terça-feira, 30 de novembro de 2010

Dia da AIDS - 1 de Dezembro

AIDS em números

Uma infecção por um vírus, HIV. O qual destrói nossas principais células de defesa, transmitido por via venosa e sexual. epois do HIV o mundo piorou, embora estudando o HIV aprendemos sobre sistema imune, mas houveram grandes modificações comportamentais, aprendemos a tratar com os retrovirais, sabemos de interromper a transmissão pelo uso da camisinha, no entanto o HIV ainda infecta e mata milhões de seres humanos.

Amanhã é o dia de falar sobre essa doença de ensinar como se prevenir, de lutar contra o preconceito, de estimular as pessoas a fazerem os teste para HIV.







The Guardian As maiores questões cientificas




Science sees further: How science will answer some of the world's biggest questions
Science is an unending quest for understanding: as old questions are settled, new ones come into sharper focus.

I've been lucky to meet and interact with a variety of people at the Royal Society, so I am most pleased to tell you all that today (30 November 2010) is the Royal Society's 350th Anniversary. Ever since November 2009, the Royal Society has been celebrating its anniversary year by working with organisations across the UK to raise the profile of science and bring scientific activities to new audiences.

To that end, they've been contemplating all sorts of interesting questions, including: Are we alone in the universe? Can we save the lives of millions with new vaccines? How can we manage the increasing demands on our planet's resources? These questions and many of the other most challenging issues for the world today are addressed by the scientific advances described in the Royal Society's new report, Science sees further, launched today.

I shamelessly stole their pretty picture catalogue index (top), which, on their site, is a clickable index of the articles that each link to one of 12 public discussions organised and hosted by the Royal Society in 2010. All the authors are experts in their fields and the articles were reviewed by an independent committee to ensure the science is accurately represented and that a clear and balanced perspective has been provided.

So if you would like to learn more about what the Royal Society has been doing and what their people have been thinking about, be sure to check out their site and read these documents.

Do sangue ao osso

Da revista Science


Developmental biology: Blood-vessel cells turn to bone

Nature 468, 479 (25 November 2010) doi:10.1038/468479a
Published online 24 November 2010
Subject terms:Developmental biology


In the rare disease fibrodysplasia ossificans progressiva (FOP), a mutation in the Alk2 gene results in the formation of bone in soft tissues. Now researchers show that the bone cells derive from others that form the inner lining of blood vessels, called endothelial cells. These become stem-like cells before re-differentiating into bone. This process could be important in normal tissue repair, suggest Damian Medici at Harvard Medical School and Bjorn Olsen at the Harvard School of Dental Medicine, both in Boston, Massachusetts, and their colleagues.

The team found that cells from bony lesions in patients with FOP expressed marker proteins specific for endothelium. And when mutant Alk2 was introduced into normal human endothelial cells, it conferred characteristics of mesenchymal stem cells. When cultured in appropriate conditions, the endothelial-derived 'stem cells' transformed into bone, cartilage and fat cells.


- Posted using BlogPress from my iPhone

AIDS na África

o Instituto de Medicina americano divulga e alerta para a grave situação da epidemia HIV-AIDS na África


Institute of Medicine urges ramp-up of AIDS prevention in Africa - November 29, 2010

A report released today by the Institute of Medicine (IOM), part of the US National Academy of Sciences, says that cases of HIV/AIDS in sub-Saharan Africa will greatly outstrip the availability of treatment by 2020. It urges nations inside and outside of Africa to intensify prevention measures as the best long-term strategy for combating the disease.

"Because treatment will only reach a fraction of those who need it…preventing new infections should be the central tenet of any long term response to HIV/AIDS in Africa," Thomas Quinn, a co-chair of the 12-member committee that wrote the report said on Monday at a press conference in Washington, DC. Quinn, who directs the Center for Global Health at Johns Hopkins University in Baltimore, Maryland, added that, by the committee's conservative projections, the number of people living with AIDS in sub-Saharan Africa will reach an "astounding" 70 million by 2050, unless intervening forces come into play (see graph).

The report, Preparing for the Future of HIV/AIDS in Africa: A Shared Responsibility, recommends that both the United States and individual African nations develop ten-year strategic "roadmaps" for combating AIDS, and that these prioritize prevention. It also urges long-term capacity building to produce the institutions and health workforce in Africa equipped to tackle the epidemic.

Building capacity "is a big challenge" in the face of the brain drain from Africa, conceded David Serwadda, the other co-chair of the committee that wrote the report. Serwadda is an infectious disease epidemiologist at the Makere University School of Public Health in Kampala, Uganda. Still, he added, building African expertise is vital because "African countries need to take greater ownersehip of this epidemic and rely less on the global community."
The magnitude of the HIV/AIDS problem is most severe in sub-Saharan Africa. According to the 2009 epidemic update update
from UNAIDS and the World Health Organisation, the region accounted for 67 percent of all HIV-infected
individuals and 91 percent of all new infections in 2008. About 33 million people globally are HIV-infected.

While about four million people in sub-Saharan Africa are receiving anti-retroviral therapy now, they represent "the tip of the iceberg," said Patrick Kelly, the director of the IOM's Board on Global Health. Because there are still at least 18 million people who are going to need treatment, he noted, "even if incidence was zero, we would still have a huge burden of care to provide over the coming decades."

The current report grew out of an earlier IOM study that assessed the first five years of implementation of the President's Emergency Plan for AIDS Relief

Graph taken from 'Preparing for the Future of HIV/AIDS in Africa:A Shared Responsibility', by the Institute of Medicine.
Posted by Meredith Wadman on November 29, 2010

segunda-feira, 29 de novembro de 2010

AIDS na África

Instituto de Medicina americano chama atenção para gravidade da epidemia HIV-AIDS na África


Bookmark in Connotea
Institute of Medicine urges ramp-up of AIDS prevention in Africa - November 29, 2010

A report released today by the Institute of Medicine (IOM), part of the US National Academy of Sciences, says that cases of HIV/AIDS in sub-Saharan Africa will greatly outstrip the availability of treatment by 2020. It urges nations inside and outside of Africa to intensify prevention measures as the best long-term strategy for combating the disease.

"Because treatment will only reach a fraction of those who need it…preventing new infections should be the central tenet of any long term response to HIV/AIDS in Africa," Thomas Quinn, a co-chair of the 12-member committee that wrote the report said on Monday at a press conference in Washington, DC. Quinn, who directs the Center for Global Health at Johns Hopkins University in Baltimore, Maryland, added that, by the committee's conservative projections, the number of people living with AIDS in sub-Saharan Africa will reach an "astounding" 70 million by 2050, unless intervening forces come into play (see graph).

The report, Preparing for the Future of HIV/AIDS in Africa: A Shared Responsibility, recommends that both the United States and individual African nations develop ten-year strategic "roadmaps" for combating AIDS, and that these prioritize prevention. It also urges long-term capacity building to produce the institutions and health workforce in Africa equipped to tackle the epidemic.

