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Rare flesh-eating cancer shock surprise after visit to dentist

Tuesday, June 20th, 2017

Ceri Jones thought she had an abscess — No- She had a rare flesh-eating cancer

Bravery of Ceri Jones

The Ceri Jones flesh eating disease story

CERI Jones thought it would just be a routine trip to the dentist. www.perfectwhiteteeth.net

The 21-year-old had a lump in her mouth she thought was an abscess, so went to the dentist for a check up. It was only then the pub chef from Wales was horrified to lean her problem was in fact a serious, very rare, form of flesh-eating cancer.

The dentist did X-rays and told her there was nothing there so sent her to hospital for more tests. She then got the devastating diagnosis.

“It was November last year when I was diagnosed with Adenoid Cystic Carcinoma and was referred to Liverpool Women’s Hospital.

“I’d never heard of anything like it, I was so shocked that I actually had it to be honest,” The Mirror reported.

Adenoid Cystic Carcinoma affects the salivary glands of the head and neck. She needed 36 hours on the operating table to remove the tumour. But she also lost her left eye.

But that wasn’t all.

The cancer was at an advanced stage after it had spread so her upper left jaw and upper left facial bones were also replaced with titanium metal and her face needed to be reconstructed.

She also lost her teeth on the left side as she had to have the muscle and skin on her right thigh grafted into her mouth.

Miss Jones told the Daily Post the horrifying detail of the operation.

“I was under sedation for two weeks while they did it and took skin and muscle from my right thigh to replace the left and side palate in my mouth, and they had to connect major arteries to blood vessels in my neck so the palate would keep alive.”

The British health system has paid for her to fly to Florida, in the United States, to undergo specialist radiotherapy for the next few months.

But she has to meet her own costs to cover day-to-day living and other expenses, so her family have launched a GoFundMe page has been set up to help with hopes to raise almost $10,000.

Her mum Sarah Evans said: “I relive this nightmare every day from the day we took Ceri to Liverpool to the day she came home and the morning she went down to theatre for the longest life-changing surgery and the complications she had thereafter.”

She said she was proud of the “bravery and strength” her daughter had shown.

“She’s an inspiration.”

Henry Sapiecha

Video below on Flesh Eating Cancer

Precision Medicine: What Is Cancer, Really? Scientists overview here.

Monday, May 22nd, 2017

The men and women who are trying to bring down cancer are starting to join forces rather than work alone. Together, they are winning a few of the battles against the world’s fiercest disease. For this unprecedented special report, we visited elite cancer research centers around the country to find out where we are in the war.

I. Precision Medicine: What Is Cancer, Really?

When you visit St. Jude Children’s Research Hospital in Memphis, Tennessee, you expect to feel devastated. It starts in the waiting room. Oh, here we go with the little red wagons, you think, observing the cattle herd of them rounded up by the entrance to the Patient Care Center. Oh, here we go with the crayon drawings of needles. The itch begins at the back of your throat, and you start blinking very fast and mentally researching how much money you could donate without starving. Near a row of arcade games, a preteen curls his face into his mother’s shoulder while she strokes his head. Oh, here we go.

But the more time you spend at St. Jude, the more that feeling is replaced with wonder. In a cruel world you’ve found a free hospital for children, started by a Hollywood entertainer as a shrine to the patron saint of lost causes. There is no other place like this. Corporations that have nothing to do with cancer—nothing to do with medicine, even—have donated vast sums of money just to be a part of it. There’s a Chili’s Care Center. The cafeteria is named for Kay Jewelers.

Scott Newman’s office is in the Brooks Brothers Computational Biology Center, where a team of researchers is applying computer science and mathematics to the question of why cancer happens to children. Like many computer people, Newman is very smart and a little quiet and doesn’t always exactly meet your eyes when he speaks to you. He works on St. Jude’s Genomes for Kids project, which invites newly diagnosed patients to have both their healthy and tumor cells genetically sequenced so researchers can poke around.

“Have you seen a circle plot before?” Newman asks, pulling out a diagram of the genes in a child’s cancer. “If I got a tattoo, it would be one of these.” Around the outside of the circle plot is something that looks like a colorful bar code. Inside, a series of city skylines. Through the center are colored arcs like those nail-and-string art projects students make in high school geometry class. The diagram represents everything that has gone wrong within a child’s cells to cause cancer. It’s beautiful.

A Genetic Disaster: This circular visualization shows real gene mutations found in 3,000 pediatric cancers at St. Jude Children’s Research Hospital. Genes with sequence mutations are labeled in blue; those with structural variations are in red; and those

“These are the genes in this particular tumor that have been hit,” Newman says in a Yorkshire accent that emphasizes the t at the end of the word hit in a quietly violent way. “And that’s just one type of thing that’s going on. Chromosomes get gained or lost in cancer. This one has gained that one, that one, that one, that one,” he taps the page over and over. “And then there are structural rearrangements where little bits of genome get switched around.” He points to the arcs sweeping across the page. “There are no clearly defined rules.”

It’s not like you don’t have cancer and then one day you just do. Cancer—or, really, cancers, because cancer is not a single disease—happens when glitches in genes cause cells to grow out of control until they overtake the body, like a kudzu plant. Genes develop glitches all the time: There are roughly twenty thousand genes in the human body, any of which can get misspelled or chopped up. Bits can be inserted or deleted. Whole copies of genes can appear and disappear, or combine to form mutants. The circle plot Newman has shown me is not even the worst the body can do. He whips out another one, a snarl of lines and blocks and colors. This one would not make a good tattoo.

