Células Tronco no cérebro

New stem cell found in the brain
Friday, April 20, 2012

Researchers at Lund University in Sweden have discovered a new stem cell in the adult brain. These cells can proliferate and form several different cell types - most importantly, they can form new brain cells. Scientists hope to take advantage of the finding to develop methods to heal and repair disease and injury in the brain.
Analyzing brain tissue from biopsies, the researchers for the first time found stem cells located around small blood vessels in the brain. The cell's specific function is still unclear, but its plastic properties suggest great potential.
"A similar cell type has been identified in several other organs where it can promote regeneration of muscle, bone, cartilage and adipose tissue," said Patrik Brundin, M.D., Ph.D., Jay Van Andel Endowed Chair in Parkinson's Research at Van Andel Research Institute (VARI), Head of the Neuronal Survival Unit at Lund University and senior author of the study.
In other organs, researchers have shown clear evidence that these types of cells contribute to repair and wound healing. Scientists suggest that the curative properties may also apply to the brain. The next step is to try to control and enhance stem cell self-healing properties with the aim of carrying out targeted therapies to a specific area of the brain.
"Our findings show that the cell capacity is much larger than we originally thought, and that these cells are very versatile," said Gesine Paul-Visse, Ph.D., Associate Professor of Neuroscience at Lund University and the study's primary author. "Most interesting is their ability to form neuronal cells, but they can also be developed for other cell types. The results contribute to better understanding of how brain cell plasticity works and opens up new opportunities to exploit these very features."
The study, published in the journal PLoS ONE, is of interest to a broad spectrum of brain research. Future possible therapeutic targets range from neurodegenerative diseases to stroke.
"We hope that our findings may lead to a new and better understanding of the brain's own repair mechanisms," said Dr. Paul-Visse. "Ultimately the goal is to strengthen these mechanisms and develop new treatments that can repair the diseased brain."
###
Link to the study here: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0035577
Van Andel Research Institute: http://www.vai.org

Músculo e gordura. New England Journal of Medicine

Hippocrates observed that “walking is man's best medicine” and thus underscored the benefits of physical activity to health. More than two millennia later, the benefits of physical activity in lowering the risk of death from any cause and improving longevity have been well documented.1 Scientists are also beginning to understand the benefits of exercise on a molecular level and to consider skeletal muscle as an endocrine organ, capable of communicating with other tissues through myokines, which are released into the circulation during physical activity. In a recent study, Boström and colleagues2 identified a new myokine, irisin, which is released into the circulation during exercise and triggers the transformation of white fat cells into brown-in-white, or brite, cells — white fat cells with a phenotype similar to that of brown fat cells.

Well over a decade ago, a transcriptional coactivator (a molecule involved in the regulation of gene expression) was identified by Lin and colleagues,3 who in a series of studies found that this transcriptional coactivator, peroxisome proliferator-activated receptor ? coactivator 1? (PGC-1?), plays a critical role in the maintenance of glucose, lipid, and energy homeostasis. They also found that PGC-1? is involved in the pathologic processes associated with obesity-related disorders, such as diabetes, cardiovascular disease, and neurodegeneration. Moreover, mice engineered to constitutively express PGC-1? in their muscles are resistant to age-related obesity and diabetes and have an increased lifespan,4 a finding that suggests that PGC-1?, in addition to its effect within the skeletal muscle, may regulate the metabolism of other tissues — notably, white adipose tissue.

The aim of the study by Boström and colleagues was to identify the language of the crosstalk between PGC-1?–expressing skeletal muscle and white adipose tissue. When comparing the genes that are expressed in the muscle of wild-type mice with those expressed in the muscle of transgenic mice (mice engineered to express high levels of PGC-1?), they observed greater expression of several genes encoding certain secreted protein products, including a protein called fibronectin type III domain containing 5 (FNDC5). The researchers observed that FNDC5 is proteolytically cleaved (dubbing its cleavage product “irisin,” after the Greek messenger goddess, Iris) and that its expression in skeletal muscle increases with exercise in both mice and humans. In humans, plasma levels of irisin after 10 weeks of regular exercise were twice as high as baseline levels.

