VATIS Update Biotechnology . Oct-Dec 2012

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Biotechnology Oct-Dec 2012

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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Boom time in the cell culture market

Cell culture is becoming the next big pharmaceutical trend, as laboratories rush to meet demand for stem cell and biologics, states a new report by healthcare experts GBI Research, the United States. Manufacturing of biopharmaceuticals involves cell culture methods, and the growing trend for biologics will boost the demand for cell culture processing. Research in the sector is largely devoted to deriving novel action mechanisms, and increasing access to newer treatments to produce potential cures and improve the quality of life for ailing people. This focus helps to generate better treatment options and earn higher revenues for pharmaceutical and biotechnological companies.

Stem cell research also has enormous potential for cell culture. Cell culture methods ensure standardized production and propagation of highly purified stem cells and their differentiated progeny. Conventional therapies manage the disease symptoms, while stem cell therapies treat the cause of the disease. From a commercial perspective, this deficit of curative treatments in conventional therapies makes stem cell research a veritable goldmine. In the past few years, stem cell research has gained more importance in cancer research, though the technique still faces many unresolved risks including the uncontrolled proliferation of transplanted cells and transmission of infectious agents.

The global cell culture market was worth US$3.4 billion in 2011, and is tipped to grow at a compound annual growth rate (CAGR) of 9.3 per cent between 2011 and 2018 to reach US$6.3 billion in 2018. However, this market has more than 90 per cent of its products manufactured by a small number of players, such as EMD Millipore, Life Technologies Corp., Sigma-Aldrich Corporation and Thermo Fisher Scientific Inc., all based in the United States. While a significant number of small players are also entering the market, especially in emerging countries, tough industry regulations limit the speed at which these companies can progress. The cell culture process requires precise handling, with any changes affecting the safety and efficacy profile of the final product. As a result of this, the processes for cell culturing are constrained by strict controls, which slow down development and act as a bottleneck to progression in cell culture processing techniques.

Drug development research in Asia poised to grow

A strong regulatory framework and high recruitment rates solidly support the Asian clinical research industry, and key pharmaceutical players are now moving beyond simple outsourcing to analyse the region’s own healthcare problems, according to new market research. The new report, published by healthcare market research company GBI Research, the United States, explains that Asia offers a promising environment for pharmaceutical development, because of low costs, a large potential trial population and regulatory support. Oncology studies, for instance, have now begun to study the Asian phenotype to understand more about the specifics of cancer.

During 2012, more than 12 per cent of global clinical trials were conducted in the seven major markets of Asia, lagging behind the United States’ share of 48.5 per cent and Europe’s 26.5 per cent. But many Western biopharma companies are beginning to exploit the potential of emerging Asian countries, where regulatory agencies are updating the clinical trial process to meet global demand for inexpensive clinical research. The vast opportunity in Asia, however, has not yet been fully utilized by the developed markets.

The cost of conducting clinical trials in Asian countries is 35-45 per cent lower than the cost of conducting similar trials in the United States, a large number of patients from urban centres are able to be recruited easily and at a low cost. The regulatory systems in Asia also offer an encouraging environment, as the adoption of Good Clinical Practice (GCP) guidelines and the establishment of Institutional Review Boards (IRBs) are helping the region to rapidly progress and incorporate with international standards. GBI Research estimates that the total size of drug discovery and development market in China, India, Japan, Singapore, Russia, Taiwan Province of China and the Republic Korea has reached a striking US$5.3 billion in 2011, following growth at a compound annual growth rate (CAGR) of 21.9 per cent from 2007. The market is expected to reach US$17.3 billion in 2018, at a CAGR of 18.4 per cent.

WHO eases rules on Indian meningitis vaccine

In a breakthrough, a key India-made meningitis vaccine can be now transported or stored for up to four days without refrigeration, which could help combat the disease in poor countries. Scientists say that the meningitis A vaccine known as MenAfriVac, created to meet the needs of Africa’s “meningitis belt”, can now be kept in a controlled temperature chain (CTC) at temperatures of up to 40°C for up to four days. The approval is the outcome of the review and decisions of the Drugs Controller General of India (DCGI), supported by a Health Canada analysis and confirmed by the World Health Organization (WHO) Vaccines Pre-qualification Programme.

The innovative vaccine, which is manufactured by Serum Institute of India Ltd. (SIIL), costs less than US$0.50 per dose and has dramatically reduced disease burden in the first countries to introduce it, according to recently published findings. The decision could help increase campaign efficiency and coverage and save funds normally spent maintaining the challenging cold chain during the “last mile” of vaccine delivery.

The regulatory approval has the effect of permitting the re-labelling of MenAfriVac, while ensuring that the vaccine remains effective and safe throughout its life cycle. MenAfriVac is the first vaccine designed specifically to help eliminate meningococcal A epidemics from Africa’s meningitis belt, which includes 26 countries from Senegal to Ethiopia.

