Archive for setembro 21st, 2012

Causas das Grandes Explosões Solares Podem estarem Nas Cavidades da Corona Solar

sexta-feira, setembro 21st, 2012

Bem… astronomos estão intringados porque existem elevadas emissões de energia que pode afetar a Terra e estas emissões parecem vir de cavidades na coroa solar das quais nada se conhece ainda. O modêlo astronomico acadêmico mais moderno em nada prevê estas cavidades, elas não são previsiveis a partir da sua teoria da formação do Sol. Por seu lado, o Modelo Astronomico da Matrix/DNA não apenas previu a 30 anos atrás como sugere ser inevitavel que existam cavidades com tais emissões. Elas seriam as ultimas remanescentes das cavidades dos gigantescos vulcões que existiam no astro quando ainda era pulsar e se umplodiu tornando-se supernova e chegando ao atual estágio de seu ciclo vital. Como me falta tempo agora para ler tudo a respeito e anlusar melhor isso tudo, deixo registrado links das noticias:

Roots of huge solar explosions may lie in ‘coronal cavities’

Read more: http://www.foxnews.com/science/2012/09/21/roots-huge-solar-explosions-may-lie-in-coronal-cavities/#ixzz279jAJWfx

Published September 21, 2012

Space.com

NASA’s STEREO…Solar Streamers Too Hot To Handle, No Dentist For These Cavities

http://www.satnews.com/cgi-bin/story.cgi?number=491056196

Astronomers try to predict huge solar blasts by studying coronal cavities

http://www.zmescience.com/research/studies/coronal-cavity-study-for-solar-blast-prediction-04123/

Incrível Descoberta Genética no Cérebro para a Busca da Solução ao Misterioso Aparecimento da Auto-Consci6encia

sexta-feira, setembro 21st, 2012

( Isto é muito interessante para as pesquisas da Matrix/DNA por isso será temporariamente copiado aqui para ser analisado item por item.)

A primeira rápida impressão que tive ao ler o artigo foi que “parece que” o mecanismo sugerido pela Matrix/DNA para a Natureza corrigir os desvios da Macro-Evolução, que envolvem processos da termodinamica dos sistemas, entropias, etc., foi aplicado aqui. Sugere que o primata na África à 2 milhões de anos atrás conseguiu um status de vida priviliegiado e se acomodou, super-especializando numa forma provisória da Evolução, fechando as portas à esta, e assim foi descartado como beco sem saída. Porem ocorreu um momento de evolução ao reverso, pelo método de redução de genes, justo daqueles recem-adquiridos e responsaveis pelos atributos do novo estilo de vida. Esta redução se dá pela fusão de genes, então genes foram fundidos enquanto os outros genes que vinham no caminho certo antes da espécie alcançar a super-especialização foram reforçados com cópias extras e estimulados a se expressarem. Desta maneira, retornando a uma espécie inferior, a Evolução pôde reencetar sua marcha progressista. Lembre-se que a Evolução em si mesma não tem propósito algum, porem o que estamos descrevendo e assistindo são os meros passos gradativos de um grande processo de reprodução universal. Ok, por enquanto é a primeira impressão…

Human brain shaped by duplicate genes

Ewen Callaway – 03 May 2012

http://www.nature.com/news/human-brain-shaped-by-duplicate-genes-1.10584

NATURE. COM

Humans walk on two feet and (mostly) lack hair-covered bodies, but the feature that sets us furthest apart from other apes is a brain capable of language, art, science, and other trappings of civilisation.

Now, two studies published online today in Cell12suggest that DNA duplication errors that happened millions of years ago might have had a pivotal role in the evolution of the complexity of the human brain. The duplications — which created new versions of a gene active in the brains of other mammals — may have endowed humans with brains that could create more neuronal connections, perhaps leading to greater computational power.

The enzymes that copy DNA sometimes slip extra copies of a gene into a chromosome, and scientists estimate that such genetic replicas make up about 5% of the human genome. However, gene duplications are notoriously difficult to study because the new genes differ little from their forebears, and tend to be overlooked.

Evan Eichler, a geneticist at the University of Washington in Seattle, and lead author of one of the Cell papers, previously found that humans have four copies of a gene called SRGAP2, and he and his colleagues decided to investigate.

In their new paper, they report that the three duplicated versions of SRGAP2 sit on chromosome 1, along with the original ancestral gene, but they are not exact copies. All of the duplications are missing a small part of the ancestral form of the gene, and at least one duplicate, SRGAP2C, seems to make a working protein. Eichler’s team has also found SRGAP2C in every individual human genome his team has examined – more than 2,000 so far – underscoring its significance.

“Ten years after the human genome was sequenced and declared done, we’re still finding new genes in new places that are really important to human brain function and evolution,” says Eichler.

Eichler’s team calculates that SRGAP2C appeared roughly 2.4 million years ago, around the time that big-brained species of Homo evolved in Africa from smaller-skulled Australopithecines, and around the time that stone tools appeared in the fossil record. These ancient hominins eventually gave rise to Homo erectus, which were the first human ancestors to wander beyond Africa, roughly 1.8 million years ago.