The researchers then injected obese mice with adenoviral particles engineered to express FNDC5; these mice had plasma irisin levels that were three to four times as high as the levels in mice injected with adenoviral particles containing a control gene. The white adipose tissue of the mice with higher irisin levels also had a high level of expression of uncoupling protein 1 (UCP1), which is characteristic of brown adipose tissue. UCP1 funnels the energy generated from respiration into heat production. This change was accompanied by an increase in total body energy expenditure, modest weight loss, and modest improvements in glucose intolerance (Figure 1

The view that adult humans possess brown fat is now well accepted. Moreover, recent evidence shows that the metabolism of brown fat is increased when adult humans are exposed to cold.5 Therefore, the finding by Boström and colleagues that exercise (through the influence of irisin) has the capacity to turn on a phenotype similar to that of brown fat is likely to be of clinical significance for human metabolism. Further supporting this conclusion is the fact that the mouse and human irisin proteins are identical, although it remains to be seen whether irisin has the same effect on white adipose tissue in humans that it has on the white adipose tissue of mice.

Boström and colleagues have provided a mechanistic explanation for one aspect of the benefit of exercise: its protection against metabolic disease. However, their study has a broader significance in that it provides a conceptual basis for understanding how muscles communicate with other tissues. Exercise stimulates the release of multiple myokines, which offers protection against a network of diseases, including cardiovascular diseases, type 2 diabetes, cancer, dementia, and osteoporosis. It will be exciting to see how these protective effects are achieved at the molecular level.

Given the antiobesity and antidiabetic effects of brown-fat formation in mice, it is possible that patients who are unable to exercise because of severe musculoskeletal or cardiovascular conditions could benefit directly from the discovery of irisin. But because exercise orchestrates the interplay of many secreted and nonsecreted proteins and has direct and indirect benefits on organs such as the brain and on the cardiovascular system, a single “exercise pill” will probably never replace the full effect of a good workout. And so, with a nod to Hippocrates, I suggest that you keep moving and activate all of your myokines.

Disclosure forms provided by the author are available with the full text of this article at NEJM.org.

References

RS Paffenbarger, RT Hyde, AL Wing, C-C HsiehPhysical activity, all-cause mortality, and longevity of college alumni.N Engl J Med1986;314:605-613
P Bostrom, J Wu, MP Jedrychowski, A PGC1-?-dependent myokine that drives brown-fat-like development of white fat and thermogenesis.Nature2012;481:463-468
J Lin, C Handschin, BM SpiegelmanMetabolic control through the PGC-1 family of transcription coactivators.Cell Metab2005;1:361-370
T Wenz, SG Rossi, RL Rotundo, BM Spiegelman, CT MoraesIncreased muscle PGC-1? expression protects from sarcopenia and metabolic disease during aging.Proc Natl Acad Sci U S A2009;106:20405-20410
V Ouellet, SM Labbe, DP Blondin, Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans.J Clin Invest2012;122:545-552
Source Information

From the Department of Infectious Diseases, Center of Inflammation and Metabolism, Rigshopitalet, and the Faculty of Health Sciences, University of Copenhagen — both in Copenhagen.

Músculo e gordura

A Muscular Twist on the Fate of Fat

Bente Klarlund Pedersen, M.D., D.M.Sc.

N Engl J Med 366:1544-1545 | April 19, 2012

Hippocrates observed that “walking is man's best medicine” and thus underscored the benefits of physical activity to health. More than two millennia later, the benefits of physical activity in lowering the risk of death from any cause and improving longevity have been well documented.1 Scientists are also beginning to understand the benefits of exercise on a molecular level and to consider skeletal muscle as an endocrine organ, capable of communicating with other tissues through myokines, which are released into the circulation during physical activity. In a recent study, Boström and colleagues2 identified a new myokine, irisin, which is released into the circulation during exercise and triggers the transformation of white fat cells into brown-in-white, or brite, cells — white fat cells with a phenotype similar to that of brown fat cells.

Well over a decade ago, a transcriptional coactivator (a molecule involved in the regulation of gene expression) was identified by Lin and colleagues,3 who in a series of studies found that this transcriptional coactivator, peroxisome proliferator-activated receptor ? coactivator 1? (PGC-1?), plays a critical role in the maintenance of glucose, lipid, and energy homeostasis. They also found that PGC-1? is involved in the pathologic processes associated with obesity-related disorders, such as diabetes, cardiovascular disease, and neurodegeneration. Moreover, mice engineered to constitutively express PGC-1? in their muscles are resistant to age-related obesity and diabetes and have an increased lifespan,4 a finding that suggests that PGC-1?, in addition to its effect within the skeletal muscle, may regulate the metabolism of other tissues — notably, white adipose tissue.

