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Heart Attack Vaccine: A single shot against heart attacks that lasts a life long?

Heart Attack Vaccine: A single shot against heart attacks that lasts a life long? | Amazing Science | Scoop.it

Harvard researchers say simple ‘genome editing’ may dramatically lower risk of such crises in future.

 

Harvard Stem Cell Institute (HSCI) scientists collaborating with researchers at the University of Pennsylvania have developed a “genome-editing” approach for permanently reducing cholesterol levels in mice through a single injection, a development that could reduce the risk of heart attacks in humans by up to 90 percent.

 

“For the first iteration of an experiment, this was pretty remarkable,” said Kiran Musunuru of HSCI, an assistant professor in Harvard’s Department of Stem Cell and Regenerative Biology (SCRB), and a cardiologist at Harvard-affiliatedBrigham and Women’s Hospital. Musunuru stressed, however, that it could take a decade of concerted effort to get this new approach for fighting heart disease from the laboratory to phase I clinical trials in humans.

 

The research was published online today by Circulation Research, a journal of the American Heart Association. Qiurong Ding, a postdoctoral fellow in Musunuru’s laboratory, is first author on the paper.

 

The work by the Musunuru team and a Penn team led by Daniel J. Rader, an authority on cholesterol metabolism and a long-time collaborator of Musunuru, focused on altering the function of a liver gene called PCSK9.

 

David T. Scadden, co-director of HSCI, co-chair of SCRB, and director of the Massachusetts General Hospital Center for Regenerative Medicine, said the work “is an outstanding example of how new approaches to disease can emerge when basic science and clinical care are creatively combined. It’s a reminder of how important it is for all of us that research is supported if we are going to come up with disruptive new thinking to solve major health problems.”

 

Musunuru and Rader’s project to turn normal PCSK9 genes into those with the “good” defect came at an inflection point in genome editing, the refinement early last year of a technology called CRISPR/Cas9, first discovered in 2007. “The biological sciences as a field got really excited by this new technology, because it makes it far easier to edit the genome in every species you can think of, from fruit flies to fish, to mice, to monkeys, to human cells,” said Musunuru, whose group was among the first to use it in stem cells.

 

“Cas9 is a protein that will create a break in DNA, and the CRISPR is an RNAcomponent that will bind to a matching sequence and directs the Cas9 to that sequence in the DNA in which you are interested,” he said. “This creates a break where you want it. The cell can then repair itself, though often with errors, which is useful if you want to disrupt a gene to create a ‘knockout’ of the gene,” which is precisely what Musunuru’s team did with PCSK9.

 

“The PCSK9 gene is expressed primarily in the liver,” explained Musunuru, “and produces a protein that is active in the bloodstream and prevents the removal of cholesterol from the blood. Several drug companies have been developing antibodies” to it, he said, but “the problem with antibody-based drugs is they don’t last forever; you’d need an injection every few weeks. The main option for reducing cholesterol is statin drugs, such as Lipitor, but many people taking statin drugs every day still have heart attacks. So there is still a great need for other approaches,” said the scientist.

 

“What we were thinking was that, with this genome-editing technology, we can do something we couldn’t do before: make permanent changes in the genome at the level of the DNA. We can actually go to the source. So the question was whether we can use genome editing to make normal people like people born with the ‘good’ mutations.” The answer, in mice, was yes.

 

“The first question was whether we could get CRISPR/Cas9 into the liver, and once we got it into the liver, would it function properly?” Musunuru asked. “And it did. It could have had no effect, but it turned out to have a dramatic effect. Within three to four days of delivering the system into the liver, the majority of the PCSK9 gene copies in all of the liver cells were disrupted, knocked out. And what we hoped to see was much less of the protein product in the bloodstream, which is what we saw.

“The other consequence that we saw was a 35 to 40 percent reduction in cholesterol levels in these mice,” which would translate in humans to a heart attack risk-reduction of as high as 90 percent.

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First Zika-linked birth defects detected in Colombia

First Zika-linked birth defects detected in Colombia | Amazing Science | Scoop.it

Cases may signal start of anticipated wave of birth defects in country hit hard by Zika virus.

 

Researchers have found Colombia's first cases of birth defects linked to the Zika virus, Nature has learned — which are likely forerunners of a widely anticipated wave of Zika-related birth defects in the country.

 

The discovery is perhaps no surprise: the virus arrived in Colombia last September, and the country is second only to Brazil in terms of the number of people infected with Zika. But Colombian researchers hope that plans put in place to closely monitor pregnant women can help to better establish the magnitude of the threat posed to fetuses by Zika. That is a crucial question that scientists have not so far been able to answer with the data from Brazil.

 

Researchers have diagnosed one newborn with microcephaly — an abnormally small head — and two others with congenital brain abnormalities, says Alfonso Rodriguez-Morales, who chairs the Colombian Collaborative Network on Zika (RECOLZIKA), which made the diagnoses. All three tested positive for the presence of Zika virus. The researchers have submitted a report of their detections to a scientific journal.

 

Rodriguez-Morales, an infectious-diseases epidemiologist at the Technological University of Pereira in western Colombia, says that he expects to see a rise in cases of Zika-linked birth defects starting in two or three months' time. The RECOLZIKA group — a network of researchers and public-health institutions across Colombia — are already investigating a handful of other suspected cases of microcephaly, which have a possible link to Zika.

 

Brazil is the only country so far to report a large surge in newborns with microcephaly that coincides with outbreaks of Zika virus. By the time the alarm over a possible microcephaly link was raised there (in October 2015), Zika infections had already peaked in many parts of the country, because the virus first reached Brazil at the beginning of last year.

In Colombia, by contrast, researchers detected the first Zika cases in September, and by December had set up national tracking programmes to monitor pregnant women for signs of infection, and to spot early signs of birth defects in fetuses. Since then, researchers have been waiting attentively to see whether their country might experience a similar rise in birth defects.

 

The true size of Brazil's surge in microcephaly cases is unknown. The country's health ministry says that 5,909 suspected microcephaly cases have been registered since early November, but only 1,687 of them have been investigated so far. Of those, 1,046 have been discarded as false positives, and 641 have been confirmed.

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Cancer-Causing HPV Rates Fall Dramatically In Teenage Girls Following Vaccination

Cancer-Causing HPV Rates Fall Dramatically In Teenage Girls Following Vaccination | Amazing Science | Scoop.it

Vaccines are the best resource in our fight against preventable diseases, and sometimes they work even better than we could have hoped for. This seems to be the emerging case for the human papillomavirus, or HPV, vaccine, which was introduced just a decade ago to combat the virus that causes cervical cancer, among others. Although there are more than 100 different strains of HPV, only a small number are associated with cancer, and it is these that the vaccine targets. More specifically, four are high risk for genital cancer.


Types 16 and 18, for instance, cause 70 percent of cervical cancers. 

According to a new study, published in Pediatrics, in the last 10 years the prevalence of the virus, or more specifically these four types, in teenage girls has fallen by 64 percent in the U.S., concomitant with the release of the vaccine. The study also highlights that among women aged 20 to 24, who had on average lower vaccination rates, the most dangerous strains of the virus fell by 34 percent. The vaccine is usually administered before puberty because HPV is sexually transmittable.


As always people have questioned the protection given by the vaccine, but the evidence for it is overwhelming. In Australia, the vaccine is offered for free to schoolgirls and that accomplished a 92 percent reduction in genital warts in women under the age of 21 over the period 2007 to 2011.


