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A Pill That Mimics the Immune System

A Pill That Mimics the Immune System | Amazing Science | Scoop.it
Synthetic antibodies with the potential to be orally ingested to fight cancer and autoimmune diseases may replace cumbersome intravenous therapeutics


For years now doctors have used antibodies and other protein-based therapies (aka biologics) to treat a range of illnesses, cancers, infections and autoimmune diseases among them.

But antibodies have their drawbacks: for one they're bulky and hence usually have to be administered intravenously as they’re often too big to be absorbed in the gastrointestinal tract. With this in mind, chemist David Spiegel and his colleagues at Yale University are out to develop compounds with the benefits of antibodies—hopefully minus the needle.


In work recently published in the Journal of the American Chemical Society Spiegel and his team have successfully developed the first synthetic molecules that behave like antibodies. Like the real thing, these so-called "synthetic antibody mimics"—or "SyAMs"—bind to both diseased cells and disease-fighting immune cells. Specifically the compounds were found to zero in on and bind to a specific antigen on prostate cancer cells. The SyAMs also bind to and activate certain immune cells that then devour the malignancy.


Spiegel’s SyAMs are produced in a way that is similar to conventional drugs, by using chemical reactions to piece together various structural features often not found in nature. As he explains, the therapeutic potential of synthetic antibodylike compounds is vast: “Because antibodies are proteins they’re difficult and expensive to produce on a large scale, can cause unwanted immune reactions and tend to aggregate and denature with long-term storage.” Spiegel speculates that SyAMs will be easier and cheaper to produce and less likely to incite aberrant immune activity. SyAMs are also one twentieth the size of antibodies—more akin to the size of most medications—and can therefore perhaps be administered orally. This could be a major boon to patients with cancers and autoimmune diseases like multiple sclerosis who have to regularly get themselves to infusion centers for monoclonal antibody therapy.


Artificial antibody research split subsequently in two directions: one camp pursued creating protein antibodies resulting in what are called monoclonal antibodies. Monoclonals are produced by natural means in a lab and are now commonly used therapeutically. The other camp, in which Spiegel falls, set out to produce smaller, nonprotein compounds with antibodylike properties.


Beyond attacking prostate cancer, Spiegel’s group has also developed SyAM-based approaches targeting HIV, various other cancers and bacterial triggers of autoimmune disease. And although SyAM research remains in the petri dish, a mouse model is in the works and human studies are not far off. A number of other labs are also researching ways to fight disease by manipulating antibodies and synthesizing molecules that act on the immune system, including Peter Schultz at the Scripps Research Institute in La Jolla, Calif. “He's probably our biggest competitor and I'm his biggest fan,” Spiegel says.


Laura Kiessling at the University of Wisconsin–Madison, who studies ways to draw natural antibodies to tumor cells, comments on the benefits of Spiegel’s approach: “It can be tailored to selectively recruit specific types of immune cells to kill tumor cells. The smaller size of the compounds could also be an asset in eliminating tumors, but the benefits would need to be looked at in vivo,” Kiessling says.

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ViaCyte Starts Stem-Cell Clinical Trial of Bioartificial Pancreas

ViaCyte Starts Stem-Cell Clinical Trial of Bioartificial Pancreas | Amazing Science | Scoop.it

Fourteen years ago, during the darkest moments of the “stem-cell wars” pitting American scientists against the White House of George W. Bush, one group of advocates could be counted on to urge research using cells from human embryos: parents of children with type 1 diabetes. Motivated by scientists who told them these cells would lead to amazing cures, they spent millions on TV ads, lobbying, and countless phone calls to Congress.


Now the first test of a type 1 diabetes treatment using stem cells has finally begun. In October, a San Diego man had two pouches of lab-grown pancreas cells, derived from human embryonic stem cells, inserted into his body through incisions in his back. Two other patients have since received the stand-in pancreas, engineered by a small San Diego company called ViaCyte.


It’s a significant step, partly because the ViaCyte study is only the third in the United States of any treatment based on embryonic stem cells. These cells, once removed from early-stage human embryos, can be grown in a lab dish and retain the ability to differentiate into any of the cells and tissue types in the body. One other study, since cancelled, treated several patients with spinal-cord injury (see “Geron Shuts Down Pioneering Stem-Cell Program” and “Stem-Cell Gamble”), while tests to transplant lab-grown retina cells into the eyes of people going blind are ongoing (see “Stem Cells Seem Safe in Treating Eye Disease”).


Douglas Melton, a biologist at Harvard University who has two children with type 1 diabetes, worries that the ViaCyte system may not work. He thinks deposits of fibrotic, scarlike tissue will glom onto the capsules, starving the cells inside of oxygen and blocking their ability to sense sugar and release insulin. Melton also thinks it might take immature cells up to three months to become fully functional. And many won’t become beta cells, winding up as other types of pancreatic cells instead.


Melton says the “inefficiency” of the system means the company “would need a device about the size of a DVD player” to have enough beta cells to effectively treat diabetes. ViaCyte says it thinks 300 million of its cells, or about eight of its capsules, would be enough. (Each capsule holds a volume of cells smaller than one M&M candy.)    Last October, Melton’s group announced it had managed to grow fully mature, functional beta cells in the lab, a scientific first that took more than 10 years of trial-and-error research. Melton thinks implanting mature cells would allow a bioartificial pancreas to start working right away.


To encapsulate his cells, Melton has been working with bioengineer Daniel Anderson at MIT to develop their own capsule. Anderson doesn’t want to say exactly how it works, but a recent patent filing from his lab describes a container made of layers of hydrogels, some containing cells and others anti-inflammatory drugs to prevent the capsule from getting covered with fibrotic tissue. Both Melton and Anderson are cagey about discussing their results. “We do have some successes we are very excited about,” Anderson says. “The bottom line is we have reason to believe it is possible to use Doug’s cells in our devices and cure diabetes in animals.”


After the stem-cell wars, and then a decade of trying to turn the technology’s promises into reality, Henry says he feels convinced that “cells in bags” of some kind are going to be the answer to type 1 diabetes. He’s aware that curing rodents doesn’t guarantee the technology will help people, but he says the clinical trial he’s running is another in a series of “small steps” toward much-improved lives for millions of people. “I am just so positive that this is the future,” he says. 

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Smoking thins vital part of brain, study finds

Smoking thins vital part of brain, study finds | Amazing Science | Scoop.it
Years ago, children were warned that smoking could stunt their growth, but now a major study by an international team including the Montreal Neurological Institute at McGill University and the University of Edinburgh shows new evidence that long-term smoking could cause thinning of the brain’s cortex. The cortex is the outer layer of the brain in which critical cognitive functions such as memory, language and perception take place. Interestingly, the findings also suggest that stopping smoking helps to restore at least part of the cortex’s thickness.

The study involved 244 male and 260 female subjects-five times larger than any previous similar research on smoking and cortical thickness. Their average age was 73. The test group included current smokers, ex-smokers and non-smokers. All of the subjects were examined as children in 1947 as part of the Scottish Mental Survey. Researchers used health data gathered during recent personal interviews with the subjects, and also analyzed data from MRI scans showing the current state of the subjects’ brain cortices.

“We found that current and ex-smokers had, at age 73, many areas of thinner brain cortex than those that never smoked. Subjects who stopped smoking seem to partially recover their cortical thickness for each year without smoking,” says the study’s lead author Dr. Sherif Karama, assistant professor of psychiatry at McGill University, psychiatrist at the Douglas Mental Health University Institute and an affiliate of the Montreal Neurological Institute. The apparent recovery process is slow, however, and incomplete. Heavy ex-smokers in the study who had given up smoking for more than 25 years still had a thinner cortex.

