High protein foods boost cardiovascular health, as much as quitting smoking or getting exercise

Eating foods rich in amino acids could be as good for your heart as stopping smoking or getting more exercise -- according to new research. 

A higher intake of protein from animal sources was linked with lower levels of arterial stiffness.

Credit: © Africa Studio / Fotolia

 

A new study published today reveals that people who eat high levels of certain amino acids found in meat and plant-based protein have lower blood pressure and arterial stiffness.
And the magnitude of the association is similar to those previously reported for lifestyle risk factors including salt intake, physical activity, alcohol consumption and smoking.
Researchers investigated the effect of seven amino acids on cardiovascular health among almost 2,000 women with a healthy BMI. Data came from TwinsUK -- the biggest UK adult twin registry of 12,000 twins which is used to study the genetic and environmental causes of age related disease.
They studied their diet and compared it to clinical measures of blood pressure and blood vessel thickness and stiffness.
They found strong evidence that those who consumed the highest amounts of amino acids had lower measures of blood pressure and arterial stiffness.
But they found that the food source was important -- with a higher intake of amino acids from plant-based sources associated with lower blood pressure, and a higher intake from animal sources associated with lower levels of arterial stiffness.
Lead researcher Dr Amy Jennings, from UEA's Norwich Medical School, said: "This research shows a protective effect of several amino acids on cardiovascular health.
"Increasing intake from protein-rich foods such as meat, fish, dairy produce, beans, lentils, broccoli and spinach could be an important and readily achievable way to reduce people's risk of cardiovascular disease.
"Results from previous studies have provided evidence that increased dietary protein may be associated with lower blood pressure. We wanted to know whether protein from animal sources or plant-based sources was more beneficial -- so we drilled down and looked at the different amino acids found in both meat and vegetables.
"We studied seven amino acids -- arginine, cysteine, glutamic acid, glycine, histidine, leucine, and tyrosine. Glutamic acid, leucine, and tyrosine are found in animal sources, and a higher intake was associated with lower levels of arterial stiffness.
"All seven amino acids, and particularly those from plant-based sources, were associated with lower blood pressure.
"The really surprising thing that we found is that amino acid intake has as much of an effect on blood pressure as established lifestyle risk factors such as salt intake, physical activity and alcohol consumption. For arterial stiffness, the association was similar to the magnitude of change previously associated with not smoking.
"High blood pressure is one of the most potent risk factors for developing cardiovascular disease. A reduction in blood pressure leads to a reduction in mortality caused by stroke or coronary heart disease -- so changing your diet to include more meat, fish, dairy produce and pulses could help both prevent and treat the condition.
"Beneficial daily amounts equate to a 75g portion of steak, a 100g salmon fillet or a 500ml glass of skimmed milk," she added.
Prof Tim Spector from the department of Twin Research at King's college London said: "The finding that eating certain meat and plant proteins are linked to healthier blood pressure is an exciting finding. We need to understand the mechanism to see if it is direct or via our gut microbes."
 

Journal Reference:

1. A. Jennings, A. MacGregor, A. Welch, P. Chowienczyk, T. Spector, A. Cassidy. Amino Acid Intake Is Inversely Associated with Arterial Stiffness and Central Blood Pressure in Women. Journal of Nutrition, 2015; DOI: 10.3945/%u200Bjn.115.214700 

Courtesy: ScienceDaily
 

 

Capturing cancer: 3-D model of solid tumors explains cancer evolution

Researchers have developed the first model of solid tumors that reflects both their three-dimensional shape and genetic evolution. The new model explains why cancer cells have a surprising number of genetic mutations in common, how driver mutations spread through the whole tumor and how drug resistance evolves. 

This is a three-dimensional model of a tumor showing cell types in varying colors.

Credit: Bartek Waclaw and Martin Nowak

 