In the United States, the vaccine is largely optional and the debate is often linked to underage sexual activities rather than cancer prevention. Dozens of cancers centers, as well as pediatrics associations, are actively endorsing the safety and effectiveness of the vaccine.


“Multiple studies have shown the importance of a strong provider recommendation for increasing vaccination coverage,” said to the New York Times Dr. Lauri E. Markowitz, a medical epidemiologist at the National Center for Immunizations and Respiratory Diseases, a division of the C.D.C., who led the research for the latest study.

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Researchers Discover New Ebola-Fighting Antibodies in Blood of Outbreak Survivor

Researchers Discover New Ebola-Fighting Antibodies in Blood of Outbreak Survivor | Amazing Science | Scoop.it

A research team that included scientists from The Scripps Research Institute (TSRI) has identified a new group of powerful antibodies to fight Ebola virus. The antibodies, isolated from the blood of a survivor of the 2014 Ebola outbreak and the largest panel reported to date, could guide the development of a vaccine or therapeutic against Ebola. The new study also revealed a previously unknown site of vulnerability in the structure of the deadly virus.


“Our Science paper describes the first in-depth view into the human antibody response to Ebola virus,” said team leader Laura Walker, senior scientist at Adimab, LLC, and an alumna of TSRI’s PhD program. “Within weeks of receiving a blood sample from a survivor of the 2014 Ebola outbreak, we were able to isolate and characterize over 300 monoclonal antibodies that reacted with the Ebola virus surface glycoprotein.”


Studies at TSRI and other institutions have shown that Ebola virus has several weak points in its structure where antibodies can target and neutralize the virus. However, the immune system typically needs a long period of trial and error to produce the right antibodies against these sites, so researchers have been working with only a small library of anti-Ebola options. Despite this limited library, researchers have had some success in designing antibody “cocktails” that target several weak points at once. One treatment in development, Mapp Biopharmaceutical Inc.’s ZMappTM, is a cocktail of three mouse antibodies modified to resemble human antibodies. This treatment was successful in primate trials and used as an experimental human treatment in the 2014 outbreak.


With ZMapp showing promise, researchers are searching for additional antibodies to fight Ebola. “These types of antibodies could be developed into different types of antibody cocktails or therapeutics, in addition to advancing vaccine design,” said Ward.

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Baldness and thinning hair are due to aging DNA and elimination of follicle stem cells

Baldness and thinning hair are due to aging DNA and elimination of follicle stem cells | Amazing Science | Scoop.it

Stem cells enable normal cell homeostasis, but they also exist in a quiescent state, ready to proliferate and differentiate after tissue damage. Now, two studies reveal features of stem cells in the hair follicle, an epithelial mini-organ of the skin that is responsible for hair growth and recycling.


During aging, most organs in mammals become smaller (miniaturize) or thinner, and their functions and regenerative capability also decline. Histologically, tissue atrophy and fibrosis are observed in many aged organs. Yet the exact mechanisms for the architectural and functional decline are unknown. Indeed, areas that are as yet underexplored include the dynamics of the constituent cells and their cellular fate, as well as determination of whether aged or damaged cells accumulate or are eliminated in tissues and organs during the aging process.


Organismal aging has been explained by various theories—such as reactive oxygen species, cellular senescence, telomere erosion, and altered metabolism—but not from the viewpoint of cellular and tissue dynamics. Stem cell systems sustain cellular and tissue turnover in most mammalian organs, but it has been difficult to experimentally test the precise fate of somatic stem cells, the cellular pool for tissues and organs. This has limited our understanding of the mechanisms of aging of tissues and organs and the existence of an aging program in mammalian organs. The hair follicle (HF) is an epithelial mini-organ of the skin that sustains cyclic hair regrowth over repeated hair cycles. Hair thinning (senescent baldness) is one of the most typical signs of aging in many long-lived mammals and is often prematurely induced by genomic instability, as in progeroid syndromes.


Wang et al. now found that the Foxc1 transcription factor is induced in activated hair follicle stem cells, which in turn promote Nfatc1 and BMP signaling, to reinforce quiescence.


Matsumura et al. analyzed hair follicle stem cells during aging. They identified type XVII collagen (COL17A1) as key to hair thinning. DNA damage-induced depletion of COL17A1 triggered cell differentiation resulting in the shedding of epidermal keratinocytes from the skin surface. These changes then caused hair follicle shrinkage and hair loss.


Science, this issue p. 559, p. 613;

see also p. 10.1126/science.aad4395

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Researchers discover a genetic mutation (SLIC19A3) that prevents diabetes complications 

Researchers discover a genetic mutation (SLIC19A3) that prevents diabetes complications  | Amazing Science | Scoop.it
A number of complications are associated with diabetes, but they are more prevalent in some patients than in others. A Finnish study has now revealed two genetic mutations which seem to lower the risk of contracting a diabetic retinal or kidney disease.

The most significant complications of diabetes include diabetic retinal disease, or retinopathy, and diabetic kidney disease, or nephropathy. Both involve damaged capillaries. The biggest risk factor associated with damage to the tiny blood vessels is high blood sugar, although genetic factors are also at play. Experiments conducted on both individual cells and laboratory animals indicate that the presence of vitamin B1 inside the cell can prevent the damage caused by high blood sugar.

Together with Professor Massimo Porta from the University of Turin, Professor Per-Henrik Groop, Principal Investigator of the FinnDiane research project at the University of Helsinki and Folkhälsan Research Centre, and his research group have studied the impact of point mutations on the genes that encode the proteins which transfer vitamin B1 into cells. The research was based on the hypothesis that the studied mutations impact the individual’s capacity to transfer vitamin B1 into cells and consequently the susceptibility for additional complications associated with diabetes.

The research used the world’s most extensive research data set of type 1 diabetes patients, compiled by Groop’s group, in which the patients are characterised based on their genetic profile and the severity of their diabetes complications. The results showed that two of the studied point mutations in the SLC19A3 gene were strongly associated with both retinopathy and the combination of retinopathy and nephropathy; thus, carriers of the genetic variant were less likely to have these complications. The protective effect of the variant remained significant even when other common risk factors were taken into account.

The study was repeated on North American patient data, and the results confirmed that the two variants protect their carriers from the combination of retinopathy and nephropathy. “Based on these results, it seems that the SLC19A3 gene has a role in the development of diabetic nephropathy and diabetic retinopathy. The results also help explain why some patients with type 1 diabetes are more likely to develop complications than others," says Iiro Toppila, the researcher responsible for analysing the data.  “However, further research is needed into the biological effects of point mutations.”

Via Integrated DNA Technologies
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Looking back: Biomedicine 2015 - Baby Engineering, Spray-On GMOs, and Cancer Cures

Looking back: Biomedicine 2015 - Baby Engineering, Spray-On GMOs, and Cancer Cures | Amazing Science | Scoop.it
During 2015, the combination of potent biotechnologies solved problems and created new ones.


Biologists often emphasize how little anyone really knows about the brain, the genome, and the mechanisms behind effective drugs. But this year their tune changed as diverse technologies–gene editing, stem cells, cloning, and DNA databases–coalesced into an immensely powerful toolkit for manipulating life. The message in 2015 seemed to be: “We can do anything.” The technology that stole the headlines was CRISPR, the versatile genetic scissors that make it easy to cut and edit DNA of living cells.


