Biotechnology News Brasil

Brasil, China e Índia Emergindo como Países Líderes em Biotecnologia

2009-06-15T13:41:00.000-07:00

Brasil, China e Índia são os três principais países do mundo que estão na liderança dos clusters emergentes de biotecnologia em condições de competir com aqueles nos Estados Unidos. Esta notícia foi divulgada em um artigo da Genetic Engineering and Biotechnology News, baseada em entrevistas conduzidas com líderes da indústria biotecnológica.

Belo Horizonte, São Paulo e Rio de Janeiro no Brasil foram identificados como sendo os três dos principais clusters emergentes de biotecnologia no Brasil onde a maioria das atividades se concentra na biotecnologia agrícola. A República Popular da China declarou que prioriza o desenvolvimento de uma indústria biotecnológica vibrante e vários parques biotecnológicos têm surgido. Xangai e Beijing hospedam os maiores agrupamentos de empresas de biotecnologia. Semelhantemente, as previsões para os próximos dois a três anos indicam que a Índia possuirá 27 parques biotecnológicos construídos através de parcerias públicas/privadas.

Vide o artigo completo em http://www.genengnews.com/articles/chitem.aspx?aid=2883

A ilha das águias gigantes

2009-05-31T15:38:00.001-07:00

No último capítulo da trilogia O Senhor dos Anéis, o resgate de Frodo Baggins e Samwise Gamgee, realizado por águias gigantescas, não é somente uma idéia gerada pela imaginação contida nas lendas ou nos contos de fadas; essas portentosas aves habitaram realmente a Nova Zelândia. Hoje extintas, a sua existência foi documentada e explicada recentemente a partir da análise de um antigo DNA dessas águias, encontrado por Michael Bunce, antropólogo da Universidade McMaster do Canadá.

O estudo, publicado pela PloS Biology da própria McMaster descreve minuciosamente a enorme Águia de Haast (Harpagornis moorei) que pesava entre 10 e 15 kg, portanto 40% mais pesada que a maior ave de presa existente hoje em dia: a Harpia ou Águia Real, com 4,5 kg de peso, 2 metros de envergadura e 90 centímetros de altura, 11 a mais que a Águia Careca Americana e bem maior que as espécies encontradas na África e na Europa; espécie que se encontra entre as aves em extinção, sendo rara sua presença no México, na Bolívia e na Argentina.

No Brasil a Harpia Amazônica resiste bravamente, sendo a Floresta Amazônica, principalmente os estados do Amapá e Roraima, na fronteira com a Guiana Francesa e a Venezuela, praticamente seu último hábitat. As águias são aves falconiformes da família dos acipitrídeos, dotadas de bico e garras de considerável robustez, predominantemente predadoras, especialmente aquelas de grande porte.

Michael Bunce extraiu o DNA de ossos fósseis que datam uns 2.000 anos. O antropólogo canadense, ao comentar sua descoberta, disse: "Quando começamos o projeto, nosso objetivo era provar que havia uma relação entre a extinta Águia de Haast e a enorme Águia Australiana de Rabo Cuneiforme (Australian Wedge-tailed Eagle). Mas os resultados dos testes de DNA foram tão radicais que, num primeiro momento, duvidamos de sua autenticidade". Tais resultados mostraram que a gigante da Nova Zelândia estava mesmo relacionada geneticamente a uma das menores águias do mundo – a Pequena Águia da Austrália e Nova Guiné, que pesa menos de 900 gramas.

Os testes de DNA do fóssil desta espécie (por comparação com o DNA de 16 espécies de águias atualmente existentes) permitiram provar que, numa surpreendentemente rápida evolução, esta espécie está estreitamente relacionada com uma outra atual, com um décimo da sua massa corporal (e que é, simultaneamente, uma das espécies analisadas de menor tamanho). Este fato ilustra a potencial rapidez e plasticidade morfológica de alteração de tamanho no mundo dos vertebrados, especialmente em ecossistemas cujo hábitat se situa em ilhas ou arquipélagos.

"Mais surpreendente ainda foi a descoberta da estreita relação genética que havia entre as duas espécies. Estimamos que o ancestral de ambas tenha vivido há menos de um milhão de anos. Isso significa que uma águia deve ter chegado à Nova Zelândia e que seu peso deve ter aumentado de 10 a 15 vezes nesse período, o que é muito rápido em termos de evolução. Tal aumento de tamanho é inédito em aves e animais", acrescentou Bunce.

Antes de ser povoada pelos seres humanos há 700 anos, a ilha de Aoteroa, cujo nome original em língua Maori significa "País das Grandes Nuvens Brancas", atual Nova Zelândia, fora três espécies dos morcegos, o arquipélago era habitado por cerca de 250 espécies de aves e não acolhia nenhum mamífero terrestre. Devido ao seu relativo isolamento, a Nova Zelândia desenvolveu um ecossistema único.

No topo da cadeia alimentar se encontrava a Águia de Haast, único falconiforme a dominar, como grande predador, esse ecossistema majoritariamente insular.

Os cientistas acreditam que esta águia se extinguiu aproximadamente dois séculos após o povoamento da Ilha. As águias caçavam as moas gigantes (Dinornis giganteus) e kiwis (Apteryx australis), uma ave encontrada comumente na Oceania. A Nova Zelândia é também a residência do tuatara, uma espécie antiga de réptil, e do weta um inseto que pode atingir mais de 8 cm de comprimento.

O Moa Gigante era uma ave gigantesca – uma das maiores que já existiram – que viveu na Ilha já na mais recente etapa do Holoceno, até desaparecer há 700 anos.

Sua extinção coincide com a chegada do Homem à Ilha; provas fósseis que consistem em ossos quebrados por ferramentas humanas, carbonizados e com marcas de dentes humanos, demonstram serem os homens os responsáveis pela extinção de magnífica ave, a qual já não possuía mais alguns ossos das asas e nem junções das asas com o corpo. Os Moas se alimentavam de folhas, viviam em pares ou em pequenos grupos familiares e não tinham predadores naturais, isto é, até a chegada do Homem. Existiam 11 espécies diferentes de Moas, a maior delas era o Dinornis maximus, que podia chegar a quase 4 metros de altura e pesar 400 kg.

Muitos dos nichos ecológicos que normalmente teriam sido ocupados por mamíferos, eram preenchidos por aves, incluindo o Kiwi (incapaz de voar) e o Moa. A Nova Zelândia é também a residência do Tuatara, uma espécie antiga de réptil e do Weta, inseto nativo que pode atingir mais de 8 cm de comprimento, muito parecido com um grilo.

Apesar de sua aparência, os Tuataras não são lagartos. Eles são os únicos membros sobreviventes da ordem Rhynchocephalia. Fósseis de Rhyncholephalianos mostram répteis de pequeno e médio porte que eram muito comuns no mundo há cerca de 225/120 milhões de anos, muito antes de o primeiro dinossauro aparecer na Terra. Com o tempo, esses animais foram desaparecendo e há cerca de 60 milhões de anos eles ficaram praticamente extintos, exceto por uma pequena população que vive na Nova Zelândia.

Os primeiros exploradores europeus a chegar à Nova Zelândia foram o holandês Abel Tasman, em 1642, e o inglês James Cook, em 1769, cujas pesquisas conduziram a uma colonização total européia a partir de 1790.

A Nova Zelândia é um arquipélago composto por duas ilhas principais e numerosas pequenas ilhas, algumas das quais bastante longínquas. A Ilha Sul é a maior massa de terra e está dividida ao longo do seu comprimento pelos Alpes do Sul, cujo maior pico é o Monte Cook com 3.754 m. Na Ilha Sul há dezoito picos com mais de três mil metros de altitude. A Ilha Norte é menos montanhosa do que a Sul, mas está marcada por um intenso vulcanismo. Na Ilha Norte, a montanha mais alta, Ruapehu (2.797 m) é um cone vulcânico ativo. A área total da Nova Zelândia, 270.500 km² é um pouco maior que a do Estado de São Paulo ou que as Ilhas Britânicas.

Muito afastada das terras mais próximas, a Nova Zelândia é, entre as massas de terra de dimensões consideráveis do Planeta aquela que está mais isolada. Os seus vizinhos mais próximos são a Austrália, para Noroeste, e a Nova Caledônia, Fiji e Tonga, para Norte.

Weta, o nome da empresa que realizou O Senhor dos Anéis, foi uma homenagem ao inseto nativo. "O Weta, que está por aqui desde a época dos dinossauros, é capaz de sobreviver mesmo em situações extremas, como o congelamento. Por essa capacidade de sobrevivência, foi escolhido como símbolo e nome da empresa de efeitos especiais como uma forma de trazer boa sorte: É o gafanhoto mais feio que existe no Planeta, enquanto é o mais belo inseto. É a melhor criaturinha para nos inspirarmos", disse Richard Taylor, o premiado maquiador e figurinista de O Senhor dos Anéis.

René Capriles - Editor da ECO 21 Revista Eco 21, ano XV, Nº 101 abril/2005.

Fonte: Ambiente Brasil

Viruses Are Sneakier Than We Thought

2009-05-31T15:13:00.001-07:00

Viruses are molecular marauders, plundering cells for the resources they need to multiply. Of central importance for viruses is the ability to commandeer cellular gene expression machinery. Several human herpesviruses put the breaks on normal cellular gene expression to divert the associated enzymes and resources towards their own viral genes. Kaposi's sarcoma-associated herpesvirus (KSHV), which causes several AIDS-associated cancers, has now been shown to do this in an unexpected way, using a process that is normally protective, called polyadenylation.

Cells decode genetic information in a process called transcription, during which the DNA is unzipped and read by enzymes. The product of this process is a piece of messenger RNA, which then emerges from the cell's nucleus (the section of the cell containing DNA) into the cell cytoplasm (the main cellular compartment) and is translated there into the protein corresponding to the DNA's message. Polyadenylation is the process whereby Poly(A) tails are added to messenger RNAs (mRNAs) in the nucleus before they are transported into the cytoplasm. These tails serve several purposes, including protecting the messages from degradation and enhancing the translation to protein. The effects of KSHV on cells was known to be caused by one of it's proteins – called SOX – but how the protein influences host cells transcription process has previously been unclear.