Although the cortex grows thinner with normal aging, the study found that smoking appears to accelerate the thinning process. A thinner brain cortex is associated with adult cognitive decline.

“Smokers should be informed that cigarettes could hasten the thinning of the brain’s cortex, which could lead to cognitive deterioration. Cortical thinning seems to persist for many years after someone stops smoking,” says Dr. Karama.
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Researchers discover novel insulin-decreasing hormone in flies and now humans

Researchers discover novel insulin-decreasing hormone in flies and now humans | Amazing Science | Scoop.it

An insulin-regulating hormone that, until now, only had been postulated to exist has been identified by researchers at the Stanford University School of MedicineThe hormone, called limostatin after the Greek goddess of starvation, Limos, tamps down circulating insulin levels during recovery from fasting or starvation. In this way, it ensures that precious nutrients remain in the blood long enough to rebuild starving tissues, rather than being rapidly squirreled away into less-accessible fat cells.


The researchers first discovered limostatin in fruit flies but then quickly identified a protein with a similar function in humans. “Starvation or famine is an ancient, ever-present specter faced by all living organisms,” said Seung Kim, MD, PhD, professor of developmental biology. “The ways to deal with it metabolically are likely to be ancient and conserved. This research clearly connects the dots between flies and humans, and identifies a new potential way to regulate insulin output in humans.”


In particular, members of a family with an inherited mutation in the human analog of limostatin exhibited many of the same physiological characteristics as flies genetically engineered to be unable to produce limostatin — namely, high levels of circulating insulin, low blood sugar levels and a tendency toward early onset obesity.


A paper describing the research findings was published Feb. 3 in Cell Metabolism. Kim is the senior author, and graduate student Ronald Alfa is the lead author. “This work has critical ramifications for our understanding of metabolism, and has the potential to transform our approach to treating diseases like diabetes,” said Domenico Accili, MD, director of theColumbia University Diabetes and Endocrinology Research Center and Columbia’s Russell Barry Foundation Professor of Diabetes.


“The discovery of limostatin, a new hormone that can act to decrease insulin release, is an important advance,” added Accili, who was not involved with the research. “The notion that mammals express a related family of intestinal hormones that can affect insulin secretion may inform new efforts to find drugs that combat diabetes in humans.”


Limostatin was identified by virtue of its response to fasting. Kim and his colleagues withheld food from their laboratory fruit flies for 24-28 hours and looked to see which genes were highly expressed during this time. They narrowed the list to those genes that encoded proteins resembling hormones, which are special signaling molecules that circulate throughout the body to affect the function of distant cells. They observed that one of these, limostatin, caused characteristics of insulin deficiency when overexpressed in flies.


Kim and his colleagues then genetically engineered a strain of flies unable to express limostatin. They found that these flies had too much circulating insulin. As a result, the animals had abnormally low levels of circulating sugars and more than the usual number of fat cells as they packed on the micro-pounds. Their life span was also shortened.


The researchers found that, in flies, limostatin is produced by nutrient-sensing cells in the gut. It then circulates through the animal to reach the cells responsible for producing insulin. In flies, these are in the brain; in humans, insulin is produced by beta cells in the pancreas. Limostatin binds to the cells via a receptor protein on their surfaces, reducing the amount of insulin they secrete. Blocking the expression of this receptor in flies, the researchers found, affected the insects in the same way as if they couldn’t express limostatin.


Limostatin belongs to a class of hormones called decretins, which have been suspected to exist for about 150 years, starting with work by the renowned French physiologist Claude Bernard. In 1932, researchers identified a class of hormones called incretins, which were expressed in the gut after a meal and stimulated insulin secretion. Other metabolic studies, including those on animals and people undergoing starvation conditions, suggested that another class of hormone might function to suppress insulin production during times of famine. A phenomenon was termed “starvation diabetes” to describe how rapid re-feeding with glucose or carbohydrate-rich foods after a fast can cause diabetes-like symptoms of abnormally high blood sugars and low insulin production.


The discovery of limostatin, a decretin, further validates the use of fruit flies as a diabetes model, according to Kim. It may also explain a puzzling phenomenon that often occurs after bariatric surgery. The procedure, which removes a portion of the stomach to enable weight loss in obese people, often rapidly reverses ongoing or incipient signs of diabetes long before any pounds are shed.

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Measles Outbreak Traced to Fully Vaccinated Patient for First Time

Measles Outbreak Traced to Fully Vaccinated Patient for First Time | Amazing Science | Scoop.it

Get the measles vaccine, and you won’t get the measles—or give it to anyone else. Right? Well, not always. A person fully vaccinated against measles has contracted the disease and passed it on to others. The startling case study contradicts received wisdom about the vaccine and suggests that a recent swell of measles outbreaks in developed nations could mean more illnesses even among the vaccinated.


When it comes to the measles vaccine, two shots are better than one. Most people in the United States are initially vaccinated against the virus shortly after their first birthday and return for a booster shot as a toddler. Less than 1% of people who get both shots will contract the potentially lethal skin and respiratory infection. And even if a fully vaccinated person does become infected—a rare situation known as “vaccine failure”—they weren’t thought to be contagious.


That’s why a fully vaccinated 22-year-old theater employee in New York City who developed the measles in 2011 was released without hospitalization or quarantine. But like Typhoid Mary, this patient turned out to be unwittingly contagious. Ultimately, she transmitted the measles to four other people, according to a recent report in Clinical Infectious Diseases that tracked symptoms in the 88 people with whom “Measles Mary” interacted while she was sick. Surprisingly, two of the secondary patients had been fully vaccinated. And although the other two had no record of receiving the vaccine, they both showed signs of previous measles exposure that should have conferred immunity.


A closer look at the blood samples taken during her treatment revealed how the immune defenses of Measles Mary broke down. As a first line of defense against the measles and other microbes, humans rely on a natural buttress of IgM antibodies. Like a wooden shield, they offer some protection from microbial assaults but aren’t impenetrable. The vaccine (or a case of the measles) prompts the body to supplement this primary buffer with a stronger armor of IgG antibodies, some of which are able to neutralize the measles virus so it can’t invade cells or spread to other patients. This secondary immune response was presumed to last for decades.


By analyzing her blood, the researchers found that Measles Mary mounted an IgM defense, as if she had never been vaccinated. Her blood also contained a potent arsenal of IgG antibodies, but a closer look revealed that none of these IgG antibodies were actually capable of neutralizing the measles virus. It seemed that her vaccine-given immunity had waned.


Although public health officials have assumed that measles immunity lasts forever, the case of Measles Mary highlights the reality that “the actual duration [of immunity] following infection or vaccination is unclear,” says Jennifer Rosen, who led the investigation as director of epidemiology and surveillance at the New York City Bureau of Immunization. The possibility of waning immunity is particularly worrisome as the virus surfaces in major U.S. hubs like Boston,Seattle, New York, and the Los Angeles area.

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Protein-based Therapy Shows Promise against Resistant Leukemia

Protein-based Therapy Shows Promise against Resistant Leukemia | Amazing Science | Scoop.it

Occurring at an annual rate of 35 to 40 cases per million people in the U.S., ALL represents approximately 25 percent of cancer diagnoses among children under the age of 15. Historically, ALL had a high mortality rate; nearly 80 percent of children who developed the disease did not survive long term. Today, those numbers have been reversed, with almost 80 percent of children affected by ALL achieving long- term survival. 

“That’s great news, unless your child is one of the 20 percent,” said the study’s principal investigator Fatih M. Uckun, MD, PhD, of the Children’s Center for Cancer and Blood Diseases at CHLA and the Norris Comprehensive Cancer Center of the University of Southern California (USC). “Despite advances in available therapies, unmet and urgent needs remain in the fight against leukemia.  We still have children with disease that our drugs can’t help enough. And for patients who relapse, their chances of long-term survival are less than 20 percent. We’ve got to do better.”


