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Historical Blindness

February 19th, 2017 6:42 am

Closer to Levins home, this militant brand of Protestantism had been stirring in Philadelphia quite a while as well. In 1831, there had been a clash in the streets when Irish Protestants paraded past an Irish Catholic church in celebration of King Williams establishment of Protestant control of Ireland in 1690. More recently, in 1842, an assemblage of Philadelphia preachers named themselves the American Protestant Association, deemed the system of Popery to be, in its principles and tendency, subversive of civil and religious liberty, and destructive to the spiritual welfare of men and resolved to unite for the purpose of defending [their] Protestant interests against the great exertionsto propagate that system in the United States.

Watching this divisive movement gain support and momentum, Levin launched another newspaper, the Daily Sun, to use as a mouthpiece for his own nativist sentiment. Levin approached nativism through the lens of temperance and his steadily increasing resentment of the established political parties, the Democrats and the Whigs. As Levin saw it, candidates for office were decided on not by the people but by party insiders, in groggeries over segars, precisely the equivalent of the perennial smoke-filled room where cabals of secretive power brokers are said to do the dark work of true governance. Levin believed party politics to be tied up in vice and corruption and asserted that only a third party would allow for true democracy; thus he attached himself to the new American Republican Party, lately victorious in the New York mayoral election. In its Philadelphian iteration, under the auspices of Levin and other proponents, this party called itself the Native American Party. While today the term "Native American" refers to indigenous peoples, then it was a term taken up with pride to distinguish those born stateside from the wretched, tempest-tossed refuse that huddled in masses on teeming foreign shores.

While only a secretary of this nascent party, Levin was perhaps the most vocal advocate of its cause and, as a publisher, the most capable of disseminating its message. In addition to regular editorials in the Daily Sun, Levin published a book expressing his feelings on the Irish Repeal Associations campaign to dissolve Irelands union with Great Britain around this time. Predictably, he did not view it as a bid for freedom, for its leader, Daniel OConnell, was a papist who would only make Ireland beholden to the Pope. And it was just this that he warned the predominately Catholic immigrants of Europe, and particularly the Irish Catholic, intended to do in America: stage a coup by voting as a block, raising up their own men to power and subverting American democracy in favor of monarchism and deference to the Catholic Church. Our only hope, as he represented it, was to stem the surging influx of indigents and criminals and papists and to defy the cronyism and corruption of the ruling parties: in short, to support Native Americanism.

*

Before we examine the most outrageous chapter of Levins life, I would like to pause for a moment to offer a caveat regarding my scholarship. I make no claims to being a rigorous historian. I am a storyteller first and foremost, an entertainer; therefore, I may sometimes give short shrift to elements of my subject matter that dont serve well the narrative I am trying to dramatize. However, my promise is that, while attempting to shape and share an engaging story, I will also make my best efforts to present the story accurately and provide reliable sources.

To that end, I should mention some other contemporary circumstances that likely contributed to the anti-immigrant sentiments of the times as well as to the general desire for a change in the status quo of party politics. All of these factors are clearly outlined in John A. Formans Lewis Charles Levin: Portrait of an American Demagogue, a comprehensive source that I have relied on heavily.

Two important dynamics beyond anti-Catholicism that exacerbated this political climate in Philadelphia were a loss of status on the national political stage and a descent into economic depression. In 1836, the most important Philadelphian in the country, Nicholas Biddle, President of the Second Bank of the United States, was stymied in his attempt to recharter the institution by President Andrew Jackson. The Bank War, as it was called, had been a prominent issue in the Presidential campaigns of 1832, and after Jackson successfully blocked the banks recertification in 36, Philadelphia and her people took it as a personal defeat. No longer the central hub of the American economy, Philadelphia lost some of its eminence, and Philadelphians became disillusioned with their political leaders and open to outsider politicians that suggested the established parties were corrupt and/or ineffectual.

Then, in 1837, an economic crisis occurred that led to years of recession. In the absence of the national bank in Philadelphia, federal capital was placed in a variety of pet banks, relocating money from the large banks that relied on it to smaller banks that certainly benefitted from it. The practical effect, however, was panic, as major banks, now carrying far less capital, could not extend credit or offer loans as they had before. In Philadelphia, as well as elsewhere, the Panic of 1837 meant hard times, and as is almost always the case when Americans suffer economic hardship, the poor immigrant, who will often work for lower pay, is blamed for the privations of by natural-born citizens.

While the loss of their national bank and the ensuing recession certainly added to the atmosphere, one issue in particular allowed Lewis Charles Levin to really rile up his audience, and this one, again, Americans will recognize: religion in schools. The debate here, however, was not about its presence but rather about what form it would take. Catholics in the Kensington district protested that the Bible used as a reader in schools was a Protestant King James Bible and contended that Catholic students should be allowed to use a Catholic text. Levin and his Native Americans misconstrued their position, perhaps willfully misrepresenting their complaint, and warned the public that the Irish Catholics of Kensington wanted to have the Bible removed from schools, which, if it were allowed, Levin argued would lead to a new generation of idle, profligate, dissolute youth. In short, the evil immigrant papists were hell bent on undermining the very moral fabric of society.

This was the background and the political narrative when, in May of 1844, Levins incitements finally erupted into violence.

*

The Native Americans rallied first in Independence Square, holding forth to crowds of supporters about the Bible issue. But perhaps that wasnt provocative enough, for next they moved their rally right into the heart if Kensington district so that the Irish Catholics themselves could hear their disparaging speeches. The first of these rallies disbanded when Irish Catholics, predictably, gathered to face their deriders. However, in the spirit of authentic agitation, Levin and the Native Americans were not discouraged from holding their rallies in the very dooryards of Irish Catholic Kensington residents but rather determined to do so again, likely hoping that violence would break out and somehow prove their dispersions against the Irish to be true.

On a stormy Monday in May, Lewis Charles Levin ascended a stage to address his audience. As if on cue, the heavens opened up with a rumble, and a downpour beganthis perhaps a gesture toward divine intervention. But Levin was undeterred. Taking shelter in a nearby marketplace, he resumed his remarks, which have ever been described as passionate and incendiary.

It must have begun as a murmur at the crowds peripherya confrontation between a nativist and an Irishman. Very quickly, then, it came to blows and graduated to full-scale rioting, as men brandished bricks and cudgels. When gunfire boomed in the marketplace, the first struck was a constable, shot in the face. Others received gunshot wounds in their sides, their hips, their legs. Stones and bricks filled the air, crashing down upon those gathered and battering the walls and windows of businesses and houses in the area. With the report of pistols, many dispersed, and others gave chase. Residents homes received barrages of rocks for no other reason than that men had fled into an adjacent alley or fallen against their doors. The damage to property was enormous, and the violence unrestrained.

The next day, the Native American convened again, no longer in Kensington, to counsel restraint. Many among their audience called for Levin, to hear what the chief instigator had to say about curbing their retaliation against the Irish rioters. Levin kept his silence, and the rioting continued for another two days. The militia had to be deployed to bring an end to it, but by then, numerous rioters on both sides as well as bystanders had been wounded, and seven were dead. When the smoke literally cleared, a seminary and two Catholic churches had been destroyed by arson, as well as some thirty private residences.

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Historical Blindness

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Russian blindness: Trump team ties troubling – The Union Leader

February 19th, 2017 6:42 am

There is no evidence that members of the Trump presidential campaign broke the law when they were in contact with various Russian officials during the campaign and transition period.

Yet that has not stopped some liberals from fantasizing about impeachment proceedings, based on unsubstantiated claims that Trump coordinated with Russian hackers to embarrass Hillary Clinton.

Voters knew months before the election that Trump advisers, including Michael Flynn, Paul Manafort and Roger Stone, had close ties to Russia. This was one of many reasons to oppose Trump's candidacy. But he won anyway. Nothing that was reported last week, all attributed to anonymous sources within the intelligence community, invalidates that result.

President Donald Trump is furious over the constant leaks from the national security apparatus that undermined former National Security Adviser Flynn.

The leaks are definitely a problem. The D.C. bureaucracy is picking out classified information to feed to the press in order to wage a guerrilla campaign against Trump. That is unacceptable.

But such bureaucratic abuse does not excuse the Trump administration's continued blindness to the threat of Vladimir Putin's regime.

Barack Obama promised to show more flexibility to Russia after he was re-elected. But the Trump administration has tied itself in knots excusing Putin's misdeeds.

Like all bullies, Putin responded to this weakness with more aggression. Russia is cruising a spy ship up and down the Eastern seaboard, and Russian planes are buzzing U.S. Navy ships in the Black Sea.