Though models have been developed that capture the spatial aspects of tumors, those models typically don't study genetic changes. Non-spatial models, meanwhile, more accurately portray tumors' evolution, but not their three-dimensional structure.
A collaboration between Harvard, Edinburgh, and Johns Hopkins Universities including Martin Nowak, Director of the Program for Evolutionary Dynamics and Professor of Mathematics and of Biology at Harvard, has now developed the first model of solid tumors that reflects both their three-dimensional shape and genetic evolution. The new model explains why cancer cells have a surprising number of genetic mutations in common, how driver mutations spread through the whole tumor and how drug resistance evolves. The study is described in an August 26 paper in Nature.
"Previously, we and others have mostly used non-spatial models to study cancer evolution," Nowak said. "But those models do not describe the spatial characteristics of solid tumors. Now, for the first time, we have a computational model that can do that."
A key insight of the new model, Nowak said, is the ability for cells to migrate locally.
"Cellular mobility makes cancers grow fast, and it makes cancers homogenous in the sense that cancer cells share a common set of mutations. It is responsible for the rapid evolution of drug resistance," Nowak said. "I further believe that the ability to form metastases, which is what actually kills patients, is a consequence of selection for local migration."
Nowak and colleagues, including Bartek Waclaw of the University of Edinburgh, who is the first author of the study, Ivana Bozic of Harvard University and Bert Vogelstein of Johns Hopkins University, set out to improve on past models, because they were unable to answer critical questions about the spatial architecture of genetic evolution.
"The majority of the mathematical models in the past counted the number of cells that have particular mutations, but not their spatial arrangement," Nowak said. Understanding that spatial structure is important, he said, because it plays a key role in how tumors grow and evolve.
In a spatial model cells divide only if they have the space to do so. This results in slow growth unless cells can migrate locally.
"By giving cells the ability to migrate locally," Nowak said, "individual cells can always find new space where they can divide.
The result isn't just faster tumor growth, but a model that helps to explain why cancer cells share an unusually high number of genetic mutations, and how drug resistance can rapidly evolve in tumors.
As they divide, all cells -- both healthy and cancerous -- accumulate mutations, Nowak said, and most are so called "passenger" mutations that have little effect on the cell.
In cancer cells, however, approximately 5 percent are what scientists call "driver" mutations -- changes that allow cells to divide faster or live longer. In addition to rapid tumor growth, those mutations carry some previous passenger mutations forward, and as a result cancer cells often have a surprising number of mutations in common.
Similarly, drug resistance emerges when cells mutate to become resistant to a particular treatment. While targeted therapies wipe out nearly all other cells, the few resistant cells begin to quickly replicate, causing a relapse of the cancer.
"This migration ability helps to explain how driver mutations are able to dominate a tumor, and also why targeted therapies fail within a few months as resistance evolves," Nowak said. "So what we have is a computer model for solid tumors, and it's this local migration that is of crucial importance."
"Our approach does not provide a miraculous cure for cancer." said Bartek Waclaw, "However, it suggests possible ways of improving cancer therapy. One of them could be targeting cellular motility (that is local migration) and not just growth as standard therapies do."
 

Journal Reference:

1. Bartlomiej Waclaw, Ivana Bozic, Meredith E. Pittman, Ralph H. Hruban, Bert Vogelstein, Martin A. Nowak. A spatial model predicts that dispersal and cell turnover limit intratumour heterogeneity. Nature, 2015; DOI: 10.1038/nature14971 

Courtesy: ScienceDaily
 

 

Microscopic fish are 3-D-printed to do more than swim

Nanoengineers at the University of California, San Diego used an innovative 3-D printing technology they developed to manufacture multipurpose fish-shaped microrobots -- called microfish -- that swim around efficiently in liquids, are chemically powered by hydrogen peroxide and magnetically controlled. These proof-of-concept synthetic microfish will inspire a new generation of 'smart' microrobots that have diverse capabilities such as detoxification, sensing and directed drug delivery, researchers said. 

3-D-printed microfish contain functional nanoparticles that enable them to be self-propelled, chemically powered and magnetically steered. The microfish are also capable of removing and sensing toxins.

Credit: J. Warner, UC San Diego Jacobs School of Engineering.

 