Building capacity "is a big challenge" in the face of the brain drain from Africa, conceded David Serwadda, the other co-chair of the committee that wrote the report. Serwadda is an infectious disease epidemiologist at the Makere University School of Public Health in Kampala, Uganda. Still, he added, building African expertise is vital because "African countries need to take greater ownersehip of this epidemic and rely less on the global community."
The magnitude of the HIV/AIDS problem is most severe in sub-Saharan Africa. According to the 2009 epidemic update update
from UNAIDS and the World Health Organisation, the region accounted for 67 percent of all HIV-infected
individuals and 91 percent of all new infections in 2008. About 33 million people globally are HIV-infected.

While about four million people in sub-Saharan Africa are receiving anti-retroviral therapy now, they represent "the tip of the iceberg," said Patrick Kelly, the director of the IOM's Board on Global Health. Because there are still at least 18 million people who are going to need treatment, he noted, "even if incidence was zero, we would still have a huge burden of care to provide over the coming decades."

The current report grew out of an earlier IOM study that assessed the first five years of implementation of the President's Emergency Plan for AIDS Relief

Graph taken from 'Preparing for the Future of HIV/AIDS in Africa:A Shared Responsibility', by the Institute of Medicine.
Posted by Meredith Wadman on November 29, 2010


domingo, 28 de novembro de 2010

O processo de envelhecimento foi interrompido em animais






Os pontos amarelos nas pontas dos cromossomos
são telômeros. O encurtamento dos telômeros é progressivo com o envelhecimento e as células morrem.

Nesse artigo da Natureza, em camundongos deficientes do gen da telomerase Os cientistas observaram que os animais tiveram varais alterações e morrem precocemente. Em um grupo desses animais sem telomerase eles repuseram a telomerase e os animais rejuveneceram.




Harvard scientists reverse the ageing process in mice – now for humans
Harvard scientists were surprised that they saw a dramatic reversal, not just a slowing down, of the ageing in mice. Now they believe they might be able to regenerate human organs>

Carol Greider of Johns Hopkins university in Baltimore, who is investigating the role of telomerase in ageing.

Scientists claim to be a step closer to reversing the ageing process after rejuvenating worn out organs in elderly mice. The experimental treatment developed by researchers at Harvard Medical School turned weak and feeble old mice into healthy animals by regenerating their aged bodies.

The surprise recovery of the animals has raised hopes among scientists that it may be possible to achieve a similar feat in humans – or at least to slow down the ageing process.

An anti-ageing therapy could have a dramatic impact on public health by reducing the burden of age-related health problems, such as dementia, stroke and heart disease, and prolonging the quality of life for an increasingly aged population.

"What we saw in these animals was not a slowing down or stabilisation of the ageing process. We saw a dramatic reversal – and that was unexpected," said Ronald DePinho, who led the study, which was published in the journal Nature.

"This could lead to strategies that enhance the regenerative potential of organs as individuals age and so increase their quality of life. Whether it serves to increase longevity is a question we are not yet in a position to answer."

The ageing process is poorly understood, but scientists know it is caused by many factors. Highly reactive particles called free radicals are made naturally in the body and cause damage to cells, while smoking, ultraviolet light and other environmental factors contribute to ageing.

The Harvard group focused on a process called telomere shortening. Most cells in the body contain 23 pairs of chromosomes, which carry our DNA. At the ends of each chromosome is a protective cap called a telomere. Each time a cell divides, the telomeres are snipped shorter, until eventually they stop working and the cell dies or goes into a suspended state called "senescence". The process is behind much of the wear and tear associated with ageing.

At Harvard, they bred genetically manipulated mice that lacked an enzyme called telomerase that stops telomeres getting shorter. Without the enzyme, the mice aged prematurely and suffered ailments, including a poor sense of smell, smaller brain size, infertility and damaged intestines and spleens. But when DePinho gave the mice injections to reactivate the enzyme, it repaired the damaged tissues and reversed the signs of ageing.

"These were severely aged animals, but after a month of treatment they showed a substantial restoration, including the growth of new neurons in their brains," said DePinho.

Repeating the trick in humans will be more difficult. Mice make telomerase throughout their lives, but the enzyme is switched off in adult humans, an evolutionary compromise that stops cells growing out of control and turning into cancer. Raising levels of telomerase in people might slow the ageing process, but it makes the risk of cancer soar.

DePinho said the treatment might be safe in humans if it were given periodically and only to younger people who do not have tiny clumps of cancer cells already living, unnoticed, in their bodies.

David Kipling, who studies ageing at Cardiff University, said: "The goal for human tissue 'rejuvenation' would be to remove senescent cells, or else compensate for the deleterious effects they have on tissues and organs. Although this is a fascinating study, it must be remembered that mice are not little men, particularly with regard to their telomeres, and it remains unclear whether a similar telomerase reactivation in adult humans would lead to the removal of senescent cells."

Lynne Cox, a biochemist at Oxford University, said the study was "extremely important" and "provides proof of principle that short-term treatment to restore telomerase in adults already showing age-related tissue degeneration can rejuvenate aged tissues and restore physiological function."

DePinho said none of Harvard's mice developed cancer after the treatment. The team is now investigating whether it extends the lifespan of mice or enables them to live healthier lives into old age.

Tom Kirkwood, director of the Institute for Ageing and Health at Newcastle University said: "The key question is what might this means for human therapies against age-related diseases? While there is some evidence that telomere erosion contributes to age-associated human pathology, it is surely not the only, or even dominant, cause, as it appears to be in mice engineered to lack telomerase. Furthermore, there is the ever-present anxiety that telomerase reactivation is a hallmark of most human cancers."

Teleférico do Complexo do Alemão é investimento do PAC







Hoje a TV explora ao máximo a questão da invasão do complexo do alemão no Rio, para quem liga a TV e observa uma comunidade de mais de 300.000 pessoas a mercê do tráfico de drogas, e sem apoio do Estado, e por muitos anos, mas isso já estava mudando, pelo menos o governo federal esta construindo uma obra pelo PAC importante para aquela comunidade - o teleférico para facilitar o transporte, faltava mesmo uma ação local que e responsável pela segurança que agora e pela emergência resolveu agir, mesmo assim com participação das forças Federais.

Neutrófilos da medula ao micróbio

Publicação Immunity
http://www.cell.com/immunity/abstract/S1074-7613(10)00417-6#Summary





Immunity, Volume 33, Issue 5, 657-670, 24 November 2010
Copyright © 2010 Elsevier Inc. All rights reserved.
10.1016/j.immuni.2010.11.011

Authors

Niels BorregaardSee Affiliations
Summary

Neutrophils are produced in the bone marrow from stem cells that proliferate and differentiate to mature neutrophils fully equipped with an armory of granules. These contain proteins that enable the neutrophil to deliver lethal hits against microorganisms, but also to cause great tissue damage. Neutrophils circulate in the blood as dormant cells. At sites of infection, endothelial cells capture bypassing neutrophils and guide them through the endothelial cell lining whereby the neutrophils are activated and tuned for the subsequent interaction with microbes. Once in tissues, neutrophils kill microorganisms by microbicidal agents liberated from granules or generated by metabolic activation. As a final act, neutrophils can extrude stands of DNA with bactericidal proteins attached that act as extracellular traps for microorganisms.

quinta-feira, 25 de novembro de 2010

Rio - uma Guerra em curso

Narcotraficantes armados nas vielas







Soldados e tanques no´pé da favela




Fumaça decorrente de incendio de caminhões na entrada da favela
De um lado os narcotraficantes e terroristas ocupando a parte alta da favel vila cruzeiro e em em baixo os policiais tentando a coupação. Em fotos a direita os controladores do morro, em baixo a policia. Pode se comparar ao filme tropa de Elite II, só que ao vido na Globo. Nas pez que próximas horas deve ocorrer intensos combates, uma vez que os narcotraficantes estarem preparados e armados e com a clara intensão de resistir.

quarta-feira, 24 de novembro de 2010

3 conselhos para manter sua pele bonita




Nutrição
Agua
Protetor solar regularmente

1) You should include a well balanced nutritional diet in your daily meals. In order to make your skin look younger, your diet should be rich in antioxidents as well. As far as possible, avoid fried and processed foods. You should also reduce your intake of sugar as it is known to hurt the collagen protein in our body.

