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Slips of the lip stay all in the family: dogs included, but not the cat

It’s happened to many of us: While looking right at someone you know very well, you open your mouth and blurt out the wrong name. The name you blurt is not just any old name, though, says new research from Duke University that finds “misnaming” follows predictable patterns.

Among people who know each other well, the wrong name is usually plucked from the same relationship category, the study finds. Friends call each other by other friends’ names, and family members by other family members’ names. And that includes the family dog.

“It’s a cognitive mistake we make, which reveals something about who we consider to be in our group,” said Duke psychology and neuroscience professor David Rubin, one of the study authors. “It’s not just random.”

The new paper, based on five separate surveys of more than 1,700 respondents, appears online this week in the journal Memory and Cognition. Many of the patterns didn’t surprise lead author Samantha Deffler, a Ph.D. student at Duke. One did, though.

In addition to mixing up sibling for sibling and daughter for son, study participants frequently called other family members by the name of the family pet — but only when the pet was a dog. Owners of cats or other pets didn’t commit such slips of the tongue. Deffler says she was surprised how consistent that finding was, and how often it happened.

“I’ll preface this by saying I have cats and I love them,” Deffler says. “But our study does seem to add to evidence about the special relationship between people and dogs.

“Also, dogs will respond to their names much more than cats, so those names are used more often. Perhaps because of that, the dog’s name seems to become more integrated with people’s conceptions of their families.”

Phonetic similarity between names helps fuel mix-ups too, the authors found. Names with the same beginning or ending sounds, such as Michael and Mitchell or Joey and Mikey, were more likely to be swapped. So were names that shared phonemes, or sounds, such as John and Bob, which share the same vowel sound.

Physical similarities between people, on the other hand, played little to no role. For instance, parents were inclined to swap their children’s names even when the children looked nothing alike and were different genders. It’s not a question of aging, either: The authors found plenty of instances of misnaming among college undergraduates.

Although misnaming is a common theme in popular culture, Deffler said the new study is one of few describing how the phenomenon works.

Deffler is no stranger to the experience in her own life. Her graduate supervisor frequently swaps the names of his two graduate assistants. And growing up, she said, her mom often called her Rebecca, Jesse or Molly — the names of her sister, brother and the family pit bull.

“I’m graduating in two weeks and my siblings will all be there,” Deffler said. “I know my mom will make mistakes.”

Now she knows why.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/05/160516181217.htm  Original web page at Science Daily

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Islet transplantation restores blood sugar awareness and control in type 1 diabetes

New clinical trial results show that transplantation of pancreatic islets–cell clusters that contain insulin-producing cells–prevents severe, potentially life-threatening drops in blood sugar in people with type 1 diabetes. Researchers found that the treatment was effective for people who experienced episodes of severe hypoglycemia–low blood sugar levels that can lead to seizures, loss of consciousness and death–despite receiving expert care.

The Phase 3 trial was funded by the National Institute of Allergy and Infectious Diseases (NIAID) and the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), both part of the National Institutes of Health, and was conducted by the NIH-sponsored Clinical Islet Transplantation (CIT) Consortium. The investigators designed the study in consultation with the U.S. Food and Drug Administration to enable potential future licensure of the manufacture of purified human pancreatic islets. The results appear online today in Diabetes Care.

“The findings suggest that for people who continue to have life-altering severe hypoglycemia despite optimal medical management, islet transplantation offers a potentially lifesaving treatment that in the majority of cases eliminates severe hypoglycemic events while conferring excellent control of blood sugar,” said NIAID Director Anthony S. Fauci, M.D.

As expected, the treatment carried risks, including infections and lowered kidney function as a result of people taking the immune-suppressing drugs needed to prevent rejection of the donor islets. Although some of the side effects were serious, none led to death or disability. In the United States, islet transplantation is currently available only in clinical trials.

“While still experimental, and with risks that must be weighed carefully, the promise of islet transplantation is undeniable and encouraging,” said NIDDK Director Griffin P. Rodgers, M.D. “Even with the best care, about 30 percent of people with type 1 diabetes aren’t aware of dangerous drops in blood glucose levels.”

In type 1 diabetes, the immune system attacks and destroys insulin-producing cells in the islets of the pancreas. People with type 1 diabetes need lifelong treatment with insulin, which helps transport the sugar glucose from the bloodstream into cells, where it serves as a key energy source. Even with insulin therapy, people with type 1 diabetes frequently experience fluctuations in blood sugar levels.

Hypoglycemia, or low blood sugar, typically is accompanied by symptoms such as tremors, sweating and heart palpitations that prompt people to eat or drink to raise their blood sugar levels. Those who do not experience these early warning signs–a condition called impaired awareness of hypoglycemia–are at increased risk for severe hypoglycemic events, during which the person is unable to treat himself or herself. Treatments such as behavioral therapies or continuous glucose-monitoring systems can prevent these events in many–but not all–people with this impaired awareness, leaving a substantial number of people at risk.

The current study enrolled 48 people who had persistent impaired awareness of hypoglycemia and experienced severe hypoglycemic events despite expert care by a diabetes specialist or endocrinologist. Investigators at eight study sites in North America used a standardized manufacturing protocol to prepare purified islets from the pancreases of deceased human donors. All study participants received at least one transplant of islets injected into the portal vein, the major vessel that carries blood from the intestine into the liver. Islet recipients currently must take immunosuppressive drugs for the rest of their lives to prevent their immune systems from rejecting the transplanted cells.

One year after the first transplant, 88 percent of study participants were free of severe hypoglycemic events, had established near-normal control of glucose levels, and had restored hypoglycemic awareness. After two years, 71 percent of participants continued to meet these criteria for transplant success.

Even a small number of functioning, insulin-producing cells can restore hypoglycemic awareness, although transplant recipients may need to continue taking insulin to fully regulate blood glucose levels. Participants who still needed insulin 75 days after transplant were eligible for another islet infusion. Twenty-five participants received a second transplant, and one received three. After one year, 52 percent of study participants no longer needed insulin therapy.

“This is the first license-enabling trial of a cellular product for treatment of type 1 diabetes,” said NIAID Transplantation Branch Chief Nancy D. Bridges, M.D., a co-author of the paper. “Licensure is critical because it will ensure the quality, consistency and safety of the islet product; provide greater patient access to islet transplantation; and accelerate continued research that we hope would make this procedure suitable for a broader population of people with type 1 diabetes.”

The researchers are continuing to follow participants to determine whether the benefits of restoring near-normal blood glucose control and protection from severe hypoglycemic events will outweigh the risks associated with chronic immunosuppression.

“For people unable to safely control type 1 diabetes, islet transplantation offers real hope for preventing severe, life-threatening hypoglycemia,” said study co-author Tom Eggerman, M.D., Ph.D., NIDDK scientific officer for the CIT Consortium. “However, as immunosuppression drugs required for transplantation can have significant adverse side effects, the treatment only makes sense for people who have frequent severe hypoglycemia despite optimal diabetes management, or for those already on immunosuppressant drugs for a kidney transplant, a group being studied in another Phase 3 trial.”

https://www.sciencedaily.com/   Science Daily

https://www.sciencedaily.com/releases/2016/04/160418120706.htm  Original web page at Science Daily

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Gene-editing research in human embryos gains momentum

Experiments are now approved in Sweden, China and the United Kingdom. At the Karolinska Institute in Stockholm, Fredrik Lanner is preparing to edit genes in human embryos. It’s the kind of research that sparked an international frenzy in April last year, when a Chinese team revealed that it had done the world’s first such experiments.

But Lanner doesn’t expect his work, which will explore early human development, to cause such a fuss. A year of discussion about the ethics of embryo-editing research, and perhaps simply the passage of time, seems to have blunted its controversial edge — although such work remains subject to the same ethical anxieties that surround other reproductive-biology experiments. “At least in the scientific community, I sense more support for basic-research applications,” says Lanner, who gained approval for his experiments last June.

His instinct seems to be borne out by the fairly muted reaction to a 6 April report of an experiment to edit human embryos — only the second to be published. A team led by Yong Fan at Guangzhou Medical University in China used the gene-editing technology CRISPR–Cas9 to try to introduce a mutation that makes humans resistant to HIV infection.

“I don’t think there is anything wrong with what these scientists have done,” says Sarah Chan, a bioethicist at the University of Edinburgh, UK. “This work isn’t seeking to do what is still ethically in question. It’s not seeking to create genetically modified human beings.”

The ethics committee of the university-affiliated hospital that approved Fan’s work says that it has green-lighted two other embryo-editing projects; such research is ethically sound because it will lead to improvements in gene-editing technology and could help to prevent diseases, a committee spokesperson says.

Last December, an international summit of scientists and ethicists declared that gene editing should not be done in human embryos that are intended for use in establishing a pregnancy — but it endorsed basic research.

“People are more understanding of this research,” says Fan, who points to UK fertility regulators’ approval in February of a proposal by developmental biologist Kathy Niakan to edit genes in healthy human embryos, at the Francis Crick Institute in London.

Fan’s team began its experiments in early 2014 and originally submitted the paper to Cell Stem Cell, Fan says. By the time the manuscript ended up on the desk of David Albertini, editor-in-chief of the Journal of Assisted Reproduction and Genetics, a different Guanghzou-based team had become the first to report human-embryo-editing experiments. That paper, which tried to correct a mutation that causes a blood disease, fed into a firestorm over the ethics of modifying human reproductive cells (or ‘germline’ modification). Some researchers called for a moratorium even on proof-of-principle research in non-viable embryos.

Albertini, a reproductive biologist at the University of Kansas Medical Center in Kansas City, felt that it was important to publish Fan’s paper to educate scientists and clinicians. He says that the manuscript went through two rounds of review over eight months — twice as long as is normal for the journal — and that he urged the researchers to discuss the ethical issues surrounding germline editing in the paper.

Fan’s paper should help to reassure international observers about the legitimacy of human-embryo-editing research in China, says Robin Lovell-Badge, a developmental biologist at the Crick. More such embryo-editing papers are likely to be published, he adds. “I know that there are papers floating around in review,” he says. “I’d much rather everything was out in the open.” (Fan says that his team is now focusing on improving the efficiency of CRISPR using human stem cells).

Research involving the editing of human embryos will begin soon elsewhere in the world, if it hasn’t done so privately already.

In a Cell paper published on 7 April, Lanner’s team analysed gene expression in 88 early human embryos and is using those data to identify genes to disrupt in embryos using CRISPR–Cas9. Lanner will discuss the work at a meeting on human gene editing organized by the US National Academy of Sciences and National Academy of Medicine this month in Paris. He says that the experiments could begin in the coming months.

Evan Snyder, a stem-cell scientist at the Sanford Burnham Prebys Medical Discovery Institute in La Jolla, California, says that he doesn’t know of anyone in the United States conducting human embryo editing. But he thinks that US scientists will inevitably take on such research, although federal funding of research on human embryos and germline modification is prohibited. It is important for such research to go forward, Snyder adds, to determine whether technical hurdles would prevent clinical applications.

Norms for conducting and publishing human-embryo-editing work are still taking shape. Snyder says that whenever possible, researchers should use alternatives, such as embryos of non-human primates. And when it is not, they should use only surplus embryos that would ordinarily be discarded from in vitro fertilization clinics.

Both Chinese teams used non-viable embryos, but Lovell-Badge says experiments in normal embryos are also important: to see, for instance, whether CRISPR–Cas9 is more or less effective in such cells.

Some scientists contend that gene-editing experiments designed to probe human development, such as those planned by Lanner and Niakan, are more valuable than experiments that are intended to lay the groundwork for creating genetically modified humans. “At the moment, there seems little point in pursuing long-term clinical goals when there’s so much not known about the technique with human embryos,” says Lovell-Badge.

But Chan thinks there should be ethical latitude for both kinds of research to proceed. “We should give the public the credit for being able to understand the difference between research into genetically modified embryos and genetically modifying human beings,” she says. “I think it’s a good thing if the hubbub dies down a bit.”

Nature 532, 289–290 (21 April 2016) doi:10.1038/532289a

http://www.nature.com/news/index.html  Nature

http://www.nature.com/news/gene-editing-research-in-human-embryos-gains-momentum-1.19767  Original web page at Nature

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What are the factors affecting whether women choose a medical research career

Unless exposed to positive research experience and role models during their medical education and training, women are unlikely to consider careers in academic medicine seriously. That’s one conclusion of an Oxford University study published in The Lancet. It asked why, when entry to medical schools is evenly split between men and women, those working in University medical departments are predominantly men.

