segunda-feira, 31 de outubro de 2011

dicas de como achar sinônimos de palavras ao ler New York Times

Ao ler o jornal NYT você sublinha a palavra e aperta a ? que aparece acima da palavra, assim abre uma nova janela com dicionário.
Veja as figs abaixo.



domingo, 30 de outubro de 2011

monócitos CD 14



    Summary

    Monocytes are effectors of the inflammatory response to microbes. Human CD14+ monocytes specialize in phagocytosis and production of reactive oxygen species and secrete inflammatory cytokines in response to a broad range of microbial cues. Here, we have characterized the functions of human monocytes that lack CD14 (CD14dim) and express CD16CD14dim monocytes were genetically distinct from natural killer cells. Gene expression analyses indicated similarities with murine patrolling Gr1dim monocytes, and they patrolled the endothelium of blood vessels after adoptive transfer, in a lymphocyte function-associated antigen-1-dependent manner. CD14dim monocytes were weak phagocytes and did not produce ROS or cytokines in response to cell-surface Toll-like receptors. Instead, they selectively produced TNF-α, IL-1β, and CCL3 in response to viruses and immune complexes containing nucleic acids, via a proinflammatory TLR7-TLR 8-MyD88-MEK pathway. Thus, CD14dim cells are bona fide monocytes involved in the innate local surveillance of tissues and the pathogenesis of autoimmune diseases.

    mon


    terça-feira, 11 de outubro de 2011

    A batalha cpntra Tb Who trz novos dados

    Battle against TB is being won, says World Health Organisation
    WHO's annual report reveals that 2010 saw lowest number of cases and of deaths for decade

    A doctor checks for a suspected case of TB in South Sudan. The World Health Organisation's annual report revealed that 2010 saw the lowest number of cases for a decade. Photograph: David Levene for the Guardian
    Sarah Boseley, health editor
    The Guardian, Tue 11 Oct 2011 16.13 BST
    The battle against what used to be known as the White Death – tuberculosis – is apparently being won, with a steady year on year decline in the numbers infected with the disease and dying from it, according to the World Health Organisation.
    The WHO's annual report says that 2010 saw the lowest number of cases and of deaths for a decade. There were 8.8 million cases of disease, down from 9 million in the peak year of 2005. Deaths dropped from 1.8 million in 2003 to 1.4 million.
    Yet the UN warned that declining funding, as donor governments retrench in response to the tough economic climate, could put this progress at risk and cause problems in dealing with the worrying rise in cases of multi drug-resistant TB (MDRTB).
    "Fewer people are dying of tuberculosis, and fewer are falling ill. This is cause for celebration," said the UN secretary-general, Ban-ki Moon. "But it is no cause for complacency. Too many millions still develop TB each year, and too many die. I urge serious and sustained support for the Stop TB Partnership in the years to come."
    Only 16% (46,000) of those with multi drug-resistant forms of the disease are being treated at the moment, which is alarming because without treatment, not only will the patient die but the disease is likely to be spread. Even ordinary TB requires a course of drugs lasting six months. MDRTB is even harder to treat because it requires years of antibiotics which are not commonly available and expensive. Of the $1bn said to be needed in 2012 to fund the fight against TB globally, $200,000 is for MDRTB.
    A new rapid test is being rolled out, which is expected to revolutionise the diagnosis of MDRTB. "But the promise of testing more people must be matched with the commitment to treat all detected. It would be a scandal to leave diagnosed patients without treatment," said Dr Mario Raviglione, director of WHO's Stop TB department.
    The best progress has been made in big countries with large numbers of people affected by TB, which is a significant killer in people with HIV. Among them are Kenya and Tanzania. Brazil has also reported a steady decline in cases and China has made dramatic progress. Overall, the death rate dropped by 40% between 1990 and 2010. If this continues, all regions except Africa are on track to cut mortality by 15% by 2015.
    In 2009, 87% of patients treated were cured, with 46 million people successfully treated and 7 million lives saved since 1995. However, a third of estimated TB cases worldwide are not notified and therefore it is unknown whether they have been diagnosed and properly treated.

    segunda-feira, 10 de outubro de 2011

    Aproveitem Graduação Sanduiche UFBa

    Assuntos Internacionais
     
    Programa Ciência sem Fronteiras na UFBA
    Programa da CAPES: Graduação Sanduíche nos EUA
     