And we do not want that to happen.That is because collagen is a vital protein that is responsible in maintaining skin health and giving us a firm, supple, pliant and elastic skin. Diets that are high in fibre are very beneficial for skin health like cabbage, spinach, brocolli, green leafy vegetables, etc.

2) Drinking plenty of water and fluids is another effective way how to make skin look younger. Avoid alcohol, sodas, soft drinks and heavy juices as far as possible. The average amount of water that you must be drinking everyday is around 8-10 glasses of pure and filtered water.

Green tea is another excellent drink that you can include in your skin care regimen. It is rich in antioxidants and helps in keeping skin look younger by preventing it from the damage caused by free radicals.

3) Another important way how to make skin look younger is using a high quality anti aging skin care cream regularly. The important thing to consider is that it should contain scientifically proven natural ingredients that help your skin in remaining young and healthy naturally.

terça-feira, 23 de novembro de 2010

TSLP Informações básicas




TSLP (Thimic stromal lymphopoietin)


TSLP é uma citocina derivada de célula epitelial identificada inicialmente, em modelo murino, no ano de 1994 como um fator bioativo secretado no sobrenadante de células da linhagem tímica (FRIEND et al, 1994). Expressa na pele, intestino, pulmão e timo, a TSLP parece ser a principal reguladora da resposta Th2 assim como responsável pela diferenciação de células T regulatórias (Treg) através da modulação da atividade de células dendríticas (DCs) ainda no timo (WATANABE et al, 2005).
Ausente na pele normal, a expressão de TSLP é restrita a queratinócitos da camada suprabasal da epiderme; já seu receptor (TSLPR) tem sido detectado em diversas células imunes, como as DCs.
Apesar de não agir em células T CD4+ de memória, estudos mostram que essa citocina age diretamente em células naive e aumentam a proliferação de célula T CD4+ naive e seu desenvolvimento em células T de memória em resposta a antígenos (AL-SHAMI et al, 2005), como também atuam em células T CD4+ ativadas. Em se tratando de Treg, a TSLP estaria envolvida em sua diferenciação de forma DCs-dependente (WATANABE et al, 2005), porém, outros estudos mostram divergências assim como na relação da TSLP com linfócitos B, mostrando a necessidade de mais estudos sobre esta molécula.
Através de sua ação em células inatas, TSLP induz a produção de citocinas Th2 e pró-inflamatórias para iniciar uma fase inata de resposta inflamatória à alergias ou agravar reações alérgicas na ausência de linfócitos T e IgE (YOO et al, 2005). Portanto, a TSLP está muito envolvida em doenças como a dermatite atópica, asma e outras doenças auto-imunes, sendo alvo de muitos estudos terapêuticos.


TSLP expression in epidermis of skin from patients with atopic dermatitis but not from healthy control. (A) No detectable TSLP expression (no red staining). in epidermis from skin of health control. (B) High expression of TSLP (red staining) in epidermis from skin lesion of atopic dermatitis. Adapted from Adv Immunol. 2009; 101:1-25

Criminalidade aumenta em Salvador




Uma situação muito preocupante e praticamente sem uma resposta dos governos Estadual, local ou mesmo Federal.
Casos de violência aumentam 177% em dez anos em Salvador; capital registra 8 assassinatos por dia
Heliana Frazão


A violência em Salvador, na Bahia, aumentou 177% nos últimos dez anos, segundo estatísticas do governo baiano. Enquanto no ano 2000 ocorreram 666 assassinatos na capital, neste ano já são 1.846 homicídios. Confirmando a tendência de crescimento, em 2007 foram 1.333 pessoas assassinadas na cidade e em 2008, 1.733. Em toda a região metropolitana, o aumento verificado no período é de 386%.
A Central de Telecomunicações das Polícias Civil e Militar (Centel) registra em média oito assassinatos por dia na Grande Salvador, a maioria decorrente de armas de fogo.
Após marcar encontro pela internet, duas adolescentes morrem na Bahia
Apenas nos últimos dias, de sábado (20), até a noite da segunda-feira (22), foram mortas 15 pessoas na Grande Salvador. Entre os crimes, dois chocaram ainda mais a população: a morte de duas adolescentes e a do menino Joel de Castro. As adolescentes, de 13 e 16 anos, que, supostamente atraídas por marginais através de sites de relacionamentos da internet, tiveram os corpos decapitado. O outro crime que chocou os baianos foi a morte do menino da Joel Conceição Castro, de 10 anos, morto com uma bala perdida na cabeça no bairro do Nordeste de Amaralina, um dos mais violentos da capital baiana.
Para a Secretaria de Segurança Pública, no entanto, a criminalidade está em queda --a SSP afirma que os números, tomados mês a mês, em 2010, comparados aos do ano passado, dão sinais de declínio.
Em setembro de 2009, por exemplo, ocorreram 170 assassinatos em Salvador, no mesmo período de 2010 foram 106. Em outubro do ano passado foram 152, contra 107 este ano. “Esta é a tendência”, afirmam assessores da SSP.
Entretanto, o professor universitário e doutor em desenvolvimento regional urbano Carlos Alberto da Costa Gomes, responsável pelo Observatório da Violência, diz que não os números falam por si. “Estão todos lá, constando das estatísticas oficiais e são irrefutáveis. Se essa enorme diferença entre os anos 2000 e 2010 não significa aumento da violência, eu não sei como definir o que pode ser”, ironiza.
LEIA MAIS
Após bala perdida matar criança em Salvador, policiais são afastados
Em quinze dias, quinze carros foram incendiados por criminosos no RJ
Quanto à explicação apresentada pela SSP, Costa Gomes afirma que, na sua opinião “não muda muita coisa”. Ele acredita que o ano de 2010 deverá findar com um total de homicídios superior ao de 2009. Ele também faz uma comparação: “Em março de 2009, 144 pessoas foram mortas, contra 178 em 2010; em abril 138 (2009) contra 136 (2010) e em maio 115 (2009) contra 170 (2010)”.
Em fevereiro de 2008, o governador Jaques Wagner (PT) mudou o secretário de Segurança Pública --saiu o delegado da Polícia Federal, Paulo Bezerra, e entrou ao atual secretário, na época superintendente da PF no Estado, César Nunes.
Reeleito este ano, Wagner não fala em mudanças nas secretarias, mas em ajustes e fusão de pastas. Segundo a assessoria do governador, toda a estrutura do governo está passando por um processo de avaliação de desempenho e somente o resultado dessa avaliação é que definirá o destino de cada pasta.
Crimes
A Polícia Militar afastou nove policiais das atividades nas ruas, que participaram da operação no Nordeste de Amaralina, que resultou no morte do garoto Joel Santana. De acordo com a PM, as armas dos policiais também foram apreendidas para serem submetidas a perícia. Joel foi sepultado na manhã desta terça-feira (23), no Cemitério do Campo Santo, no bairro da Federação.
Já com relação ao assassinato das duas adolescentes, Janaína Brito Conceição, de 16 anos, e Gabriela Alves Nunes, de 13, a polícia, depois de ouvir nove testemunhas na segunda-feira (22), informou ter dois suspeitos dos crimes, entre eles uma outra menor, que teria envolvimento traficantes de drogas da região. Segundo a polícia as meninas teriam se envolvido com os criminosos através dessa jovem, que já está sendo procurada.