In a study published in this week's issue of PLoS Biology, researchers at UC Berkeley found that the presence of SOX led to an unexpected increase in the length of cellular mRNA poly(A) tails. Mutant KSHV viruses that can't make SOX protein are unable to block cellular gene expression. SOX mutants fail to increase poly(A) tail length. This suggests that the virus uses a process normally involved in enhancement of gene expression to instead inhibit gene expression.

"We suspect that by aberrantly lengthening the poly(A) tails, the virus is sending the cell a signal that something is wrong with its messages and as a consequence they are held back in the nucleus," says Dr. Britt Glaunsinger, one of the researchers involved in this study. Indeed, similar results have been observed in yeast when mRNAs are improperly made or cannot traffic appropriately.

The researchers showed that SOX has more than one trick to play on cells - as well as preventing the export of new cellular mRNAs, SOX targets the existing messages that were made in a cell before the KSHV could turn on its SOX protein. mRNA poly(A) tails are normally bound by the cell's poly(A) binding protein (PABP), which helps guard them from degradation and facilitates their translation into protein. During KSHV infection, however, SOX removes PABP from the cytoplasm and causes it to instead accumulate in the nucleus. PABP re-localization correlates with destruction of cytoplasmic mRNA in SOX-expressing cells, perhaps because these transcripts have been 'stripped' of an important protector. "I find it fascinating that this single viral protein targets a key mRNA stabilizing element from two different angles to block cellular gene expression," says Glaunsinger. "It's yet another example of how viruses have evolved to interface so exquisitely with their hosts."

This research was supported by a Howard Temin Career Development Award and a Burroughs Wellcome Fund Investigators in the Pathogenesis of Infectious Disease Award to BG. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Source: Science Daily

Saved By Junk DNA: Vital Role In The Evolution Of Human Genome

2009-05-31T15:12:00.001-07:00

Researchers at K.U. Leuven and Harvard University show that stretches of DNA previously believed to be useless 'junk' DNA play a vital role in the evolution of our genome. They found that unstable pieces of junk DNA help tuning gene activity and enable organisms to quickly adapt to changes in their environments. The results will be published in the journal Science.

Junk DNA

"Most people do not realize that all our genes only comprise about 3% of the total human genome. The rest is basically one large black box," says Kevin Verstrepen, heading the research team. "Why do we have this DNA, what is it doing?"

Scientists used to believe that most of the DNA outside of genes, the so-called non-coding DNA, is useless trash that has sneaked into our genome and refuses to leave. One commonly known example of such 'junk DNA' are the so-called tandem repeats, short stretches of DNA that are repeated head-to-tail. "At first sight, it may seem unlikely that this stutter-DNA has any biological function," says Marcelo Vinces, one of the lead authors on the paper. "On the other hand, it seems hard to believe that nature would foster such a wasteful system."

Unstable repeats

The international team of scientists found that stretches of tandem repeats influence the activity of neighboring genes. The repeats determine how tightly the local DNA is wrapped around specific proteins called 'nucleosomes', and this packaging structure dictates to what extent genes can be activated. Interestingly, tandem repeats are very unstable -- the number of repeats changes frequently when the DNA is copied. These changes affect the local DNA packaging, which in turn alters gene activity. In this way, unstable junk DNA allows fast shifts in gene activity, which may allow organisms to tune the activity of genes to match changing environments -- a vital principle for survival in the endless evolutionary race.

Evolution in test tubes

To further test their theory, the researchers conducted a complex experiment aimed at mimicking biological evolution, using yeast cells as Darwinian guinea pigs. Their results show that when a repeat is present near a gene, it is possible to select yeast mutants that show vastly increased activity of this gene. However, when the repeat region was removed, this fast evolution was impossible. "If this was the real world," the researchers say, "only cells with the repeats would be able to swiftly adapt to changes, thereby beating their repeat-less counterparts in the game of evolution. Their junk DNA saved their lives."

The research has been funded by Human Frontier Science Program, Fund for Scientific Research Flanders, NIH, K.U. Leuven and VIB (the Flanders Institute for Biotechnology).

Source: Science Daily

One-two Punch In Battle Against HIV: New HIV Microbicide, And A Way To Mass Produce It In Plants, Developed

2009-05-31T15:11:00.001-07:00

In what could be a major pharmaceutical breakthrough, research published in The FASEB Journal describes how scientists from St George's, University of London have devised a one-two punch to stop HIV. First the report describes a new protein that can kill the virus when used as a microbicide. Then the report shows how it might be possible to manufacture this protein in quantities large enough to make it affordable for people in developing countries.

"We desperately need to control the spread of HIV, particularly in developing countries," said Julian Ma of the Department of Cellular and Molecular Medicine at St. George's and the senior researcher involved in the work. "A vaccine is still some way off, but microbicides could provide a more immediate solution, provided we can overcome major hurdles of high efficacy, low cost, and wide availability—all of which we address in this study."

In the research paper, Ma and colleagues describe how they combined two protein microbicides (b12 monoclonal antibody and cyanovirin-N) into a single "fusion" molecule and showed that this molecule is more active against HIV than either of its individual components. They designed synthetic DNA for producing this molecule and introduced this DNA into plant cells. After regenerating transgenic plants that produce the fusion molecule, they prepared the microbicide from a plant extract made by grinding the leaves.

"This study is nothing short of a breakthrough—not only does it yield a new drug to fight the spread of HIV, but it also shows us how we can produce it on the scale necessary to get it into the hands of those who need it most," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Unlike their unregulated counterparts in the dietary supplement industry, these scientists are using the engines of nature to manufacture pharmaceuticals that must undergo extensive safety and efficacy testing long before the first gel or cream is administered."

Source: Science Daily

Why Can We Talk? 'Humanized' Mice Speak Volumes About Evolutionary Past

2009-05-31T15:08:00.001-07:00

Mice carrying a "humanized version" of a gene believed to influence speech and language may not actually talk, but they nonetheless do have a lot to say about our evolutionary past, according to a report in the May 29th issue of the journal Cell, a Cell Press publication.

"In the last decade or so, we've come to realize that the mouse is really similar to humans," said Wolfgang Enard of the Max-Planck Institute for Evolutionary Anthropology. "The genes are essentially the same and they also work similarly." Because of that, scientists have learned a tremendous amount about the biology of human diseases by studying mice.

"With this study, we get the first glimpse that mice can be used to study not only disease, but also our own history."

Enard said his team is generally interested in the genomic differences that set humans apart from their primate relatives. One important difference between humans and chimpanzees they have studied are two amino acid substitutions in FOXP2. Those changes became fixed after the human lineage split from chimpanzees and earlier studies have yielded evidence that the gene underwent positive selection. That evolutionary change is thought to reflect selection for some important aspects of speech and language.

"Changes in FOXP2 occurred over the course of human evolution and are the best candidates for genetic changes that might explain why we can speak," Enard said. "The challenge is to study it functionally."

For obvious reasons, the genetic studies needed to sort that out can't be completed in humans or chimpanzees, he said. In the new study, the researchers introduced those substitutions into the FOXP2 gene of mice. They note that the mouse version of the gene is essentially identical to that of chimps, making it a reasonable model for the ancestral human version.

Mice with the human FOXP2 show changes in brain circuits that have previously been linked to human speech, the new research shows. Intriguingly enough, the genetically altered mouse pups also have qualitative differences in ultrasonic vocalizations they use when placed outside the comfort of their mothers' nests. But, Enard says, not enough is known about mouse communication to read too much yet into what exactly those changes might mean.

Although FoxP2 is active in many other tissues of the body, the altered version did not appear to have other effects on the mice, which appeared to be generally healthy.

Those differences offer a window into the evolution of speech and language capacity in the human brain. They said it will now be important to further explore the mechanistic basis of the gene's effects and their possible relationship to characteristics that differ between humans and apes.

"Currently, one can only speculate about the role these effects may have played during human evolution," they wrote. "However, since patients that carry one nonfunctional FOXP2 allele show impairments in the timing and sequencing of orofacial movements, one possibility is that the amino acid substitutions in FOXP2 contributed to an increased fine-tuning of motor control necessary for articulation, i.e., the unique human capacity to learn and coordinate the muscle movements in lungs, larynx, tongue and lips that are necessary for speech. We are confident that concerted studies of mice, humans and other primates will eventually clarify if this is the case."

Source: Science Daily

Unexpected Bacterial Diversity On Human Skin; New Approaches For Treating, Preventing Skin Diseases

2009-05-31T15:07:00.001-07:00

The health of our skin — one of the body's first lines of defense against illness and injury — depends upon the delicate balance between our own cells and the millions of bacteria and other one-celled microbes that live on its surface. To better understand this balance, National Institutes of Health researchers have set out to explore the skin's microbiome, which is all of the DNA, or genomes, of all of the microbes that inhabit human skin.

Their initial analysis, published in the journal Science, reveals that our skin is home to a much wider array of bacteria than previously thought.

The study also shows that at least among healthy people, the greatest influence on bacterial diversity appears to be body location. For example, the bacteria that live under your arms likely are more similar to those under another person's arm than they are to the bacteria that live on your forearm.

"Our work has laid an essential foundation for researchers who are working to develop new and better strategies for treating and preventing skin diseases," said Julia A. Segre, Ph.D., of the National Human Genome Research Institute (NHGRI), who was the study's senior author. "The data generated by our study are freely available to scientists around the world. We hope this will speed efforts to understand the complex genetic and environmental factors involved in eczema, psoriasis, acne, antibiotic-resistant infections and many other disorders affecting the skin."

