European Report on Concrete Measures to Avoid Mixing of GM and Conventional Maize

A report presented by Health and Consumer Policy Commissioner John Dalli to the Agriculture Council concludes that specific measures relating to storing and the application of isolation distances can help limit or avoid the co-mingling of genetically modified (GM) maize with conventional and organic maize. In particular, the Best Practice Document, prepared by the European Coexistence Bureau (ECoB) and published by the European Commission's Joint Research Centre (JRC), notes that storing seeds adequately and applying spatial isolation are the best ways to limit or avoid co-mingling. Alternative practices based on temporal isolation (shifting flowering times of GM and non-GM fields) are possible in several EU countries with specific climatic conditions.

Presenting the report to the Agriculture Council, Commissioner in charge of Health and Consumer Policy, John Dalli, said: "The suggested practises contained in this important document are applicable within the framework of the Commission's new approach to coexistence and GMO cultivation adopted in July. They are in full accordance with the spirit and aims of the proposal, which provides Member States with more flexibility to organise the co-existence of GM, conventional and organic crops." To add : "This document details a set of non-binding practices, which aim to assist Member States develop and refine their national or regional approaches to co-existence."

Best Practice

The "best practice" document covers the cultivation of GM maize up to the first point of sale. It deals with three types of productions: grain, whole plant and sweet maize. The European Coexistence Bureau (ECoB) analysed the potential sources of admixture and reached a set of consensually agreed, best agricultural management practices that will ensure coexistence while maintaining the economic and agronomic efficiency of the farm.

For example, among other practices, the ECoB proposes isolation distances of 15-50m to reduce cross-pollination between GM maize and non-GM maize and to limit GMO content in conventional food and feed to levels below 0,9% (the legal labelling threshold). Larger distances (100-500 m) are proposed for lower targets of admixture levels (e.g. 0.1%, which is the usual estimate for the limits of quantification).

The European Coexistence Bureau

In 2006, the Council invited the Commission to further work on coexistence in order to identify best practices for technical segregation measures and to develop crop-specific guidelines for coexistence. The Commission created the ECoB in 2008.

The Bureau consists of experts nominated by interested Member States (20 Member States currently participate) and a scientific secretariat provided by the Joint Research Center's Institute for Prospective and Technological Studies (IPTS).

Work on the "best practice" document was carried out in close cooperation with stakeholders and the final outcome allows EU Member States the necessary flexibility to adapt the measures to their specific regional and local conditions.

Facts & Figures

In 2009, GM crops were cultivated worldwide on 134 million hectares. The main cultivating countries are the USA (48% of global GMO area), Brazil (16%) and Argentina (16%). The four main GM crops, either insect resistant or herbicide tolerant, are: soybean (77% of global soybean crop area), cotton (49% of global cotton crop area), maize (26% of global maize crop area), and rapeseed (21% of global rapeseed crop area).

In the EU, only three GM crops have been authorised for cultivation:

• Two GM maize products, of which only the insect-resistant Bt maize MON810 is cultivated in the EU.

• One GM potato (GM starch potato, authorised March 2010).

Background

On July 13, the Commission adopted a comprehensive proposal that provides the Member States the freedom to allow, restrict or ban the cultivation of GMOs on their territory, while keeping intact the EU's science-based GM authorisation system. The adopted package consisted of a new Recommendation on co-existence of GM crops with conventional and/or organic crops and a draft Regulation proposing a small change to the GMO legislation.

The proposal for revising Directive 2001/18/EC aimed to secure legal certainty for Member States when they decide on GMO cultivation on grounds other than science. It will be adopted through co-decision with the European Parliament and the Council.

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Why Don't Monkeys Infected With HIV-Like Viruses Get AIDS?

 Many strains of monkey become naturally infected with viruses that are related to HIV. These viruses are known collectively as SIV and naturally infected monkeys do not develop AIDS. It is hoped that understanding why monkeys naturally infected with SIV do not develop AIDS might teach researchers important lessons about the mechanisms underlying the development of AIDS in humans infected with HIV and identify ways to prevent this happening.

New insight into the mechanisms that control the number of virus particles in the blood of sooty mangabeys naturally infected with SIVsmm, the strain of SIV that naturally infects sooty mangabeys, has now been provided by a team of researchers from the University of Pennsylvania, Philadelphia, and Emory University, Atlanta.