segunda-feira, 22 de novembro de 2010

Um peixe que se comporta como humano em depressão

Esse pequeno peixe denominado Zebra tem contribuído para entender alguns mecanismos de doença. Tem sido utilizado em pesquisas de biologia celular. Nesta reportagem abaixo neurobiologistas descobriram que ele também tem stress e depressão. Se um peixe é mantido em tanque isolado por varias vezes ele se torna paralisado (depressão) Isso decorre da queda de hormonios cerebrais (glicocorticóides e outros). O modelo se torna interessante porque quando adicionado na agua antidepressivos eles voltam a reagir normalmente.
Para a neurobiologia é um modelo interessante para descobrir mecanismos e novas drogas.

Veja o video no site abaixo. Peixe parado (depressão) e peixe controle
http://www.nature.com/nature/newsvideo/news.2010.624.mov


Solitary fish hit rock bottom

'Frozen' zebrafish may be first piscene model for human depression.

zebrafishKey elements of stress response in zebrafish could make them useful for drug testing.Inga Spence / Alamy

Zebrafish that stop swimming when left without company are showing promise as the first fish model of a human mood disorder.

In 2005, when neurobiologist Herwig Baier of the University of California, San Francisco, was screening thousands of zebrafish for vision problems1, he found one that seemed a bit 'off'. If alone, especially after repeated periods of isolation, the fish would 'freeze': just sit at the bottom of the tank (see video). If fish that swum normally were put in the tank, the relatively inactive fish became normal and swam around too.

Baier looked at the genetic mutations in the 'frozen' fish and found one in the glucocorticoid receptor, a protein that is found in almost every cell and that senses cortisol — a hormone involved in the stress response. In the normal response to a stressful situation, the hypothalamus in the brain sends corticotropin-releasing hormone (CRH) to the pituitary gland, which releases adrenocorticotropic hormone (ACTH) to the adrenal gland. The adrenal gland in turn produces cortisol. Cortisol then effectively reduces levels of ACTH and CRH, completing the normal response that allows both humans and zebrafish to deal with stress.

In the frozen fish, however, Baier found that levels of all three hormones — CRH, ACTH and cortisol — were higher than normal. He guessed that the animals were unable to respond properly to chronic stress — a problem that is known to trigger anxiety or depression in humans. On the basis of that diagnosis, he started putting the antidepressant fluoxetine (originally marketed as Prozac) in their water. After four days, they started swimming around normally. Other antidepressants and anxiolytics — drugs used to treat anxiety — also worked as a pick-me-up, he says. "There's a long literature on chronic stress being related to depression, but the causal link is unknown," says Baier. "Now we might be able to simulate this in fish and study it."

Mutant marvel

Discussing his results at the Society for Neuroscience meeting in San Diego, California, last week, Baier says his mutants could represent the first fish model for a mood disorder and be a useful screening model for drugs.

"The fact that the key elements of stress and stress response are conserved in zebrafish is exciting because of the many experimental advantages of that model organism," says chemical geneticist Randall Peterson of the Massachusetts General Hospital, Harvard Medical School, Charlestown.

“There’s a long literature on chronic stress being related to depression, but the causal link is unknown.”

Studies this year support the idea that zebrafish can model complex behavior. Earlier this year, Peterson and his collaborator, neuroscientist Alex Schier of Harvard University in Cambridge, Massachusetts, published the first two small-molecule screens based on zebrafish behaviour 2,3. The studies focused on motor behaviour, not mood disorders, but the team found that certain classes of psychotropic drugs, such as the antidepressants known as monoamine oxidase inhibitors, had recognizable, characteristic effects on behaviour. "So, the idea of discovering new therapeutic approaches for anxiety or depression may not be so far-fetched," says Peterson.

If that proves true, the finding could accelerate drug-discovery programmes. Chemical biology and drug discovery usually depend on screens of cells in lab dishes, for example. "But much of biology can't be easily reduced to an in vitro assay. This is particularly true for nervous-system disorders, where a complex, integrated nervous system is essential for research," says Peterson. Filling thousands of tiny wells on lab plates with zebrafish larvae and dousing them with candidate drug molecules offers the best of both worlds — high-throughput screening in a living system. "When we discover a new small molecule, we have the advantage of knowing that it works in vivo," he says.

Larval question

Baier plans to do the same sort of screening for new antidepressants and anxiolytics using his 'frozen' fish. But Peterson does sound a note of caution. Baier's experiments used adult fish, whereas most zebrafish screens use larvae. Using adult for screening would be expensive and laborious. Baier plans to use larval stages but he admits it is not clear yet whether the larval zebrafish will react in the same way as the adult mutants.

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The model will also have to convince the pharmaceutical industry that fish depression has significant similarities with the condition in people. This has not always been the case with mice, which as mammals should be a closer match to humans. "Considering the challenges of using rodents, including genetically engineered mice, to validly model human psychiatric diseases, zebrafish probably have some way to go before they are accepted as a translational model," said conference delegate Jeffrey Kogan, a behavioural neuroscientist working within the pharma industry who studies psychiatric disease.

It might, however, just take some time to sink in. In an e-mail toNature a few days later, Kogan said that zebrafish might be a useful model organism for psychiatric disease after all. The huge numbers of fish that can be used in such studies would, for example, give the zebrafish mutant an advantage over the mouse. "I may have to reconsider my opinion," he says.

  • References

    1. Muto, A., et al. PLoS Genet. 1, e66 doi:10.1371/journal.pgen.0010066 (2005).
    2. Kokel, D. et al. Nature Chem. Biol. 6, 231-237 (2010).
    3. Rihel, J. et al. Science 327, 348-351 (2010).


domingo, 21 de novembro de 2010

Angiogenese Tumoral


Tumours grow their own blood vessels

Finding explains failure of drugs that target host vasculature.

