrounding landscape, accounting for key urban features like freeways and road density.

A clear split between urban and rural coyotes emerged. Rural coyotes living among mountains and natural vegetation formed the largest, most genetically diverse group. Urban coyotes, on the other hand, made up three distinct clusters each with decreased genetic diversity. Researchers could deduce which coyotes roam wide-open spaces and which dodge city traffic.

Rural coyotes shared a similar genetic profile even across long distances, suggesting natural barriers didnt impede their movement or gene flow. Even in coyotes separated by 160 miles, rural coyotes clustered with each other instead of their urban counterparts nearby. The surrounding environment mattered more than the geographic distance.

Why this genetic split between city and country coyotes? It could stem in part from natal-biased habitat dispersal, the researchers suggest. Animals tend to prefer habitats similar to where they grew up. When an urban coyote knows how to avoid the citys hazards and harvest its resources, she is more likely to raise babies with those skills. And when generations of street-smart coyotes stick around the same spot, the genetic gap between them and their country cousins widens.

But this isnt the whole story, the researchers argue. City coyotes werent just genetically distinct from their rural relatives; their DNA also differed from that of other city coyotes. Rather than forming one large group as the rural coyotes did, urban coyotes split into three genetically distinct populations.

The cities built features help explain why. One distinct cluster of city coyotes prowled through downtown Los Angeles, lurked by the Hollywood sign, and roamed near the Long Beach Airport. The coyotes in this clusterhad both DNA and habitat in common hyper-urban areas with high road density.

Scientists found a similar pattern in Orange County. Where major highways and commercial districts sliced through the land, so did a boundary between two distinct coyote populations. Despite roaming a similar urban environment, coyotes on one side of the highway were genetically distinct from their relatives on the other side. Coyotes' genetic structure mirrored the urban terrain.

Coyote

Peter Eades / USFWS

These findings suggest humans built environment shapes coyotes movement, the researchers argue. Major freeways, dense roads, and human development prevent urban coyotes from crossing into other areas. These built barriers keep old residents in, and new migrants out and thus leave a stamp on coyotes DNA across generations.

This is important because when a population becomes isolated, their genetic diversity tends to dwindle. Genetic diversity reflects a populations overall health, as well as an ability to adapt to future changes in the environment. Think of it like a box of tools passed down for a vast, unpredictable, multi-generational home restoration project. If the roof collapses or the plumbing busts, youre going to need more than just a hammer. The more options you have, the better whether theyre hand tools orgenes. Each genetic characteristic represents another option, in a toolbox of past solutions and potential answers.

Even as individual urban coyotes thrive, their collective genetic toolbox shrinks. The citys built features restrict urban coyotes travels more than previously thought, with significant effects on their population genetics. These findings suggest that urbanization even takes a toll on creatures that seem to flourish in human environments.

This result also points to the importance of preserving natural corridors in cities not just for coyotes, but for other urban wildlife, too. Safe passageways allow diverse species to cross between habitats, enabling both physical movement and gene flow. Los Angeles County has made natural corridors a priority by identifying Significant Ecological Areas (SEAs) and planning links between them. In fact, in 2023, Los Angeles is slated to become home to the largest wildlife corridor in the world a highway overpass in the works since 2019.

Coyotes have a reputation as survivors, adaptable and enduring. But urbanization is also here to stay, and scientists are still learning about its genetic implications for our wildlife neighbors. This study highlights the value of better understanding these effects on all creatures in the urban landscape even the most versatile and wily of them all.

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'Hyper urban' coyote genomes are growing apart from their city and rural cousins - Massive Science

Why scientists are worried about a ‘Warp Speed’ COVID-19 vaccine – New Haven Register

An engineer displays an experimental vaccine for the COVID-19 during testing at the Quality Control Laboratory at Sinovac Biotech facilities in Beijing in this April file photo. A total of 27 drugmakers are working on vaccines for the disease.

