ENSP adota a política do acesso livre para material didático

Confirmando seu compromisso público de dar acesso irrestrito à produção científica da instituição, a ENSP/Fiocruz iniciou a liberação do material didático produzido no âmbito de seus cursos de educação a distância. O primeiro material a fazer parte desta ação - que já é uma política institucional - é o do Curso Nacional de Qualificação de Gestores do SUS. Este processo teve início no Seminário Internacional Acesso Livre ao Conhecimento, que inaugurou o ano letivo da ENSP, em abril, e está alinhado ao Movimento Internacional de Acesso Livre ao Conhecimento. A ideia é que, aos poucos, os materiais de todos os cursos da EAD/ENSP sejam disponibilizados.

O acesso a materiais em um repositório institucional complementa e potencializa sua função, trazendo muitos benefícios para a instituição. Atualmente, a EAD/ENSP tem mais de 60 mil alunos inscritos e quase 32 mil alunos egressos de seus 46 cursos, que abrangem todos os estados brasileiros. O Curso Nacional de Qualificação de Gestores do SUS também atinge todas as regiões do país. Nele, já foram formados mais de 5 mil alunos e sua segunda versão pretende atingir mais de 7 mil participantes. Segundo Victor Grabois, membro da coordenação nacional do CNQGS, existe uma grande demanda nacional por esta formação, e a liberação de seu material didático contribui para a disseminação desse conhecimento.

Para o diretor da ENSP, Antônio Ivo, a decisão de colocar a produção científica da Escola disponível para acesso aberto significa um "compromisso de estender e universalizar aquilo que estamos fazendo e produzindo, em especial, o nosso patrimônio de material didático já existente e publicado em educação a distância ou vinculado a outros cursos da ENSP", disse. Ele ressaltou ainda que "a nossa instituição faz parte do sistema público, e por isso temos a obrigação de devolver a sociedade o investimento aqui feito".

Material didático ficará disponível na Biblioteca Multimídia da ENSP

O material didático da EAD/ENSP será disponibilizado na Biblioteca Multimídia da Escola, que já oferece acesso aberto a todo o seu conteúdo desde 2004. A coordenadora de Comunicação Institucional da Escola, Ana Furniel, explica que a Biblioteca funciona como um repositório institucional. Segundo ela, "estamos trabalhando em uma versão bem mais complexa desta ferramenta, para que passe a ser um sistema de informação completo. Além de estocar o material, classificado e identificado, teremos também um sistema de gestão integrado, que permitirá extrair relatórios e cruzar informações com a base de currículo Lattes".

Para ela, a disponibilização do material didático reforça a importância das discussões que aconteceram durante o Seminário de Acesso Livre ao Conhecimento. "Tivemos a presença de vários especialistas, e as soluções e definições políticas de várias instituições brasileiras e estrangeiras foram apresentadas. Desde então, estamos trabalhando para que a ENSP caminhe na direção de uma definição de Política Institucional de Acesso Aberto. Para isso, a Direção da ENSP pretende formar uma Comissão de Acesso Aberto na Escola, que dará seguimento a todos os encaminhamentos e decisões sobre o tema", completou Ana.

Campo magnético "afina" o sangue para prevenir ataques cardíacos

O campo magnético polariza as células vermelhas do sangue, fazendo com que elas se liguem a cadeias curtas, melhorando a circulação do sangue.

Afinar o sangue

Se o sangue de uma pessoa se torna muito espesso, ele pode danificar os vasos sanguíneos e aumentar o risco de ataques cardíacos.

Mas um físico da Universidade Temple (EUA) descobriu que pode-se diluir o sangue humano submetendo-o a um campo magnético.

O físico Rongjia Tao foi pioneiro no uso de campos elétricos e magnéticos para diminuir a viscosidade do óleo em motores e dutos.

Agora, ele está usando os mesmos campos magnéticos para afinar o sangue humano no sistema circulatório.

Magnetismo no sangue

Como os glóbulos vermelhos contêm ferro, Tao foi capaz de reduzir a viscosidade do sangue de uma pessoa entre 20 e 30 por cento, sujeitando-o a um campo magnético de 1,3 Tesla por cerca de um minuto.