WHO to approve China’s encephalitis vaccine

The World Health Organization (WHO) is on the verge of approving a China-made vaccine for Japanese encephalitis. The grant of pre-qualification status to the vaccine will open China’s door to lucrative regional and global markets. The vaccine has been developed by Chengdu Institute, which is a part of China’s top vaccine manufacturer China National Biotech Group (CNBG). After pre-qualification, the vaccine will be eligible for quick procurement by aid agencies.

China’s national regulatory agency received a nod from WHO in March 2011, paving the way for domestic manufacturers to apply for pre-qualification for drugs and vaccines. According to a WHO spokesperson, pre-qualification for a vaccine against Japanese encephalitis, deemed a medium-term priority by WHO, was “in the pipeline”. While speaking about this development, Dr. Seth Berkley, CEO of Global Alliance for Vaccines and Immunization (GAVI), said: “We think that the first vaccine that will receive prequalification will be Japanese encephalitis, out of a Chengdu manufacturer. If that vaccine does receive pre-qualification, we will work with that company to try to get that vaccine out to more countries in Asia.”

Report linking GM corn to cancer rejected

The European Food Safety Authority (ESFA) has said that it cannot accept an “inadequate” report by a French scientist that links cancer to genetically modified (GM) corn. EFSA said an initial review showed that the “design, reporting and analysis of the study... are inadequate,” meaning that it could not “regard the authors’ conclusions as scientifically sound”. EFSA has called on the author of the study, Mr. Gilles-Eric Seralini, to provide more information before a second, final review. Mr. Seralini, however, insisted that he would not give the EFSA any additional information until it first detailed the basis of its own assessment. The scientist’s team at University of Caen, France, found that rats develop tumours when fed the United States agribusiness giant Monsanto’s NK603 corn, or when exposed to one of the company’s weed killers used with it, containing glyphosate.

India announces new biosimilar regulatory guidelines

India has announced the much-awaited new and simple regulatory guidelines for similar biologics, which have been approved and marketed in the United States or Europe for more than four years. The guidelines provide requirements for preclinical evaluation of those recombinant products that are claimed to be similar to the already approved biopharmaceutical products, referred as ‘similar biologics’. Therefore, the regulators will partly rely on the information from the already approved products for ensuring safety, purity, potency and effectiveness.

Releasing the guidelines, Dr. Maharaj K. Bhan, Secretary, Department of Biotechnology (DBT), said: “This will be good news for governments and patients alike, as it will lead to significant reductions in costs with the introduction of a similar biologic or biosimilar to the market.” For preparing the guidelines, DBT had held wide-ranging consultation with the industry, the Central Drug Standard Control Organization (CDSCO) and other stakeholders. The guidelines prescribe the quality, pre-clinical studies and clinical trial requirements of similar biologics in India.


China’s GMP-friendly biologics plant

WuXi AppTec, China, is continuing its rise to the forefront of the country’s contract research world, unveiling recently its current good manufacturing practice (cGMP) biologics manufacturing facility, a plant described as the first in the nation to meet the United States standards. Mr. Ge Li, WuXi’s CEO, said that the all-disposable facility demonstrates the company’s commitment to providing cutting-edge drug discovery and manufacturing services to its clients.

The plant announcement comes on the heels of three recent high-profile biologics deals by the company. WuXi is partnering with Open Monoclonal Technology Inc., the United States, to develop human antibodies using that company’s OmniRat platform. WuXi has also signed on with TaiMed Biologics, Taiwan Province of China, to produce its ibalizumab HIV treatment, besides inking a deal with AstraZeneca plc, based in the United Kingdom, to develop an arthritis drug called MEDI5117.

ABLE, WBBA ink MoU on healthcare, agriculture R&D

The Association of Biotechnology Led Enterprises (ABLE), India, and Washington Biotechnology & Biomedical Association (WBBA), the United States, have inked a memorandum of understanding (MoU) for broad-ranging cooperation to support “breakthrough” discoveries in healthcare, agriculture and clean energy in India. The two entities will undertake activities to further their respective mandates by providing each others’ members opportunities to cooperate as well as invest in the State of Washington and in India in the field of biotechnology.

“These activities could be the current ones that both associations are engaged in or future ones that both may decide to do individually or jointly,” said a statement from ABLE. Among others, the activities could cover technical knowledge, market research, input for policy making, internships, collaborations, seminars, exhibitions, workshops, capacity building, investment and business partnering, it said.

Mr. P.M. Murali, President of ABLE, said, “The collaboration aims to achieve breakthrough discoveries to provide affordable solutions for critical diseases, important challenges in agriculture and energy on mutually agreed topics.” Mr. Chris Rivera, President of WBBA said, “We see India as the growth engine of tomorrow and one of the fastest growing economies in the world. This collaboration with ABLE in India is significant to WBBA to facilitate best of research in biotechnology from both the countries.”