TNF-related apoptosis-inducing ligand (TRAIL) is a protein functioning as a ligand that induces apoptosis, or cell death. Produced by the immune system cells, it has the potential to cause apoptosis in tumor cells by binding to two so-called “death receptors”, also known as TRAIL-receptor 1 and TRAIL-receptor 2.

 “TRAIL is a naturally occurring part of the body’s immune system that kills cancer cells without toxicity to normal cells.  However, earlier clinical trials using TRAIL as a potential anti-cancer medicine candidate have not been successful, largely because of its propensity to bind, not only to cancer cells, but also to ‘decoy’ receptors,” explained Uckun, who is also a professor of pediatrics at Keck School of Medicine of USC. 

Uckun and collaborators discovered a previously unknown protein – CD19-Ligand – a natural ligand of human CD19, which is expressed by almost all ALL cells.  They hypothesized that fusing it by genetic bioengineering to the portion of TRAIL (known as sTRAIL) that can kill cancer cells, would produce a powerful weapon against leukemia cells.  Unlike chemotherapy drugs, this precision medicine candidate would seek out, bind and destroy only leukemia cells carrying CD19 as the target docking site.


They successfully accomplished this unique assembly of the two proteins in a single “fusion protein” and named this protein therapeutic candidate “CD19L-sTRAIL.”  In their study, Uckun and collaborators have demonstrated that their engineering converted sTRAIL into a much more potent “membrane-anchored” form that is capable of triggering apoptosis, even in the most aggressive and therapy-resistant form of human leukemia cells.

 “Due to its ability to anchor to the surface of cancer cells via CD19, CD19L-sTRAIL was 100,000-fold more potent than sTRAIL, and consistently killed more than  99 percent of aggressive leukemia cells taken directly from children with ALL –  not only in the test tube, but also in mice,” said Uckun. Administering only two or three doses of CD19L-sTRAIL significantly improved the survival outcome of mice challenged with an otherwise invariably fatal dose of human leukemia cells, without side effects.  Its therapeutic potency in mice was superior to that of standard chemotherapy combinations as well as radiation therapy.

“The biggest challenge is to cure patients who experience a recurrence of their cancer, despite intensive chemotherapy,” Uckun concluded. “We are hopeful that the knowledge gained from this study will open a new range of effective treatment opportunities for children with recurrent leukemia.”

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Ebola Cases Are Falling In West Africa

Ebola Cases Are Falling In West Africa | Amazing Science | Scoop.it

The number of people falling victim to the Ebola virus in West Africa has dropped to the lowest level in months, the World Health Organization said on Friday, but dwindling funds and a looming rainy season threaten to hamper efforts to control the disease. More than 8,668 people have died in the Ebola epidemic in West Africa, which first surfaced in Guinea more than a year ago. But the three worst-affected countries — GuineaLiberia and Sierra Leone — have now recorded falling numbers of new cases for four successive weeks, Dr. Bruce Aylward, the health organization’s assistant director general, told reporters in Geneva.


Liberia, which was struggling with more than 300 new cases a week in August and September, recorded only eight new cases in the week to Jan. 18, the organization reported. In Sierra Leone, where the infection rate is now highest, there were 118 new cases reported in that week, compared with 184 in the previous week and 248 in the week before that.


Speaking just after a visit to the region, Dr. Aylward said on Friday that the “really substantial reduction” in new cases was a direct result of last fall’s vast buildup of resources for fighting the epidemic. “This is the first time that the countries were in a position to stop Ebola,” he said.


President Ernest Bai Koroma of Sierra Leone announced on Friday that the country was lifting the travel restrictions that it had imposed in an effort to contain the virus. “Victory is in sight,” Mr. Koroma said.


Dr. Aylward cautioned that “the things that have been driving the reduction so far will not get us to zero,” and that health authorities do not yet have the spread of the disease completely under control.


The good news about falling infection rates also bore a danger, Dr. Aylward said: Pledges of international financial support for the Ebola response were falling, as well. He said that $1.5 billion was needed to fight the disease for the next six months, but that only $482 million had been committed so far. Most of those pledges were made last year.

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8B Sarah's curator insight, February 5, 2015 2:38 AM

West Africa (mostly Liberia, Sierra Leone and Guinea) has been fighting an Ebola Epidemic for a long time, and the number of deaths has finally gone down. This epidemic has been around for more than an year now. A lot of people died, and it's good that it is now getting better. 

  I am so glad the Ebola epidemic in West Africa is settling down! When I first heard there was a deadly epidemic going around during summer of 2014, I swear, I was about to have a heart attack. I told all my best friends and family that there was an epidemic was going on, and that all of us are going to die. I cried, and I begged my parents to cancel the flight to Japan because I was afraid I'd catch Ebola at the airport. Now as I think about it, it was an overreaction, but I thought the world was ending, so I was really scared. Not too long after that, I did some research and reassured myself we'll be alright for about 6 months.  

  I feel really bad for all the people that died of Ebola, and their family and friends. 1 person's death is bad enough, but like 8000? In this day and age? That's horrible. I also thought it was horrible that people cared about Ebola since it started, but nobody was really worried about it until Western people started dying. From all the news reports I've read, I felt that that's when people actually tried to do something about it. That's just racist, pathetic and awful. I'm not sure though, this is just an educated guess of what happened when I put together all the information about Ebola I've read in the past.

8A Green's curator insight, February 5, 2015 10:21 AM

       Article #1

      In West Africa, the number of people who have been infected by Ebola has dropped to the lowest level in months. The Ebola virus was surfaced in Guinea more than a year ago ,and later spread to other countries in West Africa, such as Liberia and Sierra Leone. The number of new cases of Ebola in Liberia has dropped to now only 8 new cases per week and in Sierra Leone, 118 new cases. These numbers of new cases are very low compared to the number of cases in August and September last year. The President of Sierra Leone announced that the country is lifting the travel restrictions that it had imposed in an effort to contain the virus. He said that they are running out of cash five to six months before the virus will stop because $1.5 billion was needed to fight the disease, but only $482 million had been committed so far.

      This article helps me understand the lives in Africa. It helps me know what’s going on in Africa and the diseases there. I read in the textbook that many people in Africa died because of diseases and Ebola killed many lives of Africans. I think this article is a very great news to know that less people are infected with Ebola and they are successful in fighting the disease. However, I think it is sad that they are running out of cash to make it stop. I hope the number of new cases continue to drop, and the international countries help funding for the cure.


8B Amy's curator insight, February 5, 2015 11:16 AM

#1

The article is about the decreasing of the number of people in West Africa that have to deal with the Ebola virus. The World Health Organization said that the funds and a looming rainy season threaten to hamper efforts to control the disease. More than 8,668 people have died in the Ebola epidemic in West Africa. The three worst countries that got affected are Guinea, Liberia, and Sierra Leone.


This article helps me understand more about Africa. It shows the situation they have to be in and that there are people trying to help them. Africa is a big continent and many people have to live in very bad conditions which might cause Ebola to spread easier. This virus ha been going on in the news for a long time and I am glad to hear that it is getting better.


Ebola has affected many lives but I think it is great news for people who live in West Africa. Many people suffer and sometimes die from Ebola, but I do feel better knowing that the number of people that has this disease is reducing. I hope that it will keep on decreasing like this.


