VATIS Update Biotechnology . May-Jun 2007

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Biotechnology May-Jun 2007

ISSN: 0971-5622

VATIS Update Biotechnology is published 4 times a year to keep the readers up to date of most of the relevant and latest technological developments and events in the field of Biotechnology. The Update is tailored to policy-makers, industries and technology transfer intermediaries.

Co-publisher: Biotech Consortium India Ltd
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Indian biotech industry shows impressive growth

Indias biotechnology sector, which closed at US$ 1.5 billion mark in 2005-06, is expected to touch US$5 billion by 2010. The sector is growing at a CAGR of 35 per cent. At present, India has over 300 biotech firms focusing on different aspects of value chain and their number is going to be more than double in next three to four years, says a release from Assocham.

In a paper on Biotechnology Future, Assocham points out that although much smaller in size than the IT and BPO sectors, the domestic biotech sector is witnessing similar growth and growth prospects. For instance, during 2005-06, the sector closed at around US$1.5 billion, and grew by 35 per cent for the second year in a row. Bio pharma, the largest segment of biotech industry, grew by 32 per cent to US$1 billion. Exports were at US$763 million, and accounted for 52 per cent share of total industrys revenues. Bio pharma accounted for 75 per cent of the total exports and 70 per cent of domestic sales.

Agri-biotech and bio services are registering the fastest growth. Investments in the sector have crossed US$360 million in 2005-06, growing 36 per cent over previous year, the paper reports. India has more than 300 biotech firms focusing on different aspects of the value chain. However, about half of the revenues are concentrated with the top 10 firms. The biotech sector would have the potential to attract funding from international agencies such as World Bank and International Finance Corporation, banks, venture capital funds, as well as private equity, the paper says.


Argentina to centralize research at scientific hub

The Government of Argentina plans to establish a hub of research institutions to facilitate collaboration and discussion between Latin American scientists. It plans to gather all of its scientific institutions, selected research and teaching institutes a science museum and a convention centre in the same location Palermo, Buenos Aires. The 48,000 square-metre site will host the main headquarters of the Science & Technology Secretary, the National Scientific and Technical Research Council (CONICET), and the National Scientific Promotion Agency. At least three research institutes are planned for the complex in the fields of biomedical science, technology and humanities. International centres have been invited to take part, either by establishing a laboratory within the complex or sponsoring research. Construction is due to begin in 2008 and the government hopes that the facility will be ready by 2009.

Mr. Lino Baraao, president of the National Scientific Promotion Agency, said that Germanys Max Planck Institute had already confirmed its participation. He added, We are also talking with the International Centre for Genetic Engineering and Biotechnology, which has venues in Trieste, Italy, and New Delhi, India, among other institutions.


China and Europe form new alliance in bioethics

Bioethicists and life scientists from Europe and China have formed a new expert group to promote ethical behaviour in biomedical research in both regions. The Ethical Expert Group of BIONET consisting of leading European-Chinese bioethicists and biomedical researchers was formed at a meeting in Beijing in the first week of April.

The groups chair, Dr. Christoph Rehmann-Sutter, a professor of bioethics at the University of Basel, Switzerland, said they would hold four workshops and two conferences in China over the next three years. These will discuss ethical issues raised in research fields, in which European Union (EU) and China cooperate, as well as other biomedical research. Issues discussed will include challenges and approaches to the ethical governance of advanced biological and biomedical research in China, the promotion of comparative research on ethical governance in China and the EU, and methods to improve the publics understanding of key bioethical issues. They will also cover the ethical aspects of topics such as stem cell research, reproductive technologies, clinical trials and informed consent for clinical research.

By the end of 2009, the expert group will make a series of policy recommendations for the promotion of ethical governance in biomedical research in China and the EU. I believe BIONET will help standardize [Chinas bioethics] practice so that we can protect the interests of the common people, says Dr. Lu Guangxiu, a professor of bioethics at the Institute of Human Reproduction and Stem Cell Engineering in Chinas Hunan Province. Dr. Ole Dring, a bioethics expert at the Institute of Asian Affairs in Hamburg, Germany, says that the BIONET partnership will benefit Europe too. In China, the implementation of bioethical rules is often very diversified and complicated. By learning how to cope with these situations, European countries can make more applicable and practical ethical governance in the life sciences, he says.


Egypt and Sudan strengthen scientific ties

Sudan and Egypt signed an agreement to cooperate on science and technology at a meeting of the Joint Higher Sudan-Egypt Committee in Khartoum, Sudan in April. The cooperation will be in the fields of agriculture, irrigation, environment and land reclamation, energy, industry infrastructure, health, food sciences, higher education, and information and communication technologies.

Egypt will provide assistance to the water sector in southern Sudan by developing local capacity and providing technical equipment, assessing water resources and constructing small-scale dams, and forecasting flooding and drought. The two countries will also carry out evaluations of the Jonglei Canal project a long-term water conservation initiative designed to exploit the resources of the River Nile by diverting water into the Jonglei Canal for distribution.

In addition to the existing Khartoum branch of Cairo University, Egypt will establish a branch of Alexandria University in the southern Sudanese city of Juba. The Sudanese government will donate land in Khartoum to the proposed Arab Federation of Scientific Research.

The federation will coordinate and support science organizations to establish a knowledge-based economy in the Arab world, and promote science for development. Sudan will also donate land to set up specialized scientific centres in areas such as biotechnology, nano-technology, information technology and renewable energy.


Indian tie-up to develop next generation AIDS vaccine

Indias Department of Biotechnology (DBT) and the United States-based International AIDS Vaccine Initiative (IAVI) have signed an agreement today to address a major obstacle in AIDS vaccine development: the design of candidate vaccines to elicit neutralizing antibodies against HIV. A new Indian Medicinal Chemistry Programme, jointly sponsored and funded by IAVI and the DBT, will comprise top scientists from both countries tasked with accelerating the pace of AIDS vaccine discovery and developing creative concepts for the next generation of AIDS vaccines.

