World's Most Powerful Optical Microscope: Microscope Could 'Solve the Cause of Viruses'

ScienceDaily (Mar. 2, 2011) — Scientists have produced the world's most powerful optical microscope, which could help us to understand the causes of many diseases. Writing in the journalNature Communications, the team have created a microscope which shatters the record for the smallest object the eye can see, beating the diffraction limit of light.

Scientists have created a microscope which shatters the record for the smallest object the eye can see, beating the diffraction limit of light. 

Previously, the standard optical microscope could only see items around one micrometer -- 0.001 millimeters -- clearly.

But now, by combining an optical microscope with a transparent microsphere, dubbed the 'microsphere nanoscope', the Manchester researchers can see 20 times smaller -- 50 nanometers ((5 x 10-8m) -- under normal light. This is beyond the theoretical limit of optical microscopy.

This greatly-increased capacity means the scientists, led by Professor Lin Li and Dr Zengbo Wang, could potentially examine the inside of human cells, and examine live viruses in great detail for the first time.

The scientists, from the School of Mechanical, Aerospace and Civil Engineering, now believe they can use the microscope to detect far smaller images in the future. The new method has no theoretical limit in the size of a feature that can be seen.

The new nano-imaging system is based on capturing optical, near-field virtual images, which are free from optical diffraction, and amplifying them using a microsphere, a tiny spherical particle which is further relayed and amplified by a standard optical microscope.

Professor Li, who initiated and led the research in collaboration with academics at the National University and Data Storage Institute of Singapore, believes their research could prove to be an important development.

He said: "This is a world record in terms of how small an optical microscope can go by direct imaging under a light source covering the whole range of optical spectrum.

"Not only have we been able to see items of 50 nanometers, we believe that is just the start and we will be able to see far smaller items.

"Theoretically, there is no limit on how small an object we will be able to see.

"The common way of seeing tiny items presently is with an electron microscope, and even then you cannot see inside a cell -- only the outside. Optical fluoresce microscopes can see inside the cells indirectly by dying them, but these dyes cannot penetrate viruses.

"Seeing inside a cell directly without dying and seeing living viruses directly could revolutionize the way cells are studied and allow us to examine closely viruses and biomedicine for the first time."

Among other tiny objects the scientists will be able to examine are anodized aluminum oxide nano-structures, and nano-patterns on Blue-Ray CVC disks, not previously visible with an optical microscope.

New Role Found for Cancer Protein P53

ScienceDaily (Mar. 2, 2011) — The gene for the protein p53 is the most frequently mutated in human cancer. It encodes a tumor suppressor, and traditionally researchers have assumed that it acts primarily as a regulator of how genes are made into proteins. Now, researchers at the University of Pennsylvania School of Medicine show that the protein has at least one other biochemical activity: controlling the metabolism of the sugar glucose, one of body's main sources of fuel. These new insights on a well-studied protein may be used to develop new cancer therapies.

The tumor suppressor p53 inhibits glucose-6-phosphate dehydrogenase (G6PD) by catalytically converting the active dimer to an inactive monomer. Through the inhibition of G6PD, p53 suppresses glucose consumption and biosynthesis. However, tumor-associated p53 mutants lose this function, which contributes to the Warburg effect and enhanced biosynthesis in tumor cells. The background shows images of p53 and G6PD localization in the cell.

Intriguingly, Yang and his team estimate that the level of p53 is only about 3 percent that of G6PD. So in the cell, the p53/G6PD ratio is very low. But p53 has a dramatic effect on the overall activity of G6PD. This suggests that one p53 molecule can inactivate many G6PD molecules. This qualifies p53 as a catalyst. It appears to act almost as an enzyme to convert its much more abundant binding partner into an inactive form via transient rather than stable interactions.

Normally, when one protein binds to and inhibits another, that inhibition lasts only as long as the two proteins are bound together; dissolution of the complex almost invariably activates the released proteins. But in the case of p53 and G6PD, transient interaction with p53 is sufficient to convert G6PD into an inactive form -- a property that is most often associated with enzymes. Says Yang, this enables p53, which at most is present at 10 percent the abundance of G6PD, to regulate its binding partner.

"By converting G6PD from active to inactive form, p53 also has an enzymatic function," says Yang. That kind of mechanism, he says, is "totally new" for p53, and a new paradigm for signal transduction in general.

"This non-stoichiometric effect of p53 on G6PDH is intriguing as it proposes a catalytic role for p53, something that even in the p53 world, which is accustomed to occasional twists, is surprising," wrote Eyal Gottlieb of Cancer Research UK in an accompanying editorial.