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British say yes to three-person babies

British say yes to three-person babies | Amazing Science | Scoop.it

In an historic move, MPs have voted in favor of the creation of babies with DNA from two women and one man. The UK is now set to become the first country to introduce laws to allow the creation of babies from three people. In a free vote in the Commons, 382 MPs were in favour and 128 against the technique that stops genetic diseases being passed from mother to child. During the debate, ministers said the technique was "light at the end of a dark tunnel" for families. A further vote is required in the House of Lords. It everything goes ahead then the first such baby could be born next year.


The technique, which was developed in Newcastle, should help women like Sharon Bernardi, from Sunderland, who lost all seven of her children to mitochondrial disease.  Defective mitochondria, which are passed down only from the mother, lead to brain damage, muscle wasting, heart failure and blindness. The technique uses a modified version of IVF to combine the DNA of the two parents with the healthy mitochondria of a donor woman. It results in babies with 0.1% of their DNA from the second woman and is a permanent change that would be passed down through the generations.


Prof Doug Turnbull, the director of the Wellcome Trust centre for mitochondrial research where the technique was pioneered, urged MPs to vote in favor.

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A new type of imager for cancer diagnosis: Prototype for first traceable PET-MR phantom

A new type of imager for cancer diagnosis: Prototype for first traceable PET-MR phantom | Amazing Science | Scoop.it

As cancer diagnostic tools, a new class of imagers – which combines positron-emission tomography (PET) with magnetic resonance imaging (MR or MRI) – has shown promise in the few years since these hybrid machines have been commercially available. But to thoroughly assess PET-MR scanners' clinical performance, researchers will need to calibrate the machines in a way that is traceable to a national standard.


Aiding that effort, a collaboration of NIST scientists from PML's Radioactivity and Magnetics groups has created a prototype of the world's first traceable phantom, or calibration standard, for a dedicated PET-MR imager. PET-MR scanners may become an alternative in some cases to the commonly used PET-CT scanners, which combine PET's radioactive tracer-sensitive capabilities with the anatomical detail of x-ray computed tomography (CT). Though research is still needed to identify the best role for PET-MR, one advantage is minimizing patients' exposure to the ionizing radiation of a CT scan.


To build their prototype, the NIST team adapted a phantom that had been developed for MRI calibrations. Nicknamed "Phannie," the original MRI phantom consists of a plastic sphere about the size of a person's head filled with grids of smaller plastic spheres containing salt solutions that become magnetized in a magnetic field. The new phantom prototype includes a small, calibrated amount of fluorine-18 (F-18), a radionuclide that shows up in PET images.


In initial studies carried out using NIST's PET-CT scanner, the researchers found that the PET imaging data were accurate to within 1.5%, which is good enough for most applications, though the team hopes eventually to increase this accuracy to less than 1%.


The next iteration of the prototype should be built and tested within a year and will feature a more robust and user-friendly design, including sturdier walls and an improved filling system that will make it easier and faster to introduce the radioactive solutions. The future model may also include calibrated samples of solid, longer-lived radioactive sources for tests that can further monitor PET scanner performance.

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After smallpox and rinderpest, Guinea Worm 3rd disease-causing organism to become extinct

After smallpox and rinderpest, Guinea Worm 3rd disease-causing organism to become extinct | Amazing Science | Scoop.it

The Guinea worm is inching ever closer to extinction, but unlike just about every other endangered species, no one is going to try to save it, least of all scientists. On the contrary, the worm’s disappearance would mark the scouring of a disease from the face of the earth—a feat humanity’s only been able to celebrate twice before, with the end of smallpox in 1980 and of the cattle disease rinderpest in 2011. Polio, despite the fact that a vaccine’s been around for more than half a century, has managed to hang on by its microscopic threads.


The Guinea worm is a parasite that enters the human body when the unwitting host-to-be drinks water contaminated with tiny water fleas in which Guinea worm larvae lurk. Once ingested, the fleas die and the Guinea worm larvae enter the host’s abdominal cavity and, unbeknownst to the host, begin maturing into a worm or worms that grow up to three feet in length. After about a year a painful blister forms on the host’s skin accompanied by itching and a burning sensation. Within about 10 to 15 days, one or more worms erupt from the person’s skin in a painful and drawn-out process. The emergence can occur from different parts of the body, including the roof of the mouth, the genitals, or the eye sockets, but around 90 percent of the worms emerge from the lower legs, according to the World Health Organization (WHO).


While the disease rarely kills, it can leave the host debilitated and weakened for a short or long period of time. Thanks in large part to the work of the Carter Center, the incidence of Guinea worm disease (also known as dracunculiasis, which is Latin for “affliction with little dragons”) has plummeted in recent years, falling from an estimated 3.5 million cases worldwide in the mid-1980s to just 148 in 2013 and 126 in 2014, according to the WHO.


How has such success been achieved? It’s taken the concerted effort of all involved—the scientists who have figured out how to contain it, community organizers who have helped spread the word on preventative solutions, and the people in areas where Guinea worm disease has been a big problem who are implementing the necessary changes to keep the parasite at bay.

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End of cancer-genome project prompts to rethink: Should effort switch from sequencing to functional analysis?

End of cancer-genome project prompts to rethink: Should effort switch from sequencing to functional analysis? | Amazing Science | Scoop.it

A mammoth US effort to genetically profile 10,000 tumors has officially come to an end. Started in 2006 as a US$100-million pilot, The Cancer Genome Atlas (TCGA) is now the biggest component of the International Cancer Genome Consortium, a collaboration of scientists from 16 nations that has discovered nearly 10 million cancer-related mutations.


The question is what to do next. Some researchers want to continue the focus on sequencing; others would rather expand their work to explore how the mutations that have been identified influence the development and progression of cancer.


“TCGA should be completed and declared a victory,” says Bruce Stillman, president of Cold Spring Harbor Laboratory in New York. “There will always be new mutations found that are associated with a particular cancer. The question is: what is the cost–benefit ratio?”


Stillman was an early advocate for the project, even as some researchers feared that it would drain funds away from individual grants. Initially a three-year project, it was extended for five more years. In 2009, it received an additional $100 million from the US National Institutes of Health plus $175 million from stimulus funding that was intended to spur the US economy during the global economic recession.


On 2 December, Staudt announced that once TCGA is completed, the NCI will continue to intensively sequence tumours in three cancers: ovarian, colorectal and lung adenocarcinoma. It then plans to evaluate the fruits of this extra effort before deciding whether to add back more cancers. But this time around, the studies will be able to incorporate detailed clinical information about the patient’s health, treatment history and response to therapies. Because researchers can now use paraffin-embedded samples, they can tap into data from past clinical trials, and study how mutations affect a patient’s prognosis and response to treatment. Staudt says that the NCI will be announcing a call for proposals to sequence samples taken during clinical trials using the methods and analysis pipelines established by the TCGA.


The rest of the International Cancer Gene Consortium, slated to release early plans for a second wave of projects in February, will probably take a similar tack, says co-founder Tom Hudson, president of the Ontario Institute for Cancer Research in Toronto, Canada. A focus on finding sequences that make a tumour responsive to therapy has already been embraced by government funders in several countries eager to rein in health-care costs, he says. “Cancer therapies are very expensive. It’s a priority for us to address which patients would respond to an expensive drug.”


The NCI is also backing the creation of a repository for data not only from its own projects, but also from international efforts. This is intended to bring data access and analysis tools to a wider swathe of researchers, says Staudt. At present, the cancer genomics data constitute about 20 petabytes (10**15 bytes), and are so large and unwieldy that only institutions with significant computing power can access them. Even then, it can take four months just to download them.

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Amazing Story: Man Saves Wife's Sight by 3D Printing Her Tumor

Amazing Story: Man Saves Wife's Sight by 3D Printing Her Tumor | Amazing Science | Scoop.it

Two highly motivated stakeholders (the patient and her husband) had access to the patient’s medical data and were able to enhance its value using new era tools (software and 3D printing) and bring it to the docs – clearer – so they could better apply their clinical skills. Specifically, the physicians who read the scans before had not seen the situation clearly. With the tumor printed, a better picture emerged. That is adding value in medicine.


