New Antibiotic Resistance Genes Found in Soil Microbes – The Scientist


The Scientist
New Antibiotic Resistance Genes Found in Soil Microbes
The Scientist
The particularly surprising result is the discovery of a gene that encodes for an unusual small proline-rich polypeptide that confers resistance to the macrolide antibiotics, very important in human and animal medicine, Topp says. Macrolide ...

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New Antibiotic Resistance Genes Found in Soil Microbes - The Scientist

Human tissue model developed to test colon cancer drugs – Medical Xpress

June 20, 2017 by Jane Langille This is a projection image displaying all of the colon organoid layers. The green represents cells that line the colon called epithelial cells; the red represents an increase in the number of cells that are proliferating; and the blue represents the staining of all cells. Credit: Dr. Miguel Crespo/Weill Cornell Medicine

The first-ever "disease in a Petri dish" platform that models human colon cancer derived from stem cells has been developed by Weill Cornell Medicine investigators, allowing them to identify a targeted drug treatment for a common, inherited form of the disease. The discovery also overcomes a long-standing challenge of using mice to research this form of cancer, as they do not typically develop the disease.

In the study, published June 19 in Nature Medicine, the scientists used human-induced pluripotent stem cells (iPSCs), which can in principle differentiate into any type of cell in the body, that were derived from the skin of two patients with an inherited form of colorectal disease called familial adenomatous polyposis (FAP). With FAP, large intestine cells develop into numerous polyps that for these patients eventually become colon cancer. Using iPSCs, they developed 3-D structures called colonic organoids that closely represented large intestine tissue systems and then performed drug testing.

"Creating an effective testing platform for human colon cancer has been a challenge for the entire field," said co-senior study author Todd Evans, the Peter I. Pressman, M.D. Professor in Surgery and professor of cell and developmental biology in surgery at Weill Cornell Medicine. "The protocols for modeling human colon disease for drug testing just weren't there until our team developed a stem-cell-based large intestine tissue system."

Colon and rectal cancers are the second-leading cause of cancer deaths in America. In 2017, it is estimated that 50,260 people will die from the disease and 135,430 new cases will be diagnosed.

The investigators confirmed through a variety of steps including genomic DNA sequencing and gene expression profiling that they had grown large intestine cells with either of two different FAP mutations, FAP8 or FAP9, and that a gene that when mutated allows FAP cells to grow out of control, called APC, was inactivated. They also created colonic organoids using stem cells derived from a person without FAP for comparison.

Next, they tested the colonic organoids with drugs to measure response. The researchers found that two drugs, XAV939 and rapamycin, significantly curbed cell proliferation; but also, significantly decreased growth in the organoids developed without FAP, suggesting that those drugs could harm healthy colon tissue. Another drug, geneticin, known for its ability to rescue gene activity for some types of mutations, successfully restored normal growth in the FAP9 organoids, yet had no impact on the FAP8 or healthy control organoids.

"Our results demonstrate that we can use this platform to model colon cancer and identify precision medicines that may work to target specific genetic mutations driving the disease," said co-senior author Shuibing Chen, associate professor of chemical biology in surgery and of biochemistry at Weill Cornell Medicine.

"The beauty is that we can make patient-specific organoids," Evans added, "increasing the likelihood of predicting which drugs may work and learn about any undesirable effects, all before we treat the patients."

Explore further: Three-pronged approach is key to precision medicine

More information: Miguel Crespo et al. Colonic organoids derived from human induced pluripotent stem cells for modeling colorectal cancer and drug testing, Nature Medicine (2017). DOI: 10.1038/nm.4355

Journal reference: Nature Medicine

Provided by: Cornell University

Combining genetic information from a patient's tumor cells with three-dimensional cell cultures grown from these tumors and rapidly screening approved drugs can identify the best treatment approaches in patients for whom ...

Using the gene-editing system known as CRISPR, MIT researchers have shown in mice that they can generate colon tumors that very closely resemble human tumors. This advance should help scientists learn more about how the disease ...

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The first-ever "disease in a Petri dish" platform that models human colon cancer derived from stem cells has been developed by Weill Cornell Medicine investigators, allowing them to identify a targeted drug treatment for ...

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Human tissue model developed to test colon cancer drugs - Medical Xpress

Chemistry of sea spray particles linked for first time to formation … – Phys.Org

June 19, 2017 Credit: CC0 Public Domain

A team of researchers led by the University of California San Diego has identified for the first time what drives the observed differences in the chemical make-up of sea spray particles ejected from the ocean by breaking waves.

The discovery could enable researchers to better understand how ocean chemistry and physics directly influence cloud formation processes. The improved understanding could make climate models more accurate, especially since clouds are the hardest variable to portray in current simulations.

Kimberly Prather, Distinguished Chair in Atmospheric Chemistry and a faculty member in the Department of Chemistry and Biochemistry and Scripps Institution of Oceanography at UC San Diego, led the National Science Foundation-supported study. She said its key breakthrough involved showing that the drops sent airborne by breaking waves take on different chemical characteristics depending on the physical forces induced by the waves.

"It's the first time anyone has shown that drops from seawater have different composition due to the production mechanism," said Prather. "We are uncovering how ocean biology influences the physical production processes creating sea spray aerosol. Previous studies have focused on the processes involved in the physical production of sea sprays but our studies demonstrated that chemistry is at the heart of many ocean-atmosphere transfer processes that have profound impacts on the composition of our atmosphere as well as clouds and climate."

Some sea spray aerosols are "film" drops that are laden with microbes or organic material that collects on the ocean surface. They form when bubbles at the ocean surface rupture. Researchers had largely assumed that all aerosols smaller than a micron in size were of this variety. Prather and other researchers showed, however, that there are other cloud-forming particles derived from "jet" drops that are predominantly comprised of very different chemical species including sea salt, microbes, and other biological species. These new drops are ejected in the aftermath of bubbles popping.

These two types of aerosols have different capabilities for forming ice crystals in clouds, meaning that whether a cloud actually produces no precipitation, rain, or snow can be determined by the type of microbes and associated biomolecules being ejected from the ocean. More importantly, the presence of a large bloom of phytoplankton, as happens during red tide events, alters the ratio of film to jet drops, meaning biological processes can lead to profound changes in sea spray chemistry and ultimately cloud formation.

The study, "The role of jet and film drops in controlling the mixing state of submicron sea spray aerosol particles," appears June 19 in early editions of the journal Proceedings of the National Academy of Sciences.

The researchers found that jet-produced particles can make up nearly half the total number of submicron sea spray aerosols that contribute to cloud formation. To reach this conclusion, researchers induced phytoplankton blooms in natural seawater pumped into wave-generating tanks at a Scripps laboratory. The conditions mimicked those in the ocean that produce sea spray. The scientists differentiated the film from jet drops as they rose in the air above the waves by observing their different electric charges. Jet sea spray aerosols have a greater charge than film aerosols.

The findings are the latest to come from researchers at UC San Diego on one of the most mysterious frontiers of climate: how aerosols produced on land and at sea - whether sea salt, organic material, dust, or pollution particles - determine if clouds form and whether those clouds can produce precipitation. Prather, who pioneered methods to analyze the chemical composition of airborne particles, is the director of the Center for Aerosol Impacts on Chemistry of the Environment (CAICE) at UC San Diego where the work was performed. In 2013, the National Science Foundation named CAICE an NSF Center for Chemical Innovation, one of nine such centers in the United States.

Co-authors of the study represented a range of disciplines from biochemistry to marine microbiology. Scripps oceanographers Grant Deane and Dale Stokes contributed to the study and in follow-on work will attempt to see if they can determine the composition of sea surface aerosol mixes by measuring how long bubble-filled ocean whitecaps last.

Deane said the feat of the study likely could not have been achieved by any one of the researchers working alone, making it a model for how complex environmental research is done.

"It's a truly collaborative work among chemists, biologists, and physical oceanographers," Deane said. "This is the way this kind of work has to be done."