The Indian Programme will complement the work of IAVIs antibody consortium (NAC), a team of internationally recognized scientists working on the neutralizing antibody challenge. Researchers believe an ideal AIDS vaccine must evoke an antibody response that can block HIV from entering healthy cells, as well as reduce the amount of viral dissemination through a cell-mediated immune response to HIV-infected cells. Yet today, nearly all current vaccine candidates in the pipeline are based on cell-mediated immune responses alone, failing to target the second critical arm of the human immune system. The first component of the DBT-IAVI programme will be a collaboration of researchers from different academic research laboratories to design new HIV antigens.


South African grant for phytopharma research

In South Africa, the plant biotechnology research group at the Council for Scientific and Industrial Research (CSIR) has secured a multimillion-rand research grant from the Department of Science and Technology (DST) to extend research into transgenic plants as a platform for the production of pharmaceuticals. Plant biotechnology research group leader Dr. Rachel Chikwamba reports that the substantial grant will assist the group in expanding its investigations.

The funding has been earmarked for the CSIRs contribution to the Pharma-Planta initiative, a European Commission-funded consortium, researching plant-expressed clinical-grade pharmaceuticals against various diseases, including rabies and HIV. The CSIR in collaboration with other local partners is expected to develop a transgenic plant-based platform for the production of recombinant pharmaceuticals in plants, while government and non-governmental organizations will develop the ethical and regulatory protocols.
The project is of strategic value to South Africa and the region and, if successful, could have a major impact on the local pharmaceutical industry. It will increase the competitiveness of existing local pharmaceutical industries and possibly new players in the industry. CSIRs tasks include the genetic transformation of plants with the experimental pharmaceutical molecules, growing the transgenic plants in a contained environment and subsequent downstream processing.


British and German farmers open to GM crops

New surveys suggest that fewer farmers in the United Kingdom and Germany are opposed to planting genetically modified (GM) crops than is often believed.

About 47 per cent of surveyed farmers in the United Kingdom and 33 per cent in Germany are willing to cultivate GM plants. However, 16 per cent in the United Kingdom and 29 per cent in Germany reject the concept of GM crops, while many farmers are still undecided.

The British Grassland Society, United Kingdom, polled its members on their attitude towards GM crops. Strict opposition was expressed, surprisingly, by only 16 per cent among responding farmers, half of whom are organic growers. While 47 per cent generally favour GM crops, as many as 75 per cent stated that they would grow GM plants if consumers were willing to buy them.

In another survey, 370 farmers in the German north-west were interviewed by researchers from the University of Gttingen. The majority, 38 per cent, were undecided on this issue. However, representing a fairly even split in decided attitudes, 33 per cent of farmers welcomed GM crops and 29 per cent rejected them.



Arcadia and SESVanderHave reach agreement for sugar beets development

Arcadia Biosciences Inc., the United States, and SESVanderHave, based in Belgium, have signed an agreement to develop and commercialize sugar beet varieties efficient in nitrogen use, employing Arcadia technology and SESVanderHave seed and plant breeding capabilities. Under the agreement SESVanderHave gets an exclusive global licence to develop and commercialize sugar beets using Arcadias proprietary nitrogen use efficiency (NUE) technology. Arcadia receives technology licence fees and a share of commercial revenue from future product sales. The companies will form a collaboration to optimize research, product development and commercial activities.

Todays sugar beet farmers are under significant cost and environmental pressure, said Mr. John Akers, SESVanderHaves President and CEO. Although NUE sugar beets would not be commercialized for a number of years in the future, we need to start looking for solutions now if our customers are to remain competitive and able to do their part to protect our environment.


BioServe acquires Genomics Collaborative

BioServe Clinical Research, with headquarters in India and the United States, has acquired Genomics Collaborative from SeraCare Life Sciences Inc., the United States. According to BioServe, Genomics Collaborative is a leader in facilitating biomarker discovery and validation through its Global Repository, a comprehensive library of 600,000 human DNA, tissue and serum samples linked to detailed clinical and demographic data from 140,000 patients collected on four continents.

Through this acquisition BioServe expands its pre-clinical product and service capabilities to provide organizations engaged in drug discovery and diagnostic development with a comprehensive biomaterial to validated data services platform. This service platform extends from molecular research products and services such as DNA and RNA purification reagents, DNA sequencing, oligonucleotide synthesis and genotyping to ready-made large epidemiologically sound case-control studies of inflammatory disorders, endocrine disorders, cardiovascular diseases, hypertension, diabetes, obesity, and cancers including breast, prostate, lung and colorectal.

Working with BioServe, drug discovery researchers have the flexibility to tap the Bio Repository to augment their in house sample sets, design entire genomic studies around our sample library, and further benefit from BioServes proven ability to process and analyse vast quantities of genomic content, said Mr. Rama Modali, President, BioServe. Genomics Collaborative will operate as a fully integrated division of BioServe, offering its DNA, tissue and serum Global Repository samples to BioServes customers worldwide.


Manipal Group join Malaysian Biotech for stem cell research

Manipal Education and Medical Group (MEMG) of India and Malaysian Biotechnology Corporation (MBC), a leading Biotechnology agency in Malaysia, have signed an MoU to facilitate advanced stem cell research and development in Malaysia. The MoU was signed by Dr. Ramdas Pai, MEMG Chairman, and Mr. Tan Sri Ahmad Zaharuddin Idrus from MBC, in the presence of Datuk Seri Najib Tun Razak, the Malaysian Deputy Prime Minister. This MoU will result in MEMG setting up a subsidiary in Malaysia to focus on biotechnological advancements and showcase its expertise in stem cell research.

Stempeutics, an MEMG subsidiary, is one of the leading Stem Cell research organizations in India and is dedicated to developing cell-based therapeutics to treat human diseases using human embryonic or adult stem cells. It has seven stem cell research groups and has made significant inroads and innovations in the field of mesenchymal stem cells, human embryonic stem cells, neuro regeneration, cancer biology, diabetes research and cardio-vascular research. It is currently undertaking clinical trials for the treatment of damaged myocardium, spinal cord injury and limb ischemia by autologous transplantation of bone marrow stem cells.


