Exame reduz risco de mortalidade em recém-nascidos

Fibronectina Fetal

Um estudo produzido pela Secretaria de Estado da Saúde de São Paulo apontou que o Teste Fibronectina Fetal, além de diminuir o número de internações em Unidade de Terapia Intensiva (UTI), ajuda a evitar partos prematuros e a mortalidade neonatal.

O teste consiste em detectar a presença de uma substância chamada fibronectina fetal no conteúdo vaginal da mãe, sendo aplicado entre a 22ª e a 34ª semanas de gestação.

De acordo com a Secretaria, caso seja aplicado junto ao exame de ultrassom vaginal, ele reduz, em caso de resultado negativo, para menos de 1% as chances de parto nas duas semanas seguintes a sua realização.

Risco de parto prematuro

O estudo foi feito com 63 gestantes no Hospital e Maternidade Interlagos. Em comum, elas apresentaram alto risco de prematuridade por conta gestações anteriores, cólicas abdominais, má formação uterina e contrações não acompanhadas de nítidas modificações cervicais e infecção urinária.

Segundo a pesquisa, após a realização do Teste Fibronectina Fetal, 86% das gestantes analisadas apresentaram resultado negativo. Isso significa que, apesar de apresentarem sinais e sintomas, elas não estavam em trabalho de parto, portanto não era necessário interná-las.

No caso dessas gestantes, o espaço entre a realização do exame para o parto foi, em média, de 20 dias, o que comprovou a eficiência do teste.

Já para as 14% das gestantes cujo resultado do teste foi positivo, indicando com isso a iminência de trabalho de parto, a internação foi indicada e o nascimento dos bebês aconteceu, em média, 11 dias após a realização do exame.

Evitando a prematuridade

"A principal utilidade desse teste é evitar que as gestantes sintomáticas passem por internações ou intervenções desnecessárias. Outro benefício do teste é ajudar a diminuir o número de partos prematuros que, só no primeiro semestre de 2010, correspondeu a cerca de 10% do número total de partos realizados no Hospital e Maternidade Interlagos.

Com isso, além de reduzir os custos com internações, conseguimos reduzir os riscos de mortalidade neonatal provocado por prematuridade", disse Sandra Sestokas, diretora do Hospital e Maternidade Interlagos.

Mais da metade dos casos de Alzheimer podem ser evitados

Revisão do Alzheimer

Mais da metade de todos os casos da doença de Alzheimer poderiam ser evitados por meio de mudanças do estilo de vida e do tratamento ou prevenção de doenças crônicas.

Esta é a conclusão de um estudo conduzido pela Dra. Deborah Barnes, pesquisadora de saúde mental da Universidade da Califórnia, em São Francisco, nos Estados Unidos.

O estudo, chamado de estudo de revisão, analisou de forma sistemática dados de pesquisas científicas realizadas por inúmeros grupos de pesquisa ao redor do mundo, envolvendo no total centenas de milhares de participantes.

Como evitar o Alzheimer

Barnes concluiu que, na média mundial, os principais fatores de risco para o Alzheimer que são modificáveis são, em ordem decrescente de importância:

1. baixa escolaridade
2. tabagismo
3. sedentarismo
4. depressão
5. hipertensão na meia-idade
6. diabetes
7. obesidade na meia-idade

Juntos, esses fatores de risco estão associados com 51 por cento dos casos de Alzheimer em todo o mundo (17,2 milhões de casos) e 54 por cento dos casos de Alzheimer nos Estados Unidos (2,9 milhões de casos).

Nos Estados Unidos, Barnes descobriu que os fatores de maior risco modificáveis apresentam-se em outra ordem: inatividade física, depressão, tabagismo, hipertensão na meia-idade, obesidade na meia-idade, baixa escolaridade e diabetes.

Mudanças de estilo de vida

"O que é entusiasmante é que isso sugere que algumas mudanças de estilo de vida muito simples, como o aumento da atividade física e deixar de fumar, podem ter um tremendo impacto na prevenção do Alzheimer e outras demências, nos Estados Unidos e no mundo," disse Barnes.