For the year, the number of scientific publications involving the technique doubled to more than 1,200, as scientists use gene editing to engineer extra-muscular dogs, create mosquitoes that can’t spread malaria, and alter plants so easily that companies predict it’s just a matter of years before gene-edited foods hit our dinner plates.

We can do these things, but should we? Social and ethical questions began dogging the CRISPR breakthrough early in the year, when MITTechnology Review toured readers through one emerging debate: the possibility of genetically modifying human embryos in IVF clinics to spare children from inherited disease. With an April publication from China disclosing the first edited human embryos, the debate over whether the technology is a slippery slope to eugenics exploded, and by December many of the world’s top gene-editing scientists had gathered in Washington for a will-we-or-won’t-we debate.

They concluded that we shouldn’t, not yet. It would be “irresponsible” to use CRISPR to make customized babies, the experts declared. In fact, one participant felt that our power to engineer life had outstripped our wisdom. “We are becoming masters of manipulating genes, but our understanding of their function is very limited,” said Klaus Rajewsky of the Max Delbrück Center for Molecular Medicine, in Berlin.

Yet we might know enough to cure some cancers, or solve the shortage of organs for transplant. Companies including Juno Therapeutics this year raised billions to start treating patients with genetically engineered immune cells that they have crafted into a lifesaving new treatment for leukemia. Surgeons in the U.S. smashed records for so-called “xenotransplantation” (transplants between species) by keeping a monkey alive nearly six months with a gene-modified pig kidney.

Gene technology isn’t just more powerful. It’s easier to access. Entrepreneurs started selling do-it-yourself DNA engineering kits to modify bacteria, and in October we told the story of a startup founder, Elizabeth Parrish, who claimed to be the first person to thumb her nose at the U.S. Food and Drug Administration and treat herself with anti-aging genes. “I am patient zero,” she declared.

It’s a sign that we are deep into the second generation of biotechnology. That also means some pioneering inventions are being retired. This year, Monsanto’s patents on its original herbicide-resistant soybeans expired (pound for pound, the beans are easily the most important product of the biotech era), allowing farmers to plant “generic GMOs” for the first time. But  Monsanto has new ideas in its pipeline, like genetic sprays that can kill bugs or even change the behavior of plants on contact. Those products rely on RNA interference, which was also used to create the world’s first biotech apple.

A different trend that gained traction was the use of electricity to heal the mind or treat the body. Some call these therapies “electroceuticals.” Doctors began using brain stimulation to treat cocaine addiction,obsessive-compulsive disorder, and other problems once “considered too complex and mysterious” to cure with a simple jolt of electricity. In Cleveland, meanwhile, specialists at Case Western ran wires between the brain of a paralyzed man and the muscles of his arm, allowing him to move the arm with his thoughts. We didn’t forget to check in with the brave volunteers who got us here. We learned how patients who received a previous generation of implants at Case were left without tech support, rendering the devices useless inside their bodies. One far-out scientific pioneer even decided to put an implant in his own brain.

That role Silicon Valley might play in biotechnology is also worth watching. For that, we checked in several times this year with famed Facebook investor Peter Thiel to learn about a cancer-fighting startup he funded and get his views on how drug development could be more efficient if only biotech companies acted a little more like computer startups. Thiel, who thinks there shouldn’t be so much trial and error going on, told us his goal is to “get rid of randomness.”

We also tracked tech companies attempting to disrupt the huge, unhealthy U.S. health-care system. It’s not going too well: consumers don’t trust tech companies with their health data, and wrist-worn devices aren’t too accurate. But tech companies won’t be dissuaded. This year we learned that Apple was in discussions with researchers tocollect people’s DNA data, and a San Francisco startup called Helix, bankrolled with $100 million, said it would launch the first DNA app store for consumers in 2016.

These ideas were part of an emerging boom in consumer use of genomics, which drew in figures like J. Craig Venter. Yet the economics of consumer DNA services remain unclear, partly because DNA predictions aren’t always foolproof or useful. This year, a $699 direct-to-consumer blood test for cancer got a very chilly reception, while pregnancy tests expanded into uncharted territory and sometimesfound cancer by accident. Even better-established cancer tests aren’t proven to really help patients. The leader in tumor DNA testing in the U.S., Foundation Medicine, sold a majority of its shares to Roche, a sign that its future was uncertain.

Making DNA data more useful is the goal of President Obama’s “precision medicine initiative,” a $215 million effort that includes a planned study of the health records and DNA of one million people. Only with big numbers, the government says, will the next wave of links between genes and disease be discovered. Yet big studies could cause big, unexpected problems. In March, the CEO of DeCode Genetics, a subsidiary of Amgen that runs a nationwide gene bank in Iceland, said its database was now so big that it could pinpoint each and every Icelandic woman with a dangerous breast cancer mutation. Yet because of privacy laws, DeCode complained, it is unable to tell them. 
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Cancer Spread Tracked From A Single Cell In A Live Animal

Cancer Spread Tracked From A Single Cell In A Live Animal | Amazing Science | Scoop.it

Researchers at Harvard-affiliated Boston Children’s Hospital have, for the first time, visualized the origins of cancer from the first affected cell and watched its spread in a live animal. Their work, published in the Jan. 29 issue of Science, could change the way scientists understand melanoma and other cancers and lead to new, early treatments before the cancer has taken hold.


“An important mystery has been why some cells in the body already have mutations seen in cancer, but do not yet fully behave like the cancer,” says the paper’s first author, Charles Kaufman, a postdoctoral fellow in the Zon Laboratory at Boston Children’s Hospital. “We found that the beginning of cancer occurs after activation of an oncogene or loss of a tumor suppressor, and involves a change that takes a single cell back to a stem cell state.”


That change, Kaufman and colleagues found, involves a set of genes that could be targeted to stop cancer from ever starting. The study imaged live zebrafish over time to track the development of melanoma. All the fish had the human cancer mutation BRAFV600E — found in most benign moles — and had also lost the tumor suppressor gene p53.


Kaufman and colleagues engineered the fish to light up in fluorescent green if a gene called crestin was turned on — a “beacon” indicating activation of a genetic program characteristic of stem cells. This program normally shuts off after embryonic development, but occasionally, in certain cells and for reasons not yet known, crestin and other genes in the program turn back on.


“Every so often we would see a green spot on a fish,” said Leonard Zon, director of the Stem Cell Research Program at Boston Children’s and senior investigator on the study. “When we followed them, they became tumors 100 percent of the time.”


When Kaufman, Zon, and colleagues looked to see what was different about these early cancer cells, they found that crestin and the other activated genes were the same ones turned on during zebrafish embryonic development — specifically, in the stem cells that give rise to the pigment cells known as melanocytes, within a structure called the neural crest.


“What’s amazing about this group of genes is that they also get turned on in human melanoma,” said Zon, who is also a member of the Harvard Stem Cell Instituteand a Howard Hughes Medical Institute investigator. “It’s a change in cell fate, back to neural crest status.”


Finding these cancer-originating cells was tedious. Wearing goggles and using a microscope with a fluorescent filter, Kaufman examined the fish as they swam around, shooting video with his iPhone. Scanning 50 fish could take two to three hours. In 30 fish, Kaufman spotted a small cluster of green-glowing cells about the size of the head of a Sharpie marker — and in all 30 cases, these spots grew into melanomas. In two cases, he was able to see on a single green-glowing cell and watch it divide and ultimately become a tumor mass.