An engineer displays an experimental vaccine for the COVID-19 during testing at the Quality Control Laboratory at Sinovac Biotech facilities in Beijing in this April file photo. A total of 27 drugmakers are

Photo: Nicolas Asfouri, AFP Via Getty Images

An engineer displays an experimental vaccine for the COVID-19 during testing at the Quality Control Laboratory at Sinovac Biotech facilities in Beijing in this April file photo. A total of 27 drugmakers are working on vaccines for the disease.

An engineer displays an experimental vaccine for the COVID-19 during testing at the Quality Control Laboratory at Sinovac Biotech facilities in Beijing in this April file photo. A total of 27 drugmakers are

Why scientists are worried about a 'Warp Speed' COVID-19 vaccine

As the race for a COVID-19 vaccine heads into the stretch run, scientists are tempering their enthusiasm with caution.

The biotechnology company Moderna and the National Institutes of Health have begun Phase III efficacy trials for their vaccine. The University of Oxford and Pfizer are running combined Phase II and III testing for their respective drugs. All together, drugmakers have 27 vaccines in trials.

The goal of Operation Warp Speed, the U.S. vaccine initiative, is 300 million doses of a safe, effective vaccine by January, and if realized, it would be one of the greatest scientific achievements of all time. On Tuesday, Goldman Sachs predicted the Food and Drug Administration would approve at least one vaccine before the end of the year.

Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, said last month he was hopeful a vaccine would be available by late fall or early winter.

Heres what worries scientists:

FDA regulators will likely face enormous political pressure to approve a vaccine, even one thats not proven safe and effective.

A vaccine thats less effective than billed could cause wider spread of the pandemic, Michael S. Kinch, director of the Centers for Research Innovation in Biotechnology and Drug Discovery at Washington University in St. Louis, writes in Stat News.

A merely short-term effect could encourage vaccinated individuals to resume risky behaviors, which would all but guarantee that the epidemic endures, argues Kinch, who is also a professor of biochemistry and molecular biophysics.

A vaccine would likely erode compliance of social distancing and mask wearing, measures that are proven effective against spread of the virus.

They automatically are going to say, Oh great, Im just going to get my little vaccine, and I can go back and do exactly the things I was doing last year. That is absolutely not true, Maria Elena Bottazzi, associate dean of the National School of Tropical Medicine at Baylor College of Medicine, told Business Insider in an interview.

We dont have enough data.

What we have right now is a collection of animal data, immune response data and safety data based on early trials and from similar vaccines for other diseases, writes Natalie Dean, assistant professor of biostatistics at the University of Florida, in the New York Times.

The evidence that would convince me to get a COVID-19 vaccine, or to recommend that my loved ones get vaccinated, does not yet exist, she says.

If a substandard vaccine is green-lighted without adequate testing or trials, unforeseen harmful side effects could emerge. A weak initial vaccine and/or one with dangerous side effects would likely cause confidence in all vaccines to plummet and strengthen anti-vaccine sentiments. If a safer, more effective vaccine were subsequently developed, the residual mistrust could result in fewer people getting vaccinated.Epidemiologists estimate that to tame the pandemic, at least 70 percent of the population may need to develop immunity, either by vaccine or getting infected. Millions of Americans refusing to get inoculated by a vaccine thats at least 50 percent effective (the minimum level according to the World Health Organization) could thwart that goal.

A vaccine might only provide short-term immunity because of the nature of coronaviruses. Back in April, Dr. David States, professor of human genetics and director of bioinformatics at the University of Michigan, tweeted:

If youre hoping a vaccine is going to be a knight in shining armor saving the day, you may be in for a disappointment. SARS COV2 is a highly contagious virus. A vaccine will need to induce durable high level immunity, but coronaviruses often dont induce that kind of immunity.