Explore further: How plankton and bacteria shape ocean spray

More information: Xiaofei Wang el al., "The role of jet and film drops in controlling the mixing state of submicron sea spray aerosol particles," PNAS (2017). http://www.pnas.org/cgi/doi/10.1073/pnas.1702420114

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Chemistry of sea spray particles linked for first time to formation ... - Phys.Org

Chemistry between Phillips, Swanson leads resurgent Braves – Atlanta Journal Constitution

As a senior member of the team might do instinctively, Brandon Phillips took on a mentorship role during Dansby Swansons early season struggles.

Swanson hit .186 in the Braves first two months. Fans called for theshortstops demotion as the team floundered.

But entering the Giants series this week, Swansons was hitting .317 (19-for-60) in June and his success is reflected in the teams performance. The Braves have won or tied four of their five series this month.

Swansons started to relax a little bit more, Phillips said. I keep on giving him hell. Im always going to keep on playing around with him, loosen him up so he can play a little bit focused. Everybodys coming together and its a lot of fun.

At the beginning, you can say he was trying to do a little too much. He was uptight a little bit. So I just told him, You know, relax and play the game. Be like you were in high school. Just be that ATL-ien that you are and just have fun. Hes started to swing the bat a little bit better and hes playing better.

Defensively, Phillips said he and Swanson are close to where they need to be.

Were having a good time learning each other, he said. He knows where I like to have the ball thrown at me. I know where he likes it and its just one of those relationships where we grew together. We really take pride in our defense. You have two guys who take pride in their defense and they want to excel and be great. We just have a lot of fun out there turning double plays, talking. And me being the leader, I can be a great role model for him.

Braves manager Brian Snitker has noticed the pairs dynamics as well.

You play that much together, it kind of has a way of working itself out, you know, when theyre relying on each other and theyre kind of clicking a little bit, Snitker said. You do establish a rapport with that guy thats beside you. The level of trust and everything grows with the amount of time and the number of games they play together.

And their only interaction isnt just out there on the field, either. Its inside as they talk about the game and playing the game. So its good for (Swanson) to have somebody with that experience beside him.

The clubhouse is meshing, especially during its recent success, according to Phillips. He and the other vets have embraced guiding the youth movement.

Ownership did a great job getting the right guys over here, he said. We didnt have the superstars, all those guys, but the right group of guys. We all have personality. We all get along with each other. R.A. Dickey, (Bartolo) Colon, myself, Kemp; we just all get along with each other and the young guys listen to us, follow our lead. They see our work ethic Those guys come to the field hungry, earlier than I do, in fact.

The Phillips-Swanson duo has started to gain traction since Phillips was acquired from Cincinnati to plug the second base spot before spring training. Not only has Swanson regained form, but Phillips has hit .339 since May 16. He produced back-to-back walk-off singles Saturday and Sunday to give the Braves another series win over the Marlins.

Were just having fun, Phillips said. Were still getting to know each other. Were starting to put everything together. The pitching staff is doing a great job. The bullpens looking good. Were starting to get quality hits, having great at-bats and like I said, we get to .500, theres no turning back.

Entering the week, Atlanta was 25-25 over its last 50 games. Phillips admitted he thought the road-heavy April and May hurt the team.

The only thing I can say is this: The beginning of our season has been crazy, he said. I dont like making excuses, but playing on the road, Ive never, ever had a season Ive been playing baseball for a long time Ive never seen a schedule like this before, or ever at the beginning. So whoevers listening to me and whoever made the schedule, yall need to change that. No team should go through what we just (went) through.

Despite their budding friendship, Phillips said hes tired of losing rock-paper-scissors to his protege. Phillips started a celebration where the two play the finger game on the field immediately following every win.

Im not going to lie to you, hes kicking my butt so far, Phillips said. So I got to step my rock-paper-scissors game up.

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Chemistry between Phillips, Swanson leads resurgent Braves - Atlanta Journal Constitution

Former UM president to earn $119K as chemistry professor – Great Falls Tribune

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The Associated Press 11:06 a.m. MT June 19, 2017

Royce Engstrom(Photo: File image)

MISSOULA Former University of Montana President Royce Engstrom will earn $119,000 a year when he returns to teaching as a chemistry professor.

The Missoulian reports Engstrom will the third highest-paid professor of the 10 faculty members in the universitys chemistry department.

Engrstrom resigned as president in December at the request of Commissioner of Higher Education Clayton Christian.

Engstroms 2016 salary was $303,145.

He is expected to teach an introductory chemistry course and an honors course this fall. He previously taught chemistry at the University of South Dakota.

As Engstrom prepares for his new role as a professor, the university has offered to buy out about 100 employees to ease a budget crunch.

Tuition and fees are also going up between 5 and 13 percent for students at the school.

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Former UM president to earn $119K as chemistry professor - Great Falls Tribune

Opinion: Three must-own cancer stocks for your biotechnology portfolio – MarketWatch

June should be national cancer month.

Each year around this time, oncology groups and Wall Street brokerages hold a rash of conferences where researchers reveal the latest, greatest potential cancer cures.

This year has been no exception. Above all, we learned about remarkable advances in two exciting cancer therapies and three great companies that will benefit.

Heres more detail. (Ive kept the technical language to a minimum.)

Tumors are smart. They know how to trick the immune system into missing them. But scientists are wising up to their tricks. In one evasive strategy, tumors release an enzyme that renders them invisible. If you block the enzyme, your immune system can find tumors and destroy them with the help from cancer drugs. This is the key to an early-stage cancer weapon you should invest in, known as IDO inhibitors.

IDO stands for Indoleamine 2,3-dioxygenase, an enzyme released by tumors to blind the bodys immune system. IDO is a strange drug target, because IDO inhibition by itself has no noticeable anti-cancer effect, says Tanguy Seiwert, a cancer-therapy researcher and medical doctor who teaches at the University of Chicago. Suppressing IDO, however, makes tumors vulnerable.

The best pure play in IDO inhibitors is a company whose shares I own, and have suggested since December 2011 in my stock newsletter, Brush Up on Stocks. Were up 750% in this company since 2011 ($14 to $120). But I think this stock is still a hold because there are bigger gains ahead.

Incyte Corp. INCY, +3.58% just released excellent data on its IDO inhibitor, called epacadostat, at the American Society of Clinical Oncology (ASCO) conference. In combination with cancer therapies from Merck & Co. MRK, +1.13% and Bristol-Myers Squibb Co. BMY, +1.40% it showed excellent results against several kinds of cancer.

It looks really good. I think this was a coming-out party for IDO inhibitors, says Seiwert. Besides effectiveness, one of the main positives is that epacadostat is safe. This means it can be readily used to assist many other cancer drugs. You can add it to a ton of things because the cost is low, in terms of toxicity.

Incyte is an ideal biotech company for investors because it is self-funding. It has a very profitable drug called Jakafi, for a rare blood disorder, which supports research on new drugs like the IDO inhibitor. So investors dodge dilutive financings.

So why hasnt Incytes stock shot up? Investors have three main worries. But they look like false fears.

One bit of fake news circulating is that Incyte showed success, in part, only because it omitted patients from some results, which drove up the percentage of success stories. But this is a dubious critique for two reasons. Even if you included the three patients left out, it would only lower the success rate by a few percentage points, notes J.P. Morgan analyst Cory Kasimov. Second, Incyte offered several separate data sets showing success in many types of cancer, but the omission only affected one subgroup, says Seiwert. I think this was way overblown.

The next fear: Competitor NewLink Genetics Corp. NLNK, +3.27% recently announced Roche AG RHHBY, +0.21% handed back development rights to its IDO, following lousy results in a Roche study. Some investors take this as a sign that IDO is malarkey. But William Blair analyst Katherine Xu thinks this is bullish for Incyte, since it signals a competitor may be gone. NewLinks IDO may have fared poorly because it works differently than Incytes IDO, or because Roche used an extremely sick patient population. Neither scenario reflects poorly on Incyte.