Want to print your medical image? Ask your doctor for your DICOM files and download 3D Slicer (slicer.org). Then use the Region Growing tool to segment the image. Extract a 3D mesh of the surface, save as an STL, and use ParaView (paraview.org) to simplify it to a manageable number of triangles. To see more details, check out Make: volume 42, page 83, or visit makezine.com/ projects/3d-print-your-medical-scan.


Full story is here: http://tinyurl.com/nal2oac

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Temporary tattoo could help diabetics manage their condition without daily finger pricks

Temporary tattoo could help diabetics manage their condition without daily finger pricks | Amazing Science | Scoop.it

Nanoengineers at the University of California, San Diego have tested a temporary tattoo that both extracts and measures the level of glucose in the fluid in between skin cells. This first-ever example of the flexible, easy-to-wear device could be a promising step forward in noninvasive glucose testing for patients with diabetes.


The sensor was developed and tested by graduate student Amay Bandodkar and colleagues in Professor Joseph Wang's laboratory at the NanoEngineering Department and the Center for Wearable Sensors at the Jacobs School of Engineering at UC San Diego. Bandodkar said this "proof-of-concept" tattoo could pave the way for the Center to explore other uses of the device, such as detecting other important metabolites in the body or delivering medicines through the skin.


At the moment, the tattoo doesn't provide the kind of numerical readout that a patient would need to monitor his or her own glucose. But this type of readout is being developed by electrical and computer engineering researchers in the Center for Wearable Sensors. "The readout instrument will also eventually have Bluetooth capabilities to send this information directly to the patient's doctor in real-time or store data in the cloud," said Bandodkar.


The research team is also working on ways to make the tattoo last longer while keeping its overall cost down, he noted. "Presently the tattoo sensor can easily survive for a day. These are extremely inexpensive--a few cents--and hence can be replaced without much financial burden on the patient."


A similar device called GlucoWatch from Cygnus Inc. was marketed in 2002, but the device was discontinued because it caused skin irritation, the UC San Diego researchers note. Their proof-of-concept tattoo sensor avoids this irritation by using a lower electrical current to extract the glucose.


Wang and colleagues applied the tattoo to seven men and women between the ages of 20 and 40 with no history of diabetes. None of the volunteers reported feeling discomfort during the tattoo test, and only a few people reported feeling a mild tingling in the first 10 seconds of the test.


To test how well the tattoo picked up the spike in glucose levels after a meal, the volunteers ate a carb-rich meal of a sandwich and soda in the lab. The device performed just as well at detecting this glucose spike as a traditional finger-stick monitor.


The researchers say the device could be used to measure other important chemicals such as lactate, a metabolite analyzed in athletes to monitor their fitness. The tattoo might also someday be used to test how well a medication is working by monitoring certain protein products in the intercellular fluid, or to detect alcohol or illegal drug consumption.

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Scientists create contact lens that magnifies at blink of an eye

Scientists create contact lens that magnifies at blink of an eye | Amazing Science | Scoop.it

A contact lens that magnifies objects at the wink of an eye has been created by scientists to help people with impaired vision. The lens contains an extremely thin telescope that is switched on when the wearer winks their right eye and returns to normal when they wink their left eye.


Eric Tremblay, a researcher at Switzerland’s École Polytechnique Fédérale de Lausanne (EPFL), said the lens could help people with age-related macular degeneration (AMD), which leaves them with a blind spot in the centre of their vision. The contact lens magnifies objects by 2.8 times, making road signs, facial features and other objects large enough for people with AMD to recognise with their peripheral vision.


The device was funded by DARPA, the Pentagon’s research agency, as a means of giving soldiers a form of bionic vision. “They were really interested in supervision, but the reality is more tame than that,” said Tremblay at the American Association for the Advancement of Science. So far, only five people have tested the latest version.


The device is larger and slightly thicker than a normal contact lens. It allows the wearer to see normally by correcting for short or long sight. But around the central region is a thin, ring-shaped reflective telescope, which expands the perceived size of objects like weak binoculars.


To swap between normal and magnified vision, the wearer dons a pair of liquid crystal glasses. By winking, they can switch the glasses electronically to polarise light in different planes. The contact lens is designed so that one type of polarised light goes through the normal, central part of the lens, while the other goes through the magnifying region.


More work is needed before the contact lenses are ready for patients to wear regularly. The latest lenses can only be worn for about half an hour, because they do not allow enough oxygen to pass through them and into the eye. Tremblay said he expected a working version of the contact lenses to be available in two years or so.

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ATDC/TRIM29 gene may explain why pancreatic cancer is so aggressive

ATDC/TRIM29 gene may explain why pancreatic cancer is so aggressive | Amazing Science | Scoop.it

Pancreatic cancer is so aggressive that even when diagnosed early, fewer than 1 in 3 patients survive. Now, a new study identifies ATDC as an important culprit. The study, which is published in the journal Genes and Development, suggests a gene called ATDC - also known as TRIM29 - plays a key role in helping pre-invasive pancreatic tumors progress to a metastatic state where cancer cells travel to other parts of the body. Senior author Dr. Diane M. Simeone, director of the Pancreatic Cancer Center at the University of Michigan Comprehensive Cancer Center in Ann Arbor, says: "We know that patients with the earliest stage of pancreatic cancer have a survival rate of only 30%. This suggests that even in that very early stage of invasive cancer there are already cells that have spread to distant parts of the body." The National Cancer Institute estimate there were 46,420 new cases of pancreatic cancer in the US in 2014 and 39,590 deaths from the disease. Pancreatic cancer cases represent 2.8% of all new cancer cases among Americans and 6.8% of cancer deaths.


ATDC, also known as TRIM29, is a member of the tripartite motif (TRIM) protein family consisting of 70 members. TRIM proteins have a series of conserved domains, which include a B-box type 1 (B1) and B-box type 2 (B2), followed by a coiled–coiled (CC) region. The TRIM family of proteins has been implicated in a variety of physiologic processes, such as development, oncogenesis, apoptosis, and antiviral defense.


The ATDC gene was initially described as a candidate gene responsible for the genetic disorder ataxia telangiectasia (AT) because its expression increased radiation resistance of AT5BI (AT-D) cells. However, ATDC was later dismissed as an AT gene after the gene responsible for ataxia telangiectasia mutated (ATM) was identified. We previously reported that ATDC, highly expressed in pancreatic cancer cells, promotes pancreatic tumor growth via stimulation of the β-catenin pathway. Because pancreatic cancer cells are commonly resistant to radiation therapy and ATDC may play a role in the cellular response to ionizing radiation, high expression of ATDC in pancreatic cancer cells may contribute to the radio-resistant phenotype of pancreatic cancer and may be one of the key molecular mechanisms by which this occurs.


The research team says preliminary data also suggests ATDC may play a similar role in other types of cancer, such as ovarian, bladder, colorectal and lung cancer, as well as multiple myelomaHowever, Dr. Simeone says it is important to focus on pancreatic cancer, for which new treatment options are desperately needed. The cancer is set to become the second leading cause of cancer death in the US by 2030, she notes.


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#WeAreNotWaiting: Confessions of a Diabetes Hacker

#WeAreNotWaiting: Confessions of a Diabetes Hacker | Amazing Science | Scoop.it

There is a quiet hacking revolution taking place in the Type 1 diabetes community. You can identify its followers by the popular hashtag #WeAreNotWaiting on Twitter. There are currently thousands of individuals running an app known as Nightscout to upload real-time blood glucose readings from their Dexcom continuous glucose monitors to their own private servers. This allows hundreds of parents to keep close watch over the health of children with Type 1. While this kind of customized surveillance can be done with current diabetes technology, it has yet to be approved by the FDA. Many have decided that we are not waiting for that agency’s blessing.