In the UK, women make up 55% of medical school entrants but just 28% of faculty. In the US, they are 47% of entrants but 38% of faculty. The study reviewed 52 pieces of research evidence from the last thirty years to test eight themes often proffered as reasons for women’s under-representation in the medical academic workforce.

Dr Laurel Edmunds, Senior Systematic Reviewer, said: ‘Despite the focus on encouraging women to pursue an interest in medical sciences, we still lack comprehensive research evidence on what causes them to choose or reject a career in the subject. Most studies we reviewed had methodological limitations and were predominantly from North America. Further methodologically robust research, especially outside North America, is needed to establish the consistency of our review findings.’

The team did find that research evidence consistently pointed to a lack of adequate mentors and role models for women and to the deterrent effect of gender discrimination and unconscious bias experienced while still at medical school. They also found that women who were exposed to medical research while in training were more likely to pursue a research career, and that studies showed that women were more likely to choose a teaching career over a research career.

Professor Alastair Buchan, Head of the Medical Sciences Division and Dean of Medicine at Oxford University initiated and led the research. He said: ‘For four of the themes, we found both supporting and refuting evidence. For example, suggestions that women are less interested in research than men, or that they lose interest in research as education and training progress are not consistently supported by research evidence. We also found that evidence was conflicting on whether financial considerations and work-life balance deter women from a medical research career.’

Professor Trish Greenhalgh, Professor of Primary Care Health Sciences and a practicing GP said: ‘The focus of further research should shift from individuals’ career choices to the societies, organisations, and cultures within which those choices are made. There may be important confounding factors which explain women’s choice or rejection of careers in academic medicine. For example, some of the findings of this review may be explained by the phenomenon of stereotype threat — the idea that we stereotype ourselves as less good because we pick up on society’s stereotypes, and underperform as a result.’

Dr Pavel Ovseiko, Senior Research Fellow in Health Policy and Management, said: ‘What inconsistency of findings across reviewed studies suggests is that there are significant opportunities to overcome barriers by creating a more supportive and inclusive university culture and work environment. Winning the talent war for women in academic medicine requires a combination of practical measures and inspirational leadership from both women and men.’

The research comes as Oxford launches a new website for women interested in careers in medical sciences. The site, http://www.womeninscience.ox.ac.uk, includes interviews with women scientists from Oxford at various stages of their careers, talking frankly about topics a variety of issues including obtaining funding, career progression, mentorship, and parenting.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/04/160419214200.htm  Original web page at Science Daily

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Critical to screen patients with rheumatoid arthritis for hearing impairment

Rheumatoid arthritis (RA) is the most common autoimmune arthritis, affecting 1% of the general population. Despite its main articular manifestations, RA can involve extra-articular organs including the auditory system.

HI in RA is multifactorial. Mechanism of injury and predisposing factors are not clearly understood. Sensorineural hearing loss is the most common type in RA patients with a prevalence of 25-72%. Possible pathologies are including: Synovial destruction of incudostapedial and incudomalleolar joints, rheumatoid nodules, auditory neuropathy, destruction of the cochlear hair cells and drug-induced ototoxicity. “Elderly Patients and those with long disease duration, active disease, seropositivity, elevated acute phase reactants and rheumatoid nodules are more likely to have HI,” demonstrated a recent study by Amir Emamifar, Kristine Bjørndal and Inger Marie Jensen Hansen.

Environmental factors for instance smoking, alcohol and noise can deteriorate the condition. Passive smokers are also at risk of HI. Long-term exposure to alcohol affects hearing in RA, causing harmful effects on the cochlear function.

Results of pure tone audiometry revealed that RA patients have high prevalence of HI for all frequencies. Transiently Evoked Otoacoustic Emissions (TEOAEs) test has been used widely to evaluate cochlear function, and is capable of detecting various amounts of decreases in RA patients at an early stage of the disease.

Treatment of HI in RA is empirical. Oral steroids and intensifying Disease-Modifying Antirheumatic Drugs might be an option. Anti-oxidants (eg. vitamin E) may play a protective role for the inner ear. Regular audiometric test and TEOAEs should be performed. Patients will also benefit from the cessation of smoking and alcohol. Like other causes of HI in healthy individuals, HI in RA can also be managed by use of different types of hearing aids and implantable devices.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/04/160422115526.htm  Original web page at Science Daily

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* Infection alert system in catheters could tackle hospital superbugs

A new infection alert system in catheters could prevent serious infections in millions of hospital patients worldwide. The system, detailed in a new paper in Biosensors and Bioelectronics, changes the color of the urine so patients and carers can see easily if bacteria are starting to block the catheter.

The researchers who invented the new catheter infection alert, from the University of Bath, say it could help tackle these infections. It could also be beneficial for elderly people in care homes.

A catheter drains urine from the bladder when a person can’t release urine without help or is incontinent, including following anesthesia. 100 million urinary catheters are used around the world every year, but the infections they sometimes cause can be problematic for thousands of people. Hospital acquired urinary infections affect more than 90,000 patients a year in the US alone, according to the Centers for Disease Control and Prevention.

The new system designed by Dr. Toby Jenkins and his colleagues provides a means of early detection, so the catheter can be changed and the infection treated before a person becomes unwell.

“Catheter-related infections are a serious problem, especially if the bacteria are resistant to antibiotics. We hope that with this simple to use sensor system we can ultimately make a real difference to patients’ lives,” said Dr. Jenkins.

Over time bacteria can build a layer called a biofilm inside the catheter tubes that eventually blocks them. The urine can’t escape and pushes back into the kidneys where the bacteria can cause kidney failure, body-wide infection and death. Up to half of people who use catheters long-term have problems with blockages caused by bacteria, but there is currently no way to detect potential blockages before they cause problems.

The new coating detects biofilms built by a bacterium called Proteus mirabilis, the most common cause of catheter blockage. The system gives advanced warning of a catheter blockage 10 to 12 hours before it happens.

The coating is made up of two layers. The first reacts to changes in urine caused by the bacteria, the second layer releases the dye. The dyed urine gathers in the collection bag, turning the urine bright yellow. The color change reveals the infection.

Dr. Jenkins’ team used a glass bladder, artificial urine and bacteria from patient samples to test the system. It responds to changes in the acidity, or pH, of urine caused by bacteria. As bacteria multiply, the substances they release raise the pH so the urine becomes more alkaline than acidic. This change dissolves the top layer of the coating, releasing the super-bright dye held in the second layer.

The glass bladder tests showed that when there is no bacterial infection the dye stays in the second layer despite liquid constantly flowing past it.

Biofilms built by bacteria are not easy to treat. They avoid the natural defenses of the immune system and can’t be broken down by antibiotics. Dr. Jenkins is optimistic about the benefits of the system: “Our new coating works with existing catheter designs and gives a clear, early visual warning of infection before a catheter is blocked. It could dramatically reduce the number of infections resulting from bacterial blockages.”

The authors also hope the catheter coating could be used to cut the cost of treating infection, estimated to be £120 million a year in England and Wales. The next step is to test the coating using urine collected from volunteers and then ultimately to run a clinical trial to show the system is safe and beneficial for patients.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/04/160425095523.htm  Original web page at Science Daily

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Breakthrough made in cleft lip and palate research

Leading scientists have identified an important gene that is associated with cleft lip and palate. Experts say the discovery is a step closer to understanding how this birth defect arises, and will help in the development of medical approaches to prevent the disfiguring condition.

An international team, led by Newcastle University, UK, and the University of Bonn in Germany, has found that variants near a gene called GREM1 (Gremlin1) significantly increase the risk for cleft lip and palate.

A cleft is a gap in the upper lip, the roof of the mouth, or sometimes both. Each year, approximately 250,000 babies worldwide are born with a cleft, equating to about two babies a day in the UK.

Dr Heiko Peters, who works at Newcastle University’s Institute of Genetic Medicine, is senior author of the research paper published in the journal, PLoS Genetics.

He said: “The findings reveal a link between GREM1 and specific clinical characteristics that arise in the formation of a cleft lip and palate.

“This is very important in this research area as it helps to decipher the complex interplay between genes required for the different steps and in different tissues during lip and palate development.

“A cleft lip can occur with or without a cleft palate and the genetic factors that predispose to palate involvement are largely unknown.”

The research team carried out analyses on genetic and clinical data from three large patient cohorts and identified a strong association between a region on chromosome 15 and cleft lip and palate.

Experts carried out studies on mice to investigate where GREM1 is normally active in the development of the face and how alterations in the gene’s activity may affect the lip and palate.

Results indicate that it is not the loss of GREM1 function but rather its increased activity that causes the condition.

It is the second gene which has been shown to be linked to a condition in which a cleft of the lip and a cleft of the secondary palate occur together.

Dr Peters added: “These findings provide a framework for further analyses of GREM1 in human cell systems and model organisms, broadening our understanding of the processes that regulate the face’s shape.”

Although not life-threatening for patients with access to postnatal surgery, cleft lip and palate requires additional multidisciplinary care by specialists, including ear, nose and throat experts, orthodontists and speech therapists.

Children with the condition can have dental issues, speech problems and are at increased risk of serious ear infections and hearing loss.

Currently, scientists only have a fragmented picture about which genes are required for lip and palate development, and how environmental factors might interact with genetic risk factors.

To establish effective prevention strategies scientists must identify genetic risk factors and understand how gene-gene and gene-environment interactions interfere with lip and palate development.

As the use of personalized medicine increases, understanding how genetic changes alter fetal development will become increasingly relevant.

This is particularly important for conditions such as cleft lip and palate that appear to be caused by a combination of genetic and environmental factors, such as smoking or certain medicines used by the mother.

Further studies will focus on identifying genes and environmental factors that interact with GREM1.

Dr Laura Yates, consultant in clinical genetics at Newcastle upon Tyne Hospitals NHS Foundation Trust, said: “The families we meet in genetic clinics on a daily basis generally have two common questions.

“Firstly, what is the cause of the developmental anomaly affecting their child or themselves, and secondly, can it be treated or prevented in future pregnancies?

“Studies such as this contribute vital pieces of information that enable clinicians to provide patients with answers that are relevant to them and their family, not just general statistics.

“Our understanding of how genetic factors in both mother and fetus, and external or environmental influences impact on fetal development in the womb, is far from complete.

“This study takes us one step closer to being able to identify genetic changes that increase the chance of a particular form of cleft lip and palate re-occurring in a family, therefore to studying what can be done to reduce the chance of this happening in individuals who have this genetic change.”

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160324104802.htm  Original web page at Science Daily

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* First ever vaccine for deadly parasitic infection may help prevent another global outbreak

As scientists scramble to get a Zika virus vaccine into human trials by the end of the summer, a team of researchers is working on the first-ever vaccine to prevent another insect-borne disease — Leishmaniasis — from gaining a similar foothold in the Americas.

Leishmaniasis is a parasitic infection passed on through the bite of a sand fly. Using breakthrough CRISPR-cas9 gene editing technology, the researchers — hailing from Japan, Brazil, Canada and the United States — have altered the parasite’s DNA to create a live-attenuated vaccine. If approved, the vaccine will be the first ever to combat a parasite.

“The Ebola and Zika outbreaks show how so-called ‘neglected’ tropical diseases can quickly turn into global public health issues,” says principal investigator Abhay Satoskar, MD, PhD , a microbiologist at The Ohio State University Wexner Medical Center and Center for Microbial Interface Biology. “This vaccine, which has been more than twenty years in the making, could give us the opportunity to stop Leishmania infections before they start, and prevent the type of global spread we’ve seen with other diseases.”

The parasitic protozoa typically causes disfiguring skin infections, but can also silently lurk in the bloodstream, hiding in immune cells and lodging in the spleen, liver and bone marrow with often fatal results. Out of the two million people who are infected each year, 50,000 will die. Current treatments have toxic side effects and are expensive, making effective control of Leishmaniasis in resource-scarce communities difficult. The parasite has also begun to develop resistance against the therapies.

While Leishmaniasis is primarily found in developing nations in Asia, the Middle East and Central and South America, cases have begun to crop up along the southern US border and in Puerto Rico. Thousands of troops from Desert Storm and other Middle Eastern military campaigns have returned with the disease. Sporadic outbreaks in dog kennels across the United States (the parasite is easily transferred between animals and humans) also has public health experts watching closely.