Trump's admiration and excuses for an authoritarian thug like Putin are deeply troubling. Critics should concentrate on Trump's weak foreign policy, rather than on conspiracy theories about the 2016 election.

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Prosopagnosia: What it’s like to live with ‘face blindness’ – ABC Online

February 19th, 2017 6:42 am

Posted February 19, 2017 07:14:44

Tim Hughes once caught a plane from New York to LA. Sitting next to him was a woman, a striking brunette with big hair.

Mr Hughes helped her with her bags and then sat back to enjoy the attention of the unusually solicitous airline staff. Upon landing he wished her an enjoyable stay.

"I live here," was her steely-eyed reply.

"It was only two weeks later, after I'd seen a magazine article about her, that I realised that the person I'd been sitting next to was Elizabeth Taylor," recalls Mr Hughes.

The former IT professional has a condition called prosopagnosia, sometimes known as "face blindness".

But people with prosopagnosia aren't actually blind; they know when they see a face, but their brain can't process who it belongs to.

An inability to tell the difference between two similar faces does not necessarily mean that a person has prosopagnosia, and difficulty perceiving differences is not the same as difficulty with remembering faces, though the result can be the same.

"One of the things that we think people [without prosopagnosia] do when they look at faces is to see the face more as a whole, rather than the individual parts that make up the face," says Romina Palermo, associate professor of psychology at the University of Western Sydney.

"We know that people who see faces more as wholes tend to be better at recognising faces. We also know that people who have prosopagnosia don't tend to look at a face as a whole as much, they tend to see the parts more often."

Brain injury, most often a stroke can cause prosopagnosia, but there is also a congenital, or developmental, version in which certain brain mechanisms fail to develop properly, possibly due to genetics.

The neurological explanation for prosopagnosia is complex: to recognise a face, the brain relies on a neural network of at least three core regions in the occipital and temporal lobes of the right and left brain hemispheres which supply different aspects of face processing.

"There are a number of processes, and our understanding is sketchy," says Brad Duchaine, professor in psychological and brain sciences at New Hampshire's Dartmouth College.

"In our posterior lobes we have a fairly simple, image-based representation of the face that you're seeing which is exactly what you're seeing you're encoding the values of the features of that face.

"As you move to more anterior areas in the brain, those areas are giving what's called a 'view independent' manner, where you're extracting a representation of just who a person is. It's not tied to the particular image of the face that you're seeing at that moment."

As for Mr Hughes, he first suspected something wasn't right back in Year Six.

"There were two similar looking blonde-haired boys. I never could tell them apart, even though the other kids could," he says.

Since then, Mr Hughes' inability to recognise faces has put him in some awkward situations, especially once he started dating.

"I knew my girlfriend would be getting on the same bus, and would be wearing school uniform but I was petrified I wouldn't be able to tell who she was. Luckily, she recognised me," he says.

Things didn't work out so well another time: "One time I went to my girlfriend's house to pick her up but after a short while, the woman I was talking to said, 'I think you want my sister.'"

Many people with prosopagnosia don't have as much trouble recognising family members, but unfamiliar situations can make things difficult.

"One time at the beach I thought I'd misplaced my son Stuart," says Mr Hughes. "There was a boy standing next to me who I thought was one of Stuart's friends, so I asked him if he knew where Stuart was. He replied, 'Yes, I'm Stuart.'"

People with prosopagnosia usually develop coping strategies to give them clues to the identity of the person they're interacting with.

They use extra layers of information such as gait, voice, eye colour, clothing, or hairstyle. For people with prosopagnosia, a new hairdo can be quite confusing.

Mr Hughes' coping mechanisms include examining people "top to toe" and having a friend point out who's who, or who he might expect to see at an event.

He also lets people know he has the condition and that he might not recognise them next time he sees them.

He's not a fan of the term "face blindness" because it's not accurate. He prefers to say that he has "facial recognition issues" once he puts facial features together, he can identify who a person is.

The Australian Prosopagnosia Register was begun about 10 years ago, and people can sign up for information, receive updates on research and do tests to help figure out what level of prosopagnosia they have.

There have also been studies on whether people can be trained to improve their facial recognition abilities.

They can, but it's intensive, involving tasks like looking at photos and trying to identify subtle differences in people's eyes or the distance between the eyes.

Research into prosopagnosia also opens a window on to how the human brain processes faces. Facial recognition is a specialised task utilising different areas in the brain, and information about how this happens could assist with other research.

"It's useful to know how everybody processes faces," says Professor Romina Palermo.

"When some people are unable to do it, there can be insights into how the brain works.

"Facial recognition is a specialised task utilising a distributed network of areas in the brain, and information about how this happens can assist with other areas of cognition."

Topics: health, genetic-disorders, brain-and-nervous-system, psychology, australia

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Don’t Worry You Can Save Your Eyes From Blindness If You Sit In … – Wccftech

February 19th, 2017 6:42 am

We grew up listening to our parents saying that if we use computers for a long time, it will eventually make us go blind. This my friends was something I always believed to be true, but how is it possible to not use a computer when our survival in the modern world depends on it? Computer vision syndrome is the term used for eye strain caused due to staring at a computer for too long. The symptoms, well we all know what they are; blurry vision, headaches, dry eyes, watery eyes, and tired eyes.

The symptoms are generally temporary if you stop computer usage for a while but if you are anything like me and are literally addicted to sitting in front of a computer, then these symptoms can be a problem, but then the question is, we read books too so why arent they bad for the eyes? The answer is pretty interesting actually. According to the University of Iowa, its because while we are using computers, our rate of blinking drops by a third which results in our eyes becoming dry.

According to the American Optometric Association, the contrast that exists on the screen isnt as strong as it is in books and the letters are less precisely rendered. The eyes thus have to work harder and this leaves them tired. If you are looking at a screen from a non-ideal angle then that only worsens the strain. You must be wondering what that ideal angle is. Well, ideally you must be looking slightly down at the screen at an approximate 15-20 degree angle. The computer must also be placed about 20-28 inches away from you. So get a protractor and a ruler and start measuring (no not literally).

It also helps to take breaks while you are at the computer. Every 20 minutes take a 20 second break to stare at something 20 feet away. This is referred to as the 20-20-20 rule by optometrists. If you are planning to use a computer for a longer time, then after every 2 hours take a 15 minute break from computer usage. Some people who dont usually use spectacles can benefit from computer specific glasses. These spectacles are designed to reduce glare and increase the contrast. With age our eyes also become less flexible. Interestingly people who wear contacts may suffer from increased blurriness and dryness because they already blink less because of the contacts. So do your eyes a favor and use spectacles while you are at a computer.

And one more thing, if these things arent helping then its probably the right time to pay your eye doctor a visit because something needs checking.

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Illinois senators propose biotechnology tax credits – The State Journal-Register

February 19th, 2017 6:41 am

The Associated Press

DECATUR -- Two Illinois lawmakers have proposed a plan to offer tax credits to biotechnology businesses in hopes of boosting agricultural jobs in central Illinois.

The legislation, introduced by Republican state Sen. Chapin Rose of Mahomet and Democratic state Sen. Andy Manar of Bunker Hill, would provide incentives to produce and sell new renewable products made from biomass and other renewable sources, the Herald & Reviewreported.

Manar said the state is strategically poised to lead the development of new renewable products.

"We have leading biotechnology companies, large and small, that are leading research and development efforts on these innovative products, and we have critical mass in infrastructure to produce and transport these renewables around the world," Manar said.

Rose said there's potential for Decatur to be at the center of a new $20 billion biotechnology industry. He said the intent is to utilize Decatur's production and shipping capacity through the Midwest Inland Port along with the Integrated Bioprocessing Research Lab in Urbana.

"The potential for jobs is here," Rose said. "We have something no one else has to offer. This bill will help us capitalize on this and bring these jobs to central Illinois."

The proposed legislation would provide a state tax credit to Illinois companies that produce and sell new manufactured products made from bio-based molecules of biomass feedstocks. Those products, including renewable chemicals and food additives, represent the next generation of advanced biofuels.

"These new bio-based products offer great potential to the Illinois economy across the entire state," said Warren Ribley, president and CEO of Biotechnology Innovation Organization, which is among the organizations leading the efforts in Illinois. "We need to lead now by leveraging our tremendous assets or forever be playing catch-up."

The plan's chances in the state legislature are uncertain.

Illinois' corporate tax incentive program has been under scrutiny recently with critics calling it too expensive and favorable to large businesses. Last month Republican Gov. Bruce Rauner signed an extension of the program through April but has called for replacing the program, known as EDGE, or Economic Development for a Growing Economy.