Almost four decades ago, Judah Folkman, a cell biologist at Harvard Medical School in Boston, Massachusetts, proposed that tumours were dependent on the blood vessels surrounding them, and that choking off that blood supply would kill the cancer1. Bevacizumab (Avastin), the first drug to block blood-vessel growth, was approved in 2004, but it and other 'angiogenesis inhibitors' have proved disappointing in the clinic, extending patients' lives for at best a few months.

Now two studies published online today in Nature2,3 have identified blood vessels grown directly from cancer cells. So Avastin and drugs like it may be targeting a pathway that is not present in those tumour-made vessels, says David Cheresh, a cancer biologist at the University of California, San Diego, who was not involved in either study.

When it comes to treatment, "most people agree that a single pathway is not going to do it," he says.

Telltale markers

In both studies, researchers worked with tumour samples from patients with an aggressive type of brain cancer called glioblastoma. They found that many of the blood-vessel cells within the tumours contained genetic markers characteristic of the cancer cells, suggesting that the blood vessels were of tumour origin.

The researchers then used markers to identify a subset of tumour cells known to have stem-cell-like properties — that is, the ability to develop into cells with different functions. In a dish, these cells could make blood vessels and, when they were injected into the brains of mice, tumours developed with blood vessels that clearly came from the original human cells. Those stem-like cells, the researchers concluded, could form both tumour and blood vessel.

Such cells seemed to be first making blood-vessel precursor cells, and then differentiating into blood-vessel cells. One of the groups, led by Viviane Tabar, a neurosurgeon and stem-cell researcher at the Memorial Sloan-Kettering Cancer Center in New York City, applied Avastin to cells in a dish to try to block these events. Although the drug did affect differentiation into blood-vessel cells, "we found that Avastin does not alter that first process whatsoever," says Tabar.

In the second study, Ruggero De Maria from the Italian National Institute of Health in Rome and his colleagues selectively killed the tumour-related blood-vessel cells. This caused the tumours to shrink, showing their reliance on those blood vessels. However, the number of tumour-derived blood-vessel cells in each tumour sample varied from 20% to 90%, suggesting that blood-vessel formation was more important for some tumour cells than others.

Tabar says that it is not clear whether this self-vascularizing capacity is widely present in other tumour types, although there are some hints that this is the case. "It would be very exciting if other tumour cells exhibit the same phenomenon," she says.

Two-pronged attack

This isn't the first time researchers have suggested that cancer cells can make their own blood vessels. In 1999, Mary Hendrix, a cancer researcher now at Northwestern University in Chicago, Illinois, and her colleagues reported a similar effect in melanoma cells which they called "vascular mimicry"4.

At the time, says Hendrix, her group predicted that these vascular cells would prevent drugs such as Avastin from being fully effective, but their findings were controversial. The two latest studies support the idea's validity, she says, as well as demonstrating "an example of the functional plasticity of tumour cells".

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Such plasticity means that researchers must look for a combination therapy that can target both the host vasculature, as Avastin does, and the stem-like cancer cells that can create both vasculature and tumour tissue, Hendrix adds.

Cheresh agrees. Today's findings in glioblastoma are not the only recent strike against anti-angiogenesis drugs. In the last two years, a handful of studies have reported that, counterintuitively, such drugs can speed tumour growth (see Cutting off cancer's supply lines, 2009)5,6,7,8. But that doesn't mean that the strategy of targeting the blood supply is inherently faulty, says Cheresh, who co-authored two such studies


"There are many more ways to affect the vasculature" than through such drugs, he notes: "It means we need to identify either more than one drug" to shut down blood vessels of tumour and non-tumour origin, "or a common molecular mechanism affecting both the tumour and the vasculature".

  • References

    1. Folkman, J. N. Engl. J. Med. 285, 1182-1186 (1971).
    2. Wang, R. et al. Nature advance online publication doi:10.1038/nature09624 (2010).
    3. Ricci-Vitiani, L. et al. Nature advance online publication doi:10.1038/nature09557 (2010).
    4. Maniotis, E. J.[/author] et al. Am J. Pathol 155, 739-752 1999.
    5. Pàez-Ribes, M. et al. Cancer Cell 15, 220-231 (2009).
    6. Ebos, J. M. L. et al. Cancer Cell 15, 232-239 (2009).
    7. Greenberg, J. I. et al. Nature 456, 809-813 (2008).
    8. Stockmann, C. et al. Nature 456, 814-818 (2008).

sábado, 20 de novembro de 2010

Maria Eugênia - Companheiro - Abertura da novela Araguaia

Etanol, Brasil deve triplicar produção - Reportagem da Nat Geo






This story is part of a special series that explores energy issues. For more, visit The Great Energy Challenge.

Brazil, which has done more than any other nation to displace oil with ethanol, is poised as never before to ramp up production of its sugarcane-based fuel and, it hopes, to market its “sweeter alternative” around the world.

Brightening Brazil’s prospects to solidify its position as world biofuel powerhouse are billions of dollars of new foreign investment and the possible fall of a long-standing trade barrier in the United States, a huge potential market.


Brazil Mines and Energy Minister Marcio Zimmerman said in recent weeks that South America’s largest country plans to more than double its ethanol production, from 7 billion gallons (26 billion liters) annually to 17 billion gallons (64 billion liters), by 2019. The plan may sound especially ambitious in light of the depressed ethanol production of the past two years. But it was the global economic downturn—and resulting low prices—that set the stage for a wave of mergers and outside investment in Brazilian companies that were in need of cash.

In August, Shell* signed a $12 billion joint venture with Brazil sugar and ethanol maker Cosan, S.A. Earlier in the year, BP, which already has a two-year-old stake in Brazilian ethanol, announced plans to expand its investments by $5 billion to $6 billion in the next decade, and media reports in São Paulo this month were buzzing with rumors of a pending deal. The U.S. agricultural company, Bunge Ltd., and France's Louis Dreyfus Commodities both expanded their presence in the Brazil with acquisitions of ethanol companies last year. The dizzying succession of deals helps fortify Brazil’s ethanol industry to invest in needed infrastructure, especially a long-discussed pipeline from the producing regions in the interior of the country to the population centers of Rio de Janeiro and São Paulo.

Also, Brazil now has money and access to worldwide distribution networks that would allow it to increase exports. Certainly, most of Brazil’s ethanol still will be consumed domestically—half of the nation’s car and light truck transport is now fueled by ethanol, and that level is bound to increase, because most cars sold in the country are flex-fuel vehicles that can run on 100 percent ethanol.

Ethanol sales in Brazil are very sensitive to prices, however, due both to the flexibility of the vehicles and the fact that Brazilian consumers have a choice at the pump—pure ethanol or a blend that is 80 percent gasoline. If the price of gasoline is low relative to the price of ethanol, consumers will choose the “gasohol” blend, said Carla Silva Cohen, a Latin American specialist with the energy consulting group IHS CERA. In fact, Silva said, because ethanol delivers less mileage per gallon, ethanol has to be selling for 25 percent less than gasoline for Brazilian consumers to choose to put the alternative fuel in their tanks. “It’s important for producers to have an alternative to the domestic market, because the price domestically will be capped naturally by the price of gasoline,” she said.