Drawing on the power of modern DNA sequencing technology and computational analysis, the research team from NHGRI, the National Cancer Institute (NCI) and the NIH Clinical Center uncovered a far more diverse collection of microbes on human skin than had been detected by traditional methods that involved growing microbial samples in the laboratory.

The NIH study involved taking skin samples from 20 sites on the bodies of 10 healthy volunteers. "We selected skin sites predisposed to certain dermatological disorders in which microbes have long been thought to play a role in disease activity," said study coauthor Maria L. Turner, M.D., senior clinician in NCI's Dermatology Branch.

The researchers extracted DNA from each sample and sequenced the 16S ribosomal RNA genes, which are a type of gene that is specific to bacteria. The researchers identified more than 112,000 bacterial gene sequences, which they then classified and compared. The analysis detected bacteria belonging to 19 different phyla and 205 different genera, with diversity at the species level being much greater than expected.

To gauge how much the skin microbiome differs among healthy people, the researchers studied many different parameters. They found considerable variation in the number of bacteria species at different sites, with the most diversity being seen on the forearm (44 species on average) and the least diversity behind the ear (19 species on average).

The research also generated information that may prove useful in efforts to combat the growing problem of methicillin-resistant Staphylococcus aureus (MRSA), a bacterium that can cause serious, even life-threatening, infections. While it is known that a significant proportion of people have colonies of S. aureus inside their noses, the NIH team checked to see where else on the body surface that these bacteria thrive. They found that the crease of skin outside the nose is the site with the microbial community most similar to that found inside the nose.

"Not only does our work shed new light on understanding an important aspect of skin biology, it provides yet another example of how genomic approaches can be applied to study important problems in biomedical research," said NHGRI's Scientific Director Eric D. Green, M.D., Ph.D., who is a co-author of the study. "This also demonstrates what can be achieved through efforts that pull together researchers from across NIH."

NIH recently launched the Human Microbiome Project, a part of the NIH Roadmap for Medical Research, to discover what microbial communities exist in different parts of the human body and to explore how these communities change with disease. In addition to skin and nose, that project is sampling the digestive tract, the mouth and the vagina.

The skin sites selected for the Science study represent three microenvironments: oily, moist and dry. The oily sites included between the eyebrows, beside the nose, inside the ear, back of the scalp, and upper chest and back. Moist areas were inside the nose, armpit, inner elbow, webbed area between the middle and ring fingers, side of the groin, top fold of the buttocks, behind the knee, bottom of the foot and the navel. Dry areas included the inside surface of the mid-forearm, the palm of the hand and the buttock. Researchers found that dry and moist skin had a broader variety of microbes than did oily skin. Oily skin contained the most uniform mix of microbes.

To look for changes that may occur in the skin microbiome over time, the researchers sampled some volunteers twice, with the samples being taken about four to six months apart. Most of the re-sampled volunteers were more like themselves over time than they were like other volunteers. However, the stability of the microbial community was dependent on the site surveyed. The greatest stability was found in samples from inside the ear and nose, and the least stability was found in samples from behind the knee.

"Our results underscore that skin is home to vibrant communities of microbial life, which may significantly influence our health," said the study's first author, Elizabeth Grice, Ph.D., who is a postdoctoral fellow at NHGRI.

For more information on the Human Microbiome Project, go to http://nihroadmap.nih.gov/hmp/

Source: Science Daily

Scientists Engineer Cellular Circuits That Count Events

2009-05-31T15:04:00.001-07:00

MIT and Boston University engineers have designed cells that can count and "remember" cellular events, using simple circuits in which a series of genes are activated in a specific order.

Such circuits, which mimic those found on computer chips, could be used to count the number of times a cell divides, or to study a sequence of developmental stages. They could also serve as biosensors that count exposures to different toxins.

The team developed two types of cellular counters, both described in the May 29 issue of Science. Though the cellular circuits resemble computer circuits, the researchers are not trying to create tiny living computers.

"I don't think computational circuits in biology will ever match what we can do with a computer," said Timothy Lu, a graduate student in the Harvard-MIT Division of Health Sciences and Technology (HST) and one of two lead authors of the paper.

Performing very elaborate computing inside cells would be extremely difficult because living cells are much harder to control than silicon chips. Instead, the researchers are focusing on designing small circuit components to accomplish specific tasks.

"Our goal is to build simple design tools that perform some aspect of cellular function," said Lu.

Ari Friedland, a graduate student at Boston University, is also a lead author of the Science paper. Other authors are Xiao Wang, postdoctoral associate at BU; David Shi, BU undergraduate; George Church, faculty member at Harvard Medical School and HST; and James Collins, professor of biomedical engineering at BU.

Learning to count

To demonstrate their concept, the team built circuits that count up to three cellular events, but in theory, the counters could go much higher.

The first counter, dubbed the RTC (Riboregulated Transcriptional Cascade) Counter, consists of a series of genes, each of which produces a protein that activates the next gene in the sequence.

With the first stimulus — for example, an influx of sugar into the cell — the cell produces the first protein in the sequence, an RNA polymerase (an enzyme that controls transcription of another gene). During the second influx, the first RNA polymerase initiates production of the second protein, a different RNA polymerase.

The number of steps in the sequence is, in theory, limited only by the number of distinct bacterial RNA polymerases. "Our goal is to use a library of these genes to create larger and larger cascades," said Lu.

The counter's timescale is minutes or hours, making it suitable for keeping track of cell divisions. Such a counter would be potentially useful in studies of aging.

The RTC Counter can be "reset" to start counting the same series over again, but it has no way to "remember" what it has counted. The team's second counter, called the DIC (DNA Invertase Cascade) Counter, can encode digital memory, storing a series of "bits" of information.

The process relies on an enzyme known as invertase, which chops out a specific section of double-stranded DNA, flips it over and re-inserts it, altering the sequence in a predictable way.

The DIC Counter consists of a series of DNA sequences. Each sequence includes a gene for a different invertase enzyme. When the first activation occurs, the first invertase gene is transcribed and assembled. It then binds the DNA and flips it over, ending its own transcription and setting up the gene for the second invertase to be transcribed next.

When the second stimulus is received, the cycle repeats: The second invertase is produced, then flips the DNA, setting up the third invertase gene for transcription. The output of the system can be determined when an output gene, such as the gene for green fluorescent protein, is inserted into the cascade and is produced after a certain number of inputs or by sequencing the cell's DNA.

This circuit could in theory go up to 100 steps (the number of different invertases that have been identified). Because it tracks a specific sequence of stimuli, such a counter could be useful for studying the unfolding of events that occur during embryonic development, said Lu.

Other potential applications include programming cells to act as environmental sensors for pollutants such as arsenic. Engineers would also be able to specify the length of time an input needs to be present to be counted, and the length of time that can fall between two inputs so they are counted as two events instead of one.

They could also design the cells to die after a certain number of cell divisions or night-day cycles.

"There's a lot of concern about engineered organisms — if you put them in the environment, what will happen?" said Collins, who is also a Howard Hughes Medical Institute investigator. These counters "could serve as a programmed expiration date for engineered organisms."

The research was funded by the National Institute of Health Director's Pioneer Award Program, the National Science Foundation FIBR program, and the Howard Hughes Medical Institute.

Source: Science Daily

'Glowing' Transgenic Monkeys Carrying Green Fluorescent Protein Gene Pave Way For New Disease Models

2009-05-31T15:02:00.001-07:00

A transgenic line of monkeys carrying a gene encoding green fluorescent protein fully integrated into their DNA has been created for the first time. The research, published in the journal Nature, marks the first such feat in non-human primates and paves the way for developing new models of human diseases.

Scientists reported the first transgenic monkeys last year — a model of Huntington's disease — but in these animals, the gene did not fully integrate into the monkey's own DNA and was not passed down to their offspring. In this report, Erika Sasaki and colleagues used viral DNA as a delivery vehicle to introduce the gene for GFP into the DNA of the common marmoset Callithrix jacchus. They show that the gene integrated into the monkey's DNA and was successfully passed down to their offspring, which were healthy and all expressed the new gene.

Transgenic mice have contributed immensely to biomedical research, but for many diseases they are too dissimilar from humans for the results to be meaningful. Non-human primates hold great promise for the study of several human diseases, particularly neurological disorders, for which there are currently no appropriate experimental models. This study marks an important milestone on the road to developing the means to investigate these diseases.

In an accompanying news story, Nature News reporter David Cyranoski explains why other transgenic monkeys have failed to reproduce so far, and describes the 5-year Japanese project to develop alternative animal models of which Sasaki's research is a part. Also in this issue, an editorial calls for researchers working on transgenic primates to go much further than they have so far in articulating the ethical aspects both of their research and its potential applications. Engagement in public discussion is essential to avoid inappropriate regulation.

Source: Science Daily

New Cellular Targets For HIV Drug Development

2009-05-31T14:56:00.001-07:00

Focusing HIV drug development on immune cells called macrophages instead of traditionally targeted T cells could bring us closer to eradicating the disease, according to new research from University of Florida and five other institutions.

In the largest study of its kind, researchers found that in diseased cells — such as cancer cells — that are also infected with HIV, almost all the virus was packed into macrophages, whose job is to "eat" invading disease agents.

What's more, up to half of those macrophages were hybrids, formed when pieces of genetic material from several parent HIV viruses combined to form new strains.

Such "recombination" is responsible for formation of mutants that easily elude immune system surveillance and escape from anti-HIV drugs.

"Macrophages are these little factories producing new hybrid particles of the virus, making the virus probably even more aggressive over time," said study co-author Marco Salemi, Ph.D., an assistant professor in the department of pathology, immunology and laboratory medicine at the UF College of Medicine. "If we want to eradicate HIV we need to find a way to actually target the virus specifically infecting the macrophages."

At least 1.1 million people in the United States and 33 million in the world are living with HIV/AIDS, according to the Kaiser Family Foundation.

The researchers set out to see if HIV populations that infect abnormal tissues are different from those that infect normal ones, and whether particular strains are associated with certain types of illness.