The aim of the study by Boström and colleagues was to identify the language of the crosstalk between PGC-1?–expressing skeletal muscle and white adipose tissue. When comparing the genes that are expressed in the muscle of wild-type mice with those expressed in the muscle of transgenic mice (mice engineered to express high levels of PGC-1?), they observed greater expression of several genes encoding certain secreted protein products, including a protein called fibronectin type III domain containing 5 (FNDC5). The researchers observed that FNDC5 is proteolytically cleaved (dubbing its cleavage product “irisin,” after the Greek messenger goddess, Iris) and that its expression in skeletal muscle increases with exercise in both mice and humans. In humans, plasma levels of irisin after 10 weeks of regular exercise were twice as high as baseline levels.

The researchers then injected obese mice with adenoviral particles engineered to express FNDC5; these mice had plasma irisin levels that were three to four times as high as the levels in mice injected with adenoviral particles containing a control gene. The white adipose tissue of the mice with higher irisin levels also had a high level of expression of uncoupling protein 1 (UCP1), which is characteristic of brown adipose tissue. UCP1 funnels the energy generated from respiration into heat production. This change was accompanied by an increase in total body energy expenditure, modest weight loss, and modest improvements in glucose intolerance (Figure 1).

Figure 1


Cross-Talk between Muscle and Fat.

The view that adult humans possess brown fat is now well accepted. Moreover, recent evidence shows that the metabolism of brown fat is increased when adult humans are exposed to cold.5 Therefore, the finding by Boström and colleagues that exercise (through the influence of irisin) has the capacity to turn on a phenotype similar to that of brown fat is likely to be of clinical significance for human metabolism. Further supporting this conclusion is the fact that the mouse and human irisin proteins are identical, although it remains to be seen whether irisin has the same effect on white adipose tissue in humans that it has on the white adipose tissue of mice.

Boström and colleagues have provided a mechanistic explanation for one aspect of the benefit of exercise: its protection against metabolic disease. However, their study has a broader significance in that it provides a conceptual basis for understanding how muscles communicate with other tissues. Exercise stimulates the release of multiple myokines, which offers protection against a network of diseases, including cardiovascular diseases, type 2 diabetes, cancer, dementia, and osteoporosis. It will be exciting to see how these protective effects are achieved at the molecular level.

Given the antiobesity and antidiabetic effects of brown-fat formation in mice, it is possible that patients who are unable to exercise because of severe musculoskeletal or cardiovascular conditions could benefit directly from the discovery of irisin. But because exercise orchestrates the interplay of many secreted and nonsecreted proteins and has direct and indirect benefits on organs such as the brain and on the cardiovascular system, a single “exercise pill” will probably never replace the full effect of a good workout. And so, with a nod to Hippocrates, I suggest that you keep moving and activate all of your myokines.

Disclosure forms provided by the author are available with the full text of this article at NEJM.org.

References

RS Paffenbarger, RT Hyde, AL Wing, C-C HsiehPhysical activity, all-cause mortality, and longevity of college alumni.N Engl J Med1986;314:605-613
P Bostrom, J Wu, MP Jedrychowski, A PGC1-?-dependent myokine that drives brown-fat-like development of white fat and thermogenesis.Nature2012;481:463-468
J Lin, C Handschin, BM SpiegelmanMetabolic control through the PGC-1 family of transcription coactivators.Cell Metab2005;1:361-370
T Wenz, SG Rossi, RL Rotundo, BM Spiegelman, CT MoraesIncreased muscle PGC-1? expression protects from sarcopenia and metabolic disease during aging.Proc Natl Acad Sci U S A2009;106:20405-20410
V Ouellet, SM Labbe, DP Blondin, Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans.J Clin Invest2012;122:545-552
Source Information

From the Department of Infectious Diseases, Center of Inflammation and Metabolism, Rigshopitalet, and the Faculty of Health Sciences, University of Copenhagen — both in Copenhagen.