“As a tumor becomes cancerous and grows, it can accumulate many thousands of genetic mutations. When we do whole genome sequencing, we see all of them,” Newman says. To whittle down the complexity, he applies algorithms that pop out gene mutations most likely to be cancer-related, based on a database of all the mutations researchers have already found. Then, a genome analyst manually determines whether each specific change the algorithm found seems likely to cause problems. Finally, the department brings its list of potentially important changes to a committee of St. Jude’s top scientists to discuss and assign a triage score. The mutations that seem most likely to be important get investigated first.

It took thirteen years and cost $2.7 billion to sequence the first genome, which was completed in 2003. Today, it costs $1,000 and takes less than a week. Over the last two decades, as researchers like Newman have uncovered more and more of the individual genetic malfunctions that cause cancer, teams of researchers have begun to tinker with those mutations, trying to reverse the chaos they cause. (The first big success in precision medicine was Gleevec, a drug that treats leukemias that are positive for a common structural rearrangement called the Philadelphia chromosome. Its launch in 2001 was revolutionary.) Today, there are eleven genes that can be targeted with hyperspecific cancer therapies, and at least thirty more being studied. At Memorial Sloan Kettering Cancer Center in New York City, 30 to 40 percent of incoming patients now qualify for precision medicine studies.

Charles Mullighan,a tall, serious Australian who also works at St. Jude, is perhaps the ideal person to illustrate how difficult it will be to cure cancer using precision medicine. After patients’ cancer cells are sequenced, and the wonky mutations identified, Mullighan’s lab replicates those mutations in mice, then calls St. Jude’s chemical library to track down molecules—some of them approved medicines from all over the world, others compounds that can illuminate the biology of tumors—to see if any might help.

New York: Britta Weigelt and Jorge Reis-Filho use police forensics techniques to repair old tumor samples at Memorial Sloan Kettering so the samples can be genetically profiled.

If Mullighan is lucky, one of the compounds he finds will benefit the mice, and he’ll have the opportunity to test it in humans. Then he’ll hope there are no unexpected side effects, and that the cancer won’t develop resistance, which it often does when you futz with genetics. There are about twenty subtypes of the leukemia Mullighan studies, and that leukemia is one of a hundred different subtypes of cancer. This is the kind of precision required in precision cancer treatment—even if Mullighan succeeds in identifying a treatment that works as well as Gleevec, with the help of an entire, well-funded hospital, it still will work for only a tiny proportion of patients.

Cancer is not an ordinary disease. Cancer is the disease—a phenomenon that contains the whole of genetics and biology and human life in a single cell. It will take an army of researchers to defeat it.

Luckily, we’ve got one.

Interlude

“I used to do this job out in L.A.,” says the attendant at the Hertz counter at Houston’s George Bush Intercontinental Airport. “There, everyone is going on vacation. They’re going to the beaach or Disneyland or Hollywood or wherever.

“Because of MD Anderson, I see more cancer patients here. They’re so skinny. When they come through this counter, they’re leaning on someone’s arm. They can’t drive themselves. You think, there is no way this person will survive. And then they’re back in three weeks, and in six months, and a year. I’m sure I miss some, who don’t come through anymore because they’ve died. But the rest? They come back.”

II. Checkpoint Inhibitor Therapy: You Have the Power Within You!

On a bookshelf in Jim Allison’s office at MD Anderson Cancer Center in Houston (and on the floor surrounding it) are so many awards that some still sit in the boxes they came in. The Lasker-DeBakey Clinical Medical Research Award looks like the Winged Victory statue in the Louvre. The Breakthrough Prize in Life Sciences, whose benefactors include Sergey Brin, Anne Wojcicki, and Mark Zuckerberg, came with $3 million.

“I gotta tidy that up sometime,” Allison says.

Allison has just returned to the office from back surgery that fused his L3, L4, and L5 vertebrae, which has slightly diminished his Texas rambunctiousness. Even on painkillers, though, he can explain the work that many of his contemporaries believe will earn him the Nobel Prize: He figured out how to turn the immune system against tumors.

“One day, the miracles won’t be miracles at all. They’ll just be what happens.”

Allison is a basic scientist. He has a Ph.D., rather than an M.D., and works primarily with cells and molecules rather than patients. When T-cells, the most powerful “killer cells” in the immune system, became better understood in the late 1960s, Allison became fascinated with them. He wanted to know how it was possible that a cell roaming around your body knew to kill infected cells but not healthy ones. In the mid-1990s, both Allison’s lab and the lab of Jeffrey Bluestone at the University of Chicago noticed that a molecule called CTLA-4 acted as a brake on T-cells, preventing them from wildly attacking the body’s own cells, as they do in autoimmune diseases.

Allison’s mother died of lymphoma when he was a child and he has since lost two uncles and a brother to the disease. “Every time I found something new about how the immune system works, I would think, I wonder how this works on cancer?” he says. When the scientific world discovered that CTLA-4 was a brake, Allison alone wondered if it might be important in cancer treatment. He launched an experiment to see if blocking CTLA-4 would allow the immune system to attack cancer tumors in mice. Not only did the mice’s tumors disappear, the mice were thereafter immune to cancer of the same type.

Ipilimumab (“ipi” for short) was the name a small drug company called Medarex gave the compound it created to shut off CTLA-4 in humans. Early trials of the drug, designed just to show whether ipi was safe, succeeded so wildly that Bristol Myers Squibb bought Medarex for $2.4 billion. Ipilimumab (now marketed as Yervoy) became the first “checkpoint inhibitor”: It blocks one of the brakes, or checkpoints, the immune system has in place to prevent it from attacking healthy cells. Without the brakes the immune system can suddenly, incredibly, recognize cancer as the enemy.

“You see the picture of that woman over there?” Allison points over at his desk. Past his lumbar-support chair, the desk is covered in papers and awards and knickknacks and frames, including one containing a black card with the words “Never never never give up” printed on it. Finally, the photo reveals itself, on a little piece of blue card stock.