The technique used to fabricate the microfish provides numerous improvements over other methods traditionally employed to create microrobots with various locomotion mechanisms, such as microjet engines, microdrillers and microrockets. Most of these microrobots are incapable of performing more sophisticated tasks because they feature simple designs -- such as spherical or cylindrical structures -- and are made of homogeneous inorganic materials. In this new study, researchers demonstrated a simple way to create more complex microrobots.
The research, led by Professors Shaochen Chen and Joseph Wang of the NanoEngineering Department at the UC San Diego, was published in the Aug. 12 issue of the journal Advanced Materials.
By combining Chen's 3D printing technology with Wang's expertise in microrobots, the team was able to custom-build microfish that can do more than simply swim around when placed in a solution containing hydrogen peroxide. Nanoengineers were able to easily add functional nanoparticles into certain parts of the microfish bodies. They installed platinum nanoparticles in the tails, which react with hydrogen peroxide to propel the microfish forward, and magnetic iron oxide nanoparticles in the heads, which allowed them to be steered with magnets.
"We have developed an entirely new method to engineer nature-inspired microscopic swimmers that have complex geometric structures and are smaller than the width of a human hair. With this method, we can easily integrate different functions inside these tiny robotic swimmers for a broad spectrum of applications," said the co-first author Wei Zhu, a nanoengineering Ph.D. student in Chen's research group at the Jacobs School of Engineering at UC San Diego.
As a proof-of-concept demonstration, the researchers incorporated toxin-neutralizing nanoparticles throughout the bodies of the microfish. Specifically, the researchers mixed in polydiacetylene (PDA) nanoparticles, which capture harmful pore-forming toxins such as the ones found in bee venom. The researchers noted that the powerful swimming of the microfish in solution greatly enhanced their ability to clean up toxins. When the PDA nanoparticles bind with toxin molecules, they become fluorescent and emit red-colored light. The team was able to monitor the detoxification ability of the microfish by the intensity of their red glow.
"The neat thing about this experiment is that it shows how the microfish can doubly serve as detoxification systems and as toxin sensors," said Zhu.
"Another exciting possibility we could explore is to encapsulate medicines inside the microfish and use them for directed drug delivery," said Jinxing Li, the other co-first author of the study and a nanoengineering Ph.D. student in Wang's research group.
How this new 3D printing technology works
The new microfish fabrication method is based on a rapid, high-resolution 3D printing technology called microscale continuous optical printing (μCOP), which was developed in Chen's lab. Some of the benefits of the μCOP technology are speed, scalability, precision and flexibility. Within seconds, the researchers can print an array containing hundreds of microfish, each measuring 120 microns long and 30 microns thick. This process also does not require the use of harsh chemicals. Because the μCOP technology is digitized, the researchers could easily experiment with different designs for their microfish, including shark and manta ray shapes.
"With our 3D printing technology, we are not limited to just fish shapes. We can rapidly build microrobots inspired by other biological organisms such as birds," said Zhu.
The key component of the μCOP technology is a digital micromirror array device (DMD) chip, which contains approximately two million micromirrors. Each micromirror is individually controlled to project UV light in the desired pattern (in this case, a fish shape) onto a photosensitive material, which solidifies upon exposure to UV light. The microfish are built using a photosensitive material and are constructed one layer at a time, allowing each set of functional nanoparticles to be "printed" into specific parts of the fish bodies.
"This method has made it easier for us to test different designs for these microrobots and to test different nanoparticles to insert new functional elements into these tiny structures. It's my personal hope to further this research to eventually develop surgical microrobots that operate safer and with more precision," said Li.
 

Journal Reference:

1. Wei Zhu, Jinxing Li, Yew J. Leong, Isaac Rozen, Xin Qu, Renfeng Dong, Zhiguang Wu, Wei Gao, Peter H. Chung, Joseph Wang, Shaochen Chen. 3D-Printed Artificial Microfish. Advanced Materials, 2015; 27 (30): 4411 DOI: 10.1002/adma.201501372 

Courtesy: ScienceDaily
 

 

Revealed: Helicobacter pylori's secret weapon

Is the game up for Helicobactor pylori? Researchers have identified the molecular mechanism that the bacterium's best-known adhesion protein uses to attach to stomach sugars and evade the body's attempts to 'flush' it away. 

Discovered in 1982, Helicobacter pylori (H. pylori) is a disease-causing bacterium that survives in our stomachs despite the harsh acidic conditions. It is estimated that one in two people have got it, though most won't ever experience any problems. Even so, it is considered one of the most common bacterial infections worldwide and a leading cause of dyspepsia, peptic ulceration and gastric cancer.

Through unique evolutionary adaptations, H. pylori is able to evade the antiseptic effect of our stomach acid by hiding within the thick acid-resistant layer of mucus that coats the stomach wall. Once within the mucus layer, the bacterium latches onto sugars naturally found on the stomach wall using its adhesion proteins. This attachment is so effective that the bacterium can resist attempts by the body to 'flush' it away, allowing the pathogen to colonise with impunity.
But the game could be up for H. pylori. Researchers in the School of Pharmacy, at The University of Nottingham and AstraZeneca R&D have identified the molecular mechanism that the bacterium's best-known adhesion protein uses to attach to stomach sugars. The research is published today, August 14 2015, in the scientific journal Science Advances.
Powerful x-rays reveal special 'groove'
Finding the molecular interactions that make this pathogen so successful in such a harsh environment has, until now, proved elusive.
Naim Hage, the postgraduate researcher who worked on this project as part of his doctoral thesis, said: "Although it's still very early, the insight we've gained from this study is already very exciting news for patients."
Using extremely powerful x-rays, the scientists were able to study the interactions between the H. pylori adhesion protein BabA and Lewisb sugars of the gastric mucosa at the atomic level. They found that, right at its tip, BabA possesses a specific groove that enables it to securely attach to Lewisb using a network of hydrogen bonds (the same kind of interactions that keep water molecules together).
First exciting step
The research team also found that this network is finely tuned -- if a few of the hydrogen bonds are disrupted, the network doesn't function and binding can no longer occur. This insight into the molecular interactions required for adhesion is a promising lead for the development of new strategies for the treatment of H. pylori infections.
This study now forms the foundation for future research between The University of Nottingham and AstraZeneca R&D into "anti-adhesion strategies" that would work by clearing H. pylori out of the stomach through dislodging the bacterium off the stomach wall using BabA:Lewisb inhibitors. Such novel strategies are needed to help treat H. pylori infections, which are globally gaining resistance to conventional antibiotic therapies.
Naim said: "Because BabA is unique to H. pylori, we can specifically target, and hopefully eradicate, this bacterium without affecting the other good bacteria in our normal flora. If successful, this therapeutic strategy will also be extremely useful for treating H. pylori infections that are already resistant to antibiotics."
More research to be done
The principal investigator behind the project, Dr Franco Falcone, said: "While this study answers long-standing questions about how H. pylori colonises the stomach, it represents the very first step in the development of novel therapies. The next few years of laboratory-based research will be crucial to determine if an anti-BabA adhesion approach is viable and can progress to clinical development. A similar approach is already showing promising results for the treatment of urinary tract infections in preclinical models. Looking forward, we are excited to continue working closely with AstraZeneca R&D who have provided a tremendous amount of support to achieve this discovery."
 