     
    Prezados Docentes e Estudantes,
     
    A Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (Capes) lançou a primeira chamada pública no âmbito do programa Ciência sem Fronteiras: Chamada Pública 01/2011 - Graduação Sanduíche nos EUA.
    Nesta primeira chamada, as bolsas serão disponibilizadas na modalidade graduação-sanduíche nos Estados Unidos da América (EUA). A ida dos estudantes terá início a partir de janeiro de 2012. A chamada pública propicia que as instituições de ensino superior brasileiras (IES) selecionem estudantes brasileiros de graduação em áreas de estudo e trabalho de interesse para o Brasil, por meio da realização de disciplinas ou de estágio em instituições norte-americanas.
    Os alunos participantes receberão uma bolsa de estudos pelo período de 12 meses, pagamento das taxas escolares norte-americanas, nos casos em que couber, além de passagens aéreas para o traslado Brasil/EUA/Brasil.
    Para se inscrever, os candidatos devem ter, entre outros requisitos: nacionalidade brasileira; apresentar bom rendimento acadêmico; ter concluído, no mínimo, 50% e, no máximo, 80% do currículo previsto para o curso de graduação no momento de início da viagem de estudos; e ter obtido nota mínima de 79 pontos no exame TOEFL/IBT Test. Os candidatos poderão encaminhar comprovantes de inscrição para realização do TOEFL agendados até 10 de outubro.
    Para realizar a inscrição, os alunos devem acessar o site da CAPES: http://www.capes.gov.br/cienciasemfronteiras/html/graduacao.html. Atenção especial deve ser dada para os temas e áreas de interesse priorizadas pelo programa Ciência sem Fronteiras.
    Serão aceitos, além do TOEFL IBT com nota mínima de 79 pontos, também os testes de proficiência TOEFL Paper Based com nota mínima de 550 pontos e IELTS com nota mínima igual a 6.0.
    Além dos critérios do programa Ciência sem Fronteiras, os estudantes devem atender também ao que dispõe o Regulamento do Ensino de Graduação da UFBA (disponível em http://www.ufba.br/legislacao), com atenção especial à Seção III: Da Matrícula Decorrente de Convênio, Intercâmbio ou Acordo Cultural (Artigo 15 a Artigo 21 do REG).
    Caberá à CAPES implementar as propostas das IES, respeitadas as disponibilidades orçamentária e de absorção dos alunos pelas universidades norte-americanas.
    O contato com a Capes deverá ser realizado pelo endereço eletrônico graduacaosemfronteiras.usa@capes.gov.br