AB-Biotics in licence pact with HanAll BioPharma

Spanish biotech firm AB-Biotics has signed a 10-year licence agreement with HanAll BioPharma of the Republic of Korea. The agreement gives HanAll exclusive rights to distribute AB-Biotics’ cholesterol-lowering probiotic AB-Life in the Republic of Korea. According to a clinical trial supported by the ethics committee of Hospital Puerta del Hierro, Spain, AB-Life reduces the total cholesterol levels by 14-18 per cent.

“This contract marks a significant milestone for AB-Biotics, since Korea opens the Asian door for our international expansion, and thanks to HanAll BioPharma we can enter there with a local and very well-positioned partnership,” said Mr. Miquel Angel Bonachera, co-founder and CEO of AB-Biotics. The pact with HanAll BioPharma is the fifth international licence agreement signed by AB-Biotics so far this year. The probiotic AB-LIFE already has licence agreements in Brazil, Mexico, Venezuela, Canada, the United States and Southeast Europe.

Novartis to invest US$500 million in new Singapore facility

Novartis, Switzerland, will pay more than US$500 million to construct a new biotech production site in Singapore to support its growing pipeline of biologics. The project, which was first announced in 2007 and then put on hold after Novartis formed a biologics production partnership with Lonza in Switzerland, has now been revived. Construction of the new site is planned to start in early 2013, and the facility is expected to be operational by the end of 2016.

The new facility will focus on drug substance manufacturing based on cell culture technology, such as monoclonal antibodies treatments for cancers and autoimmune and respiratory diseases. The new facility will be based at the same location as Novartis’ existing pharmaceutical production facility. It will be designed to operate in a flexible manner to handle small and large-scale volumes and to support clinical and commercial production of potential new products. Novartis already has several operations in Singapore, including its tropical diseases institute, the Asia-Pacific head offices, and two production facilities for its eye-care unit Alcon.

Cipla Ltd. offers to buy into Cipla Medpro

Indian drug manufacturer Cipla Ltd. plans to offer US$215 million for a majority stake in Cipla Medpro, South Africa, to broaden its presence in Africa’s rapidly growing market for cheap, generic versions of branded drugs. The proposed bid for 51 per cent stake in South Africa’s third largest drug company highlights the Indian pharmaceutical firms’ growing interest in the continent, particularly as a market for low price versions of medicines that are off patent. Cipla Ltd. supplies the bulk of Cipla Medpro’s drugs but has so far not owned a stake in the business. Cipla plans to offer 8.55 rand (US$75) a share, Cipla Medpro said in a statement, adding that it would express a view to its shareholders on the Indian firm’s proposal upon receiving a firm offer. Cipla said it would fund the deal using its own cash.

Life Technologies acquires cancer bioinformatics firm

In the United States, Life Technologies has acquired Compendia Bioscience, a major cancer bioinformatics company that is widely used by the pharmaceutical industry to identify novel gene targets for drug discovery and development. Compedia’s oncology expertise and proprietary assets will augment Life Technologies’ diagnostic development capabilities across multiple platforms, such as next-generation sequencing, quantitative polymerase chain reaction (qPCR) and proteome analysis.

Compendia’s current business adds an established base of pharmaceutical industry customers for Life Technologies’ platforms. The oncology data of the company is utilized by major pharmaceutical firms in their drug development research, and will extend Life Technologies’ abilities to both develop its own tests and to partner with pharmaceutical companies in companion diagnostic development. Life Technologies plans to utilize the extensive content in Compendia to move into different areas of oncology. Compendia has one of the world’s largest and most comprehensive sets of mutation profiles, gene expression data as well as cellular biomarkers that have been gathered from more than 62,000 cancer patients.

GSK buys Human Genome Sciences for US$3 billion

GlaxoSmithKline (GSK), based in the United Kingdom, has acquired Human Genome Sciences (HGS), the United States. The final deal size was about US$3 billion net of cash and debt. GlobalData, an international market research firm based in the United Kingdom, said the acquisition of HGS gives GSK full rights to three main drugs – Benlysta (belimumab), albiglutide, and darapladib.

As the first approved therapy for systemic lupus erythematosus in more than 50 years, there were high potential for Benlysta sales. Unfortunately, certain comments by the United States Food and Drug Administration (FDA) noted during the approval process are said to have dampened the sales of Benlysta in its first year on the market. Since then, though the sales have improved, they remain considerably below what was originally forecast. Albiglutide, a GLP-1 analog, is scheduled for FDA filing in early 2013 in the treatment of type 2 diabetes. While Albiglutide has a longer half-life than other GLP-1 analogs on the market, results from several head-to-head studies are pending. Darapladib, a phospholipase A2 inhibitor, is in phase III for coronary heart disease. Initial trial results are not expected until the end of 2013.

Biocon picks BMS as oral insulin partner

Biocon Ltd., India, has announced that it has signed an ‘option’ agreement with the United States drug major Bristol-Myers Squibb (BMS) to develop and market its ambitious oral insulin candidate drug. BMS and Biocon are old partners; BMS started its dedicated research and development centre at Biocon’s Syngene over three years ago.

