sábado, 27 de abril de 2013

PEC 33 - tentativa da CCJ em modificar as decisões do STF

25/04/2013 15h46 - Atualizado em 25/04/2013 19h56



O deputado federal pelo PT Nazareno Fontelles do Piaui (foto acima) propos esta semana uma PEC denominada 33, que revelou o que é o PT nas suas entranhas e os objetivos de uma camera de deputados desacreditada e oportunistas que já pouco serve a DEMOCRACIA.


As coligações partidarias, as compras de deputados pelo mensalão e tantas artimanhas do palacio do Planalto ocupado pelo PT nesses últimos anos criou uma camara legislativa somente fisiologista de interesses pessoais que agora revela também seu interesse golpista, tirando o poder do STF. 

Todas as artimanhas lideradas pelo poder executivo nesses anos tenta desacreditar a Justiça em especial após a condenação do dos integrantes do MENSALÃO.


Entenda a PEC 33, que pretende reduzir os poderes do STF

Proposta de emenda constitucional impõe limites ao poder do Supremo.
Deputado Nazareno Fontelles (PT-PI) apresentou proposta em 2011.

O que é
A proposta de emenda constitucional número 33, a chamada PEC 33 (leia a íntegra), impõe limites ao poder do Supremo Tribunal Federal. Na prática, o STF deixaria de ter a última palavra sobre mudanças na Constituição.
Quem propôs
A PEC foi protocolada em 2011 pelo deputado federal Nazareno Fontelles (PT-PI).
Os argumentos
Na justificativa da proposta, Nazareno Fontelles aponta "ativismo judicial" do Supremo, isto é, ao decidir, o tribunal estaria criando normas que seriam de competência do Legislativo. Para o parlamentar, o ativismo representa "grave violação ao regime democrático e aos princípios constitucionais".

Os pontos principais da PEC
A PEC modifica três artigos da Constituição e estabelece que:
 - passam a ser necessários os votos de quatro quintos dos membros dos tribunais para que uma lei seja considerada inconstitucional. No caso do Supremo, seriam necessários os votos de nove dos 11 ministros (em vez de seis, como atualmente).
- em ações que questionam a legalidade de emendas à Constituição Federal, a decisão do Supremo não será mais definitiva. Depois do julgamento pelo STF, o Congresso terá de dizer se concorda ou não com a decisão. Se discordar, o assunto será submetido a plebiscito.
- fica transferido do Supremo para o Congresso a aprovação de súmulas vinculantes. Esse mecanismo obriga juízes de todos os tribunais a seguirem um único entendimento acerca de normas cuja interpretação seja objeto de controvérsia no Judiciário. A aprovação de uma súmula pelo Congresso dependeria do voto favorável de pelo menos 257 deputados e 41 senadores.

A tramitação
A PEC foi aprovada em 24 de abril de 2013 pela Comissão de Constituição e Justiça (CCJ) da Câmara dos Deputados. Por se tratar de emenda à Constituição, a próxima etapa de tramitação é a formação de uma comissão especial para análise do projeto, conforme determina o Regimento Interno da Câmara. Aprovada na comissão especial, a PEC será votada no plenário.

A favor e contra -Parte dos deputados defende a proposta; ministros do Supremo TribunalFederal já se manifestaram contra
 

quinta-feira, 25 de abril de 2013

60 anos da descoberta do DNA


DNA: the 'smartest' molecule in existence?

Composite image of zip, ladder, DNA strand, Morse code (courtesy Porthcurno Telegraph Museum) and telephone coil. Other images via GettyDNA is structured like a ladder, opens and closes like a zip, codes data like Morse code and coils tightly

Related Stories

DNA is the molecule that contains and passes on our genetic information. The publication of its structure on the 25th of April 1953 was vital to understanding how it achieves this task with such startling efficiency.
In fact, it's hard to think of another molecule that performs so many intelligent functions so effortlessly. So what is it that makes DNA so smart?