The third knock on Incyte is the one to watch. While Seiwert is impressed with Incytes IDO results, he points out the Phase II results are early-stage, and longer-term studies are needed to learn more about patient survival. Those studies are in the works. Incyte has nine Phase III studies planned with Merck and Bristol-Myers Squibb, says Xu. The outcomes here are key, since about $50 worth of the current $120 Incyte stock price is linked to IDO.

In another key advance in cancer therapy in the past two years, doctors have learned how to extract a patients blood and genetically tweak white blood cells so they override evasive tactics used by tumors.

Then the cells are reproduced in a lab to expand the supply, and put back in the patients body so they can move in for the kill. Hopefully, the cells then continue to proliferate and thrive and stay on hand to fight any more cancer that comes along.

Known as chimeric antigen receptor T-cell therapy (CAR-T), this approach has produced remarkable results against blood cancers in patients who otherwise had almost no hope of survival. CAR-T works by unblocking cancer cell receptors normally sought out by the immune system.

This is one of the most exciting therapies in immunotherapy, said Jae Park, a Memorial Sloan Kettering Cancer Center cancer researcher and medical doctor, at the Jefferies 2017 Global Healthcare Conference in early June.

Probably the best pure play here is Kite Pharma Inc. KITE, +1.64% At the Jefferies conference, Kite CEO Arie Belldegrun showed images of a patients body riddled with tumors, which disappeared about a month after treatment began. The patient showed no sign of the disease a year later.

Kite has a product coming on the market by the end of this year, and probably many more on the way, says Brad Loncar, the cancer research expert behind the Loncar Cancer Immunotherapy CNCR, +2.93% exchange traded fund. This is pretty good progress for a therapy that was considered science fiction two years ago.

I suggested Kite in my stock letter at around $71 on May 17, and I think its still a hold even though it has already risen to $87, because this promises to be a blockbuster therapy. At the time, insiders were big buyers as the stock sold off on news of the death of a patient in one of its studies.

That unfortunate death highlights one of the key risks here. CAR-T patients have died because the therapy can cause brain swelling. Doctors are getting better at staving off adverse side effects, says Park. But they still dont fully understand what causes them, which should raise a yellow flag for investors.

Kite also faces competition from other companies developing CAR-T, including power players like Novartis AG NVS, +0.75% Pfizer Inc. PFE, +0.76% Johnson & Johnson JNJ, -0.21% and GlaxoSmithKline PLC GSK, -0.09% as well as Juno Therapeutics Inc. JUNO, +3.91% Cellectis SA CLLS, +0.00% Adaptimmune Therapeutics PLC ADAP, -0.44% and two privately held companies called Poseida Therapeutics and Nanjing Legend Biotech.

Any of these efforts may pan out nicely, but my pick as a third CAR-T play is bluebird bio BLUE, +3.59% which is partnering with Celgene Corp. CELG, +2.29% Bluebird just announced really impressive results for its CAR-T candidate called bb2121. In early studies, just released at ASCO, this therapy produced an overall response rate of 90% to 100% among hospice-type patients whose cancer was so bad that seven different attempts to cure them, on average, had failed.

To generate efficacy data on this level with an overall very tolerable safety profile is highly impressive, says Kasimov, at J.P. Morgan. With more key updates to come in 2017, we would continue to add to positions in bluebird bio.

At the time of publication, Michael Brush held INCY. Brush has suggested INCY and KITE in his stock newsletter Brush Up on Stocks. Brush is a Manhattan-based financial writer who has covered business for the New York Times and The Economist group, and he attended Columbia Business School in the Knight-Bagehot program.

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Opinion: Three must-own cancer stocks for your biotechnology portfolio - MarketWatch

Mystery science – Gazette

Students from local high schools descended on the Department of Biochemistry recently to try out their scientific and detective skills.

For the first time, the department opened its doors to students from ODonel and Holy Heart for a daylong field trip. It saw them role play as junior crime scene investigation agents tasked with determining if a local fisherman had a freezer full of flounder or near extinct Atlantic Bluefin tuna.

Using a procedure called the Biuret method, students compared the composition of both fish species by measuring protein content.

Our equipment is basically gathering dust over the summer, so this was an opportunity to introduce high school students to biochemistry, let them see the lab and apply some modern techniques to the things theyve been learning in class, said Dr. Mark Berry, head, Department of Biochemistry.

Jamie Parsons is a science teacher at Holy Heart and an alumnus of the biochemistry department; he participated in the field trip with students from his Grade 11 international baccalaureate (IB) biology class.

He says he speaks really highlyof the biochemistry program at Memorial.

This allows my students to get a glimpse of the kind of fun stuff they can learn about and hopefully it will plant the seed that will get them to come to Memorial, said Mr. Parsons. They think away is better, but Ive been telling them Memorial is a great school. Theres a natural tendency to want to go and explore, and I get that. But its also okay to stay here. Many of us who stay here also do well.

Photo: Chris Hammond

Mr. Parsons also says that he and the students cant do everything theyd like to in their labs and that this was a chance to expose some of Holy Hearts top students to Memorial and the biochemistry department in particular.

Dr. Berry is hoping to repeat the field trip in future years with other schools.

Im in preliminary discussions with the biology and chemistry departments to see if we can put together a Natural Sciences and Engineering Research Council of Canada Promo Science proposal, he said. Id love to see this expand to a week or two of visits from other school groups, both high school and junior high.

The program was funded by Memorials Quick Start Fund for Public Engagement. It supports small projects that support activities that foster public engagement and collaboration.

Kelly Foss is a communications advisor with the Faculty of Science. She can be reached at kfoss@mun.ca.

Continued here:
Mystery science - Gazette

Anatomy of a Goal: Higuain’s Equalizer – Massive Report

Welcome to the Anatomy of a Goal, where each week we dissect one goal (or near goal) from Columbus Crew SCs previous match.

For match 17 of the 2017 MLS Season, we take a look at Federico Higuains 26th minute equalizer as part of the 3-1 loss to Atlanta United on Saturday.

Heres a look at the finish from Columbus No.1 10.

Crew SC gave up the first goal in this match on a turnover created by the Atlanta high press. While its tempting to review that goal, we have covered the Black & Golds struggles with pressure in their defensive third multiple times this season.

Columbus lone goal of the game is another example of just how good the Gregg Berhalter system can be when it works like it should. This goal is the result of nine passes, eight of which were simple and one that required a bit of individual skill. Only the final pass was defended and the goal-scoring shot came from right about the United penalty marker.

Higuains equalizer begins with Jukka Raitala receiving the ball on the left. Raitala immediately has Justin Meram and Wil Trapp open, and must quickly get rid of the ball before the aggressive Atlanta press is able to take effect.

Raitala picks out Trapp, surrounded by United attackers ready to pounce. Again, Trapp must decide whether to play a quick pass back to Jonathan Mensah or to play a quick ball into the path of a wide open Artur.

Trapp gets the pass off to Artur who immediately sees Higuain standing, unmarked, near midfield. The Atlanta press, which never really got started, has already been broken by these three quick, simple passes, all of which moved forward toward the midfield rather than backward toward the Columbus goal. Back passes can be valuable, and are a linchpin of Berhalters possession based system, but on Saturday these passes led to multiple turnovers.

As Higuain prepares to receive Arturs ball, that was just a bit overhit, he notices Ethan Finlay running in an open position. Higuain makes a dummy run (a run where the player pretends to receive the ball but lets it pass by him) and allows Finlay to receive this pass.

Harrison Afful, sensing that the offensive break is on, makes the intelligent decision to begin his run downfield toward the attacking end. Afful will make the cross that sets up Ola Kamaras assist.

As Finlay feels the pressure from Atlanta left back Greg Garza, he immediately passes the ball back to Higuain who has had the opportunity to survey the field and his passing options. Afful continues his unmarked run up the right flank.