Journal Reference:

1. Franco H. Falcone et al. Structural basis of Lewisb antigen binding by the Helicobacter pylori adhesin BabA. Science Advances, August 2015 DOI: 10.1126/sciadv.1500315 

Courtesy: ScienceDaily
 

Promising drug for Parkinson's disease: Study supports fast track to clinical trials

A drug which has already been in use for decades to treat liver disease could be an effective treatment to slow down progression of Parkinson's disease, scientists have discovered. 

The pioneering research led by academics from the Sheffield Institute of Translational Neuroscience (SITraN), in collaboration with scientists from the University of York, supports the fast-tracking of the drug ursodeoxycholic acid (UDCA) for a clinical trial in Parkinson's patients.
Dr Heather Mortiboys, Parkinson's UK Senior Research Fellow from the University of Sheffield, explained: "We demonstrated the beneficial effects of UDCA in the tissue of LRRK2 carriers with Parkinson's disease as well as currently asymptomatic LRRK2 carriers. In both cases, UDCA improved mitochondrial function as demonstrated by the increase in oxygen consumption and cellular energy levels."
Oliver Bandmann, Professor of Movement Disorders Neurology at the University of Sheffield and Honorary Consultant Neurologist at Sheffield Teaching Hospitals NHS Foundation Trust, added: "Whilst we have been looking at Parkinson's patients who carry the LRRK2 mutation, mitochondrial defects are also present in other inherited and sporadic forms of Parkinson's, where we do not know the causes yet. Our hope is therefore, that UDCA might be beneficial for other types of Parkinson's disease and might also show benefits in other neurodegenerative diseases."
The research is also the first to demonstrate beneficial effects of UDCA on dopaminergic neurons, the nerve cells affected in Parkinson's disease, in a fly model of Parkinson's disease which carries the same genetic change as some patients with the condition.
The study published in the journal Neurology is funded by Parkinson's UK, the Wellcome Trust and the Norwegian Parkinson Foundation.
A mutation in the LRRK2 gene is the single most common inherited cause of Parkinson's disease. However, the precise mechanism that leads to Parkinson's is still unclear.
Defects in mitochondria, and as a consequence reduced energy levels, are a factor in a number of diseases that affect the nervous system including Parkinson's and Motor Neuron Disease. Nerve cells have a particularly high energy demands, therefore defects in the cell's energy generators will crucially affect their survival.
Professor Bandmann added: "Following on from the promising results of our in vitro drug screen, we were keen to further investigate and confirm the potential of UDCA in vivo -- in a living organism.
"UDCA has been in clinical use for decades and thus could be advanced to the clinic rapidly if it proves beneficial in clinical trials."
Collaborators Rebecca Furmston, White Rose PhD student, and Dr Chris Elliott, from the University of York's Department of Biology, demonstrated the beneficial effects of UDCA in vivo using the fruit fly (Drosophila melanogaster). In fruit flies, the mitochondrial defects caused by the LRRK2 mutation to dopaminergic neurons can be monitored through the progressive loss of visual function. Flies carrying the mutation maintained their visual response when fed with UDCA.
Dr Elliott said: "The treatment of fruit flies carrying the faulty LRRK2 gene with UDCA showed a profound rescue of dopaminergic signalling. Feeding the flies with UDCA partway through their life slows the rate at which the fly brain then degenerates. Thus, mitochondrial rescue agents may be a promising novel strategy for disease-modifying therapy in LRRK2-related Parkinson's."
Dr Arthur Roach, Director of Research and Development at Parkinson's UK, which part-funded the study, said: "There is a tremendous need for new treatments that can slow or stop Parkinson's.
"Because of this urgency, the testing of drugs like UCDA, which are already approved for other uses, is extremely valuable. It can save years, and hundreds of millions of pounds.
"It's particularly encouraging in this study that even at relatively low concentrations the liver drug still had an effect on Parkinson's cells grown in the lab.
"This type of cutting-edge research is the best hope of finding better treatments for people with Parkinson's in years, not decades."
 