That’s the first patient I met,” Allison says. “She was about twenty-four years old. She had metastatic melanoma. It was in her brain, her lungs, her liver. She had failed everything. She had just graduated from college, just gotten married. They gave her a month.”

The woman, Sharon Belvin, enrolled in a phase-two trial of ipilimumab at Memorial Sloan Kettering, where Allison worked at the time. Today, Belvin is thirty-five, cancer- free, and the mother of two children. When Allison won the Lasker prize, in 2015, the committee flew Belvin to New York City with her husband and her parents to see him receive it. “She picked me up and started squeezing me,” Allison says. “I walked back to my lab and thought, Wow, I cure mice of tumors and all they do is bite me.” He adds, dryly, “Of course, we gave them the tumors in the first place.”

After ipi, Allison could have taken a break and waited for his Nobel, driving his Porsche Boxster with the license plate CTLA-4 around Houston and playing the occasional harmonica gig. (Allison, who grew up in rural Texas, has played since he was a teenager and once performed “Blue Eyes Crying in the Rain” onstage with Willie Nelson.) Instead, his focus has become one of two serious problems with immunotherapy: It only works for some people.

So far, the beneficiaries of immune checkpoint therapy appear to be those with cancer that develops after repeated genetic mutations—metastatic melanoma, non-small-cell lung cancer, and bladder cancer, for example. These are cancers that often result from bad habits like smoking and sun exposure. But even within these types of cancer, immune checkpoint therapies improve long-term survival in only about 20 to 25 percent of patients. In the rest the treatment fails, and researchers have no idea why.

Lately, Allison considers immune checkpoint therapy a “platform”—a menu of treatments that can be amended and combined to increase the percentage of people for whom it works. A newer drug called Keytruda that acts on a different immune checkpoint, PD-1, knocked former president Jimmy Carter’s metastatic melanoma into remission in 2015. Recent trials that blocked both PD-1 and CTLA-4 in combination improved long-term survival in 60 percent of melanoma patients. Now, doctors are combining checkpoint therapies with precision cancer drugs, or with radiation, or with chemotherapy. Allison refers to this as “one from column A, and one from column B.”

The thing about checkpoint inhibitor therapy that is so exciting—despite the circumscribed group of patients for whom it works, and despite sometimes mortal side effects from the immune system going buck-wild once the brakes come off—is the length of time it can potentially give people. Before therapies that exploited the immune system, response rates were measured in a few extra months of life. Checkpoint inhibitor therapy helps extremely sick people live for years. So what if it doesn’t work for everyone? Every cancer patient you can add to the success pile is essentially cured.

Jennifer Wargo and team remove lymph nodes from a melanoma patient.

Italian neuroscientist intends bringing frozen brains back to life

Friday, April 28th, 2017

London: A neuroscientist claims he will be able to “wake up” people who have been cryogenically frozen within three years, by transferring their brains to donor bodies.

Sergio Canavero, director of the Turin Advanced Neuromodulation Group, has already announced plans to carry out the first human head transplant, an operation which he claims is just 10 months away.

But he is now thinking further ahead, and wants to begin brain transplants within three years.

If the procedures are successful, he believes that frozen brains could be thawed and inserted into a donor, effectively bringing “dead” people back to life.

Hundreds of people who were dying or paralysed have had their bodies or brains cryogenically preserved in the hope that medical science will one day be able to cure their conditions.

Although many experts are sceptical that the brain can be thawed without damage, Professor Canavero said he planned to awaken patients frozen by the Alcor Life Extension Foundation, which is based in Arizona.

“As soon as the first human head transplant has taken place, no later than 2018, we will be able to attempt to reawaken the first frozen head,” he said.

“We are currently planning the world’s first brain transplant, and I consider it realistic that we will be ready in three years at the latest.”

British scientists are sceptical about whether the brain could be fully restored from frozen.

Clive Coen, professor of neuroscience at King’s College London, said the chances of bringing a brain back was “infinitesimal”.

Dr Channa Jayasena, clinical senior lecturer at Imperial College London added: “It is currently not possible to freeze and thaw human tissue without killing many cells contained within it.”

Professor Canavero is working with a Chinese team of doctors led by Dr Ren Xiaoping, of Harbin Medical Centre, who helped perform the first successful hand transplant in the US.

Although Russian computer scientist Valery Spiridonov, who has spinal muscular atrophy, had volunteered to become the first head transplant patient, the team expects the first operation to be with a Chinese donor and patient.

Last year, the team announced a successful head transplant performed on a monkey.

Telegraph, London

Just Hours after this photo was taken, she tragically died

Sunday, March 19th, 2017

Gabrielle Marsh died hours after this photo was taken. She was celebrating her upcoming 20th birthday at home with friends when she suffered a catastrophic brain bleed image www.newcures.info

Gabrielle Marsh died hours after this photo was taken. She was celebrating her upcoming 20th birthday at home with friends when she suffered a catastrophic brain bleed

IT WAS supposed to be a fun night with her friends celebrating her 20th birthday – and when Gabrielle Marsh started to get a headache, no one suspected she would be dead hours later.

Photos of the night show the young Auckland woman raising a toast with her best friends, showing off the platter of food she’d thoughtfully planned and created for the night.

Two hours after those photos were taken Gabby, as she was known, was lying on the floor of her home in agony, her mother Kathryn at her side and an ambulance on its way.

Later that night as Gabby lay hooked up to life support machines Auckland City Hospital staff delivered the heartbreaking news to her family – she had suffered a brain haemorrhage and was unlikely to survive.

The next day a decision was made. Gabby was to be taken off life support – but not until her organs had been donated.