Esse campo magnético tem aproximadamente a mesma intensidade da usada em um exame de ressonância magnética (MRI).

Depois de testarem diversas amostras de sangue em laboratório, os pesquisadores descobriram que o campo magnético polariza as células vermelhas do sangue, fazendo com que elas se liguem a cadeias curtas, melhorando a circulação.

Como essas cadeias são maiores do que as células do sangue individuais, elas fluem para o centro, reduzindo o atrito contra as paredes dos vasos sanguíneos.

Os efeitos combinados reduzem a viscosidade do sangue, ajudando-o a fluir mais livremente.

Viscosidade do sangue

Quando o campo magnético é retirado, a viscosidade inicial do sangue lentamente retorna, mas em um período de várias horas.

A técnica é conhecida como magneto-reológica e, sendo reversível, aponta para uma possibilidade de uso em situações críticas ou na prevenção de ataques cardíacos - os campos magnéticos podem ser reaplicados e a viscosidade reduzida novamente.

"Selecionando uma intensidade do campo magnético e uma duração de pulso adequadas, podemos controlar o tamanho das cadeias agregadas de hemácias, controlando, portanto, a viscosidade do sangue," disse Tao.

Método do campo magnético

Atualmente, o único método para diluir o sangue é através de drogas, como a aspirina. No entanto, essas drogas frequentemente produzem efeitos colaterais indesejados.

Tao afirma que o método do campo magnético não é apenas mais seguro, mas também pode ser aplicado repetidas vezes.

Ele também acrescentou que a redução da viscosidade não afeta a função normal das células vermelhas do sangue.

O pesquisador alerta que mais estudos serão necessários e que ele espera conseguir transformar esta tecnologia em uma terapia para prevenir doenças cardíacas, que seja aceita pelas autoridades de saúde.

Dieta ioiô é mais saudável do que manter-se obeso

Efeito sanfona

Um estudo que comparou a obesidade ao longo da vida com as flutuações de peso da chamada dieta ioiô sugere que é melhor tentar perder peso, apesar de vários insucessos, do que ficar obeso sem qualquer tentativa.

"É claro que manter uma dieta estável e saudável dá os melhores resultados para a saúde e a longevidade," afirma o Dr. Edward List, da Universidade de Ohio (EUA).

Entretanto, indivíduos obesos geralmente têm ciclos de peso, o chamado efeito sanfona, repetindo etapas de emagrecimento com outras de recuperação do peso.

Apesar de sempre apontada como prejudicial à saúde, essa dieta ioiô, causadora do efeito sanfona, tem sido pouco estudada de forma consistente.

Dieta ioiô

Para descobrir os efeitos da dieta ioiô sobre a saúde, a longo prazo, List e seus colegas fizeram o que eles chamaram de "o primeiro estudo controlado de um regime de dieta ioiô por uma vida inteira."

Como é extremamente difícil e demorado realizar um estudo de alimentação de longo prazo em humanos, os cientistas usaram camundongos para testar se a variação de peso devido à dieta ioiô é tão prejudicial quanto a obesidade ao longo de toda a vida.

Os animais foram separados em grupos segundo a alimentação - alimentação saudável, alimentação rica em gordura e dieta ioiô - ao longo de toda a sua vida.

Nesse período, foram acompanhadas todas as "medidas de saúde" tradicionais, incluindo peso corporal, gordura corporal e níveis de glicemia (açúcar) níveis.

Saúde média

A dieta ioiô resultou em grandes flutuações nesses indicadores de saúde - um verdadeiro efeito sanfona nos exames.

Os resultados melhoravam durante o período com alimentação saudável e pioravam até um estado diabético durante a alimentação rica em gordura.

Mas quando se tira uma média dos indicadores de saúde durante os períodos de boa alimentação e má alimentação, a "saúde média" ficou melhor do que a dos camundongos continuamente obesos.

Benefícios da dieta ioiô

Um resultado que resume bem os benefícios da dieta ioiô em relação a não fazer nenhuma dieta é que os camundongos cujos pesos ficaram oscilando entre saudável e não-saudável viveram quase 35 por cento mais do que os camundongos obesos.