With the ball at his feet and the a full view of the attacking half, Higuain has three options as he is closed down by Jeff Larentowicz: a slotted pass to Afful, a pass into space for Finlay or a more difficult ball over the top to Kamara.

Higuain keeps with the trend and makes the easy pass to Afful who immediately has three options: a give-and-go back to Higuain, a pass to Finlay in the space between Garza and Larentowicz or dribble forward until Garza begins to defend him.

Afful decides to carry the ball up the field until Garza decides to leave Finlay and mark the Black & Golds right back. Marked by Garza, Afful can either make a difficult pass to Higuain or pass to Finlay on the wing.

Notice former Crew SC captain Michael Parkhurst standing with his left foot on the top of the penalty box. Parkhurst will keep Finlay onside during the next pass, much to the dismay of fellow center-back Leandro Gonzalez Pirez.

Afful makes the simple pass to Finlay as Gonzalez Pirez mistakenly argues for offside. Garza shifts back to the speedy Columbus winger, leaving Afful open as a safety valve.

Feeling the pressure of two Atlanta defenders, Finlay passes right back to Afful. As the fullback sees a defender approaching to his left, he must decide if he should make a quick pass, attempt to beat the defenders off the dribble or look for a safety valve at his back.

Both Kamara and Higuain, the assist man and goalscorer, are both surrounded by Atlanta defenders, but not tightly marked. Parkhurst is generally aware of Kamaras positioning as Tyrone Mears shifts toward Justin Meram.

Afful, potentially noticing that Kamara has a few yards of space behind Parkhurst, decides to send in an early cross.

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Affuls cross will hit the mark, but Kamaras movement and positioning are the real keys to this portion of the goal. In the above highlight you can see Kamara, who was just onside as the ball was played, contort his body around Parkhurst and knock the ball into the path of Higuain with the outside of his right foot.

Thus far, every pass in the goal sequence was simple but this goal still requires a bit of individual brilliance from Kamara.

As the ball bounces near Kamara, who is already getting in position around Parkhurst, Higuain is surprisingly unmarked inside the United penalty box.

Even as Kamara gets to the ball, Higuain is still open.

Your browser does not support HTML5 video.

Though Kamara knocks the ball back into the path of Higuain, his pass did not take Parkhurst out of the play. As the ball approaches Higuain, he is defended by Parkurst and has to quickly decide whether he will hit a one time shot or try to beat Parkhurst off the dribble.

The above highlight shows Higuain fake a first touch volley and take the ball just to the left of Parkhurst where hell slot home the equalizer.

Parkhurst does well to recover onto Higuain, who is faced with the decision between a first-touch shot and taking the Atlanta center back off the dribble.

Higuains fake volley sets Parkhurt just off balance enough to allow the Crew SC attacker the time to get around the defender.

Around Parkhurst, Higuain makes a quick shot to the keepers right. Kamara is absolutely offside but arguably does not interfere with the play.

Higuains right-footed-shot levels the match.

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Anatomy of a Goal: Higuain's Equalizer - Massive Report

Spotted: Millie Bobby Brown Playing Doctor On ‘Grey’s Anatomy’ – Konbini US

The year is 2015. For the past two years Millie Bobby Brown, yet to become a household name, has been discovering the joys of acting.

The third child of a family of four kids, Millie's family emigrated to Orlando, Florida, when the futureactress was four years old.

Kelly and Robert Brown started to notice their daughter's star talent at a young age, deciding to invest everything in taking Millie to auditions around the country.

A worthwhile investment, it was to turn out, as in 2013, Millie Bobby Brown found her first role in Alice in Wonderland spin-off Once Upon a Time.

From there she bagged a regular double role as a brother and sister duo on BBC America'sIntruders.

After makingbrief appearances in NCIS and Modern Family, Millie Bobby Brown touched down atGrey Sloan Memorial Hospital for a spot inGreys Anatomyinwhat wouldturn out to be her last role as an unknown actor.

In the episode "I Feel the Earth Move" of Grey's Anatomy season eleven, the city of Seattle is hit by a serious earthquake which rocks the roots of Grey Sloan Memorial Hospital. As a result, Maggie and Ethan find themselves stuck in a lift while Meredith takes over a series of tricky operations.

With the emergency services inundated with calls, Owen receives a call directly to the hospital from a panicked young girl called Ruby. Her mother has fallen and is unconscious, prompting Owen to join forces with the police to track the call and come to the girl's aid.

Owen and Amelia team up to help Ruby's mother over the telephone and discover that her airways are blocked.

(Photo: ABC)

Things quickly go from bad to worse when the woman's lips start turning blue. The young girl examines her mother's throat in an attempt to get rid of any obstacles but nothing works.

Finally, the doctors realize that the woman is suffering from a tension pneumothorax and the little girl is forced to pierce her mother's throat to release the trapped air.

While the operation works briefly, the woman loses consciousness again and Owen has to teach Ruby how to perform CPR (to the rhythm of the Bee Gee's "Stayin' Alive", of course).

In the end, the family is finally rescued and helicoptered into the hospital. Of course, Ruby's mother survives and in classic Grey's Anatomy style, Owen and Ruby come together for an emotional reunion.

Following the success of her role as Eleven in the breakout hit Stranger Things, Millie Bobby Brown is in for a seriously busy year. Along with her young colleagues from the Netflix original show, she's been reeling off appearances on talk shows and panels like nobody's business.

Everywhere she lands, she seems to unveil a new talent from singing at the Emmysto rapping with Jimmy Fallon. She's also been picked to face a Calvin Klein line and collaborated with Converse. The most impressive part of it all: she's still only 13 years old.

With filming of Stranger Things season two done and dusted, Millie is ready to break the world of Hollywood blockbusters, starting withGodzilla: Kings of the Monstersset for a 2019 release.

Ready to hit Netflix on October 31, here's hoping Stranger Things manages to avoid Netflix's recent cancellation spree and live on for another few seasons.

Read More ->Why 'Flaritza' was the most powerful ship of OITNB season 5

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Spotted: Millie Bobby Brown Playing Doctor On 'Grey's Anatomy' - Konbini US

Empire Medical Training Attends the AANP 2017 National Conference – Benzinga

Empire Medical Training is excited to announce their attendance at the American Association of Nurse Practitioners 2017 National Conference. Those interested may visit booth 375 for more information on all of the Continuing Medical Education courses that Empire Medical Training has to offer.

Philadelphia, PA (PRWEB) June 19, 2017

The Pennsylvania Convention Center in Philadelphia, PA will be holding the American Association of Nurse Practitioners (AANP) 2017 National Conference from June 20-25, 2017. Empire Medical Training has announced they will be in attendance and will have an information booth at the event.

Empire Medical Training invites attendees to visit booth 375 to learn more about their 32 accredited CME courses and the variety of locations that are offered. With topics like "Revolutionizing Health Care," Empire Medical Training is proud to offer their workshops to help medical professionals continue to expand their business.

As President and Founder of Empire Medical Training, Dr. Stephen Cosentino, DO, states, "We have over 27 trained physicians and other specialists in key areas, so Empire Medial Training is able to offer a unique curriculum for topics including aesthetics, pain management, and anti-aging." With over 19 years in the business, Empire Medical Training is offering American Medical Association and Physician's Recognition Award Category 1 accredited programs nationwide.

Empire Medical Training has been training Physicians and Health Care Practitioners since 1998, longer than any other procedural training institution. With over 45,000 graduates in specialties such as Aesthetics, Anti Aging/Weight Management Medicine, and Pain Management, Empire Medical Training is renowned throughout the United States and abroad as the premier academy for providing academic excellence. Dr. Stephen Cosentino pioneered ways to add new procedures and services as well as business strategies to a practice and improve patient care. With Dr. Cosentino's commitment and dedication to the specialty and the field of medicine, Empire Medical Training is steadfast to developing new training programs and topics to broaden the scope of the primary care practitioner. All Empire courses are created through mainstream medicine using the most current technologies and standards of care.