They tackled the question using frozen post-autopsy tissue samples, pathology results and advanced computational techniques. They analyzed 780 HIV sequences from 53 normal and abnormal tissues from seven patients who had died between 1995 and 2003 from various AIDS-related conditions, including HIV-associated dementia, non-Hodgkin's lymphoma and generalized infections throughout the body. Four patients had been treated with highly active antiretroviral therapy, called HAART, at or near the time of death.

The researchers compared brain and lymphoma tissues, which had heavy concentrations of macrophages, with lymphoid tissues — such as from the spleen and lymph nodes— that had a mix of HIV-infected macrophages and T cells.

The analyses revealed great diversity in the HIV strains present, with different tissues having hybrid viruses made up of slightly different sets of genes. A high frequency of such recombinant viruses was also found in tissues generally associated with disease processes, such as the meninges, spleen and lymph nodes.

The researchers concluded that HIV-infected macrophages might be implicated in tumor-producing mechanisms.

The higher frequency of recombinant virus in diseased tissues likely is because macrophages multiply as a result of an inflammatory response, the researchers said.

"The study points to macrophages as a site of recombination in active disease," said neurobiologist Kenneth C. Williams, Ph.D., a Boston College associate professor and AIDS expert who was not involved in the study. "So people can say this is one spot where these viruses come from."

T cells — the so-called conductors of the immune system orchestra, whose decline is the hallmark of HIV disease — are an obvious target for HIV drug development because they die soon after infection, and are readily sampled from the blood and cultured. But although current drugs are effective at blocking infection of new cells and lowering viral loads to barely detectable levels, they never reduce the viral level in an infected person to zero.

"Where is it coming from?" said Michael S. McGrath, the University of California, San Francisco, professor who led the research team. "We believe it's coming from these macrophages."

Macrophages, like T cells, can be infected multiple times by HIV. But unlike T cells, when they get infected, they don't die within days, but live for several months, all the while being re-infected with multiple viruses of different genetic makeup. That situation is ripe for the emergence of hybrids.

"Most people who look at viral sequences assume that evolution of the virus is linear. In the real world that doesn't happen — large parts of the virus are swapped in and out. This group has shown that in this model," Williams said. "It sort of overturns the old way of trying to match virus sequence with pathology."

McGrath's group is now developing macrophage-targeting drugs that, through a grant from the National Institute of Mental Health, should be in human clinical trials in a few years.

"This is one of the last frontiers — killing off what we believe is a so far untouched reservoir," he said.

The work was published recently in the journal PLoS One.

Source: Science Daily

Antibiotic Multi-resistance: Why Bacteria Are So Effective

2009-05-31T14:51:00.001-07:00

In an article published in Science, teams from the Institut Pasteurand the University of Limoges, associated with the CNRS and Inserm, decipher for the first time the molecular mechanism that enables bacteria to acquire multi-resistance to antibiotics, and that even allows them to adapt this resistance to their environment. This discovery highlights the difficulties that will have to be tackled by public health strategies if they are to address the problems created by multi-resistance.

Multiresistance of bacteria to antibiotics is a phenomenon that appeared when these drugs began to be used in the 1950s. It was subsequently discovered that resistance genes were easily captured, disseminated and exchanged from one bacterium to another by a system involving genetic "copying and pasting" of the structures containing these genes, known as integrons. But the dynamics of these exchanges, which governs the multi -resistance development in bacteria, remained unknown.

The work of researchers from the Institut Pasteur associated with the CNRS (Bacterial Genome Plasticity unit, CNRS URA 2171) and from Inserm, within the Limoges Faculty of Medicine (EA3175, Inserm, Avenir Team), in cooperation with Spanish teams, reveals for the first time today how bacteria acquire these multi -resistance properties. It is actually the antibiotics themselves that trigger the synthesis of the bacterial enzyme that captures the resistance genes and enables their expression in the integron.

This enzyme also promotes the random rearrangement of the resistance genes within the integron. The order of these genes in the integron determines the degree of priority for their expression: the first are expressed most highly and give the bacteria the corresponding resistance. The last remain silent, although they are kept in reserve. When a new rearrangement occurs, triggered by taking an antibiotic, for example, they are likely to be moved to the first positions, and give the bacteria the required resistance to this drug. The bacteria with the right "combination" of genes will therefore be able to survive and ensure that the resistance potential is maintained from generation to generation.

This work shows the extent to which strategies of bacterial adaptation to antibiotics are effective, in both the short and the long term. It therefore clearly demonstrates the difficulties associated with bacterial genetics that future public health measures will have to take into account if they are to tackle the problem of multi-resistance.

Source: Science Daily

Slicing Chromosomes Leads To New Insights Into Cell Division

2009-05-31T14:47:00.001-07:00

By using ultrafast laser pulses to slice off pieces of chromosomes and observe how the chromosomes behave, biomedical engineers at the University of Michigan have gained pivotal insights into mitosis, the process of cell division.

Their findings could help scientists better understand genetic diseases, aging and cancer.

Cells in plants, fungi, and animals—including those in the human body—divide through mitosis, during which the DNA-containing chromosomes separate between the resulting daughter cells. Forces in a structure called the mitotic spindle guide the replicated chromosomes to opposing sides as one cell eventually becomes two.

"Each cell needs the right number of chromosomes. It's central to life in general and very important in terms of disease," said Alan Hunt, an associate professor in the Department of Biomedical Engineering and an author of a paper describing these findings published in Current Biology.

"One of the really important fundamental questions in biology is how do chromosomes get properly segregated when cells divide. What are the forces that move chromosomes around during this process? Where do they come from and what guides the movements?"

Hunt's results validate the theory that "polar ejection forces" are at play. Scientists had hypothesized that the direction and magnitude of these forces might provide physical cues guiding chromosome movements. In this capacity, polar ejection forces would play a central role separating chromosomes in dividing cells, but no one had established a direct link until now.

Polar ejection forces are thought to arise out of the interaction between protein motors on the arms of chromosomes that push against cells' microtubules. Microtubules are long, thin tubes that form a central component of the cytoskeleton and the mitotic spindle. They serve as intracellular structural supports and as railways along which molecular motors move cargoes such as chromosomes.

Hunt's group hypothesized that polar ejection forces should be proportional to the chromosome's size, and therefore could be predictably changed by altering the size of the chromosomes. Using newts as a model organism, they cut off pieces of the chromosomes' arms.

"We asked what the relationship is between the size of the fragment we removed and the direction the chromosome moved," Hunt said. "Not only did we observe a relationship, we established that polar ejection forces were in fact a direct cue that guided chromosomal movements in mitosis."

To achieve this, Hunt performed "nanoscale surgery," as he calls it, taking advantage of the unprecedented precision of femtosecond pulses of laser light. A femtosecond is one billionth of one millionth of a second. The chromosomes he altered were only micrometers long, and the slices across the chromosomes were only nanometers thick. A nanometer is one-billionth of a meter, about a million times thinner than a human hair.

Understanding how chromosome guidance occurs allows scientists to determine how failures lead to genetic diseases, aging and cancer. When cells don't properly divide, they usually die. But survival can cause cancer or aging-related disorders. Likewise, genetic diseases such as Down's syndrome result from improper chromosome segregation.

Mitosis, Hunt says, is one of the most important targets of chemotherapy.

"By knowing how chromosomes move, we can better understand how these drugs interfere with those movements and we can design experiments to screen for new drugs," Hunt said. "It will also allow us to have a better handle on what makes these drugs work. There are a lot of drugs that interfere with mitosis, but only a few are good for cancer therapy."

This research is funded by the National Science Foundation, the National Institutes of Health and the Cellular Biotechnology Training Grant at the University of Michigan. Hunt is also an assistant research scientist in the U-M Institute of Gerontology, and director of the Biomedical Lab at the Center for Ultrafast Optical Sciences.

Source: Science Daily

Sugarcoating Fruit Fly Development: Sugar Tags On Nuclear Proteins Have An Important Developmental Function

2009-05-31T14:45:00.001-07:00

Proteins are the executive agents that carry out all processes in a cell. Their activity is controlled and modified with the help of small chemical tags that can be dynamically added to and removed from the protein. 25 years after its first discovery, researchers at the European Molecular Biology Laboratory (EMBL) in Heidelberg have now gained insight into the role of one of these tags, a small sugar residue, that is found on many different proteins across species.

In the current online issue of Science, they report that the addition of this sugar tag to proteins in the nucleus of a cell is vital for normal development in fruit flies.

Over 25 years ago scientists discovered that many proteins in the nucleus and cytoplasm have a small sugar molecule, called GlcNAc, attached to them. The enzyme that adds this sugar is called Ogt but since its discovery it has remained elusive why attaching GlcNAc to proteins is important. Researchers in the group of Jürg Müller at EMBL have now discovered that flies lacking Ogt show dramatic developmental defects. In the absence of Ogt cells do not develop into the appropriate cell types and body segments do not differentiate according to plan.

"Expressing the right genes at the right time is critical for a developing organism," says Jürg Müller. "It is the appropriate combination of genes that tells a cell to turn into muscle, nerve or skin. This is why a tight control system regulates gene expression throughout development."

One important component of this control system is a group of regulatory proteins, called Polycomb proteins. They switch off developmental genes when and where their activity is not needed and thereby prevent the formation of specialised tissues and organs in the wrong places.

The scientists found that in the absence of Ogt, Polycomb proteins are no longer able to inactivate developmental genes. They showed that one specific Polycomb protein, called Polyhomeotic, is modified with the sugar tag by Ogt and might be the link between Ogt and development. Further investigations are necessary to find out how the sugar tag affects the function of Polyhomeotic.

"Our findings were very surprising. GlcNAc has been found on so many different proteins in mammalian cells that we expected many processes to go wrong in a fly lacking Ogt. Instead we see a very specific effect on development in fruit flies that is likely brought about by a single nuclear protein that needs the sugar tag to function properly," says Maria Cristina Gambetta, who carried out the research in Müller's lab.