Melhor ainda, isso manteve os animais da dieta ioiô com a mesma média de vida que os animais saudáveis, que nunca foram obesos.

"O medo de conseqüências negativas para a saúde devido ao efeito sanfona pode estar superestimado," concluiu List. "De acordo com o nosso estudo, parece que é melhor continuar a incentivar a perda de peso, independentemente do número de tentativas e fracassos."

Curativo com células-tronco começa a ser testado em pacientes

Cartilagem crescida em laboratório a partir de células-tronco adultas clonadas, que são a base do curativo de células-tronco desenvolvido para tratar o rompimento do menisco.

Rompimento dos meniscos

Se os ensaios clínicos forem bem-sucedidos, milhões de pessoas com lesões nos joelhos poderão se beneficiar de um novo tipo de curativo contendo células-tronco.

O primeiro teste clínico do mundo com o curativo com células-tronco acaba de receber aprovação do órgão regulador de saúde do Reino Unido.

O tratamento inédito está sendo proposto para pacientes com danos severos na cartilagem do menisco, o chamado rompimento dos meniscos.

Curativo com células-tronco

O tratamento atual para a maioria das lesões é a retirada do menisco, um procedimento que muitas vezes resulta no aparecimento precoce da osteoartrite.

O chamado Ensaio de Fase I, um dos primeiros a serem aprovados com o uso de células-tronco, vai tratar o rasgo meniscal com uma bandagem celular, semeada com células-tronco do próprio paciente, depois de passarem por um processo de "expansão" em laboratório.

A bandagem celular, produzida pela Azellon Ltd, uma empresa emergente criada por cientistas da Universidade de Bristol, explora uma tecnologia chamada células-tronco autólogas (do próprio paciente).

Nos testes in vitro (cultura de tecidos) essa técnica mostrou-se promissora para a cura dos meniscos rompidos.

O ensaio vai testar sobretudo o perfil de segurança do curativo com células-tronco em dez pacientes com rompimento do menisco. Mas será possível obter algumas informações preliminares sobre sua eficácia.

Tratamento do menisco

O curativo, contendo as células-tronco do próprio paciente, será implantado em um procedimento cirúrgico simples, usando um instrumento especialmente projetado para essa operação.

Os pacientes serão monitorados de perto ao longo de cinco anos.

O objetivo final é que o curativo com células-tronco seja um tratamento de primeira linha, em lugar da remoção do menisco.

"As células-tronco são muito promissoras em termos científicos e médicos, mas só podemos saber se elas funcionam ou não testando-as em ensaios clínicos," disse o Dr. Anthony Hollander, coordenador da pesquisa.

'Catch and Release' Program Could Improve Nanoparticle Safety Assessment

ScienceDaily (June 8, 2011) — Depending on whom you ask, nanoparticles are, potentially, either one of the most promising or the most perilous creations of science. These tiny objects can deliver drugs efficiently and enhance the properties of many materials, but what if they also are hazardous to your health in some way? Now, scientists at the National Institute of Standards and Technology (NIST) have found a way to manipulate nanoparticles so that questions like this can be answered.

After gold nanoparticles are trapped on the brown collection surface (left), the NIST team can apply a mild electric field and release most of them (right). The ability to trap and release particles in this fashion could aid in studying their properties, particularly with respect to their effects on human health.

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The team has developed a method of attracting and capturing metal-based nanoparticles on a surface and releasing them at the desired moment. The method, which uses a mild electric current to influence the particles' behavior, could allow scientists to expose cell cultures to nanoparticles so that any lurking hazards they might cause to living cells can be assessed effectively.

The method also has the advantage of collecting the particles in a layer only one particle thick, which allows them to be evenly dispersed into a fluid sample, thereby reducing clumping -- a common problem that can mask the properties they exhibit when they encounter living tissue. According to NIST physicist Darwin Reyes, these combined advantages should make the new method especially useful in toxicology studies.

"Many other methods of trapping require that you modify the surface of the nanoparticles in some way so that you can control them more easily," Reyes says. "We take nanoparticles as they are, so that you can explore what you've actually got. Using this method, you can release them into a cell culture and watch how the cells react, which can give you a better idea of how cells in the body will respond."