For more information on attending the AANP 2017 National Conference please visit their website and for more information on Empire Medical Training call 866-366-1576.

For the original version on PRWeb visit: http://www.prweb.com/releases/2016/06/prweb13514018.htm

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Potential anti-aging Cardax Astaxanthin compound selected for NIH research – UH System Current News

Zanthosyn, an Astaxanthin product marketed by Cardax

The proprietary Cardax astaxanthin compound CDX-085 developed by the University of Hawaii at Mnoa John A. Burns School of Medicine (JABSOM) and Hawaii based life sciences company Cardax, Inc. was selected by the National Institute on Aging for its anti-aging Interventions Testing Program. The institute is part of the National Institutes of Health (NIH).

Getting into the Interventions Testing Program with the National Institute on Aging is a game-changer, said Bradley Willcox, professor and director of research at JABSOMs Department of Geriatric Medicine. It puts CDX-085, Cardaxs proprietary astaxanthin compound, into a very elite club of compounds that have the potential to become true anti-aging therapies. Willcox is principal investigator of the NIH-funded Kuakini Hawaii LIFESPAN and HEALTHSPAN Studies and Cardax Scientific Advisory Board member.

In March of this year, JABSOM and Cardax jointly announced that CDX-085 showed the ability to significantly activate the FOXO3 gene in mice, which plays a proven role in longevity.

Out of all the compounds they could have chosen, they chose ours, said David G. Watumull, Cardax CEO. Its an important validation of the work that weve done here in Hawaii.

The National Institute on Aging ranked the proposal submitted by Willcox and Richard Allsopp, associate professor at JABSOMs Institute for Biogenesis Research, a high priority, its highest ranking.

The information we get from the ITP is going to be quite significant and should greatly enhance our knowledge of how astaxanthin/CDX-085 affects aging, said Allsopp.

The National Institute on Aging funds the rigorous and extensive studies included in the ITP, which are conducted at several labs across the country.

The ITP will build upon the research by JABSOM and Cardax demonstrating the ability of CDX-085 to activate the important anti-aging gene FOXO3 in mice. CDX-085, like the companys first generation dietary supplement, ZanthoSyn, delivers astaxanthin to the bloodstream with optimal absorption and purity.

Read more about the astaxanthin research at the JABSOM website.

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Potential anti-aging Cardax Astaxanthin compound selected for NIH research - UH System Current News

Green chemistry efforts honored – Chemical & Engineering News

The 12 Principles of Green Chemistry are a how-to guide written 20 years ago for chemists and chemical engineers. They provide insight on developing new chemicals and chemical processes and revitalizing existing ones so that they achieve their desired function while being environmentally and economically friendly. Its a creative challenge to put the 12 principles into action.

Five technologies that have succeeded in meeting that creative challenge are being recognized with 2017 Green Chemistry Challenge Awards. Merck, Dow Chemical, Koehler, Amgen, Bachem, UniEnergy Technologies, and University of Pennsylvania chemistry professor Eric J. Schelter were honored for their achievements at a ceremony held on June 12 at the National Academy of Sciences in Washington, D.C.

The Environmental Protection Agency established the Green Chemistry Challenge Awards program in 1995 as a competitive effort to promote chemical products and manufacturing processes that help the agency achieve federal goals set by the Pollution Prevention Act of 1990. The program is administered by EPAs Green Chemistry Program and is supported by partners from industry, government, academia, and other organizations, including the ACS Green Chemistry Institute.

EPA has now presented 114 of the awards to scientists and companies selected from more than 1,700 nominations. The work described in the award nominations must have been carried out or demonstrated in the U.S. in the preceding five years. An independent panel selected by ACS, which publishes C&EN, judges the nominations and selects the award winners.

Among this years winners, Merck took home the Greener Synthetic Pathways Award for developing a streamlined synthesis of the antiviral drug letermovir, which is currently in Phase III clinical trials. The new synthesis reduces the process mass intensity for making the drug, a sustainability measure of raw materials used per amount of product made, by 73% compared with the original synthesis.

Dow and papermaker Koehler jointly landed the Designing Greener Chemicals Award for a new technology that uses a polymer coating on paper to create air pockets that collapse during printing to create an image stemming from the altered refractive index of the coating. This physical process replaces chemical dyes and image developers such as bisphenol A in the production of thermal paper used for printing receipts.

Amgen and Bachem teamed up to receive the Greener Reaction Conditions Award for an improved peptide manufacturing technology to make the drug etelcalcetide, a calcium inhibitor to help control activity of the thyroid gland in patients with kidney disease. The new process produces more peptide in less time while drastically cutting solvent and water use.

UniEnergy Technologies garnered the Small Business Award for its design of a vanadium-based redox flow battery for grid-scale energy storage. The new battery has double the energy density of previous flow battery technology even though its smaller and uses smaller amounts of chemicals.

Schelter got the nod for the Academic Award for developing a process that uses tailored ligands to separate mixtures of rare-earth metals during the recycling of consumer lighting and electronics. Scientists expect the approach to reduce energy use and the waste generated during recycling of rare-earth metals and help minimize new rare-earth metal mining.

The Green Chemistry Challenge Awards highlight the importance of sustainable chemistry and its impact across a range of disciplines, says Princeton Universitys Paul J. Chirik, a 2016 award recipient. Striking features common among many of the winners is that green chemistry often results in an improved product or a cost savings, demonstrating that environmentally responsible science does not have to come with reduced performance or added cost.

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Concrete Chemistry Pioneer Bill Hime is Dead at 91 – Engineering News-Record (subscription)

William G. "Bill" Hime, one of the nation's first and premier experts in cement chemistry and a pioneer in failure analysis of concrete and construction materials, died on June 6 in Glenview, Ill. He was 91.

The death of the former senior principal of structural and forensics engineer Wiss, Janney, Elstner Associates Inc. follows by just 10 days that of the Illinois firm's former president John M. Hanson.

Hime joined Wiss, Janney in 1984 with its acquisition of Erlin, Hime Associates, which he had co-founded 12 years earlier with Bernard Erlin. It specialized in chemical and petrographic analyses of construction materials.

The chemist had previously been a chemistry assistant professor at Louisiana Tech University, and also laboratory chief and manager of chemical and petrographic research at the Portland Cement Association.

Among other things, while at Erlin, Himes, he was widely consulted to offer analysis on the use of Sarabond as a concrete mortar additive that was linked to masonry cracking, according to a March 1986 ENR article.

Himes said the Sarabond leached out chloride ions when in contact with unprotected steel in a building, which, in turn, had accelerated corrosion. He said excessive buildup of rust pushed outward on the masonry, eventually cracking and displacing bricks.

In a 1983 article related to ongoing litigation, the New York Times said Sarabond had been used in about 2,000 buildings.

Hime published more than 100 professional articles in books and magazines and received numerous industry group awards. He remained a Wiss, Janney principal until he was 81 and "was a champion" in cement burn prevention, said the firm.

"When there was a need for analytical work, [Hime] enthusiastically beamed when he did hands-on 'wet chemistry' to get data that more [sophisticated] instrumental methods would miss, or not be as accurate," said former partner Erlin in a 2007 interview in Concrete Construction magazine, referring to him as "one of the greatest chemical and technological minds of our industry."

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Trumann student starting ABI biotechnology research internship – Democrat Tribune

Dustin Rhoads of Trumann is participating in Biotechnology Research Internship at Arkansas Biosciences Institute. (Photo provided)

Five Arkansas State University students are pursuing their interest in science this summer through the Biotechnology Research Internship Program at the Arkansas Biosciences Institute (ABI) facility on campus. One of those students, Dustin Rhoads, is from Trumann.

The program provides basic support for A-State undergraduate science majors who want research experience in life sciences or applications of life sciences during the summer of their sophomore or junior years.

Each student is matched with a faculty mentor who is conducting research related to biotechnology or biology from one of several departments and colleges, based largely on the student's interests. Selection also is based on academic credentials.