Biotechnica and Interphex announce partnership

Biotechnica is partnering with the Interphex in 2008 to create a global meeting-place for companies engaged in the core pharmaceutical and biotech sectors, including process development and R&D through services, manufacturing and packaging. The agreement between Deutsche Messe, Germany, and Reed Exhibitions, the United States, further integrates the pharmaceutical and biotech industries by offering a single venue that serves as a platform for the entire marketplace.
The event shall be the biggest gathering of the life sciences industry on the North American continent.

Biotechnica and Interphex will provide an entire spectrum of R&D and upstream and downstream processing technologies. Biotechnica and Interphex debut at the Pennsylvania Convention Centre, Philadelphia, from 26-28 March 2008. By virtue of this co-operation agreement the Biotechnica product family will now be represented on three important continents: Europe, North America and Asia, said the Director of Deutsche Messe, Mr. Jrgen Frstenberg-Brock.


Lexicon-Genentech collaboration for potential therapeutic targets

A collaboration between Lexicon Genetics Inc. and Genentech Inc., both in the United States, has yielded potential therapeutic targets. Lexicon has developed antibodies for one of these targets, designated LG842, which it is now advancing through pre-clinical research. Data revealed that the deletion or neutralization of LG842, a circulating protein expressed predominantly in adipose tissue, placenta, pancreas and liver, resulted in lower triglycerides and cholesterol in vivo models. We believe that our collaboration with Genentech has been enormously fruitful. We have been able to elucidate the function of a number of genes that have shown promise in important areas of medicine, said Dr. Brian P. Zambrowicz, Lexicons chief scientific officer. Lexicon can choose six targets from the collaboration to advance into biotherapeutics drug discovery efforts. LG842 was the first of the two targets chosen by Lexicon for internal development.


BASF and Monsanto in R&D and commercialization deal

BASF and Monsanto Company have announced a long-term joint research and development and commercialization collaboration in plant biotechnology that will focus on the development of high-yielding crops and crops that are more tolerant to adverse environmental conditions such as drought. The collaboration is effective immediately. Over the life of the collaboration, the two companies will invest a joint budget of about US$1.5 billion to fund a dedicated pipeline of high-yield and stress-tolerance traits for corn, soybeans, cotton and canola. The first product developed as part of this collaboration would be commercialized in the first half of the next decade.
Under this collaboration, the companies will share profits associated with commercialized products, with Monsanto receiving 60 per cent and BASF 40 per cent of net profits. Other aspects are:
  • The companies will establish and collaboratively manage a dedicated pipeline that will focus on the development of crops with higher yields and crops that lead to consistent yields under adverse environmental conditions such as drought.
  • Each company will additionally maintain independent trait discovery programmes.
  • From the various programmes, each company will nominate specific candidate genes and the most promising candidates will be advanced for accelerated joint development and for commercialization in the Monsanto pipeline.
  • The companies expect to generate a greater number of viable research projects than they could have done on their own, accelerate the development of new products, and bring a greater number of traits to the market at a faster speed.
  • The nominated projects will be jointly funded at a 50-50 cost sharing through each phase of development, as the candidate gene works its way towards commercial status.
  • Monsanto will commercialize the products that emerge from the joint development.



The gene behind sophisticated brain function

Researchers from the Yale University School of Medicine, the United States, have reported a gene, found exclusively and at high levels in the brain, that appears to be a key player in enabling more sophisticated brain function. The finding about the gene, dynamin 1, could have widespread implications since members of the dynamin gene family are needed for the body to absorb nutrients, to grow, to respond to insulin, and even for viruses to gain entry into cells.

Dynamin 1 encodes a protein implicated in endocytosis, cells absorbing material from the outside by engulfing it with their cell membranes. There has been considerable evidence that dynamin 1 is required for a specialized form of endocytosis in brain cells that is responsible for generating the synaptic vesicles that store and release neurotransmitter. The researchers disrupted the gene in mice to test this hypothesis, and found that the mice developed normally up until the time of birth. They were initially able to move and feed just like the other mice.

Only subsequently did the mutant mice develop neurological impairments and a failure to thrive that led to death within two weeks after birth.

It was quite striking that their nervous system could support synaptic transmission in the absence of dynamin 1, which is by far the major brain dynamin, said Prof. Pietro DeCamilli of Howard Hughes Medical Institute, who led the study. He said the properties of dynamin 1 and its binding partners that make them optimally adapted to function in the context of a simulated synapse are being investigated. It is expected that these studies will reveal new important features of synaptic physiology.


Master regulatory gene of epithelial stem cells

The skins ability to replace the tissue it sloughs off is controlled by a variety of genes. A new study from Harvard Medical School, the United States, has identified a master regulator of this regeneration process not only for skin, but also for many epithelial tissues including breast, prostate and urogenital tract. This master regulator of epithelial stem cells turns out to be the p63 gene, a close relative to p53, the gene known as a tumour suppressor. Without p63, mutant mice run out of the regenerative epithelial stem cells. The findings also have implications for cancers of the skin, breast and prostate, which are among the most common human malignancies.

The role of p63 in epithelial stem cells has been controversial. Some studies found that p63 maintains a steady pool of the regenerative cells, while other studies argued that p63 has more to do with causing the cells to differentiate into particular types of tissue. The study, which was led by Dr. Frank McKeon, a professor of cell biology, shows that p63s role is not in tissue differentiation but rather to impart stemness to the regenerative cells in these tissues.

Having established that p63 was only important to the maintenance of stem cells, Dr. McKeon and his team used the epithelial stem cell cloning methods developed by his colleague Dr. Howard Green to show that p63s key function was to provide the enhanced potential of stem cells to divide. The fact that p63 is essential for these epithelial stem cells, while other master regulators have been identified for blood stem cells and spermatocyte stem cells, suggests a fundamental requirement for tissue specificity of these regulators that we dont understand, said Dr. McKeon.


Zorro-LNA, new agent to fight genetic disorders

A study by researchers from the Karolinska Institute in Stockholm, Sweden, has described the development of Zorro-locked nucleic acid (Zorro-LNA) to bind with both strands of a genes DNA simultaneously, thereby effectively disabling that gene. This development has clinical implications for virtually every human condition caused by or worsened by dominant defective genes, such as: Huntingtons disease, familial high cholesterol, polycystic kidney disease, certain instances of glaucoma and colorectal cancer, and neurofibromatosis.