“The sand fly is here. Millions of people travel each year to areas with Leishmaniasis and 90% of those who are infected with the visceral form of the infection don’t have any symptoms,” says co-investigator Hira Nakhasi, PhD, a researcher with the US Food & Drug Administration (FDA) who has been studying Leishmaniasis for decades in order to keep the nation’s blood supply parasite-free. “Diseases don’t recognize borders. Either we can stop Leishmaniasis before it gets here, or we can try to deal with it after. We’re hopeful this vaccine will give us a good head start.”

The idea that a vaccine could be developed for Leishmaniasis is not new. For hundreds of years, rural communities have observed that people who had Leishmaniasis skin infections (which typically do not require medical intervention) were less likely to get the deadly, visceral form of the parasite. Some cultures adopted a crude vaccination method where disease-free children were deliberately exposed to pus from sores to establish immunity — a tradition that has carried over into modern times.

“The Leishmanization process practiced by these villages gave us the idea that a vaccine was possible, but we also wanted to truly understand how and why this immune memory develops,” says Satoskar.

As one of the first steps, the team created the first animal model of visceral leishmaniasis using natural mode of infection through an infected sand fly bite. Previously, Nakhasi’s lab at the FDA made a critical discovery that Leishmanias growth is dependent on the production of a protein called centrin in the amastigote form of the parasite which is responsible for infectivity. When the gene that triggers centrin production is removed, the parasite is unable to develop, and is cleared out of the immune cells within a few weeks.

Further, Nakhasi’s lab successfully removed the centrin gene from a deadly strain of Leishmania and used it to create a live-attenuated vaccine that ultimately protected dogs, hamsters and mice from the deadly visceral type of Leishmaniasis. The group, along with Dr. Satoskar’s lab, showed that this live-attenuated vaccine also provided cross-protection against the two other types of Leishmanias that cause non-deadly skin infections. Recently, the Canadian member of the research team removed the centrin gene from the Leishmanias that cause non-deadly skin infections using CRISPR-Cas9 gene editing technology and showed that they do not cause skin infections in mice.

There are inherent risks with live-attenuated vaccines, which use a weakened version of the pathogen in order to trigger an immune response without causing full blown disease. But the researchers are confident that the vaccine based on the altered Leishmaniasis parasites could join a line of successful live-attenuated vaccines that have been used to control yellow fever, polio, Rubella, Measles, Mumps and smallpox.

“The team’s cross-functional expertise in immunology, microbiology, parasitology and genetics along with a deep understanding of vaccine manufacturing methods means we aren’t just creating a vaccine that works, but all of the biomarker tests needed to ensure it’s safe and effective,” says Nakhasi.

The team has already identified a manufacturer in India that is capable of making the live-attenuated vaccine and meets FDA production standards. India bears about 80% of the world’s Leishmaniasis burden.

“It’s one thing to create a vaccine in a sterile, academic lab,” says Satoskar. “When we can do it successfully in resource-scarce areas, it helps ensure greater access for people who need it the most,”

The vaccine wasn’t designed to work in just animal models, but also to be effective against natural infection through sand fly bites. Past research has shown that sand fly saliva contains a protein that slows the human immune system down, which gives the parasite a better chance at surviving. Many studies so far simply start an infection by delivering the parasite via intravenous injection (IV), but this method does not measure the potential immune impact of the sand fly saliva.

In the last few years the team has pioneered procedures that emulate the sand fly bite in order to better understand the role saliva has in producing an immune response, and importantly, antibodies against future infection.

In a study recently published in PLoS Neglected Tropical Diseases, the team discovered that a vaccine augmented with a salivary protein delivered via the skin provided a better immunity against visceral Leishmaniasis than just the vaccine or the salivary protein alone.

“It’s not enough to simply find a vaccine that works. We want to know the exact mechanisms that are generating immunity, how and why,” says Satoskar. “That increases our likelihood of developing a safe, effective vaccine and the diagnostics needed to measure both.” The team expects human trials of the vaccine to begin within the next five years.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/04/160426092455.htm  Original web page at Science Daily

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* Analysis of dog genome will provide insight into human disease

An important model in studying human disease, the non-coding RNA of the canine genome is an essential starting point for evolutionary and biomedical studies, according to a new study led by The Genome Analysis Centre (TGAC).

New research published today in PLOS ONE reveals an improved annotation of microRNAs in the dog genome to further understand its biological role. Providing a platform for future studies into biomedicine, evolution and the domestication of important animals including dogs, cows, horses and pigs.

MicroRNAs (miRNAs) are small non-coding RNA molecules that play a crucial role in regulating gene expression in animals and plants. Using the latest dog genome assembly and small RNA sequences of nine different dog tissues including skin, blood, ovaries and testes, scientists from TGAC have identified 91 novel miRNAs.

This discovery provides a significant opportunity not only to enhance our understanding of how miRNAs regulate a variety of biological processes in an important model species for studying human diseases, but can lead to further, similar research into the role that miRNAs play in animal domestication.

Lead researcher, Dr Luca Penso Dolfin from TGAC’s Vertebrate & Health Genomics Group, said: “As miRNAs are so important in orchestrating a variety of cellular processes, the discovery of these 91 novel miRNAs provides a vital starting point to explore their potentially major effects on gene regulation.”

Overall, 811 miRNAs were analysed by Dr Penso-Dolfin: 91 novel microRNA sequences and 720 conserved (that is, common to other organisms). Among these conserved loci, 207 had not previously been identified as canine microRNAs.

Dr Penso-Dolfin, added: “Our results represent a clear improvement in our knowledge of the dog genome, paving the way for further research on the evolution of gene regulation, and the contribution of microRNAs to pathological conditions. We are now looking at additional data for dog and a variety of farm animals, combining microRNA discovery to the investigation of their possible role in domestication.”

The domestic dog, Canis familiaris, is the result of wolf (Canis lupus) domestication, which started around 10,000 years ago. Since then, hundreds of dog breeds have been artificially selected, leading to very high levels of morphological and behavioural variation. Having shared the environment with humans ever since its appearance, the dog has been exposed to similar pathogens, and therefore represents an important model system for the study of human diseases.

The publication of the latest Canine genome build and annotation, CanFam3.1 provides an opportunity to enhance our understanding of gene regulation across tissues in the dog model system.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/04/160427164134.htm  Original web page at Science Daily

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Researchers push for personalized tumour vaccines

It is precision medicine taken to the extreme: cancer-fighting vaccines that are custom designed for each patient according to the mutations in their individual tumours. With early clinical trials showing promise, that extreme could one day become commonplace — but only if drug developers can scale up and speed up the production of their tailored medicines.

The topic was front and centre at the American Association for Cancer Research (AACR) annual meeting in New Orleans, Louisiana, on 16–20 April. Researchers there described early data from clinical trials suggesting that personalized vaccines can trigger immune responses against cancer cells. Investors seem optimistic that those results will translate into benefits for patients; over the past year, venture capitalists have pumped cash into biotechnology start-ups that are pursuing the approach.

But some researchers worry that the excitement is too much, too soon for an approach that still faces many technical challenges. “What I do really puzzle at is the level of what I would call irrational exuberance,” says Drew Pardoll, a cancer immunologist at Johns Hopkins University in Baltimore, Maryland.

The concept of a vaccine to treat cancer has intrinsic appeal. Some tumour proteins are either mutated or expressed at different levels than in normal tissue. This raises the possibility that the immune system could recognize these unusual proteins as foreign — especially if it were alerted to their presence by a vaccine containing fragments of the mutated protein. The immune system’s army of T cells could then seek out and destroy cancer cells bearing the protein.

Decades of research into cancer-treatment vaccines have thus far yielded disappointing clinical trial results, but recent advances — including a suite of drugs that may amplify the effects of cancer vaccines — have rekindled hope for the field. And DNA sequencing of tumour genomes has revealed a staggering diversity of mutations, producing proteins that could serve as ‘antigens’ by alerting the immune system.

Last year, researchers reported that they had triggered an immune response in three patients with melanoma by administering a vaccine tailored to their potential tumour antigens. The vaccines’ effects on tumour growth are not yet clear, but by the end of 2015, several companies had announced their intention to enter the field. Gritstone Oncology, a start-up firm in Emeryville, California, raised US$102 million to pursue the approach, and Neon Therapeutics of Cambridge, Massachusetts, raised $55 million. A third company, Caperna, spun out of a prominent biotechnology company called Moderna Therapeutics, also in Cambridge.

Academic groups are also moving quickly. At the AACR meeting, Robert Schreiber of Washington University in St. Louis described six ongoing studies at his institution in cancers ranging from melanoma to pancreatic. Cancer researcher Catherine Wu of the Dana-Farber Cancer Institute in Boston, Massachusetts, also presented data from a trial in melanoma, showing signs of T-cell responses to the vaccine.

But it takes Wu’s team about 12 weeks to generate a vaccine, and the Washington University team needs about 8 weeks. That could limit the treatment to slow-growing cancers, says Wu.

There is also a reason that so many researchers choose melanoma for proof-of-principle trials. Melanoma tumours tend to harbour many mutations — sometimes thousands — which provide scientists with ample opportunity to select those that may serve as antigens. Some researchers worry that tumours with fewer mutations may not be as suitable for personalized vaccines.

But Schrieber notes that researchers have been able to design a vaccine for a woman with the brain tumour glioblastoma — which often has relatively few mutations. In that case, however, the tumour had many mutations, some of which may have been caused by her previous cancer treatment.

The number of potential antigens could be crucial. At the AACR meeting, Ton Schumacher, an immunologist at the Netherlands Cancer Institute in Amsterdam, noted that many of the mutant proteins that his group has found are not required for tumour survival. As a result, a tumour could maintain its cancerous lifestyle but become resistant to the vaccine if the proteins used to design the vaccine mutate again. “We will need to attack tumours from many different sides,” he says.

Pardoll, meanwhile, is concerned that the field is shifting too quickly to the personalized-vaccine approach and leaving behind decades of research on antigens that might be shared across tumours — an approach that has not borne out in clinical trials thus far, but would be much simpler to manufacture and deploy on a large scale. “I will be the happiest person in the world to be proven wrong on these,” he says of personalized vaccines. “But I think one has to nonetheless be cognizant of where the challenges are.”

Nature 532, 425 (28 April 2016) doi:10.1038/nature.2016.19801

http://www.nature.com/news/index.html  Nature

http://www.nature.com/news/researchers-push-for-personalized-tumour-vaccines-1.19801  Original web page at Nature

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Treating myasthenia gravis with autologous hematopoietic stem cell transplants

A report on seven cases of severe myasthenia gravis (an autoimmune disease characterized by severe muscle weakness) suggests that autologous hematopoietic stem cell transplantation (when a patient’s own stem cells are used) may result in long-term remission that is symptom and treatment free, according to an article published online by JAMA Neurology.

The study by Harold Atkins, M.D., F.R.C.P.C., of the University of Ottawa and the Ottawa Hospital, Canada, and coauthors reports outcomes at the Ottawa Hospital from 2001 through 2014.

All of the patients who were treated had persistent severe or life-threatening symptoms related to myasthenia gravis (MG), although they had used intensive immunosuppressive therapies.

“The ability to control autoimmunity by autologous HSCT [hematopoietic stem cell transplantation] has been demonstrated in other treatment-refractory autoimmune conditions, including neurologic diseases. … The role of autologous HSCT for MG warrants further exploration with prospective testing,” the authors conclude.

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https://www.sciencedaily.com/releases/2016/04/160404133932.htm  Original web page at Science Daily

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* New esophagus tissue reconstructed

US doctors report reconstructing new esophagus tissue in a critically ill patient. Writing in The Lancet, US doctors report the first case of a human patient whose severely damaged esophagus was reconstructed using commercially available FDA approved stents and skin tissue. Seven years after the reconstruction and 4 years after the stents were removed, the patient continues to eat a normal diet and maintain his weight with no swallowing problems.

Until now, this regeneration technique has only been tested in animals. The authors, reporting on the outcome of the procedure, say that research, including animal studies and clinical trials, are now needed to investigate whether the technique can be reproduced and used in other similar cases.

Professor Kulwinder Dua from the Medical College of Wisconsin, Milwaukee, USA, and colleagues report using metal stents as a non-biological scaffold and a regenerative tissue matrix from donated human skin to rebuild a full-thickness 5cm defect in the esophagus of a 24-year-old man. The patient was urgently admitted to hospital with a disrupted esophagus resulting in life-threatening infection and inability to swallow following complications from an earlier car accident which had left him partially paralysed. Despite several surgeries, the defect in the esophagus was too large to repair.