The students, along with their future plans and comments from their applications are:

Dustin Rhoads plans to go to dental school after completing his degree at A-State. His faculty mentor also is Dr. Malathi Srivatsan.

"I chose to apply for this internship mostly because of my interest in the field," Rhoads said. "Neurology has always been and interest of mine. Furthermore, the research we are doing at Dr. Srivatsan's Lab could be used to help so many people. Neuroregeneration could impact the lives of millions, and to be a part of something that could do that is very special to me. What sparked my interest in science was the way it's completely unique from all other academic fields, it has no sense of complacency, and is forever evolving. Im the kind of person who would rather study how things work as opposed to memorizing hard set facts, so the sciences are definitely for me regarding that aspect. I chose Arkansas State University because growing up I was always around it, almost developing it as a second home before even leaving high school, also accompanied with the report of its programs, made it a complete match for me."

The other students are Madalyn Rose Weiner of Little Rock, Oliver Dozier of Paragould, Kayleigh Nelson of Marion, and Aylin Villalpa-Arroyo of Hidalgo, Mexico.

Each internship is valued at $2,500. The students work 20 hours per week for 10 weeks. An additional $500 is provided to the supporting laboratory for research supplies.

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Trumann student starting ABI biotechnology research internship - Democrat Tribune

Puma Biotechnology Inc (PBYI) Receives Buy Rating from Citigroup Inc. – The Cerbat Gem


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Puma Biotechnology Inc (PBYI) Receives Buy Rating from Citigroup Inc.
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Puma Biotechnology logo Puma Biotechnology Inc (NYSE:PBYI)'s stock had its buy rating reissued by investment analysts at Citigroup Inc. in a research report issued to clients and investors on Monday, May 22nd, MarketBeat Ratings reports. They ...
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Puma Biotechnology Inc (PBYI) Receives Buy Rating from Citigroup Inc. - The Cerbat Gem

The anatomy of Caliphate colonialism (5) – Vanguard

By Douglas Anele

But despite their remarkable capacity for creative ingenuity and accomplishments, the Igbo as a group, according to Prof. Chinua Achebe, have the deadly flaws of hubris, overweening pride, obsession with material success and irritatingly noisy exhibitionism or showiness which tend toinvite envy from members of other ethnic groups. Yet, those flaws do not justify their being massacred periodically by northerners or treated as second class citizens in their own country. The May riots of 1966, Ironsis gruesome murder and massacre of Ndigbo afterwards led to a radical rethinking of their attitude to the idea of a unified Nigerian nation. The Igbo began to realise that their belief in a strong central authority that provides a level playing field which enables Nigerians from every ethnic group to actualise the ideal of one nation, one citizenship, and one destiny was a delusion.

The belated Igbo questioning of One Nigeria was consistent with the memorandum submitted by the northern delegation to the Nigerian ad hoc constitutional conference of September 1966. In it, northern representatives claimed that We have pretended for too long that there are no differences between the peoples of this country. The hard fact which we must honestly accept as of paramount importance in the Nigerian experiment especially for the future is that we are different peoples brought together by recent accidents of history. To pretend otherwise would be folly. The north even went further to demand that in any new constitution a secession clause should be inserted granting any member state the right to unilaterally secede completely from the union, and to make arrangements for cooperation with other members of the union in such a manner as they may severally or individually deem fit. Now, from what transpired later, it became clear that northerners were only interested in regional autonomy as long as it favours the north.

We have noted that the civil war that lasted from July 1967 to January 1970 proves the deadly extent caliphate colonialists can go to maintain its dominance in Nigeria. But before the war proper, a last ditch attempt was made in Ghana to save the country from disintegration occasioned by the fallouts of the two military coups in 1966. The Aburi meeting hosted by Ghanas military ruler, Lt. Gen. Joseph Ankrah and attended by senior military and police officers as well as government secretaries, resolved that each region should be responsible for its own affairs, and that the federal government would be responsible for issues dealing with the whole country, such as defence, currency and external affairs. In my opinion, if the Aburi accord had been implemented, the Biafran war would have been averted because eastern region would not have seceded. The agreement collapsed because ab initio there was a mismatch between the delegation led by Gowon and the one from eastern region headed by its military governor, Lt. Col. Chukwuemeka Odumegwu Ojukwu: whereas Gowon and delegates from other regions apart from the east arrived Aburi with the vague idea that somehow Nigeria must remain as one country, Ojukwu and his group came with a well-articulated detailed vision of what the future political architecture of Nigeria should be. Thus, although the eastern position was eventually adopted, the two parties left Aburi with different ideas of what the agreement meant in practice. As a corollary, some aspects of the accord, especially those dealing with the issue of power relations between the central government and the regions, were unrealistic and impractical to implement given the growing domination of the army and political power by the north, coupled with the strained relations between the Igbo and northerners as a result of pogroms against Ndigbo resident in the north. Moreover, top federal civil servants in Lagos vehemently opposed the accord, and convinced Gowon that it was unworkable. The problem was aggravated by the all-or-nothing attitude to the contents of the accord by Gowon and Ojukwu, which was unnecessarily rigid and myopic. Gowons unilateral repudiation of the agreement was matched by Ojukwus insistence on its full implementation as quickly as possible: both men failed to realise that a give-and-take approach and compromises are required forsuccessful implementation of agreement on troublesome political conflicts.

The non-implementation of the Aburi accord by the federal military government heralded the end of the concept of regional autonomy and self-sufficiency in Nigeria, leading to the consolidation of caliphate colonialism. After Gowon had emerged as military head of state, he started implementing measures that effectively turned Nigeria into a unitarist federation, which increased the powers of the federal government over the federating units beyond what was allowed by the unification decree promulgated when Ironsi was in power and which was used by northern soldiers and their civilian collaborators to justify the bloodthirsty coup of July 29, 1966. Interestingly, northern emirs who had for long opposed the creation of states mainly in order not to compromise the norths geographical and political domination of Nigeria suddenly urged Gowon to create states. Gowon complied with the demand. The creation of states was more detrimental to solidarity among the three regions in the south than to the northern region because southern Nigeria did not have the equivalents of the theocratic emirate system, Islam and a dominant language (Hausa) which tended to unify different ethnic nationalities in the north. Besides, by concentrating more power at the centre ostensibly to keep Nigeria as one united country, Gowon also ensured that the federal government dominated by northerners controlled all revenues from recently discovered large deposits of petroleum mostly in the eastern region. As a result, Gowon not only expanded the pre-independent policy of using resources from the south to develop the north, he instigated the bizarre practice of northern preponderance in the ownership of oil wells in oil-bearing communities. One can claim justifiably that some of the most significant pre-war decisions taken by the federal government headed by Gowon are responsible for the extremely damaging effects of caliphate colonialism in Nigeria since 1967.

Any student of Nigerian history who blames the eastern region, particularly Ndigbo, for seeking self-determination after the horrendous atrocities they suffered in northern Nigeria is either a pathological misanthrope or moron. It is difficult to imagine a self-respecting ethnic nationality with the quantum of human and natural resources of the defunct eastern region that would not desire to take its destiny in its own hands. As Prof. Achebe observed, The Nigeria that meant so much for [Ndigbo] was not reciprocating the affection we had for it. The country had not embraced us, the Igbo people and other easterners, as full-fledged members of the Nigerian family. Hence, on May 30, 1967, when Ojukwu, on behalf of the 335-member Consultative Assembly of Chiefs and Elders who unanimously mandated him to pull out the east from the rest of Nigeria at an early practicable date, announced the secession of Biafra, he was actually demanding that Igbo people and their immediate neighbours be allowed to develop at their own pace untrammelled by the yoke of caliphate colonisation. Many uninformed Nigerians believe the pernicious falsehood that the Igbo declared war on the rest of Nigeria. Far from it because, as I have stated earlier, if there is any group that have contributed most to the building of modern Nigeria and lived the concept of One Nigeria (and still does, admittedly,to its own detriment) it is the Igbo. Therefore, it is in Ndigbos interest that Nigeria continues to exist and prosper. When the eastern region seceded, caliphate colonialists led by Gowon decided to respond with a short, surgical strike through what he called a police action.