Other means of studying nanoparticle toxicity do not enable such precise delivery of the particles to the cells. In the NIST method, the particles can be released in a controlled fashion into a fluid stream that flows over a colony of cells, mimicking the way the particles would encounter cells inside the body -- allowing scientists to monitor how cells react over time, for example, or whether responses vary with changes in particle concentration.

For this particular study, the team used a gold surface covered by long, positively charged molecules, which stretch up from the gold like wheat in a field. The nanoparticles, which are also made of gold, are coated with citrate molecules that have a slight negative charge, which draws them to the surface covering, an attraction that can be broken with a slight electric current. Reyes says that because the surface covering can be designed to attract different materials, a variety of nanoparticles could be captured and released with the technique.

Blood Simpler: Researchers Parse the Origins of Hematopoietic Stem Cells

ScienceDaily (June 8, 2011) — Researchers at the University of California, San Diego School of Medicine have identified a gene and a novel signaling pathway, both critical for making the first hematopoietic stem cells (HSCs) in developing vertebrate embryos. The discovery has implications for developing stem cell-based therapies for diseases like leukemia and congenital blood disorders.

A scanning electron microscope image depicting normal circulating human blood, which includes round, dimpled red blood cells and several types of white blood cells, including lymphocytes, a monocyte and a neutrophil, and many small, disc-shaped platelets.

"What we need is the ability to generate self-renewing HSCs from patients for treatments," said David Traver, PhD, an associate professor in UCSD's Department of Cellular and Molecular Medicine. "But accomplishing this goal means first understanding the mechanisms involved in creating HSCs during embryonic development."HSCs are multipotent stem cells that give rise to all blood cell types, including red blood and immune cells. Existing medical treatments using HSCs are hampered by cell shortages and finding compatible matches between donors and recipients. Currently, it is not possible to create HSCs from converted embryonic stem cells or induced pluripotent stem cells -- pluripotent cells artificially derived from non-pluripotent cells, such as skin cells.

One of those mechanisms is described for the first time in a paper published by Traver and colleagues in the June 9 issue of the journal Nature.

The researchers focused on a family of 19 known genes called Wnts, which had previously been recognized as important players in other aspects of embryogenesis. "Wnt signaling is involved in virtually all aspects of development," said Traver. The scientists eventually narrowed their efforts to a single, largely unstudied gene called Wnt16, which they found residing close to HSC precursors in the somites of vertebrate embryos. A somite is an early body segment in the developing embryo that gives rise to most of the adult body muscle and skeleton.

They determined that Wnt16 controls a novel genetic regulatory network necessary for HSC specification. The gene turns on key binding molecules, or ligands, that are required to definitively establish blood cell production. Knocking out Wnt16 in zebrafish, a powerful model of vertebrate development, resulted in embryos lacking HSCs.

Identifying Wnt16 as a vital factor in HSC production dramatically expands what's known about how HSCs are formed and provides new insight into what tissues talk to each other to achieve the end-goal of producing the adult blood system. "We're on the cusp of understanding something that people have been wondering about for decades," said Wilson K. Clements, first author of the study and a postdoctoral fellow in Traver's lab.

Other authors of the paper are Albert D. Kim and Karen G. Ong, UCSD Department of Cellular and Molecular Medicine and Section of Cell and Developmental Biology; John C. Moore and Nathan Lawson, University of Massachusetts Medical School.

Funding for this research came, in part, from the California Institute for Regenerative Medicine, the National Institutes of Health and the American Heart Association.

Genes Provide Landmarks on the Roadmap of Autism

ScienceDaily (June 8, 2011) — Many roads can lead to the same place, often crossing over one another and sometimes passing the same landmarks.

The figure illustrates a partial component of the autism interaction network showing how proteins encoded by autism associated genes (red circles) share many partners (white circles)

In a report in the current issue of the journal Science Translational Medicine, Dr. Huda Zoghbi, director of the Neurological Research Institute and professor of neurology, neuroscience, molecular and human genetics and pediatrics at BCM, and her colleagues describe the network that identifies hundreds of new interactions among proteins encoded by genes associated with autism spectrum disorder.The interactome or protein interaction network for autism spectrum disorders developed by researchers at Baylor College of Medicine and the Jan and Dan Duncan Neurological Research Institute at Texas Children's Hospital in collaboration with scientists at the Center for Cancer Systems Biology (CCSB) at Dana-Farber Cancer Institute demonstrates how protein pathways converge, diverge and interact to arrive at the same devastating condition.