Rauner's spokeswoman Eleni Demertzis saidMondaythat the bill is "under review."

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National Agri-Food Biotechnology Institute celebrates seventh foundation day – The Indian Express

February 19th, 2017 6:41 am

By: Express News Service | Mohali | Published:February 19, 2017 4:43 am The National Agri-Food Biotechnology Institute, Mohali, on Saturday observed its 7th foundation day.

The National Agri-Food Biotechnology Institute, Mohali, on Saturday observed its 7th foundation day at the NABI premises at Phase 8 in Mohali. The NABI is an autonomous institute aided by the department of Biotechnology, Government of India, and carries out research in the area of biotechnological applications at the intersection of agriculture, food and nutritional biotechnology.

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A gathering of heads of the institutes and faculty from the Tricity region joined the function. More than 200 scientists, students and staff participated in the foundation day ceremony. Prof. Nagendra Kumar Singh, national professor, B P Pal chair and project director, ICAR National Research Centre on Plant Bioterchnology, New Delhi was the chief guest.

He delivered the foundation day lecture on Decoding the genomes of crop plants uniquely important for India. Dr T R Sharma, executive director, NABI highlighted the achievements of NABI and mentioned that NABI is poised to play an important role in generating world-class knowledge in the area of agri-food and health security. NABI is working on strategies to overcome anti-nutritional activity, and make food crops a better quality source for nutrition.

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The Puma Biotechnology Inc (PBYI) Stock Rating Decreased by the Zacks Investment Research – DailyQuint

February 19th, 2017 6:41 am

Puma Biotechnology Inc (NYSE:PBYI) was downgraded by Zacks Investment Research from a buy rating to a hold rating in a research note issued to investors on Tuesday.

According to Zacks, Pumas progress with the lead candidate, neratinib, has been impressive. Currently, neratinib is under review in both the U.S. and the EU for the treatment of HER2-positive breast cancer. An approval would be a huge boost for the company given the immense commercial potential in the target market. Several additional studies on neratinib targeting different types of breast cancer patient populations are currently underway. Being a development-stage company, Puma does not have any approved product in its portfolio yet. Thus, the company is totally dependent on neratinib for growth. Puma has had its share of setbacks related to neratinib. With so much depending on the successful development and approval of neratinib, any further kind of development or regulatory setback could hamper the companys growth prospects and the stock adversely. Shares of the company have underperformed that of the industry in the past one year.

Other equities research analysts have also recently issued reports about the company. Citigroup Inc. set a $88.00 price target on Puma Biotechnology and gave the company a buy rating in a research note on Tuesday, January 3rd. Stifel Nicolaus reiterated a buy rating and issued a $88.00 price target on shares of Puma Biotechnology in a research note on Wednesday, November 30th. J P Morgan Chase & Co set a $89.00 price target on Puma Biotechnology and gave the company a buy rating in a research note on Monday, November 14th. Cowen and Company restated a market perform rating on shares of Puma Biotechnology in a research note on Tuesday, November 15th. Finally, Credit Suisse Group restated an outperform rating and set a $111.00 target price on shares of Puma Biotechnology in a research note on Tuesday, November 15th. One investment analyst has rated the stock with a sell rating, four have issued a hold rating and four have assigned a buy rating to the company. The stock presently has an average rating of Hold and an average price target of $68.56.

Puma Biotechnology (NYSE:PBYI) traded up 0.73% on Tuesday, hitting $34.60. Puma Biotechnology has a one year low of $19.74 and a one year high of $73.27. The firms 50-day moving average is $37.28 and its 200-day moving average is $45.81. The companys market capitalization is $1.27 billion.

Several hedge funds and other institutional investors have recently made changes to their positions in the company. Canada Pension Plan Investment Board increased its position in shares of Puma Biotechnology by 53.2% in the third quarter. Canada Pension Plan Investment Board now owns 16,700 shares of the biopharmaceutical companys stock valued at $1,120,000 after buying an additional 5,800 shares during the period. BNP Paribas Arbitrage SA increased its position in shares of Puma Biotechnology by 112.0% in the third quarter. BNP Paribas Arbitrage SA now owns 2,133 shares of the biopharmaceutical companys stock valued at $143,000 after buying an additional 1,127 shares during the period. Northern Capital Management LLC increased its position in shares of Puma Biotechnology by 1.2% in the second quarter. Northern Capital Management LLC now owns 16,288 shares of the biopharmaceutical companys stock valued at $485,000 after buying an additional 190 shares during the period. Traynor Capital Management Inc. bought a new position in shares of Puma Biotechnology during the second quarter valued at about $246,000. Finally, JPMorgan Chase & Co. increased its position in shares of Puma Biotechnology by 31.4% in the second quarter. JPMorgan Chase & Co. now owns 231,875 shares of the biopharmaceutical companys stock valued at $6,907,000 after buying an additional 55,345 shares during the period. Institutional investors own 80.98% of the companys stock.

About Puma Biotechnology

Puma Biotechnology, Inc is a biopharmaceutical company that focuses on the development and commercialization of products for the treatment of cancer. The Company focuses on in-licensing the global development and commercialization rights to over three drug candidates, including PB272 (neratinib (oral)), which the Company is developing for the treatment of patients with human epidermal growth factor receptor type 2 (HER2), positive breast cancer, and patients with non-small cell lung cancer, breast cancer and other solid tumors that have a HER2 mutation; PB272 (neratinib (intravenous)), which the Company is developing for the treatment of patients with advanced cancer, and PB357, which is an orally administered agent.

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Children get arthritis, too – Star2.com

February 19th, 2017 6:41 am

The US Centers for Disease Control and Prevention (CDC) published in 2015 that one in 250 children have some form of joint pain that may be related to either an autoimmune condition or infection.

If the pain is due to an underlying infection, treating the child would usually result in complete resolution of the arthritis.

However, some of these children may have an autoimmune cause for their arthritis. These children would have seen many doctors and the pain doesnt appear to go away with standard painkillers. At times, the pain can be so severe that they cannot do normal activities in school, or worse, they will skip school completely as they are unable to get up from bed and walk.

When the joint pain lasts more than six weeks, the child may have a condition called childhood arthritis (know medically as Juvenile Idiopathic Arthritis or JIA), and it affects children and teenagers up to the age of 16.

This is a chronic condition and is due to the immune system attacking the joint capsule or synovium, leading to overt inflammation. This inflammation will lead to pain, swelling and increased warmth on the skin surface.

The pain is usually associated with early morning stiffness, i.e. the child will have difficulty straightening or bending the affected joint in the morning.

These children will move around with bent knees or elbows, and sometimes, they can be seen walking with a limp. The exact cause of this condition is still unknown.

Unfortunately, due to lack of awareness, many of these children only get referred many months later to a paediatric rheumatologist.

JIA is an aggressive condition, and if not managed early, can lead to long-term damage to the structures within and surrounding the joint. As these children are growing, this disease can affect their growth plate, leading to shortening of their limbs.

Worse still is that when the bones are completely damaged, they will not be able to bend their joints.

It is very important to get these children treated as soon as possible to prevent long-term damage to all these vital structures in their body.

There are eight sub-types of JIA, namely oligoarthritis, rheumatoid-factor-positive polyarthritis, rheumatoid-factor-negative polyarthritis, systemic arthritis, juvenile psoriatic arthritis, systemic arthritis, enthesitis-related arthritis and undifferentiated arthritis.

Oligoarthritis occurs when four joints or less are affected and it usually affects children below the age of five. This condition mainly targets larger joints like the knees, ankles and elbows.

Patients with this subtype are prone to suffer eye inflammation called uveitis and will need to have regular follow-up with the eye specialist.

For rheumatoid-factor-positive polyarthritis and rheumatoid-factor-negative polyarthritis, more than four joints are inflamed. The difference is only whether or not there is an autoantibody called rheumatoid factor present.

If this autoantibody is present, the child is likely to have a worse outcome as the disease is more aggressive and will probably need the newer drugs for control.

These two subtypes usually affect children above five years of age.

Girls are more likely to have polyarthritis than boys.

Systemic arthritis usually affects children below five and is a severe form of arthritis, as these children usually present with high grade fever and rash, which cannot be explained or have no source of infection.

This subtype is due to uncontrolled inflammation within the body and can lead to swelling of the heart, lungs, liver and spleen. It can cause a severe drop in the white blood cells, red blood cells and platelets, leading to a medical emergency called Macrophage Activation Syndrome. This condition can lead to death if not identified early, and as such, should be managed urgently by a paediatric rheumatologist.

Enthesitis-related arthritis is a form of arthritis that affects not only the joints but also the enthesis, which is the part where the ligaments or tendons attach to the bones.