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Mike Moffitt is an SFGATE Reporter. Email: moffitt@sfgate.com. Twitter: @Mike_at_SFGate

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Why scientists are worried about a 'Warp Speed' COVID-19 vaccine - New Haven Register

Gyroscope Announces Appointment of Leaders in Retinal Disease, Gene Therapy and the Complement System to Its Clinical and Scientific Advisory Boards -…

LONDON--(BUSINESS WIRE)--Gyroscope Therapeutics Limited, a clinical-stage retinal gene therapy company, today announced the appointment of leading experts in retinal disease, gene therapy and the complement system to its Clinical and Scientific Advisory Boards. The newly appointed boards will help guide the development of the company's lead investigational gene therapy, GT005, a one-time therapy being developed to potentially slow the progression of dry age-related macular degeneration (AMD), as well as novel gene therapy delivery systems and additional pipeline candidates.

This is an exciting time for Gyroscope and we are honoured to have a group of highly esteemed leaders in retinal surgery, ophthalmology and gene therapy join our Clinical Advisory Board, said Nadia Waheed, M.D., Chief Medical Officer of Gyroscope. We look forward to working with these leaders as we advance the clinical development of GT005 and our proprietary delivery system, with the ultimate goal of helping preserve the sight of millions of people who suffer from vision loss as a result of dry AMD.

We have embarked upon an ambitious journey exploring the potential of gene therapy beyond rare disease and building a pipeline of potential medicines for one of the worlds leading causes of blindness, said Jane Hughes, Ph.D., Chief Scientific Officer of Gyroscope. We are excited to welcome our Scientific Advisory Board members to Gyroscope and to benefit from the insights of some of the worlds leading experts as we advance our understanding of the role of the complement system in retinal diseases.

Members of the Gyroscope Therapeutics Clinical Advisory Board include:

Professor Jacque Duncan, M.D. Professor of Ophthalmology at the University of California, San Francisco School of Medicine.

Jeffrey Heier, M.D. Co-President and Medical Director, Director of the Vitreoretinal Service and Director of Retina Research at Ophthalmic Consultants of Boston.

Professor Allen Ho, M.D. Professor of Ophthalmology at Sidney Kimmel Medical College of Thomas Jefferson University, and Attending Surgeon and Director of Retina Research at Wills Eye Hospital in Philadelphia.

Professor Nancy Holekamp, M.D. Director of Retina Services at Pepose Vision Institute and Professor of Clinical Ophthalmology at the Washington University School of Medicine in St. Louis.

Arshad Khanani, M.D., M.A. Managing Partner, Director of Clinical Research and Director of Fellowship at Sierra Eye Associates, and Clinical Associate Professor at the University of Nevada, Reno School of Medicine.

Professor Robert MacLaren Professor of Ophthalmology at the University of Oxford in the United Kingdom, Consultant Ophthalmologist at the Oxford Eye Hospital, Honorary Professor of Ophthalmology at the UCL Institute of Ophthalmology, Honorary Consultant Vitreoretinal Surgeon at Moorfields Eye Hospital, and an NIHR Senior Investigator. Professor MacLaren is also a member of the Scientific Advisory Board.

Professor Sir Keith Peters, M.D. Senior Consultant to The Francis Crick Institute in London and Regius Professor of Physic Emeritus at the University of Cambridge in the United Kingdom. Professor Peters is also a member of the Scientific Advisory Board.

Professor Hendrik Scholl, M.D. Founder and Director of the Institute of Molecular and Clinical Ophthalmology Basel in Switzerland, and Professor and Chairman of the Department of Ophthalmology at the University of Basel.

Professor David Steel, M.D., MBBS, FRCOphth Consultant Ophthalmologist at Sunderland Eye Infirmary in the United Kingdom and Honorary Professor of Retinal Surgery at Newcastle University in Newcastle upon Tyne, United Kingdom. Professor Steel is also a member of the Scientific Advisory Board.

Professor Bernhard Weber, Ph.D. Head of Institute of Human Genetics, Head of Institute of Clinical Human Genetics, and Director of the Diagnostics Unit for DNA Testing and Vice President of Research of the University of Regensburg, Germany.

Charles Wykoff, M.D., Ph.D. Director of Research at Retina Consultants of Houston, Deputy Chair for Ophthalmology at Blanton Eye Institute, and Clinical Associate Professor of Ophthalmology Weill Cornell Medical College at Houston Methodist Hospital.