Novos Ca de Mama

The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups

Christina Curtis, Sohrab P. Shah, Suet-Feung Chin, Gulisa Turashvili, Oscar M. Rueda, Mark J. Dunning, Doug Speed, Andy G. Lynch, Shamith Samarajiwa, Yinyin Yuan, Stefan Gräf, Gavin Ha, Gholamreza Haffari, Ali Bashashati, Roslin Russell, Steven McKinney, METABRIC Group, Anita Langerød, Andrew Green, Elena Provenzano, Gordon Wishart, Sarah Pinder, Peter Watson, Florian Markowetz, Leigh Murphy et al.
AffiliationsContributionsCorresponding authors
Nature (2012) doi:10.1038/nature10983
Received 24 April 2011 Accepted 22 February 2012 Published online 18 April 2012
Abstract
Abstract Author information Supplementary information Comments
The elucidation of breast cancer subgroups and their molecular drivers requires integrated views of the genome and transcriptome from representative numbers of patients. We present an integrated analysis of copy number and gene expression in a discovery and validation set of 997 and 995 primary breast tumours, respectively, with long-term clinical follow-up. Inherited variants (copy number variants and single nucleotide polymorphisms) and acquired somatic copy number aberrations (CNAs) were associated with expression in ~40% of genes, with the landscape dominated by cis- and trans-acting CNAs. By delineating expression outlier genes driven in cis by CNAs, we identified putative cancer genes, including deletions in PPP2R2A, MTAP and MAP2K4. Unsupervised analysis of paired DNA–RNA profiles revealed novel subgroups with distinct clinical outcomes, which reproduced in the validation cohort. These include a high-risk, oestrogen-receptor-positive 11q13/14 cis-acting subgroup and a favourable prognosis subgroup devoid of CNAs. Trans-acting aberration hotspots were found to modulate subgroup-specific gene networks, including a TCR deletion-mediated adaptive immune response in the ‘CNA-devoid’ subgroup and a basal-specific chromosome 5 deletion-associated mitotic network. Our results provide a novel molecular stratification of the breast cancer population, derived from the impact of somatic CNAs on the transcriptome.

Mais um passo para cura da calvície

Regenerative medicine repairs mice from top to toe

Three separate studies in mice show normal function can be restored to hair, eye and heart cells.

At the turn of the twentieth century, the promise of regenerating damaged tissue was so far-fetched that Thomas Hunt Morgan, despairing that his work on earthworms could ever be applied to humans, abandoned the field to study heredity instead. Though he won the Nobel Prize in 1933 for his work on the role of chromosomes in inheritance, if he lived today, the advances in regenerative medicine may have tempted him to reconsider.

Three studies published this week show that introducing new cells into mice can replace diseased cells — whether hair, eye or heart — and help to restore the normal function of those cells. These proof-of-principle studies now have researchers setting their sights on clinical trials to see if the procedures could work in humans.

Transplanting bioengineered stem cells into nude mice enabled them to grow hair.

Takashi Tsuji/Tokyo University of Science

“You can grow cells in a Petri dish, but that’s not regenerative medicine,” says Robin Ali, a geneticist at University College London, who led the eye study. “You have to think about the biology of repair in a living system.”

Sprouting hair

In work published in Nature Communications, Japanese researchers grew different types of hair on nude mice, using stem cells from normal mice and balding humans to recreate the follicles from which hair normally emerges¹. Takashi Tsuji, a regenerative-medicine specialist at Tokyo University of Science who led the study, says that the technique holds promise for treating male pattern baldness.

The team used a specialized nylon sheath to guide the hair through the skin layers, enabling it to erupt from the skin of the mice in 94% of all grafts. The hairs took between 2 and 5 weeks to emerge, and behaved as normal: they underwent normal growth cycles and established connections to the muscles and nerves underneath the skin. The hairs also lifted up from the skin in response to acetylcholine, a neurotransmitter known to cause hairs to stand on end.

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Mayumi Ito, a dermatologist at New York University, says that this is the first report to reconstitute hair follicles using human cells. But for the technique to be effective, the researchers need to show that they can expand the number of hair follicles that they are able to grow.