BMS would fund the development of the drug, code-named IN-105, through Phase II trials. Depending on the result of the clinical trials, it would have an exclusive option to further develop and commercialize the candidate, according to a company statement. Biocon would retain exclusive rights to IN-105 within India. It will conduct clinical studies to further characterize IN-105’s clinical profile up to the completion of Phase II trials, which may take up to two years, a company spokesperson said.


New light on embryonic stem cells

A significant breakthrough in the understanding of embryonic stem (ES) cells has been made by scientists from the Smurfit Institute of Genetics at Trinity College Dublin, Ireland. The new research describes the process whereby genes that are ‘on’ in ES cells are switched ‘off’. This process is essential in order to convert ES cells into different cell types such as neurons, blood or heart cells and therefore represents a key breakthrough in the area of regenerative medicine.

This new research explores the role of PHF19, a ‘polycomb group protein’, in mouse ES cells. Mr. Gerard Brien, the lead author of the paper and PhD student in the laboratory of Dr. Adrian Bracken, demonstrated that without PHF19, ES cells are incapable of generating specialized cells such as those of the heart, lung or brain. He then established that PHF19 plays a critical role in switching the ES cell genes from an ‘on’ to an ‘off’ state during conversion into specialized cells. PHF19 does this by reading an ‘epigenetic mark’ called H3K36me3, which is only found on genes that are ‘on’. It then recruits additional ‘polycomb’ and other proteins, which replace H3K36me3 with another mark, H3K27me3, that is found on genes that are ‘off’.

Commenting on the findings, Dr. Bracken stated: “This discovery about PHF19 is an important step forward in our understanding of how stem cells specialize. In addition to its relevance in regenerative medicine, it may also have implications in future cancer therapies. We are also studying a related ‘polycomb group protein’ called EZH2, which is mutated in lymphoma, a type of blood cancer. a number of novel drugs have been developed to target EZH2 and treat these patients. Our new results suggest that these patients could also be treated by inhibitors of PHF19.”

The barley genome is bigger than human genome

As part of an international consortium, scientists led by plant sciences professor Dr. Rod Wing of University of Arizona (UA) College of Agriculture & Life Sciences, the United States, have helped decipher the genome of the barley plant. This is the largest plant genome to be sequenced and paves the way for tackling the wheat genome, the last frontier in the world’s most important cereal crops. Higher yield, better pest and disease resistance and enhanced nutritional value are among potential benefits of the international scientific research effort that has resulted in an integrated physical, functional and genetic sequence assembly of the barley genome. Dr. Wing, who is also Director of UA Arizona Genomics Institute, and several of his colleagues are part of the International Barley Sequencing Consortium (IBSC).

The new resource will facilitate the development of better barley varieties able to cope with the demands of climate change, said IBSC. It should also aid in the fight against cereal crop diseases, which cause heavy losses every year. First cultivated more than 10,000 years ago, barley belongs to the Triticeae family – which includes wheat and rye – and that together provides around 30 per cent of the calories consumed worldwide. Barley is the world’s fourth most important cereal crop both in terms of area of cultivation and in quantity of grain produced.

At 5 billion nucleic acid base pairs, the barley genome is almost twice the size of that of humans, and determining the sequence of its DNA has presented a major challenge. This is mainly because its genome contains a large proportion of closely related sequences, which are difficult to piece together. “The larger the genome, the more repetitive its sequence is,” Dr. Wing said. His group laid an important piece of the groundwork for the sequencing project by constructing a library containing the genetic sequences of large chunks of the genome. Built in 2000, that library was the largest of its kind at the time. In the current effort, those pieces helped the consortium determine the locations of the genetic sequences obtained by the participating centres so that they could construct a map of the barley genome. “We know where most of the genes reside in the barley genome. If the sequence were a text, we would have almost all the words in the right order, but every 100 words or so, there would be one that is missing, Dr. Wing said.

The genome sequence provides a detailed overview of the functional portions of the barley genome, revealing the order and structure of most of its 32,000 genes and a detailed analysis of where and when genes are switched on in different tissues and at different stages of development. They describe the location of dynamic regions of the genome that carry genes conferring resistance to diseases. Dr. Wing said the sequenced barley genome would serve as a guide for wheat, the last of the world’s most important cereal crops yet to be sequenced, with a genome about three times larger than barley.

Gene ‘bursting’ plays key role in protein production

At the Gladstone Institutes, the United States, researchers have mapped the precise frequency by which genes get turned on across the human genome, providing new insight into the most fundamental of cellular processes and revealing clues as to what happens when this process goes awry. Gladstone researcher Dr. Leor Weinberger and his research team describe how a gene’s on-and-off switching – called “bursting” – is the predominant method by which genes make proteins. This discovery that provides an understanding of this underlying mechanism has the potential to vastly help researchers learn what happens at the molecular level when this mechanism is disrupted – such as in cancer or when exposed to a particular drug.