Via Steven Krohn
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WHO Extremely Alarmed by Zika, Cases Could Reach 4 Million

WHO Extremely Alarmed by Zika, Cases Could Reach 4 Million | Amazing Science | Scoop.it

From October 2015 to January 2016, there were almost 4,000 cases of babies born with microcephaly in Brazil. Before then, there were just 150 cases per year. The suspected culprit is a mosquito-borne virus called Zika. Officials in Colombia, Ecuador, El Salvador and Jamaica have suggested that women delay becoming pregnant. And the Centers for Disease Control and Prevention has advised pregnant women to postpone travel to countries where Zika is active. Zika virus was first detected in Zika Forest in Uganda in 1947 in a rhesus monkey, and again in 1948 in the mosquito Aedes africanus, which is the forest relative of Aedes aegyptiAedes aegypti and Aedes albopictus can both spread Zika. Sexual transmission between people has also been reported.


The World Health Organization says it is likely that the virus will spread, as the mosquitoes that carry the virus are found in almost every country in the Americas. Zika virus was discovered almost 70 years ago, but wasn’t associated with outbreaks until 2007.


The World Health Organization (WHO) expects the Zika virus, which is spreading through the Americas, to affect between three million and four million people, a disease expert said recently. The WHO's director-general said the spread of the mosquito-borne disease had gone from a mild threat to one of alarming proportions.


Marcos Espinal, an infectious disease expert at the WHO's Americas regional office, said: "We can expect 3 to 4 million cases of Zika virus disease". He gave no time frame. There is no vaccine or treatment for Zika, which is a close cousin of dengue and chikungunya and causes mild fever, rash and red eyes. An estimated 80 percent of people infected have no symptoms, making it difficult for pregnant women to know whether they have been infected.


WHO Director-General Margaret Chan said the organization's will convene an emergency committee on Monday to help determine the level of the international response to an outbreak of the virus spreading from Brazil that is believed to be linked to severe birth defects.


"The level of alarm is extremely high," Chan told WHO executive board members at a meeting in Geneva. "As of today, cases have been reported in 23 countries and territories in the (Americas) region."


Brazil's Health Ministry said in November 2015 that Zika was linked to a fetal deformation known as microcephaly, in which infants are born with abnormally small heads Brazil has reported 3,893 suspected cases of microcephaly, the WHO said last week, more than 30 times more than in any year since 2010 and equivalent to 1-2 percent of all newborns in the state of Pernambuco, one of the worst-hit areas.

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Leonardo Wild's curator insight, February 3, 8:24 AM

Of course WHO would. Not much when it comes to drugs that have negative side effects, though, not necessarily blatant death, but certainly can destroy lives. That, though, is a taboo subject ever since Pasteur came on the scene.

8A Saumya's curator insight, February 10, 2:34 AM

                       This article is about the disease Zika virus .Zika was first detected in 1947 in a rhesus monkey. The world health organization says that it is going to spread in every country.There is no vaccine or treatment for this disease. Zika virus causes fever, rash, joint pain and bloodshot eyes in about 20 per cent of the people.It is a common disease in Africa as well as Asia. Zika virus was discovered almost 70 years ago, but wasn't associated with outbreaks until 2007. An estimated 80 percent of people infected have no symptoms, making it difficult for pregnant women to know whether they have been infected.In this disease the head of a new born baby become more shorter compared to another new born baby. 

                   From this article I learned that their are lots of diseases going on in Africa.People in Africa struggles a lot with harmful diseases like Zika virus which doesn't have any vaccine or treatment.I also get to know that lot people are struggling their with diseases caused like dengue and  malaria and chicken guinea.I also learned this is because of dirty water,pollution and maybe lack of resources.I could also guess they need some more facilities like hospital,school and at least food from everyone.This tells me that how struggling and hard it would be to live in Africa.  

                         

http://www.lifehacker.com.au/2016/02/your-non-alarmist-guide-to-the-zika-virus/ 

http://www.scientificamerican.com/article/who-extremely-alarmed-by-zika-cases-could-reach-4-million/

 

 

 

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Bed bugs have recently developed a resistance to the most widely used insecticide

Bed bugs have recently developed a resistance to the most widely used insecticide | Amazing Science | Scoop.it

Bed bugs have developed a resistance to neonicotinoids, a group of the most widely used insecticides, according to a new study published in the Journal of Medical EntomologyIf neonicotinoids no longer work against the elusive and resilient creatures, bed bugs will continue to thrive despite exterminators’ efforts.


Products developed over the past few years to control bed bugs combine neonicotinoids, or neonics, with pyrethroids, another class of insecticide. The newly found resistance to neonics has real implications for people who need to control the pest, which are most often found in human dwellings such as apartments or condominiums, single-family homes and hotels or motels, according to the 2015 Bugs Without Borders Survey.


Neonics are the most commonly used insecticide to fight the already elusive and resilient bed bugs, and if they no longer work, bed bugs will continue to thrive despite exterminators’ efforts. Study authors Alvaro Romero, from New Mexico State University, and Troy Anderson, from Virginia Tech, discovered the resistance by collecting bed bugs from human dwellings in Cincinnati and Michigan and exposing them to four different neonics: acetamiprid, dinotefuran, imidacloprid and thiamethoxam.


Romero and Anderson applied the same neonics to a bed bug colony kept by entomologist Harold Harlan for more than 30 years without exposure to insecticide, and to a pyrethroid-resistant population from Jersey City, New Jersey, that had not been exposed to neonics since 2008.


Harlan’s bed bugs died after exposure to small amounts of neonics. The Jersey City bed bugs died when exposed to imidacloprid and thiamethoxam but resisted the other two neonics. According to Romero and Anderson, the neonic resistance in the Jersey City bed bugs could be credited to pre-existing resistance mechanisms. Bed bugs produce “detoxifying enzymes” to counter exposure to insecticides, and the researchers found that the Jersey City bed bugs had higher levels of the enzymes than did the Harlan bed bugs.

“Elevated levels of detoxifying enzymes induced by other classes of insecticides might affect the performance of newer insecticides,” Romero said.


The bed bugs collected from Cincinnati and Michigan proved to be tougher, with a much higher resistance to neonics than the Harlan and Jersey City bed bugs. Compared with Harlan’s bed bugs, the Michigan creatures were 462 times more resistant to imidacloprid, 198 times more resistant to dinotefuran, 546 times more resistant to thiamethoxam and 33,333 times more resistant to acetamiprid.

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Using CRISPR-CAS and Precision Medicine to Treat Vision Loss and Blindness

Using CRISPR-CAS and Precision Medicine to Treat Vision Loss and Blindness | Amazing Science | Scoop.it

Columbia University Medical Center (CUMC) and University of Iowa scientists have used a new gene-editing technology called CRISPR to repair a genetic mutation responsible for retinitis pigmentosa (RP), an inherited condition that causes the retina to degrade and leads to blindness in at least 1.5 million cases worldwide.


The study was published in Scientific Reports, and marks the first time researchers have replaced a defective gene associated with a sensory disease in stem cells that were derived from a patient’s tissue.


Our vision is to develop a personalized approach to treating eye disease,” says Stephen Tsang, MD, PhD, the László Z. Bitó Associate Professor of Ophthalmology and associate professor of Pathology & Cell Biology at CUMC, ophthalmologist at NewYork-Presbyterian/Columbia, and one of the study’s senior authors. “We still have some way to go, but we believe that the first therapeutic use of CRISPR will be to treat an eye disease. Here we have demonstrated that the initial steps are feasible.”