This subtype usually affects school-going children and can lead to severe back pain due to inflammation of the sacroiliac joint. This is a joint that forms between the tail bone and the hip bone.

Children with inflammatory bowel disease, which is an autoimmune disease causing inflammation in the intestines, are at greater risk of developing this subtype.

Examples of swelling in childhood arthritis.

Juvenile psoriatic arthritis affects 20% of children who have psoriasis (an autoimmune skin disease where the skin flakes excessively due to rapid skin cell turnover) or have parents or siblings who have psoriasis themselves.

It usually affects the fingers or toes of children above the age of five, leading to sausage-shaped fingers called dactylitis.

Treatment for JIA aims to control the disease as early as possible to prevent further damage to the childs joints.

It can start with targeted injections into the joints with potent anti-inflammatory medications such as triamcinolone (if there are only a few joints involved), to combination treatment with disease-modifying anti-rheumatic drugs (DMARDs) for those with more severe forms of the disease.

Most recently, there are more targeted therapies against certain inflammatory molecules in the body, called biologics, which add to the arsenal of treatments against JIA.

With all these medications, the cure rate for JIA is good, especially if treated early, and more than 80% of children with JIA can lead normal, active lifestyles similar to other children.

In a nutshell:

Children and teenagers can have arthritis too.

If a child has joint pain for more than six weeks, the child will need to seek medical help from a paediatric rheumatologist as soon as possible as it may be JIA.

JIA is a chronic, autoimmune disease that can lead to life-long disability if not adequately treated.

JIA has no exact known cause.

There are many subtypes of JIA and each subtype has different levels of severity.

Children with unexplained fever for weeks without a known source may have a severe form of JIA.

Children with psoriasis can also have arthritis.

Early treatment is very important to prevent damage to the joint and growth plate.

Current treatment regimens have a good success rate and most children can lead normal and active lives.

Parents and the paediatric rheumatologist play an essential role in helping children with JIA cope with this disease, which requires long-term care and treatment.

Dr Cham Weng Tarng is a consultant paediatrician and paediatric rheumatologist. This article is courtesy of the Malaysian Paediatric Associations Positive Parenting programme in collaboration with expert partners. This article is supported by an educational grant from Sunway Medical Centre. For further information, visit http://www.mypositiveparenting.org. The information provided is for educational and communication purposes only and it should not be construed as personal medical advice. Information published in this article is not intended to replace, supplant or augment a consultation with a health professional regarding the readers own medical care. The Star does not give any warranty on accuracy, completeness, functionality, usefulness or other assurances as to the content appearing in this column. The Star disclaims all responsibility for any losses, damage to property or personal injury suffered directly or indirectly from reliance on such information.

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Osteopenia (bone loss) update: natural treatment, anti-inflammatory diet, diabetes, psoriatic arthritis – Bel Marra Health

February 19th, 2017 6:41 am

Home Bone Health Osteopenia (bone loss) update: natural treatment, anti-inflammatory diet, diabetes, psoriatic arthritis

In case you missed it, here is Bel Marra Healths roundup on osteopenia decreased bone densityfeaturing information on what factors contribute to bone loss, natural treatment options, anti-inflammatory diet tips for stronger bones, and how psoriasis affects bone density.

Bone loss, and more specifically osteoporosis, is often identified as a female health problem, but men are not immune to losing bone density. There are many factors that can contribute to bone loss, so practicing bone-boosting habits is essential, especially as you age.

Bones are composed of minerals, the most predominant being calcium. The body goes through a process called resorption, meaning it breaks down old bone and creates newer, stronger ones. Unfortunately, as we age, this becomes more difficult. The quicker old bone breaks down the more the need for new bone increases, but older adults simply do not create new bone as quickly as someone who is young. Bone loss can lead to osteopenia, which can evolve into osteoporosis. Bone disease can increase fractures and breaks and can negatively impact a persons life. Here are four factors that can contribute to bone loss, aside from aging, and what you can do to prevent bone loss. Continue reading

Many people are familiar with the term osteoporosis, but fewer have heard the term osteopenia, which means lower bone density than normal. If you have osteopenia, your bone density may be lower than normal peak level, but it isnt low enough to be considered osteoporosis.

Bone density is simply the measurement of how dense and strong bones are. Lower bone density puts you at a higher risk of eventually getting osteoporosis.

Low bone density is often associated with the elderly. As we grow older, bones become thinner due to the fact that the body reabsorbs bone cells faster than new bone is made. Other diseases or treatments can also cause osteopenia. Continue reading

New research published in the Journal of Bone and Mineral Research suggests that women who consume a diet high in anti-inflammatories experience less bone loss than their peers.

The study examined data from the Womens Health Initiative and compared inflammatory elements of participants diets to their bone mineral density and fractures, discovering a connection between food and bone health. Continue reading

Diabetes can increase the risk of bone loss, and the severity of diabetes can determine its impact on bone health. Osteoporosis is a consequence of diabetes, and both diabetes and osteoporosis have a high prevalence in America. The likelihood of developing both conditions increases with aging.

Type 1 diabetes causes bone mineral density loss, weakening the bones and leading to osteoporosis. In type 2 diabetes, though, there isnt a great loss in bone mineral density. In fact, type 2 diabetics tend to have higher bone mass density than average. Unfortunately, many of these patients tend to be overweight, and that extra weight contributes to bone loss and bone weakening over time. Many studies have even shown that type 2 diabetics, even with above average bone mineral density, are still at a higher risk for bone fractures. Continue reading

Psoriasis or psoriatic arthritis patients show higher osteoporosis and osteopenia prevalence, according to research. M. Elaine Husni, director of the Arthritis and Musculoskeletal Center at Cleveland Clinic, said Clinicians who treat patients with psoriasis or psoriatic arthritis should be on alert for an association with osteopenia and osteoporosis. The researchers suggest there is strong evidence to link psoriatic arthritis to bone loss, and there is an independent association between psoriasis and low mineral density. Continue reading

Related: Bone loss linked with serious illness

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INDYCAR legend Foyt plans to have stem cell therapy – IndyCar.com – INDYCAR

February 19th, 2017 6:40 am

(This story originally appeared as exclusive content on the Verizon INDYCAR Mobile app. To download the app for smartphones, click here.)

AVONDALE, Ariz. At 82, A.J. Foyt's body has literally been beaten beyond his years.

The first four-time winner of the Indianapolis 500 has experienced everything from a broken back at a 1964 NASCAR race in Riverside, California, to two badly broken feet and legs in a horrible crash at Road America in a 1990 Indy car race.

Foyt retired from racing on pole qualifying day at the 1993 Indianapolis 500, but retirement hasn't been much easier. He was stung more than 200 times from an attack of killer bees in 2005, trapped under an overturned bulldozer on his Texas ranch in 2007 and had knee replacements and a hip replacement. In November 2014, Foyt underwent triple-bypass heart surgery and remained in the hospital for weeks afterward because of complications.

Foyt has survived it all but not without a struggle. He now is looking for a fountain of youth and told the Verizon INDYCAR Mobile App that he will undergo stem cell therapy in Cancun, Mexico.

They have to cut away some of the tissue from my stomach and it takes 8-10 weeks for it to grow back to produce the stem cells, Foyt said in an exclusive interview. I'll probably have it done soon so that we can begin the treatment within the next two to three months.

Adult stem cells are able to grow and become a cell for a specific tissue or organ, according to the National Institutes of Health. They are different from embryonic stem cells, which come from fertilized eggs or aborted fetuses. Embryonic stem cells can turn into cells for nearly any tissue in the body.

The procedure is not performed in the United States, so Foyt has found a medical facility in Mexico that can do the treatment that regenerates newer and younger cells. He said he will have stem cells injected into each ankle and shoulder, as well as into his blood.

It used to be you would have to go to Germany to get this procedure, but now it's available in Cancun and that is probably where I'll have it done, Foyt said Saturday during the Verizon IndyCar Series open test at Phoenix Raceway. I'm not in good health like I used to be and, if my son Larry hadn't taken over (running) the team four years ago, I would have had to shut it down. It's something he likes to do and I'm backing him 100 percent.

Foyt said he feels good to be his age after all the crap that I've been through.

I feel better this year than I did last year, Foyt continued. If I get to feeling bad, I probably won't show up at the race. But I'm going to do that stem cell deal. My wife, Lucy, has been pretty sick lately. Dan Pastorini (the former NFL quarterback) did it and it helped him. Peyton Manning (the former Indianapolis Colts and Denver Broncos quarterback) did it for his neck and it really helped him. Tony Dorsett (the former Dallas Cowboys running back) did it, so I think we should try it.