Now, says Yang, the question is whether this new role for p53 can be exploited to yield novel anticancer therapies. "Previously," he says, "people were hesitant to target the inefficient pathway because they thought it was stimulatory. Our data suggests the pathway is a good target."

The research was supported by the China National Natural Science Foundation, the Chinese Ministry of Science and Technology, the Chinese Academy of Sciences, the US National Cancer Institute and the US Department of Defense. Peng Jiang, PhD, and Wenjing Du, PhD, postdoctoral fellows in the Yang lab, were co-first authors on the paper.

Protein Identified That Serves as a Switch in a Key Pathway of Programmed Cell Death

ScienceDaily (Mar. 2, 2011) — Work led by St. Jude Children's Research Hospital scientists identified how cells flip a switch between cell survival and cell death that involves a protein called FLIP.

The findings solve a riddle that has puzzled scientists for more than a decade regarding the dual nature of caspase-8, an enzyme intimately linked to the cell's suicide pathway but also essential for cell survival during embryonic development and the immune response. Researchers identified FLIP and the silencing of another enzyme, named RIPK3, as playing pivotal roles. The study was published in the March 2 advance online edition of Nature.

Douglas Green, Ph.D., the paper's senior author and chair of the St. Jude Department of Immunology, said work is already underway to use the findings to generate new cancer treatment targets and fresh insight into the missteps that give rise to certain tumors as well as evidence of how some virus-infected cells escape the pathways designed to dispatch such threats.

"It is a pretty rare thing to 'cure' a lethal mutation in an animal by removing another gene. When that happens, the biology shouts out to us that this is important. We just have to listen," Green said.

FLIP's role was identified after investigators bred mice that lacked genes for both caspase-8 and RIPK3. Previous research identified RIPK3 as responsible for orchestrating cell death via programmed necrosis. Once viewed as an uncontrolled form of cell death, programmed necrosis is now recognized as a distinct form of cell suicide. The body relies on both programmed necrosis and apoptosis, the more common process, to rid itself of damaged, dangerous or unneeded cells.

While loss of caspase-8 was known to be lethal during embryonic development, in this study investigators showed mice that lacked both caspase-8 and RIPK3 were born at normal rates and appeared developmentally normal early in life.

Investigators went on to show that caspase-8 prevents programmed necrosis by combining with FLIP to form an enzyme complex that disrupts RIPK3 functioning and so prevents death via programmed necrosis. The work also demonstrated that FLIP expression prevents caspase-8 from triggering cell death via apoptosis, although the exact mechanism must still be determined. Apoptosis relies on caspase enzymes and other molecules to ensure the cell self destructs.

Green said the findings provide insight into the mechanisms at work in neuroblastoma and other tumors that suffer a loss of caspase-8. "We are beginning collaborative experiments to examine these tumors to see if RIPK3 is deleted or blocked," he said. Neuroblastoma arises in cells of the sympathetic nervous system. It is the most common solid tumor in children, accounting for up to 10 percent of all childhood cancers.

Andrew Oberst, a St. Jude postdoctoral fellow, is the study's first author. The other authors are Christopher Dillon, Ricardo Weinlich, Laura McCormick and Patrick Fitzgerald, all of St. Jude; Cristina Pop and Guy Salvesen, of Sanford-Burnham Medical Research Institute, La Jolla; and Razq Hakem, of the University of Toronto.

The research was supported in part by the National Institutes of Health, the Canadian Institutes of Health Research, the Sass Foundation for Medical Research and ALSAC.