It also relays new information about idiopathic autism, which has no known cause. It does this by building on what is known about syndromic autism that often occurs as a symptom of a broader genetic disorder such as fragile X, tuberous sclerosis and Phelan-McDermid syndrome. The three core features of autism present in both idiopathic and syndromic cases include impaired social skills, delayed language and repetitive behaviors.

"The interactome is a more functional approach," said Zoghbi. "It can help us understand how mutations in different genes can cause similar clinical symptoms."

When the study started, she and her colleagues began with 26 genes known to be associated with syndromic autism. Studying each of those singly and devising a therapy would take a lifetime, said Zoghbi. Together, they account for no more than 30 percent of autism cases. (There are now more than 60 genes associated with autism spectrum disorder, a sign of advances in the field).

"We had these 26 genes that seemed to have little to do with each other but still resulted in autism-like symptoms," said Zoghbi. "We thought that perhaps they cause autism by interacting with some shared partners that function in pathways that lead to similar phenotypes (similar characteristics)."

They took each protein associated with autism and determined the proteins with which they interacted. The complicated network that resulted encompasses 539 proteins that interact with the 26 proteins associated with syndromic autism spectrum disorders. These protein interactions include a variety of genes including transcription factors, RNA-binding proteins, cell adhesion molecules and enzymes involved in modifying and degrading proteins.

Compiling the interactome was a massive undertaking, said Dr. Chad A. Shaw, assistant professor of molecular and human genetics at BCM and a computational scientist who was a co-corresponding author of the study.

"One of the most important contributions of this interactome is that it provides a deep, experimentally driven foundation that can be used to understand complicated genetic variation," he said.

He credits the paper's first author, Dr. Yasunari Sakai, with important work in constructing the interactome itself which Shaw and his laboratory then analyzed; Sakai also validated random selections of interactions in the laboratory, an exacting, time-consuming task. Sakai was a postdoctoral fellow in Zoghbi's laboratory.

The network confirmed many previously known or hypothesized connections and revealed previously unsuspected connectivity between two syndromic autism spectrum disorder proteins -- SHANK3 (SH3 and multiple ankyrin repeat domains 3) and TSC (tuberous sclerosis protein 1).

Shaw compared the information in the network to information from published studies on chromosomal differences known as copy number variations (duplications or deletions of genetic information from chromosomes) that had been observed both in normal subjects and in patients with non-syndromic or idiopathic autism spectrum disorder. He looked for genes that were present both in their network and in the copy number variations in the individuals within the normal and autism groups.

The autism patients had a greater rate of copy number variations that included the genes in the interactome than did the control group.

The team also performed microarray or gene chip analysis for all of the genes in the network on tissue from 288 subjects with idiopathic autism collected by the Simons Foundation Simplex Collection. None of these subjects had any of the symptoms associated with syndromic autism and their intellectual capacities were fairly high.

They identified three previously unrecognized copy number variations that involve three genes found in the network, further confirming the protein interaction network as a framework for identifying as-yet unknown causes of autism and understanding the molecular pathways that involve both syndromic and idiopathic autism.

"We are at a point in time of being able to measure people's complete genotype," said Shaw. "We can measure more variation than we can interpret. The interactome lets us tag variations to a disease-relevant network. That's why resources like the interactome are important. They help tie the complexity together. If you are trying to diagnose a person, you don't have to have a research study around each gene."

Others who took part in the research include Brian C. Dawson, Dr. Diana V. Dugas and Dr. Zaina Al-Mohtaseb all of BCM and Dr. David E. Hill of Dana Farber Cancer Institute.

Funding for this work came from the Howard Hughes Medical Institute, the Simons Foundation, and the Ellison Foundation.

Citrate Key in Bone's Nanostructure

ScienceDaily (June 8, 2011) — Bone is one of nature's surprising "building materials." Pound-for-pound it's stronger than steel, tough yet resilient. Scientists at the U.S. Department of Energy's Ames Laboratory have identified the composition that gives bone its outstanding properties and the important role citrate plays, work that may help science better understand and treat or prevent bone diseases such as osteoporosis.