Seeing at night

A second study using regenerative techniques helped to restore some vision to mice with congenital stationary night blindness, an inherited disease of the retina — the part of the eye that is sensitive to light ². The research, published in Nature, could potentially be used for treating macular degeneration, which causes damage to the retina.

Ali and his colleagues transplanted precursor rod cells, which have a role in night-time vision, into the retinas of mice lacking α-transducin, a protein needed to see in dim light. Around 26,000 new rods were delivered into each eye, which normally contains 6 million rods. Only 10–15% of the rods integrated into the retina, but they still improved vision.

The researchers measured the effect of the transplant by placing the mice in front of a rotating grating of black and white lines and showing that they demonstrated more sensitivity to changing levels of contrast and spaces between the lines compared to blind mice that did not receive a transplant. The mice with transplanted rod cells also took less time to complete a water maze that used a visual cue to reveal the escape route.

Ali acknowledges that further animal studies are needed before beginning a clinical trial. He and his colleagues are now testing embryonic stem cells and other models of macular degeneration in which there is damage to the cones, another type of retinal cell.

Beating hearts

But stem-cell transplants aren't always straightforward: if the cells fail to integrate into the desired tissue, they can form tumours instead. To avoid this problem, researchers have been trying to reprogram fully developed adult cells directly so that they form other cell types. Now, in a study published in Nature³, a team of researchers at the University of California, San Francisco (UCSF), has managed to achieve just that using cardiac fibroblasts.

Deepak Srivastava, director of the UCSF Gladstone Institute of Cardiovascular Disease, led a team in reprogramming cardiac fibroblasts into cardiomyocytes — the muscle cells of the heart that are permanently lost after a heart attack. The team used a retrovirus to deliver three transcription factors that induced the reprogramming in adult mice, and improved their cardiac function. This study follows on from work in 2003, when Srivastava and his colleagues discovered that a mutation in one of these transcription factors, GATA4, caused heart disease in several generations of a family under his care⁴. “What I do clinically, motivates me. Absolutely, every day,” he says.

Robert Lanza, a regenerative-medicine specialist at Advanced Cell Technologies, a biotechnology firm headquartered in Santa Monica, California, reiterates that regenerative medicine has come a long way since Morgan's time, and is a field that holds much promise for the future. “These three papers are just the tip of the iceberg. By the time we grow old, doctors are going to look back and say, ‘Can you believe people used to go bald, go blind or even have their leg cut off from vascular disease?’ — and then the doctor will treat the problem with an injection of cells.”

As melhores Universidades Americanas oferecem cursos online de graça

Drop In! Top Schools from Berkeley to Yale Now Offer Free Online Courses
04/18/12 by Sarah Kessler

On average, it will cost $55,600 to attend Princeton, Penn, Michigan or Stanford next year. But now you can enroll in online courses at all four universities online for free.

The universities won’t just be posting lectures online like MIT’s OpenCourseWare project, Yale’s Open Yale Courses and the University of California at Berkeley’s Webcast. Rather, courses will require deadlines, evaluations, discussions and, in some cases, a statement of achievement.

“The technology as well as the sociology have finally matured to the point where we are ready for this,” says Daphne Koller, a co-founder of Coursera, the for-profit platform classes will run on.

“This is a group that didn’t grow up at a time when there weren’t browsers,” Koller adds. “They have the mental state that allows them to say, ‘I’m willing to get a good portion of my education online.’”

Coursera grew out of an experiment in Stanford’s computer science department that opened up a handful of classes to non-Stanford students via the Internet. The online students received a signed letter from the instructor (but no credit) upon completion.

Both Koller and her co-founder Andrew Ng taught classes in the experiment, which ended up enrolling between 100,000 and 160,000 online students in each class. Ng says that more than half of the 160,000 students in his class attempted one particular problem, and about 23,000 of them completed the work.

Koller and Ng are the second pair of Stanford professors attempting to scale the idea past Stanford. The first pair launched a portal for online classes called Udacity last year.


Stanford professors are not the only group pushing the limits of free, virtual education. University of the People, for instance, enrolls more than a thousand students in 115 different countries in its free degree programs. For-profit learning site Udemy has recruited professors from universities such as Stanford, Yale, Northwestern and Dartmouth to teach video-based courses on its free platform.