“Much like flicking on a light switch, genes get ‘switched on’ at specific intervals to initiate the fundamental biological process of protein synthesis,” said Dr. Weinberger, who is also an associate professor at the University of California, San Francisco (UCSF). “Until recently, the process was thought to be continuous – once a gene is switched on, it stays on, churning out protein products at a steady pace like a garden hose. But recently, some studies have suggested the opposite – that DNA produces RNA molecules in rapid-fire ‘staccato’ bursts. We decided to investigate how common this rapid-fire bursting was across the genome.”

In lab experiments, Dr. Weinberger’s team inserted a green fluorescent protein (vector) into the DNA of Jurkat T lymphocytes – a type of white blood cell that helps maintain a healthy human immune system. From this, they generated new cells in which the vector was integrated into any one of thousands of gene segments – with each segment glowing green when it was activated, or “switched on”. This allowed the researchers to see exactly how gene activation occurred across the entire human genome.

“Our analysis reveals support for the ‘bursting’ hypothesis – the genes acted as a sort of strobe light – transcribing RNA in rapid-fire bursts,” said Dr. Roy Dar, a Gladstone post-doctoral fellow and one of the paper’s lead authors. “We observed that the bursting frequency increases until, over time, it reaches a particular threshold. At that point, higher protein levels are reached by increasing the size of the bursts, eventually coming to a halt when no more protein product is needed. These results are a huge step towards understanding the basic molecular mechanism behind gene regulation.” The team believes that this new-found understanding of this fundamental biological process – that genomic bursts account for the majority of instances of protein production – holds vital clues to discovering how the disruption of these bursts could be harmful.

Embryo survival gene may fight range of diseases

A gene that keeps embryos alive appears to control the immune system and determine how it fights chronic diseases like hepatitis and human immunovirus (HIV), as well as autoimmune diseases like rheumatoid arthritis, say scientists at the Walter and Eliza Hall Institute of Medical Research in Australia. Although the studies on the gene Arih2 were conducted using mice, the scientists hope that the gene can be used as a target for drugs eventually to fight a spectrum of currently incurable diseases. Lead author Mr. Marc Pellegrini said the gene appears to act like a switch, flipping the immune system on and off – if the gene is on, it dampens the immune response; if it is off, it greatly enhances immune responses. “It is probably one of the few genes and pathways that is very targetable and could lead to a drug very quickly,” Mr. Pellegrini said.

Arih2, first identified in the fruit fly, drew the interest of Mr. Pellegrini’s team because of its suspected links to the immune system. The scientists removed the gene from adult mice and noticed how their immune systems were boosted for a short period. But then it quickly went into an overdrive and started attacking the rodents’ own healthy cells, skin and organs. The scientists hope that the gene would be studied further for use as a drug target to fight a large spectrum of diseases. “In infectious diseases, you want to slam on the brakes on this gene, and for autoimmune diseases, you want to push the accelerator to make it work much harder to stop the whole immune response,” said Mr. Pellegrini.

A gene that maintains bones in health

An international study that involved more than 50 researchers across Europe, North America and Australia has identified a special gene with a strong link to bone density and so-called cortical bone thickness, which is decisive to bone strength. The gene, Wnt16, can be used as a risk marker for fractures and opens up opportunities for preventive medicine against fractures. The international study – led by Associate Professor Dr. Mattias Lorentzon and Professor Dr. Claes Ohlsson at the Sahlgrenska Academy, University of Gothenburg, Sweden – was based on extensive genetic analyses of the genetic material of 10,000 patients and experimental studies in mice.

The genetic variation studied by the international research network could predict, for example, the risk of a forearm fracture in a large patient group of older women. In an experimental study, the research team established that the gene has a crucial effect on the thickness and density of the femur. The team found that the strength of the femur was up to 61 per cent lower in mice without the Wnt16 gene. The discovery opens up opportunities to develop new medicines to prevent the most common fractures.

Genome analysis of tumours reveals new pathways

Recent genomic analysis of pancreatic tumours has revealed two new pathways involved in the disease – information that could be capitalized on to develop new and earlier diagnostic tests for the disease, stated Dr. William Fisher, Professor of surgery at Baylor College of Medicine (BCM) and Director of BCM Elkins Pancreas Centre, the United States, who was part of the local team that took part in the international effort. “We now know every gene involved in pancreatic cancer,” said Dr. Fisher. “This study ushers in a whole new era of taking care of patients with pancreatic cancer.”

BCM Human Genome Sequencing Centre was one of three sequencing centres worldwide that analysed the genomes of pancreatic tumours and normal tissues taken from 142 patients with the disease. Along with Australian Pancreatic Centre Genome Initiative and Canadian Ontario Institute for Cancer Research Pancreatic Cancer Genome Study, the Centre studied in detail 99 tumours, identifying 1,982 mutations that resulted in a change to a protein and 1,628 significant copy number variations events in which the structure of the chromosomes themselves were changed.