This diagram shows the effect of citrate concentration on the size of hydroxyapatite crystals fabricated with self-assembling block copolymer templates. Just as it does with actual bone structure, as the concentration of citrate increases, the thickness of the nanocrystals decreases and the thinner nanocrystals appear to make the bone more resistant to stress cracking.

By understanding the nanostructure of naturally occurring materials, researchers may be able to develop new light-weight, high-strength materials that will require less energy to manufacture and that could make the products in which they are used more energy efficient.Using nuclear magnetic resonance (NMR) spectroscopy, Ames Laboratory scientist and Iowa State University chemistry professor Klaus Schmidt-Rohr and his colleagues studied bone, an organic-inorganic nanocomposite whose stiffness is provided by thin nanocrystals of carbonated apatite, a calcium phosphate, imbedded in an organic matrix of mostly collagen, a fibrous protein.

"The organic, collagen matrix is what makes bones tough," Schmidt-Rohr said, "while the inorganic apatite nanocrystals provide the stiffness. And the small thickness -- about 3 nanometers -- of these nanocrystals appears to provide favorable mechanical properties, primarily in prevention of crack propagation."

While bone structure has been studied extensively, how these apatite nanocrystals form and what prevents them from growing thicker was a mystery. Some research pointed to sugars being involved, but that didn't match with the NMR spectra that Schmidt-Rohr was seeing.

"We can see all the peaks clearly," he says of a spectral graph which shows the points at which specific components in bone samples resonate; these specific signatures are the key to NMR technology, "even those at the organic-inorganic interface, where the organic material's signal strength is relatively weak."

After studying bone structure over a five-year period, it was actually serendipitous that Schmidt-Rohr came across a signature that appeared to match what he was seeing.

"We had gotten some crystalline collagen samples to study," he said, "and it turned out that the supplier, Sigma-Aldrich, had used citrate to dissolve the collagen. And the citrate signature in the collagen samples matched the signature we were seeing in bone."

According to Schmidt-Rohr, the role of citrate in bone had been studied up until about 1975, but since that time, no mention was made in any of the newer literature on bone. So in essence, his research team had to rediscover it.

The case for citrate was made most convincingly when graduate research assistant Yanyan Hu was able to extract citrate from cow bone and replace it with carbon 13 (C13) -enriched citrate, resulting in a 30-fold enhancement of the NMR signals of the bone sample. The peaks matched exactly, confirming the presence of citrate on the surface where the apatite nanocrystals had formed.

Schmidt-Rohr further hypothesized that, since citrate is too large to be incorporated into the apatite crystal lattice, it must be bound to the nanocrystals' surface where it stabilizes the nanocrystals' size by preventing their further growth. The findings were published in the Dec. 28, 2010 issue of theProceedings of the National Academy of Sciences.

"Based on the old literature, we looked at the citrate levels in a variety of types of bone and found that herring spine had the highest citrate concentration -- about 13 percent by weight," Schmidt-Rohr said. "So it should hold that the citrate signal for herring spine should be three times higher than for cow bone, and indeed it was."

In further studies, the group found that higher concentration of citrate, the thinner the apatite nanocrystals in bone. This was further confirmed on bone-mimetic nanocomposites in a collaboration with Ames Lab faculty scientists Surya Mallapragada and Muffit Akinc, using a polymer template with various concentrations of citrate to synthesize apatite nanocrystals. At higher concentrations, the nanocrystals that formed were thinner and should therefore be more resistant to crack propagation. This work was published in the April 12 issue of Chemistry of Materials.

"At this point, we feel that citrate probably also has a role in the biomineralization of the apatite," Schmidt-Rohr said. "It's also been noted in the literature that as an organism ages, the nanocrystal thickness increases and the citrate concentration goes down," Schmidt-Rohr said, "and there's also support from clinical studies that citrate is good for bones," adding that one of the leading supplements for bone strength contains calcium citrate.

"While calcium loss is a major symptom in osteoporosis, the decline of citrate concentration may also contribute to bone brittleness," he said.