Journal Reference:

1. H. Mortiboys, R. Furmston, G. Bronstad, J. Aasly, C. Elliott, O. Bandmann. UDCA exerts beneficial effect on mitochondrial dysfunction in LRRK2G2019S carriers and in vivo. Neurology, 2015; DOI: 10.1212/WNL.0000000000001905 

Courtesy: ScienceDaily
 

Modern parenting may hinder brain development, research suggests

Social practices and cultural beliefs of modern life are preventing healthy brain and emotional development in children, according to an interdisciplinary body of research. 

"Life outcomes for American youth are worsening, especially in comparison to 50 years ago," says Darcia Narvaez, Notre Dame professor of psychology who specializes in moral development in children and how early life experiences can influence brain development.
"Ill-advised practices and beliefs have become commonplace in our culture, such as the use of infant formula, the isolation of infants in their own rooms or the belief that responding too quickly to a fussing baby will 'spoil' it," Narvaez says.
This new research links certain early, nurturing parenting practices -- the kind common in foraging hunter-gatherer societies -- to specific, healthy emotional outcomes in adulthood, and has many experts rethinking some of our modern, cultural child-rearing "norms."
"Breast-feeding infants, responsiveness to crying, almost constant touch and having multiple adult caregivers are some of the nurturing ancestral parenting practices that are shown to positively impact the developing brain, which not only shapes personality, but also helps physical health and moral development," says Narvaez.
Studies show that responding to a baby's needs (not letting a baby "cry it out") has been shown to influence the development of conscience; positive touch affects stress reactivity, impulse control and empathy; free play in nature influences social capacities and aggression; and a set of supportive caregivers (beyond the mother alone) predicts IQ and ego resilience as well as empathy.
The United States has been on a downward trajectory on all of these care characteristics, according to Narvaez. Instead of being held, infants spend much more time in carriers, car seats and strollers than they did in the past. Only about 15 percent of mothers are breast-feeding at all by 12 months, extended families are broken up and free play allowed by parents has decreased dramatically since 1970.
Whether the corollary to these modern practices or the result of other forces, an epidemic of anxiety and depression among all age groups, including young children; rising rates of aggressive behavior and delinquency in young children; and decreasing empathy, the backbone of compassionate, moral behavior, among college students, are shown in research.
According to Narvaez, however, other relatives and teachers also can have a beneficial impact when a child feels safe in their presence. Also, early deficits can be made up later, she says.
"The right brain, which governs much of our self-regulation, creativity and empathy, can grow throughout life. The right brain grows though full-body experience like rough-and-tumble play, dancing or freelance artistic creation. So at any point, a parent can take up a creative activity with a child and they can grow together."
Further information: http://ccf.nd.edu/symposium/2012-symposium-presentations/
 

Story Source:
The above post is reprinted from materials provided by University of Notre Dame. The original item was written by Susan Guibert. Note: Materials may be edited for content and length.
 

Courtesy: ScienceDaily

 

Ebola vaccine efficacy trial suggest vaccine provides high protection against disease

Tests of the experimental Ebola vaccine VSV-ZEBOV in over 7500 participants in Guinea suggest that the vaccine provides high protection against the disease as early as ten days after vaccination, in adults who have potentially been exposed to the virus by coming in close contact with a recently infected person. 

New research suggests that the vaccine is safe, and also provides the first evidence that unvaccinated people may be indirectly protected from Ebola virus disease (EVD) when the VSV-ZEBOV vaccine is delivered using a ring vaccination strategy.