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Roundup: News from the Advanced Technologies & Treatments for … – MobiHealthNews

February 18th, 2017 12:45 pm

This week in Paris, companies in the diabetes managment space came together at theAdvanced Technologies and Treatments for Diabetes conference to share news and, mostly, a lot of efficacy data. It's an exciting time for the space as closed-loop systems that allow people with diabetes to monitor their glucose continuously and automatically manage their insulin dosing get closer and closer to becoming a validated, regulated reality for people with Type 1 diabetes. We didn't make it out to Paris ourselves, but we're covering the news. We've written up some of the bigger stories from the conference earlier this week. Look below for a roundup of other digital health news from the show.

Nonprofit organizationT1D Exchangepublished a major study in Diabetes Care yesterday (and presented the research at the conference).The data re-affirmsthe FDA's recent clearance ofDexcom's CGM for insulin dosing. The study looked at 226 adult CGM users for six months. Of those, 149 dosed their insulin using the CGM and 77 used a fingerstick glucometer in addition, as is currently required for most CGMs. There was no difference in outcomes between the two groups.

"This study is an important step to support regulatory pathways for the automation of insulin delivery for people with type 1 diabetes, Dana Ball, executive director and co-founder of T1D Exchange, said in a statement. These data are supportive of the recent FDA decision to approve the Dexcom G5 indication for insulin dosing and removes a key obstacle that has prevented reimbursement of CGM by Medicare.

Integrity Applications, makers of GlucoTrak, a novel non-invasive glucose monitor that clips onto the ear lobe, presented data showing that their device has improved in accuracy from previous generations. The data shows GlucoTrak has increased its tracking consistency, with different devices on opposite earlobes of the same subject returning the same results. They've also corrected for previous inaccuracies in readings before and after meals.

Aspire Ventures announced that its portfolio company Tempo Health's Rhythm system, based on Aspire's A2I adaptive artifical intelligence platform, performed well in an observational study at Diabeter, a specialized treatment center in Europe. Rhythm uses A2I toforecast and manage blood glucose levels of people with diabetes, based on data from non-invasive biometric sensors. In seven out of eight patients in the study, Rhythm would have helped them to achieve a 20 percent increase in time in range, and a 9 percent reduction in low glucose ratings, as compared to the actual results achieved by active monitoring by Diabeter doctors and their diabetes teams using patient-activated remote monitoring.

Waltham, Massachusetts-based Glytec,which makes a personalized therapy and decision support module for patients with diabetes, presented two studies about its Glucommander system. One study sawA1C levels drop from a baseline average of 10.2 percent to 7.7 percent at three months and 7.6 percent at six months. Another study looked at the use of Glucommander for patients prescribed subcutaneous insulin.Among 5,718 patients, the median time to prescribed glucose target was 0.8 days. Once in the target range, 67.9 percent of all blood glucose readings remained between 70 and 180 mg/dL.

Insulet, maker of the Omnipod line of tubeless insulin pumps, presented data about its own closed-loop system, a hybrid system called OmniPod Horizon.The 36-hour, 24-person study used a modified version of Omnipod, a Dexcom CGM sensor, and Insulets personalized model predictive control algorithm. Use of the system was associated with significantly less time spent in hypoglycemic blood glucose range compared to ranges prior to the study, the company said. Additionally, patients stayed in the target blood glucose control range 69 percent of the time over the course of the study, including staying in range 90 percent of the time at night.

Valeritas, which makes a wearable, disposable insulin-delivery device called V-Go, shared data showing the device helped lower A1c and insulin dosage better than insulin pens for people with type 2 diabetes. In a retrospective study of 107 people, split roughly in half by use of V-Go versus insulin pens, V-Go users had their A1c levels down by 1.96 percent to insulin pen users 1.23 percent reduction. V-Go users also had fewer insulin doses than insulin pen users, with 56 units per day versus 77, respectively, and insulin pen users had to go through 3.6 needle sticks per day while V-Go users only required one.

UK-based device company Nemaura Medicalshowcased sugarBEAT, its still-in-development continuous glucose-monitoring patch. In a poster session, the company demonstrated the needle-free disposable patch, which is about 1 millimeter thick and uses a small electronic sensor to measure blood sugar levels and streams the data via Bluetooth to a companion smartphone app. They expect to launch at a "cost-competitive" price point next year.

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Pilot study shows stable insulin production in type 1 diabetes – Science Daily

February 18th, 2017 12:45 pm

A small pilot study in which researchers attempted to slow attacks mounted by the immune system on insulin-producing cells in type 1 diabetes has given promising results. The study by researchers at Linkping University in Sweden has been published in the scientific journal New England Journal of Medicine.

Type 1 diabetes is an autoimmune disease in which the body loses its ability to produce insulin. During the development of the disease, the body's own immune system attacks the insulin-producing beta cells in the pancreas. This often gives rise to the presence of antibodies against the body's own proteins in the beta cells. One of these proteins is GAD65 (glutamic acid decarboxylase), and several clinical trials are underway of a drug known as GAD-alum, based on GAD65.

In the study reported here, DIAGNODE, researchers from Linkping University have injected GAD-alum directly into lymph nodes in the groin, rather than under the skin, in order to determine whether this causes the immune response to become more tolerant towards the body's own GAD protein. This method is similar to one known as "allergen immunotherapy" used in certain treatments for allergy, where it induces tolerance against an allergenic substance.

Six patients aged 20-22 years who had been diagnosed with type 1 diabetes up to 6 months previously were included in the study. They were injected with a small dose of GAD-alum on three occasions, and took vitamin D supplements during the period of the study. The latter can reduce the inflammatory response of the immune system.

"The results for these six patients are very promising. Type 1 diabetes usually progresses gradually as the patient loses the ability to produce insulin, but this has not happened in these patients. We must follow them for a longer period and we must include more patients before we can say anything about the effectiveness of the treatment, but the results so far are extremely exciting," says Johnny Ludvigsson, senior professor at Linkping University and principal investigator for the study.

The pilot study does not contain a control group of patients who do not receive the treatment being tested. The report instead compares the results with those from other studies of untreated patients. The long-term blood sugar level (HbA1c) and the need to inject extra insulin both fell in the patients in the current study. Their natural production of insulin remained at a stable level. The six patients were followed for at least six months; four of them for more than 15 months.

The researchers are now planning to continue the study by increasing the number of participants, and including younger patients.

"If these results are confirmed when we test more patients, it would be an extremely important advance. The way in which type 1 diabetes progresses differs between individuals for many reasons, and this means that it is not necessary to find a treatment that has excellent effects for everyone. Even if it helps only half of patients, this would be a major step forward," says Johnny Ludvigsson.

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Gestational Diabetes Poses Risks for Mom, Baby – WebMD – WebMD

February 18th, 2017 12:45 pm

By Robert Preidt

HealthDay Reporter

THURSDAY, Feb. 16, 2017 (HealthDay News) -- Diabetes that develops during pregnancy -- known as gestational diabetes -- carries health risks for both the mom-to-be and her baby, new research confirms.

A team of French researchers analyzed data from more than 700,000 births in France occurring after 28 weeks of pregnancy in 2012.

Compared to other pregnant women, those with gestational diabetes were 30 percent more likely to experience preterm birth, 40 percent more likely to require a C-section, and 70 percent more likely to have preeclampsia/eclampsia, a dangerous spike in blood pressure.

Risks weren't confined to the mother, however. Babies born to women with gestational diabetes were 80 percent more likely to be of significantly larger-than-average size at birth; 10 percent more likely to suffer respiratory issues; 30 percent more likely to experience a traumatic birth, and 30 percent more likely to have heart defects, the study found.

Babies born after 37 weeks to women with gestational diabetes also had an increased risk of death, compared to babies born to women without the condition, the study authors said.

The study clearly shows that gestational diabetes "is a disease related to adverse pregnancy outcomes," concluded a team led by Dr. Sophie Jacqueminet, of the Pitie-Salpetriere Hospital in Paris.

Two experts in diabetes care weren't surprised by the findings, and they noted that while a woman's weight isn't always a factor, the odds for gestational diabetes go up in the obese.

"Gestational diabetes is a dangerous entity, and the child is at risk," said Dr. Robert Courgi, an endocrinologist at Northwell Health's Southside Hospital, in Bay Shore, N.Y.

"As obesity increases, so does [the risk of] diabetes," he added. "We need to do a better job at diagnosing and treating gestational diabetes."

The study also found that the risk of death was 30 percent higher among babies born to women whose gestational diabetes was treated with a special diet. There was no increased risk of death among babies born to women whose gestational diabetes was treated with insulin, however.