HIV and SIV infect immune cells known as CD4+ T cells. So, the authors set out to determine how CD4+ T cells affected the number of virus particles in the blood of sooty mangabeys naturally infected with SIVsmm -- did they provide immune control of the number of virus particles or did they simply provide a place to live a replicate.

The number of SIVsmm particles in the blood of naturally infected sooty mangabeys decreased when the monkeys were depleted of CD4+ T cells and then increased again as the number of proliferating CD4+ T cells rebounded.

So, it was concluded that availability of proliferating CD4+ T cells is a key determinant of how many SIVsmm particles can be detected in the blood of naturally infected sooty mangabeys, rather than CD4+ T cells providing immune control of the virus.

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Malaria's Newest Pathway Into Human Cells Identified

Development of an effective vaccine for malaria is a step closer following identification of a key pathway used by the malaria parasite to infect human cells. The discovery, by researchers at The Walter and Eliza Hall Institute, provides a new vaccine target through which infection with the deadly disease could be prevented

Each year more than 400 million people contract malaria, and more than one million, mostly children, die from the disease. The most lethal form of malaria is caused by the parasite Plasmodium falciparum. Part of the parasite's success lies in its ability to deploy multiple ways to invade red blood cells, a process essential for the survival of the parasite within the human host.

Professor Alan Cowman, head of the institute's Infection and Immunity division, led the research with Dr Wai-Hong Tham, Dr Danny Wilson, Mr Sash Lopaticki, Mr Jason Corbin, Dr Dave Richard, Dr James Beeson from the institute and collaborators at the University of Edinburgh.

For decades, it has been known that malaria parasites use proteins called glycophorins as a means of entering red blood cells. This new research reveals an alternative pathway used by the parasite to enter red blood cells. The pathway does not involve glycophorins, instead requiring the binding of a parasite molecule named PfRh4 to Complement Receptor 1 (CR1), a common protein found on the surface of red blood cells.

"The parasite is like a master burglar - it will try a variety of different methods to get into the house, not just the front door," Professor Cowman said. "Although the human body has evolved a variety of methods to keep the parasite out, it keeps finding new ways to get in."

Professor Cowman said the PfRh family of surface proteins is involved in the recognition of red blood cell receptors, which allows the parasite to attach to the red blood cell surface and gain entry.

"We think that the parasite uses this protein to correctly identify the red blood cell and say 'Yes, this is the one we want to invade', it's like a quality assurance process," Professor Cowman said.

"The PfRh4-CR1 pathway is one of the most important of the pathways we've identified for entry of malaria parasites into cells," Professor Cowman said. "We are now at the stage where we have identified the best combination of proteins for a vaccine, and are ready to start clinical development.

"When both glycophorin and CR1 pathways are blocked, there is a 90 per cent decrease in infection of the cells with the parasite. These results suggest that if a vaccine were to stimulate the immune system to recognise and generate antibodies to the prevalent invasion pathways, there is a good chance it would lead to a significant decrease in malaria infection."

The research was published in the journal Proceedings of the National Academy of Sciences. The study was supported by the National Health and Medical Research Council of Australia, the Darwin Trust of Edinburgh, the Wellcome Trust and the Victorian Government.

Professor Alan Cowman has identified a new pathway used by the malaria parasite to infect human cells. (Credit: Image courtesy of Walter and Eliza Hall Institute)

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Interview Questions asked in Biotech Companies & Institutes Part 2

1. what is the difference between defined, characterised and standard serum? (JNU)
2. what is the difference between fermentor and bioreactor? (TITAN BIOTECH)
3. what is regenrative medicine?
4. Why is the RBC called as a cell even though it dont have all the characteristic features of a complete cell?
5. what are the shine-dalgarno sequences in organism other than E.coli.?
6. why life span of RBC IS GREATER THEN THE WBC?
7. Dubai is desert how it is possible it is becaming greenary
8. Size of Normal Land and bhosada
9. L-Tryptophan produced by a genetically modified bacteria caused many illnesses and deaths. Does this not prove that genetic modification can result in the production of toxic substances?
    