In the study, the researchers created stem cells from a sample of skin that was taken from a patient with retinitis pigmentosa. As the patient-derived stem cells still harbored the disease-causing mutation, the teams used CRISPR to repair the defective gene. The stem cells can potentially be transformed into healthy retinal cells and transplanted back into the same patient to treat vision loss.


“The X-linked form of retinitis pigmentosa is an ideal candidate for a precision medicine approach because a common mutation accounts for 90% cases,” Tsang explains. Using CRISPR —which is easily adaptable to diverse sequences of DNA, and allows for fast and accurate editing —scientists can take a patient’s own cells and make pinpoint repairs specific to that individual’s genome.


Because the corrections are made in cells derived from the patient’s own tissue, doctors can re-transplant the cells with fewer fears of rejection by the immune system. Previous clinical trials have shown that generating retinal cells from embryonic stem cells and using them for transplantation is a safe and potentially effective procedure.

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New handheld miniature microscope could ID cancer cells in doctor’s offices and operating rooms

New handheld miniature microscope could ID cancer cells in doctor’s offices and operating rooms | Amazing Science | Scoop.it

A miniature handheld microscope being developed by University of Washington mechanical engineers could allow neurosurgeons to differentiate cancerous from normal brain tissue at cellular level in real time in the operating room and determine where to stop cutting.


The new technology is intended to solve a critical problem in brain surgery: to definitively distinguish between cancerous and normal brain cells, during an operation, neurosurgeons would have stop the operation and send tissue samples to a pathology lab — where they are typically frozen, sliced, stained, mounted on slides and investigated under a bulky microscope.


Developed in collaboration with Memorial Sloan Kettering Cancer Center, Stanford University and the Barrow Neurological Institute, the new microscope is outlined in an open-access paper published in January in the journalBiomedical Optics Express.


“Surgeons don’t have a very good way of knowing when they’re done cutting out a tumor,” said senior author Jonathan Liu, UW assistant professor of mechanical engineering. “They’re using their sense of sight, their sense of touch, and pre-operative images of the brain — and oftentimes it’s pretty subjective. “Being able to zoom and see at the cellular level during the surgery would really help them to accurately differentiate between tumor and normal tissues and improve patient outcomes.”


The handheld microscope, roughly the size of a pen, combines technologies in a novel way to deliver high-quality images at faster speeds than existing devices. Researchers expect to begin testing it as a cancer-screening tool in clinical settings next year.

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Searching for Cancer Maps in Free-Floating Cell-Free DNA

Searching for Cancer Maps in Free-Floating Cell-Free DNA | Amazing Science | Scoop.it
A new study suggests that one day a simple blood test may tell doctors whether you have the disease and, if so, where it is.


Loose pieces of DNA course through our veins. As cells in our body die, they cast off fragments of genes, some of which end up in the bloodstream, saliva and urine. Cell-free DNA (cfDNA) is like a message in a bottle, delivering secrets about what’s happening inside our bodies. Pregnant women, for example, carry cell-free DNA from their fetuses. A test that analyzes fetal DNA has proved to be more accurate in screening for Down syndrome than standard blood tests.


In 2012, Jay Shendure, a geneticist at the University of Washington, and his colleagues were able to reconstruct the entire genome of a fetus from cell-free DNA in a pregnant woman’s saliva. A team of Stanford University researchers collected DNA fragments from the blood of patients who had received heart transplants and managed to find DNA from their donated hearts. Tellingly, levels were highest in patients who were rejecting their hearts.


These days, scientists are especially excited by the prospect of using cell-free DNA to test for cancer. Instead of relying on invasive biopsies, they hope to find blood-borne fragments that carry distinctive cancer mutations.


Unfortunately, the genetic sequence of a piece of cell-free DNA doesn’t tell researchers where in the body it originated — a valuable clue for doctors looking for diseases. “Knowing the origin of circulating DNA is of great importance,” said Alain R. Thierry, director of research at France’s National Institute of Health and Medical Research.


All the cells in our body typically descend from a single fertilized egg, and they inherit all the same genes. The reason we aren’t uniform sacs of protoplasm is that our cells turn those same genes on and off in distinctive patterns, thereby developing into different tissues. In a study published on Thursday in the journal Cell, Dr. Shendure and his colleagues took some important steps toward identifying the origins of free-floating DNA. To do so, they took advantage of a way that cells control their genes.


As it turns out, different types of cells squirrel away different stretches of DNA in nucleosomes. One of Dr. Shendure’s graduate students, Matthew W. Snyder, wondered what happened to those nucleosomes in dying cells. A cell ending its useful life is shredded by enzymes. But nucleosomes, Mr. Snyder suggested, might shield the DNA they’ve hidden. If so, then much of the cell-free DNA that scientists collect from blood samples should have come from nucleosomes. They could reveal the pattern of nucleosomes in the cells they came from — and thus tell researchers which kind of cell produced it.


Mr. Snyder and his colleagues put the idea to the test. They searched the blood of healthy individuals for cell-free DNA, and then searched a map of the human genome to figure out where each fragment came from. Much of the cell-free DNA came from regions in or around nucleosomes, just as Mr. Snyder had suggested. The scientists then looked at the patterns of nucleosomes in different types of cells. They found that all the healthy subjects produced cell-free DNA that mainly came from nucleosomes found in blood cells.


But when they looked at cell-free DNA from people with advanced cancer, the picture was different. In a patient with lung cancer, for example, the team found that the cell-free DNA fit a different pattern — one belonging to a type of lung cancer cell. The researchers went on to match cell-free DNA in other cancer patients to the types of cancer they had.


Dr. Thierry, who was not involved in the research, said the findings might eventually make it possible to use cell-free DNA to find important clues about diseases. Doctors might be able to use it to figure out the location of hard-to-find cancers, for example. It could provide clues to diseases other than cancers as well. Free-floating genes shed by the heart, for example, might reveal damage from a heart attack. Cell-free DNA from neurons might signal a stroke.

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Optics Supervision: Can we one day do whole body imaging with regular light?

Optics Supervision: Can we one day do whole body imaging with regular light? | Amazing Science | Scoop.it

It seemed too good to be true, says Allard Mosk. It was 2007, and he was working with Ivo Vellekoop, a student in his group at the University of Twente in Enschede, the Netherlands, to shine a beam of visible light through a 'solid wall' — a glass slide covered with white paint — and then focus it on the other side. They did not have a particular application in mind. “I really just wanted to try this because it had never been done before,” Mosk says. And in truth, the two researchers did not expect to pick up much more than a faint blur.

 

But as it turned out, their very first attempt1 produced a sharp pinprick of light a hundred times brighter than they had hoped for. “This just doesn't happen on the first day of your experiment,” exclaims Mosk. “We thought we'd made a mistake and there must be a hole in our slide letting the light through!”

 

But there was no hole. Instead, their experiment became the first of two independent studies1, 2that were carried out that year pioneering ways to see through opaque barriers. So far it is still a laboratory exercise. But progress has been rapid.

 

Researchers have now managed to obtain good-quality images through thin tissues such as mouse ears3, and are working on ways to go deeper. And if they can meet the still-daunting challenges, such as dealing with tissues that move or stretch, potential applications abound. Visible-light images obtained from deep within the body might eliminate the need for intrusive biopsies, for example. Or laser light could be focused to treat aneurysms in the brain or target inoperable tumours without the need for surgery.

 

“Just ten years ago, we couldn't imagine high-resolution imaging down to even 1 centimetre in the body with optical light, but now that has now become a reality,” says Lihong Wang, a biomedical engineer at Washington University in St. Louis, Missouri. “Call me crazy, but I believe that we will eventually be doing whole-body imaging with optical light.”