The esophagus is a hollow muscular tube that connects the mouth to the stomach carrying food and liquids. Removal of the esophagus (esophagectomy) to treat cancer or injury requires reconnecting the remaining part of the esophagus to the stomach to allow swallowing and the passage of food. Part of the stomach or colon is used to make this connection. However, the procedure was not possible in this case because the defect in the esophagus was too large, and the patient too ill to undergo the procedure.

The team hypothesized that if the three-dimensional shape of the esophagus could be maintained in its natural environment for an extended period of time while stimulating regeneration using techniques previously validated in animals, esophageal reconstruction may be possible.

They used commercially available, FDA-approved, materials to repair the defect. To maintain the shape of the esophagus and bridge the large defect, they used an endoscope to place self-expanding metal stents. The defect was then surgically covered with regenerative tissue matrix and sprayed with a platelet-rich plasma gel produced from the patient’s own blood to deliver high concentrations of growth factors that not only stimulate growth but also attract stem cells to stimulate healing and regeneration. The sternocleidomastoid, a muscle running along the side of the neck, was placed over the matrix and the adhesive platelet-rich plasma gel.

The team planned on removing the stent 12 weeks after reconstruction, but the patient delayed the procedure for three and a half years because of fears of developing a narrowing or leakage in the esophagus. One year after the stents were removed, endoscopic ultrasound images showed areas of fibrosis (scarring) and regeneration of all five layers of the esophageal wall. Full recovery of functioning was also established by swallowing tests showing that esophageal muscles were able to propel water and liquid along the esophagus into the stomach in both upright and 45° sitting positions. But, how long the regeneration process took is unclear because the patient delayed stent removal for several years.

According to Professor Dua, “This is a first in human operation and one that we undertook as a life-saving measure once we had exhausted all other options available to us and the patient. The use of this procedure in routine clinical care is still a long way off as it requires rigorous assessment in large animal studies and phase 1 and 2 clinical trials. The approach we used is novel because we used commercially available products which are already approved for use in in the human body and hence didn’t require complex tissue engineering.”

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https://www.sciencedaily.com/releases/2016/04/160409091725.htm  Original web page at Science Daily

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New assay offers improved detection of deadly prion diseases

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are a family of rare progressive, neurodegenerative illnesses that affect both humans and animals. TSE surveillance is important for public health and food safety because TSEs have the potential of crossing from animals to humans, as seen with the spread of mad cow disease, or bovine spongiform encephalopathy (BSE). A study in The Journal of Molecular Diagnostics describes an advanced assay that offers better sensitivity than currently available tests for detecting a prion disease affecting elk.

Timed amyloid seeding assay achieves or surpasses sensitivity of currently available tests for transmissible spongiform encephalopathies, according to report in The Journal of Molecular Diagnostics.

Transmissible spongiform encephalopathies (TSEs), or prion diseases, are a family of rare progressive, neurodegenerative illnesses that affect both humans and animals. TSE surveillance is important for public health and food safety because TSEs have the potential of crossing from animals to humans, as seen with the spread of mad cow disease, or bovine spongiform encephalopathy (BSE). A study in The Journal of Molecular Diagnostics describes an advanced assay that offers better sensitivity than currently available tests for detecting a prion disease affecting elk.

“The significance of TSEs on human health was not entirely realized until cases of variant Creutzfeldt-Jakob disease (vCJD) in humans had been discovered in the years following the BSE outbreak in the United Kingdom. These vCJD cases were associated with consuming meat products contaminated with BSE prions,” explained lead investigator Stefanie Czub, DVM, PhD, of the Canadian BSE Reference Lab, Canadian Food Inspection Agency, Lethbridge Laboratory, Lethbridge, Alberta (Canada). “The result is that many countries have enacted TSE surveillance programs, aiming to eradicate livestock-related TSEs.”

Surveillance programs rely on highly sensitive diagnostic methods to detect infections early. Addressing the need to define steadfast analytical performance criteria for prion amyloid seeding assays (ASAs), researchers developed a method to measure prion protein conversion time (from normal cellular form to prion form) by a combination of statistical analyses to obtain a prion-detecting ASA with a known degree of confidence. They compared the sensitivity of the new assay technique, the timed prion seeding assay (tASA), to other currently available tests (two bioassays in laboratory rodents and three commercially available TSE rapid tests).

The test samples came from elk brains infected experimentally with chronic wasting disease (CWD), a prion disease that affects cervids (hoofed ruminant mammals in the deer family). The investigators were able to define clear cut-off criteria, allowing determination of TSE-positive and TSE-negative states. Unlike TSE rapid tests, ASAs also have the potential to detect and measure TSE infection in blood, saliva, or urine. This would offer clinical advantages, such as the ability to sample blood instead of relying on more invasive tissue biopsy and to screen blood donations for contamination.

“We found that the tASA was at least as sensitive as two rodent bioassays and up to 16 times more sensitive than three different TSE rapid tests,” noted lead author John G. Gray, MS, Canadian BSE Reference Lab, Canadian Food Inspection Agency. “This study should further advance ASAs as recognized prion detection systems. We believe this methodology represents the future for prion diagnostics, especially concerning human health, for example in screening blood donations.”

The tASA is an in vitro method that mimics the conjectured mechanism of prion propagation in vivo. It is a conversion assay that uses recombinant prion-related protein as a substrate and detects conversion via changes in fluorescence. The report describes time specifications for the assay to help avoid false-positive results (30 hours) or false-negative results in weakly-positive samples (48 hours), as well as the number of replications necessary for adequate sensitivity (2-12).

“This study represents an important first step for the tASA diagnostic protocol to gain regulatory approval for its use in TSE surveillance programs targeting CWD in cervids,” commented noted authority Holger Wille, PhD, of the University of Alberta Department of Biochemistry and Centre for Prions and Protein Folding Diseases in Edmonton, Alberta (Canada). “Additional work will also be needed to fine-tune and test tASA for the detection of prions in peripheral organs and environmental samples, which represent a substantial unmet need to track the spread of CWD prions among North America cervids as well as in the environment.”

Prions are abnormal, transmissible pathogenic agents that induce abnormal folding of specific, normal cellular proteins. Because these proteins are concentrated in brain tissue, brain damage is characteristic of prion diseases. Prion diseases generally progress rapidly and are associated with high mortality. Prion disease occurs when the normal cellular form of prion-related protein converts or conformationally changes to the disease form. Once the disease form is introduced, it becomes self-perpetuating as it converts the normal form into more of the disease form. CWD is currently spreading throughout the U.S. and Canada, is also present in South Korea, and was just diagnosed in a first reindeer in Norway.

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https://www.sciencedaily.com/releases/2016/04/160408112336.htm  Original web page at Science Daily

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Test run finds no cancer risk from stem cell therapy

Therapeutic stem cells can be made without introducing genetic changes that could later lead to cancer, a study in PLOS Genetics has found.

The discovery, made by researchers at the Wellcome Trust Sanger Institute, is a boost for scientists working on ways to make regenerative medicines from induced pluripotent stem (iPS) cells; a type of stem cell made by reprogramming healthy body cells.

It is the first time scientists have tracked the genetic mutations gathered by iPS cells as they are grown in the laboratory.

The idea behind the research was to follow the whole journey iPS cells will take when used in clinical therapy. The Sanger Institute team, led by Professor Allan Bradley and Dr Kosuke Yusa, started with blood cells donated by a 57-year-old man.

As a person grows from embryo, to child, to adult, and as they age, the cells in their body generate a mosaic of tiny genetic changes. Most of these mutations have no effect but some can lead to cancer. The Sanger Institute team traced the history of genetic changes in both the donated blood cell and the iPS cells created from it.

The results reveal that mutations arise 10 times less often in iPS cells than they do in lab-grown blood cells and that none of the iPS cell mutations are in genes known to cause cancer.

Lead researcher Dr Foad Rouhani said: “None of the mutations we found in induced pluripotent stem cells were cancer-driver mutations or mutations in cancer-causing genes. We didn’t find anything that would preclude the use of iPS cells in therapeutic medicine.”

In addition, the team used the iPS cells, reprogrammed from the donated blood cell, to trace the history of every mutation that one cell had developed from the time it was a fertilised egg all the way up to the moment it was taken out of the body.

This is the first time that mutation rates of both types of cells, the donor cell and iPS cell, have been calculated and compared.

Professor Allan Bradley said: “Until now the question of whether generating iPS cells and growing them in cell culture creates mutations has not been addressed in detail. If human cells are really to be reprogrammed on a large scale for use in regenerative medicine then understanding the mutations the donor cells carry will be a crucial step. We now have the tools to do this.”

The ability to track the genetic changes in cells over a lifetime could also improve scientists’ understanding of how, when and why mutations can lead to cancer.

Dr Kosuke Yusa said: “One of the exciting things is that we have found a way to use iPS cells as a tool to look at the genetic history of a single cell. It also underlines the fact that before you use these cells you really need to characterise them to a high degree to know where the mutations that have been introduced are.”

The team also found that the genetic changes that do take place in iPS cells in the lab might be caused by a mechanism known as oxidative stress. They hope this knowledge will help to find ways to improve the process of making iPS cells.

Researchers from the University of Cambridge and the European Bioinformatics Institute also contributed to the study.

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https://www.sciencedaily.com/releases/2016/04/160407150325.htm  Original web page at Science Daily

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Why do cells rush to heal a wound? Mysteries of wound healing unlocked

Researchers at the University of Arizona have discovered what causes and regulates collective cell migration, one of the most universal but least understood biological processes in all living organisms.

The findings, published in the March 13, 2015, edition of Nature Communications, shed light on the mechanisms of cell migration, particularly in the wound-healing process. The results represent a major advancement for regenerative medicine, in which biomedical engineers and other researchers manipulate cells’ form and function to create new tissues, and even organs, to repair, restore or replace those damaged by injury or disease.

“The results significantly increase our understanding of how tissue regeneration is regulated and advance our ability to guide these processes,” said Pak Kin Wong, UA associate professor of mechanical and aerospace engineering and lead investigator of the research.

“In recent years, researchers have gained a better understanding of the molecular machinery of cell migration, but not what directs it to happen in the first place,” he said. “What, exactly, is orchestrating this system common to all living organisms?”

The answer, it turns out, involves delicate interactions between biomechanical stress, or force, which living cells exert on one another, and biochemical signaling.

The UA researchers discovered that when mechanical force disappears — for example at a wound site where cells have been destroyed, leaving empty, cell-free space — a protein molecule, known as DII4, coordinates nearby cells to migrate to a wound site and collectively cover it with new tissue. What’s more, they found, this process causes identical cells to specialize into leader and follower cells. Researchers had previously assumed leader cells formed randomly.

Wong’s team observed that when cells collectively migrate toward a wound, leader cells expressing a form of messenger RNA, or mRNA, genetic code specific to the DII4 protein emerge at the front of the pack, or migrating tip. The leader cells, in turn, send signals to follower cells, which do not express the genetic messenger. This elaborate autoregulatory system remains activated until new tissue has covered a wound.

The same migration processes for wound healing and tissue development also apply to cancer spreading, the researchers noted. The combination of mechanical force and genetic signaling stimulates cancer cells to collectively migrate and invade healthy tissue.

Biologists have known of the existence of leader cells and the DII4 protein for some years and have suspected they might be important in collective cell migration. But precisely how leader cells formed, what controlled their behavior, and their genetic makeup were all mysteries — until now.

“Knowing the genetic makeup of leader cells and understanding their formation and behavior gives us the ability to alter cell migration,” Wong said.

With this new knowledge, researchers can re-create, at the cellular and molecular levels, the chain of events that brings about the formation of human tissue. Bioengineers now have the information they need to direct normal cells to heal damaged tissue, or prevent cancer cells from invading healthy tissue.

The UA team’s findings have major implications for people with a variety of diseases and conditions. For example, the discoveries may lead to better treatments for non-healing diabetic wounds, the No. 1 cause of lower limb amputations in the United States; for plaque buildup in arteries, a major cause of heart disease; and for slowing or even stopping the spread of cancer, which is what makes it so deadly.

The research also has the potential to speed up development of bioengineered tissues and organs that can be successfully transplanted in humans.