Barnes adverte que suas conclusões são baseadas no pressuposto de que existe uma relação causal entre cada fator de risco e a doença de Alzheimer.

"Nós estamos assumindo que, quando você altera o fator de risco, então você altera o risco," explicou ela. "O que precisamos fazer agora é descobrir se essa suposição é correta."

Os resultados do estudo foram publicados na conceituada revista The Lancet Neurology.

Ômega-3 reduz ansiedade de estudantes

Resposta imunológica inflamatória

O ácido graxo ômega 3 levou a uma redução tanto na inflamação quanto na ansiedade dos estudantes durante o conturbado período das provas.

Inúmeros dos efeitos dos óleos ômega-3 para a saúde já são bem conhecidos e bem documentados pela ciência.

Agora, em uma descoberta surpreendente, cientistas verificaram que o óleo de peixe tem um forte efeito sobre a ansiedade em pessoas jovens saudáveis.

O efeito parece se dar em associação com a diminuição na resposta imunológica inflamatória, que tanto pode ser uma reação normal do organismo para se defender quanto uma característica associada com vários tipos de doenças.

As descobertas sugerem que, se pacientes jovens são beneficiados por um suplemento alimentar tão específico, os benefícios para os pacientes mais idosos podem ser ainda maiores.

Imunidade e estresse

O trabalho é mais um a documentar uma ligação entre a imunidade - a resposta inflamatória - e o estresse psicológico.

Os ácidos graxos poli-insaturados ômega-3 - incluindo o ácido eicosapentanoico (EPA) e docosahexanoico (DHA) - são considerados aditivos importantes para a dieta.

Pesquisas anteriores sugeriram que esses compostos têm um papel importante na redução dos níveis de citoquinas no corpo - as citoquinas são compostos que promovem a inflamação e com uma ação redutora dos sintomas da depressão.

Como o estresse psicológico tem uma forte associação com a produção de citoquinas, os pesquisadores da Universidade de Ohio, nos Estados Unidos, queriam saber se o ômega-3 poderia inibir esse processo, reduzindo a resposta inflamatória.

Ômega-3 contra o estresse

"Nós levantamos a hipótese de que os suplementos de ômega-3 poderiam diminuir a produção das citoquinas pró-inflamatórias," explicou Janice Kiecolt-Glaser, uma das autoras da pesquisa. "Nós imaginamos que o ômega-3 poderia reduzir o aumento das citoquinas induzidas pelo estresse, que normalmente vem com o nervosismo associado com as provas."

As provas a que a pesquisadora se refere são provas escolares feitas pelos estudantes de medicina, que serviram como voluntários para os testes.

Embora a inflamação seja uma resposta imunológica natural que ajuda o corpo a se curar, ela também desempenha um papel perigoso em doenças que vão da artrite às doenças do coração e até ao câncer.

O grupo de estudantes que tomou os suplementos de ômega-3, que continham de três a quatro vezes a quantidade de ômega-3 encontrada em uma porção de peixe, teve uma redução tanto na inflamação quanto na ansiedade, comprovando a hipótese dos cientistas.

Making Blood Sucking Deadly for Mosquitoes

ScienceDaily (July 20, 2011) — Mosquitoes die soon after a blood meal if certain protein components are experimentally disrupted, a team of biochemists at the University of Arizona has discovered. The approach could be used as an additional strategy in the worldwide effort to curb mosquito-borne diseases like dengue fever, yellow fever and malaria.

Recognized by white markings on the legs, a mosquito of the species Aedes aegypti feeds on human blood.

When the researchers blocked a cellular process known as vesicle transport, on which the mosquitoes rely to release digestive enzymes into the gut among other functions, it caused the affected animals to die within two days of blood feeding.

"The idea behind our research is this: If we can kill the mosquito after she bites the first person, she won't be able to bite and infect a second," said Roger Miesfeld, a professor in the UA's department of chemistry and biochemistry, who led the research project.

"We do this by blocking the mosquito's ability to digest its blood meal," said Miesfeld, also a member of the UA's BIO5 Institute.

The research team's findings were recently published in Proceedings of the National Academy of Sciences, or PNAS.