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First gene for grey hair found

First gene for grey hair found | Amazing Science | Scoop.it

Published in Nature Communications, the BBSRC-funded study analysed a population of over 6,000 people with varied ancestry across Latin America to identify new genes associated with hair color, greying, density and shape, i.e. straight or curly. “We already know several genes involved in balding and hair color but this is the first time a gene for greying has been identified in humans, as well as other genes influencing hair shape and density,” said lead author, Dr Kaustubh Adhikari, UCL Cell & Developmental Biology.

 

“It was only possible because we analysed a diverse melting pot of people, which hasn’t been done before on this scale. These findings have potential forensic and cosmetic applications as we increase our knowledge on how genes influence the way we look.”

 

The findings could help develop forensic DNA technologies that build visual profiles based on an individual’s genetic makeup. Research in this field has previously used samples from people of European descent, but these new results could help forensic reconstructions in Latin America and East Asia.

 

The gene identified for grey hair – IRF4 – is known to play a role in hair color but this is the first time it has been associated with the greying of hair. This gene is involved in regulating production and storage of melanin, the pigment that determines hair, skin and eye color.

 

Hair greying is caused by an absence of melanin in hair so the scientists want to find out IRF4’s role in this process. Understanding how IRF4 influences hair greying could help the development of new cosmetic applications that change the appearance of hair as it grows in the follicle by slowing or blocking the greying of hair.

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Cancer cell imaging in 3D

Cancer cell imaging in 3D | Amazing Science | Scoop.it

Cancer cells don’t live on glass slides. Yet the vast majority of images related to cancer biology come from the cells being photographed on flat, two-dimensional surfaces — images sometimes used to draw conclusions about the behavior of cells that normally reside in a more complex environment.


Now a new high-resolution microscope, presented (open access) February 22 in Developmental Cell, makes it possible to visualize cancer cells in 3D and record how they are signaling to other parts of their environment — revealing previously unappreciated biology of how cancer cells survive and disperse within living things. Based on ”microenvironmental selective plane illumination microscopy” (meSPIM),  the new microscope is designed to image cells in microenvironments free of hard surfaces near the sample.


“There is clear evidence that the environment strongly affects cellular behavior — thus, the value of cell culture experiments on glass must at least be questioned,” says senior author Reto Fiolka, an optical scientist at the University of Texas Southwestern Medical Center. “Our microscope is one tool that may bring us a deeper understanding of the molecular mechanisms that drive cancer cell behavior, since it enables high-resolution imaging in more realistic tumor environments.”


In their study, Fiolka and colleagues, including co-senior author Gaudenz Danuser, and co-first authors Meghan Driscoll and Erik Welf, also of UT Southwestern, used their microscope to image different kinds of skin cancer cells from patients. They found that in a 3D environment (where cells normally reside), unlike a glass slide, multiple melanoma cell lines and primary melanoma cells (from patients with varied genetic mutations) form many small protrusions called blebs.


One hypothesis is that this blebbing may help the cancer cells survive or move around and could thus play a role in skin cancer cell invasiveness or drug resistance in patients.


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This 3D Printer Prints Bone, Cartilage, and Muscle

This 3D Printer Prints Bone, Cartilage, and Muscle | Amazing Science | Scoop.it

A team of biomedical researchers at Wake Forest Institute for Regenerative Medicine has just completed an invention 10 years in the making. It's a 3D printer that can craft relatively simple tissues like cartilage into large complex shapes—like an infant's ear. Using cartridges that are brimming with biodegradable plastic and human cells bound up in gel, this new kind of 3D printer builds complex chunks of growing muscle, cartilage, and even bone. When implanted into animals, these simple fabricated tissues survive and thrive indefinitely.


The scientists led by Anthony Atala surmounted two particularly thorny challenges that have long impeded the futuristic goal of printing living human tissues. First, their new device manufactures large, stable chunks of printed tissue that don't fall apart. Second, it keeps those large structures alive and growing. The new 3D printer is unveiled and outlined today in the journal Nature Biotechnology.


"This is the first bioprinter that can print tissue at the large scales relevant for human implantation,"  Atala says. "Basically, once we've printed a structure, we can keep it alive for several weeks before we implant it. Now the next step is to test these [printed tissues] for safety so we can implant them in the future in patients."


Atala's new device—named the Integrated Tissue and Organ Printing System, or ITOP—is straightforward. The programmed printer slowly squirts out layer upon layer of a rapidly hardening material in the form of tiny droplets. Like other 3D printers, this layered approach allows ITOP to print highly complex shapes in three dimensions with incredible detail. The materials ITOP uses, and the way it structures the tissues that it builds, are what make this machine revoutionary.

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tt2561's curator insight, May 1, 10:47 AM

Regenerative medicine...

 

Astounding!

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We Have the Technology to Destroy All Zika Virus Spreading Mosquitoes

We Have the Technology to Destroy All Zika Virus Spreading Mosquitoes | Amazing Science | Scoop.it

A controversial genetic technology able to wipe out the mosquito carrying the Zika virus will be available within months, scientists say. The technology, called a “gene drive,” was demonstrated only last year in yeast cells, fruit flies, and a species of mosquito that transmits malaria. It uses the gene-snipping technology CRISPR to force a genetic change to spread through a population as it reproduces.


Three U.S. labs that handle mosquitoes, two in California and one in Virginia, say they are already working toward a gene drive for Aedes aegypti, the type of mosquito blamed for spreading Zika. If deployed, the technology could theoretically drive the species to extinction.

“We could have it easily within a year,” says Anthony James, a molecular biologist at the University of California, Irvine.


Any release of a gene drive in the wild would be hotly debated by ecologists. So far, no public health agency has thrown its weight behind the idea. But with Zika sowing fear across Latin America and beyond, the technology is likely to get a closer look. “Four weeks ago we were trying to justify why we are doing this. Now they’re saying ‘Get the lead out,’” says James. “It’s absolutely going to chan­­­­­­­­­ge the conversation.”


The Zika virus is now spreading “explosively" in the Americas, according to the World Health Organization, which last week declared a global health emergency. While the virus causes only a mild rash, the epidemic is frightening because of a suspected link to 4,000 children born in Brazil with microcephaly, or shrunken heads.


There’s no easy way to stop Zika. There is no vaccine and developing one could take several years. Brazil is sending 220,000 soldiers door-to-door to check for mosquitoes breeding in old tires and swimming pools. Women are being asked to delay pregnancy. Gene-drive technology could be ready sooner than a vaccine, but it’s no quick fix, either, scientists caution. Self-annihilating mosquitoes will first have to undergo tests in the lab, then perhaps on an island, before they could be released more broadly. Regulations and public debate could stretch the time line out for years.


The Aedes aegypti mosquito is not native to the Americas. It’s an invasive species that is now found from Florida to Argentina and whose range could expand with climate change. In addition to the Zika virus, its bite also transmits the chikinguya and dengue viruses. Dengue fever causes 100 million people to fall ill each year. Because of the extent of the problems Aedesaegypti causes, some scientists favor using advanced technology to drive the species to extinction, at least in the Americas. “These mosquitoes truly have little value,” says Zach Adelman, an entomologist at Virginia Tech who works with Aedes aegypti. “People in favor of eradication are going to be able to plead their case.”