In the UA Systematic Bioengineering Laboratory, which Wong directs, researchers used a combination of single-cell gene expression analysis, computational modeling and time-lapse microscopy to track leader cell formation and behavior in vitro in human breast cancer cells and in vivo in mice epithelial cells under a confocal microscope.

Their work included manipulating leader cells through pharmacological, laser and other means to see how they would react.

“Amazingly, when we directed a laser at individual leader cells and destroyed them, new ones quickly emerged at the migrating tip to take their place,” said Wong, who likened the mysteries of cell migration and leader cell formation to the processes in nature that cause geese to fly in V-formation or ants to build a colony.

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https://www.sciencedaily.com/releases/2015/03/150313094551.htm  Original web page at Science Daily

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Dressed to kill: Tailoring a suit for tumor-penetrating cancer medications

For more than a decade, biomedical researchers have been looking for better ways to deliver cancer-killing medication directly to tumors in the body. Tiny capsules, called nanoparticles, are now being used to transport chemotherapy medicine through the bloodstream, to the doorstep of cancerous tumors. But figuring out the best way for the particles to get past the tumor’s “velvet rope” and enter the tumor is a challenge scientists are still working out. Drexel University researchers believe that the trick to gaining access to the pernicious cellular masses is to give the nanoparticles a new look — and that dressing to impress will be able to get them past the tumor’s biological bouncers.

Targeted cancer therapy is most effective when the medication is released as close as possible to the interior of a tumor, to increase its odds of penetrating and killing off cancerous cells. The challenge that has faced cancer researchers for years is making a delivery vehicle that is sturdy enough to safely get the medication through the bloodstream to tumors — which is no smooth ride — but is also lithe enough to squeeze through the tumor’s dense extra cellular space — a matrix stuffed with sugars called hyaluronic acid.

In research recently published in the journal Nano Letters, lead author Hao Cheng, PhD, an assistant professor with an appointment in Drexel’s College of Engineering, and affiliation with School of Biomedical Engineering, Science and Health Systems; reports that the way to get past the tumor’s front door has everything to do with how the tiny particle is suited up for the journey.

“What we’ve reported here is a strategy to overcome biological barriers that plague delivery of medication, such as nonvehicle clearance in the bloodstream by the host immune system, and ineffective diffusion in the extracellular matrix of tumor cells,” Cheng said. “It’s a unique strategy that involves the decoration of nanovehicles with enzymes known to break down hyaluronic acid, which is a main barrier in the extracellular space, and the addition of an extra layer of polyethylene glycol to partially cover the enzymes.”

In the paper entitled “Hyaluronidase Embedded in Nanocarrier PEG Shell for Enhanced Tumor Penetration and Highly Efficient Antitumor Efficacy,” the group reports that their method is four times more effective at sending nanoparticles into a solid tumor than one of the best strategies currently in use. When cancer medication is loaded in the tiny particle, it has been shown to inhibit the growth of a type of aggressive breast cancer.

The team, which also included researchers Wilbur Bowne, MD, an associate professor in Drexel’s College of Medicine; Dimitrios Arhontoulis, an undergraduate in Drexel’s School of Biomedical Engineering, Science and Health Systems; lead author Hao Zhou and Zhiyuan Fan, doctoral candidates, Junjie Deng, PhD, postdoctoral researchers, and Pelin Lemons, a graduate student, all in the Materials Science and Engineering Department in the College of Engineering, created its nanoparticle suit by starting with one that is common in this area of cancer research and making some key alterations.

“In the general design of nanoparticles, bioactive molecules — not limited to enzymes — were attached on the outermost layer of particles,” Cheng said. “These enzymes can degrade the extra cellular matrix and enhance the nanoparticle’s ability to penetrate solid tumors.”

But in the body, this extra cargo can cause problems. One issue is that attaching enzymes to nanoparticles could cause them to come up short of the tumor and be cleared by the bloodstream before delivering the medication. There’s also a chance that the trip through the bloodstream could render the enzymes inert.

To counter these issues and keep the nanoparticles on course, the team decided to add an extra layer that not only protects the precious payload, but also positions the enzymes for maximum impact.

“The novelty of our design is that we partially embedded the hyaluronidase enzymes in a second polyethylene glycol layer to form the outer shell of the nanoparticle,” Cheng said. “This design dramatically reduces the enzymes’ effect on slowing the particle’s circulation and allows enzymes to maintain their function after the particle diffuses into the tumor.”

Embedding the enzymes in the layers of polyethylene glycol (PEG) ensures that the nanoparticle’s appearance tricks the immune system into leaving it alone during its trip to the tumor, yet and still allows the particle to deal with any hyaluronic acid it encounters on its penetration of the tumor. Other researchers have tested a theory that exposes tumors to the enzymes first, and then to nanoparticles, but this is not nearly as effective as Cheng’s method, because the nanoparticles developed at Drexel retain the enzymes through the duration of their diffusion into tumors, minimizing unnecessary hyaluronic acid degradation.

“The degradation of hyaluronic acid removes the barrier for nanoparticles to diffuse and allows them to access more cancer cells,” Cheng said. “The enhanced diffusion also increases the accumulation of nanoparticles in tumors, and the more nanoparticles that get into tumors the more effective they are at reducing its size.”

As part of the research, the team tested their nanoparticle against competitors that did not have a second layer of polyethylene glycol and ones that did not have the ECM-degrading enzymes. It was no surprise that their nanoparticle performed better in both penetrating tumors and accumulating in the cancerous cells.

“This exciting, novel nanoparticle drug delivery system will improve delivery of anti-cancer agents, enhancing anti-cancer activity to improve patient outcomes,” said Bowne. He foresees enormous potential for this strategy in the neoadjuvant and adjuvant setting for a number difficult to treat cancers such as locally advanced breast, pancreatic and mucin-producing gastrointestinal cancers.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/04/160408163824.htm  Original web page at Science Daily

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Radiation improves survival in older patients with soft tissue sarcomas

UC Davis researchers have shown that radiation therapy following surgery benefits older patients more than their younger counterparts, a surprising finding that could change the way some patients are treated for soft tissue sarcomas (STS).

The study, published in the journal Anticancer Research, used data from the Surveillance, Epidemiology, and End Results (SEER) program to assess whether radiation treatments after surgery improved disease-specific and overall survival in patients with non-metastatic sarcomas.

They found that radiation did increase survival compared to surgery alone, but the improvements mostly benefited patients 65 and older. This is the first time these outcomes have been analyzed on such a granular level, factoring in both age and cancer subtype.

“We found that older patients had a survival benefit with radiation, but in younger patients, many of those benefits went away,” said Robert Canter, associate professor in the Department of Surgery and principal investigator on the paper. “It seems that older patients respond better to the combination of surgery and radiation.”

There are more than 50 different types of soft-tissue sarcomas, which develop in muscles, fat and other cell types. While these conditions are generally treated surgically, it was not clear whether radiation therapy after surgery improved survival.

To clarify the issue, Canter and colleagues crunched data from SEER, which has gathered detailed cancer statistics since the 1970s. Analyzing data collected between 1990 and 2011, the team identified 15,380 non-pediatric patients with non-metastatic STS who were treated with surgery alone or with surgery and radiation.

The group pulled data on the tumor site, grade, size, cancer subtype and year of diagnosis, as well as the patient’s age, gender and other demographic information.

The team found significant improvements in overall survival and disease-specific survival in older patients across the majority of sarcomas. This was particularly true of the 12 major STS subtypes, including rhabdomyosarcoma, fibrosarcoma and synovial sarcoma. Younger patients benefited much less from radiation.

These results were somewhat surprising, as the researchers expected radiotherapy to primarily improve survival for younger patients.

“We were thinking it would be the opposite,” said Canter. “If the benefit is immune-mediated, younger patients should respond better since they have stronger immune systems.”

While younger patients did not receive the same level of benefit from radiotherapy as the older groups, they still had better overall and disease-specific survival from STS. The improvements among the older groups were compared to other older patients with similar disease who did not receive radiation.

Canter notes that more work must be done to validate the findings and illuminate the mechanisms that drive these age-related radiotherapy benefits. However, the work does offer a path to improve STS treatments for older patients.

“We sometimes don’t want to treat older people with radiation because we’re worried about the side effects,” said Canter. “However, these results indicate these patients should really be receiving it if they are candidates.”

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https://www.sciencedaily.com/releases/2016/04/160411134812.htm  Original web page at Science Daily

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Scientists discover how the brain repurposes itself to learn scientific concepts

The human brain was initially used for basic survival tasks, such as staying safe and hunting and gathering. Yet, 200,000 years later, the same human brain is able to learn abstract concepts, like momentum, energy and gravity, which have only been formally defined in the last few centuries.

New research from Carnegie Mellon University has now uncovered how the brain is able to acquire brand new types of ideas. Published in Psychological Science, scientists Robert Mason and Marcel Just used neural-decoding techniques developed at CMU to identify specific physics concepts that advanced students recalled when prompted. The brain activation patterns while thinking about the physics concepts indicated that all of the students’ brains used the ancient brain systems the same way, and the patterns revealed how the new knowledge was formed — by repurposing existing neural systems.

The findings could be used to improve science instruction. “If science teachers know how the brain is going to encode a new science concept, then they can define and elaborate that concept in ways that match the encoding. They can teach to the brain by using the brain’s language,” said Mason, a senior research associate in the Dietrich College of Humanities and Social Sciences’ Department of Psychology.

Mason and Just, the D. O. Hebb University Professor of Psychology, recruited nine advanced physics and engineering students to participate in the study. Each student’s brain was scanned at CMU’s Scientific Imaging and Brain Research (SIBR) Center while they were shown a set of 30 familiar concepts, such as gravity, entropy, inertia, refraction and velocity.

Using a machine learning program, Mason and Just were able to identify which of the 30 concepts a student was thinking about because the thought of each concept created its own brain activation pattern. They also could break down the patterns into the different neural pieces used to build the full concepts.

The research showed for the first time how learning physics concepts is accomplished by repurposing neural structures that were originally used for general everyday purposes. More specifically, the brain is able to learn physics concepts because of its ability to understand the four fundamental concepts of causal motion, periodicity, energy flow and algebraic (sentence-like) representations.

Brain systems that process rhythmic periodicity when hearing a horse gallop also support the understanding of wave concepts in physics. Similarly, understanding gravity involves visualizing causal motion, like an apple falling from a tree; energy flow uses the same system as sensing warmth from a fire or the sun; and understanding how one concept relates to others in an equation uses the same brain systems that are used to comprehend sentences describing quantities.

“This is why humans have been able to move ahead and innovate — because we can use our brain for new purposes,” Just said. “Human brains haven’t changed much over a few thousand years, but new fields like aeronautics, genetics, medicine and computer science have been developed and continuously change. Our findings explain how the brain is able to learn and discover new types of concepts.”

These findings are examples of the many brain research breakthroughs at Carnegie Mellon. CMU has created some of the first cognitive tutors, helped to develop the Jeopardy-winning Watson, founded a groundbreaking doctoral program in neural computation, and is the birthplace of artificial intelligence and cognitive psychology. Building on its strengths in biology, computer science, psychology, statistics and engineering, CMU launched BrainHub, an initiative that focuses on how the structure and activity of the brain give rise to complex behaviors.

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https://www.sciencedaily.com/releases/2016/04/160412132608.htm Original web page at Science Daily

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Precision medicine’s potential to define the genetics of autoimmune disease

Precision medicine is an emerging field that aims to deliver highly personalized health care by understanding how individual differences in genetics, environment, and lifestyle impact health and disease.

SLE, commonly called lupus, is a serious, potentially fatal autoimmune disease that the National Institutes of Health reports affects nine times more women than men, and is more likely to strike young African-American, Hispanic, Asian, and Native American women. The disease often begins between the ages of 15 and 44.

“SLE starts when the immune system attacks multiple organ systems in the body, which can result in a complex array of symptoms that are difficult to manage clinically and can lead to organ damage,” said Dr. Edward Wakeland, Chair of Immunology at UT Southwestern and co-senior author of the study posted online recently in the journal eLife. “Our findings support the potential of precision medicine to provide clinically relevant information about genetic susceptibility that may ultimately improve diagnosis and treatment.”

The study also may have implications for other systemic autoimmune diseases, a category of diseases that affect multiple body systems and includes Type 1 diabetes, rheumatoid arthritis, and multiple sclerosis, he said.