And on Monday March 6, on her 20th birthday, after her family had said their goodbyes, Gabby was taken to surgery.

“The woman at the hospital called me and said it was all done, and the donation was taking place as we speak,” Kathryn Marsh told the NZ Herald.

“Gabby loved doing things for other people, and that was her biggest, most amazing gift.”

Gabby’s organs saved the lives of at least six people; her kidney, pancreas, lungs, liver and heart valves were all successfully donated.

“Of course, more than anything, we would love to have her here, but that’s not to be,” said Kathryn.

“But if anything good can come out of it, if she has helped people, then that’s comforting.”

Gabby was the eldest of three children and is survived by Jacob, 18 and 16-year-old Victoria.

Her death was the second tragedy for her family, her father Shayne died just 17 months ago after a long illness.

“It’s still not really sunken in, it was so sudden,” Kathryn said.

“Shayne was sick for 14 months and we all had time to get used to the idea, but with Gabby it was the complete opposite. It’s left us all a bit shell-shocked.”

Gabby was born and raised in Auckland, attending Mount Albert Grammar School before enrolling at Auckland University.

She was about to start her third year of a double degree in commerce and law when she died.

“She was a really good sister, she was kind, generous and she was like a second mum to me,” Jacob said.

Her family described her as extremely thoughtful and loving, adventurous, caring, a “rock star academic” and a young woman motivated and driven with a lot of energy.

“She had a killer smile that came easy and often,” her aunt Michelle Cliffe said.

Kathryn said she didn’t know where to begin when asked what was special about her eldest child.

“She just made people feel at ease and she was easy to be around. There was something special about Gabby,” she said.

After Shayne died, Gabby was a “phenomenal help” to Kathryn, stepping up to do her share of cooking, cleaning and helping with her siblings.

“She just got stuff done, she was pragmatic, hard working and so organised,” Michelle said.

The day Gabby died she woke early and went for a walk with Kathryn – something they did most days together.

Then the pair went to Newmarket shopping and Gabby helped her mother choose a new swimsuit for an extended family holiday to Fiji in April.

The family ate lunch together and Gabby went to watch her boyfriend Bradley play softball before returning home to prepare for her party.

She didn’t drink alcohol, but prepared pina colada cocktails for her three best friends, making a rum-free version for herself.

The girls had planned to go out in the city that night; Gabby loved old music so wanted to go dancing at Irish bar Danny Doolans.

Bradley was going to pick them up and drive them to town.

Then, Gabby started to complain about having a headache.

“It was getting worse and worse,” Kathryn said.

“She just wanted to lie down. Her friends left, they told her it was okay, that they would celebrate with her another time and they called Bradley to tell him.”

After the girls left, Gabby started throwing up and became agitated and slurring her words.

Kathryn suspected a severe migraine, and called an ambulance.

As the paramedics arrived – and Bradley – Gabby lost consciousness.

She never woke up.

Doctors have told her family they believe she had a arteriovenous malformation (AVM), a tangle of abnormal blood vessels connecting arteries and veins in the brain.

It is likely she was born with the condition and there was nothing her family could have done to detect or prevent her death.

“She was healthy, she exercised, she didn’t drink,” said Kathryn, shaking her head.

“The specialist said it was like a ticking time bomb,” Jacob added.

The family said the decision to donate Gabby’s organs was easy; they knew it was what she wanted as she specified it on her licence, and she was a generous young woman.

“She had such a bright future in front of her and I would have just loved to see her future unfold,” Kathryn said.

“We said goodbye to her and we knew that she was then going off to theatre – that she was the one giving the gifts on her birthday.

“She’s given life to more than six people on her birthday, that is her legacy.”

Jacob was brimming with pride over his sister’s final gift.

“It’s like she is living on in other people,” he said.

The Marsh family urged people to openly discuss organ donation with loved ones and make their wishes known.

They hoped to one day meet some of the people that Gabby’s organs helped.

The Gabby Marsh Scholarship

Gabby’s university friends have started a Givealittle page to fund a scholarship in her name, with the support of her family.

“Gabby was passionate, fun loving and kind. She smiled easily and often. She was selfless, considerate and generous.

She was someone who impacted everyone she met,” her friends said.

“Gabby changed the lives of so many around her, and we dream for her character and kindness to continue changing the life of others.

“To honour her academic ability, her exceptional character and her future cut tragically short, the Gabby Marsh Scholarship will be established and offered annually to enable a young school leaver demonstrating exceptional character and service to fulfil their dream of studying commerce at the University of Auckland.”

More than $20,000 has been donated so far.

To donate or read more, click here.

Thanks to the generosity of 503 deceased organ donors and their families a record 1,447 Australians were given a second chance at life in 2016. There were an additional 267 living donors, including 44 under the Australian Kidney Exchange Program.

To register on the Australian Organ Donor Register, click here.

www.goodgirlsgo.com

club-libido-banner-kelly-lies-in-blue-sheets

Henry Sapiecha

Nobel Prize for Medicine Goes to Discovery of Cells’ Garbage Disposal System Article-1 of 2

Monday, October 3rd, 2016

Japanese biologist Yoshinori Ohsumi won the Nobel Prize in medicine image www.newcures.info

STOCKHOLM (AP) — Japanese biologist Yoshinori Ohsumi won the Nobel Prize in medicine on Monday for discoveries on how cells break down and recycle content, a garbage disposal system that scientists hope to harness in the fight against cancer, Alzheimer’s and other diseases.

The Karolinska Institute honored Ohsumi for “brilliant experiments” in the 1990s on autophagy, a phenomenon that literally means “self-eating” and describes how cells gobble up damaged content and provide building blocks for renewal.