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Some Interview questions asked in Biotech Companies & Institutes

1. wat is the composition of glutathione? (BIOCON)
2. how much vol of sample u've 2 take to make 6mM solution.. if the Molr Wt is 164? (BIOCON)
3. Explain Gram Staining method?(BIOCON)
4. if protein in unknown solution,how will you determine it is protein?(IIT)
5. For which purpose Immunoblotting technique is used?(Biological.e.limited)
6. The absorbance of protein at 280 nm is due to which amino acid?(IGCAR)
7. The number of chromosomes in the triploid variety of a plant is 72...what is the number of chromosomes in a diploid genome of the same plant?? (IGCAR)
8. Who is the real father of biotechnology?

You all can also post the questions which you encountered in your interview

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New technique uncovers hidden insecticide resistance

A new technique pioneered at Liverpool School of Tropical Medicine (LSTM) is improving the detection and monitoring of insecticide resistance in field populations of an important malaria-carrying mosquito.

Researchers at LSTM, led by Dr Charles Wondji have developed a new technique which encourages the female Anopheles funestus mosquitoes to lay eggs which are then reared into adult mosquitoes to provide sufficient numbers to determine levels of insecticide resistance and to characterise the underlying mechanisms.

Explaining the significance, John Morgan, who designed the technique, said: "Malaria is the main cause of death in Uganda with some 12 million cases recorded annually. The Ministry of Health relies heavily on insecticide treated nets and spraying to control mosquitoes. The effectiveness of those control programmes depends on the ability to detect and monitor insecticide resistance. "

The An. funestus mosquito is difficult to collect and rear from the field and hence published studies of insecticide resistance in this species are limited. This new forced egg laying technique encourages the females to lay eggs which we were then able to rear into viable populations.

"This allowed us to study levels of resistance to particular insecticides and in doing so, we have been able to find the first documented resistance to pyrethroid/DDT insecticides in East Africa. This will enable researchers to map the distribution of this resistance and allow the Ministry of Health to modify its vector control programme, thereby increasing its effectiveness and helping to reduce the transmission of malaria."

Source: The paper is published in PLoS ONE. Provided by Liverpool School of Tropical Medicine

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Acute Pain Is Eased With the Touch of a Hand, Study Shows

There may be a very good reason that people naturally clutch their hand after receiving an injury. A new report published online Sept. 23 in Current Biology shows that self-touch offers significant relief for acute pain under experimental conditions. The researchers suggest that the relief comes from a change in the brain's representation of the rest of the body.

"Pain is quite an important, but also complicated, experience and can be caused in many different ways," said Patrick Haggard of University College London. "We show that levels of acute pain depend not just on the signals sent to the brain, but also on how the brain integrates these signals into a coherent representation of the body as a whole."

Haggard and his colleague Marjolein Kammers, also of University College London, made the discovery by studying the effects of self-touch in people who were made to feel pain using an experimental condition known as the thermal grill illusion (TGI). "The TGI is one of the best-established laboratory methods for studying pain perception," Haggard explained. "In our version, the index and ring fingers are placed in warm water and the middle finger in cold water. This generates a paradoxical feeling that the middle finger is painfully hot." That's ideal because it allows scientists to study the experience of pain without actually causing any injury to those who participate in the studies.

When TGI was induced in an individual's two hands and then the three fingers of one hand were touched to the same fingers on the other hand immediately afterwards, the painful heat experienced by the middle finger dropped by 64 percent compared to a condition without self-touch. That relief didn't come when only one hand was placed under TGI conditions. Partial self-touch in which only one or two fingers were pressed against each other didn't work either. Nor did it work to press the affected hand against an experimenter's hand that had also been warmed and cooled in the same way.

"In sum," the researchers wrote, "TGI was reduced only when thermosensory and tactile information from all three fingers was fully integrated. That is, TGI reduction required a highly coherent somatosensory pattern, including coherence between tactile and thermal patterns and coherence of stimuli between the two hands."

Haggard said that earlier studies of chronic pain had suggested the importance of body representation in the experience of pain. For example, the phantom pain that is often felt following amputation of a limb appears to lessen with time as the brain converges on an updated representation of the body. Haggard said the new findings extend the important role of body representation to acute pain and may lead to a better understanding of the brain mechanisms involved in chronic pain as well.