Boosting brains

According to a second study, also published in Cell2, the emergence of SRGAP2C could have helped our ancestors to boost the power of their bigger brains, which may have been created by other, unknown changes in the genome.

“It’s got to play some important function,” says Franck Polleux, a neurobiologist at the Scripps Research Institute in La Jolla, California, and senior author of the second paper in Cell.

Surprisingly, the SRGAP2C protein blocks the action of the ancestral protein, Polleux’s team discovered, effectively rendering humans as ‘knockouts’ for the ancestral SRGAP2 gene. The team then expressed the human form of SRGAP2C in the neurons of developing mice. The change didn’t cause the mice brains to enlarge, but their neurons produced denser arrays of brain cell structures, called dendritic spines, that forge connections with neighbouring neurons.

“If you’re increasing the total number of connections, you’re probably increasing the ability of this network to handle information,” Polleux says. “It’s like increasing the number of processors in a computer.”

In mice, the gene also increased the migration speed of neurons across the developing brain. Polleux’s team speculates that this trait could also have helped neurons to travel long distances in the enlarged brains of human ancestors.

“One has to be cautious about putting too much emphasis on the role of one gene in brain evolution,” says Genevieve Konopka, a neuroscientist at the University of Texas Southwestern Medical Center in Dallas. But she thinks that the two papers make a good case that duplication ofSRGAP2 influenced human cognition.

James Sikela, an evolutionary geneticist at the University of Colorado, Denver, adds that theSRGAP2 duplications are likely to be one of a multitude of genetic changes that moulded the human brain. His team has identified dozens of duplicated genes unique to humans3, many of them expressed in the brain. “Finding the genes that make us human may be challenging,” he says, “but the resources we now have to ask such questions are unprecedented.”

Nature
doi:10.1038/nature.2012.10584

( Êste artigo foi extraído de dois papers cientificos, que preciso comprar para ler:

1) Evolution of Human-Specific Neural SRGAP2 Genes by Incomplete Segmental Duplication

http://www.cell.com/retrieve/pii/S0092867412004618 – ( ver figura no artigo)

  • Highlights
  • Missing SRGAP2 human-specific genes sequenced by using haploid hydatidiform mole DNA
  • SRGAP2 duplicated three times in the human lineage ∼1.0–3.4 million years ago
  • One duplicate is expressed in the brain and is fixed in copy number in all humans
  • The incomplete initial duplication likely antagonized the parent gene at birth

Summary

Gene duplication is an important source of phenotypic change and adaptive evolution. We leverage a haploid hydatidiform mole to identify highly identical sequences missing from the reference genome, confirming that the cortical development gene Slit-Robo Rho GTPase-activating protein 2 (SRGAP2) duplicated three times exclusively in humans. We show that the promoter and first nine exons of SRGAP2 duplicated from 1q32.1 (SRGAP2A) to 1q21.1 (SRGAP2B) ∼3.4 million years ago (mya). Two larger duplications later copiedSRGAP2B to chromosome 1p12 (SRGAP2C) and to proximal 1q21.1 (SRGAP2D) ∼2.4 and ∼1 mya, respectively. Sequence and expression analyses show that SRGAP2C is the most likely duplicate to encode a functional protein and is among the most fixed human-specific duplicate genes. Our data suggest a mechanism where incomplete duplication created a novel gene function—antagonizing parental SRGAP2 function—immediately “at birth” 2–3 mya, which is a time corresponding to the transition from Australopithecus to Homo and the beginning of neocortex expansion

2)

Inhibition of SRGAP2 Function by Its Human-Specific Paralogs Induces Neoteny during Spine Maturation

http://www.cell.com/retrieve/pii/S009286741200462X – Ver figura no artigo

  • Highlights
  • SRGAP2 has undergone two partial duplications, specifically in the human genome
  • One copy (SRGAP2C) is expressed in the human brain and antagonizes ancestral SRGAP2
  • Ancestral SRGAP2 promotes dendritic spine maturation and limits spine density in vivo
  • Human SRGAP2C induces neoteny and leads to higher density of spines with longer necks

Summary

Structural genomic variations represent a major driving force of evolution, and a burst of large segmental gene duplications occurred in the human lineage during its separation from nonhuman primates. SRGAP2, a gene recently implicated in neocortical development, has undergone two human-specific duplications. Here, we find that both duplications (SRGAP2B and SRGAP2C) are partial and encode a truncated F-BAR domain. SRGAP2C is expressed in the developing and adult human brain and dimerizes with ancestral SRGAP2 to inhibit its function. In the mouse neocortex, SRGAP2 promotes spine maturation and limits spine density. Expression of SRGAP2C phenocopies SRGAP2 deficiency. It underlies sustained radial migration and leads to the emergence of human-specific features, including neoteny during spine maturation and increased density of longer spines. These results suggest that inhibition of SRGAP2 function by its human-specific paralogs has contributed to the evolution of the human neocortex and plays an important role during human brain development.