Disrupted autophagy (aw-TAH’-fuh-jee) has been linked to several diseases including Parkinson’s, diabetes and cancer, the prize committee said.

“Intense research is now ongoing to develop drugs that can target autophagy in various diseases,” it said in itscitation .

Ohsumi, 71, from Fukuoka, Japan, is a professor at the Tokyo Institute of Technology. In 2012, he won the Kyoto Prize, Japan’s highest private award for global achievement.

Ohsumi said he never thought he would win a Nobel Prize for his work, which he said involved studying yeast in a microscope day after day for decades.

“As a boy, the Nobel Prize was a dream, but after starting my research, it was out of my picture,” he told reporters in Tokyo.

“I don’t feel comfortable competing with many people, and instead I find it more enjoyable doing something nobody else is doing,” Ohsumi added. “In a way, that’s what science is all about, and the joy of finding something inspires me.”

Nobel committee secretary Thomas Perlmann said Ohsumi seemed surprised when he was informed he had won theNobel Prize.

“The first thing he said was ‘ahhh.’ He was very, very pleased,” Perlmann said.

Nobel judges often award discoveries made decades ago, to make sure they have stood the test of time.

Though scientists have known that autophagy exists for more than 50 years, its fundamental significance was only recognized after Ohsumi’s “paradigm-shifting research” on yeast in the 1990s, the committee said.

“Thanks to Ohsumi and others following in his footsteps, we now know that autophagy controls important physiological functions where cellular components need to be degraded and recycled,” it said.

The term autophagy was coined in 1963 by Belgian scientist Christian de Duve, who shared the 1974 Nobel Prize in medicine for discoveries on cell structure and organization.

But before Ohsumi’s research, scientists “didn’t know what it did, they didn’t know how it was controlled and they didn’t know what it was relevant for,” said David Rubinsztein, deputy director of the Institute for Medical Research at the University of Cambridge.

Now “we know that autophagy is important for a host of important mammalian functions.” For example, it protects against starvation in the period when a newborn animal hasn’t yet started breastfeeding, by providing energy, he said.

It also removes proteins that clump together abnormally in brain cells, which is important in conditions like Huntington’s and Parkinson’s diseases and some forms of dementia. If autophagy didn’t do that job, “the diseases would appear more early and be more aggressive,” he said.

Animal studies suggest that boosting autophagy can ease and delay such diseases, said Rubinsztein, whose lab is pursuing that approach for therapy.

“As time goes on, people are finding connections with more and more diseases” and normal cellular operations, he said.

In 1993 Ohsumi published his “seminal discovery” of 15 genes crucial to autophagy, and cloned several of those genes in yeast and mammalian cells in subsequent studies, the Nobel committee said.

“He actually unraveled which are the components which actually perform this whole process,” said Rune Toftgard, chairman of the Nobel Assembly. “Having those components at hand were also important tools to … do functional experiments to understand how important it was for different types of processes in the body.”

In Tokyo, Ohsumi said many details of autophagy are yet to be understood and that he hoped younger scientists would join him in looking for the answers.

“There is no finish line for science. When I find an answer to one question, another question comes up. I have never thought I have solved all the questions,” he said. “So I have to keep asking questions to yeast.”

It was the 107th award in the medicine category since the first Nobel Prizes were handed out in 1905.

Last year’s prize was shared by three scientists who developed treatments for malaria and other tropical diseases.

The announcements continue with physics on Tuesday, chemistry on Wednesday and the Nobel Peace Prize on Friday. The economics and literature awards will be announced next week.

Each prize is worth 8 million kronor ($930,000). The awards will be handed out at prize ceremonies in Stockholm and Oslo on Dec. 10, the anniversary of prize founder Alfred Nobel’s death in 1896.

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Henry Sapiecha

Japanese Scientist Wins Nobel Prize in showing How Human Cells Cannibalize Worn Out Parts

Monday, October 3rd, 2016

yoshinori_osumi_nobel-prize-recipient image www.newcures.info

Even the best-man made machines eventually break down. And the human body, made up of millions of tiny machine-like cells, is no different. Over the years, cells gradually wear from the grueling work of keeping you alive. To restore themselves, they devour their own broken parts. This morning, cell biologist Yoshinori Ohsumi was awarded the Nobel Prize in Physiology or Medicine for identifying the genes and underlying mechanisms that keep our cells in tip-top shape.

The cellular process known as “autophagy” (Greek for “self-eating”) has been known since the 1960s. As far as biological processes go, it’s one of the most important ones. Without being able to tear apart old, broken-down cells for parts, we would age much faster and be more vulnerable to diseases like cancer caused by error-riddled cells running amok.

In the 1950s, scientists discovered that cells of plants and animals are packed with tiny structures called organelles, which are responsible for cellular functions such as generating energy. Researchers noticed, however, that one of these organelles also contained bits and pieces of proteins and structures from the cell itself, “like a garbage dump,” write Gina Kolata and Sewell Chan for the New York Times. This trash pile, dubbed the “lysosome,” cannibalizes worn out parts of the cell for the raw materials to build anew, according to the Nobel Assembly at Stockholm’s Karolinska Institutet.

Before Ohsumi’s work, however, cellular biologists didn’t have a firm understanding of the inner workings of this process. Scientists knew that cells built little sacs around worn-out proteins and organelles for transport to the lysosome. But beyond this basic process, the cellular recycling remained a mystery, Ariana Eunjung Cha and Anna Fifield report for The Washington Post. By studying the inner workings of small, simple yeast cells, Ohsumi was able to identify the genes that make autophagy possible, how cells determine which parts need replacing and what happens when things go wrong.

“Looking into bodily processes, I found that we have an ongoing renewal process without which living organisms can’t survive,” Ohsumi tells the Japanese broadcaster NHK. “This recycling process did not receive as much attention as it deserved, but I discovered that we should be paying more attention to this autophagy process.”