The findings might be put to practical use, the researchers say. "Our work suggests that therapies aimed at strengthening the multisensory representation of the body may be effective in reducing pain," Haggard said.

The researchers include Marjolein P.M. Kammers, Institute of Cognitive Neuroscience, University College London, Alexandra House, London, UK; Frederique de Vignemont, Institut Jean-Nicod, CNRS/EHESS/ENS, Paris, France; Transitions NYU-CNRS, New York, NY; and Patrick Haggard, Institute of Cognitive Neuroscience, University College London, Alexandra House, London, UK.

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Hybrid Protein Developed as Tools for Gene Cutting, Editing

A U.S. team of researchers has developed a kind of hybrid proteins that can make double-strand DNA breaks at specific sites in living cells, potentially leading to better gene replacement and gene editing therapies.

Dr. Bing Yang, assistant professor of genetics, development and cell biology at Iowa State University (ISU; Ames, USA;), and his colleagues developed the hybrid protein by joining parts of two different bacterial proteins. One is called a TAL (transcription activator-like) effector, which functions to find the specific site on the gene that needs to be cut, and the other is an enzyme called a nuclease that cuts the DNA strands. Dr. Yang hopes this study will lead to the ability to engineer genomes by cutting out defective or undesirable parts of DNA, or by replacing defective or undesirable gene segments with a functioning piece of replacement DNA--a process called homologous recombination.

Dr. Yang reported that these hybrid proteins could be constructed to locate specific segments of the DNA in any sort of organism. "This breakthrough could eventually make it possible to efficiently modify plant, animal and even human genomes," said Dr. Yang. "It should be effective in a range of organisms."

The proteins function by binding onto the specific segment of DNA the researcher needs to change. These proteins do this by reading the DNA sequence and finding the specific area to be cut. Once the protein binds onto the DNA at the correct spot, the other half of the protein then cuts the double-stranded DNA. Bad or undesirable DNA can be resected and good or more desirable DNA can be introduced. When the DNA heals, the good DNA is included in the gene.

Dr. Yang began his project approximately one year ago after seeing the results of research by Dr. Adam Bogdanove, ISU associate professor of plant pathology, showing that TAL effectors use a very clear-cut code to bind to a specific DNA sequence. This discovery allowed Dr. Yang to predict precisely where the TAL effector nuclease will bind on the DNA to make the cut. Another study had similar results.

The conecept has also been validated by Dr. Bogdanove and Dr. Dan Voytas, collaborator in genetics, development, and cell biology at Iowa State, and director of the Center for Genome Engineering at the University of Minnesota (Twin Cities, USA). The TAL effector-nuclease approach improves on tools currently available for genome modification. It should be faster and less expensive to make TAL effector nucleases, and simpler to design them to recognize specific DNA sequences, according to Dr. Yang.

Yang's findings appeared in August 2010 in the online version of the journal Nucleic Acids Research. Dr. Voytas' and Bogdanove's study also appeared in August 2010 the journal Genetics. Dr. Voytas and Dr. Bogdanove were also able to demonstrate that the TAL effector part of the hybrid protein can be modified to target new DNA sequences.

The above story is reprinted from materials provided by USDA/Agricultural Research Service. The original article was written by Dennis O'Brien.

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Structure That Allows Bacteria to Resist Drugs Identified

A research team led by Edward Yu of Iowa State University and the Ames Laboratory has discovered the crystal structures of pumps that remove heavy metal toxins from bacteria, making them resistant to antibiotics.

The findings are published in the Sept. 23 issue of the journal Nature.

Yu -- an Iowa State associate professor of chemistry, of physics and astronomy, of biochemistry, biophysics and molecular biology and an associate of the U.S. Department of Energy's Ames Laboratory -- said the finding gives researchers a better understanding of bacterial resistance to antibiotics. Ultimately it could help drug researchers develop treatments to combat that resistance.

To make their findings, the researchers purified and crystallized the membrane proteins that make up an efflux pump of E. coli bacteria. The researchers prepared some samples that contained the toxic heavy metals copper and silver and some that did not.

The researchers used X-ray crystallography to compare the various structures, identify the differences and understand the mechanism that removes heavy-metal toxins from cells.

Their paper specifically describes the crystal structure of CusA, one of three parts of the pumps responsible for removing toxins from bacteria. Yu said CusA is an inner membrane transporter which belongs to the resistance-nodulation-division protein superfamily. It consists of 1,047 amino acid residues and spans the inner membrane 12 times.