Stephen Black reports: "I was diagnosed with Type 1 four months ago. At that time, I knew nothing about diabetes. I was in disbelief when I discovered that if I wanted to see my glucose levels in real time, I would need to carry around an extra, bulky device in my pocket. If I wanted to see that data anywhere else, I would need to plug it into a computer and upload it. If a loved one wanted to check in to see if I was doing alright, they would need to call me and hope I answered. This seemed anachronistic in the wireless age. I promptly got to work on a project I have dubbed DexDrip, a wireless bluetooth bridge that would allow real-time blood glucose readings from a sensor to be delivered straight to my phone. I started by researching the Nightscout project. After doing some digging, I soon discovered an underground community of individuals working on similar projects to mine. Skirting just outside the peripheral vision of the FDA, they are working on all sorts of projects, including their own closed-loop artificial pancreas systems. Some are working in groups, others are working alone, but all share the same goal of making lives for people with diabetes easier, better, and (although they are taking personal risks) safer. Finding these people was difficult because many want to remain anonymous, but I was amazed by the community; everyone was there to help me. Once I discovered how to intercept transmissions from my Dexcom transmitter, it was pretty straightforward to steer the signal to my smartphone. The math presents a bigger challenge. Every 12 hours, the Dexcom receiver asks the user to enter his or her current blood glucose value so it can recalibrate. I couldn’t find a way to work around this automatic recalibration request. If I was going to cut the receiver out of the equation, I would need to write my own calibration algorithm."


Read Stephen Black's full report here

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U.S. proposes effort to analyze genome from 1 million people

U.S. proposes effort to analyze genome from 1 million people | Amazing Science | Scoop.it

The United States has proposed analyzing genetic information from more than 1 million American volunteers as part of a new initiative to understand human disease and develop medicines targeted to an individual’s genetic make-up.


At the heart of the “precision medicine” initiative, announced on Friday by President Barack Obama, is the creation of a pool of people – healthy and ill, men and women, old and young – who would be studied to learn how genetic variants affect health and disease.


Officials hope genetic data from several hundred thousand participants in ongoing genetic studies would be used and other volunteers recruited to reach the 1 million total.


“Precision medicine gives us one of the greatest opportunities for new medical breakthroughs we’ve ever seen,” Obama said, promising that it would “lay a foundation for a new era of life-saving discoveries.”


The near-term goal is to create more and better treatments for cancer, Dr. Francis Collins, director of the National Institutes of Health (NIH), told reporters on a conference call on Thursday. Longer term, he said, the project would provide information on how to individualize treatment for a range of diseases.


The initial focus on cancer, he said, reflects the lethality of the disease and the significant advances against cancer that precision medicine has already made, though more work is needed.


The president proposed $215 million in his 2016 budget for the initiative. Of that, $130 million would go to the NIH to fund the research cohort and $70 million to NIH’s National Cancer Institute to intensify efforts to identify molecular drivers of cancer and apply that knowledge to drug development.


A further $10 million would go to the Food and Drug Administration to develop databases on which to build an appropriate regulatory structure; $5 million would go to the Office of the National Coordinator for Health Information Technology to develop privacy standards and ensure the secure exchange of data.


The effort may raise alarm bells for privacy rights advocates who have questioned the government’s ability to guarantee that DNA information is kept anonymous. Obama promised that “privacy will be built in from day one.”

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Risto Suoknuuti's curator insight, February 13, 2015 6:59 PM

I wellcome this inititive in the name of all camcer patients who have suffered current hard and heavy teatments exspeacially remembering those of us who did not survive. Give them more hope.

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Shattered chromosome (chromothripsis) cures woman of immune disease

Shattered chromosome (chromothripsis) cures woman of immune disease | Amazing Science | Scoop.it

Call it a scientific oddity—or a medical miracle. A girl who grew up with a serious genetic immune disease was apparently cured in her 30s by one of her chromosomes shattering into pieces and reassembling. Scientists traced the woman’s improvement to the removal of a harmful gene through this scrambling of DNA in one of her blood stem cells—a recently identified phenomenon that until now had only been linked to cancer.


As a child, the woman was suffering from WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome, and extremely rare disease—only about 60 cases are known worldwide—patients live into adulthood, but they can develop lung scarring, hearing loss, and other health problems from the frequent infections.


In 2003, researchers linked WHIM to a gene called CXCR4, which codes for a cell surface protein that immune cells use to recognize chemical messengers called chemokines. In WHIM, patients have one normal copy of CXCR4 and a defective copy that causes the receptor to be overactive—it doesn’t shut off when it’s supposed to.


This somehow causes white blood cells to “get stuck” in the bone marrow instead of entering the bloodstream, says Philip Murphy, an immunologist at the National Institute of Allergy and Infectious Diseases in Bethesda, Maryland. Murphy and colleagues have studied WHIM patients at the National Institutes of Health’s (NIH’s) Clinical Center to better understand the disease and develop a possible treatment with a drug that inhibits CXCR4. Two years ago, they heard from a woman who said she wanted to bring in her two daughters for evaluation because they had inherited the disease.


The woman was that first WHIM patient, now 59 years old. Her two daughters in their early 20s did indeed have classic symptoms of WHIM, such as warts on their hands, and their blood cells carried the mutation in CXCR4 that usually causes it. But as for their mother, “When we asked a very simple question—‘How was she doing?’—she said she was fine,” Murphy recalls. She had not had warts or serious infections since her late 30s. “At this point we got very, very interested,” he says.


The NIH team began sleuthing. To its surprise, the woman’s white blood cells no longer had the faulty CXCR4 mutation, although other cell types still carried it. Examining the chromosomes in her apparently normal white blood cells, they found an anomaly: One copy of chromosome 2 was about 15% shorter than the other copy. Whole-genome sequencing revealed that it had become scrambled and lost a chunk that included the defective CXCR4and 163 other normal genes.


The explanation seems to be chromothripsis, a phenomenon discovered only 4 years ago in a leukemia patient and occasionally seen in other cancers. A chromosome somehow shatters during cell replication, then reassembles with the pieces in a different order. Presumably, the cells typically die as a result of this damage, Murphy says. If the cell survives, the scrambled genes may contribute to cancer.


In this case, however, the chromosome shattering seems to have occurred in a blood stem cell, which then replicated to give her a supply of normal white blood cells. The missing copy ofCXCR4 also appears to explain why the cells now constitute all of her white blood cells, the NIH researchers say. They showed that transplants of stem cells lacking one copy of CXCR4engraft better in mice than stem cells with two normal copies or a normal copy and the WHIM version, they report online today in Cell.

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Could you re-grow your own bones? Clinical trial is beginning

Could you re-grow your own bones? Clinical trial is beginning | Amazing Science | Scoop.it

A pioneering stem cell treatment could avoid thousands of hip replacements - by helping patients 'regrow' damaged bone. Five NHS hospitals in the UK will trial the jabs, which doctors claim can regenerate damaged tissue after just one injection.


And a leading specialist says it has the potential to be 'life-changing' for those with bone disease avascular necrosis (AVN). Patients often face years of pain before being considered for a hip replacement. Zameer Shah, a consultant orthopaedic and trauma surgeon at London's Guy's and St Thomas' NHS Foundation Trust, says: 'A treatment that doesn't involve surgery could be a real game-changer.'