Source: Science Daily

To Spread, Skin Cancer Attacks Immune Dendritic Cells

2009-05-31T14:44:00.001-07:00

Dendritic cells are the sentinels of the immune system. When they're alert and on guard, they will marshal the body's immunosoldiers, T cells, to battle at the sight of harmful pathogens. But some diseases, such as cancer, are able to escape their watchful eye. By knocking out or beguiling dendritic cells, they slip the defenses of the immune system and sack the unsuspecting body.

New research shows that one of the most common types of skin cancer has learned such a trick, finding a way to disable apparently healthy dendritic cells, which then allow cancer cell nests to spread around them without calling T cells to the fight.

The work was led by Michelle Lowes, an assistant professor of clinical investigation in the Laboratory for Investigative Dermatology at Rockefeller University, and John Carucci, associate professor of dermatology and director of Mohs Micrographic and Dermatologic Surgery at Weill Cornell Medical College. Their research shows that dendritic cells taken from squamous cell carcinomas have most of the known genetic and physiologic hallmarks of their able-bodied fellows in healthy skin tissue. But they do not behave the same at all, says Carucci, a former postdoc in the lab of Rockefeller professor Ralph M. Steinman, who discovered dendritic cells in 1973. "They are impotent," he says. "They just can't be turned on."

Curucci is an expert in surgical treatment of aggressive carcinomas and an immunologist who focuses on tumor biology. Lowes, whose usual focus is psoriasis, an inflammatory skin disorder in which dendritic cells are implicated, helped Carucci and colleagues adapt her methods for the detailed study of dendritic cells in squamous cell carcinoma. It is the second most common type of skin cancer, afflicting about 250,000 people in the United States in 2007. The work, funded by a Dana Foundation grant supporting collaborative immunological research likely to lead to clinical treatments, involved genetic and biochemical testing of dendritic cell samples from carcinoma nests, bordering tissue and healthy skin.

Under normal circumstances, mature dendritic cells present pathogens to T cells, stimulating the production of an army of T cells specialized to neutralize the threat. Certain kinds of immunoregulatory proteins called cytokines are known to normally increase dendrtic cells' ability to muster that army. But Lowes and Carucci found that dendritic cells from the squamous cell carcinomas, although appearing mature and ready, could not be boosted with a cytokine cocktail to do much of anything at all. Similar-looking dendritic cells from healthy skin responded positively to the booster, and dendritic cells from skin bordering the cancer nests fell somewhere in between. The researchers do not yet know why; they're investigating that now. "First we need to find out what switched the dendritic cells off, then we'll look at how to turn them on," Lowes says. "If you can stimulate the right T cell response, you could mount a robust antitumor response," says Carucci. "If we can do that, we might actually be able to treat so-called inoperable cancers. This could truly have some clinical applications."

Source: Science Daily

eBooks

2009-05-23T09:54:00.001-07:00

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On this post, I`ll upgrade with news eBooks... Have fun, but remember. The BNB DON`T AGREE WITH THE PIRACY. So, after you read and use it for yours scholar porpoise, delete it. We don´t host any of those eBooks. They are found out Worldwide in the web. We only research for them, and link it from here. We don´t have any responsibility for the bad usage of this content.
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General Biology

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http://rapidshare.com/files/37258811/0130892416.rar

Biology - Science for life

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Parte 1: http://rapidshare.com/files/156974310/ELS.part1.rar

Parte 2: http://rapidshare.com/files/156977815/ELS.part2.rar

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Encyclopedia of Life Sciences [26 volumes]

Número de páginas: 18348

Ano de publicação: 2007

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Parte 2: http://rapidshare.com/files/37707261/Variation__First_Edition_.part2.rar

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Variation - A central concept in biology

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Concepts in Biology

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Ano de publicação: 2003

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Oxford Dictionary of Science

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Ano de publicação: 2005

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http://www.filefactory.com/file/020610/n/0195089626_rar

Migration- The biology of live on the move

Número de páginas: 480

Ano de publicação: 1996

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http://www.mma.gov.br/sitio/index.php?ido=conteudo.monta&idEstrutura=148&idConteudo=1918

Cerrado: Ecologia, Biodiversidade e Conservação

Coletânea de publicações sobre ecologia, biodiversidade e conservação do Cerrado Brasileiro, distribuída gratuitamente pelo MMA, através de capítulos para download.

:: Aldicir Scariot, José Carlos Sousa-Silva, Jeanini Maria Felfini

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Mapas de Cobertura Vegetal dos Biomas Brasileiros

http://www.mma.gov.br/estruturas/sbf_chm_rbbio/_arquivos/mapas_cobertura_vegetal.pdf

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http://www.4shared.com/file/45013927/bdee9d8/TuToMaNiA_51934_317765_O378.html

Vocabulário básico de recursos naturais e meio ambiente

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http://www.megaupload.com/?d=7KCVT53L

Título: O manejo da paisagem e a paisagem do manejo

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Título: Fundamentos da Biologia Moderna

Autor: Amabis e Martho

Formato: Programa

Tamanho do arquivo: 80 MB

CD-ROM que acompanha o livro Fundamentos da Biologia Moderna. Ele contém animações, atividades, exercícios, etc.

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http://rapidshare.com/files/172571675/Floresta_em_Chamas.pdf

Título: Floresta em Chamas: origens, impactos e prevenção do fogo na Amazônia

Autores: Nepstad, D. C., A. Moreira & A. A. Alencar

Idioma: Português

Formato: PDF

Número de Páginas: 204

Tamanho do arquivo: 1,5 MB

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http://rapidshare.com/files/172572153/Dossie_Mata_Atlantica_2001.pdf

Título: Dossiê Mata Atlântica 2001

Idioma: Português

Formato: PDF

Número de Páginas: 409

Tamanho do arquivo: 3 MB

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http://rapidshare.com/files/170160261/Biology_6ed_-_Raven.pdf

Título: Biology (Biologia)

Autor: Raven & Johnson

Idioma: Inglês

Formato: PDF

Número de Páginas: 1239

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Descrição: Uma abordagem geral, mas de nível acadêmico, da Biologia.

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Marine Biology

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Advances in Marine Biology - Vol. 50

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Ano de publicação: 2006

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Marine Biology

Ano de publicação: 2003

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http://www.megaupload.com/?d=2X0YUJNL

Simulador de ecossistema aquático onde você pode manipular fatores abioticos e bioticos.

Formato: RAR

Tamanho: 1,67 MB

http://www.publish.csiro.au/samples/LagoonDEMO_MANUAL.pdf

Manual do programa acima

Formato: Pdf

Tamanho: 870 kb

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Título: Dolphins, Whales and Porpoises (Golfinhos e Baleias)

Autores: Reeves et. al.

Idioma: Inglês

Formato: PDF

Número de Páginas: 147

Tamanho do arquivo: 2 MB

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Título: The Biology of Sea Turtles vol. II

Autor: Lutz et al.

Idioma: Inglês

Formato: PDF

Número de Páginas: 472

Tamanho do arquivo: 9,07 MB

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Parte 1: http://rapidshare.com/files/174489976/Territorio_Selvagem_-_Tubaroes.part1.rar

Parte 2: http://rapidshare.com/files/174533458/Territorio_Selvagem_-_Tubaroes.part2.rar

Parte 3: http://rapidshare.com/files/174553464/Territorio_Selvagem_-_Tubaroes.part3.rar

Título: Território Selvagem: Tubarão

Autor: Superinteressante e BBC

Idioma: Audio em Português

Formato: AVI

Duração: 49 min

Tamanho do arquivo: 233 MB

Molecular Biology

----------------------------------------------------

Plant Genomics and Proteomics

ZIP - 1,0 MB

http://rapidshare.com/files/162035361/ebook.Plant_Genomics_and_Proteomics.0471373141.zip

RapidShare

Molecular Biology of the Gene - 5 ed. + CD-Rom

Molecular Biology of the Gene, 5th ed
Autor: James D. Watson / Tania A. Baker / Stephen P. Bell / Alexander Gann / Michael Levine / Richard Losick
Idioma: Inglês
Número de páginas: 830
Formato: DJVU
Tamanho do arquivo: 21MB

Livro

http://rapidshare.com/files/63095165/MBGbyRohan.rar

CD-Rom que acompanha o livro

Formato: RAR

Tamanho do arquivo: 62MB

CD-Rom

http://rapidshare.com/files/68177006/MBG_CD.rar

Molecular Modelling: Principles and Applications - 2 ed.

http://rapidshare.com/files/8958979/Molecular_Modelling_-_Principles_and_Applications__2e_-_A_R_Leach__2001__WW.djvu.html

Molecular Cloning - A Laboratory Manual - 3 ed.
Autor: Joseph Sambrook, David W. Russell
Idioma: Inglês
Número de páginas: 1448
Formato: PDF
Tamanho do arquivo: 62MB
http://www.filefactory.com/file/e7e663/n/Molecular_Cloning_A_Laboratory_Manual_On_The_Web_Maniatis_pdf

Título: Encyclopedia of Molecular Cell Biology and Molecular Medicine, 1e

Autor: Robert A. Meyers

Idioma: Inglês

Número de páginas: 9932

Formato: PDF

Tamanho do arquivo: 291
MB

Parte 1http://rapidshare.com/files/151857567/EMCBMM.part1.rar

Parte 2http://rapidshare.com/files/151863354/EMCBMM.part2.rar

Parte 3http://rapidshare.com/files/151867850/EMCBMM.part3.rar

Título: Current Protocols in Molecular Biology, 1 ed.

Autor: Frederick M. Ausubel, Roger Brent, Robert E. Kingston, David D. Moore, J.G. Seidman, John A. Smith, Kevin Struhl

Idioma: Inglês

Número de páginas: 4410

Formato: PDF

Tamanho do arquivo: 50
MB

RAR* - 50 MB

http://rapidshare.com/files/136281593/CPiMB.rar

*Senha para Descompressão: www.forumakademi.org

Título: Biologia Celular e Molecular - 6 ed.