The work was supported by DOE's Office of Science. The Ames Laboratory is a U.S. Department of Energy Office of Science national laboratory operated by Iowa State University.

Protein Folding Made Easy

ScienceDaily (June 8, 2011) — Protein folding is one of the central questions in biochemistry. Protein folding is the continual and universal process whereby the long, coiled strings of amino acids that make up proteins in all living things fold into more complex three-dimensional structures. By understanding how proteins fold, and what structures they are likely to assume in their final form, researchers are then able to move closer to predicting their function.

Protein folding is the continual and universal process whereby the long, coiled strings of amino acids that make up proteins in all living things fold into more complex three-dimensional structures. By understanding how proteins fold, and what structures they are likely to assume in their final form, researchers are then able to move closer to predicting their function.

Computational methods of modelling protein folding have existed for a couple of decades. But what McGill researcher Jérôme Waldispühl of the McGill Centre for Bioinformatics has done, working with collaborators from MIT, is to develop algorithms that can work from a laptop computer to examine a protein's fundamental chemical properties and then scan a number of possible protein shapes before predicting the final form that the protein is likely to take.This is important because incorrectly folded proteins in humans result in such devastating diseases as Alzheimer's, Parkinson's, Huntington's, emphysema and cystic fibrosis. Developing better modelling techniques for protein folding is crucial to creating more effective pharmaceutical treatments for these and other diseases.

The results have been impressive. Whereas classical techniques for predicting protein folding pathways required hundreds of thousands of CPU hours to compute the folding dynamics of 40 amino acids proteins, the program tFolder implemented by Solomon Shenker -- a former McGill undergraduate student now at Cornell -- has been able to predict correctly in 10 minutes on a single laptop, a coarse-grained representation of the folding pathways of a protein with 60 amino acids.

Waldispühl and his students continue to work on their algorithm to improve its success rate at predicting protein folding with broader categories of proteins including some that are important in DNA-binding. The research was recently presented at the 15th Annual International Conference in Research in Computational Molecular Biology (RECOMB 2011).

Using Magnets to Help Prevent Heart Attacks: Magnetic Field Can Reduce Blood Viscosity, Physicist Discovers

ScienceDaily (June 8, 2011) — If a person's blood becomes too thick it can damage blood vessels and increase the risk of heart attacks. But a Temple University physicist has discovered that he can thin the human blood by subjecting it to a magnetic field.

Aggregated red-cell clusters have a streamlined shape, leading to further viscosity reduction.

Because red blood cells contain iron, Tao has been able to reduce a person's blood viscosity by 20-30 percent by subjecting it to a magnetic field of 1.3 Telsa (about the same as an MRI) for about one minute.Rongjia Tao, professor and chair of physics at Temple University, has pioneered the use of electric or magnetic fields to decrease the viscosity of oil in engines and pipelines. Now, he is using the same magnetic fields to thin human blood in the circulation system.

Tao and his collaborator tested numerous blood samples in a Temple lab and found that the magnetic field polarizes the red blood cells causing them to link together in short chains, streamlining the movement of the blood. Because these chains are larger than the single blood cells, they flow down the center, reducing the friction against the walls of the blood vessels. The combined effects reduce the viscosity of the blood, helping it to flow more freely.

When the magnetic field was taken away, the blood's original viscosity state slowly returned, but over a period of several hours.

"By selecting a suitable magnetic field strength and pulse duration, we will be able to control the size of the aggregated red-cell chains, hence to control the blood's viscosity," said Tao. "This method of magneto-rheology provides an effective way to control the blood viscosity within a selected range."

Currently, the only method for thinning blood is through drugs such as aspirin; however, these drugs often produce unwanted side effects. Tao said that the magnetic field method is not only safer, it is repeatable. The magnetic fields may be reapplied and the viscosity reduced again. He also added that the viscosity reduction does not affect the red blood cells' normal function.

Tao said that further studies are needed and that he hopes to ultimately develop this technology into an acceptable therapy to prevent heart disease.

Tao and his former graduate student, Ke "Colin" Huang, now a medical physics resident in the Department of Radiation Oncology at the University of Michigan, are publishing their findings in the journal Physical Review E.