AVN is a disease where bone tissue dies and eventually collapses due to the loss of blood supply to the area. The cause is unknown but triggers include injury and rheumatoid arthritis. It can also be a side effect of treatments such as steroids, chemotherapy or radiotherapy.


AVN is particularly common in the hip, with 150,000 AVN patients undergoing a total hip replacement in Europe and the US every year. Radio 4 presenter Jenni Murray, who suffers from AVN, had both hips replaced in 2008. The new trial will compare the effectiveness of the osteoblastic (bone-forming) product Preob to other treatments, and the trusts taking part - Cambridge University Hospitals, King's College Hospital London, Newcastle upon Tyne Hospitals, University Hospital Southampton and the Royal Orthopaedic Hospital Birmingham - are among 37 centres across Europe involved. The trial will run until late 2017.

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What does measles actually do and why is the disease back?

What does measles actually do and why is the disease back? | Amazing Science | Scoop.it

The United States is now experiencing what promises to be one of the worst outbreaks of measles since the virus was declared eliminated from the country in 2000.  It began in early January at Disneyland Resort in Anaheim, California, and has since spread to 14 states and infected 84 people, according to the U.S. Centers for Disease Control and Prevention (CDC).


Measles, caused by a paramyxovirus from the genus Morbillivirus, is one of the most contagious diseases in the world, infecting more than 90% of susceptible hosts that come in contact with an afflicted individual. In the absence of widespread vaccination, the average person with measles will infect an average of 12 to 18 other people; in contrast, Ebola is typically transmitted to 1.5 to 2.5 people. Children, in particular, are more likely to experience complications as a result of a measles infection. Although the overall mortality rate for children who get measles is only between 0.1% and 0.2%, as many as one out of every 20 children will also develop pneumonia. The disease symptoms can be managed with common anti-inflammatory drugs, hydration, and rest, but like many other viral illnesses, there is no cure and antibiotics will have no effect. Death rates are much higher in developing countries.


The Measles virus is spread from person to person through the air in coughed-out aerosolized droplets that are inhaled. The virus typically first comes in contact with host lung tissue, where it infects immune cells called macrophages and dendritic cells, which serve as an early defense and warning system. From there, the infected cells migrate to the lymph nodes where they transfer the virus to B and T cells. A surface protein on these white blood cells, known as CD150, serves as the virus’s point of entry during this critical step. The infected B and T cells then migrate throughout the body releasing virus particles into the blood. The spleen, lymph nodes, liver, thymus, skin, and lungs are eventual destinations for the virus. In rare instances (about one in 1000 cases), the virus can cross the blood-brain barrier and cause dangerous swelling of the brain; infection of lung cells causes a hacking cough that keeps the virus circulating in the population.


Why is measles back?

Measles has actually been back since quite a while. Last year was one of the worst years in recent history for the United States: CDC reported 644 cases from 23 separate outbreaks during 2014; between 2001 and 2013, no single year saw more than 250 cases. (Because measles was declared “eliminated” in the United States in 2000, outbreaks have been triggered by virus “imported” from other countries, which then finds an unvaccinated person.) With 84 people infected already in 2015, things are not off to the best start. Part of the reason for the resurgence is a rise in the number of parents who refuse to vaccinate their children against the virus. Despite an overwhelming amount of scientific and medical evidence demonstrating both the safety and efficacy of the measles vaccine, some parents refuse to vaccinate their children for reasons of personal belief. The problem is compounded because many like-minded parents are geographically clustered. For the entire state of California, the vaccine refusal rate is only 2.6%, indicating that most citizens are cognizant of the benefits of immunization. However, a recent study of pediatric health records revealed that in some areas the vaccine refusal rate is as high as 13.5%. Other factors such as a lack of time, education, or money can cause parents to inadvertently fall behind on their children’s immunizations.


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Ed Rybicki's comment, February 5, 2015 7:44 AM
People - especially people in California - are stupid about vaccinations.
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Promising use of nanodiamonds to kill chemoresistant cancer stem cells more effectively

Promising use of nanodiamonds to kill chemoresistant cancer stem cells more effectively | Amazing Science | Scoop.it

A study led by the National University of Singapore (NUS) found that attaching chemotherapy drug Epirubicin to nanodiamonds effectively eliminates chemoresistant cancer stem cells. The findings were first published online in ACS Nano, the official journal of the American Chemical Society, in December 2014.


The research team, led by Assistant Professor Edward Chow, Junior Principal Investigator at the Cancer Science Institute of Singapore (CSI Singapore) at NUS, demonstrated the use of nanotechnology to repurpose existing chemotherapy drugs as effective agents against chemoresistant cancer stem cells. Chemoresistance, which is the ability of cancer cells to escape chemotherapy treatment, is a primary cause of treatment failure in cancer. Cancer stem cells, a type of cancer cell which initiates the formation of tumours, are commonly found to be more resistant to chemotherapy than the rest of the bulk tumour, which can lead to cancer recurrence following chemotherapy treatment. As such, there is intense interest in developing new drugs or treatment strategies that overcome chemoresistance, particularly in cancer stem cells.


In this study, widely-used chemotherapy drug Epirubicin was attached to nanodiamonds, carbon structures with a diameter of about five nanometres, to develop a nanodiamond-Epirubicin drug delivery complex (EPND). The researchers found that while both standard Epirubicin as well as EPND were capable of killing normal cancer cells, only EPND was capable of killing chemoresistant cancer stem cells and preventing secondary tumour formation in xenograft models of liver cancer.


Compared to other approaches such as combinatorial therapy of chemotherapy drugs with inhibitors of chemoresistance pathways, delivery of existing chemotherapy drugs with nanomaterials, in this case nanodiamonds, provide a broader range of protection in a package that is both safer and more effective. The study showed that delivery of Epirubicin by nanodiamonds resulted in a normally lethal dosage of Epirubicin becoming a safe and effective dosage. As such, delivery of chemotherapy drugs by nanodiamonds not only enables enhanced killing of chemoresistant cancer stem cells, but may be a useful alternative for patients who cannot tolerate the toxic side effects of standard chemotherapy drugs.


Furthermore, the versatility of the nanodiamond-based drug delivery platform opens up the possibility of future applications of nanodiamonds such as the addition of other similar drugs as well as active targeting components such as antibodies or peptides against tumour cell surface proteins for targeted drug release. In addition, the application of a nanodiamond-drug delivery system is not limited to liver cancer. It offers a promising approach to treating a broad range of difficult cancers, particularly those driven by chemoresistant cancer stem cells. In collaboration with Professor Dean Ho at the University of California Los Angeles and Professor Li Jianzhong at Peking University, Asst Prof Chow's group is working towards completing preclinical work on anthracycline delivery by nanodiamonds and hope to begin clinical trials in the near future.

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GLG Pharma's curator insight, February 6, 2015 7:54 AM

Cool new technology!

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4-Year-Old Australian Boy Receives World’s First Version of an Artificial Pancreas

4-Year-Old Australian Boy Receives World’s First Version of an Artificial Pancreas | Amazing Science | Scoop.it

In 2013 alone, over 79,000 children around the globe were diagnosed with type 1 diabetes: an autoimmune disorder that affects the amount of insulin produced by the pancreas. Receiving insulin therapy through a traditional pump or injections can require a lot of work to ensure blood sugar levels are safe, particularly during the night. A tremendous step forward has been made in the treatment of this disease when a 4-year-old boy from Australia was fitted with the world’s first commercially-available artificial pancreas which automatically regulates his insulin levels. With the device managing insulin output, diabetics who typically test their blood sugar up to eight times a day will need to do so less frequently.


Xavier Hames from Perth received the device from Princess Margaret Hospital for Children, where he has been receiving treatment for his diabetes since he was 22 months old. This is also where clinical trials for the device have been ongoing for several years. Xavier is the first person to receive the pump commercially, which is available for AUS$10,000 (US$8,100).