MIT announced its plans for online courses in December, though it doesn’t plan to launch a prototype until Spring.

Research suggests that online learning can be just as effective as classroom learning. In a 2009 report based on 50 independent studies, the U.S. Department of Education found that students who studied in online learning environments performed modestly better than peers who were receiving face-to-face instruction.

When it comes to creating open online courses that reflect the classroom experience, however, it pays to be a professor of computer science. Coursera’s founders are well equipped to solve problems such as automatic grading, peer grading and 1,000-student class discussions that make an online class size of 100,000 students manageable.

But no matter how elegant the solution, universities don’t believe their course offerings on Coursera will ever equate to the $55,000 classroom version — or they would not agree to give them away.

“I don’t think any of these universities think their value proposition to their students is the lectures,” Koller says, citing interaction with peers and professors as one reason students would still want to pay $55,000 for courses they can access online for free.

A startup called 2tor has helped universities such as the University of North Carolina at Chapel Hill and the University of Southern California monetize their virtual classrooms. Those programs grant degrees, but limit class size and charge standard tuition.

Coursera announced on Tuesday that it has raised a $16 million round of funding, which means that it will also be installing a business model at some point. But Ng and Koller say the company will not charge for classes.

“It opens doors to people who wouldn’t have had them opened otherwise,” Koller says. “Education is a real equalizer, even if it doesn’t come with a degree attached to it.”

Corte no orçamento em Ciência e Tecnologia

Retirado do site da Academia Brasileira de Ciências
4/04/2012

Os cortes propostos pelo governo federal ao orçamento do Ministério da Ciência, Tecnologia e Inovação (MCTI) podem colocar a perder muitos dos significativos avanços obtidos nos últimos anos e vão na contramão de outras medidas adotadas pela própria União em tempos recentes, como a expansão da infraestrutura de ensino público universitário e a busca pela internacionalização da ciência brasileira.

Esse é o diagnóstico quase unânime dos cientistas ao tratar da redução em cerca de 22% na verba federal destinada ao sistema de C,T&I brasileiro para 2012. É o segundo ano consecutivo em que há contingenciamento de recursos destinados ao MCTI. Somados, os dois cortes fizeram o valor disponível ao Ministério cair de R$ 7,8 bilhões, em 2010, para R$ 5,2 bilhões, neste ano. Mesmo sem levar em conta a inflação no período (que tornaria a situação ainda mais alarmante), o orçamento foi reduzido a dois terços do valor do último ano do governo Lula.

O anúncio dos cortes, justificado no governo pela crise financeira internacional, foi veementemente criticado por representantes da comunidade científica. A Sociedade Brasileira para o Progresso da Ciência (SBPC), a Sociedade Brasileira de Física (SBF) e a Sociedade Brasileira de Astronomia (SAB) estiveram entre as entidades que divulgaram notas de repúdio à ação federal.

Os protestos não se limitaram à esfera científica. Representantes do setor industrial, preocupados com o impacto dos cortes no estímulo à inovação - fator essencial para a preservação da competitividade da indústria brasileira no cenário internacional - também se manifestaram contrários à restrição de recursos.

"No momento em que o Brasil começa a se afirmar no cenário internacional, consideramos tal redução orçamentária um grave retrocesso para a política de formação de recursos humanos qualificados e o desenvolvimento científico nacional", afirma o Acadêmico Celso de Melo, presidente da SBF. "É desanimador constatar que, pelo segundo ano consecutivo, cai a fração do PIB aplicada em ciência, tecnologia e inovação, o que nos coloca cada vez mais distante dos percentuais observados para o setor nos países desenvolvidos."

Contraste internacional - Mais do que aumentar a distância entre nós e as nações mais avançadas, a decisão - que os cientistas ainda esperam reverter - coloca o Brasil em forte contraste com outros países em estágio similar de desenvolvimento. Na China, por exemplo, a despeito de uma expectativa menor de crescimento (a exemplo do que ocorre aqui), o primeiro-ministro Wen Jibao anunciou em março um aumento de 12,4% no orçamento para ciência e tecnologia, atingindo a expressiva soma de US$ 36 bilhões. Dentre as medidas adotadas, incluem-se uma elevação de 26% nas verbas voltadas à pesquisa básica e um incremento de 24% no montante de recursos destinados às universidades de elite.