Members of the Gyroscope Scientific Advisory Board include:

Professor Alberto Auricchio, M.D. Professor of Medical Genetics at the Department of Advanced Biomedicine, Federico II University in Naples, and Coordinator of the Molecular Therapy Program at Telethon Institute of Genetics and Medicine (TIGEM) in Pozzuoli (NA), in Italy.

Professor Pete Coffey, DPhil Theme Lead of Development, Ageing and Disease at University College Londons Institute of Ophthalmology and the Co-Executive Director of Translation at the University of California Santa Barbaras Center for Stem Cell Biology and Engineering.

Professor Claire Harris Professor of Molecular Immunology at Newcastle University.

Professor David Kavanagh, Ph.D., FRCP Professor of Complement Therapeutics at the National Renal Complement Therapeutics Centre (NRCTC), Newcastle University.

Professor Sir Peter Lachmann, FRS, FMEDSCI Emeritus Sheila Joan Smith Professor of Immunology, University of Cambridge.

Professor Robert MacLaren Professor MacLaren is also a member of the Clinical Advisory Board.

Professor Sir Keith Peters, M.D. Professor Peters is also a member of the Clinical Advisory Board.

Professor Matthew Pickering, Ph.D., M.B., B.S. Professor of Rheumatology, Imperial College LondonHonorary Consultant Rheumatologist, Imperial College Healthcare NHS Trust, and Wellcome Trust Senior Fellow in Clinical Science.

Professor David Steel, M.D., MBBS, FRCOphth Professor Steel is also a member of the Clinical Advisory Board.

Professor Timothy Stout, M.D. Sid W. Richardson Professor and Margarett Root Brown Chair of the Department of Ophthalmology, and Director of the Cullen Eye Institute at Baylor College of Medicine in Houston.

Full biographies for members of the Gyroscope Advisory Boards are available at http://www.gyroscopetx.com.

About Gyroscope Therapeutics: Vision for Life

Gyroscope Therapeutics is a clinical-stage retinal gene therapy company developing and delivering gene therapy beyond rare disease to treat a leading cause of blindness, dry age-related macular degeneration (AMD). Currently, there are no approved treatments for dry AMD.

Our investigational gene therapy, GT005, is designed to restore balance to a part of our immune system called the complement system. An overactive complement system leads to inflammation that damages healthy eye tissues. Our ultimate goal is to slow the progression of dry AMD. Patients in our Phase I/II clinical trial, known as the FOCUS study, receive a single dose of GT005 through an injection under their retina.

Syncona Ltd, our lead investor, helped us create the only retinal gene therapy company to combine discovery, research, drug development, a manufacturing platform, and surgical delivery capabilities. Headquartered in London with locations in Philadelphia and San Francisco, our mission is to preserve sight and fight the devastating impact of blindness. For more information, visit http://www.gyroscopetx.com and follow us on Twitter (@GyroscopeTx) and on LinkedIn.

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Gyroscope Announces Appointment of Leaders in Retinal Disease, Gene Therapy and the Complement System to Its Clinical and Scientific Advisory Boards -...

Noel Rose, Who Demonstrated Autoimmunity Exists, Dies at 92 – The Scientist

Noel Rose, an immunologist and microbiologist whose early experiments underpinned the molecular mechanisms of autoimmune disease, died of a stroke July 30. He was 92.

As a young medical student, Rose worked alongside his mentor, Ernest Witebsky of the University at Buffalo, studying organ-specific antigens. The prevailing hypothesis for the last half century had been that the body was incapable of producing antigens against itself, an idea known as horror autotoxicus. Witebskys own academic lineage stretched back to the ideas original progenitor, Paul Ehrlich, who had coined the term in the 18th century.

But Rose showed that rabbits injected with their own thyroid-derived antigens mounted an immune response against the invading molecules that damaged or destroyed the animals thyroid. The body was indeed capable of attacking itself. The results were so outlandish that the first journals refused to publish the findings, and it took years of careful experimentation to finally topple the paradigm of horror autotoxicus.Over the next several decades, Rose would further characterize the genetic and environmental causes of autoimmune diseases, publishing more than 880 articles and book chapters on the subject, according to Johns Hopkins University.