Credit: © Anton Gvozdikov / Fotolia

The research, published in The Lancet, suggests that the vaccine is safe, and also provides the first evidence that unvaccinated people may be indirectly protected from Ebola virus disease (EVD) when the VSV-ZEBOV vaccine is delivered using a ring vaccination strategy.  The study was sponsored and led by the World Health Organisation (WHO).
Ring vaccination, which was used in the past to eradicate smallpox, is intended to create a buffer of protection to prevent the spread of the disease, by vaccinating and monitoring the contacts, and contacts of contacts (the “ring”), of each newly diagnosed Ebola case.
The Ebola ça Suffit (translation: “Ebola this is Enough”) trial took place in Basse-Guinea, the only area in Guinea with new Ebola cases at the start of the study on April 1, 2015. When a new (index) Ebola case was diagnosed, the researchers traced all individuals who may have been in close contact with this first case [2].  Adult contacts aged 18 or older (not pregnant or breastfeeding) were offered the vaccine. If consent was given, adults in the ring were randomised to receive either immediate or delayed (21 days after randomisation [3]) vaccination. Vaccinated volunteers were then visited at home on days 3, 14, 21, 42, 63, and 84 after vaccination to record any adverse events.
The study reports the incidence of EVD in the immediate rings compared to the delayed rings up to 20 July, 2015. In the 90 clusters who received either immediate vaccination (48; 4123 adults vaccinated) or delayed vaccination (42; 3528 adults vaccinated on day 21), a single intramuscular injection of VSV-ZEBOV gave complete (100%) protection against EVD 10 days after randomisation [4]. No cases of EVD were recorded 10 days after randomisation in the immediate group, compared to 16 cases in the delayed vaccination clusters (table 2).
“Before the trial started, in most clusters there had been a series of Ebola cases over the weeks prior to randomisation.  However, since the trial started, we have seen no new cases in vaccinated volunteers within 10 days of vaccination, regardless of whether vaccination was immediate or delayed,” explains co-author Dr Marie Paule Kieny, from the World Health Organisation (WHO) in Geneva, Switzerland.
Secondary analysis for the trial suggests that ring vaccination also reduced the risk of contracting EVD for non-vaccinated individuals in the clusters. The overall effectiveness of the vaccine in adults, including both those who consented to vaccination and those who did not, was 75% against EVD.  Additionally, in all members of the clusters, including non-vaccinated children and pregnant women, the risk of testing positive for EVD was reduced by around 76% (table 2 and figure 3).
The vaccine was well-tolerated – one vaccinated patient experienced an episode of fever, classed as a serious adverse event, that was found to be related to the vaccine.  Assessment of serious adverse events is ongoing as the trial progresses.
According to study co-author Professor John-Arne Røttingen, from the University of Oslo, Norway, “Our results are encouraging in that they suggest that ring vaccination could substantially reduce rates of Ebola virus disease in the community. Because the way that Ebola virus transmits has been shown to be consistent across countries and regions, we believe that these results are likely to be applicable to other regions of Guinea and to Sierra Leone and Liberia.  But whether this candidate vaccine could become a licensed vaccine for widespread use against Ebola outbreaks is still uncertain, and further evidence is needed to evaluate the safety and efficacy of the vaccine before it is used outside of a clinical trial setting.”
The study is an interim analysis of results from the Ebola ça Suffit trial, and the trial is now continuing in order to generate more data for the assessment of vaccine efficacy and safety.
A Lancet Editorial accompanying the Article states that, “This study will be the subject of intense scientific scrutiny and debate. But what do the results mean for those most at risk of Ebola virus infection in west Africa? The vaccine is not yet licensed. More data on efficacy are needed before it can be widely deployed. But if the evidence proves sufficient for licensing, a Global Ebola Vaccine Implementation Team, also under WHO's leadership, has been preparing the ground for its introduction-creating guidelines for the vaccine's use, strategies for community engagement, and mechanisms to expand country capacity for the vaccine's distribution and delivery. In addition, the GAVI Alliance has approved substantial funding for the procurement and deployment of the vaccine.”
The sponsor of the study is the World Health Organization (WHO); it is implemented by the Ministry of Health of Guinea, Médecins sans Frontières (MSF), EPICENTRE, the Norwegian Institute of Public Health and WHO. The trial is funded by WHO, with support from the Wellcome Trust (United Kingdom); MSF; the Norwegian Ministry of Foreign Affairs through the Research Council of Norway; and the Canadian government through the Public Health Agency of Canada, Canadian Institutes of Health Research, International Development Research Centre and Department of Foreign Affairs, Trade and Development. The trial team includes researchers from the University of Bern, the University of Florida, the London School of Hygiene and Tropical Medicine, Public Health England, and the European Mobile Laboratory among others.
FOOTNOTES:
[1] VSV-ZEBOV was developed by the Public Health Agency of Canada and is licensed to NewLink Genetics and Merck. The vaccine works by replacing a gene from a harmless virus known as vesicular stomatitis virus (VSV) with a gene encoding an Ebola virus surface protein. The vaccine does not contain any live Ebola virus. Earlier trials have shown VSV-ZEBOV to be safe and to produce consistently powerful immune responses in adults, thought to be important for protection against Ebola.
[2] This included contacts and contacts of contacts of the index case, around 50-100 people. Contacts included individuals who, within the last 21 days, lived in the same household, were visited by the index case after the onset of symptoms, or were in close physical contact with the patients’ body or body fluids, linen or clothes.
[3] This method is an alternative to using a placebo, but allows all consenting contacts to be vaccinated during the trial. The delayed vaccination group acts as a control group.
[4] Analyses of vaccine efficacy were restricted to events occurring 10 days or more after randomisation to account for the incubation period of Ebola and the unknown time for the vaccine to develop protective immunity.
 