Dr. Wakeland and colleagues sequenced millions of DNA base pairs from more than 1,700 people, which allowed precise identification of the genetic variations contributing to SLE, he said. Specifically, the researchers identified 1,206 DNA variations located in 16 different regions of the human genome associated with increased susceptibility to SLE. They then showed that almost all of them (1,199) modify the level of expression of specific molecules that regulate immune responses, he said.

In addition, the two-year study identified many of the specific regulatory variations that were changed in SLE patients and demonstrated that accurately identifying such so-called causal variants increased the accuracy of the genetic association of individual SLE risk genes with susceptibility to SLE.

“Prior to our study, such a comprehensive sequence analysis had not been done and little was known about the exact genetic variations that modify the functions of the genes that cause SLE,” added Dr. Wakeland, who holds the Edwin L. Cox Distinguished Chair in Immunology and Genetics.

The scientists began their comprehensive sequence analysis using the DNA samples of 1,349 American Europeans (773 with SLE disease and 576 without) from sample collections at UT Southwestern, the University of Southern California, UCLA, Oklahoma Medical Research Foundation, and the Université Catholique de Louvain in Belgium.

They then determined the precise DNA sequences at SLE-associated genetic regions scattered throughout the genome. They found that SLE risk is associated with specific clusters of DNA variations, commonly called haplotypes, and that some haplotypes increased the risk for SLE while others provided protection from SLE.

After identifying the sets of DNA variants that increased SLE susceptibility in Caucasians, they used multiple public databases, including the international 1000 Genomes Project (2,504 genomic samples from the global human population) to determine whether these haplotypes also were found in South American, South Asian, African, and East Asian populations.

They discovered that the variants and haplotypes were distributed across subpopulations worldwide. Their findings indicate that many common haplotypes in the immune system are shared at different frequencies throughout the global population, suggesting that these variations in the immune system have ancient origins and persist in populations for long periods, Dr. Wakeland said.

“We thank the many SLE patients and control participants whose sample contributions were essential for these studies,” the researchers wrote.

Dr. Wakeland and colleagues plan to continue the research by obtaining more DNA samples and expanding their analysis to additional SLE risk genes with the goal of obtaining a data set that can be used to predict an individual’s unique risk of SLE, as well as the likelihood of benefiting from specific treatments.

“It is feasible that this same type of genetic analysis will allow the clustering of SLE patients into specific groups, based on their genetic predispositions, which would improve clinical management and potentially allow the development of more targeted therapies,” Dr. Wakeland said.

Earlier this month, UT Southwestern announced that Dr. Wakeland, whose laboratory has long served as the institution’s Genomics and Microarray Core Facility, will be leading a large DNA-sequencing initiative to address important clinical challenges. The new clinical sequencing facility, in collaboration with the Department of Pathology, will provide panel sequencing for cancer and other diagnoses, and eventually expand to whole-exome and whole-genome sequence analysis for a variety of patients. The laboratory will be established in the BioCenter on the East Campus. To commit full effort to this initiative, Dr. Wakeland will step down as Chair of Immunology, but will remain in this role until his successor is named.

“This clinical sequencing core facility will generate laboratory data to be used for the evaluation of patient tumors. I hope we will someday expand to genotyping patients to identify potential susceptibility to autoimmune disease and many other conditions as the field of precision medicine develops,” Dr. Wakeland said.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160318144531.htm  Original web page at Science Daily

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New compounds discovered as candidates for new antimicrobial drugs against Listeria infection

Scientists at Umeå Centre for Microbial Research (UCMR) have discovered chemical compounds which are able to attenuate the virulence of the bacterial human pathogen Listeria monocytogenes. Their findings are published today in the high impact journal Cell Chemical Biology.

The dramatic increase of antibiotic resistance makes new antimicrobial strategies necessary. The researchers at Umeå University in Sweden are studying an alternative approach, to inhibit the disease capacity (virulence) of bacteria but not their viability. Compared with traditional antibiotics, which often kill the bacteria, the risk of resistance development in disarmed bacteria is lower, since their survival does not depend on resistance against the new drug.

A Listeria infection can be very severe, particularly among patients such as elderly, infants, immunocompromised or pregnant women. Although disease occurrence is relatively low, Listeria‘s severe and sometimes fatal health consequences make it among the most serious foodborne infections, with a mortality of 30%. Listeria is found in unpasteurized dairy products and various ready-to-eat foods, and can grow at refrigeration temperatures. In Sweden, 60-90 people per year get infected and the statistics show that the number of outbreaks is increasing.

The study involved several different Umeå University research groups with diverse specialties: Microbiology, Chemistry and Structural Biology. The group of Jörgen Johansson, professor at the laboratory for Molecular Infection Medicine Sweden (MIMS) and the Department of Molecular Biology collaborated with the research groups of Elisabeth Sauer-Eriksson and Fredrik Almqvist, both professors at the Department of Chemistry.

The researchers tested a large number of possible candidates, which could inhibit expression of the Listeria virulence factors. For the test, they screened Listeria infection of human cells with a collection of ring-fused 2-pyridones. The scientists could prove that the ring-fused 2-pyridones could both attenuate the uptake of Listeria in the cell and the activity of the virulence regulator PrfA, which control the pathogenic abilities of Listeria.

The researchers also identified the first crystal structure of PrfA together with an inhibitor. Binding of the inhibitor to PrfA blocked its ability to interact with DNA, thereby preventing expression of virulence factors. As a consequence, Listeria bacteria were not able to bind and infect the human cells.

“This study means a lot for future development of ‘disarming compounds’, not only in Listeria. In fact, our study is the first example on a structural level of an inhibition of any virulence regulator in bacteria,” says Jörgen Johansson about the impact of the findings.

“The first results are very promising. We have been able to use the structural information to design and synthesize new improved candidates that are now being evaluated,” added Fredrik Almqvist.

“We now know that this class of compounds (2-pyridones) constitute a great platform for the development of virulence blocking compounds. We have developed methods that allow us to fine-tune the substitution pattern and compound properties in such a way that we can direct these compounds towards several different pathogens e.g. E. coli and Chlamydia. And more studies are ongoing with other pathogens,” adds Fredrik Almqvist.

“Through this very fruitful research collaboration, we showed that Umeå has all the tools and expertise needed to understand and develop new antimicrobial strategies,” says Elisabeth Sauer-Eriksson.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160317151130.htm  Original web page at Science Daily

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Memories retrieved in mutant ‘Alzheimer’s’ mice

People with Alzheimer’s disease may forget faces or where they left familiar objects because their brains cannot find where they put those memories, a study in mice suggests.

The study, reported in Nature, contradicts the notion that Alzheimer’s prevents the brain from making new memories. It also suggests that brain stimulation might temporarily improve the memories of patients in the early stages of the disease.

The research builds on earlier work by lead author Susumu Tonegawa, a neuroscientist, and his colleagues at Massachusetts Institute of Technology in Cambridge. Last year, they showed that in certain types of amnesia, memories were stored but could not be retrieved.

It is difficult to detect the difference between a stored and a retrieved memory in humans, as the only way to test memory is to ask patients to recall information. But memories can be manipulated in mice, so Tonegawa and his colleagues tested their theory using two strains of mice with mutations in genes linked to Alzheimer’s disease.

These mice develop amyloid protein clusters, or plaques, in their brains and eventually lose their memories — just as humans with Alzheimer’s disease do. The researchers demonstrated this memory loss by placing the mice in a box in which they received an electric shock. Normal mice learned to fear the box, but the mutant mice did not, because they did not remember being shocked.

The researchers engineered the mutant mice to make a light-sensitive protein in neurons in the hippocampus, the part of the brain that encodes short-term memories. Then the scientists placed the mice back into the box, shining a light onto the animals’ brains to force the modified neurons to fire. This caused the mice to recall the memory of being shocked, and the animals froze — suggesting that the memory had been encoded in the first place. But the next day, the mice had again forgotten their fear of the box.

Next, the scientists pulsed the light, mimicking a process that occurs naturally as a memory is accessed repeatedly over time. This strengthened the connections between the hippocampus and another brain region called the entorhinal cortex, a connection that serves as long-term memory storage. With the memories now firmly embedded, the mice remembered to be afraid of the box, even when the light was off.

When the researchers dissected the animals’ brains, they found that the pulsing stimulation had created more connections between the hippocampus and the entorhinal cortex — connections that are lost as Alzheimer’s disease progresses. But the researchers expect that the technique would only work for a few months in mice, or two to three years in humans, before the disease advances enough to erase any gains.

This theory about how Alzheimer’s affects the brain agrees with symptoms seen in patients. For unknown reasons, the hippocampus is particularly vulnerable to the ravages of Alzheimer’s, which is why a person with the disease first forgets new memories, such as where he left his car. As the disease worsens, other parts of the brain are destroyed, causing patients to forget long-term information such as family members’ names.

“It’s a beautifully executed study,” says Itzhak Fried, a neurosurgeon at the University of California Los Angeles. But he cautions that the findings may not translate to human brains, because mice do not develop amyloid plaques in the same way as humans do. And it is impossible to test whether the memory-retrieval hypothesis holds true in humans, because researchers have not worked out how to stimulate human brains using light.

Christine Denny, a neurobiologist at Columbia University in New York City, says that electrical stimulation may succeed where optogenetics has not. Early trials suggest that deep-brain stimulation of the hippocampus prompts the creation of neurons and improves memory in some Alzheimer’s patients. But no one knows how it works.

Tonegawa’s findings may allow more targeted stimulation, especially once researchers understand what happens to memories after they leave the hippocampus. Several groups, including Fried’s, are already implanting such fine-tuned micro-stimulation devices into the entorhinal cortices of epilepsy patients with brain injuries in the hope of restoring memory abilities.

Fried says that it might soon be time to test microstimulation in very small groups of people with Alzheimer’s disease. Although he acknowledges that it is important to do more animal work, especially in primates, “at the same time we’re crying for relief of clinical symptoms in patients who are really suffering”.

Nature doi:10.1038/nature.2016.19574

http://www.nature.com/news/index.html   Nature

http://www.nature.com/news/memories-retrieved-in-mutant-alzheimer-s-mice-1.19574  Original web page at Nature

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Stem cells used to identify cellular processes related to glaucoma

Using stem cells derived from human skin cells, researchers led by Jason Meyer, assistant professor of biology, along with graduate student Sarah Ohlemacher of the School of Science at Indiana University-Purdue University Indianapolis, have successfully demonstrated the ability to turn stem cells into retinal ganglion cells (RGCs), the neurons that conduct visual information from the eye to the brain. Their goal is the development of therapies to prevent or cure glaucoma.

In addition to glaucoma, a group of degenerative diseases that damage the eye’s optic nerve and can result in vision loss and blindness, this work has potential implications for treatment of optic- nerve injuries of the types incurred by soldiers in combat or athletes in contact sports.

In the study, which appears online in advance of publication in the journal Stem Cells, the IUPUI investigators took skin cells biopsied from volunteers with an inherited form of glaucoma and from volunteers without the disease and genetically reprogrammed them to become pluripotent stem cells, meaning they are able to differentiate into any cell type in the body. The researchers then directed the stem cells to become RGCs at which point the cells began adopting features specific to RGCs — features that were different in the cells of individuals with glaucoma than in the cells that came from healthy individuals.

Glaucoma is the most common disease that affects RGCs, which serve as the connection between the eye and the brain, sending information taken in by the eye to the brain for interpretation. When these cells are damaged or severed, the brain cannot receive critical information, leading to blindness. The National Institutes of Health’s National Eye Institute estimates that glaucoma affects more than 2.7 million people in the United States and more than 60 million worldwide.

“Skin cells from individuals with glaucoma are no different from skin cells of those without glaucoma,” said Meyer, a cell biologist and stem cell researcher, who also holds an appointment as a primary investigator with the Stark Neurosciences Research Institute at the Indiana University School of Medicine. “However, when we turned glaucoma patients’ skin cells into stem cells and then into RGCs, the cells became unhealthy and started dying off at a much faster rate than those of healthy individuals.

“Now that we have produced cells that develop features of glaucoma in culture dishes, we want to see if compounds we add to these RGCs can slow down the degeneration process or prevent these cells from dying off. We already have found candidates that look promising and are studying them. In the more distant future, we may be able to use healthy patient cells as substitute cells as we learn how to replace cells lost to the disease. It’s a significant challenge, but it’s the ultimate — and, we think, not unrealistic — long-range goal.”

https://www.sciencedaily.com/   Science Daily

https://www.sciencedaily.com/releases/2016/03/160321081227.htm  Original web page at Science Daily

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Individualized cancer treatment targeting the tumor, not the whole body, a step closer

They look like small, translucent gems but these tiny ‘gel’ slivers hold the world of a patient’s tumour in microcosm ready for trials of anti-cancer drugs to find the best match between treatment and tumour.