In the United States, where the vast majority of ethanol sold is in a 10 percent blend with gasoline, and consumers have little choice of a higher blend in most locations, Brazil producers can sell their ethanol at a higher price when gas prices are low.

Looking to Overseas

Certainly, Brazil already is an exporter—sending about 18 percent of its production overseas, mostly to the United States, Japan, and Europe, according to the most recent data from the U.S. Energy Information Administration. But trade barriers have limited those sales.

For years, a 54-cent-per-gallon tariff has discouraged imports of ethanol at U.S. borders, even though fuel alcohol from Brazilian sugarcane is generally cheaper than the U.S. alternative grown from corn. Zeal to protect the heartland corn industry, source of most of the ethanol sold in the United States, still runs high in Washington, D.C. But tax- and energy-policy gridlock on Capitol Hill may well work to Brazil’s advantage. The ethanol import tariff is one of 65 provisions in the U.S. tax code that are set to expire on the last day of the year.

(Related: “Ethanol Future Still Looking for Fuel”)

And until the U.S. Congress decides what to do about the most controversial of those measures—the federal income tax breaks enacted early in the Bush administration—observers think it unlikely that lawmakers will tackle the lower-profile battles over the tariff or another key ethanol provision, the 45-cent-per-gallon tax credit paid to refiners for blending ethanol into the U.S. fuel mix. The blenders’ credit, paid directly to oil refiners, is expected to cost taxpayers $7.6 billion this year.

The enthusiasm for these developments in the United States is clear on Sweeteralternative.com, the website of the Brazilian Sugarcane Industry Association (UNICA) export campaign, where a calendar is counting down the days to “cleaner, more affordable energy” beginning on January 1. UNICA’s chief representative in North America, Joel Velasco, a dual national of Brazil and the United States and former personal aide to Vice President Al Gore, has spent much of the year taking on the U.S. corn ethanol industry lobby with vigor and wit.

“The subsidies [that favor domestic producers] were created to build an ethanol industry,” Velasco says. “The baby now can walk and talk and has a job. But they [corn growers] are saying ‘Let’s keep the training wheels on this.’ ”

Velasco says that without import tariffs, the average American could save about a nickel per gallon using gasoline blended with sugarcane ethanol.

The U.S. ethanol industry lobbying group, the Renewable Fuels Association, has warned that ending government support for what has been the nation’s most important alternative transportation fuel will result in the loss of 112,000 jobs, a 38 percent decline in domestic ethanol production, and a $6.6 billion drop in spending by the U.S. ethanol industry.

But UNICA has battled back, funding a study by Iowa State University indicating that hundreds of jobs would be lost, not tens of thousands of jobs. “A change in ethanol policy would not have major implications for the U.S. employment picture,” the report said, though it did note that the study did not factor in indirect job losses associated with a possible decline in ethanol production.

Brazil’s ethanol industry also is looking at a possibly expanding market for its product across the Atlantic Ocean. Although Europe has had an even higher ethanol tariff than the United States—about 19 Euro cents per liter (about 72 Euro cents per gallon)—the European Union member states are moving to increase their use of ethanol. The EU has adopted a renewables directive requiring its member nations to increase the renewable fuel content in their energy use to 20 percent by 2020.

Environmental Impact

Much of the debate in both Europe and the United States over sugarcane ethanol has turned on the question of whether it is, as Brazil argues, an environmentally friendly alternative, or whether its true impact on land use and the planet’s greenhouse gas burden is far worse than previously understood.

(Related: “Green Dreams: Making fuel from crops could be good for the
planet—after a breakthrough or two.”)

Earlier this year, Brazil got a boost when the U.S. Environmental Protection Agency determined that sugarcane ethanol was a so-called “advanced” biofuel, with life-cycle greenhouse gas emissions 61 percent lower than fossil fuels. Corn ethanol, in contrast, has life-cycle greenhouse gas emissions just 23 percent less than oil, according to EPA calculations.

That determination is key, because under the energy policy reform that Congress passed in 2007, advanced biofuel is favored in the mandates that seek to increase the amount of ethanol used in the United States from about 10 billion gallons in 2009 to 36 billion gallons by 2020. “Sugarcane ethanol is a first-generation biofuel, but with generation two efficiency,” says Velasco.

But not everyone agrees. Kate McMahon, biofuels campaign coordinator for Friends of the Earth in Washington, D.C., said the group is concerned about the Brazilian sugarcane industry, particularly about land use and food crop replacement, and the industry’s impact on the Amazonian rain forest. Estimates are that rain-forest destruction is responsible for at least one-quarter of the atmosphere’s carbon overload. Even though sugarcane is not directly planted onto rain-forest land, critics are concerned that it will displace other crops—especially soybeans—that will then take over important ecosystems in a domino effect.

(Related: “Ethanol Production Could Be Eco-Disaster, Brazil's Critics Say”)

“Historically it is always natural ecosystems that pay for rising demands,” McMahon said. “We have insatiable energy demands and ultimately what we need to be doing is reducing that demand, not just using up Brazil’s land to meet the energy demand of the United States.”

But Izabella Teixeira, Brazil’s environment minister, said her country could produce more sugarcane ethanol without hurting the delicate ecosystems. This year, she said, the amount of deforestation in Brazil will likely be 1,540 square miles (4,000 square kilometers), down dramatically from the peak of 9,270 square miles (24,000 square kilometers) in 2004. “Brazil is doing more to reduce its carbon footprint than any other country,” she said.

(Related: “Brazil to Crack Down on Amazon Clearing” and “Brazil grasps the nettle of climate mitigation”)

“The soy land has stopped taking the rainforest. The domino hypothesis is thwarted,” Velasco said.

Perhaps. But due to the indirect land use question, the European Union is considering environmental criteria for ethanol imports that could restrict Brazil’s access to the market. Further analysis on indirect land use also is under way at the U.S. EPA. As a result, earlier this month, UNICA President Marcos Jank said the industry might go to the World Trade Organization to protest such calculations as a nontariff trade barrier. Before the “sweeter alternative” makes its way to more markets, there could be a bitter battle ahead.

* This report is produced as part of National Geographic’s Great Energy Challenge initiative, sponsored by Shell. National Geographic maintains autonomy over content.