Journal Reference:

1. Ana Maria Henao-Restrepo, Ira M Longini, Matthias Egger, Natalie E Dean, W John Edmunds, Anton Camacho, Miles W Carroll, Moussa Doumbia, Bertrand Draguez, Sophie Duraffour, Godwin Enwere, Rebecca Grais, Stephan Gunther, Stefanie Hossmann, Mandy Kader Kondé, Souleymane Kone, Eeva Kuisma, Myron M Levine, Sema Mandal, Gunnstein Norheim, Ximena Riveros, Aboubacar Soumah, Sven Trelle, Andrea S Vicari, Conall H Watson, Sakoba Kéïta, Marie Paule Kieny, John-Arne Røttingen. Efficacy and effectiveness of an rVSV-vectored vaccine expressing Ebola surface glycoprotein: interim results from the Guinea ring vaccination cluster-randomised trial. The Lancet, 2015 DOI: 10.1016/S0140-6736(15)61117-5 

Courtesy: ScienceDaily
 

How bees naturally vaccinate their babies

When it comes to vaccinating their babies, bees don't have a choice -- they naturally immunize their offspring against specific diseases found in their environments. Now for the first time, scientists have discovered how they do it. This opens the door for researchers to develop the first-ever vaccine for insects. This is particularly important for bees since they help keep fruit, nuts and vegetables in our diets and have been declining in numbers for six decades. 

With the discovery of how bees naturally vaccinate their babies, researchers can now develop the first vaccine for insects. This vaccine could be used to fight serious diseases that decimate beehives. This is an important development for food production.

Credit: Christofer Bang

Researchers from Arizona State University, University of Helsinki, University of Jyväskylä and Norwegian University of Life Sciences made the discovery after studying a bee blood protein called vitellogenin. The scientists found that this protein plays a critical, but previously unknown role in providing bee babies protection against disease.
The findings appear in the journal PLOS Pathogens.
"The process by which bees transfer immunity to their babies was a big mystery until now. What we found is that it's as simple as eating," said Gro Amdam, a professor with ASU's School of Life Sciences and co-author of the paper. "Our amazing discovery was made possible because of 15 years of basic research on vitellogenin. This exemplifies how long-term investments in basic research pay off."
Co-author Dalial Freitak, a postdoctoral researcher with University of Helsinki adds: "I have been working on bee immune priming since the start of my doctoral studies. Now almost 10 years later, I feel like I've solved an important part of the puzzle. It's a wonderful and very rewarding feeling!"
How it works
In a honey bee colony, the queen rarely leaves the nest, so worker bees must bring food to her. Forager bees can pick up pathogens in the environment while gathering pollen and nectar. Back in the hive, worker bees use this same pollen to create "royal jelly" -- a food made just for the queen that incidentally contains bacteria from the outside environment.
After eating these bacteria, the pathogens are digested in the gut and transferred to the body cavity; there they are stored in the queen's 'fat body' -- an organ similar to a liver. Pieces of the bacteria are then bound to vitellogenin -- a protein -- and carried via blood to the developing eggs. Because of this, bee babies are 'vaccinated' and their immune systems better prepared to fight diseases found in their environment once they are born.
Vitellogenin is the carrier of these immune-priming signals, something researchers did not know until now.
First edible vaccines for bees
While bees vaccinate their babies against some diseases, many pathogens are deadly and the insects are unable to fight them.
But now that Amdam and Freitak understand how bees vaccinate their babies, this opens the door to creating the first edible and natural vaccine for insects.
"We are patenting a way to produce a harmless vaccine, as well as how to cultivate the vaccines and introduce them to bee hives through a cocktail the bees would eat. They would then be able to stave off disease," said Freitak.
One destructive disease that affects bees is American Foul Brood, which spreads quickly and destroys hives. The bacterium infects bee larvae as they ingest food contaminated with its spores. These spores get their nourishment from the larvae, eventually killing them.
This disease is just one example where the researchers say a vaccine would be extremely beneficial.
Why this discovery is important to humans
It's widely known that pollinators, including bees, are facing serious environmental dangers.
During the past six decades, managed honey bee colonies in the United States have declined from 6 million in 1947 to only 2.5 million today. Not only are bees affected by diseases, they have been decimated by a phenomenon called colony collapse disorder. Researchers don't know exactly what causes this, but pesticides, pests, pathogens and nutrition problems may all be contributing factors.
According to a 2014 report by the U.S. government, pollinators are instrumental for a healthy economy and critical to food security, contributing 35 percent of global food production. In North America, insects pollinate 87 of the top 115 food crops and honey bees are vital in keeping fruits, nuts and vegetables in our diets.
Humans depend on bees and other pollinating insects for a huge portion of their food supply. Insect vaccines could play an important role in helping to combat colony collapse disorder, in addition to fighting a variety of diseases.
All egg-laying species have vitellogenin
This discovery could have far-reaching benefits for other species, as well as substantial, positive impacts on food production. All egg-laying species including fish, poultry, reptiles, amphibians and insects have vitellogenin in their bodies.
The food industry could implement the use of natural vaccines that would not only be inexpensive to produce, they could easily be used in developing countries.
"Because this vaccination process is naturally occurring, this process would be cheap and ultimately simple to implement. It has the potential to both improve and secure food production for humans," said Amdam.