What those pumps do, Yu wrote in a summary of his research, is "recognize and actively export these substances out of bacterial cells, thereby allowing the bugs to survive in extremely toxic conditions."

The research project was supported by the National Institutes of Health. In addition to Yu, the research team includes Robert Jernigan, an Iowa State professor of biochemistry, biophysics and molecular biology and director of Iowa State's Laurence H. Baker Center for Bioinformatics and Biological Statistics; Kanagalaghatta Rajashankar, the operations team leader for the Northeastern Collaborative Access Team facility at Argonne National Laboratory in Argonne, Ill., that's managed by Cornell University in Ithaca, N.Y.; Iowa State post-doctoral researchers Feng Long and Chih-Chia Su; and Iowa State graduate students Michael Zimmermann and Scott Boyken.

"This work reports the first detailed structure of a unique heavy metal transporter that enables bacteria to survive the toxic effects of silver and copper," said Jean Chin, Ph.D., who oversees this and other structural biology grants at the National Institutes of Health. "By detailing the exact steps that a metal ion is likely to take through the transporter, this study suggests how we might block the pathway and render pathogenic bacteria sensitive to heavy metal toxins."

Yu, who has been studying bacterial resistance to antibiotics for nearly a decade, said direct information about how bacteria handle heavy-metal toxins is important information for biomedical researchers.

"We want to understand the mechanisms of these heavy-metal pumps," he said. "And that could allow biotechnology researchers to make inhibitors to stop the pump and the antibiotic resistance."

Journal Reference:

1. Feng Long, Chih-Chia Su, Michael T. Zimmermann, Scott E. Boyken, Kanagalaghatta R. Rajashankar, Robert L. Jernigan, Edward W. Yu. Crystal structures of the CusA efflux pump suggest methionine-mediated metal transport. Nature, 2010; 467 (7314): 484 DOI:10.1038/nature09395

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Can Stress Control Our Genes ?

People  experience stress as something that affects  their  entire body and mind, the causes of which are plentiful. But if we zoom in on the building bricks of the body, our cells, stress and its causes are defined somewhat differently. Stress can arise at the cellular level after exposure to pollution, tobacco smoke, bacterial toxins etc, where stressed cells have to react to survive and maintain their normal function. In worst case scenario, cellular stress can lead to development of disease.

    Researchers from Dr. Klaus Hansen's group at BRIC, University of Copenhagen, have just shown that external factors can stress our cells through the control of our genes.

    "We found that stress-activating factors can control our genes by turning on certain genes that were supposed to be silenced. It is very important that some genes are on and others are off in order to ensure normal foetal development and correct function of our cells later in life," says Hansen.
         Simmi Gehani, PhD-student in the Hansen group, found that exposing human cells to a stress-activating compound turned on silenced genes. Even brief changes in gene activation can be disastrous during foetal development as establishment of correct cellular identity can be disturbed in our cells. But altered gene activity can also have consequences in the adult body. "For example, one could imagine that prolonged stress causes nerve cells in the brain to produce hormones and other signalling molecules they do not normally produce and this can disturb normal brain function," says Gehani.
        The Hansen research group is very interested in understanding how our genes are turned on and off. "We know that different protein complexes can associate with specific proteins (histones) to which DNA is wound around and thereby determine whether the genes are active or inactive. Small chemical groups can cause protein complexes to bind to histones and these can control gene activity" says Hansen. The researchers have studied in detail a complex called PRC2. PRC2 can attach small chemical groups -- methyl groups -- to the histones. Protective complexes can bind to the histones when this marker is present and the genes are turned off. Their new results show that the protective complexes are lost and selected genes turned on when cells are exposed to external stress factors. The reason why the complexes are lost is that the stress factors instruct an enzyme named MSK to attach another chemical group -- a phosphate group -- to the histones neighbouring the methyl group. The phosphate group neutralises the effect of the methyl group and turns specific genes on.

 "The consequence is that genes that should be turned off are now active and this may disturb cellular development, identity and growth," says Gehani. This means that without damaging our genetic code external stress factors can control the activity of our genes.
  The results are published in the journal Molecular Cell
 

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