Autor(es): Junqueira & Carneiro

Idioma: Português

Formato: PDF

Número de Páginas: 302

Tamanho do arquivo: 80 MB

http://rapidshare.com/files/171422307/Biologia_Celular_e_Molecular_6ed_-_Junqueira_e_Carneiro.PDF

Título: Molecular Biology of the Cell (Biologia Molecular da Célula) 4º Ediçao

Autor(es): Alberts et al.

Idioma: Inglês

Formato: PDF

Número de Páginas: 4301

Tamanho do arquivo: 70 MB

Parte 1: http://rapidshare.com/files/174845979/Molecular_Biology_of_the_Cell_4ed_-_Alberts.part1.rar

Parte 2: http://rapidshare.com/files/174861431/Molecular_Biology_of_the_Cell_4ed_-_Alberts.part2.rar

Título: Oxford Dictionary of Biochemistry and Molecular Biology (Dicionário Oxford de Bioquímica e Biologia Molecular)

Autor: Cammack

Idioma: Inglês

Formato: PDF

Número de Páginas: 738

Tamanho do arquivo: 7,5 MB

http://rapidshare.com/files/175173432/Oxford_Dictionary_of_Biochemistry_and_Molecular_Biology_-_Cammack.pdf

Título: Ecología Molecular

Autor: Eguiarte et al.

Idioma: Espanhol

Formato: PDF

Número de Páginas: 608

Tamanho do arquivo: 6,2 MB

http://rapidshare.com/files/171752829/Ecologia_Molecular_-_Eguiarte.pdf

Title: The Biomass Assessment Handbook: Bioenergy for a Sustainable Environment
Number of Pages : 291

Introduccion: Responding to the need for reliable and detailed information on biomass consumption and supply and overcoming the lack of standardized measurement and accounting procedures, this handbook provides the skills to understand the biomass resource base and the tools to assess the resource and the pros and cons of exploitation. Topics covered include assessment methods for woody and herbaceous biomass, biomass supply and consumption, and remote sensing techniques. International case studies, ranging from techniques for measuring tree volume to transporting biomass, help to illustrate step-by-step methods and are based on fieldwork experience. A set of technical appendices offer a glossary of terms, energy units, and other valuable reference data. The Biomass Assessment Handbook will be invaluable reading for energy consultants, agronomists, foresters, project developers, natural and social scientists, environmental policy analysts, and students interested in bioenergy and environmental studies.

http://rapidshare.com/files/62563630/TheBAH2007.rar.html
http://mihd.net/kgj5am
http://www.mediafire.com/?31bof1ltmjj

Industry and Research Centers worldwide

2009-05-22T21:05:00.001-07:00

United States of America

Bio-Link Centers

National Bio-Link Center

Elaine A. Johnson

Bio-Link
City College of San Francisco
1855 Folsom St, Ste 643
San Francisco, CA 94103
(415) 487-2472
ejohnson@biolink.ucsf.edu

Northcentral Region Bio-Link Center

Lisa Seidman
Madison Area Technical College

3550 Anderson Street
Madison WI 53704-2599
(608) 246-6204
lseidman@matcmadison.edu

Northeast Region Bio-Link Center
Sonia Wallman
Director, Great Bay CC Biotechnology Center,
Northeast Biomanufacturing Collaborative
Great Bay Community College
320 Corporate Drive
Portsmouth NH 03801
(603) 559-1581 Voice
(603) 334-6308 FAX
swallman@ccsnh.edu

Northwest Region Bio-Link Center

Guy Hamilton

Shoreline Community College

16101 Greenwood Ave N
Shoreline WA 98133
(206) 546-4786
ghamilto@shoreline.edu

Southcentral Region Bio-Link Center

Patricia Phelps

Austin Community College

3401 Webberville Rd.
Austin, Texas 78702
(512) 223-5914
pphelps@austincc.edu

Southeast Region Bio-Link Center
Bill Woodruff
Director of Biotechnology
Alamance Community College
PO Box 8000
Graham, NC 27253
(336) 506-4224 Voice
(336) 578-1987 Fax
woodruff@alamancecc.edu

Southwest Region Bio-Link Center

Jim Dekloe

Solano Community College

4000 Suisun Valley Rd
Fairfield CA 94534-3197
(707) 864-7000 x351
james.dekloe@solano.edu

Biotechnology Education, Organizations, and Industry in Alabama

EDUCATION

Calhoun Community College
P.O. Box 2216
Decatur, AL 35609
256-306-2500
800-626-3628

University of Alabama in Huntsville
301 Sparkman Drive
Huntsville, AL 35899
USA
256-824-3192
(f): 256-824-6349

ORGANIZATIONS

Alabama Partnership for Biotechnology Research

Alabama Technology Network
2601 Carson Road
Birmingham, Alabama 35215
205... Voice
205... Fax

Biotechnology Association of Alabama
500 Beacon Parkway West
Birmingham, AL 35209
205... Voice
205... Fax

INDUSTRY

Absorbable Polymer International
2683 Pelham Parkway
Pelham, Alabama 35124
205... Voice

Allvivo Inc
2800 Milan Court
Suite 119
Birmingham, Alabama 35211-6908
949... Voice

Atrion Medical Products
1426 Curt Francis Road
Arab, Alabama 35016
256... Voice

Avanti Polar Lipids Inc
700 Industrial Park Drive
Alabaster, AL 35007
205... Voice
Diagnostics

Axcan-Scandipharm
22 Inverness Center Parkway
Suite 310
Birmingham, Alabama 35242
205... Voice

BioCryst Pharmaceuticals Inc
2190 Parkway Lake Drive, Suite B
Birmingham, AL 35244
205... Voice
Therapeutics

Bioelastic Research
2800 Milan Court
Suite 386
Birmingham, Alabama 35211

BioFlage
500 Beacon Parkway West
Birmingham, Alabama 35209

BioHorizons Implant Systems Inc
1 Perimeter Park South
Suite 230 South
Birmingham, Alabama 35243
205... Voice

CAMgate Laboratories
2800 Milan Court
Suite 385
Birmingham, Alabama 35211

Cebert Pharmaceuticals
1200 Corporate Drive
Birmingham, Alabama 35242
1-8... Voice

Center Macromolecular Crystallography
1918 University Blvd.
Birmingham, AL 35294
205... Voice

Darius Pharmaceutical Research
1007 East Samford Road
Auburn, Alabama 36830

Emerging Technology Partners LLC
500 Beacon Parkway West
Birmingham, Alabama 35209
205... Voice

ErgoScience
4131 Cliff Road
Birmingham, Alabama 35222

Erythrogen
4687 Bridgewater Road
Birmingham, Alabama 35242

Folia Inc
2800 Milan Court
Suite 115
Birmingham, Alabama 35211
205... Voice

Galenica Pharmaceuticals Inc
One Chase Corporate Drive
Suite 490
Birmingham, Alabama 35244-1026

Gem Pharmaceuticals Inc
180 Chandalar Place Drive
Birmingham, AL 35124
205... Voice
Therapeutics

Genaco Biomedical Products
2707 Artie St. Building 100
Suite 20
Huntsville, AL 35805

Gryphus Diagnostics
2800 Milan Court
Suite 285
Birmingham, Alabama 35211

IBBEX
2800 Milan Court
Suite 373
Birmingham, Alabama 35211

International Medical Innovations
2800 Milan Court
Suite 369
Birmingham, Alabama 35211

International Pharmacy Management
300 Corporate Parkway
Suite One
Birmingham, Alabama 35242

Medmined
2800 Milan Court
Suite 123
Birmingham, Alabama 35211
877... Voice

Molecular Diagnostics of Alabama
3124 Woodhave Drive
Birmingham, Alabama 35243

Monoclonal Partnerships
P.O. Box 532032
Birmingham, Alabama 35253
205... Voice

Monomer Sciences, Inc.
Nature's Way
P.O. Box 520
New Market, AL 35761
256... Voice

New Century Pharmaceuticals Inc
895 Martin Road
Huntsville, AL 35824
205... Voice

Oculus Pharmaceuticals
262 Basic Health Sciences Bldg
1918 University Blvd.
Birmingham, Alabama 35294-0005

Omega Pharmaecuticals
1000 Urban Center Drive
Suite 450
Birmingham, Alabama 35242

PNP Therapeutics
4363 1st Avenue North
Birmingham, Alabama 35222
205... Voice

Replicon Technologies Inc
Cahaba Rd, SUITE 240
Birmingham AL 35223
205... Voice

Seatrace Pharmaceuticals
503 Hickman Street
Gadsden, Alabama 35906

Southern BioSystems Inc
756 Tom Martin Drive
Birmingham, AL 35211
205... Voice
Therapeutics

Southern Biotechnology Associates Inc
P.O. Box 26221
Birmingham, Alabama 35260
205... Voice

Southern Microbiology Associates
4204 Edmonton Drive
Bessemer, Alabama 35023

Southeast Pharmaceuticals
704A Troy Highway
Post Office Box 415
Elba, Alabama 36323

TransMolecular
3800 Colonnade Parkway
Suite 240
Birmingham, Alabama 35243
205... Voice

Tranzyme Inc
500 Beacon Parkway West
Birmingham, Alabama 35209
205... Voice

UAB Center for Macromolecular Crystallography
1530 3rd Avenue South
MCLM 262
Birmingham, Alabama 35294-0005
205-975-5469 Voice

United Douglas Pharm Inc
72 Jane Drive
Luverne, Alabama 36049

Vaxin, Inc
2800 Milan Court, Suite 231
Birmingham, AL 35211-6916
Voice: 205-943-6655
Fax: 205-943-6656

VectorLogics Inc
824 Linwood Road
Birmingham, Alabama 35222
205-934-8627 Voice

VistaPharm
120 Corporate Drive
Birmingham, Alabama 35242
205-981-1387 Voice

Vintage Pharmaceuticals
130 Vintage Drive
Huntsville, Alabama 35811

Interferencia Genética na Cardiologia

2009-05-20T17:06:00.001-07:00

A hipertensão arterial pode ser considerada como uma doença ou como um fator de risco para o desenvolvimento de enfermidades do coração, pois, na grande maioria das vezes, não provoca sintomas ou o quadro sintomático é confundido com o de outras moléstias.