Multi-millennial survivor

For such a huge molecule, DNA is very stable so if it's kept in cold, dry and dark conditions, it can last for a very, very long time. This is why we have been able to extract and analyse DNA taken from species that have been extinct for thousands of years.
Illustration of a woolly mammothScientists have 'resurrected' blood protein from preserved mammoths after harvesting their DNA
It's the double-stranded, double-helix structure of DNA that stops it falling apart.
DNA's structure is a bit like a twisted ladder. The twisted 'rails' are made of sugar-phosphate, which give DNA its shape and protect the information carrying 'rungs' inside. Each sugar-phosphate unit is joined to the next by a tough covalent bond, which needs a lot of energy to break.
In between the 'rails', weaker hydrogen bonds link the two halves of the rungs together. Individually each hydrogen bond is weak - but there are thousands of hydrogen bonds within a single DNA molecule, so the combined effect is an extremely powerful stabilising force.
It's this collective strength of DNA that has allowed biologists to study genes of ancient species like the woolly mammoth - extinct but preserved in the permafrost.
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This short animation explains everything else you need to know about DNA.

Clever facsimile machine

Our cells need to divide so we can grow and re-build, but every cell needs to have the instructions to know 'how to be' a cell.

Intelligent error correction

Brain Zip
The consequences of wrongly read or copied information can be disastrous and cause deformities in the proteins.
So as DNA replicates, enzymes carry out a proof-reading job and fix any rare errors.
They tend to repair about 99% of these types of errors, with further checks taking place later.
DNA provides those instructions - so a new copy of itself must be made before a cell divides.
It's the super-smart structure that makes this easy. The 'rungs' of the DNA ladder are made from one of four nitrogen-based molecules, commonly known as A, T, G and C. These form complementary pairs - A always joins with T and G always joins with C.
So one side of the double-stranded DNA helix can be used as a template to produce a new side that perfectly complements it. A bit like making a new coat zip, but by using half of the old zip as a template.
The original side and the new one combine together to form a new DNA double helix, which is identical to the original.
Cleverly, human DNA can unzip and 'replicate' at hundreds of places along the structure at the same time - speeding up the process for a very long molecule.

Molecular contortionist

coiled telephone cordTwo metres of DNA coils like a telephone cord to fit into each cell
DNA is one of the longest molecules in the natural world. You possess enough DNA, stretched out in a line, to reach from here to the sun and back more than 300 times.
Yet each cell nucleus must contain two metres of DNA, so it has to be very flexible. It coils - much like a telephone cord - into tight complex structures called chromatins without corrupting the vital information within.

DNA bases - vital rungs in the ladder

There are four different nucleotide bases in each DNA molecule:
  • Adenine (A)
  • Thymine (T)
  • Guanine (G)
  • Cytosine (C)
These small molecules join DNA together and encode our genetic information.
And despite being packed in so tightly, the genetic material can still be accessed to create new copies and proteins as required.
Human cells contain 23 pairs of chromosomes, with each containing one long DNA molecule as well as the proteins which package it. It's no wonder DNA needs to be extremely supple.
Amazingly, this folded and packed form of DNA is approximately 10,000 times shorter than the linear DNA strand would be if it was pulled taut.
This is why we have the 'luxury' of having the plans for our entire body in nearly every cell.

Biological database

DNA storage

Morse code
research team has encoded data in artificially produced segments of DNA, including:
  • A 26-second snippet of Martin Luther King's classic anti-racism address from 1963
  • A .pdf" of the seminal 1953 paper by Crick and Watson describing DNA' structure
The total data package was equivalent to 760 kilobytes on a computer drive. Physically, the DNA carrying all that information is no bigger than a speck of dust.
Genes are made up of stretches of the DNA molecule which contain information about how to build proteins - the building blocks of life which make up everything about us.
Different sequences of the four types of DNA bases make 'codes' which can be translated into the components of proteins, called amino acids. These amino acids, in different combinations can produce at least 20,000 different proteins in the human body.
Think of it like Morse Code. It too uses only four symbols (dot, dash, short spaces and long spaces), but it's possible to spell out entire encyclopaedias with that simple code.
Just one gram of DNA can hold about two petabytes of data - the equivalent of about three million CDs.
That's pretty smart, especially when you compare it to other information-storing molecules. Using the same amount of space, DNA can store 140,000 times more data than iron (III) oxide molecules, which stores information on computer hard drives.
DNA may be tiny but with properties including stability, flexibility, replication and the ability to store vast amounts of data, there's a reason why it must be one of the smartest known molecules.
With huge quantities of data being produced by ever-growing computer systems, traditional data storage solutions, like magnetic hard drives are becoming bulky and cumbersome. Researchers have now used DNA to store artificially-produced information, but could this be the future of data storage?