"During a blood meal, a mosquito ingests its body weight in blood. It's the equivalent of a 125-pound human consuming a 12-gallon smoothie made from 25 pounds of hamburger meat plus a half pound of butter and two tablespoons of sugar," Miesfeld said.

Miesfeld and the research team had previously shown that the blood feeding process poses a huge metabolic challenge to the female mosquito.

"By disrupting any number of biochemical processes needed to fully utilize the blood meal, the mosquito has a very difficult time completing the egg production cycle," he added.

To maintain their bodily needs, the insects rely on sugary nectar from flowers, but when the time to make eggs comes, they need large amounts of protein. Only female mosquitoes bite and feed on the blood of humans or warm-blooded animals.

If a mosquito finds enough victims to bite and avoids being squashed, it can live as long as three weeks. During that time, it may lay up to five clutches of more than 100 eggs each.

For their studies, the team used mosquitoes of the species Aedes aegypti, which originally hails from the sub-tropical and tropical regions of Africa. These mosquitoes are now found in many parts of the world and are particularly abundant in towns and cities where the climate is warm and water is plentiful. A. aegypti mosquitoes buzz about at dawn and dusk in search of their next blood meal, preferably from people's ankles.

A. aegypti mosquitoes are the main vector for dengue fever, now the most common viral disease transmitted by mosquitoes. Dengue fever has made a comeback especially in subtropical and tropical regions due to the geographical spread of the mosquitoes and the virus. Four strains, or serotypes, of disease-causing dengue viruses are known.

When infected for the first time, most people suffer through a bout of high and painful fever, but usually the illness is not life threatening and renders them immune to that particular strain of dengue virus. However, a subsequent infection with any of the other dengue virus strains often triggers an all-out immune response that leads to a much more severe form, called dengue hemorrhagic fever, which can be fatal.

Miesfeld said most mosquito-borne pathogens are not passed down from the female mosquito to her offspring, but instead picked up by the mosquitoes when they bite an infected human.

In the case of A. aegypti mosquitoes, the pathogen is often dengue or yellow fever viruses, whereas the Anopheles gambiae mosquito, which is found in many parts of Africa, transmits the more deadly malaria parasite. Miesfeld further explained that malaria and dengue pathogens take about 10 to 12 days to complete their life cycle within the mosquito before they can be transmitted to humans through blood feeding.

"The most dangerous mosquitoes are the older ones," Miesfeld said.

His team used a technique called RNAi to specifically target genes that are required for the digestion process. The researchers homed in on a protein complex called COPI, which stands for coatomer protein 1.

COPI consists of several subunits that together make up the envelope of the vesicles on which the cell relies for internal transport and for secretion of enzymes into the gut.

When a female mosquito takes a blood meal, the cells lining its gut secrete enzymes to break down the blood proteins. The secretion process involves packaging the enzymes in small droplets called vesicles that the cells then release into the gut.

"We thought, 'Why don't we knock out the whole process that allows the proteases to be secreted?' That's where we got this amazing result," Miesfeld said. "Not only did we eliminate her ability to secrete anything, we were surprised to find that about 90 percent of those mosquitoes died within two days after feeding on blood."

The COPI RNAi does not have an adverse effect on the female mosquitoes for 10 days -- unless they decide to take a blood meal.

"When she does, all hell starts breaking loose, biochemically and anatomically speaking," Miesfeld said.

"What we think is happening is that if there is protein in her gut, it induces the secretory machinery. It initiates this huge secretion process but it's defective and causes cells to disintegrate," he added. "The whole lining of the gut starts to fall apart, allowing the blood to seep into her body."

In looking at the potential causes, Miesfeld said his team found that removing any one of the COPI subunits causes the whole complex to fall apart.

"Based on what we know about the COPI system, it shouldn't have that strong of an effect," he said.

"As scientists have been knocking out COPI to learn more about its function over the past couple of years, they have achieved some interesting results," Miesfeld added. "Together with our findings they suggest that COPI does a lot more than what people thought."

Miesfeld envisions that the ultimate goal of this research is to develop a small molecule that works in place of injected RNAi and acts as a specific inhibitor of the secretion process.