J. Okray is a reporter for Medill News Service in Washington, D.C.

(Related: Brazil Photos from National Geographic Travel)

vacinas para Tuberculose por Kaufmann







-Future Vaccination Strategies against Tuberculosis: Thinking outside the Box
Immunity, Volume 33, Issue 4, 567-577, 29 October 2010


Authors

Stefan H.E. Kaufmann
Summary

With almost a dozen vaccine candidates in clinical trials, tuberculosis (TB) research and development is finally reaping the first fruits of its labors. Vaccine candidates in clinical trials may prevent TB disease reactivation by efficiently containing the pathogen Mycobacterium tuberculosis (Mtb). Future research should target vaccines that achieve sterile eradication of Mtb or even prevent stable infection. These are ambitious goals that can be reached only by highly cooperative engagement of basic immunologists, vaccinologists, and clinical researchersor in other words, by translation from basic immunology to vaccine research and development, as well as reverse translation of insights from clinical trials back to hypothesis-driven research in the basic laboratory. Here, we review current and future strategies toward the rational design of novel vaccines against TB, as well as the progress made thus far, and the hurdles that need to be overcome in the near and distant future.








sexta-feira, 19 de novembro de 2010

Dia da consciência negra -






100 anos da Revolta da Chibata - João Cândido, o almirante negro da esquadra revoltosa

100 anos da Revolta da Chibata - João Cândido, o almirante negro da esquadra revoltosa
Luiz Carcerelli

Após a decretação da Lei de Terras, em 1850, ficou determinado que a terra só poderia ser adquirida pela compra e os ex-escravos ficaram impossibilitados de ter acesso à terra. Com a publicação da "Lei Áurea" em 1888, uma alternativa para os negros passou a ser o trabalho, como marujo, na Marinha de Guerra do Brasil. Nos navios, no entanto, as humilhações, exploração e brutalidade do tempo da escravidão não haviam findado, eram permitidos os castigos físicos contra os marinheiros que infringissem as regras draconianas. Obviamente, para o oficialato as regras eram outras. Tal fato diminuía o número de voluntários, que eram supridos com o recrutamento forçado, feito pela polícia. Tais castigos foram abolidos quando da Proclamação da República e restabelecidos um ano depois. Estavam previstas as seguintes penalidades:

"Para as faltas leves, prisão a ferro na solitária, por um a cinco dias, a pão e água; faltas leves repetidas, idem, por seis dias, no mínimo; faltas graves, vinte e cinco chibatadas, no mínimo."
AS MELHORES INFLUÊNCIAS

Em 15 anos de carreira militar, João Cândido fez várias viagens pelo Brasil e por vários países, mas a que maior influência teve sobre ele foi para a Grã Bretanha em 1909, para acompanhar o final da construção de navios de guerra encomendados pelo governo brasileiro. Lá, além de vivenciar a diferença com a qual eram tratados os marujos britânicos e os brasileiros, tomou consciência da revolta do navio russo Encouraçado Potenkin, em 1905.

Ainda na Inglaterra, João Cândido montou clandestinamente um Comitê Geral para preparar a revolta. Esse comitê se ramificou em vários comitês revolucionários em diferentes navios. Em 1910, no Rio de Janeiro, se junta ao comitê Francisco Dias Martins, o Mão Negra, que havia ficado conhecido pela carta que escreveu sob este pseudônimo, denunciando a chibata.

Na noite de 22 de novembro de 1910, amotinou-se a tripulação do Encouraçado Minas Gerais. Quando o comandante retornou de um jantar em navio francês, tentou resistir e foi morto a tiros e coronhadas. Além deles, outros cinco oficiais foram executados. Alertados por um tenente ferido, os oficiais do Encouraçado São Paulo debandaram para terra e essa unidade da Armada também aderiu ao levante. O mesmo aconteceu com o Deodoro e com o Cruzador Bahia, além de embarcações menores, fundeadas na Baía de Guanabara.

Na manhã do dia 23, de posse dos navios e das armas, os marinheiros sublevados apresentaram ultimatum, ameaçando abrir fogo sobre a Capital Federal. João Cândido, o Almirante Negro, como ficou conhecido, liderava a revolta e a redação do documento foi de Francisco Dias Martins. Dizia a carta:

"O governo tem que acabar com os castigos corporais, melhorar nossa comida e dar anistia a todos os revoltosos. Senão, a gente bombardeia a cidade, dentro de 12 horas."
E mais abaixo:

"Não queremos a volta da chibata. Isso pedimos ao presidente da República e ao ministro da Marinha. Queremos a resposta já e já. Caso não a tenhamos, bombardearemos as cidades e os navios que não se revoltarem."
A Marinha esboçou um ataque com dois navios menores, prontamente repelidos pelos revoltosos que abriram fogo contra a Ilha das Cobras (base naval) e dispararam tiros de advertência sobre o Palácio do Catete (sede do executivo).

Surpreendido e temendo o combate, o Estado brasileiro na pessoa do marechal Hermes da Fonseca, então presidente da República, aceitou as exigências dos revoltosos. Mas a estratégia do governo ficaria clara alguns dias depois.

Hermes da Fonseca abole os castigos físicos e promete anistia para os que se entregassem. Os marinheiros depõem as armas e sucede-se o que sempre acontece quando se confia em um Estado reacionário.

A reação desencadeou feroz perseguição aos marinheiros revoltosos. Às dezenas, os marujos foram encarcerados em porões de navios ou nas masmorras da Ilha das Cobras. O barco de guerra Satélite foi palco de numerosos fuzilamentos.

Já no dia 28 de novembro, alguns marujos são expulsos da Armada por serem "inconvenientes à disciplina". No dia 4 de dezembro, quatro marinheiros foram presos acusados de conspiração. Muito desorganizados, no dia 9, os fuzileiros navais da Ilha das Cobras sublevam-se e são duramente bombardeados, mesmo tendo hasteado a bandeira branca. Dos 600, sobrevivem apenas cem. Na sequência, vários foram desterrados e condenados a trabalhos forçados nos seringais da Amazônia, sendo que sete foram assassinados no caminho.

Mas esses monstruosos crimes não foram capazes de quebrar a rebeldia dos marinheiros. Muitos participantes da rebelião de 1910 ligaram-se anos depois ao movimento revolucionário. O marinheiro Normando, comandante de um dos barcos rebelados, ingressou nas fileiras do Partido Comunista do Brasil – PCB. Em 1924, os marinheiros novamente sublevaram-se no encouraçado São Paulo. Em 1935, incorporaram-se às centenas à luta da Aliança Nacional Libertadora e mais tarde, em 1964, compuseram a linha de frente da resistência contra o gerenciamento militar-fascista.

O ódio zoológico nutrido pela oficialidade da Marinha a João Cândido manteve-se irretocado e foi renovado ano após ano. Em 6 de dezembro de 1969, o líder da rebelião da esquadra de 1910 faleceu sem receber nenhum centavo da marinha.

Ainda na década de 1970, a reação destilava seu veneno contra João Cândido e seus companheiros. A censura do gerenciamento militar mutilou a bela música de João Bosco e Aldir Blanc, O mestre sala dos mares, trocando as palavras marinheiro por feiticeiro, almirante por navegante, bloco de fragatas por alegria das regatas, e outras mais, tirando muito de sua força.

Em 22 de Novembro de 2007, quando se completaram 97 anos da Revolta, foi inaugurada uma estátua em homenagem ao "Almirante Negro" nos jardins do Museu da República, antigo Palácio do Catete. A estátua, de corpo inteiro, de João Cândido com o leme em suas mãos, foi afixada de frente para o mar.


Em 24 de julho de 2008, 39 anos depois da morte de João Cândido, publicou-se, no Diário Oficial da União, a Lei Nº 11.756 que concedeu "anistia" ao líder da Revolta da Chibata e a seus companheiros. No entanto, a lei foi vetada na parte em que determinava a reintegração de João Cândido à Marinha do Brasil o reconhecimento de sua patente e devidas promoções e o pagamento de todos os seus direitos e de seus familiares.