The researchers discovered mutations in genes involved in chromatin modification – affecting the way DNA is packaged inside the cell – and axon guidance – the process that guides the axon to grow to its proper target. “This is a category of genes not previously linked to pancreatic cancer,” Dr. Fisher said. This study is the first to report findings from primary tumours in the disease.

Gene discovery chip detects gene variants involved obesity

An international study has identified three new gene variants associated with body mass index (BMI) levels in adults. The scientific consortium, numbering approximately 200 researchers, performed a meta-analysis of 46 studies, covering gene data from around 109,000 adults from four ethnic groups. In discovering intriguing links to lipid-related diseases, type 2 diabetes and other disorders, the IBC 50K SNP Array BMI Consortium’s study may provide fundamental insights into the biology of adult obesity.

The study used the CardioChip, a gene array containing probes for some 50,000 genetic variants in 2,100 genes relevant to cardiovascular and metabolic functions. The researchers first analysed a dataset of around 51,000 individuals of European ancestry (EA) to discover initial gene signals, and then performed replication studies in another 27,000 EA subjects, as well as 14,500 additional EA individuals. Further analyses of data from approximately 12,300 African Americans, 2,600 Hispanics and 1,100 East Asians strengthened the team’s findings.

Three novel signals were uncovered from the genes TOMM40-APOE-APOC1, SREBF2 and NTRK2, that were significantly associated with BMI in adults. All had previously been linked to other important disorders. The APOE locus is well known to be involved in blood lipid regulation and circulation, and Alzheimer’s disease. The SREBF2 gene is linked to type 2 diabetes. NTRK2 codes for a receptor of the BDNF protein, which is known to be related to BMI and is associated with anorexia. The researchers also discovered that two genes, BDNF and MC4R, each harbour two independent signals for BMI. The two genes were among eight genes previously associated with BMI that the current study was able to replicate, including FTO, SH2B1 and COL4A3BP-HMGCR.


New insights into herpes virus proteome

Researchers had already sequenced the herpes virus genome 20 years ago, thinking they could then predict all proteins that the virus produces (virus proteome). Now scientists from the Max Planck Institute of Biochemistry (MPIB), Germany, and their collaboration partners at University of California–San Francisco (UCSF), the United States, have identified several hundred novel proteins, many of which are surprisingly small, in herpes virus proteome.

To carry out their study, the scientists infected cells with herpes virus and observed which proteins the virus produced inside the cell over a period of 72 hours. In order for proteins to be produced at all, the cell machinery must first make copies of the genetic material as intermediate products (RNA). In the case of the herpes virus, the UCSF scientists discovered many novel RNA molecules that were in large part surprisingly short. They also found that the organization of information required for protein production in the virus genome was far more complex than previously assumed. Dr. Annette Michalski, a scientist in the MPIB Department of Proteomics and Signal Transduction, subsequently confirmed the predicted viral proteins in the infected cell using mass spectrometry.

The results of the joint research provide detailed insight into the complex mechanisms used by the virus. “We showed that it is not enough merely to know the virus genome to understand the biology of the herpes virus,” Dr. Michalski said. “What is important is to look at the products actually produced from the genome.” Even human genes may be much more complex than the genome sequence itself indicates, said the scientists.

Bacterial protein structures reveal a biochemical secret

The structures of key bacterial proteins have revealed one of the biochemical secrets that enable bacteria to outwit antibiotics. At Duke University School of Medicine, the United States, scientists studied multi-drug tolerance, a phenomenon that allows bacteria to become dormant and tolerate antibiotics, only to later awaken and re-infect the host. Multi-drug tolerance starts with a protein kinase molecule called HipA, which drives a few bacterial cells into dormancy. Eventually, these so-called “persister” cells – one in a million in the bacterial population – awaken to begin growing and starting the cycle of infection all over again.

By analysing the structural and biochemical components at work in the HipA-mediated system, the Duke team was able to get to the bottom of how this protein works. Dr. Maria A. Schumacher, Professor of biochemistry and lead author of the study, used X-ray crystallography to produce an atomic-level 3-D structure of HipA. This structure was pivotal to understand how this simple modification affected HipA’s activity.

HipA carries out phosphorylation, which affects the activities of other molecules that control dormancy, Dr. Schumacher said. When phosphorylation is in excess, HipA turns itself off by an unusual self-modification, causing the modified region to become disordered. “In fact, this normally internal part of the protein is ejected to the outside. To the best of our knowledge, this had never been seen before in any protein of this type, and it is an incredibly unusual mechanism for how it works,” Dr. Schumacher said.

Multi-drug tolerance is different from the better-known multi-drug resistance. “In multi-drug resistance, bacteria evolve by a number of mechanisms to become strains that are resistant to higher and higher concentrations of antibiotics,” explains Dr. Richard G. Brennan, Professor and Chairman of Department of Biochemistry and senior author of the study. “In multi-drug tolerance, the drugs do not work because the bacteria are dormant. The persister cells simply evade most drugs until it is safe for them to re-emerge and re-infect, without having mutated.”