The ‘gel’ is a new 3D printable material developed by QUT researchers that opens the way to rapid, personalised cancer treatment by enabling multiple, simultaneous tests to find the correct therapy to target a particular tumour.

Professor Dietmar W. Hutmacher from QUT’s Institute of Health and Biomedical Innovation said the new material was a gelatine-based hydrogel that mimicked human tissue. The method for producing the gelatine-based hydrogel is published in the journal Nature Protocols.

“Hydrogel is a biomaterial used by thousands of researchers around the globe; gelatine is based on collagen, one of the most common tissues in the human body. We have modified the gelatine to engineer 3D tumour microenvironments,” Professor Hutmacher said.

“Our big breakthrough is we can produce this high-quality material on a very large scale inexpensively.

“It is highly reproducible which means we have been able to produce this hydrogel hundreds of times, not just once or twice in the lab, so researchers worldwide will be able to create it.”

Professor Hutmacher said the new hydrogel could be used as a ‘bioink’ to print 3D ‘microenvironments’ or models of a tumour to test different anti-cancer drugs.

“We will be able to use this hydrogel infused with tumour cells to quickly create a number of models of patient-specific tumours.

“Instead of the sometimes hit and miss chemotherapy that affects every cell in the body this will allow us to test different anti-cancer drugs and different combinations of them all at once so that we can pinpoint an individualised treatment that will hit only the cancer cells.

“It will cut the process of finding a personalised treatment for each patient down to a week or two.” Because the hydrogel can be modified to mimic the firmness of cartilage or softness of breast tissue it can be used to create models for all types of cancer and also for research on stem cells and tissue engineering.

The IHBI research team includes Dr Daniela Loessner, Associate Professor Travis Klein and PhD student Christoph Meinert. The study, Functionalization, preparation and use of cell-laden gelatin methacryloyl-based hydrogels as modular tissue culture platforms was published this week.

The new hydrogel discovery is part of Biofabrication Research led by Professor Hutmacher at IHBI, which launched the world’s first Master of Biofabrication, a dual Australian and European master degree.

“We are seeking more students for the masters course at IHBI from all science and technology disciplines,” Professor Hutmacher says.

“Biofabrication is the future of medicine. It is a multidisciplinary area of research that requires an understanding of chemistry, physics, biology, medicine, robotics and computer science and we welcome graduates from any of these fields to apply for the master degree.”

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160321110301.htm  Original web page at Science Daily

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* Anatomy of pain

Grimacing, we flinch when we see someone accidentally hit their thumb with a hammer. But is it really pain we feel? Researchers at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig and other institutions have now proposed a new theory that describes pain as a multi-layered gradual event which consists of specific pain components, such as a burning sensation in the hand, and more general components, such as negative emotions. A comparison of the brain activation patterns during both experiences could clarify which components the empathic response shares with real pain.

Imagine you’re driving a nail into a wall with a hammer and accidentally bang your finger. You would probably injure finger tissue, feel physical distress, focus all your attention on your injured finger and take care not to repeat the misfortune. All this describes physical and psychological manifestations of “pain” — specifically, so-called nociceptive pain experienced by your body, which is caused by the stimulation of pain receptors.

Now imagine that you see a friend injure him or herself in the same way. You would again literally wince and feel pain, empathetic pain in this case. Although you yourself have not sustained any injury, to some extent you would experience the same symptoms: You would feel anxiety; you may recoil to put distance between yourself and the source of the pain; and you would store information about the context of the experience in order to avoid pain in the future.

Previous studies have shown that the same brain structures — namely the anterior insula and the cingulate cortex — are activated, irrespective of whether the pain is personally experienced or empathetic. However, despite this congruence in the underlying activated areas of the brain, the extent to which the two forms of pain really are similar remains a matter of considerable controversy.

To help shed light on the matter, neuroscientists, including Tania Singer, Director at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, have now proposed a new theory: “We need to get away from this either-or question, whether the pain is genuine or not.”

Instead, it should be seen as a complex interaction of multiple elements, which together form the complex experience we call “pain.” The elements include sensory processes, which determine, for example, where the pain stimulus was triggered: in the hand or in the foot? In addition, emotional processes, such as the negative feeling experienced during pain, also come into play. “The decisive point is that the individual processes can also play a role in other experiences, albeit in a different activation pattern,” Singer explains — for example, if someone tickles your hand or foot, or you see images of people suffering on television. Other processes, such as the stimulation of pain receptors, are probably highly specific to pain. The neuroscientists therefore propose comparing the elements of direct and empathetic pain: Which elements are shared and which, by contrast, are specific and unique to the each form of pain?

A study that was published almost simultaneously by scientists from the Max Planck Institute for Human Cognitive and Brain Sciences and the University of Geneva has provided strong proof of this theory: They were able to demonstrate for the first time that during painful experiences the anterior insula region and the cingulate cortex process both general components, which also occur during other negative experiences such as disgust or indignation, and specific pain information — whether the pain is direct or empathic.

The general components signal that an experience is in fact unpleasant and not joyful. The specific information, in turn, tells us that pain — not disgust or indignation — is involved, and whether the pain is being experienced by you or someone else. “Both the nonspecific and the specific information are processed in parallel in the brain structures responsible for pain. But the activation patterns are different,” says Anita Tusche, also a neuroscientist at the Max Planck Institute in Leipzig and one of the authors of the study.

Thanks to the fact that our brain deals with these components in parallel, we can process various unpleasant experiences in a time-saving and energy-saving manner. At the same time, however, we are able register detailed information quickly, so that we know exactly what kind of unpleasant event has occurred — and whether it affects us directly or vicariously. “The fact that our brain processes pain and other unpleasant events simultaneously for the most part, no matter if they are experienced by us or someone else, is very important for social interactions,” Tusche says, “because it helps to us understand what others are experiencing.”

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160323115915.htm  Original web page at Science Daily

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Researchers identify new cause of inherited neuropathy

Neurology researchers link mutations in myelin protein to Charcot-Marie-Tooth Disease.

Charcot-Marie-Tooth Disease (CMT) is a family of inherited disorders of the peripheral nervous system, affecting approximately one in 2,500 Americans. Its most common iteration, CMT1, comes in many forms, most of which have to date been linked to a small set of causative genes. New research from the department of Neurology at the Perelman School of Medicine at the University of Pennsylvania and the Children’s Hospital of Philadelphia recently spanned the globe to uncover a new genetic cause of CMT1. Their findings are published online in Brain.

Their findings expand the number of genes known to cause CMT1, further helping neurologists and patients find the genetic underpinnings of their neuropathy.

Charcot-Marie Tooth Disease is a progressive debilitating neurodegenerative disorder that strikes in the second or third decade of life. This disease results in numbness and weakness in the hands and feet. There are two categories of CMT: those caused by the loss of axons in the peripheral nerves (CMT2) and those characterized by a malfunction in the Schwann cells that make up the myelin sheath, the protective coating that surrounds the nerve fibers and allows them to conduct nerve signals at high speeds (CMT1).

Penn neurologists studied a father and son with CMT1 who were treated at the Hospital of the University of Pennsylvania and Children’s Hospital of Philadelphia, respectively, and did not carry a mutation in any of the five genes known to cause CMT1. The father’s parents did not have the disease, suggesting that a new random mutation occurred, not shared by either parent, which he then passed on to one of his three sons.

Through complex genetic sequencing of the father’s 20,000 genes, the team was able to identify 49 mutations that could be the cause of the pair’s CMT. One mutation, a change in the peripheral myelin protein 2 gene (PMP2), emerged as the most likely culprit. PMP2 encodes a protein that transports fatty acids, which are the building blocks of the myelin sheath and known to be one of the most abundant proteins in peripheral nervous system myelin. Further testing of the father’s living siblings, parents and two other sons showed that he and his one affected son were the only family members to carry this mutation. This was strong evidence that mutations in PMP2 cause CMT1, slowing nerve conduction and resulting in weakness and numbness in the hands and feet.

“Next-generation sequencing technology has allowed us to find new causes of genetic diseases in much smaller families,” explained the study’s lead author, William Motley, MD, PhD, a resident physician in Medicine. “The fact that his parents did not have the disease allowed us to narrow the number of possible mutations, as so few arise between generations. We are fortunate to have these tools to help us provide genetic diagnoses to our patients, sometimes even in cases where the patients have no mutations in known causes of their disease. Traditional genetic techniques would never have allowed us to find the cause of this family’s CMT.”

To provide further evidence of an association between PMP2 mutation and CMT1, the Penn team reached out to an international consortium of CMT researchers to find patients with mutations in the same gene. Working with collaborators at the University of Antwerp, an additional 136 European families with CMT1 were screened for mutations in PMP2. These identified an Austrian family with several affected members who share a mutation in PMP2. Interestingly, the mutation was adjacent to the mutation in the family seen at Penn.

“This has been a highly fulfilling effort. We were able to track down the cause of this family’s CMT, help another family, and find a new genetic cause of CMT in the process,” said senior author, Steven S. Scherer, MD, PhD, the Ruth Wagner Van Meter and J. Ray Van Meter Professor of Neurology and Chief of the Neuromuscular division in the department of Neurology. “The participation of the family, the clinicians, and the scientists, from Penn and around the world, makes this success even sweeter.”

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160323185657.htm  Original web page at Science Daily

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New proteins discovered that link obesity-driven diabetes to cancer

For the first time, researchers have determined how bromodomain (BRD) proteins work in type 2 diabetes, which may lead to a better understanding of the link between adult-onset diabetes and certain cancers.

The findings, which appear in PLOS ONE, show that reducing levels in pancreatic beta cells of individual BRDs, called BET proteins, previously shown to play a role in cancer, may also help patients who are obese and diabetic.

The research was led by Gerald V. Denis, PhD, associate professor of pharmacology and medicine at Boston University School of Medicine, who was the first to show that BET protein functions are important in cancer development.

Adult-onset diabetes has been known for decades to increase the risk for specific cancers. The three main members of the BET protein family, BRD2, BRD3 and BRD4, are closely related to each other and often cooperate. However at times, they work independently and sometimes against each other.

According to the researchers new small molecule BET inhibitors have been developed that block all three BET proteins in cancer cells, but they interfere with too many functions.

“The BET proteins provide a new pathway to connect adult-onset diabetes with cancer, so properly targeting BET proteins may be helpful for both,” explained Denis, who is the corresponding author of the study.

He believes this discovery shows the need for deeper analysis of individual BET proteins in all human cell types, starting with boosting insulin and improving metabolism in the pancreas of adults who are obese.

“Without better targeted drugs, some ongoing cancer clinical trials for BET inhibitors are premature. These new results offer useful insight into drug treatments that have failed so far to appreciate the complexities in the BET family.”

https://www.sciencedaily.com/   Science Daily

https://www.sciencedaily.com/releases/2016/03/160323151852.htm  Original web page at Science Daily

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New clue to fighting acute myeloid leukemia found

A study led by researchers from the Cancer Science Institute of Singapore (CSI Singapore) at the National University of Singapore (NUS) has uncovered a new clue that may help fight acute myeloid leukemia (AML), the most common form of cancer of the blood and bone marrow, and an aggressive type of cancer. The findings open a new door to treating the disease more effectively.

AML usually originates from the bone marrow, where blood cells are produced. It is characterized by an overproduction of impaired white blood cells. The differentiation of immature white blood cell precursors into functional white blood cells is an essential process mediating the body’s immunity.

The research team found that an enzyme, GCN5, is able to inactivate a protein called C/EBPa in myeloid precursor cells. This prevents immature myeloid white blood cells from maturing into granulocytes — which make up about 70 per cent of white blood cells in the body. As a result, healthy white blood cells formation is disrupted.

The team, which includes Professor Daniel Tenen, Director of CSI Singapore, Ms Kwok Hui Si, PhD student at the Institute, as well as Dr Deepak Bararia, a former Postdoctoral Fellow at the Institute, discovered that the inactivation of the C/EBPa protein is carried out by acetylation, which is a process by which GCN5 adds an acetyl group onto C/EBPa reducing the ability of C/EBPa to bind to DNA and modulating its transcriptional activity in the cell. The findings of the study were published in the journal Nature Communications on 24 March 2016.