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Corie Rosen's curator insight, February 10, 11:15 PM

I hate mosquitoes as much as the next person, but from an ecological perspective, this is not a good idea. The Aedes aegypti does cause a lot of damage and suffering, and that is truly awful, but who are we to play God? Why should we decide what species lives and dies? As much as we hate them, mosquitoes provide an ecological niche. Even Aedes aegypti does. Even if we wipe them out, there is no telling what the consequences of that will be. Mother Nature may unleash a creature even worse than Aedes aegypti to take over that niche, and we don’t want or need that to happen! There is also the possibility of these mosquitoes becoming resistant to genetic modification. Should that end up happening, then what would we be left with? The problem is that we just don’t know, nor can scientists predict, what would happen if we go through with this, and that is scary!

 

I found this article to be pretty biased. As I stated before, I hate mosquitos as much as the next guy, but the article seems to suggest that this is the best solution we have to combat the Zika virus, which is ironic seeing as how they also mention the possibility of a vaccine in the same article! Vaccines have protected mankind from thousands of disease-causing organisms for decades, so I for one don't buy the whole controversy linking them to autism. Even if it takes awhile for one to be produced, that would be far safer than potentially causing environmental harm using CRISPR.

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Hydrogels can put stem cells to sleep

Hydrogels can put stem cells to sleep | Amazing Science | Scoop.it

Unlike normal cells, stem cells are pluripotent -- they can become any cell type, which makes them powerful potential treatments for diseases such as diabetes, leukemia and age-related blindness. However, maintaining this versatility until the time is right is a major challenge. This week in ACS Central Science, researchers reveal that mimicking a natural process called diapause can halt stem cells, effectively putting them to sleep for up to two weeks.


Recently, scientists have shown that growing pluripotent stem cells (PSCs) on different kinds of surfaces can cause them to differentiate into specific cell types. Based on these observations, Steve Armes, Harry Moore, Irene Canton, Nick Warren and colleagues postulated that the right sort of environment could stop them from differentiating altogether. They were inspired by the fact that certain mammals such as kangaroos can choose to delay gestation, a process known as embryonic diapause, in order to make sure that their offspring are born when conditions are most favorable. Embryos exhibiting diapause are often covered in a soft protective layer of mucus, so the team created very soft hydrogels using a synthetic polymer that mimicked this natural material. When pluripotent stem cells were placed within the hydrogel, the cells essentially stopped growing and differentiating at human body temperature. Cooling turned the gel into a liquid, enabling the stem cells to be easily removed when required. On removal, the cells 'woke up' and began proliferating again within one day. Such hydrogels could be used to store and ship stem cells much more easily and cheaply than at present. Further, the team notes that human embryos also appear to enter diapause when placed in such hydrogels. This suggests that simply creating the right physical environment may be sufficient to delay gestation, which has not previously been observed for human embryos.


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Future of drug delivery in a crystal ball 100 times stronger than liposomes

Future of drug delivery in a crystal ball 100 times stronger than liposomes | Amazing Science | Scoop.it

A Drexel University materials scientist has discovered a way to encapsulate medication to deliver it more effectively inside the body. Until now, crystals have grown in rigid, structured formations (like the snowflake) — with a web of straight lines connecting to making a grid that grows into the crystalline flake.*


But the formation of a crystal is affected by the environment in which it forms. And Christopher Li, PhD, a professor in the College of Engineering and head of the Soft Materials Lab in the Department of Materials Science & Engineering, uses this workaround to engineer hollow crystal spheres. He recently reported his finding in Nature Communications(open access).


Li was able to overcome crystal’s edge-forming tendencies by creating a tiny bubble of oil to encase water molecules. When the surfactant bubble was cooled to the appropriate temperature, the molecules inside began to crystalize. But rather than forming an angular web of connections, the molecules, instead, lined up along the interior of the oil bubble — crystallizing in a hollow, spherical shape.


Early tests indicate that Li’s “crystalsome” (named for their similarity to liposomes — tiny bubbles with the same membrane as cells that are being explored for use as biological packages for delivering drug treatments) is a few hundred times stronger than liposomes, making them a sturdier option for medicine encapsulation.

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No more insulin injections? Encapsulated pancreatic cells offer new possibilities

No more insulin injections? Encapsulated pancreatic cells offer new possibilities | Amazing Science | Scoop.it
Researchers have designed a material that prevents transplanted human islet cells from being attacked by the immune system in patients with Type 1 diabetes. The advance could help patients control their blood sugar without taking drugs.


Since the 1980s, a standard treatment for diabetic patients has been injections of insulin produced by genetically engineered bacteria. While effective, this type of treatment requires great effort by the patient and can generate large swings in blood sugar levels.


At the urging of JDRF director Julia Greenstein, Anderson, Langer, and colleagues set out several years ago to come up with a way to make encapsulated islet cell transplantation a viable therapeutic approach. They began by exploring chemical derivatives of alginate, a material originally isolated from brown algae. Alginate gels can be made to encapsulate cells without harming them, and also allow molecules such as sugar and proteins to move through, making it possible for cells inside to sense and respond to biological signals.


However, previous research has shown that when alginate capsules are implanted in primates and humans, scar tissue eventually builds up around the capsules, making the devices ineffective. The MIT/Children’s Hospital team decided to try to modify alginate to make it less likely to provoke this kind of immune response.


“We decided to take an approach where you cast a very wide net and see what you can catch,” says Arturo Vegas, a former MIT and Boston Children’s Hospital postdoc who is now an assistant professor at Boston University. Vegas is the first author of the Nature Biotechnology paper and co-first author of the Nature Medicine paper.


“We made all these derivatives of alginate by attaching different small molecules to the polymer chain, in hopes that these small molecule modifications would somehow give it the ability to prevent recognition by the immune system.”


After creating a library of nearly 800 alginate derivatives, the researchers performed several rounds of tests in mice and nonhuman primates. One of the best of those, known as triazole-thiomorpholine dioxide (TMTD), they decided to study further in tests of diabetic mice. They chose a strain of mice with a strong immune system and implanted human islet cells encapsulated in TMTD into a region of the abdominal cavity known as the intraperitoneal space.


The pancreatic islet cells used in this study were generated from human stem cells using a technique recently developed by Douglas Melton, a professor at Harvard University who is an author of the Nature Medicine paper. Following implantation, the cells immediately began producing insulin in response to blood sugar levels and were able to keep blood sugar under control for the length of the study, 174 days.


“The really exciting part of this was being able to show, in an immune-competent mouse, that when encapsulated these cells do survive for a long period of time, at least six months,” says Omid Veiseh, a senior postdoc at the Koch Institute and Boston Children’s hospital, co-first author of the Nature Medicine paper, and an author of the Nature Biotechnology paper. “The cells can sense glucose and secrete insulin in a controlled manner, alleviating the mice’s need for injected insulin.”

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New gadget analyses your sweat - and it could replace blood tests in future

New gadget analyses your sweat - and it could replace blood tests in future | Amazing Science | Scoop.it

Researchers have developed a prototype that packs five sensors onto a flexible circuit board. The wearable device is able to measure biomarkers in sweat and could one day replace health-monitoring blood tests, scientists have said. By analyzing a person's sweat, the device can measure glucose, lactate - a marker of low oxygen levels in the body - sodium, potassium and skin temperature. The results can be transmitted to wi-fi devices such as smart phones.