In every aspect, [Rose] is the father of autoimmunity, George Tsokos, a professor of rheumatology at Harvard Medical School, told The Scientist in a profile of Rose this year. The man opened a whole chapter in the book of medicine.

Currently, there are more than 80 recognized autoimmune diseases, including lupus, type 1 diabetes, rheumatoid arthritis, and AIDS, that have sickened more than 20 million Americans. Speaking to The Washington Post in 1995, Rose called autoimmune diseases one of the big three, meaning cancer, heart disease, and autoimmune disease.

Rose was born December 3, 1927, in Stamford, Connecticut. His father, a physician who served during World War II, became a specialist in treating rheumatic fever, now considered to be an autoimmune disease, the Post reports.

Prior to his groundbreaking work, Rose frequently brushed up against the limitations of medical knowledge at the time. When he began his undergraduate degree at Yale University in the mid-1940s, he wanted to study microbiology, but he was only able to attend a handful of classes on the topic. Instead, he majored in zoology and took the electives in microbiology, which were taught by botanistsbacteria were largely thought to be plants at the time, The Scientist reported in June.

Rose decided to complete a PhD ahead of attending medical school. He joined the lab of microbiologist Harry Morton at the University of Pennsylvania in 1948, where he spent the next several years studying the flagella-like motor structures of Treponema pallidum, the bacterium that causes syphilis.

Next, Rose enrolled as a medical student at the University at Buffalo, where he would make many of his most important medical discoveries. It was here, working alongside Witebsky, that he first demonstrated autoimmunity in rabbits.

Rose extracted a protein called thyroglobulin from humans, horses, and pigs, treated it with a solution called Freunds adjuvant to induce an immune response, and injected it into rabbits. Even though the injected thyroglobulin was similar to the protein already in the rabbits body, the animals still produced protective antibodies. This was true even when the protein, primed by the adjuvant that induces an immune response, came from another rabbit, and most surprisingly, when the protein was extracted and re-injected into the same animal. When he looked at the thyroids of these rabbits, he found that they were often damaged, and sometimes destroyed, by the bodys own immune response.

After having their findings rejected during peer review, Witebsky and Rose turned to studying autoimmunity in humans, determined to replicate and refine their work. They focused on Hashimotos disease, a rare thyroid condition with no identifiable cause, showing that serum taken from patients developed the same type of antibodies when exposed to thyroglobulin that they had seen in rabbits. We went ahead and showed that this same destruction applies to humans and that you could induce a disease in an organ by immunizing it with a specific antigen of the same species, Rose had told The Scientist. And that was autoimmunity.

Having overturned the idea of horror autotoxicus, Rose says, the work came out of the walls, and he spent the next several decades furthering the study of autoimmune diseases. He graduated with his MD in 1964 and remained at the University at Buffalo. According to a memorial page by Johns Hopkins University, where his career would eventually take him, his lab at Buffalo was the first to show that the genes for the major histocompatibility complex, closely linked on human chromosome six, contain the primary genes that determine the risk for autoimmune diseases.

Rose moved his lab to Wayne State University in 1973, where he remained for almost a decade before finally accepting a position at Johns Hopkins in 1981 in the Bloomberg School of Public Health. There, Rose focused on environmental conditions that could trigger disease. In many diseases, Rose told The Scientist, genetics was always less than half the risk. We thought something from the environment must be involved.

His later work focused on myocarditis, an inflammation of the heart muscle, and Rose was still working up until his death. He found great promise in the advent of big data and using it to analyze hundreds or thousands and patients to identify the best possible treatments and preventives. What we want to do is avoid the train wreck from the beginning, and I think we can begin to do that, Rose told The Scientist. Thats what Im excited about.

Rose is survived by his wife of 69 years, Deborah, two sons, two daughters, 10 grandchildren, and five great-grandchildren.

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Noel Rose, Who Demonstrated Autoimmunity Exists, Dies at 92 - The Scientist