A detailed view of brain protein structure

Researchers have published the first highly detailed description of how neurotensin, a neuropeptide hormone that modulates nerve cell activity in the brain, interacts with its receptor. Their results suggest that neuropeptide hormones use a novel binding mechanism to activate a class of receptors called G-protein coupled receptors (GPCRs). “The knowledge of how the peptide binds to its receptor should help scientists design better drugs,” said Dr. Reinhard Grisshammer, a scientist at the National Institute of Neurological Disorders and Stroke (NINDS), the United States National Institutes of Health (NIH).

Dr. Grisshammer and his colleagues used X-ray crystallography to show what the receptor looks like in atomic detail when it is bound to neurotensin. Their results provide the most direct and detailed views describing this interaction, which may change the way scientists develop drugs targeting similar neuropeptide receptors. Neurotensin receptors and other GPCRs belong to a large class of membrane proteins that are activated by ligands. Previous X-ray crystallography studies showed that smaller ligands, such as adrenaline and retinal, bind in the middle of their respective GPCRs and well below the receptor’s surface. In contrast, Dr. Grisshammer’s group found that neurotensin binds to the outer part of its receptor, just at the receptor surface. These results suggest that neuropeptides activate GPCRs in a different way compared with the smaller ligands.

3-D model of tuberculosis protein

Researchers at Johns Hopkins University, the United States, have figured out the 3-D shape of the protein responsible for creating unique bonds within the cell wall of the bacteria that cause tuberculosis (TB). The bonds make the bacteria resistant to all currently available drug therapies. With the protein structure in hand, the scientists say, drug designers have a clear way forward for weakening the cell wall and terminating these deadly bacteria. The Johns Hopkins team used X-ray crystallography to scatter radiation off a specially prepared portion of the enzyme that forms the unique molecular bonds within the cell wall of Mycobacterium tuberculosis. They then used information about the direction and intensity of the radiation scattered to build a 3-D model of the arrangement of atoms in the enzyme.

Dr. Mario A. Bianchet, Assistant Professor of neurology at Johns Hopkins and a member of the research team, says that roughly 1 per cent of bacteria persists after the first week of a patient’s treatment. “The ‘persisters’ resist in part because of unique bonds within their cell walls. Their cell walls form a thick, three-layered boundary between the bacteria and the outside world, including a middle layer of interlocking molecules, called peptidoglycans, that form a network resembling a chain-link fence,” says Dr. Bianchet.

Peptidoglycans are long chains of sugar molecules with short protein branches extending from every other sugar on alternating sides of the chain. Specific enzymes bond the protein branches to each other to create a meshwork. In most bacterial species, the majority of the bonds between these branches are created between position 4 on one branch and position 3 on an opposing branch. In M. tuberculosis, however, the majority of the bonds are created between positions 3 on both branches. The most common antibiotics interfere with the enzyme that creates the 4-3 bonds, which is enough to destabilize the cell wall and kill most TB bacteria.

The bacteria that persist have a particularly high level of 3-3 bonds between the peptidoglycan chains in their cell walls. These 3-3 bonds are created by a different enzyme, which is not specifically targeted by any current drugs.

A protein that helps cells repair DNA damage

In the United States, University at Buffalo (UB) scientists have discovered the role that a protein called Transcription Factor II B (TFIIB) plays in helping cells repair DNA damage, a critical function for preventing growth of tumours. TFIIB is a protein that binds to DNA in cells to initiate the transcription process, which is vital for building new proteins. When DNA damage occurs, TFIIB is altered in a way that halts general transcription, enabling a cell to give priority to repair, the researchers found. With the shut-down in effect, cells are able to prioritize the vital functions carried out by a tumour-suppressing protein called p53, said lead author Dr. Jayasha Shandilya, a post-doctoral researcher in UB’s Department of Biological Sciences.

About half of all cancer cases involve a mutation or deletion of the p53 gene. When DNA is damaged, it activates p53, which not only stimulates the DNA repair pathway, but also triggers the synthesis of proteins that stop cells from dividing before problems are fixed, Dr. Shandilya said. In cases where the damage is not reparable, p53 initiates apoptosis or programmed cell death. Dr. Shandilya and her colleagues report that for normal transcription to occur, TFIIB must undergo phosphorylation, in which a phosphate group is attached to the protein. But in cells treated with DNA damaging agents, the scientists found that TFIIB was dephosphorylated, preventing general transcription and enabling the cells to focus resources on helping p53 carry out its tumour suppressing functions. In essence, p53 can bypass the need for TFIIB phosphorylation to activate transcription of its target genes, which are vital for DNA damage response.