Ohsumi’s discoveries shed new light on some of the most important processes our cells use to stay healthy. By understanding how autophagy works, scientists hope to better understand the role it plays in aging and disease. Yet despite his accomplishments, Ohsumi remains humble, calling himself “just a basic researcher in yeast,” in an interview with the Canadian newspaper TThe Globe and Mail last year after he received the Canada Gairdner International Award. Perhaps—but some yeast researchers clearly rise to the top more than others.

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Henry Sapiecha

British researchers get the go ahead to genetically modify human embryos

Monday, July 11th, 2016

IS THIS THE START OF WORLD BABY FACTORIES MANUFACTURING BABIES TO ORDER??

Scientists investigating miscarriage will not be able to implant embryos or study them for more than two weeks, says HFEA

Dr Kathy Niakan wants to look at the first few days of fertilisation-image www.newcures.info

Dr Kathy Niakan wants to look at the first few days of fertilisation.

Photograph: Francis Crick Institute

Britain’s first genetically modified human embryos could be created within months, after scientists were granted permission by the fertility regulator to carry out the procedure.

The Human Fertilisation and Embryology Authority (HFEA) regulator approved a licence application by Kathy Niakan, a stem cell scientist at the Francis Crick Institute in London, to perform so-called genome editing – also called gene editing – on human embryos.

The decision permits Niakan to study the embryos for 14 days for research purposes only. It does not permit them to be implanted into women. Niakan’s research is aimed at finding the genes at play in the early days of human fertilisation.

The decision was greeted positively by the Francis Crick Institute and British scientists but was met with anger and dismay by those concerned that rapid advances in the field of genome editing is precluding proper consideration of the ethical implications.

Paul Nurse, director of the institute, said: “I am delighted that the HFEA has approved Dr Niakan’s application. Dr Niakan’s proposed research is important for understanding how a healthy human embryo develops and will enhance our understanding of IVF success rates, by looking at the very earliest stage of human development – one to seven days.”

The work, using embryos donated by couples with a surplus after IVF treatment, will look at the fertilised egg’s development from a single cell to about 250 cells. The basic research could help scientists understand why some women lose their babies before term and provide better clinical treatments for infertility, using conventional medical methods.

Niakan will use a powerful genome editing procedure called Crispr-Cas9 to switch genes on and off in early stage human embryos. She will then look for the effects the modifications have on the development of the cells that go on to form the placenta.

Crispr-Cas9 has revolutionised biomedical research since its invention three years ago. It allows scientists to make precise changes to DNA, and has the potential to transform the treatment of genetic disorders by correcting faulty genes.

Prof Robin Lovell-Badge, group leader at the Francis Crick Institute, said: “

The approval of her [Niakan’s] licence gives the exciting prospect that we will at last begin to understand how the different cell types are specified at these pre-implantation stages in the human embryo.”

Lovell-Badge said it would also provide invaluable information about the accuracy and efficiency of the technique, helping to inform the debate about whether genome editing could be used in future to correct faulty genes that cause devastating diseases.

That prospect remains a long way off but is already a subject of concern.

Dr David King, director of Human Genetics Alert, said: “This is the first step in a well mapped-out process leading to GM babies, and a future of consumer eugenics.” He claimed the government’s scientific advisers had already decided they were comfortable with the prospect of so-called “designer babies”.

Anne Scanlan, from the anti-abortion organisation Life, said: “The HFEA now has the reputation of being the first regulator in the world to approve this uncertain and dangerous technology. It has ignored the warnings of over 100 scientists worldwide and given permission for a procedure that could have damaging far-reaching implications for human beings.”

There are fears that changes to an embryo’s DNA could have unknown harmful consequences throughout a person’s body and be passed on down the generations.

Last year, leading UK funders called for a national debate on whether editing human embryos could ever be justified in the clinic. Some fear that a public backlash could derail less controversial uses of genome editing, which could lead to radical new treatments for conditions such as muscular dystrophy and sickle cell disease.

The US National Institutes of Health will not fund any genome editing research on human embryos at present.

But supporters of the HFEA’s decision said it had arrived at the right conclusion, balancing the benefits to research and ethical considerations.

“The ruling by the HFEA is a triumph for common sense,” said Darren Griffin, a professor of genetics at the University of Kent.While it is certain that the prospect of gene editing in human embryos raised a series of ethical issues and challenges, the problem has been dealt with in a balanced manner. It is clear that the potential benefits of the work proposed far outweigh the foreseen risks.”

Sarah Norcross, director of Progress Educational Trust, called it a victory for level-headed regulation over moral panic”.

Dr Sarah Chan, chancellor’s fellow at Usher Institute for Population Health Sciences and Informatics, University of Edinburgh, said: “We should feel confident that our regulatory system in this area is functioning well to keep science aligned with social interests.”

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Henry Sapiecha

DOCTORS CURE & TREATMENT KILLED HIS PATIENT COURT FINDS & AWARDS COMPENSATION

Wednesday, June 22nd, 2016

Newcastle Private Hospital.image www.newcures.info

Newcastle Private Hospital.NSW.Australia. Photo: Fiona Morris

Colleen Stefanyszyn, of the Newcastle suburb Merewether, vomited faecal material for several days before her death following surgery at Newcastle Private Hospital in December, 2008.

It was “the worst red flag that a surgeon would see”, a medical expert said during a NSW Supreme Court hearing that resulted in negligence findings against her gynaecologist and the hospital, and the possibility of contempt action against the hospital relating to the Supreme Court proceedings.