This difference in death risk could be because women with diet-treated gestational diabetes tend to give birth later than those who are insulin-treated, the research team said.

Outcomes were worse for mothers with gestational diabetes "who gave birth later because the baby was exposed to higher blood sugar levels for a longer period of time," Courgi explained.

Dr. Gerald Bernstein coordinates the diabetes program at Lenox Hill Hospital in New York City. He stressed that gestational diabetes requires prompt and proper treatment.

"Once diagnosed, treatment is geared to maintain normal blood sugar but without the risk of hypoglycemia [low blood sugar]," Bernstein explained. "This may range from nutritional and other lifestyle changes to the addition of insulin. The goal is to give the baby a maximum opportunity for growth and development without an unusual early delivery, so that key organs are as mature as possible.

"Most patients are followed by an endocrinologist, a high-risk ob-gyn and diabetes educators in various disciplines," Bernstein added. "To reduce birth complications, early diagnosis along with aggressive therapy with a full health care team is essential."

The study was published Feb. 15 in the journal Diabetologia.

WebMD News from HealthDay

SOURCES: Robert Courgi, M.D., endocrinologist, Northwell Health's Southside Hospital, Bay Shore, N.Y.; Gerald Bernstein, M.D., endocrinologist and coordinator, Friedman Diabetes Program, Lenox Hill Hospital, New York City; Dibatetologia, news release, Feb. 15, 2017

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Fat tissue can ‘talk’ to other organs, paving way for possible treatments for diabetes, obesity – Science Magazine

February 18th, 2017 12:45 pm

Fat cells can regulate genes in distant organs like the liver by sending out molecular messengers.

Steve Gschmeissner/Science Source

By Emma HiolskiFeb. 16, 2017 , 6:00 PM

Theres more to those love handles than meets the eye. Fat tissue can communicate with other organs from afar, sending out tiny molecules that control gene activity in other parts of the body, according to a new study. This novel route of cell-to-cell communication could indicate fat plays a much bigger role in regulating metabolism than previously thought. It could also mean new treatment options for diseases such as obesity and diabetes.

I found this very interesting and, frankly, very exciting, says Robert Freishtat of Childrens National Health System in Washington, D.C., a pediatrician and researcher who has worked with metabolic conditions like obesity and diabetes. Scientists have long known that fat is associated with all sorts of disease processes, he says, but they dont fully understand how the much-reviled tissue affects distant organs and their functions. Scientists have identified hormones made by fat that signal the brain to regulate eating, but this new studyin which Freishtat was not involvedtakes a fresh look at another possible messenger: small snippets of genetic material called microRNAs, or miRNAs.

MiRNAs, tiny pieces of RNA made inside cells, help control the expression of genes and, consequently, protein production throughout the body. But some tumble freely through the bloodstream, bundled into tiny packets called exomes. There, high levels of some miRNAs have been associated with obesity, diabetes, cancer, and cardiovascular disease.

To understand how miRNAs function in fat, a team of researchers led by Thomas Thomou, a diabetes researcher at Joslin Diabetes Center and Harvard Medical School in Boston, studied a genetically engineered strain of mice in which fat cells lacked a critical miRNA-processing enzyme. These rodents had less fat tissue, and they couldnt process glucose as effectively as nonengineered mice. They also had low circulating miRNA levels overall, suggesting that most of the miRNAs in exosomes come from fat tissue, the researchers reported this week in Nature.

By transplanting fat from normal mice, the researchers restored the previously low miRNA levels in the modified mice. Transplants of brown fatspecialized energy-burning fat that regulates temperaturehelped restore glucose processing in the genetically modified mice, whereas white fatenergy-storing fattransplants did not.

In a previous study with the mice whose fat had impaired miRNA production, the researchers also noticed that other organsincluding the heart and liverwere affected, even though the genetic modification didnt alter those tissues directly. So they decided to investigate whether fat uses miRNAs to communicate with other tissues, Thomou says. They developed a method to measure cross-talk using a human miRNA. In one group of mice, they engineered brown fat cells to produce the human miRNA and package it in exosomes; in another, they engineered liver cells to produce a fluorescent molecular target for the miRNA. Injecting exosomes from the first group of mice into mice from the second group caused a drastic drop in liver cell fluorescence, because the miRNA bound to the fluorescent target and suppressed its production. This confirmed that fat tissue, through exosomes, can communicate with the liver and regulate gene expression. Exosomal miRNAs from brown fat were also found to regulate expression of an important metabolism gene, Fgf21, in liver cells.

This finding will provide not only insights into new pathways of tissue communication, but also pathways that can be altered in disease states, says study co-author C. Ronald Kahn, a diabetes researcher and physician at Harvard University. If researchers can figure out how to engineer exomes to target specific cell types, adds Thomou, they might one day use the vesicles to deliver drugs and other therapies. But its far from clear, he notes, whether exomes target specific cell typesusing a kind of molecular ZIP code that could help them travel from point A to point B.

Thomou and his team plan to continue identifying specific miRNA signatures from different tissues to determine what other factors, besides miRNAs, are bundled into exosomes. For Freishtat, the new work offers an exciting way to begin filling a gap between mouse models and human patient studies. This is a big deal, he says. Were just beginning to scratch the surface of exosomes and how they regulate processes in the body.

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Marshall researcher lands grant for diabetes – The Independent

February 18th, 2017 12:45 pm

HUNTINGTON A health professor and researcher at the Department of Family and Community Health at Marshall University has received a $1.3 million grant to support health care work for high-risk diabetes patients.

Dr. Richard Crespo said the funds from the Appalachian Regional Commission will aid community health workers in Kentucky, West Virginia, and Ohio. He said the grant supports the creation of care coordination teams, which work with patients in their homes and communities.

What community health workers can do is invaluable, especially with patients with chronic conditions who are at high risk, Crespo said. What we are doing with this project is engaging the health insurance companies in coming up with a system for reimbursing the health care agencies who are doing this care coordination for the high-risk patients.

Crespo said community health workers rely on grants for much of their funding, so the project is important to the continued care of patients.

The critical outcome of this grant is sustainable employment for the community health workers, he said.

Crespo estimated the funds will support approximately 25 community health workers care for about 625 high-risk diabetes patients with the goal of providing them with self-management skills to control their condition.

In Kentucky, he is working with Big Sandy Healthcare, which operates in Magoffin, Martin and Pike counties.

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Gastric bypass controls diabetes long term better than other methods – Science News

February 18th, 2017 12:45 pm

People who undergo gastric bypass surgery are more likely to experience a remission of their diabetes than patients who receive a gastric sleeve or intensive management of diet and exercise, according to a new study. Bypass surgery had already shown better results for diabetes than other weight-loss methods in the short term, but the new research followed patients for five years.

We knew that surgery had a powerful effect on diabetes, says Philip Schauer of the Bariatric & Metabolic Institute at the Cleveland Clinic. What this study says is that the effect of surgery is durable. The results were published online February 15 in the New England Journal of Medicine.

The study followed 134 people with type 2 diabetes for five years in a head-to-head comparison of weight-loss methods. At the end of that time, two of 38 patients who only followed intensive diet and exercise plans were no longer in need of insulin to manage blood sugar levels. For comparison, 11 of 47 patients who had a gastric sleeve, which reduces the size of the stomach, and 14 of 49 who underwent gastric bypass, a procedure that both makes the stomach smaller and shortens digestion time, did not need the insulin anymore. In general, patients who had been diabetic for fewer than eight years were more likely to be cured, Schauer says.

Even those surgical patients who still needed to take insulin had greater weight loss and lower median glucose levels than others in the study. This study was also one of the few to show that bariatric surgery could help those with only mild obesity, defined as a body mass index between 27 and 34. How bariatric surgery might improve diabetes is still unknown, but scientists have pointed to effects on the bodys metabolism (SN: 8/24/13, p. 14) and gut microbes (SN: 9/5/15, p. 16).

Over five years, gastric bypass patients showed bettercontrol ofblood sugar levels than patients whoused a gastric sleeve or medical management such as intensive diet and exercise plans.

The same research team had published similar results at one and three years after surgery, but few studies looked further, says Kristoffel Dumon, a bariatric surgeon with the University of Pennsylvania Health System in Philadelphia. The criticism of bariatric research has been that there are no good long-term results. With weight-loss surgery, you often see rapid initial results, but you want to see that to a five-year time point.

Dumon also notes that the patients who received only intensive medical therapy did not report an improvement in their quality of life, and their emotional well-being worsened. People in the surgical group reported improvements in quality of life, but not in emotional well-being, a finding that Schauer says has more to do with stress management and other characteristics that wouldnt necessarily be affected by surgery.