In every war, it is always plausible to argue, after the fact, that it could have be
en averted or avoided if the combatants had shown more restraint. The Biafran case is not anexception. The war was led by two young military officers in their early thirties, Ojukwu and Gowon. Perhaps, older and more experienced statesmen could have handled the complex issues that led to the bloody conflict much better in a manner that would have led to a peaceful resolution, although it would have been extremely difficult, judging by the horrors they suffered in the hands of their northern compatriots, to persuade the eastern populace shortly before the civil war broke out that they are equal stakeholders in the Nigerian project.

Now, northern hardliners such as MurtalaMohammed wanted full-blown war as the final solution to teach the Igbo a brutal lesson and consolidate the norths domination of federal power, whereas Gowon saw it as an opportunity to cut the arrogant and rebellious Ojukwu to size. Eastern leaders who mandated Ojukwu to secede at the earliest practicable opportunity were desperate and confused, and the people themselves were emotionally exhausted and disillusioned. In such a psychologically charged atmosphere, critical thinking and logic would be replaced by the exciting logic of war hysteria such that anyone who questions the extreme measures taken by Ojukwu in response to Gowons prevarications and provocations or expresses doubt concerning the propriety of secession without adequate preparation for war would bebranded a spineless coward or saboteur. To be continued.

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The anatomy of Caliphate colonialism (5) - Vanguard

ANATOMY OF AGITATIONS – Oherald

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From industries to bridges, mega projects to widening of roads and pipelines, it sometimes seems that everywhere you look, some group in Goa is rallying against something.

What is behind this new opposition-ism? Goans social values, and their evolution over the past few decades, tell an important part of the story.

Social values are the deep-seated beliefs and orientations that underline our opinions on the issues of the day.

While at one time many Goans would conform to the expectations of authority figures, and follow the customs and demands of institutions and ideologies, these days they are increasingly unwilling, or uncomfortable, deferring to authority and instead are interested in making their own choices onwhat they want.

The people want development they want motorable roads, uninterrupted water and power supply what they dont want is an abrupt change in their lives wrought about by a project that they are unlikely to ever benefit from.

Goans do not generally accept the notion that pollution is inevitable, or acceptable, in an industrial society.

Second, Goans do not tend to hold the belief that environmental damage is an acceptable price to pay for economic growth.

Third, Goans, by and large, tend to see environmental activists as reasonable people who have Goan interest at heart , rather than extremists out to take away livelihoods

While this combination of values sounds pretty daunting for those wanting to move forward with infrastructure or other developments, there are ways to ensure that these projects are aligned with the communitys values and expectations.

While the agitation against the casinos and many a mega projects besides polluting industries is understandable the recent agitation which led to shifting of the plans to set up Indian Institute of Technology (IIT) at Loliem is highly debatable.

This is not the first time that a project or projects proposed by the government have been deposed by the people. In the past decades, especially since the early 1980s, very few projects proposed by the government have met with the approval of the people. Some have been bulldozed through despite opposition and others have been scratched from the planning board after some long and bitter agitations.

The Nylon 6,6 project and the Special Economic Zones are examples of the latter.

Against this background of agitations, it would have been smart on the part of the government to first take into confidence the people on any project and then give its approval for the venture, rather than push forward its plans and agendas without knowing the mind of the people.

This would portray that the government was sensitive to the wishes and opinions of the people and that this was a government that would act positively only on such projects that met with the approval of the affected people.

But this is just not happening in Goa. At regular intervals the government will propose a project that the people will oppose and then the fight begins.

While the IIT at Loliem is a justified project, it is nowbeing moved to Ponda, because all stakeholders were not taken into confidence at the project clearing stage.

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ANATOMY OF AGITATIONS - Oherald

What If (Almost) Every Gene Affects (Almost) Everything? – The Atlantic

In 1999, a group of scientists scoured the genomes of around 150 pairs of siblings in an attempt to find genes that are involved in autism. They came up empty. They reasoned that this was because the risk of autism is not governed by a small number of powerful genes, which their study would have uncovered. Instead, its likely affected by a large number of genes that each have a small effect. Perhaps, they wrote, there might be 15 such genes or more.

Two decades later, that figure seems absurdly and naively low. If you told a modern geneticist that a complex traitwhether a physical characteristic like height or weight, or the risk of a disease like cancer or schizophreniawas the work of just 15 genes, theyd probably laugh. Its now thought that such traits are the work of thousands of genetic variants, working in concert. The vast majority of them have only tiny effects, but together, they can dramatically shape our bodies and our health. Theyre weak individually, but powerful en masse.

But Evan Boyle, Yang Li, and Jonathan Pritchard from Stanford University think that this framework doesnt go far enough.

They note that researchers often assume that those thousands of weakly-acting genetic variants will all cluster together in relevant genes. For example, you might expect that height-associated variants will affect genes that control the growth of bones. Similarly, schizophrenia-associated variants might affect genes that are involved in the nervous system. Theres been this notion that for every gene thats involved in a trait, thered be a story connecting that gene to the trait, says Pritchard. And he thinks thats only partly true.

Yes, he says, there will be core genes that follow this pattern. They will affect traits in ways that make biological sense. But genes dont work in isolation. They influence each other in large networks, so that if a variant changes any one gene, it could change an entire gene network, says Boyle. He believes that these networks are so thoroughly interconnected that every gene is just a few degrees of separation away from every other. Which means that changes in basically any gene will ripple inwards to affect the core genes for a particular trait.

The Stanford trio call this the omnigenic model. In the simplest terms, theyre saying that most genes matter for most things.

More specifically, it means that all the genes that are switched on in a particular type of cellsay, a neuron or a heart muscle cellare probably involved in almost every complex trait that involves those cells. So, for example, nearly every gene thats switched on in neurons would play some role in defining a persons intelligence, or risk of dementia, or propensity to learn. Some of these roles may be starring parts. Others might be mere cameos. But few genes would be left out of the production altogether.

This might explain why the search for genetic variants behind complex traits has been so arduous. For example, a giant study called er GIANT looked at the genomes of 250,000 people and identified 700 variants that affect our height. As predicted, each has a tiny effect, raising a persons stature by just a millimeter. And collectively, they explain just 16 percent of the variation in heights that you see in people of European ancestry. Thats not very much, especially when scientists estimate that some 80 percent of all human height variation can be explained by genetic factors. Wheres that missing fraction?

Pritchards team re-analyzed the GIANT data and calculated that there are probably more than 100,000 variants that affect our height, and most of these shift it by just a seventh of a millimeter. Theyre so minuscule in their effects that its hard to tell them apart from statistical noise, which is why geneticists typically ignore them. And yet, Pritchards team noted that many of these weak signals cropped up consistently across different studies, which suggests that they are real results. And since these variants are spread evenly across the entire genome, they implicate a substantial fraction of all genes, Pritchard says.

The team found more evidence for their omnigenic model by analyzing other large genetic studies of rheumatoid arthritis, schizophrenia, and Crohns disease. Many of the variants identified by these studies seem relevant to the disease in question. For example, some of the schizophrenia variants affect genes involved in the nervous system. But mostly, the variants affect genes that dont make for compelling stories, and that do pretty generic things. According to the omnigenic model, theyre only contributing to the risk of disease in incidental ways, by rippling across to the more relevant core genes. Its the only model I can come up with that make all the data fit, Pritchard says.

Pritchards a very perceptive investigator, who looks beyond what most people do, says Aravinda Chakravarti, a geneticist at John Hopkins Medicine. Do I believe this all correct? No, but its very compelling. Its a serious hypothesis that weve got to prove or disprove.