No Brasil, de acordo com dados do Ministério de Saúde, a hipertensão afeta cerca de 31 milhões de brasileiros. Apesar do índice já ser elevado, este pode estar subestimado e, para a Sociedade Brasileira de Cardiologia, 50% dos hipertensos do país não sabem que sofrem da enfermidade. Nos Estados Unidos e na Europa, a hipertensão é também uma patologia com elevada prevalência e caracterizada por uma identificação deficiente dos pacientes.

Na busca pelo conhecimento mais aprofundado da dinâmica da hipertensão e da regulação da pressão arterial, pesquisadores da Johns Hopkins University School of Medicine, Estados Unidos, através de um programa de colaboração internacional, identificaram modificações genéticas que possibilitam um novo campo de percepção para o controle da pressão arterial e para o progresso de novos tratamentos para hipertensão.

Para a identificação dos genes envolvidos, os cientistas analisaram particularidades nos genomas de quase 30.000 indivíduos com um histórico hereditário europeu, cujas pressões sanguíneas sistólicas médias variaram de 118 milímetros hectograma (mmhg) a 143 mmhg, e as pressões sanguíneas diastólicas médias sofreram variações de 72 milímetros hectograma a 83 mmhg. Os pesquisadores procuraram as diferenças genéticas que se relacionaram com a hipertensão e encontraram 11 variações na sequência de DNA que parecem regular os níveis de pressão sanguínea.

As alterações no gene ATP2B1 foram associadas à pressão sanguínea e à hipertensão. Esse componente genético codifica uma proteína que bombeia o cálcio para fora de células localizadas no interior de vasos sanguíneos. As mudanças em SH2B3, uma proteína envolvida na resposta imune, foram igualmente relacionadas ao aumento da pressão sanguínea. Os cientistas também identificaram mudanças nos genes relacionados com o crescimento celular, assim como nos genes necessários para o desenvolvimento correto do coração.

As diferenças genéticas encontradas na pesquisa representam uma característica comum da população e causam somente pequenas alterações na pressão sanguínea. O estudo, entretanto, suporta a idéia de que alterações em muitos genes contribuem para a incidência de hipertensão e pressão alta. A combinação de mudanças múltiplas, em genes diferentes, pode aumentar a pressão sanguínea significativamente, todavia a influência de cada alteração gênica individual, na pressão sanguínea, é reduzida.

O estudo da hipertensão é difícil, pois trata-se, em primeiro lugar, de uma característica sujeita a contribuição de fatores diferenciados. Os resultados dessa pesquisa demonstram vias importantes para a manutenção da pressão sanguínea e podem conduzir à melhorias na terapia da hipertensão e à formação de sistemas de identificação precoce da enfermidade.

New Way Of Treating The Flu

2009-05-20T17:02:00.001-07:00

What happens if the next big influenza mutation proves resistant to the available anti-viral drugs? This question is presenting itself right now to scientists and health officials this week at the World Health Assembly in Geneva, Switzerland, as they continue to do battle with H1N1, the so-called swine flu, and prepare for the next iteration of the ever-changing flu virus. Promising new research announced by Rensselaer Polytechnic Institute could provide an entirely new tool to combat the flu. The discovery is a one-two punch against the illness that targets the illness on two fronts, going one critical step further than any currently available flu drug. "We have been fortunate with H1N1 because it has been responding well to available drugs. But if the virus mutates substantially, the currently available drugs might be ineffective because they only target one portion of the virus," said Robert Linhardt, the Ann and John H. Broadbent Jr. '59 Senior Constellation Professor of Biocatalysis and Metabolic Engineering at Rensselaer. "By targeting both portions of the virus, the H and the N, we can interfere with both the initial attachment to the cell that is being infected and the release of the budding virus from the cell that has been affected." The findings of the team, which have broad implications for future flu drugs, will be featured on the cover of the June edition of European Journal of Organic Chemistry. The influenza A virus is classified based on the form of two of its outer proteins, hemagglutinin (H) and neuraminidase (N). Each classification – for example H5NI "bird flu" or H1N1 "swine flu" – represents a different mutation of hemagglutinin and neuraminidase or H and N. Flu drugs currently on the market target only the neuraminidase proteins, and disrupt the ability of the virus to escape an infected cell and move elsewhere to infect other healthy cells. The new process developed by Linhardt is already showing strong binding potential to hemagglutinin, which binds to sialic acid on the surface of a healthy cell, allowing the virus to entire the cell.

"We are seeing promising preliminary results that the chemistry of this approach will be effective in blocking the hemagglutinin portion of the disease that is currently not targeted by any drug on the market," he said. In addition, Linhardt and his team have shown their compound to be just as effective at targeting neuraminidase as the most popular drugs on the market, according to Linhardt. The approach can also be modified to specifically target the neuraminidase or the hemagglutinin, or both, depending on the type of mutation that is present in the current version of the flu, according to Linhardt. In the next steps of his research, Linhardt will look at how their compounds bind to hemagglutinin, and he will test the ability to block the virus first in cell cultures and then in infected animal models. "It is still early in the process," he said. "We are several steps away from a new drug, but this technique is allowing us to move very quickly in creating and testing these compounds." The technique that Linhardt used is the increasingly popular technique of "click chemistry." Linhardt is among the first researchers in the world to utilize the technique to create new anti-viral agents. The process allows chemists to join small units of a substance together quickly to create a new, full substance.In this case, Linhardt used the technique to quickly build a new derivative of sialic acid. Because it is chemically very similar to the sialic acid found on the surface of a cell, the virus could mistake the compound as the real sialic acid and bind to it instead of the cell, eliminating the connections to hemagglutinin and neuraminidase that are required for initial infection and spread of the infection in the body. The currently available drugs are translation-state inhibitors whose chemical structure allows them to only effectively target the neuraminidase. The research was funded by the National Institutes of Health. Linhardt was joined in the research by Michel Weïwer, Chi-Chang Chen, and Melissa Kemp of Rensselaer.

Gene Transfer Technology May Lead To HIV Vaccine

2009-05-17T17:02:00.001-07:00

ScienceDaily (May 17, 2009) — A research team may have broken the stubborn impasse that has frustrated the invention of an effective HIV vaccine, by using an approach that bypasses the usual path followed by vaccine developers. By using gene transfer technology that produces molecules that block infection, the scientists protected monkeys from infection by a virus closely related to HIV—the simian immunodeficiency virus, or SIV—that causes AIDS in rhesus monkeys.

"We used a leapfrog strategy, bypassing the natural immune system response that was the target of all previous HIV and SIV vaccine candidates," said study leader Philip R. Johnson, M.D., chief scientific officer at The Children's Hospital of Philadelphia. Johnson developed the novel approach over a ten-year period, collaborating with K. Reed Clark, Ph.D., a molecular virologist at Nationwide Children's Hospital in Columbus, Ohio.

Johnson cautioned that many hurdles remain before the technique used in this animal study might be translated into an HIV vaccine for humans. If the technique leads to an effective HIV vaccine, such a vaccine may be years away from realization.

Most attempts at developing an HIV vaccine have used substances aimed at stimulating the body's immune system to produce antibodies or killer cells that would eliminate the virus before or after it infected cells in the body. However, clinical trials have been disappointing. HIV vaccines have not elicited protective immune responses, just as the body fails on its own to produce an effective response against HIV during natural HIV infection.

The approach taken in the current study was divided into two phases. In the first phase, the research team created antibody-like proteins (called immunoadhesins) that were specifically designed to bind to SIV and block it from infecting cells. Once proven to work against SIV in the laboratory, DNA representing SIV-specific immunoadhesins was engineered into a carrier virus designed to deliver the DNA to monkeys. The researchers chose adeno-associated virus (AAV) as the carrier virus because it is a very effective way to insert DNA into the cells of a monkey or human.

In the second part of the study, the team injected AAV carriers into the muscles of monkeys, where the imported DNA produced immunoadhesins that entered the blood circulation. One month after administration of the AAV carriers, the immunized monkeys were injected with live, AIDS-causing SIV. The majority of the immunized monkeys were completely protected from SIV infection, and all were protected from AIDS. In contrast, a group of unimmunized monkeys were all infected by SIV, and two-thirds died of AIDS complications. High concentrations of the SIV-specific immunoadhesins remained in the blood for over a year.

Further studies need to be conducted if this technique is to become an actual preventive measure against HIV infection in people, Johnson said. "To ultimately succeed, more and better molecules that work against HIV, including human monoclonal antibodies, will be needed," he and his co-authors conclude. Finally, added Johnson, their approach may also have potential use in preventing other infectious diseases, such as malaria.

Grants from the National Institute of Allergic and Infectious Diseases of the National Institutes of Health supported this study. Johnson's collaborators, in addition to Clark, were Jianchao Zhang, of Nationwide Children's Hospital, Columbus, Ohio; Eloisa Yuste and Ronald C. Desrosiers of the New England Primate Research Center and Harvard Medical School; and Bruce C. Schnepp, Mary J. Connell, and Sean M. Greene, of Children's Hospital and the University of Pennsylvania School of Medicine. Johnson also is on the University of Pennsylvania faculty.

Journal reference:

Johnson et al. Vector-mediated gene transfer engenders long-lived neutralizing activity and protection against SIV infection in monkeys. Nature Medicine, May 17, 2009 DOI: 10.1038/nm.1967

Adapted from materials provided by Children's Hospital of Philadelphia.