The findings of this study significantly raise the possibility that new therapies could arise where defective DNA is deactivated more completely and more thoroughly than ever before. For instance, Zorro-LNA could be used in combination with RNA interference (RNAi). Like Zorro-LNA, RNAi has the ability to deactivate genes, but does so by degrading the genes RNA. In addition, Zorro-LNA could be used to deactivate certain genes in stem cells, which could eventually lead to the development of new cells, tissues or organs.

One might say these researchers have found a gene-hunters Holy Grail for which scientists have been hunting for many years, said Dr. Gerald Weissmann, Editor-in-Chief of The FASEB Journal in which the study appeared.


Gene that specifically links calorie restriction to longevity

Earlier studies had shown that mice and many other species subsisting on a severely calorie-restricted diet have consistently outlive their well-fed peers by as much as 40 per cent. But just how such a diet extends lifespan has remained elusive. Now, researchers at the Salk Institute for Biological Studies, the United States, have identified a critical gene that specifically links calorie restriction (CR) to longevity. This opens the door to development of drugs that mimic the effects of calorie restriction and might allow people to reap health benefits without having to adhere to an austere regimen.

The researchers led by Dr. Andrew Dillin from the Molecular and Cell Biology Laboratory found that in the roundworm Caenorhabditis elegans, signals that passed down the insulin/IGF-1 pathway regulate a DNA-binding protein called DAF-16, which belongs to the forkhead family. DAF-16 then regulated expression of genes associated with longevity, it was believed. Dr. Dillin had also identified SMK-1, a co-regulator in the pathway that apparently worked with DAF-16. The scientists were surprised to find that SMK-1, not DAF-16, was necessary for CR-mediated longevity.

The researchers then set out to find which of the 15 other forkhead-like factors expressed in C. elegans teams up with SMK-1 to delay aging in the CR-response. They discovered that the loss of only one gene that encodes the protein PHA-4 negates the effect of CR in worms. PHA-4s over-expression in worms enhanced the longevity effect, thus confirming their finding. Humans have three genes highly similar to worm PHA-4, all belonging to what is called the Foxa family. All three play an important role in development and then later on in the regulation of glucagon, a pancreatic hormone that, unlike insulin, increases the concentration of blood sugar and maintains the bodys energy balance, especially during fasting.


Trigger for genetic shut down in healthy immune cells

Researchers at University of Pittsburgh School of Medicine, the United States, have discovered a fundamental genetic mechanism, called somatic stop-codon mutation, that shuts down an important gene in healthy immune system cells. This kind of loss-of-function mutation can be very dangerous, and it is the first such mutation that has been identified in normal immune cells in blood, said Dr. Bora E. Baysal, assistant professor of obstetrics, gynaecology & reproductive sciences at the university. The finding could lead to new therapies against infections and cancers.

Dr. Baysal and his team tested 180 samples, including blood from healthy individuals and other material from those with childhood leukaemia, looking at specific portions of DNA in immune cells known as monocytes, natural killer cells and lymphocytes cells that are key to the bodys immune response against infection and disease. They found somatic stop-codon mutations in an average of 5.8 per cent of crucial portions of genetic material that deliver instructions from DNA, called messenger RNA (mRNA), in normal blood samples and in a quarter of leukaemia samples.

Dr. Baysal said that stop-codon mutation is a kind of permanent off switch that has escaped DNA repair. Earlier research on the mutated gene had suggested the stop-codon mutation might be part of the programmed adaptive response to oxygen deprivation. This mutation and its location are unusual because it predicts loss of function, it targets a classical tumour-suppressor gene, and it occurs in peripheral blood mononuclear cells, said Dr. Baysal, adding that the mutation is present at much higher levels in mRNA compared with DNA. He sees it as a tool to modify the immune cells survival in a low oxygen environment, to help the cells to survive and fight infections and tumours.


New light on long-sought cold sensation gene

A discovery at the Scripps Research Institute, the United States, might one day lead to the development of drugs that induce cold sensation as an analgesic, or block it to prevent certain forms of chronic pain associated with cold sensation. The study represents the first demonstration that a single gene, TRPM8, is responsible for most cool temperature sensation. The gene was discovered by Dr. Ardem Patapoutian and his team, who proposed it as a key gene controlling cold sensation. It codes for an ion channel found at the tips of sensory neurons, which innervate the skin. When opened, ions flowing through TRPM8 lead to the activation of the sensory neuron, which in turn sends a signal to the brain.

In experiments, mice without TRPM8 showed no preference in the temperature range of 18 to 31C, suggesting their ability to sense this range was completely disabled without the gene. Normal mice, on the contrary, found cold temperature unpleasant, clearly preferring warmer areas. The altered mice also showed little response to the application of acetone, which causes cold sensation, to their hind paw, while the acetone caused normal mice to flick their paw and lick them.

TRPM8 acts as a gate, says Dr. Ajay Dhaka, lead author of the study. At warm temperature it remains closed, but opens when exposed to cool temperature. The TRPM8-deficient mice did not lose their ability to feel pain in response to extreme cold, suggesting that other genes are responsible for this facet of cold sensation. The researchers also tested the analgesic effect of cold. They injected the mice with small amounts of a pain-causing chemical, formalin, and then exposed the affected paw to a cold plate. Cold plate reduced the acute pain felt by control mice, while TRPM8-deficient mice had no pain relief, suggesting that cold activation of TRPM8 can mediate some of the analgesic effects of cold.



Some degenerative diseases similar at molecular level

Alzheimers disease, Parkinsons disease, type 2 diabetes, the human version of mad cow disease, and other degenerative diseases are more closely related at the molecular level than previously realized, says a team of researchers. While still preliminary, the research could help scientists develop tools for diagnosing such diseases, and potentially for treating them through structure-based drug design, said a research team member Dr. David Eisenberg, a molecular biologist and a chemist at the University of California Los Angeles, the United States.