For this to be an effective mosquito-selective insecticide, it must not have any effect on humans.

The simplest use would be to soak it into mosquito nets like currently available insecticides that target the mosquito's nervous system. A slightly more complex strategy would be to include it in a pill that humans take, so the mosquitoes pick up the inhibitor drug when they bite. As part of this strategy, the researchers are looking for genes that are unique to the mosquito and could serve as targets without affecting human health.

To explain, Miesfeld said to imagine a village in the tropics during a rainy season.

"As the mosquitoes hatch in large numbers, the whole population of villagers is ready," he explained. "As soon as the insects start biting, they take up the inhibitor and by the time they bite again, they die in large numbers. Over a few seasons, that can make a difference."

Miesfeld added it is unlikely there would ever be a silver bullet eliminating mosquito-transmitted diseases like malaria and dengue fever altogether.

"One potential issue with our strategy is genetic changes rendering the mosquitoes immune over time," Miesfeld said. "Many approaches from different angles will be necessary, and ours could be another tool in the toolbox."

New Lung-Cancer Gene Found: Cancer Biologists Identify a Driving Force Behind the Spread of an Aggressive Type of Lung Cancer

ScienceDaily (July 20, 2011) — A major challenge for cancer biologists is figuring out which among the hundreds of genetic mutations found in a cancer cell are most important for driving the cancer's spread.

X-ray image of a chest. Both sides of the lungs are visible with a growth on the left side of the lung, which could possibly be lung cancer. Researchers have pinpointed a gene that appears to drive progression of small cell lung cancer. 

Using a new technique called whole-genome profiling, MIT scientists have now pinpointed a gene that appears to drive progression of small cell lung cancer, an aggressive form of lung cancer accounting for about 15 percent of lung cancer cases.

The gene, which the researchers found overexpressed in both mouse and human lung tumors, could lead to new drug targets, says Alison Dooley, a recent PhD recipient in the lab of Tyler Jacks, director of MIT's David H. Koch Institute for Integrative Cancer Research. Dooley is the lead author of a paper describing the finding in the July 15 issue of Genes and Development.

Small cell lung cancer kills about 95 percent of patients within five years of diagnosis; scientists do not yet have a good understanding of which genes control it. Dooley and her colleagues studied the disease's progression using a strain of mice, developed in the laboratory of Anton Berns at the Netherlands Cancer Institute, that deletes two key tumor-suppressor genes, p53 and Rb.

"The mouse model recapitulates what is seen in human disease. It develops very aggressive lung tumors, which metastasize to sites where metastases are often seen in humans," such as the liver and adrenal glands, Dooley says.

This kind of model allows scientists to follow the disease progression from beginning to end, which can't normally be done with humans because the fast-spreading disease is often diagnosed very late. Using whole-genome profiling, the researchers were able to identify sections of chromosomes that had been duplicated or deleted in mice with cancer.

They found extra copies of a few short stretches of DNA, including a segment of chromosome 4 that turned out to include a single gene called Nuclear Factor I/B (NFIB). This is the first time NFIB has been implicated in small cell lung cancer, though it has been seen in a mouse study of prostate cancer. The gene's exact function is not known, but it is involved in the development of lung cells.

Researchers in Jacks' lab collaborated with scientists in Matthew Meyerson's lab at the Dana-Farber Cancer Institute and the Broad Institute to analyze human cancer cells, and found that NFIB is also amplified in human small cell lung tumors.

That makes a convincing case that the gene truly is playing an important role in human small cell lung cancer, says Barry Nelkin, a professor of oncology at Johns Hopkins University School of Medicine, who was not involved in this research.

"The question, always, with mouse models is whether they can tell you anything about a human disease," Nelkin says. "Some tell you something, but in others, there may be only a similarity in behavior, and the genetic changes are nothing like what is seen in humans."

The NFIB gene codes for a transcription factor, meaning it controls the expression of other genes, so researchers in Jacks' lab are now looking for the genes controlled by NFIB. "If we find what genes NFIB is regulating, that could provide new targets for small cell lung cancer therapy," Dooley says.