Journal Reference:

1. Heli Salmela, Gro V. Amdam, Dalial Freitak. Transfer of Immunity from Mother to Offspring Is Mediated via Egg-Yolk Protein Vitellogenin. PLOS Pathogens, 2015; 11 (7): e1005015 DOI: 10.1371/journal.ppat.1005015 

Courtesy: ScienceDaily

Can we restart the heart?

What if you could use the proliferative and survival properties of cancer-prone cells to rejuvenate cardiac progenitor cells and get them dividing again, without forming tumors? Researchers are exploring the results of taking an enzyme, Pim, known to be associated with growth and survival of certain types of cancer cells, and causing it to be overexpressed in cardiac progenitor cells in mice. 

 

These photomicrograph cardiac stem cells isolated from mouse hearts clustered together in the shape of a heart.

Credit: Mark Sussman

This is all very simplified, of course, but it's the basic model described by Mark Sussman, chief research scientist at the San Diego State University Heart Institute, who was recently selected by the American Heart Association's Basic Cardiovascular Science division to receive this year's Distinguished Achievement Award.
The heart in particular seems to be resistant to developing cancerous cells.
"When's the last time you heard of anyone having heart cancer? It's almost unheard of," said Sussman.
That's not surprising from an evolutionary standpoint. If heart cells make a grave transcription error during cell division and your ticker ticks its last tock, there's no fixing the problem. So it makes sense that heart cells are incredibly careful when it comes to proliferating.
But it's this very meticulousness that makes heart disease such an intractable problem, Sussman explained. Over time, the cells burn themselves out. Their ability to repair themselves and generate fresh replacements gets progressively worse. By the time you reach old age and start experiencing symptoms of age-related heart disease, your cardiac cells are running on fumes and aren't able to properly divide into new cells.
"There's a razor's edge balancing cellular aging and cancer risk," he said.
What if you could use biotechnology to walk that razor's edge? To use the proliferative and survival properties of cancer-prone cells to rejuvenate cardiac progenitor cells -- a rare type of stem cell that replicates indefinitely into new heart cells--and get them dividing again, without forming tumors?
That's the aim of one arm of Sussman's research at SDSU. Sussman and his colleagues published a paper in the May 29 issue of the Journal of Biological Chemistry exploring the results of taking an enzyme, Pim, known to be associated with growth and survival of certain types of cancer cells, and causing it to be overexpressed in cardiac progenitor cells in mice.
In healthy cells, Pim helps facilitate chromosome splitting, a key part of the cellular division process.
The gene that encodes the production of this enzyme, PIM1, is what's known as a proto-oncogene. That means that by itself, the gene doesn't cause cancer. But when it teams up with another gene, Myc, tumors are likely to form.
Fortunately, the Pim/Myc combination isn't an issue in heart progenitor cells, meaning you could tweak those cells to overexpress the PIM1 gene without raising the risk of cancer.
That's exactly what Sussman's team did. They modified mouse heart progenitor cells to overexpress PIM1 in specific locations within the cell, targeting specific locations with more of the critical Pim enzyme in hopes that it would protect against aging-related heart disease.
And it worked. Compared to controls, the mice with overexpressed PIM1 lived longer and showed stronger cell proliferation. But interestingly, the way it worked was different depending on where in the cell the gene was overexpressed.
If the researchers caused PIM1 to be overexpressed in the progenitor cell's nucleus, they saw increased proliferation into new cells. If they overexpressed the gene in a different region of the cell, the mitochondria, they found that the enzyme inhibited the cell's natural self-destruct signals, causing them to live longer.
One technique enhanced cell division, the other warded off cell death. In humans, depending on a person's individual circumstance, either or both of these effects might help restore their cardiac cells to a younger, healthier state.
Sussman and his colleagues have replicated the results with human tissue obtained from people whose hearts have failed and who are living on a ventricular assist device that pumps their blood for them. The research team is currently trying to obtain funding to do human clinical trials wherein they obtain a patient's own cardiac progenitor cells, modify them to overexpress PIM1, then put them back into the patient's heart in hopes of rejuvenating the tissue and spurring the heart to repair itself.
"We're trying to dial back the clock to when their cells had more regenerative potential," Sussman said. "By understanding how and where Pim affe
cts these cells, we can create specialized Pim molecules that get you all the benefits of youthfulness without the risk of cancer."
 

Journal Reference:

1. Kaitlen Samse, Jacqueline Emathinger, Nirmala Hariharan, Pearl Quijada, Kelli Ilves, Mirko Völkers, Lucia Ormachea, Andrea De La Torre, Amabel M. Orogo, Roberto Alvarez, Shabana Din, Sadia Mohsin, Megan Monsanto, Kimberlee M. Fischer, Walter P. Dembitsky, Åsa B. Gustafsson, Mark A. Sussman. Functional Effect of Pim1 Depends upon Intracellular Localization in Human Cardiac Progenitor Cells. Journal of Biological Chemistry, 2015; 290 (22): 13935 DOI: 10.1074/jbc.M114.617431 

Courtesy: ScienceDaily