sábado, 20 de abril de 2013

Raio X, e progresso da medicina

X-ray vision: how a chance discovery revolutionised medicine http://www.guardian.co.uk/science/video/2013/apr/19/x-ray-vision-discovery-medicine

sábado, 13 de abril de 2013

H7N9

RSPECTIVE
Global Concerns Regarding Novel Influenza A (H7N9) Virus Infectio
Timothy M. Uyeki, M.D., M.P.H., M.P.P., and Nancy J. Cox, Ph.D.
April 11, 2013
10.1056/NEJMp1304661
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Comments open through May 29, 2013
Available on the NEJM.org full site.
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Severe disease in humans caused by a novel influenza A virus that is distinct from circulating human influenza A viruses is a seminal event. It might herald sporadic human infections from an animal source — e.g., highly pathogenic avian influenza (HPAI) A (H5N1) virus; or it might signal the start of an influenza pandemic — e.g., influenza A(H1N1)pdm09 virus. Therefore, the discovery of novel influenza A (H7N9) virus infections in three critically ill patients reported in the Journal by Gao and colleagues is of major public health significance. Chinese scientists are to be congratulated for the apparent speed with which the H7N9 virus was identified, and whole viral genome sequences were made publicly available in relatively short order. Because this H7N9 virus has not been detected in humans or animals previously, the situation raises many urgent questions and global public health concerns.

The key question for pandemic risk assessment is whether there is evidence of either limited or, more important, sustained human-to-human transmission — the latter being indicative of an emerging pandemic. If human-to-human transmission occurs, transmission dynamics, modes of transmission, basic reproductive number, and incubation period must all be determined. It is possible that these severely ill patients represent the tip of the iceberg and that there are many more as-yet-undetected mild and asymptomatic infections. Determining the spectrum of illness will help us understand the scope of the problem and assess severity. Enhanced surveillance for H7N9 virus infection is therefore urgently needed among hospitalized patients and outpatients of all ages with less severe respiratory illness. Other useful information can be derived from monitoring close contacts of patients with confirmed H7N9 cases to assess whether family members or health care personnel who provided care for patients with H7N9 virus infection have respiratory illness and laboratory-confirmed H7N9 virus infection. Such investigations will clarify whether H7N9 virus transmission in people appears efficient, or whether limited, nonsustained human-to-human transmission is occurring in persons with prolonged unprotected exposures, such as in clusters of HPAI H5N1 cases in blood-related family members. So far, the information provided by Chinese health officials provides reassurance that sustained human-to-human transmission is not occurring.

In addition to causing severe illness and deaths, the novel H7N9 viruses reported by Gao and colleagues have genetic characteristics that are of concern for public health. The hemagglutinin (HA) sequence data suggest that these H7N9 viruses are a low-pathogenic avian influenza A virus and that infection of wild birds and domestic poultry would therefore result in asymptomatic or mild avian disease, potentially leading to a “silent” widespread epizootic in China and neighboring countries. If H7N9 virus infection is primarily zoonotic, as reports currently suggest, transmission is expected to occur through exposure to clinically normal but infected poultry, in contrast to HPAI H5N1 virus infection, which typically causes rapid death in infected chickens.

The gene sequences also indicate that these viruses may be better adapted than other avian influenza viruses to infecting mammals. For example, the presence of Q226L in the HA protein has been associated with reduced binding to avian-like receptors bearing sialic acids linked to galactose by α-2,3 linkages found in the human lower respiratory tract,1 and potentially an enhanced ability to bind to mammalian-like receptors bearing sialic acids linked to galactose by α-2,6 linkages located in the human upper airway.1 Equally troubling is that Q226L in HA has been shown to be associated with transmission of HPAI H5N1 viruses by respiratory droplets in ferrets, one of the animal models for assessing pathogenicity and transmissibility of influenza viruses.2,3 These H7N9 viruses also possess the E627K substitution in the PB2 protein, which has also been associated with mammalian adaptation and respiratory-droplet transmission of HPAI H5N1 virus in ferrets.3 This H7N9 virus is a novel reassortant with HA and neuraminidase (NA) genes from an ancestral avian H7N9 virus and the six other genes from an avian H9N2 virus. The animal reservoir now appears to be birds, but many experts are asking whether these viruses might also be able to infect pigs, another common reservoir for zoonotic infections. The viral sequence data indicate antiviral resistance to the adamantanes and susceptibility to neuraminidase inhibitors, except for a 292K mutation in the NA protein of the A/Shanghai/1/2012 virus. Because this mutation has been associated with in vitro resistance to neuraminidase inhibitors in another N9 NA subtype virus, additional analyses must be undertaken to understand its significance. It is not known whether this mutation arose de novo in the host or is associated with oseltamivir treatment. Ongoing surveillance is crucial to assessing the emergence and prevalence of H7N9 viruses resistant to available antivirals.