Schauer hopes to have even longer-term data in the future. His team will combine their results with those from similar research at three other U.S. sites with the goal of following patients for up to 10 years.

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Experimental Therapy May Slow Type 1 Diabetes – Live Science

February 18th, 2017 12:45 pm

It may be possible to slow the progression of type 1 diabetes, according to a new pilot study that used an experimental therapy that centers on the immune system.

In the new study, researchers in Sweden tested a new method to train the immune system to stop attacking the body's own insulin-producing cells, according to the findings published today (Feb. 15) in the New England Journal of Medicine. With only six participants, the study was small, but experts called these early results exciting.

In people with type I diabetes, the immune system mistakenly recognizes certain proteins in beta cellsas foreign invaders and wages a war against them. Once the beta cells have been killed, the pancreas produces little or no insulin, the hormone that regulates how the body absorbs sugar from the blood to use for energy. As a result, patients need to follow lifelong treatments such as insulin injections to keep their blood sugar levels at normal ranges. [9 Healthy Habits You Can Do in 1 Minute (Or Less)]

This destruction of beta cells doesn't happen overnight, however. Although the majority of them are gone by the time someone is diagnosed, some cells manage to dodge the attacks and continue to produce some insulin. That's why several research teams have been working on finding ways to rescue the remaining cells, or delay their destruction in people who have been recently diagnosed with the condition.

In the new study, the researchers injected a protein normally found on beta cells directly into the patients' lymph nodes.

"This method has shown the best efficacy so far," at slowing the disease's progression, said Dr. Johnny Ludvigsson, senior professor of pediatrics at Linkping University and the study's lead investigator. "But we have to be cautious. The number of patients is small."

If confirmed in larger trials, the therapy could bring a number of benefits to patients. The ability to make insulin secretion, even if only at very low levels, dramatically decreases people's risk of complications, such as episodes of dangerously low blood sugar levels, Ludvigsson told Live Science.

The small amount of insulin that the patients in the study could produce would also make it easier for the patients to maintain a good blood sugar balance, improving their quality of life. It would also reduce their risk of long-term complications of the disease, such as heart attack, stroke, neuropathy, kidney problems and eye disease.

"These are exciting results," said Dr. Lawrence Steinman, a professor of pediatrics and neurological sciences at Stanford University, who was not involved with the study. Steinman echoed Ludvigsson's warning that the study is small, and said that trials with more people and which include a control group of patients who are given a placebo are needed to confirm the findings.

The injections that the researchers gave to the patients in the study contained a protein called GAD, which is normally found in the beta cells. Ludvigsson and his colleagues injected this protein into the patients' lymph nodes near the groin. Lymph nodes contain many immune cells, and the idea behind the treatment is that exposing the body's immune cells to larger amounts of GAD than they normally encounter will cause the immune cells to become more tolerant of GAD, and halt their attack on it.

The participants in the study were ages 20 to 22, and all had been diagnosed with type 1 diabetes within the last six months. The researchers followed up with the patients six to 15 months after the treatment, and found that the functioning of the pancreas had not declined, as expected in the typical course of the disease, but remained stable.

Previously, Ludvigsson's team had tried the same treatment, but had injected the protein under the skin. The new results suggest that an injection directly into the lymph nodes better exposes immune cells to the self-antigen.

"With a much lower dose, we got a very strong desired effect on the immune system," Ludvigsson said.

The team is now planning to repeat the study in a larger number of people, which would take a few years, Ludvigsson said.

Although these results are far too early to be applied to patients, they lend promising evidence to a relatively new line of research that aims to modify the immune system with high precision to treat or perhaps even cure type 1 diabetes.

"A few approaches are in clinical trials, but nothing is yet on the market," Steinman said. "Antigen-based therapy [which was used in the new study] is a sought-after approach, but only a few in the world are attempting this."

In his own work, Steinman has focused on another protein, called proinsulin, which also becomes a target of the immune system in people with type 1 diabetes.

In a 2012 clinical trial with 80 people, Steinman and his team injected participants with a chunk of DNA-encoding proinsulin, in an attempt to desensitize the immune system to proinsulin. The researchers found that the function of the pancreas not only stabilized, but actually improved. It is possible, Steinman said, that some beta cells somehow hide from the immune attacks by going into hibernation, and that once the attacks are eased, they recover and resume function. Plans for the next trial are ongoing, Steinman said.

An immune therapy for type 1 diabetes in the future might combine some of the various approaches that different research teams have tried.

"So far, almost all studies have been performed testing one drug at a time, and they have not been effective enough," Ludvigsson said. "My opinion is that we need a combination of different approaches. For example, different drugs, given in a planned scheme, as is done in oncology. And not until just recently has that idea started to become accepted."

Originally published on Live Science.

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More lessons from Dolly the sheep: Is a clone really born at age zero? – San Francisco Chronicle

February 18th, 2017 12:42 pm

(THE CONVERSATION) In 1997 Dolly the sheep was introduced to the world by biologists Keith Campbell, Ian Wilmut and colleagues. Not just any lamb, Dolly was a clone. Rather than being made from a sperm and an egg, she originated from a mammary gland cell of another, no-longer-living, six-year-old Fynn Dorset ewe.

With her birth, a scientific and societal revolution was also born.

Some prominent scientists raised doubts; it was too good to be true. But more animals were cloned: first the laboratory mouse, then cows, goats, pigs, horses, even dogs, ferrets and camels. By early 2000, the issue was settled: Dolly was real and cloning adults was possible.

The implications of cloning animals in our society were self-evident from the start. Our advancing ability to reprogram adult, already specialized cells and start them over as something new may one day be the key to creating cells and organs that match the immune system of each individual patient in need of replacements.

But what somehow got lost was the fact that a clone was born at day zero created from the cell of another animal that was six years old. Researchers have spent the past 20 years trying to untangle the mysteries of how clones age. How old, biologically, are these animals born from other adult animals cells?

Dolly became an international celebrity, but she was not the first vertebrate to be cloned from a cell taken from the body of another animal. In 1962, developmental biologist John Gurdoncloned the first adult animal by taking a cell from the intestine of one frog and injecting it into an egg of another. Gurdons work did not go unnoticed he went on to share the 2012 Nobel Prize in Physiology or Medicine. But it was Dolly who had captured our imagination. Was it because she was a warm-blooded animal, a mammal, much closer to human? If you could do it in a sheep, you could do it on us!

Dolly, along with Gurdons frogs from 35 years earlier and all the other experiments in between, redirected our scientific studies. It was amazing to see a differentiated cell an adult cell specialized to do its particular job transform into an embryonic one that could go on to give rise to all the other cells of a normal body. We researchers wondered if we could go further: Could we in the lab make an adult cell once again undifferentiated, without needing to make a cloned embryo?

A decade after Dolly was announced, stem cell researcher Shynia Yamanakas team did just that. He went on to be the Nobel corecipient with Gurdon for showing that mature cells could be reprogrammed to become pluripotent: able to develop into any specialized adult cell.

Now we have the possibility of making individualized replacement cells potentially any kind to replace tissue damaged due to injury, genetic disorders and degeneration. Not only cells; we may soon be able to have our own organs grown in a nonhuman host, ready to be transplanted when needed.

If Dolly was responsible for unleashing the events that culminate with new methods of making fully compatible cells and organs, then her legacy would be to improve the health of practically all human beings on this planet. And yet, I am convinced that there are even better things to come.

In the winter of 2013, I found myself driving on the wrong side of the road through the Nottingham countryside. In contrast to the luscious landscape, I was in a state gloom; I was on my way to see Keith Campbells family after his sudden death a few weeks earlier. Keith was a smart, fun, loving friend who, along with Ian Wilmut and colleagues at the Roslin Institute, had brought us Dolly 15 years earlier. We had met at a conference in the early 1990s, when we were both budding scientists playing around with cloning, Keith with sheep, me with cows. An extrovert by nature, he quickly dazzled me with his wit, self-deprecating humor and nonstop chat, all delivered in a thick West Midlands accent. Our friendship that began then continued until his death.

When I knocked at the door of his quaint farmhouse, my plan was to stay just a few minutes, pay my respects to his wife and leave. Five hours and several Guinnesses later, I left feeling grateful. Keith could do that to you, but this time it wasnt him, it was his latest work speaking for him. Thats because his wife very generously told me the project Keith was working on at the time of his death. I couldnt hide my excitement: Could it be possible that after 20 years, the most striking aspect of Dollys legacy was not yet revealed?