The researchers studied the harmful rope-like structures known as amyloid fibrils, linked protein molecules that form in the brain. The fibrils have a stack of watertight molecular zippers. With each disease, a different protein transforms into amyloid fibrils, but all those diseases are similar at the molecular level, says Dr. Eisenberg. If the molecular zipper is universal in amyloid fibrils, it might be possible to pry open the zipper or prevent its formation. His research team used X-ray analysis and a sophisticated computer algorithm to study proteins known to be associated with human diseases. When the computer said a protein will form an amyloid fibril, it almost always did.


Vaccine protection against vCJD

Scientists say they have a vaccine that stops mice getting a brain disease similar to bovine spongiform encephalopathy (BSE) in cattle and which may ultimately protect humans against variant Creutzfeldt-Jakob disease (vCJD), BSEs human version. A vaccine that checks the spread of prion disease in animals would reduce the risk of spread in humans too, says the New York University team, led by Dr. Thomas Wisniewski.
BSE and vCJD are caused by abnormal versions of prion proteins in the brain, which accumulate and cause brain damage, leading to dementia and abnormal limb movements. As the infection takes hold, prion proteins invade brain tissue and force normal proteins to adopt their own mis-folded shape. The prototype that Dr. Wisniewski and his team tested was made from prion proteins attached to a genetically modified strain of Salmonella, the bacterium that is used in several animal and human vaccines.

Many of the mice that received the oral vaccine had no symptoms of the disease after 400 days, while others had delayed disease onset. Without the vaccine, it would normally take a mouse 120 days to develop the disease. Dr. Wisniewski and his team are now redesigning the vaccine so that it could be used on deer and cattle, and possibly humans too.


A novel compound that kills tuberculosis bacteria

VASTox plc, the United Kingdom, has reported positive results in its tuberculosis (TB) drug discovery programme. The company has identified from its proprietary screening libraries several novel series of small, drug-like molecules that show high in vitro efficacy against Mycobacterium tuberculosis. The results from these efficacy studies have been validated in three world-class laboratories.

VASTox targets N-acetyltransferase, an enzyme implicated in the growth of M. tuberculosis. It says compounds that inhibit the target enzyme are also active against M. tuberculosis resulting in cell death. Following the success of the initial screens, a chemical optimization programme is now aiming to further enhance the efficacy of the identified compounds.

VASTox has already increased the value of the active compounds through safety and toxicity screening in the companys market-leading zebrafish technology platform, in advance of a series of in vivo studies.


Cure for hepatitis C found

The use of peginterferon alone, or in combination with ribavirin, points to a cure for hepatitis C, the leading cause of cirrhosis, liver cancer and the need for liver transplant, according to Dr. Mitchell Shiffman, Medical Director of the Liver Transplant Programme at Virginia Commonwealth University Medical Centre, the United States.

Researchers have reported that 99 per cent of patients with hepatitis C who were treated successfully with peginterferon alone or together with ribavirin, had no detectable virus up to seven years later. Researchers say this data validate the use of the word cure when describing hepatitis C treatment. The long-term follow-up study reviewed 997 patients, either mono-infected with chronic HCV or co-infected HCV and HIV, who achieved a sustained viral response following treatment with either peginterferon alfa-2a alone or in combination with ribavirin.

After successful treatment, the researchers monitored serum levels of HCV once a year for an average of 4.1 years (range 0.4 to 7 years). Of the 997 patients, 989 maintained undetectable levels of HCV. The remaining eight patients tested positive for HCV at an average of two years following treatment completion. The study found that these eight patients exhibited no consistency in age, gender or HCV genotype, and it has not yet been determined if these patients experienced a relapse or if they were re-infected with HCV.


Stem cells provide clues to cancer spread

Scientists at the University of Manchester, the United Kingdom, have made a breakthrough in understanding how cancers spread in what could lead to new ways of beating the disease. The study, led by Dr. Chris Ward at the Universitys Faculty of Medical and Human Sciences, used embryonic stem (ES) cells to investigate how some tumours are able to migrate to other parts of the body, which makes the treatment of cancer much more difficult.

Eepithelial cells normal as well as early cancer cells bind tightly to each other forming stable tissue. As a tumour becomes more advanced, some of the cells become mesenchymal cells, which do not bind to each other, forming more disorganized tissues in which the cells can move around. Since this crucial change, known as the epithelial-mesenchymal transition, was first noted in the early embryo, Dr. Ward postulates that embryonic stem cells might undergo a similar process.

The study used ES cells to investigate how the protein E-cadherin stopped cells from migrating during normal growth. The team found that, besides helping cells stick together, this protein also blocked the action of another protein known to increase cell mobility. This important dual function of E-cadherin opens up the potential for new targets to prevent tumours from spreading.


New strategy for preventing brain diseases

Scientists at the Gladstone Institute of Neurological Disease (GIND), the United States, have discovered that reducing levels of the protein tau can prevent seizures and neurological deficits related to Alzheimers disease (AD). They found that when tau is removed from mice genetically engineered to simulate AD, the memory function of the mice is retained and they live a normal lifespan. Reducing tau levels also made mice more resistant to epileptic seizures. If this strategy also works in humans, it could enable a major leap forward in our ability to treat and prevent devastating neurological diseases, said Dr. Lennart Mucke, GIND Director and a professor of neurology at the University of California San Francisco (UCSF) and senior author of the study.

Unlike many investigational therapies for AD that aim to reduce levels of amyloid A proteins (AA), the UCSF scientists pursued a complementary strategy to make the brain more resistant to AA. They found that even a partial reduction of tau prevented memory problems and early deaths in AD mice, even though their brains were full of AA. The key finding was that cognitive and neuronal deficits in these mice were prevented when one or both copies of the tau gene were eliminated.

Tau is made normally by brain cells and regulates the stability of their internal skeleton. In AD, tau is altered in a way that makes it aggregate into clumps, called tangles. A lot of effort has been devoted to finding ways to specifically eliminate these abnormal forms of tau, but this has been difficult. A breakthrough came when the scientists identified a tau reduction mechanism that could protect the brain. They found that reduction of tau protects brain cells from over-stimulation, which can interfere with the brains normal functioning and even cause epileptic seizures.