Source: Science Daily

eBooks de Biotecnologia

2009-05-15T15:21:00.001-07:00

On this post, I`ll upgrade with news eBooks... Have fun, but remember. The BNB DON`T AGREE WITH THE PIRACY. So, after you read and use it for yours scholar porpouse, delete it.
Thank you.

-------------------------------------------------------------------------------------------------------------

The Biomass Assessment Handbook: Bioenergy for a Sustainable Environment
Quantidade de Páginas (Number of Pages) : 291

Introduçao(Introduccion): Responding to the need for reliable and detailed information on biomass consumption and supply and overcoming the lack of standardized measurement and accounting procedures, this handbook provides the skills to understand the biomass resource base and the tools to assess the resource and the pros and cons of exploitation. Topics covered include assessment methods for woody and herbaceous biomass, biomass supply and consumption, and remote sensing techniques. International case studies, ranging from techniques for measuring tree volume to transporting biomass, help to illustrate step-by-step methods and are based on fieldwork experience. A set of technical appendices offer a glossary of terms, energy units, and other valuable reference data.

OBS: The Biomass Assessment Handbook will be invaluable reading for energy consultants, agronomists, foresters, project developers, natural and social scientists, environmental policy analysts, and students interested in bioenergy and environmental studies.

http://rapidshare.com/files/62563630/TheBAH2007.rar.html
http://mihd.net/kgj5am
http://www.mediafire.com/?31bof1ltmjj

-------------------------------------------------------------------------------------------------------------

How An Enzyme Tells Stem Cells Which Way To Divide

2009-05-14T14:41:00.001-07:00

ScienceDaily (May 13, 2009) — Driving Miranda, a protein in fruit flies crucial to switch a stem cell's fate, is not as complex as biologists thought, according to University of Oregon biochemists. They've found that one enzyme (aPKC) stands alone and acts as a traffic cop that directs which roads daughter cells will take.

"Wherever aPKC is at on a cell's cortex or membrane, Miranda isn't," says Kenneth E. Prehoda, a professor in the chemistry department and member of the UO's Institute of Molecular Biology. When a stem cell duplicates into daughter cells, the side, or cortical domain, containing aPKC (atypical protein kinase C) continues as a stem cell, while the other domain with Miranda becomes a differentiated cell such as a neuron that forms the central nervous system.

Prehoda and co-author Scott X. Atwood, who studied in Prehoda's lab and recently earned his doctorate, describe how the mechanism works in the May 12 issue of the journal Current Biology.

Instead of a complex cascade of protein deactivation steps that many biologists have theorized, Prehoda said, aPKC strips phosphate off an energy-transfer nucleotide known as ATP and then attaches it to Miranda. This process forces Miranda away from aPKC and helps determine the fates of subsequent daughter cells.

"This process is pretty simple," he said, when viewed from a biochemical perspective. "What happens is that Miranda gets phosphorylated by aPKC, turning it into an inactivated substrate and pushing it into another location in the cell."

Much of the paper in Current Biology is devoted to why the more complex scenarios are not accurate. "There have been a lot of ideas on how this works, and most seemed to be really complicated and difficult to explain. We have found it's a much simpler mechanism," Prehoda said, adding that the mechanism likely is similar in many other types of cells, not just stem cells.

"It's a basic-research question. How does this polarity occur? In order to develop stem cell-specific therapeutics based on a rational methodology you have to understand the mechanism," he said.

If Miranda is improperly isolated into other regions by aPKC, the stem cell divides symmetrically, with both daughter cells adopting the same fate, In turn, Prehoda said, these cells can become tumorous as they continue to rapidly divide without proper polarization.

The National Institutes of Health supported the research through a Developmental Biology Training Grant to Atwood and a research grant to Prehoda.

Source:Science Daily

Nanotechnology: Self-assembly Of Building Blocks Of DNA Can Now Be Easily Controlled

2009-05-14T11:37:00.001-07:00

ScienceDaily (May 14, 2009) — Nature has long perfected the construction of nanomachines, but David González and his fellow researchers from Eindhoven University of Technology and Utrecht University under the leadership of Spinoza Award winner Bert Meijer, have brought the construction of artificial supramolecular structures a step closer. The researchers managed to carefully control the self-assembly of guanosine, one of the building blocks of DNA.

The natural world is a shining example when it comes to the self-assembly of molecules. However, it has not disclosed all of its secrets yet. Controlling the shape and structure of self-assembled systems continues to be a stumbling block for scientists. Yet such structures, in which the different molecules cooperate with each other, can have unrivaled characteristics. Self-assembly could provide the way forward for the future mass production of nanomaterials, nanodrugs and nanoelectronics.

Control

A quadruplex of four DNA strands is an example of such a self-assembling structure. Guanosine molecules bind together to form such a G-quadruplex. The researchers managed to influence the formation of G-quadruplexes, using Coulombic interactions. They produced structures with 8, 12, 16, or even 24 guanosine molecules.

During the formation of G-quadruplexes, positively charged alkali metal ions are incorporated in the interior of the structure. Negatively charged anions, however, fall on the outside of the structure and are therefore exposed to the surrounding medium. Coulomb's law describes the forces that two electrical charges exert on each other. According to this law, that force depends on the distance between the negatively and positively charged ions and on the stabilizing characteristics of the solution in which the self-assembly takes place. The negatively charged ions on the outside of the structure are of course exposed to this solution, as a result of which the solution determines the stability of the structure to a large extent.

By varying the two different factors, distance and solution, the researchers could regulate the formation of the G-quadruplexes. For example, they could build structures with different numbers of molecules. A structure with exactly 24 guanosine molecules had not previously been artificially constructed. This new perspective therefore provides opportunities for the regulation of self-assembling structures.

The research was performed by the Institute for Complex Molecular Structures at Eindhoven University of Technology in cooperation with Utrecht University. Part of the research was financed by the NWO/Spinoza Award of Bert Meyer.

Source: ScienceDaily (May 14, 2009)

Novidades no portal

2009-05-14T10:52:00.000-07:00

Caros leitores!
Como podem ver, estamos com as novidades prometidas no inicio do ano!
um design TOTALMENTE novo, baseado no design do portal http://www.cahayabiru.com/, que é um asiático que esta transformando templates de WordPress, para o estilo Blogger.

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Old Genes Can Learn New Tricks, Horned Beetles Show

2009-05-13T15:19:00.000-07:00

A popular view among evolutionary biologists that fundamental genes do not acquire new functions has been challenged by a new study in the Proceedings of the National Academy of Sciences.

Indiana University Bloomington biologist Armin Moczek and research associate Debra Rose report that two ancient genes were "co-opted" to help build a new trait in beetles -- the fancy antlers that give horned beetles their name. The genes, Distal-less and homothorax, touch most aspects of insect larval development, and have therefore been considered off-limits to the evolution of new traits.

In the two horned beetle species Moczek and Rose studied, the genetic sequences of Distal-less and homothorax were hardly different, suggesting the two genes have retained their unique identities because of selective pressures not to change. What changed was not the genes themselves, but when and where they are turned on.

"Evolutionary biologists have a good idea of what it takes to change the shape of a wing, the length of a leg, or the anatomy of an eye," Moczek said. "What we have struggled with, though, is how these traits originate in the first place. How do you evolve that first wing, limb or photoreceptor from a flightless, limbless and blind ancestor?"

To investigate these questions, Moczek and Rose examined three development genes that are so old, all insects have them: Distal-less, homothorax and a third, dachshund. The genes were first characterized in fruit flies, and are categorized as "upstream" regulatory genes because they influence a wide variety of genetic processes in insect cells, such as the development of legs, antennae and wings. Moczek said that in horned beetles, each of the three genes is likely to have hundreds to thousands of downstream targets.

A tenuous consensus among evolutionary biologists was that such genes -- upon which so many different and important processes depend -- could not be easily modified, because any modification would affect countless aspects of the insect's development, any one of which could be bad for the individual insect, reducing its fitness relative to its peers.

Moczek and Rose's PNAS paper confirms one aspect of this idea. All three genes were sequenced and found to be highly conserved, or unchanged, not only among the individuals of each beetle species they examined, but also between the two species, Onthophagus taurus (Italy) and Onthophagus binodis (South Africa), whose lineages diverged about 24 million years ago. But that isn't the whole story.

To understand the effects of the three genes on horned beetle development, Moczek and Rose employed a new and promising technique, RNA interference, which disables the action of specific genes without compromising other genetic processes. Humans are only mimicking nature here; RNA interference is also a natural method of gene regulation in eukaryotes.

Moczek and Rose divided beetle larvae of both species into three treatment groups: no injection, buffer injection with nonsense RNA and buffer injection with RNA interference transcripts designed to disrupt one of three crucial developmental genes.

Moczek and Rose learned that two of the three genes, Distal-less and homothorax, are used by both O. taurus and O. binodis in the development of beetle horns. While Distal-less was found to affect both the development of thorax horns (which form just behind the head) and head horns, homothorax was only found to influence thorax horn development. The gene dachshund appears to have no effect whatsoever on horn development in either species.

"The evolution of novel features does not require the evolution of novel genes," Moczek said. "A lot of innovation can grow from within the organism's genetic toolbox."

More importantly, Moczek and Rose learned all developmental genes are candidates for such recruitment, not just the genes whose development functions are considered non-essential or limited in their effects.

Moczek also says the PNAS paper may compel evolutionary biologists to revisit pleiotropy, the foundational concept of one gene influencing many traits.

"It may be that our understanding of pleiotropy is too simplistic," Moczek said. "Now that we know fundamental development genes can acquire new and diverse functions with relative ease, pleiotropy may not be nearly as constraining as we have thought."

Research described in the PNAS paper was supported by grants from the National Science Foundation (IOS 0445661 and IOS 0718522). Source : ScienceDaily (May 13, 2009)

The project

2009-05-13T07:10:00.000-07:00

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