See, when Dolly was cloned, she was created using a cell from a six-year-old sheep. And she died at age six and a half, a premature death for a breed that lives an average of nine years or more. People assumed that an offspring cloned from an adult was starting at an age disadvantage; rather than truly being a newborn, it seemed like a clones internal age would be more advanced that the length of its own life would suggest. Thus the notion that clones biological age and their chronological one were out of sync, and that cloned animals will die young.

Some of us were convinced that if the cloning procedure was done properly, the biological clock should be reset a newborn clone would truly start at zero. We worked very hard to prove our point. We were not convinced by a single DNA analysis done in Dolly showing slightly shorter telomeres the repetitive DNA sequences at the end of chromosomes that count how many times a cell divides. We presented strong scientific evidence showing that cloned cows had all the same molecular signs of aging as a nonclone, predicting a normal lifespan. Others showed the same in cloned mice. But we couldnt ignore reports from colleagues interpreting biological signs in cloned animals that they attributed to incomplete resetting of the biological clock. So the jury was out.

Aging studies are very hard to do because there are only two data points that really count: date of birth and date of death. If you want to know the lifespan of an individual you have to wait until its natural death. Little did I know, that is what Keith was doing back in 2012.

That Saturday afternoon I spent in Keiths house in Nottingham, I saw a photo of the animals in Keiths latest study: several cloned Dollies, all much older than Dolly at the time she had died, and they looked terrific. I was in awe.

The data were confidential, so I had to remain silent until late last year when the work was posthumously published. Keiths coauthors humbly said: For those clones that survive beyond the perinatal period [] the emerging consensus, supported by the current data, is that they are healthy and seem to age normally.

These findings became even more relevant when last December researchers at the Scripps Research Institute found that induced pluripotent stem cells reprogrammed using the Yamanaka factors retain the aging epigenetic signature of the donor individual. In other words, using these four genes to attempt to reprogram the cells does not seem to reset the biological clock.

The new Dollies are now telling us that if we take a cell from an animal of any age, and we introduce its nucleus into a nonfertilized mature egg, we can have an individual born with its lifespan fully restored. They confirmed that all signs of biological and chronological age matched between cloned and noncloned sheep.

There seems to be a natural built-in mechanism in the eggs that can rejuvenate a cell. We dont know what it is yet, but it is there. Our group as well as others are hard at work, and as soon as someone finds it, the most astonishing legacy of Dolly will be realized.

This article was originally published on The Conversation. Read the original article here: http://theconversation.com/more-lessons-from-dolly-the-sheep-is-a-clone-really-born-at-age-zero-73031.

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More lessons from Dolly the sheep: Is a clone really born at age zero? - San Francisco Chronicle

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Genome surgery with CRISPR-Cas9 to prevent blindness – Science Daily

February 18th, 2017 12:42 pm

It is estimated that almost one in every ten people over 65 has some signs of age-related macular degeneration (AMD), and its prevalence is likely to increase as a consequence of the aging population. AMD is a form of blindness, common in Caucasians, which causes distorted vision and blind spots. Scientists at the Center for Genome Engineering, within the Institute for Basic Science (IBS) report the use of CRISPR-Cas9 in performing "gene surgery" in the layer of tissue that supports the retina of living mice. Published in Genome Research, this study combines basic research and mouse model applications.

The most common retinopathies causing blindness are 'retinopathy of prematurity' in children, 'diabetic retinopathy' and 'AMD' in older adults. In these diseases, abnormally high levels of the Vascular Endothelial Growth Factor (VEGF) are secreted. In AMD, VEGF causes the formation of new blood vessels in the eyes but also leads to leakages of blood and fluid into the eye, damaging an area at the center of the retina called macula.

Injections of anti-VEGF drugs are the most common treatment against AMD, but at least seven injections per year are required, because VEGF is continuously overexpressed by the cells of the diseased retinal pigment epithelium. Instead of such invasive treatments, IBS scientists believe that gene therapy with the third generation gene editing tool CRISPR-Cas9 could improve the situation. "The injections tackle the effects, but not the main cause of the problem. By editing the VEGF gene, we can achieve a longer-term cure," explains KIM Jin-Soo, Director of the Center for Genome Engineering.

CRISPR-Cas9 can precisely cut and correct DNA at the desired site in the genome. The CRISPR-Cas9 system works by cutting DNA at a target site, in this case, inside the VEGF gene. Two year ago, IBS scientists proved that a pre-assembled version of CRISPR-Cas9, a.k.a, Cas9 ribonucleoprotein (RNP), can be delivered to cells and stem cells to modify target genes. The pre-assembled complex works rapidly and degrades before the body has time to build up an immune response against it. Despite these advantages and previous successes, the difficulty in delivering pre-assembled CRISPR-Cas9 has limited its use in therapeutic applications.

In this study, the research team successfully injected CRISPR-Cas9 into the eyes of a mice model with wet AMD and locally modified the VEGF gene. Initially they found that the delivery of the pre-assembled CRISPR-Cas9 complex is more efficient that the delivery of the same components in a plasmid form. Secondly, the complex disappeared after just 72 hours. Scientists assessed the whole genome of the animals and found the CRISPR-Cas9 complex modified only the VEGF gene and did not affect other genes. The progression of the eye disease was monitored by looking at choroidal neovascularization (CNV), the creation of new blood vessels between the retina and the sclera -- a common problem of 'wet' macular degeneration -- and researchers found the CNV area reduced by 58%. Moreover, a likely side effect, namely cone dysfunction, that takes only 3 days to show in these mice, did not occur a week after the treatment.

"We have developed a treatment to suppress CNV by inactivating the VEGF gene, one of the causes of AMD. We envision that, in the future, surgeons will be able to cut and paste disease-causing genetic elements in patients," explains Kim Jin-Soo.

While CRISPR-Cas9 is conventionally used to correct mutations causing hereditary diseases or cancer, this study suggests a new therapy for non-hereditary degenerative disease."We believe that this is a new therapeutic modality for the treatment of non-hereditary degenerative diseases," points out Professor KIM Jeong Hun (Seoul National University), "We confirmed the effect on the animal models of the disease and now we wish to continue with preclinical trials."

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Genome surgery with CRISPR-Cas9 to prevent blindness - Science Daily

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Non-profit seeking to cure blindness up for $100M grant – SFGate

February 18th, 2017 12:42 pm

Wilson Ring, Associated Press

Non-profit seeking to cure blindness up for $100M grant

WATERBURY, Vt. (AP) A Vermont-based nonprofit group that works to cure blindness in Nepal and other developing countries is one of eight semifinalists for a $100 million grant from the John D. and Catherine T. MacArthur Foundation.

The Waterbury-based Himalayan Cataract Project, based out of a rented office in a church parsonage, has been working for years to train local health care providers to perform cataract and laser surgery in Nepal and other countries.

The organization was co-founded in 1995 by Nepalese Dr. Sanduk Ruit and Dr. Geoff Tabin, formerly of the University of Vermont Medical Center and now at the University of Utah.

"They had a shared motivation that the right to sight is a human right and that no one anywhere in the world should receive care of a different or lower quality," said Job Heintz, the chief executive officer of the nonprofit, formed in 2003 to carry out the vision of the doctors. It now has 10 employees and an annual budget of about $9 million.

Over the years the organization has provided eye care for thousands of patients by training health care providers and providing equipment and other infrastructure.

"The quality of eye health care has dramatically risen, nowhere better than in Nepal," Heintz said on Thursday.

The Chicago-based MacArthur Foundation announced Wednesday that the Cataract Project was one of eight organizations chosen as semifinalists from among 1,904 proposals, for the $100 million grant program. The foundation says the competition is for "proposals promising real progress toward solving a critical problem of our time in any field or any location."

The winner would receive the entire $100 million.

Other semifinalists include Catholic Relief Services in Baltimore, which is working to change the way children are cared for in orphanages, and The Carter Center in Atlanta, which is working to eliminate river blindness in Nigeria.

The winner will be chosen in December.

The Cataract Project got its start at the Tilganga Eye Centre in Kathmandu, Nepal, which performed its first outpatient cataract surgery in 1994. Ruit and Tabin started the Cataract Project a year later.

At the Tilganga Centre providers now see about 1,000 patients a day for a variety of eye care needs.

Tabin worked at what is now the University of Vermont Medical Center from 1995 to 2005. The project opened Vermont offices in Waterbury and Norwich in 2003

The Cataract Project already has expanded its operations to a number of other countries, but the grant would be to expand operations in Nepal, Ethiopia and Ghana.

If they win the grant, the organization would increase the work it currently does, such as training doctors and support staff in their home countries and at other locations, including the United States.

"We know what we would do with every dollar," Heintz said.

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Non-profit seeking to cure blindness up for $100M grant - SFGate

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