Salmonella-based vaccine against aerosolized anthrax

A joint effort by scientists from the United States and elsewhere has resulted in the development of an orally administered Salmonella-based vaccine that protects mice against aerosolized anthrax and may also have human implications. Currently, there is an effective anthrax vaccine, but it needs multiple injections over several months, is costly to produce and is not openly available.

The researchers produced Salmonella enterica serovar Typhimurium, expressing differing levels of the needed protective antigen to induce anthrax immunity and orally immunized groups of mice. Following immunization, the mice were challenged with aerosolized anthrax spores. Five of the six mice that received the vaccine containing full expression of the antigen were protected against infection, while the vaccine with reduced antigen levels only provided up to 25 per cent protection.


Development of insulin-producing cells

A study, by researchers from Imperial College London and an INSERM Unit at Necker Hospital in Paris, has revealed how embryos create the cells that secrete insulin. The research reveals that glucose plays a key role in enabling healthy beta cells, which secrete insulin, to develop in the pancreas of an embryo.

Glucose prompts a gene called Neurogenin3 to switch on another gene, known as NeuroD, which is crucial for the normal development of beta cells. If the glucose levels are low this gene is not switched on.

Knowing how to switch on the gene that produces beta cells could eventually enable researchers to create these cells from stem cells and transplant them into patients with type 1 diabetes. In this type of diabetes, the immune system destroys patients beta cells. At present, only very few patients with the condition are able to have beta cell transplants, because the cells have to be taken from deceased donors. The research may also help scientists to eventually develop drug therapies that enhance the action of glucose and thus encourage the growth of healthy beta cells.



Brain protein linked to increased blood pressure

A brain protein is linked to rise in blood pressure, according to a study that scientists say could lead to new ways of treating the condition. Prof. Julian Paton and colleagues at Bristol University, the United Kingdom, isolated a protein, JAM-1, located in the walls of blood vessels in the brain. In studies done on rats by the scientists, it was seen that JAM-1 is linked to raised blood pressure. JAM-1 appeared to trap white blood cells obstructing blood flow. This can cause inflammation and result in poor oxygen supply to the brain, the scientists say. The future challenge will be to understand the type of inflammation within the vessels in the brain. The scientists are now looking at the human brain to understand more.


Special proteins level critical to proper muscle formation

A study at the University of Texas Medical Branch (UTMB) at Galveston, the United States, has revealed that proper formation of the proteins that power heart and skeletal muscle depends on the precise concentration of a chaperone protein known as UNC-45. Chaperone proteins guide other newly formed proteins into the shapes that enable them to perform their specific functions. The UTMB discovery may have important implications for understanding and eventually treating heart failure and muscle wasting elsewhere in the body resulting from burns, brain trauma, diabetes, cancer and the effects of aging.

In muscle cells, UNC-45 acts as a chaperone for myosin proteins, helping them fold into long, thin stable structures, which clump together to form the thicker filaments that give heart and skeletal muscle its striated appearance. Chemical signals cause these myosin filaments to contract, producing, for example, a heartbeat or an arm movement. Scientists knew that a shortage of UNC-45 disrupts myosin formation, leading to muscle paralysis. But the UTMB study showed that an over-supply of UNC-45 is also a problem: it interferes with myosin accumulation and assembly, explains Dr. Henry Epstein, chairman of UTMBs Department of Neuroscience and Cell Biology and senior author of the study.

Dr. Epsteins group made the discovery using Caenorhabiditis elegans worms genetically engineered to produce more UNC-45 than do normal worms. Being over-chaperoned by extra UNC-45, the researchers found, prevents the myosin proteins from binding into thick filaments, and leaves them free-floating and vulnerable to the ubiquitin/proteasome system, a cellular clean-up squad that breaks unstable proteins down into their amino acid components. The result is a partially paralysed worm whose muscles show visibly smaller fibres. It now looks as though precise levels of UNC-45 are critical during myosin formation, said Dr. Epstein.


Study of protein folds gives clue to metabolic evolution

Researchers led by Dr. Gustavo Caetano-Anolls, professor of crop sciences at the University of Illinois, the United States, have constructed the first global family tree of metabolic protein architecture. Their work relied on established techniques of phylogenetic analysis developed in the past decade to plot the evolution of genes and organisms, but which have never before been used to work out the evolutionary history of protein architecture across biological networks. They studied metabolic proteins at the level of their component structures: easily identifiable folds in the proteins that have known enzymatic activities. These protein domains catalyse several functions, breaking down or combining metabolites.

The findings of the researchers relied on a basic assumption: that the most widely utilized protein folds were also the most ancient. The team used data from the metabolic pathways database of the Kyoto Encyclopedia of Genes and Genomes, and the Structural Classification of Proteins database. They combined these two data sets with phylogenetic reconstructions, or family trees, of protein fold architectures in metabolism to create a new database, called the Molecular Ancestry Network, which links these data sources into a global network diagram of metabolic pathways.

To represent evolutionary age, the researchers added colour to their diagrams of metabolic networks. The result is a multi-coloured mosaic of protein fold evolution. The mosaic shows that modern metabolic networks and even individual enzymes are composed of both ancient and more recent protein architectures.

This finding supports the hypothesis that protein architectures that perform one function are often recruited to perform new tasks. The new, global family tree of protein architecture also revealed that many metabolic protein folds are quite ancient. These architectures were found to be quite common in all the species of bacteria, animals, plants, fungi, protists and archaea the researchers analysed. Of the 776 metabolic protein folds surveyed, 16 were found to be omnipresent, and nine of those occurred in the earliest branches of the newly constructed tree.

The analysis also found that the most ancient metabolic protein folds are important to RNA metabolism, specifically the interconversion of the purine and pyrimidine nucleotides that compose the core of the RNA molecule. This discovery supports the hypothesis of an RNA world in which RNA molecules were among the earliest catalysts of life.


Survival protein that aids leukaemia identified

In the United States, researchers at the Ohio State University Comprehensive Cancer Centre have identified a specific protein, inactivation of which may offer a cure for leukaemia. The identified protein called Mcl1 helps keep normal cells healthy, and is involved in the development of immune system components, but it can also help prolong survival of cancer cells. Cells with an overabundance of Mcl1 are also more resistant to anti-cancer drugs, such as rituximab.