"É interessante notar que o aumento do orçamento para pesquisa e a redução do crescimento foram anunciados no mesmo discurso, o que indica uma consciência muito clara sobre o papel da ciência, da tecnologia e da inovação no futuro da China", comenta o diretor da ABC Luiz Davidovich, pesquisador da Universidade Federal do Rio de Janeiro (UFRJ). "Infelizmente, não podemos dizer o mesmo do Brasil."

Impactos imediatos - Em alguns estados da federação, como São Paulo e Rio de Janeiro, há uma "rede de proteção" estadual consistente que pode amenizar um pouco os impactos, com fundações de amparo à pesquisa (Faps) consolidadas e financiando importantes trabalhos das comunidades científicas locais. Contudo, nas regiões menos desenvolvidas do País, como o Centro-Oeste, o Nordeste e, sobretudo, o Norte, essa estrutura local ainda não tem participação tão significativa nas verbas destinadas ao sistema de CTI, e o resultado dos cortes pode ser ainda mais dramático.

"O financiamento do MCTI constitui a parte mais significativa do investimento na região", diz o Acadêmico Luís Carlos Bassalo Crispino, físico da Universidade Federal do Pará (UFPA). "Isso acontece porque as fundações de amparo à pesquisa do Norte, quando existem, são muito jovens e ainda não apresentam continuidade em seus investimentos. Para que se tenha uma ideia, nem mesmo todos os estados da região possuem uma Fap."

O estrangulamento do orçamento nacional para pesquisa cria ainda mais complicações com o recente movimento do governo brasileiro de ampliar a rede de universidades federais - um esforço para democratizar o acesso ao ensino superior público de qualidade e abrir vagas para os doutores formados no País.

"Atraídos por essa nova oferta de emprego, diversos brasileiros foram repatriados. Em um prazo de dois anos tivemos um aumento de cerca de 20% no número de professores em diversos departamentos de física no País", afirma Marcia Barbosa, diretora do Instituto de Física da Universidade Federal do Rio Grande do Sul (UFRGS) e vice-presidente da IUPAP (International Union of Pure and Applied Physics). "O Brasil se tornou um celeiro de empregos e atraiu pesquisadores de todo o mundo que se interessavam a vir aqui para estágios de pós-doutorado."

Contudo, com o corte de recursos para a pesquisa nos últimos dois anos, esse tiro pode acabar saindo pela culatra. Os doutores recém-formados absorvidos nas vagas de docência nessas instituições estão sendo obrigados a abandonar seus esforços de pesquisa, sem verba que estão para conduzi-los.

"Aliás, esses jovens já estão sofrendo um verdadeiro massacre, pois em várias instituições nacionais devem lecionar 12 ou mais horas de aula por semana. Em instituições de pesquisa de países desenvolvidos, a carga horária típica semanal em sala de aula de um professor é de cerca de três horas por semana", diz Davidovich.

"Com a atual carga horária, e um fraco apoio às atividades de pesquisa, estamos liquidando o que há de mais precioso nos ambientes de pesquisa: o vigor e a criatividade de jovens pesquisadores. Nessas condições, fica difícil competir com os países mais desenvolvidos", completa.

Corre-se o risco de as novas universidades públicas replicarem o modelo do ensino superior privado, que, salvo poucas e louváveis exceções, se dedica única e exclusivamente à emissão de diplomas, sem se preocupar com a produção de conhecimento.

Sem Fronteiras e Sem Futuro - O estrangulamento dos orçamentos de pesquisa também entra em rota de colisão direta com uma das grandes bandeiras recentes do governo brasileiro, o programa Ciência Sem Fronteiras, destinado a financiar bolsas de estudo em universidades estrangeiras. "Uma consequência direta desses cortes é que teremos uma geração de jovens que vieram de experiências produtivas no exterior e que, sem a infraestrutura apropriada, se tornarão profissionais frustrados", diz Marcia Barbosa.

"O problema não é somente a descontinuidade das pesquisas em andamento, mas sobretudo o efeito desmotivador que isso produz nos estudantes de pós-graduação e nos cientistas mais jovens", complementa José Wellington Tabosa, físico da Universidade Federal de Pernambuco (UFPE). "Um mínimo de regularidade orçamentária é fundamental para o planejamento de qualquer atividade, principalmente em ciência e tecnologia, onde a interrupção de um projeto de pesquisa, mesmo por um curto tempo, pode significar o seu fim."