Identification of this molecular pathway provides clues towards targeting the GCN5-mediated acetylation of C/EBPa in the treatment of leukemia.

Prof Tenen said, “As AML is a fast-growing cancer, timely treatment soon after diagnosis could increase patients’ chances of survival. The current main treatment strategy for AML is cytotoxic chemotherapy. Our research results form the basis of an alternative therapeutic strategy that could potentially reduce remission risks and improve cure rates. Moving forward, the team is looking into designing effective GCN5 inhibitors for therapeutic purposes by studying GCN5 in AML further in depth.”

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160329101534.htm  Original web page at Science Daily

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Moments of acute stress can cause molecular alterations in immune response

Chronic psychosocial and emotional stress has well-documented negative effects upon the human immune system, measurably increasing the risk of disease. Much less is known about the health effects of acute but transitory episodes of stress, such as jumping out of an airplane. Do these panic-inducing moments also raise the risk of stress-related conditions and disorders, such as cardiovascular disease, sleep dysfunction, impaired wound healing, depression and obesity?

A team of researchers at University of California, San Diego School of Medicine, Stony Brook University in New York and elsewhere addressed that question by asking study participants to literally jump out of a plane, taking blood samples before and after to measure key immune response indicators. Their findings are published in the March 4 issue of Brain, Behavior and Immunity.

“In our everyday lives, acute stress is manageable and does not cause physiological damage,” said study co-author Brinda Rana, PhD, associate professor in the Department of Psychiatry at UC San Diego School of Medicine. “However, for those who experience it frequently, it can be a risk for chronic diseases and disorders, such as cardiovascular and immune modulated inflammation. And since the health of the immune system is crucial to protection against pathogens and other diseases, it’s important to understand the impact of stressful life events on the ability of our immune system to properly do its job.”

The study involved 39 individuals (24 males, 15 females) who had independently contacted a New York-area skydiving school to schedule a first-time tandem sky dive in which the student skydiver was connected by harness to an instructor who guided the student through the jump, freefall and landing.

All of the participants were healthy adults with no history of cardiac or mental illness. They were divided into two groups: 13 would have their RNA expression profiles measured to understand molecular signatures associated with stress, and 26 would be studied by flow cytometry to access changes in immune cell composition in blood.

Blood sampling was precisely scheduled by the lab of co-author Lilianne R. Mujica-Parodi, PhD, associate professor in the Department of Biomedical Engineering at Stony Brook University. Participants provided a baseline blood sample at 9:15 a.m. within one week prior to or one day after the sky dive. On the day of the skydive, all participants awoke at 6:30 a.m. and arrived at Stony Brook University Hospital at 7:30 a.m. where “pre-boarding” samples were collected at 9:15 a.m., one hour before take-off.

The actual jump occurred at 10:30 a.m., when the airplane reached an altitude of 11,550 feet. Skydivers landed five minutes later, with post-landing samples taken at 10:45 a.m. and again at 11:30 a.m. back at the hospital.

“Our tandem skydive instructor is also a phlebotomist,” said Mujica-Parodi. “He carried the blood draw supplies with him on the jump and was poised to draw blood as soon as the skydivers hit the ground.”

In addition, saliva samples were collected every 15 minutes from 9:15 a.m. to 11:30 a.m. on both the day of the sky dive and the baseline hospital day

Previous research has shown that acute, short-term stress provokes a mixed bag of immune responses, some beneficial, some not. For example, numbers of natural killer cells, which are part of the innate immune response, increase, but skin healing capacity is reduced. The novelty of the study, said Rana, is leveraging advanced computational and molecular tools to assess large-scale immune system responses, to more finely detail the effects of acute, short-term stress.

“Our study is the first to probe the rapid transcriptomic (messenger RNA) changes in white blood cells that occur before and after an acute psychological stressor,” said Rana. “We identified specific genes and pathways involved in both the innate and the adaptive immune response that were dysregulated in response to the acute stress of the sky dive, and which returned rapidly to natural baseline levels one hour after the jump.”

Interestingly, the researchers noted that modules of coordinately expressed genes responding to stress were different between male and female skydivers, which they say may help explain gender differences observed in development of stress related cardiovascular and autoimmune disorders, as well as conditions like post-traumatic stress disorder (which is twice as common in women).

Nadejda Beliakova-Bethell, PhD, first co-author of the study and an assistant project scientist at UC San Diego, with background in infectious diseases, said while the research was exploratory, it laid the foundation for future, more detailed experiments to elucidate the contribution of stressful life events and exposure to pathogens to the functioning of the immune system.

“The immune response to stress is similar to the response to pathogens,” said Beliakova-Bethell. “An instance of an acute stress or infection activates the immune system, while chronic stress or infection results in the exhaustion of the immune system, making it less effective at responding to new stressful events or new pathogens. The effects on the transcriptome of white blood cells, observed in this study, were very transient, returning to baseline levels within one hour after landing, but with repeated acute or chronic stress, these transcriptomic changes would be expected to be more permanent, and may be similar, at least in part, to the effects of chronic viral infection.

“Future studies could make an important contribution to identifying gene targets for developing therapeutic strategies that would help people to cope with the prolonged effects of a stressor or to fight new infections. This would be specifically important for the elderly, who would have accumulated effects of stressors and infections throughout their lifetimes.”

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160301174009.htm  Original web page at Science Daily

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Fungal pathogen sheds gene silencing machinery and becomes more dangerous

For more than a decade, a rare but potentially deadly fungus called Cryptococcus deuterogatti has taken up residence in the Pacific Northwest and Vancouver Island. Unlike its cousin Cryptococcus neoformans, which mostly infects patients with compromised immune systems, this fungus has sickened hundreds of otherwise healthy people.

Now, researchers have found that the pathogen tossed aside over a dozen different genes on its way to becoming a new, more virulent species. Surprisingly, most of these discarded genes play a part in RNA interference or RNAi, a defense mechanism employed by fungi and other organisms to protect the integrity of their genomes. The study was published March 4 in PLOS Genetics.

“Genome instability is a bad thing in terms of human health, because it is linked to cancer and other diseases,” said Blake Billmyre, lead study author and a graduate student in Joseph Heitman’s lab at Duke University School of Medicine. “But it could be good thing for single-celled organisms like Cryptococcus, because it enables them to mutate, evolve and adapt to survive under different conditions.”

Cryptococcus deuterogatti was largely confined to tropical climates until 1999, when it showed up on Vancouver Island and began spreading throughout southwest Canada and into Washington and Oregon. The emerging fungal pathogen causes severe pulmonary and central nervous system infections, and is fatal if left untreated.

Five years ago, researchers in the Heitman lab participated in an international collaborative consortium to sequence the genome of this outbreak species and discovered that it had lost two genes involved in RNAi, a process previously thought to be key to its survival.

The RNAi gene-silencing machinery normally shreds the genetic instructions for harmful viruses or silences rogue genes that might contaminate the fungus’ genome. But Cryptococcus deuterogatti had holes in its genome where the two RNAi genes should have been.

Armed with this information, Billmyre hypothesized that other genes in this missing set of genes might also function in RNAi. He and his colleagues compared the genomes of Cryptococcus deuterogatti with less potent cousins like Cryptococcus neoformans, which predominantly infects immunocompromised individuals. They found that C. deuterogatti has lost 14 genes compared to the other, less pathogenic, species.

The researchers then conducted a number of genetic and molecular analyses to determine if any of these lost genes played a role in RNAi. They mutated each of the genes in Cryptococcus neoformans, which has fully functioning RNAi machinery, to see if these genes were needed for the fungi to silence extra genetic material.

Joseph Heitman, the James B. Duke professor and chair of Molecular Genetics and Microbiology, said he expected to find maybe one or two other genes involved in RNAi. To his surprise, they found that 11 of the 14 missing genes they surveyed were involved in gene silencing.

“We could have imagined that the species lost a couple of RNAi genes, and then a smattering of genes involved in all other kinds of processes,” said Heitman. “Instead, the one glaring difference between these more and less virulent species seems to be the loss of the RNAi pathway.”

Though the researchers don’t know why shedding the RNAi machinery could help Cryptococcus assume a deadlier form, they do have some ideas. It could enable the fungi to cohabitate with killer viruses that pump out powerful toxins to poison competing organisms. Or it could allow them to accumulate mutations or even extra chromosomes to gain resistance against antifungal medications.

Whatever the reason, the discovery could pave the way for future studies using comparative genomics to identify other sets of related genes. Once one gene in a pathway is lost, the researchers hypothesize that an organism can find itself on a slippery evolutionary slope as other genes that are no longer of benefit are lost in quick succession. Only a few other examples of this system-wide pattern of gene loss, called systems polymorphisms, have been described so far.

“There is so much you can learn from looking for things that are missing,” said Billmyre. “It’s true what they say, you don’t know what you’ve got ’till it’s gone.”

https://www.sciencedaily.com/   Science Daily

https://www.sciencedaily.com/releases/2016/03/160304160348.htm  Original web page At Science Daily

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Likely biological link found between Zika virus, microcephaly

Working with lab-grown human stem cells, a team of researchers suspect they have discovered how the Zika virus probably causes microcephaly in fetuses. The virus selectively infects cells that form the brain’s cortex, or outer layer, making them more likely to die and less likely to divide normally and make new brain cells.

The researchers say their experiments also suggest these highly-susceptible lab-grown cells could be used to screen for drugs that protect the cells or ease existing infections.

“Studies of fetuses and babies with the telltale small brains and heads of microcephaly in Zika-affected areas have found abnormalities in the cortex, and Zika virus has been found in the fetal tissue,” says Guo-li Ming, M.D., Ph.D., a professor of neurology, neuroscience, and psychiatry and behavioral science at Johns Hopkins’ Institute for Cell Engineering. “While this study doesn’t definitely prove that Zika virus causes microcephaly, it’s very telling that the cells that form the cortex are potentially susceptible to the virus, and their growth could be disrupted by the virus.” Ming led the research team along with Hongjun Song, Ph.D., a professor of neurology and neuroscience in the Institute for Cell Engineering, and Hengli Tang, Ph.D., a virologist at Florida State University.

Results of the experiments, conducted by researchers at the Johns Hopkins University School of Medicine, Florida State University, and Emory University, are described online March 4 in the journal Cell Stem Cell.

In a quickly executed study that reflects the global public health threat posed by Zika, the researchers compared Zika’s effect on cells known as cortical neural progenitor cells to two other cell types: induced pluripotent stem cells and immature neurons. Induced pluripotent stem cells are made by reprogramming mature cells, and can give rise to any cell type in the body, including cortical neural progenitor cells. Cortical neural progenitor cells in turn give rise to immature neurons.

The experiments, conducted in less than a month, began when Tang reached out to Ming and Song, who use stem cells to study early brain development. The Johns Hopkins labs sent team members and cells to Tang’s lab, where the cells were exposed to Zika virus. Then the cells’ genetic expression — evidence of which genes were being used by the cells and which weren’t — were analyzed in Peng Jin’s laboratory at Emory University.

According to Tang, three days after exposure to the virus, 90 percent of the cortical neural progenitor cells were infected, and had been hijacked to churn out new copies of the virus. Furthermore, the genes needed to fight viruses had still not been switched on, which is highly unusual, he adds. Many of the infected cells died, and others showed disrupted expression of genes that control cell division, indicating that new cells could not be made effectively.

Using specific, known types of cells allowed the researchers to see where the developing brain is most vulnerable, Song says. He and Ming are now using the cells to find out more about the effects of Zika infection on the developing cortex. “Now that we know cortical neural progenitor cells are the vulnerable cells, they can likely also be used to quickly screen potential new therapies for effectiveness,” Song adds.

Zika virus has recently emerged as a public health concern, but it was first discovered in Uganda in the 1940s. Since then, small outbreaks have appeared in Asia and Africa, but symptoms were generally mild and did not appear to have any long-term effects. Carried by infected Aedes aegypti mosquitos, Zika is largely transmitted through bites, but can also occur through intrauterine infection or sexual transmission.

In 2015, the Zika virus began spreading throughout the Americas and a potential link was seen between the virus and a significant increase in cases of fetal microcephaly, as well as other neurologic abnormalities. This connection and the proliferation in cases led to the World Health Organization declaring Zika virus an international public health emergency.

https://www.sciencedaily.com/  Science Daily

https://www.sciencedaily.com/releases/2016/03/160304163404.htm  Original web page at Science Daily