Mrs Stefanyszyn’s death was preventable, NSW Supreme Court Justice Monika Schmidt found in a decision on Tuesday that was highly critical of the hospital and its breaches of duty of care that contributed to Mrs Stefanyszyn’s death.

Justice Schmidt accepted Newcastle gynaecologist and obstetrician Dr Oliver Brown’s admission that he breached his duty of care to Mrs Stefanyszyn and that it had resulted in her death.

Mrs Stefanyszyn’s death “could have been prevented, had available surgical steps been taken”, Justice Schmidt said.

Mrs Stefanyszyn, 61, had vaginal hysterectomy elective surgery at the hospital on December 1, 2008.

During the operation a loop of suture material “inadvertently looped around Mrs Stefanyszyn’s bowel”, resulting in a blockage, Justice Schmidt said.

She lived for just four days after the surgery, vomiting faecal matter from the third day, starting with a “coffee-coloured fluid” on the night of December 3.

While Dr Brown’s response to Mrs Stefanyszyn’s symptoms until the third day was reasonable, it was the medical experts’ common ground that his approach to her subsequent care “was not only wrong, but inexplicable, given her deteriorating condition” that included continued faecal vomiting, Justice Schmidt found.

“Despite Mrs Stefanyszyn not recovering from the surgery as was expected and her deteriorating condition, the cause of her symptoms was not investigated, the blockage was not identified and surgical steps necessary to remove it were not taken, with her death the result,” Justice Schmidt found.

“The result was that the blockage was not identified or addressed; infection set in; she repeatedly vomited faecal material; she inhaled some of that material with resulting pneumonia; her electrolytic balance became disordered; her oxygen levels deteriorated; and finally, she suffered a fatal cardiac arrest.”

Justice Schmidt was highly critical of the hospital, its breaches of duty to Mrs Stefanyszyn which were “more extensive than it finally admitted”, the failure of its staff to record observations of Mrs Stefanyszyn on the three days before her death, and the hospital’s decision not to call evidence to address issues of its breaches.

Dr Brown’s “failure to give evidence in support of his own case and the hospital’s failure to call evidence in its, is that such evidence would not have assisted their respective cases”, Justice Schmidt found.

The hospital’s failures “did not give rise to a mere possibility of injury, but actually materially contributed to the death which resulted from both its failures and those of Dr Brown”, Justice Schmidt found.

The matter returns to court on Friday where Justice Schmidt will consider whether the hospital should face contempt proceedings over aspects of the court case.

Justice Schmidt noted the hospital, Mrs Stefanyszyn’s husband Walter and daughters Leigh and Megan had settled a compensation case.

In a notice in the Newcastle Herald on the second anniversary of his wife’s death Mr Stefanyszyn wrote: “I have lost my soul’s companion, a life linked with my own. Day by day I miss you more, as I walk through life alone. Forever Wal.”

Her daughters wrote: “What is home without a mother? All things this world may send, but when we lost our darling mother, we lost our dearest friend. Love Leigh and Megan.”

Newcastle Herald

www.ozrural.com.au

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Henry Sapiecha

‘It Eats Cancer Cells’:Melanoma Treatment Explained for footballer Jarryd Roughead

Wednesday, June 1st, 2016

footballer Jarryd Roughead's Melanoma Treatment image www.newcures.info

Immunotherapy. Nope, we’d never heard of it either.

Radiotherapy and chemotherapy are two well known forms of cancer treatment. But immunotherapy? What exactly is that?

The Huffington Post Australia contacted Cancer Council Australia to learn more about the revolutionary treatment which Hawthorn star Jarryd Roughead is set to undergo to tackle his melanoma.

We spoke to Cancer Council CEO, Professor Sanchia Aranda, who explained that it’s a relatively new treatment which has been worked on for decades by both Australian and international experts. But only recently has it come into common usage.

“Generally immunotherapy is the use of medicines in a way that stimulates your own immune system to recognise and destroy cancer cells,” Aranda explained.

“Your immune system is killing off cells all the time that have the potential to become cancer. The immunotherapy drugs [of which there are two classes — and we don’t know which Roughead is taking] basically boost the immune response.

“They cause immune cells or T-cells — which are a particular a particular type of white blood cells — to attack the melanoma cells. They recognise a particular protein expressed by the cancer cell, and they attach to that and then basically gobble the cancer cells up.”

Aranda said there were some side effects, which could include fatigue, itching, skin rash pain in joints and sometimes diarrhoea.

“But not hair falling out and not quite so much vomiting and those kind of things,” she said.

Fan favourite Jarryd Roughead celebrates after winning the 2015 Grand Final. image www.newcures.info

Fan favourite: Jarryd Roughead celebrates after winning the 2015 Grand Final.

Like any cancer treatment, there is no 100 percent certainty of success. But immunotherapy has been proven to work in many cases.

The treatment was in its infancy just seven years ago when AFL legend Jim Stynes was diagnosed with melanoma which metastasised to his brain. Aranda is well familiar with his case, and said he lived for three years thanks to immunotherapy, where most patients with his diagnosis would expect to live less than a year.

Seven years down the track, the fledgling field of immunotherapy has hugely advanced.

“In melanoma some of these drugs lead to complete remission,” Aranda said. “It’s important to understand that the state of of play regarding treating melanoma is changing on a daily basis. There’s been a sudden and dramatic shift.”

Aranda said further good news for Roughhead is that he is in the “very best place”, the Peter MacCallum Cancer Centre in Melbourne, which is known to most people as just “Peter Mac”. Aranda described Peter Mac lead researcher Professor Grant McArthur as a “world leader” in the field.

Sanchia-Aranda & Jarryd's in a very good place image www.newcures.info

Sanchia Aranda & Jarryd’s in a very good place.

Roughead would also have a fantastic nurse on his side, in Dr Donna Milne. Milne has a PhD in the field of cancer care, which is why she’s a nurse with a doctor in her title.