"O Ciência Sem Fronteiras é um programa para treinar no exterior pesquisadores para o futuro. Mas não haverá futuro se agora não construirmos a infraestrutura científica necessária", prossegue Marcia Barbosa.

Mais ameaças no horizonte - Além de seu impacto imediato no financiamento à pesquisa, com todos os malefícios que ele traz no fomento a uma estrutura robusta de C,T&I no País, os cortes prejudicam muito programas de pesquisa que, por sua própria natureza, exigem comprometimento constante e de longo prazo.

"Um exemplo é o caso da Física Experimental de Altas Energias onde os projetos levam anos para serem implementados, e os experimentos operam por dezenas de anos", menciona Sergio Novaes, físico da Universidade Estadual Paulista (Unesp) envolvido com um dos experimentos instalados no LHC (Large Hadron Collider), o maior acelerador de partículas do mundo, instalado no Centro Europeu para Física de Partículas (Cern), na divisa entre a França e a Suíça.

"O envolvimento nesses experimentos requer compromissos de longo prazo, que exigem acima de tudo uma estabilidade no financiamento", diz Novaes. "Não cumprir com as responsabilidades assumidas compromete a credibilidade da ciência brasileira perante os grupos e laboratórios internacionais e vai na contramão dos esforços brasileiros recentes de internacionalização da ciência produzida no País."

Interessante lembrar que o Brasil iniciou um esforço consistente de inserção de sua ciência no contexto internacional, buscando parcerias com instituições como o Cern e o ESO, que constituem o que há de mais relevante em seus segmentos (física de partículas e astronomia). A instabilidade orçamentária, se não leva diretamente à inadimplência, certamente criará trepidações nas relações com os países participantes desses consórcios, que podem temer que o Brasil não cumpra com suas obrigações depois de negociar seu ingresso nas organizações.

Nano-orçamento - Outra área que está na fronteira da ciência hoje e que pode ser prejudicada fortemente pelos cortes orçamentários é o desenvolvimento da nanotecnologia. O País teve a chance de embarcar nessa onda - que ambiciona o desenvolvimento de dispositivos e materiais construídos nas menores escalas possíveis, muitas vezes feitas de alguns poucos átomos, com potencial tecnológico revolucionário -, mas não conseguiu. "Infelizmente nessa área o País vem patinando há vários anos, com mudanças constantes de coordenação e políticas desconcertadas", afirma o Acadêmico Marcos Pimenta, especialista em nanotecnologia na Universidade Federal de Minas Gerais (UFMG).

Mesmo em sua plenitude, o orçamento nacional dedicado às "nanos" sempre foi modesto, se comparado a outros países. "Só para termos um parâmetro de comparação, Singapura está gastando US$ 100 milhões só em um centro para estudar e desenvolver tecnologias baseadas no grafeno [forma molecular de carbono que o torna extremamente promissor para aplicações]", diz Fernando Lázaro, diretor do Centro Brasileiro de Pesquisas Físicas (CBPF). "No Brasil, em 2011, devemos ter gasto ou prometido gastar menos que 10% desse valor em todas as diferentes vertentes das nanociências. Se essa situação não for revertida rapidamente, o Brasil não vai ter um papel minimamente relevante nesse segmento."

O Acadêmico Adalberto Fazzio, físico da USP, assumiu em 2011 a coordenação da área de nanotecnologia no MCTI e tem feito grande esforço para finalmente organizar as ações nessa área. "Ele propôs inclusive um arranjo interministerial para uma política geral do governo sobre nanotecnologia", diz Pimenta. "Mas o corte no orçamento pode vir a prejudicar seu trabalho."

A busca pela reversão - O MCTI ainda está por anunciar publicamente em que áreas especificamente os cortes incidirão, mas nesse momento Luiz Davidovich acha que o foco da comunidade científica deve ser em enfaticamente mobilizar governo e sociedade civil para impedir que o contingenciamento venha a acontecer de fato. "Temos de protestar veementemente contra essa política, que compromete o futuro de nosso País."