If Pritchard is right, it has big implications for genetics as a field. Geneticists are running ever-bigger and more expensive searches to identify the variants behind all kinds of traits and diseases, in the specific hope that their results will tell them something biologically interesting. They could show us more about how our bodies develop, for example, or point to new approaches for treating disease. But if Pritchard is right, then most variants will not provide such leads because they exert their influence in incidental ways.

Put it this way: The Atlantic is produced by all of us who work here, but our lives are also affected by all the people we encounterfriends, roommates, partners, taxi drivers, passers-by etc. If you listed everyone who influences what happens at The Atlantic, even in small ways, all of those peripheral people would show up on the list. But almost none of them would tell you much about how we do journalism. They're important, but also not actually that relevant. Pritchard thinks the same is true for our genes. And if thats the case, he says, its not clear to me that increasing your study size is going to help very much.

The alternative, he says, is to map the networks of genes that operate within different cells. Once we know those, well be better placed to understand the results from the forthcoming mega-studies. It is a really hard problem, says Boyle. Historically, even understanding the role of one gene in one disease has been considered a major success. Now we have to somehow understand how combinations of seemingly hundreds or thousands of genes work together in very complicated ways. Its beyond our current ability.

There are, however, projects that are trying to do exactly that. Im very excited about trying to understand whether these network ideas are correct, says Pritchard. I think its telling us something profound about how our cells work.

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What If (Almost) Every Gene Affects (Almost) Everything? - The Atlantic

Scientists Find Genetic Mutation That Could Increase the Male Lifespan – Gizmodo

Jiroemon Kimura, the oldest man ever (Image: YouTube/Screenshot)

Professor S. Jay Olshansky once told Gizmodo, In the world of aging sciences, if you want to live a long life, choose long-lived parents. So genetic markers linked to longevity are interesting as hell. But if youve got the wrong genes, then the wrong moves might do you in.

A team of researchers from universities in the United States wanted to figure out the role of genetics in human lifespan, specifically relating to growth hormone. The researchers work shows two main things: first, that a mutation in mens DNA relating to growth hormone might lead to a longer lifespan. And secondly, that treating older people with growth hormone might be dangerous if they dont have the variation.

Gil Atzmon, the studys principal investigator from Albert Einstein College of Medicine and the University of Haifa in Israel, was most excited by how a slight change in DNA could have such a big impact. Delete a few base pairs, and you still have a functional protein that now makes people live longer, he said. I think this is phenomenal.

This is complex, so Im going to take it slow and possibly oversimplify things. Basically, theres one system in question, the IGF-1/GH axis. Each of these are genes that code for different molecules in your body.

Researchers have already had a hunch that IGF-1 can regulate height at the expense of longevity, like the case in dogs. More IGF-1 means taller but shorter lifespan and less IGF-1 means shorter but longer lifespan. This should make senseits akin to the way big dogs live shorter lives than small dogs.

The researchers studied 800 men and women from across four populations and found something surprising. Indeed, the IGF-1 levels were lower in the centenarians, but many of the men were also taller. The data showed the researchers that theres more than just IGF-1 at play.

Centenarian males were often missing a specific snippet of DNA in their GHR gene. These people seem to be more sensitive to growth hormone and grow taller. So, even though their IGF-1 levels were lower (they lived longer), they still grew taller from their special GH gene. The people with this mutation seemed to live ten years longer, on average.

And the study really was huge. The replication across the four different populations makes our result more accurate and globally translated.

Atzmon himself admitted that all this is pretty complex. But its definitely new, important evidence pointing to the role that this IGF-1/GH axis plays in simultaneously determining your height and your lifespan, explained Andrzej Bartke, Professor of Physiology and Internal Medicine at Southern Illinois University School of Medicine, in a conversation with Gizmodo.

But were not at some level of life-hacking clarity. Clearly more research is needed to understand exactly why this type of GH receptor favors extreme longevity, why the effect was seen only in men and why the results in people studied by these investigators differ from some of the previous findings in different groups of human subjects with the same type of receptors, said Bartke.

Theres a catch to all this. Their results seemed to show that folks who dont have the GH variation might actually be sensitive to growth hormone therapy. This is a stark reminder that administering growth hormone as an intervention to slow agingwhich is still being done in the anti-aging medicine industry is not warranted by the scientific literature, Olshansky told Gizmodo. In fact, could actually be harmful.

So, youre still going to die one day. But as to when, that answer probably doesnt reside in what you eat (or in young blood) nearly as much as it does in what your DNA looks like.

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Scientists Find Genetic Mutation That Could Increase the Male Lifespan - Gizmodo

How population health will benefit from the journey to precision medicine – MedCity News

Population health and precision medicine seem like such polar opposites standing 180 degrees apart. But the path to fully realizing the benefits of precision medicine stands to reap rewards for population health along the way. That was the takeaway from an interview with India Hook-Barnard, the director of research strategy and associate director of Precision Medicine at the University of California San Francisco. She talked about the balance between the two areas of healthcare in an interview in Boston after she spoke at HIMSS Precision Medicine Summit this week.

Hook-Barnard called attention to a list of projects related to precision medicine. They included the Cell Cancer Map Initiative to discover molecular networks of cancer, the University of California Data Warehouse to connect 15 million electronic health records across the University of California health system, a Biobank that seeks to simplify the informed consent process and the Scalable Precision Open Knowledge Engine.

All of these projects are helping to advance precision medicine in different ways. They will enable us to more quickly make discoveries, provide better care, but also make better decisions in public health.

She called attention to some of the work of her colleagues. Atul Butte is the first director for the Institute of Computational Health Sciences. Among his many roles, he is one of the leaders of the University of California Data Warehouse. Among their tasks are to address privacy and security issues for making data from those records accessible across health systems plugged into the University of California network.

Theyre looking at being able to repurpose drugs, what will really provide better outcomes. It will be really huge being able to connect that kind of data and use it in a healthcare space and research space.

The San Francisco Cancer Initiative, is about sharing information for what works and what doesnt work for five types of cancer with the highest cost burden: prostate, breast, liver, colorectal and tobacco-related cancers. Each will be assigned a taskforce, Hook-Barnard said. The public-private partnership launched last year with a $3 million investment from a donor to the UCSF Helen Diller Family Comprehensive Cancer Center. The initiative is led by Dr. Robert Hiatt, the chair of the Department of Epidemiology and Biostatistics at UCSF. He authored a report on health disparities for cancer treatment outcomes.

Hook-Barnard described what the program seeks to accomplish using tobacco-related cancer as an example, and highlighted some of the questions the initiative seeks to address in this area. Social determinants of health will also come into play.

We know the dangers of smoking and the impact of it, yet there are certain communitiesthat are still developing lung cancer at much higher rate than others. Why is that? Is the messaging on prevention not resonating? Are cessation efforts not tailored enough to be effective? Is access to early screening for detection in certain neighborhoods [the problem]? Being able to tailor those kinds of preventive messaging, early screenings, diagnostics and access, could improve earlier access to treatment.

The Molecular Oncology initiative led by Michael Korn of UCSF is yet another initiative. The website offers this description of the UCSF500 gene panel assay the laboratory conducts.

a cutting-edge sequencing test that, in contrast with commercial cancer gene panel tests, sequences tumor DNA and the patients germline (inherited) DNA. This unique component of the UCSF500 molecular diagnostic test enables identification of genetic changes (mutations) in the DNA of a patients cancer, which helps oncologists improve treatment by identifying targeted therapies, or appropriate clinical trials, or in some cases clarify the exact type of cancer a patient has.

Although it is about using genomics in the clinic to get a more precise diagnosis, the goal of the initiative is to solve some of the wider questions that often go unanswered and to make sure that data isnt locked in a silo somewhere. What treatment(s) worked and why?

How do we capture that information to make sure that is shared and duplicated? We want to make sure those lessons, those findingsonce you have that piece of knowledge, how do you make sure it is shared with other medical centers? For precision medicine to work, it is about these different kinds of data and acquiring knowledge we need to enable data sharing.

Photo: Getty Images

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How population health will benefit from the journey to precision medicine - MedCity News