The artificial pancreas features a sensor that reads blood sugar levels and communicates to the pump, which is connected to the body underneath the skin to administer the insulin. Unlike traditional pumps, this new technology does not deliver a constant stream of insulin to the body. Instead, the artificial pancreas uses an algorithm to track blood sugar levels over time, predicting when insulin is no longer required. This reduces the risk of dangerously low blood sugar levels, known as hypoglycemia.


Symptoms of a hypoglycemic attack can be mild and include sweating or fatigue, but in more serious cases, weakness, temporary unconsciousness, organ damage, coma, or death can occur. These typically happen while the person is sleeping (and therefore not eating) because the insulin is still working in their body, bringing their blood sugar to dangerously low levels. Diabetics often have to wake up several times each night in order to monitor their blood sugar.


"The majority of hypoglycemic attacks occur at night when a person is asleep and they might not be able to react or recognize the attack," Professor Tim Jones from Princess Margaret Hospital told The West Australian. "This device can predict hypoglycemia before it happens and stop insulin delivery before a predicted event. This, coupled with the fact that the pump automatically resumes insulin when glucose levels recover, is a real medical breakthrough.”


It is not clear exactly when Xavier was fitted with the pump, but his mother has already said that she expects it to greatly impact his day-to-day life. Because the pump stops administering insulin automatically, Xavier (and his parents) will be able to sleep more soundly when he would normally be at risk for hypoglycemia. Additionally, it will also allow him to act more like a kid and occasionally indulge in high carbohydrate foods such as pasta or snack foods. The device is also waterproof, meaning that Xavier can wear it in the bathtub or while swimming.

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Melissa Wright's curator insight, February 10, 2015 2:09 PM

Research Question: #2

I believe this is a very good website that tells a good story. It also gives many good and interesting facts.

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Top Rated Electronic Health Record Software Is Free

Top Rated Electronic Health Record Software Is Free | Amazing Science | Scoop.it

Earlier this month, Medscape published the results of their recent survey (here) which asked 18,575 physicians across 25 specialties to rate their Electronic Health Record (EHR) system. For overall satisfaction, the #1 ranked EHR solution was the VA’s Computerized Patient Record System ‒ also known as VistA. It was built using open‒source software and is therefore license free.


There’s also a publicly available version of VistA called OpenVista and several companies leverage a services-only business model for larger OpenVista installations. For smaller installations, a YouTube video (here) suggests the free OpenVista software can be installed in about 10 minutes ‒ bring your own hardware.


Of course free software licensing doesn’t make the hardware, installation or maintenance free, but the lack of any software licensing fees at all does reduce the overall cost ‒ especially for large installations ‒ and that can typically save millions of dollars.


Open-source software also charts a much different course for design changes that are not dependent on the resources, budgets (or revenue requirements) of independent software vendors (ISV’s).


In many ways, VistA’s top rating is no surprise because it’s the only EHR installation in the U.S. with a truly national footprint. As a single software solution, VistA is designed to support almost 9 million vets through about 1,700 different care sites around the country.

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Kris Prendergast's curator insight, March 9, 2015 10:01 AM

How vendor-lock in drains customers

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Ebola In The Air: What Science Says About How The Virus Spreads

Ebola In The Air: What Science Says About How The Virus Spreads | Amazing Science | Scoop.it

Turns out, Ebola is transmitted through the air, but it's not very good at spreading through the airborne route. What in the heck does that mean?


Viruses can spread through the air in two ways: inside large droplets that fall quickly to the ground (red), or inside tiny droplets that float in the air (gray). In the first route, called droplet transmission, the virus can spread only about 3 to 6 feet from an infected person. In the second route, called airborne transmission, the virus can travel 30 feet or more.


Viruses that move through the second route — the airborne route — can travel more than 30 feet and can stay in the air for minutes, even hours, when the humidity and temperature are right. That means you don't even have to see the person to catch a virus from him or her. An infected person could sneeze, walk out of the room and leave an infectious mist behind.


A few viruses, such as measles and chickenpox, spread this way (that's why they have such high R0s). What about Ebola? In the lab, scientists can infect monkeys with Ebola virus through the airborne route. They essentially stick a monkey's head in a plastic tube and spray the animal's face with a mist infused with Ebola. If the humidity and temperature are right in the tube, the monkey can get Ebola. But scientists haven't found evidence that Ebola spreads through the airborne route in real outbreaks, with real people. Does that mean Ebola never catches a ride on tiny, floating droplets? No.

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Your Odds Of Surviving Cancer Depend Very Much On Where You Live

Your Odds Of Surviving Cancer Depend Very Much On Where You Live | Amazing Science | Scoop.it
The largest study of cancer patients reveals a huge gulf in survival rates around the world. And in some countries, there may only be one cancer doctor for the entire population.


In the United States, 9 out of 10 kids diagnosed with acute lymphoblastic leukemia will live. In Jordan, the survival rate is 16 percent. And while cervical cancer patients have a five-year survival rate of over 70 percent in countries like Mauritius and Norway, the rate in Libya is under 40 percent.


That's the sobering news from the largest cancer study ever published. It surveyed more than 25.7 million patients and reveals a huge gulf in cancer survival worldwide. But there's good news as well. "In most countries, survival from some of the commonest cancers has been improving," says Dr. Michel Coleman from the London School of Hygiene and Tropical Medicine, one of the study's authors.


More people are surviving breast cancer, colon cancer and stomach cancer than ever before, especially in the U.S. and Europe. The survival rate for breast cancer in France and Finland, for example, is 87 percent. The data from other regions are also encouraging. Brazil's breast cancer survival rate has gone up from 78 percent in 1995-99 to 87 percent in 2005-09.


The reason that some countries lag behind is not surprising; it's a matter of how much is invested in cancer care. Dr. Corey Casper, head of global oncology at the Fred Hutchinson Cancer Research Center in Seattle, met a doctor in Uganda a few years ago who was then seeing 10,000 patients a year "in a facility that had ... no roof, inconsistent electricity and no meds." What's more, says Casper, he was the only cancer doctor in Uganda and four surrounding countries.


In summary, the study found that 5-year survival from colon, rectal, and breast cancers has increased steadily in most developed countries. For patients diagnosed during 2005–09, survival for colon and rectal cancer reached 60% or more in 22 countries around the world; for breast cancer, 5-year survival rose to 85% or higher in 17 countries worldwide. Liver and lung cancer remain lethal in all nations: for both cancers, 5-year survival is below 20% everywhere in Europe, in the range 15–19% in North America, and as low as 7–9% in Mongolia and Thailand. Striking rises in 5-year survival from prostate cancer have occurred in many countries: survival rose by 10–20% between 1995–99 and 2005–09 in 22 countries in South America, Asia, and Europe, but survival still varies widely around the world, from less than 60% in Bulgaria and Thailand to 95% or more in Brazil, Puerto Rico, and the USA. For cervical cancer, national estimates of 5-year survival range from less than 50% to more than 70%; regional variations are much wider, and improvements between 1995–99 and 2005–09 have generally been slight. For women diagnosed with ovarian cancer in 2005–09, 5-year survival was 40% or higher only in Ecuador, the USA, and 17 countries in Asia and Europe. 5-year survival for stomach cancer in 2005–09 was high (54–58%) in Japan and South Korea, compared with less than 40% in other countries. By contrast, 5-year survival from adult leukaemia in Japan and South Korea (18–23%) is lower than in most other countries. 5-year survival from childhood acute lymphoblastic leukaemia is less than 60% in several countries, but as high as 90% in Canada and four European countries, which suggests major deficiencies in the management of a largely curable disease.

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