“She’s really smart,” Aranda said. “And she’s a Hawthorn supporter too.”

creams

Henry Sapiecha

Families hope ‘Frankenstein science’ activists will not stop gene cure for mitochondrial disease

Saturday, May 28th, 2016

Deniz-Safak-died 23 yrs image www.newcures.info

Deniz Safak’s condition continued to worsen until he died last year at the age of 23.

Deniz Safak was five years old when he first displayed symptoms of the disease that would later take his life. “He started being sick and had intense, stroke-like seizures,” his mother, Ruth, recalled.

Doctors were baffled by the boy’s condition and it took months before a diagnosis was made. Ruth and her husband, Erdhal, were told that Deniz was suffering from mitochondrial disease, an incurable condition that is passed from mother to child and can often be fatal.

Deniz’s condition continued to worsen. By the time he died last year at the age of 23, he had become deaf, suffered intense migraines and was confined to a wheelchair. “That is how he spent his life at the end,” said Ruth, who lives in Sunderland. “He was very bright and he knew what he was missing from life.” There is no cure for mitochondrial disease and, although its symptoms vary in their severity, the condition is often fatal. Health officials estimate that there are several thousand people in Britain affected by the condition, which is caused by mutations in the DNA in the mitochondria, which exist inside the cells of their bodies.

“Mitochondria are the little power packs that provide our cells with energy and they have their own DNA,” said Professor Douglas Turnbull, director of the Wellcome Trust Centre for Mitochondrial Research at Newcastle University. “The disease particularly affects cells that use a lot of energy, including those involved in hearing, pumping blood and firing nerves. About a third to a half of those who have the condition face an early death.”

It is a grim scenario. However, hopes of tackling mitochondrial disease will be raised in a few weeks when the government announces regulations that will permit the use of an IVF technique that should rid affected families of the disorder. If these plans are approved by parliament, Britain will become the first nation to permit germ-line gene therapy, which will change the DNA of future generations in order to eradicate the condition.

The technique involves taking an egg with healthy mitochondria from a donor female. Its main set of nuclear genes is then scooped out and replaced with those of a woman affected by mitochondrial disease but whose basic nuclear DNA is healthy. The egg is then fertilised using her partner’s sperm. In this way an embryo is created that has the central genes of the two parents but no longer carries the mutated mitochondrial DNA once carried by the mother. The technique is known as mitochondrial replacement. It has never been tried on humans, but has worked in animal studies.

Most scientists and doctors, particularly those who work with families touched by mitochondrial disease, support the introduction of the technique. However, some groups vociferously oppose its use. “The social benefits for a relatively small number of women … do not come near to justifying the potential health risks from these techniques to the child and the risks to global society that stem from human genetic engineering,” said the campaign group Human Genetics Alert.

Anti-abortion groups also oppose mitochondrial replacement, while some tabloid newspapers have described the creation of embryos using the nuclear DNA of two parents and the mitochondrial DNA of a third-party donor as “three-parent babies” and have claimed that this represents a slippery slope to a “Frankenstein future”.

This last claim particularly infuriates researchers. “It is wrong to say this produces three-parent babies,” said Turnbull. “More than 99.9% of DNA is nuclear DNA and that will not be affected. Mitochondrial DNA accounts for around 0.1% of our total DNA. We are changing only mitochondrial DNA. We are not changing a person’s hair or height or eye colour.”

The potential of mitochondrial replacement is demonstrated through another of Turnbull’s patients: Marie Austen, also from Sunderland. Her son, Adam, was seven when he was diagnosed with mitochondrial DNA disease. His heart was subsequently found to have been damaged but, before he could have a transplant, Adam’s condition worsened and he died last year at the age of 13. “I wanted to see Adam grow up, but that has been taken from me,” said Marie.

Austen has another child, a daughter, who at present has no symptoms. However, the disease varies in the severity of its symptoms as it passes from generation to generation. This poses problems for Marie’s daughter. “One day she may want to have her own kids, but she will not be able to have them safe in the knowledge that this disease will not kill them when they are young. That is why I want this new technique to be given the go-ahead, so my daughter will have healthy mitochondria and can have children who will not die when they are teenagers, as her brother Adam did.”

The disease is passed through the maternal line because men do not pass on mitochondrial DNA to future generations. Only women do that. However, the mutated versions do so with unpredictable consequences. Both Ruth and Marie have severe hearing problems, for example. However, the version picked up by their sons was far worse in its effects.

Last year the Human Fertilisation and Embryology Authority (HFEA) completed an extensive public consultation on mitochondrial replacement and found widespread support for it. Now the proposed regulations that will allow it to be carried out, under licence from the HFEA, are to published. Interested parties will give their views on these regulations before they are debated by parliament, probably on a free vote, later this year.

Alison Murdoch, professor of reproductive medicine at Newcastle University,hopes that parliament will approve the new regulations – though she is only cautiously hopeful. “This is controversial in some people’s eyes and there will be attempts to block the regulations. My fear is that the government could still get cold feet and delay the vote, which would not be good news given we will have a general election next year.

“The trouble is that the people who oppose this work are much better organised and proactive than the people that actually need the treatment,” Murdoch said. “They claim that around 30% of the population is against this kind of medical intervention. But when you actually sit down with a group of people and explain what you want to do, they all say the same thing: why not?”

Ruth Safak will also be watching the forthcoming battle over the implementation of mitochondrial replacement therapy. She is passionately in favour of the procedure. “When you lose a child, there is not enough time to get over it. This thing wipes out your life. The point is that if this treatment had become available for me when I was beginning my family, I could have had Deniz and he would still be with me now.”

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Henry Sapiecha