The researchers suggest that a drug that can block the activities of the survival protein may offer an effective therapy for drug-resistant forms of chronic lymphocytic leukaemia (CLL) and acute lymphoblastic leukaemia (ALL), when used in combination with other drugs. The investigators led by Dr. John C. Byrd, professor of internal medicine and director of the hematologic malignancies programme, placed molecules called small interference RNA (siRNA) inside the cells. They found that the molecules greatly reduced the amount of the survival protein, thereby causing many of the cells to die. The effect was the same even in cells that came from patients with advanced cancer or from patients with tumours that resisted conventional treatment.

Upon treatment of cells with both siRNA and the drug rituximab, it was noted that the combination killed significantly more leukaemia cells than the drug alone.


The trick of toxoplasmosis infection explained

Toxoplasmosis is a parasitic disease, primarily carried by cats. It is transmitted to humans by eating undercooked meat or through contact with cat faeces. It is particularly dangerous for pregnant women, whose foetuses can be infected via the placenta, and those with a weakened immune system, such as people infected with HIV. In its severity, toxoplasmosis can cause damage to the brain and eyes, and even death.

The parasite that causes toxoplasmosis, Toxoplasma gondii, is one of the worlds most common parasites.
Scientists from London and Geneva have determined, for the first time, the atomic structure of a key protein, which is released onto the surface of T. gondii just before it invades host cells in the human body. They found that the protein known as TgMIC1 binds to certain sugars on the surface of the host cell, assisting the parasite to stick to, and then enter the human cell.

Using a novel carbohydrate microarray, the team was able to identify the precise sugars to which the parasite protein binds. Following this, the team was able to characterise the behaviour and interactions of the parasite protein and host cell sugars, to get a detailed picture of T. gondiis invasion mechanism.

Professor Steve Matthews from Imperial College Londons Division of Molecular Biosciences, one of the papers authors, explained the significance of the research, Now that we understand that it is a key interaction between a protein on the parasites surface and sugars on the human cell which lead to the cells invasion, there is potential to develop therapeutics that are targeted at disrupting this mechanism, therefore thwarting infection.



Gene switches for a plants self-pollination ability

The ability to self-pollinate turns up in cultivated tomatoes and canola, among other major crops, and can be a nuisance for plant breeders and seed producers trying to develop hybrid varieties and produce hybrid seed on a commercial scale. To get hybrid seed, two different varieties are planted in the same field and allowed to cross-pollinate. If either variety can self-pollinate, then the pollen sacs (anthers) have to be removed from the flowers by hand to prevent selfing a very labour-intensive process. Now researchers from Cornell University, the United States, are zeroing in on genes that turn a plants ability to self-pollinate on and off.

The research group of Dr. June Nasrallah, a plant biology professor Cornell, is working with Arabidopsis thaliana to understand how self-pollination is inhibited in self-incompatible plants, which are unable to self-pollinate because their stigmas can recognize and reject their own pollen. The group had earlier shown that two genes, known as SCR and SRK, are key to self-incompatibility. SCR codes for a protein on the surface of pollen grains, and SRK codes for a receptor in the cell membranes of stigma cells. When both proteins come from the same plant, the stigma rejects the pollen and fertilization does not occur.

The researchers inserted SCR and SRK genes from a self-incompatible species, A. lyrata, and created A. thaliana varieties that ranged from self-incompatible to pseudo self-compatible, where a plant resists self-pollination for a while, but if it is not pollinated from another plant it will eventually accept its own pollen. The team mapped the genomes of several varieties of transgenic A. thaliana in fine detail and isolated a gene known as PUB8 that seems to regulate the expression of SRK whether or not it is turned on to manufacture its protein.

PUB8 is very close to SCR and SRK on the genome: it is unusual to find a regulatory gene so close to the gene it regulates. The gene shows some variation from one variety of A. thaliana to another. The degree to which self-incompatibility is turned on in the plant seems to correlate with these variations.


GM crops survive weed-whacking herbicide

Genetically modified (GM) crops resistant to specific herbicides have found favour with farmers, as these can be applied with abandon, cutting costs and reducing the need for tilling. But this advantage of GM crops has also sown the seeds of destruction by speeding the evolution of weeds into varieties that have inborn resistance to the herbicide. Now researchers at the University of Nebraska, the United States, have successfully modified crops to resist yet another herbicide dicamba that would eradicate the pernicious weeds.

We can now spray dicamba on a number of different plants and have no visible symptoms at all, says plant molecular biologist Dr. Donald Weeks. The researchers first isolated a soil bacterium that disposes of dicamba, a herbicide that works by mimicking plant hormones and causing broad-leaved greenery to grow out of control as if every one of its cells had turned cancerous. The plant grows itself to death, explains Dr. Weeks. The organization becomes so disrupted that the plant can no longer nourish itself properly.

The soil bacterium Pseudomonas maltophilia (strain DI-6) quickly breaks down dicamba. As the herbicide does not build up in the soil, farmers prefer it to control broad-leaved weeds. However, as broad-leaved weeds and broad-leaved crops are so similar, it could not be used with plants like soybeans. Dr. Weeks and his team used a virus that afflicts groundnut plants to carry the dicamba-disarming gene into the cells of tobacco plants.

Tobacco plants are extremely sensitive to decamba, succumbing to just one one-thousandth of a pound per acre. With the new gene producing the enzyme that breaks down dicamba, the plants resisted as much as 20 pounds per acre. Researchers for the past three years have also been able to grow dicamba-resistant soybeans and other broad-leaved crops. The plants carry the genetic information in their chloroplasts, which seems to make the enzyme very effective in disposing of dicamba.


Plant enzyme that could make ethanol production efficient

Researchers at the Cornell University, the United States, have discovered a class of plant enzymes that potentially could allow plant materials such as cellulose to be broken down more efficiently than is possible using current technologies. This could make mass-production of ethanol from cellulose to be competitive in terms of costs with corn-based ethanol production.