Since available diagnostic assays used in clinical care (e.g., rapid influenza diagnostic tests) may lack sensitivity to identify H7N9 virus and since existing molecular assays will identify H7N9 virus as a nonsubtypeable influenza A virus, a critical public health issue is the rapid development, validation, and deployment of molecular diagnostic assays that can specifically detect H7N9 viral RNA. Such assays have been developed in China and are in development in many countries including the United States, and they will be deployed as they were for the 2009 H1N1 pandemic.4 Having available H7-specific assays will facilitate surveillance of H7N9 virus infections and help address key questions such as the duration of viral shedding, the infectious period, the optimal clinical specimens for laboratory confirmation, and the spectrum of clinical illness.

The clinical features described in the three patients with H7N9 virus infection, including fulminant pneumonia, respiratory failure, acute respiratory distress syndrome (ARDS), septic shock, multiorgan failure, rhabdomyolysis, and encephalopathy, are very troubling. Clinical care of severely ill patients should be focused on evidence-based supportive management of complications such as ARDS. Adherence to recommended infection-control measures in clinical settings to reduce the risk of nosocomial transmission cannot be overemphasized.

All three patients with H7N9 virus infection reported by Gao and colleagues received late treatment with oseltamivir starting on day 7 or 8 of illness while critically ill. Data related to human infections with seasonal, pandemic, and HPAI H5N1 viruses indicate that the earlier antiviral treatment is initiated, the greater the clinical benefit. Therefore, oral oseltamivir or inhaled zanamivir should be administered to patients with suspected or confirmed H7N9 virus infection as soon as possible. Secondary invasive bacterial infections associated with influenza can cause severe and fatal complications, and appropriate empirical antibiotic treatment for community-acquired bacterial infections may be indicated for initial management of severe H7N9 pneumonia. Caution should be exercised regarding the use of glucocorticoids, which are not indicated for routine treatment of influenza. Clinical research, including randomized, controlled trials and observational studies, is urgently needed on new antiviral agents, including parenteral neuraminidase inhibitors and drugs with different mechanisms of action, combination antiviral treatment, and immunotherapy. To inform clinical management, rapid clinical data collection, data sharing, analysis, and timely feedback are needed worldwide.5

Because H7N9 virus infections have not occurred in humans before, it is expected that persons of all ages might be susceptible worldwide. Serologic assays must be developed so that studies can be conducted to determine whether some people have cross-reactive antibodies to these viruses from prior influenza A virus infections. Existing H7-vaccine viruses are not well matched to this novel H7N9 virus, and extensive efforts are under way to develop potential H7N9 vaccines as quickly as possible. These efforts have started worldwide using the H7N9 sequence data obtained from these early cases, and sharing of H7N9 viruses will further facilitate vaccine development. There are many challenges to making H7N9 vaccines available. Previously studied H7 vaccines were poorly immunogenic in humans, and clinical trials to assess the safety and immunogenicity of H7N9 vaccine candidates will be needed. But even if new vaccine manufacturing technologies, such as tissue-cell-culture–derived vaccine antigens, are utilized, the process from vaccine development to availability will probably take many months.

The 2009 H1N1 pandemic taught us many lessons, including that a pandemic virus can emerge from an animal reservoir in an unexpected location and be spread rapidly through air travel. The focus on critically ill adults early in the pandemic led to elevated public concern about pandemic severity. Clear communication of key messages to the public and the clinical community is critical in implementing successful prevention and control activities. The detection of human H7N9 virus infections is yet another reminder that we must continue to prepare for the next influenza pandemic. The coming weeks will reveal whether the epidemiology reflects only a widespread zoonosis, whether an H7N9 pandemic is beginning, or something in between. The key is intensified surveillance for H7N9 virus in humans and animals to help answer important questions. We cannot rest our guard.