Em 20 de Novembro de 2008, a estátua do Almirante Negro foi retirada do Palácio Catete e colocada na Praça Quinze de Novembro, no Centro da cidade do Rio de Janeiro. Lá, às margens da Baia da Guanabara, a imponente figura de João Cândido certamente está mais à vontade, entre os populares que passam e param para lhe render homenagem, entre tantos filhos do povo como ele negros, pobres, explorados, revoltosos.

O Mestre Sala dos Mares

(João Bosco / Aldir Blanc)
Composição original

Há muito tempo nas águas da Guanabara
O dragão do mar reapareceu
Na figura de um bravo marinheiro
A quem a história não esqueceu
Conhecido como o almirante negro
Tinha a dignidade de um mestre sala
E ao navegar pelo mar com seu bloco de fragatas
Foi saudado no porto pelas mocinhas francesas
Jovens polacas e por batalhões de mulatas
Rubras cascatas jorravam das costas
dos negros pelas pontas das chibatas
Inundando o coração de toda tripulação
Que a exemplo do marinheiro gritava então
Glória aos piratas, às mulatas, às sereias
Glória à farofa, à cachaça, às baleias
Glória a todas as lutas inglórias
Que através da nossa história
Não esquecemos jamais
Salve o almirante negro
Que tem por monumento
As pedras pisadas do cais
Mas faz muito tempo

Preocupante essa ordem de credibilidade nas Instituções

http://globonews.globo.com/Jornalismo/GN/0,,MUL1631007-17665,00.html

Veja reportagem da Globo News sobre o ranking das Instituições que os brasileiros mais acreditam. Os comentários masi bem elaborados são feitos por Lenador Kampal

quinta-feira, 18 de novembro de 2010

A crise financeira continua, mas na Irlanda. The Economist




As dificuldades financeiras dos PIGS, (Portugal, Irlanda, Grecia, Espanha)
continuam, mesmo com apoio do Fundo europeu , ainda o FMI vai ter que entrar para emprestar a esses paises. Esse socorro causa desestabilidade do Euro ( €)

Saving the euro
Ireland’s woes are largely of its own making but German bungling has made matters worse


Nov 18th 2010


HERE we go again. Barely six months since Greece was bailed out, a familiar story is emerging. Investors nervous about a small European country with ballooning debts and uncertain prospects, start selling its bonds. A surge in bond yields infects other countries in a similar (if less urgent) bind. A looming local poll—this time a by-election in Donegal—feeds the doubts. The mixed messages and bungling of Germany’s politicians plunge a bad situation into outright peril.

And three horribly familiar questions emerge. Who is to blame for this mess? What is the way out? And what on earth does it mean for the euro, the common currency at the heart of the world’s biggest economic region? At least there are limits to the parallels with Greece; Ireland is more likely to generate the growth that will one day allow it to service its debts.

On the first question, the original sin lies with Ireland. The Celtic tiger roared ahead, but it paid too little attention to its gung-ho banks and asset markets. A property bubble blew up, and Ireland became dangerously dependent on the revenues that flowed from it. The country’s financial regulators were incompetent at best, cronies at worst. And at the first sign of trouble, the government made the mistake of issuing a blanket guarantee for all its banks’ debts, which now means that taxpayers have to bear the catastrophic losses on property bets made by Anglo Irish Bank and others, pushing the budget deficit to 32% of GDP this year (see article).

So Ireland has long been flirting with a debt crisis of its own. But it has not been helped by the other euro-zone members. To begin with, the rescue of Greece was a botch: it fudged the obvious issue that Greece will never fully be able to repay its debts on time. And the temporary support scheme cobbled together for the rest of the euro zone was equally flawed: in particular, it was too easy on private creditors. But although all this was troubling, Angela Merkel’s attempt to fix it has been spectacularly clumsy.

At an EU summit at the end of October the German chancellor won agreement that any future euro-zone rescue scheme should include a mechanism for an orderly sovereign-debt default. The principle was absolutely right: unless default is a possibility, bond investors have no reason to distinguish between good and bad credits. But the idea of making bondholders lose money when sovereign credits turn sour was aired without any guidance about how and when it might apply. Astonishingly, the Germans failed to put together a detailed proposal for the summit.

The timing was dreadful, with Ireland, Greece and Portugal trying to fashion austere budgets for 2011. Bond investors were invited to fear the worst. Ever since, the Irish have been on the run, and the Greeks and others on tenterhooks. An Irish problem has quickly become a euro-zone problem—and a British headache, too, given the close links between the neighbours.

The second question—the solution—shows how different Ireland in fact is from Greece, which was pleading for money from a reluctant Mrs Merkel. This time the argument is between the Irish, who have insisted they do not need a bail-out, and large euro-zone countries which insist they must take one.

Both sides are being disingenuous (see article). The Irish are right that they have enough money to last until the middle of next year (the treasury has around €20 billion of cash squirrelled away). But they could face bank runs long before then.

On the other hand, the Irish are also right to be suspicious of intentions in Brussels and Berlin. Too much of the EU’s motivation seems to be to punish Ireland for its Anglo-Saxon ways—especially its highly competitive 12.5% tax rate on corporate profits, which helps it attract foreign firms. Raising this would be madness. Ireland is planning budget cuts for next year of 3.8% of GDP; any economy would struggle against that headwind. But its hopes are anchored in those new foreign arrivals. The sort of foreign direct investment (FDI) on which the prosperity of the 1990s was built is flooding in once again. IDA Ireland, the agency that targets such investors, says FDI in 2010 will be the best for seven years. A new generation of firms, including computer-gaming outfits like Activision Blizzard and Zynga, are joining the established operations of Intel and Google. Ireland’s workforce is young, skilled and adaptable. Rents are coming down even faster than wages.

If only both sides gave up posturing, they would agree that the European rescue funds should be used to stabilise Ireland’s banks, insisting only on certain budget targets in return. Such a deal should satisfy Ireland’s euro-zone partners, which want an end to the uncertainty, and the European Central Bank (ECB), on which Ireland’s banks have become overly reliant for funding. It would also be wise to offer a similar deal to Portugal. Its banks are dependent on ECB support, and it too is in the bond markets’ sights.


Green and bear it

That leaves the third question: the euro. For all the talk of the euro failing to survive this sovereign-debt crisis, it should struggle through. Despite the troubles on its periphery, the public debt of the euro zone as a whole is not notably high by rich-country standards. The real problems are the absence of a credible plan to deal with errant countries (as the Germans have recognised), the structural imbalances between Germany and the less competitive southern members and, most of all, the miserable growth prospects for those poorer, weaker southerners, made worse by their fiscal retrenchment. Denied the possibility of devaluation, slow-growing countries like Portugal and now Spain should be looking for structural reforms that can reduce their labour costs, enhance enterprise, stimulate competition and regain competitiveness.

Ironically Ireland looks more likely to find that growth than the Mediterranean countries. None of that excuses the mess it has made of its banking system. But the real question for Europe is whether it wants a slow succession of Greeces and Irelands—or whether it is ready to move beyond government rescues and focus on growth.

- Posted using BlogPress from my iPad