A critical step in producing cellulosic ethanol involves breaking down a plants cell wall material and fermenting the sugars that are released. Current technologies use microbial enzymes called cellulases to digest the cellulose in grasses and such rapidly growing trees as poplars. The microbial enzymes have a structure that makes them very efficient at binding to and digesting plant cell wall material called lignocellulose, potentially offering researchers new properties for producing ethanol more efficiently. The bottleneck for conversion of lignocellulose into ethanol is efficient cellulose degradation, said Dr. Jocelyn Rose, assistant professor of plant biology. The discovery of these enzymes suggests there might be sets of new plant enzymes to improve the efficiency of cellulose degradation.


Pumpkin pectin may offer novel gelling opportunities

The chemical fine structure of pectin dictates its functionality. The majority of pectins used currently come from citrus peel and apple pomace. Other sources of the ingredient have remained largely unexploited because of certain undesirable structural properties. Pectin extracted from pumpkin and then modified using an enzyme could offer an interesting alternative for jams and confectionery, suggests new research carried out by the Saratov State Agarian Vavilov University and the Moscow State University of Applied Biotechnology in Russia.

Using enzymes cultured from Aspergillus awamori, the researchers enzymatically modified pectin extracted from pumpkin. The pectin was classified as a high-methoxy pectin with a degree of esterification greater than 50 per cent, which does not conform with the food industry standard of using pectins with DE greater than 60 per cent. However, the researchers point out that the biopectin can form gels with a 60 per cent sucrose solution, making its use feasible in confectionary, baked items, fruit jelly products and soft drinks. The researchers also state that pectins with DE less than 60 per cent can bind and remove heavy metals from the body, making the pumpkin pectin interesting as a nutritional recommendation for those who work with such metals.


Researchers find out how plants manufacture Vitamin C

In the United States, a group of researchers from University of California Los Angeles and Dartmouth Medical School have discovered GDP-L-galactose phosphorylase, the controlling enzyme that serves as the biosynthetic pathway by which plants manufacture vitamin C. The discovery now makes clear the entire 10-step process by which plants convert glucose into vitamin C.

The research team, while working on a particular type of gene in worms, discovered a similarity between the worm gene and the product of the VTC2 gene of Arabidopis thaliana. Mutations in this plant gene have been previously linked to low levels of vitamin C. The researchers were able to express and purify the plant VTC2 enzyme from bacteria. They then produced the GDP-L-galactose substrate and reconstituted in test tubes the long-sought seventh step in vitamin C synthesis. The team has expressed hope that their discovery might lead to new strategies for increasing vitamin C levels in food crops, which could mean more nutritious foods and potentially higher crop yields.


Scientists look to grow electricity with platinum

A group of scientists in the United States are examining the possibility of growing electricity by using small amounts of platinum. As part of the effort to reduce emissions in energy production, Prof. Barry Bruce and his team at the University of Tennessees Centre for Environmental Biotechnology are looking at developing energy in the same way as nature through photosynthesis. They are collecting particles from photosynthetic plants and bacteria together in nano-clusters on small assemblages of platinum. These photosystems then produce high-energy electrons that can be used for direct electrical power, or to stimulate the production of hydrogen for fuel cell applications.


Watermelon juice may be novel amino acid source

Watermelon juice may provide a novel source of the essential amino acid arginine, says a new study in the United States that shows the juice is a rich source of its metabolic precursor. Arginine is a precursor for nitric oxide, which has been shown to lower blood pressure, reduce blood clotting and protect against myocardial infarction and strokes. Researchers from the Agricultural Research Service, Texas A&M University, the University of Nevada and Oklahoma State University have reported increased blood arginine levels after three weeks of drinking watermelon juice with every meal.

Some studies have reported that high oral doses of arginine were associated with nausea, gastrointestinal discomfort and diarrhoea in humans. A solution to this potentially severe problem may be the alternative use of l-citrulline, an effective precursor for arginine synthesis, explained the lead scientist Dr. Julie Collins.

L-citrullines conversion to arginine consumes ammonia, said Dr. Collins, meaning the amino acid could be useful for those with elevated ammonia levels, arginine transport problems or enhanced intestinal arginine breakdown, as is found in people with stress or infection.

The researchers tested the theory using healthy volunteers who received set daily doses of watermelon juice. After the three weeks of intervention, they found that fasting blood levels of arginine had increased by 22 per cent for those who received high dose (1,560 g) of juice. Levels of ornithine, a product of arginine catabolism, also increased in the high-dose watermelon juice group by 18 per cent after three weeks. While previous studies with animals have reported that citrulline administration may be detrimental to levels of other amino acids, no such results were seen in this human study.



Cancer Genomics and Proteomics: Methods and Protocols

Cancer Genomics and Proteomics: Methods and Protocols provides a compendium of techniques and applications that will be of profound use to researchers interested in gene identification and function. The approaches described in this book are state-of-the-art and can be tailored to ongoing individual or planned research projects. Reviews are written by experts gene identification and full-length gene cloning, gene profiling (microarrays), chromatin modification of gene regulation, bacterial artificial chromosomes, cancer cytogenetic analyses, and gene methylation, etc.

Contact: Humana Press, 999 Riverview Drive, Suite 208 Totowa, NJ 07512, United States of America. Tel: +1 (973) 256 1699; Fax: +1 (973) 256 8341


Molecular Genetics of Recombination

Genetic recombination is an important process involved in shaping the genetic make-up of progeny. Until recently, most knowledge on the mechanisms of genetic recombination has come from studies of prokaryotic and simple eukaryotic fungal systems. These studies have now been extended to mammals, and a comparative picture of the general factors and mechanisms of genetic recombination is beginning to emerge. Genetic and biochemical studies have led to the isolation and characterization of many of the recombination-repair proteins in bacteria, which led to the identification of their human homologues. This book, No. 17 in the Topics in Current Genetics series, captures all these new information in detail.

Contact: Ms. Eileen Purelis, Springer Science+ Business Media LLC, 233 Spring Street, New York, NY 10013-1578, United States of America. Tel: +1 (212) 460 1507; Fax: +1 (212) 460 1581



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