    sábado, 8 de outubro de 2011

    Neuroimunologia - Science


    IMMUNOLOGY

    Neuroimmune Communication

    1. Ephraim F. Trakhtenberg
    2. Jeffrey L. Goldberg
    +Author Affiliations
    1. Bascom Palmer Eye Institute, Interdisciplinary Stem Cell Institute, Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
    1. E-mail: jgoldberg@med.miami.edu
    Our immune and nervous systems influence each other, both locally and at a distance (14). Locally, immune responses in the central nervous system (CNS) include activation of resident glia cells and macrophages (36), and infiltration of circulating immune cells (5). Many responses rely on cytokines secreted by immune cells for communicating not only to immune cells but also to neurons and glia to control synaptic pruning (7), neuroplasticity (8), and neuroprotection (3). Molecules important in the immune system, such as major histocompatibility complex (MHC) proteins, are also expressed by neurons and glia and likely contribute to neural function. Can the nervous system communicate with the immune system through neurotransmitters—chemicals that relay signals from neurons to target cells—to regulate inflammation and immunity, or even to feed back and regulate the nervous system itself? Two papers in this issue, by Rosas-Ballina et al. on page 98 (9) and Wong et al. on page 101 (10), demonstrate how neurotransmitters directly modulate specific cells and cellular responses in the immune system at a distance.
    Previous work pointed to pathways of direct, long-distance neuroimmune cross-talk. For example, stimulation of the vagus nerve, which originates in the brainstem and innervates visceral organs, inhibits cytokine release and attenuates inflammatory damage in endotoxemia and sepsis. The vagus nerve stimulates celiac ganglion adrenergic neurons that innervate the spleen, leading to release of the neurotransmitter acetylcholine (ACh) and activation of the nicotinic ACh receptor (nAChR) on splenic macrophages. This blocks production of the proinflammatory cytokine tumor necrosis factor–α (TNF-α). How does stimulation of adrenergic neurons induce ACh release in the spleen? Rosas-Ballina et al. show that a splenic T cell capable of synthesizing and secreting ACh fulfills this role (see the figure). The authors identified a subpopulation of CD4+ T cells that secrete ACh, express β-adrenergic receptors, and are located adjacent to adrenergic nerve endings in the spleen. Transplanting these T cells into mutant mice devoid of T cells and with endotoxemia rescued the attenuation of TNF-α by vagus nerve stimulation. Furthermore, reducing expression by small interfering RNA of choline acetyltransferase, an enzyme required for ACh biosynthesis, in these T cells before transplantation blocked rescue of TNF-α attenuation after vagus nerve stimulation. Thus, ACh secretion by these T cells is required in this inflammatory reflex. Considering the roles of TNF-α in CNS inflammation (11), this pathway should also be explored with CNS injury and disease models.
    Neuroimmune cross-talk.
    Noradrenaline-secreted from peripheral nerve terminals in the spleen and liver regulates pro- and anti-inflammatory cytokine secretion by stimulating specialized T cells. These immune cells and cytokines, in turn, could feed back into the nervous system and regulate neuroinflammation and neural function. APC, antigen-presenting cell.
    CREDIT: B. STRAUCH/SCIENCE
    Long-distance neuroimmune communication also occurs in poststroke immunosuppression, which protects the brain from inflammatory damage (12) but leaves the body prone to infection, a major cause of stroke-related death (13). Although the fundamental mechanism of this immunosuppression is not known, Wong et al. focused on stroke-activated hepatic invariant natural killer T (iNKT) cells to address how stroke modulates immunosuppression. Using a mouse stroke model, they observed that mice deficient in iNKT cells developed peripheral infection earlier and had higher mortality, suggesting that iNKT cells normally attenuate stroke-induced immunosuppression. They then found that noradrenergic innervation in the liver, rather than a circulating molecule, signals hepatic iNKT cells after stroke to promote systemic immunosuppression. Either depletion of noradrenergic nerve terminals in the liver or blockade of β-adrenergic receptors with propranolol altered the cytokines secreted by iNKT cells, thereby attenuating immunosuppression, bacterial infection, and mortality in wild-type mice. Conversely, noradrenaline injected directly into the liver activated iNKT cells and increased immunosuppression and infection. Unexpectedly, Wong et al. found that another iNKT cell activator, the glycolipid antigen α-galactoceramide (α-GalCer), which acts through MHC proteins, also reduced bacterial infection after stroke. Together, these data suggest that the determining factor in iNKT cell-mediated immunosuppression after stroke may not simply be their activation, but adrenergic regulation of a shift from proinflammatory T helper cell 1 (TH1)–type cytokines [such as interferon-γ (IFN-γ)] to antiinflammatory TH2-type cytokines [such as interleukin-10 (IL-10)]. Pretreatment of mice with IL-10 led to increased lung infections, whereas administration of propranolol and α-GalCer reversed cytokine production from IL-10 back to IFN-γ after stroke. Demonstrating stroke-induced increase in noradrenergic signaling in the liver would bolster this hypothesis.
    The findings of Rosas-Ballina et al. and Wong et al. raise the possibility of leveraging specific pathways to extinguish damaging neuroinflammation without compromising the ability to fight infection—for example, by activating nAChR in the spleen and blocking β-adrenergic receptors and activating MHC receptors in the liver. Furthermore, these findings raise several questions: Are T cells and noradrenaline specialized for mediating long-distance cross-talk between the immune and nervous systems, or do other subpopulations of immune cells participate? Various brain insults and neurodegenerative diseases may range from subclinical involvement to primary or secondary damage from inflammation—are these regulated by long-distance feedback loops between the CNS and peripheral immune organs, in addition to local interactions within the nervous system? For example, although noradrenaline in the spleen increased damaging neuroinflammation, and noradrenaline as well as IL-10 in the liver increased infection, both are neuroprotective in the CNS (56). Neuroactivated immune cells and their cytokine signals may enter the CNS and modulate neuronal and/or glial function, prompting investigation of “immunoneurobiology” pathways in which the peripheral immune system may regulate neural plasticity and behavior.

    References and Notes

    1.  
       
    2.  
    3.  
       
    4.  
       
    5.  
       
    6.  
    7.  
       
    8.  
       
    9.  
       
    10.  
       
    11.  
       
    12.  
       
    13.  
       
    14. We acknowledge support from the American Heart Association (grant 11PRE7310069 to E.F.T.), NIH (grants EY020913, EY020297, NS061348, and NS074490 to J.L.G.; grant P30-EY014081 from the University of Miami), and an unrestricted grant from Research to Prevent Blindness (University of Miami).