Inventor Professor Ali Javey, from the University of California at Berkeley (UC Berkeley), US, said: "Human sweat contains physiologically rich information, thus making it an attractive body fluid for non-invasive wearable sensors. However, sweat is complex and it is necessary to measure multiple targets to extract meaningful information about your state of health. In this regard, we have developed a fully integrated system that simultaneously and selectively measures multiple sweat analytes, and wirelessly transmits the processed data to a smartphone. Our work presents a technology platform for sweat-based health monitors."


Colleague Professor George Brooks, also from UC Berkeley, said: "Having a wearable sweat sensor is really incredible because the metabolites and electrolytes measured by the Javey device are vitally important for the health and well-being of an individual. He explains: "When studying the effects of exercise on human physiology, we typically take blood samples. With this non-invasive technology, someday it may be possible to know what's going on physiologically without needle sticks or attaching little disposable cups on you."

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ATF6 Gene Mutation: A New Color Blindness Cause Identified

ATF6 Gene Mutation: A New Color Blindness Cause Identified | Amazing Science | Scoop.it
A rare eye disorder marked by color blindness, light sensitivity, and other vision problems can result from a newly discovered gene mutation identified by an international research team, including scientists from Columbia University Medical Center (CUMC). The findings, which were published today in the online edition of Nature Genetics, could lead to new, targeted treatments for this form of color blindness.

The researchers found that mutations to a gene called ATF6, a key regulator of the unfolded protein response, can lead to achromatopsia, a hereditary visual disorder characterized by color blindness, decreased vision, light sensitivity, and uncontrolled eye movement in children.

The unfolded protein response is a mechanism cells use to prevent the dangerous accumulation of unfolded or mis-folded proteins.

Based on mouse studies, the researchers suspect that the cone cells of people with achromatopsia are not permanently damaged and could be revived by enhancing the pathway that regulates the unfolded protein response. “Several drugs that activate this pathway have already been approved by the FDA for other conditions and could potentially benefit patients with achromatopsia,” said one of the study leaders, Stephen Tsang, MD, PhD, who is the Laszlo Z. Bito Associate Professor of Ophthalmology, and is affiliated with the Institute of Human Nutrition, at CUMC.

“Dr. Tsang’s innovative research continues to unfold the genetic basis for a variety of ocular diseases. This finding is an example of the finest clinically based science that will ultimately allow us to overcome preventable vision loss,” said George A. Cioffi, MD, Edward S. Harness Chairman and Ophthalmologist-in-Chief at NewYork-Presbyterian Hospital/Columbia University Medical Center.

“Five genes had previously been linked to achromatopsia; however, they accounted for only about half of all cases,” said Dr. Tsang. “Using next-generation gene sequencing on a small group of patients, we found that mutations in a sixth gene—ATF6—can independently lead to the disease.”
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University of Iowa researchers reveal how cancer cells form tumors

University of Iowa researchers reveal how cancer cells form tumors | Amazing Science | Scoop.it



Two University of Iowa studies offer key insights by recording in real time, and in 3–D, the movements of cancerous human breast tissue cells. It's believed to be the first time cancer cells' motion and accretion into tumors has been continuously tracked. (See accompanying videos.)


The team discovered that cancerous cells actively recruit healthy cells into tumors by extending a cable of sorts to grab their neighbors—both cancerous and healthy—and reel them in. Moreover, the Iowa researchers report that as little as five percent of cancerous cells are needed to form the tumors, a ratio that heretofore had been unknown. “It’s not like things sticking to each other,” said David Soll, biology professor at the UI and corresponding author on the paper, published in the American Journal of Cancer Research. “It’s that these cells go out and actively recruit. It’s complicated stuff, and it’s not passive. No one had a clue that there were specialized cells in this process, and that it’s a small number that pulls all the rest in.”


The findings could lead to a more precise identification of tumorigenic cells (those that form tumors) and testing which antibodies would be best equipped to eliminate them. Soll's Monoclonal Antibody Research Institute and the Developmental Studies Hybridoma Bank, created by the National Institutes of Health as a national resource, directed by Soll and housed at the UI, together contain one of the world’s largest collections of antibodies that could be used for the anti-cancer testing, based on the new findings.


In a paper published last spring in the journal PLOS One, Soll’s team showed that only cancerous cells (from a variety of cancers, including lung, skin, and aggressive brain tumors known as glioblastomas) engaged in tumor formation by actively soliciting other cells. Like evil-minded envoys, individual cancer cells extend themselves outward from the original cluster, probing for other cells in the area, the researchers observed. Once it detects one, the extended cell latches on and pulls it in, forming a larger mass. The activity continues, the cancerous extensions drawing in more and more cells—including healthy cells—as the tumor enlarges. “There’s nothing but tumorigenic cells in the bridge (between cells),” Soll said, “and that’s the discovery. The tumorigenic cells know what they’re doing. They make tumors.”


The question is how these cells know what to do. Soll hypothesizes they’re reaching back to a primitive past, when these cells were programmed to form embryos. If true, perhaps the cancerous cells—masquerading as embryo-forming cells—recruit other cells to make tissue that then forms the layered, self-sustaining architecture needed for a tumor to form and thrive.



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How the GyroGlove Steadies Hands of Parkinson’s Patients

How the GyroGlove Steadies Hands of Parkinson’s Patients | Amazing Science | Scoop.it
A wearable device promises to help steady hand tremors by using an old technology—gyroscopes.


When he was a 24-year-old medical student living in London, Faii Ong was assigned to care for a 103-year-old patient who suffered from Parkinson’s, the progressive neurological condition that affects a person’s ease of movement. After watching her struggle to eat a bowl of soup, Ong asked another nurse what more could be done to help the woman. “There’s nothing,” he was grimly told.


Ong, now 26, didn’t accept the answer. He began to search for a solution that might offset the tremulous symptoms of Parkinson’s, a disease that affects one in 500 people, not through drugs but physics. After evaluating the use of elastic bands, weights, springs, hydraulics, and even soft robotics, Ong settled on a simpler solution, one that he recognized from childhood toys. “Mechanical gyroscopes are like spinning tops: they always try to stay upright by conserving angular momentum,” he explains. “My idea was to use gyroscopes to instantaneously and proportionally resist a person’s hand movement, thereby dampening any tremors in the wearer’s hand.”


Together with a number of other students from Imperial College London, Ong worked in the university’s prototyping laboratory to run numerous tests. An early prototype of a device, called GyroGlove, proved his instinct correct. Patients report that wearing the GyroGlove, which Ong believes to be the first wearable treatment solution for hand tremors, is like plunging your hand into thick syrup, where movement is free but simultaneously slowed. In benchtop tests, the team found the glove reduces tremors by up to 90 percent.


GyroGlove’s design is simple. It uses a miniature, dynamically adjustable gyroscope, which sits on the back of the hand, within a plastic casing attached to the glove’s material. When the device is switched on, the battery-powered gyroscope whirs to life. Its orientation is adjusted by a precession hinge and turntable, both controlled by a small circuit board, thereby pushing back against the wearer’s movements as the gyroscope tries to right itself.


While the initial prototypes of the device still require refinements to size and noise, Alison McGregor, professor of musculoskeletal biodynamics at Imperial College, who has been a mentor to the team, says the device “holds great promise and could have a significant impact on users’ quality of life.” Helen Matthews of the Cure Parkinson’s Trust agrees: “GyroGlove will make everyday tasks such as using a computer, writing, cooking, and driving possible for sufferers,” she says.

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Mike Oehme's curator insight, January 26, 2:47 AM

Interesting idea, unfortunately I don't have a gyro trainer at home anymore