Métodos de coleta de material para diagnóstico de doenças de peixes

CURSOS PROVET 2011

Métodos de coleta de material para diagnóstico de doenças de peixes Coordenação: Dra. Agar Costa Alexandrino de Pérez Data: 01 a 03 de Abril de 2011 Carga horária: 16h Objetivo: Apresentar ao médico veterinário as técnicas de coleta de material para diagnóstico de doenças de peixes Investimento: Médicos Veterinários: R$450,00 Graduandos: R$390,00 Docentes: Dra. Agar Costa Alexandrino de Pérez, Dra. Mariana Vaz Rodriguez, Dra. Silvia Napoleão, Dr. Roberto Ishikawa e Dr. Augusto Pérez Montano Programação Sexta-feira 01.04.2011  18:00h às 20:00h - Elementos de anatomia, fisiologia e semiologia 20:00h às 20:15h - Coffee break 20:15h às 22:00h - Principais doenças em peixes Sábado 02.04.2011  08:00h às 10:00h - Contenção e eutanásia 10:00h às 10:15h - Coffee break 10:15h às 12:00h - Técnica de necropsia e coleta de material para exame parasitológico 12:00h às 13:00h - Almoço 13:00h às 15:00h - Coleta de material para exame hematológico e microbiológico 15:00h às 15:15h - Coffee break 15:15h às 17:00h - Coleta de material para exame histopatológico e biópsia Domingo 03.04.2011 Programação Prática: 08:00h às 10:00h - Anatomia e coleta de amostras para os diferentes exames 10:00h às 10:15h - Coffee break 10:15h às 12:00h - Anatomia e coleta de amostras para os diferentes exames Inscrições Para efetuar sua inscrição Clique Aqui! Contato: Talita Miyamura 55 11 3579-1431 55 11 7865-1175 ID Nextel: 82*22891 e-mail: cursos@provet.com.br

Pesquisa encontra vírus HPV em 50% dos homens

A metade dos homens saudáveis está infectada com HPV, indica um dos maiores estudos já feitos sobre a incidência da doença no sexo masculino. Os resultados são publicados nesta terça-feira no "Lancet".

O HPV (papiloma vírus humano) é transmitido por relações sexuais na maioria das vezes, e pode causar lesões na pele e nas mucosas.

A pesquisa acompanhou por quatro anos 4.074 homens de 18 a 70 anos do Brasil, dos EUA e do México.

Eles tiveram amostras recolhidas do pênis e do escroto submetidas a análise. Dos 50% com HPV, 30% tinham o vírus que pode levar a câncer, 38% tinham o não cancerígeno, e o restante tinha mais de um tipo de HPV.

Há mais de cem tipos de HPV, mas a maioria é inofensiva e assintomática.

As altas taxas de contaminação nos homens, superiores às das mulheres, surpreendem. Na população feminina, mais associada ao HPV, a taxa média de contaminação é de 14%, compara a pesquisadora Luisa Villa, do Instituto Ludwig, responsável pelo estudo no Brasil.

"Antes, acreditava-se que os homens tinham menos HPV, que as infecções ocorriam em menor proporção. Mas eles também têm infecções, e em taxas mais elevadas do que as mulheres."

Apenas recentemente é que começou a se estudar sobre o HPV no homem. Um dos motivos para isso é que, nas mulheres, as consequências das contaminações são mais graves, como o câncer de colo de útero -segundo tumor mais frequente, depois do de câncer de mama.

"Os homens foram deixados de lado. São o vetor do vírus, mas as mulheres têm mais doenças por causa dele", diz Glauco Baiocchi Neto, diretor de ginecologia oncológica do A.C. Camargo.

O risco aumenta com o número elevado de parceiras e com a prática de sexo anal.

As chances de ter HPV que pode evoluir para um câncer aumentaram 2,4 vezes em homens que tinham tido mais de 50 parceiras, e 2,6 vezes em homens com pelo menos três parceiros.

Clique na imagem para visualizar

MAIS IMUNIDADE

Outra novidade da pesquisa é que, entre os homens, o risco de adquirir o vírus é constante, dos 18 a 70 anos. Entre as mulheres, o risco é maior até os 25 anos e tende a diminuir com o tempo.

Segundo o estudo, ainda não se sabe o porquê dessa diferença, mas há hipóteses.

Uma é que o número de parceiras sexuais do homem é constante por toda a vida, o que faz com que aumente sua exposição. Por outro lado, essa maior exposição poderia criar uma resposta imune que os protege de outras infecções subsequentes.

PREVENÇÃO

O estudo frisa a importância da vacinação contra HPV em homens de todas as idades, como prevenção.

Estudo recente publicado no "New England" e feito em mais de 18 países, incluindo o Brasil, mostrou que a vacina contra o HPV pode ser eficaz também em homens.

Mas sua aplicação em homens só foi aprovada em alguns países, como EUA, Panamá, Equador e Austrália.

O Brasil usa dois tipos de vacina contra o HPV, só em mulheres. São encontradas em clínicas particulares e indicadas a meninas e mulheres entre nove e 26 anos, mas não excluem a necessidade do Papanicolaou para prevenção do câncer.

Camisinha reduz o risco, mas, diz o urologista Alvaro Sarkis, não protege 100%.

Para Jorge Hallak, professor de urologia da USP, a melhor prevenção é a circuncisão, que diminui em mais de 70% as chances de contágio.