New technique can identify cell-secreted proteins

Researchers from North Carolina State University, the United States, have developed a new technique to identify the proteins secreted by a cell. The new approach should help researchers collect precise data on cell biology, which is critical in fields ranging from zoology to cancer research. The work is important because cells communicate by secreting proteins. Some of the proteins act on the cell itself, telling it to grow or multiply, for example. But the proteins can also interact with other cells, influencing them to perform any biological function.

The new approach takes advantage of the fact that each cell packages its proteins in its “secretory pathway”. Each cell synthesizes the protein and passes it through this pathway, essentially placing it in a bag-like membrane before it is passed out of the cell. In their new technique, researchers take a sample of cells and isolate the secretory pathway organelles that contain the proteins. They then use mass spectrometry to analyse the contents of the organelles to see which proteins are being secreted by the cell. The researchers were thus able to identify proteins that are secreted by human embryonic stem cells.

“This gives us a snapshot of exactly what a cell was secreting at that point in time,” says Dr. Balaji Rao, an assistant professor of chemical and biomolecular engineering and co-author of a paper describing the work. This new method eliminates the problems related to the proteins found in cell culture media. It also allows researchers to track changes in the proteins released by a cell in response to a stimulus, such as exposure to a chemical. In principle, this technique would also allow researchers to identify which proteins any specific type of cell is secreting when in a mixed population of cells.

Protein that plays a role in immunity decline in the aged

Scientists at Stanford University School of Medicine in the United States have found that blocking the action of a single protein, whose levels in human immune cells creep steadily upwards with age, can restore those cells’ response to a vaccine. Vaccine failure among seniors poses a serious health problem. This discovery holds important long-term therapeutic ramifications, said Dr. Jorg Goronzy, Professor of rheumatology and immunology and the senior author of the study. The Stanford team fingered a protein called DUSP6 that interferes with the capacity of an important class of immune cells to respond to the presence of a foreign substance, such as those appearing on the surface of an invading pathogen or in a vaccine designed to stifle that invasion. The researchers also identified a potential lead compound that, by inhibiting DUSP6’s action, restores those cells’ responsiveness to a more youthful state.

Older people’s T-helper cells, an important type of “beat cop” of the immune system, have diminished capacity to activate, proliferate and secrete vital signalling chemicals in response to infections or vaccines. This limits even an adjuvant-containing vaccine’s efficacy. Dr. Goronzy’s team had shown that faulty regulation in memory T-helper cells (cells that have previously encountered an antigen), owing to aging-related increased levels of a protein called DUSP4, inhibits the activation of those cells, with their consequent failure to ignite a good antibody-producing response from B-cells, which play a key role in the body’s response to infection-preventing vaccines.

This time around, the investigators uncovered a similar effect with a related protein, DUSP6, on naive T-helper cells (cells that have not known an antigen before). DUSP6 is an enzyme that works by hacking phosphate groups off other enzymes, thus reducing their activity. The “downstream” enzymes are crucial to naive T-helper cell activation. DUSP6 levels are much higher in older people’s naive T-helper cells, due to an age-related easing up on a brake pedal called miR-181a, one among hundreds of microRNAs that regulate protein production. miR-181a directly interferes with DUSP6 production. The amount of miRNA-181 in naive T-helper cells declines steadily with age, causing DUSP6 levels of in these cells to increase. Artificially boosting miRNA-181a levels in naive T-helper cells causes DUSP6 levels to plummet, commensurately raising those cells’ readiness to activate on exposure to vaccine. In contrast, artificially increasing the levels of DUSP6 blocked the beneficial effects of heightened miR-181a levels.


Alzheimer’s drug improves cognitive function

In the United States, Washington State University (WSU) researchers have developed a new drug candidate that improves cognitive function dramatically in rats with Alzheimer’s-like mental impairment. The new compound, which is intended to repair brain damage that has already occurred, is a significant departure from the current Alzheimer’s treatments, which either slow the process of cell death or inhibit cholinesterase, an enzyme believed to break down a key neurotransmitter involved in learning and memory development.

In 1992, Prof. Joe Harding from WSU College of Veterinary Medicine and Prof. Jay Wright from WSU College of Arts and Sciences began looking at the impact of the peptide angiotensin IV on the hippocampus, a brain region involved in spatial learning and short-term memory. The scientists noted that angiotensin IV, or early drug candidates based on it, were capable of reversing learning deficits seen in many models of dementia. However, as these compounds were not stable enough to cross the blood-brain barrier, the practical utility of these early drug candidates was severely limited.

Then, Prof. Harding designed a smaller and stable version of the molecule called Dihexa. Not only Dihexa can cross the blood-brain barrier, but it can also move from the gut into the blood – that is, it can be taken in pill form. The researchers tested the drug on a number of rats treated with scopolamine, a chemical that interferes with a neurotransmitter critical to learning and memory. After receiving the WSU drug directly in the brain, orally or through an injection, the cognitive function of the rats greatly improved.

The current “gold standard” compound for creating neuron connections is brain-derived neurotrophic factor (BDNF), a growth-promoting protein associated with normal brain development and learning. Autopsies of Alzheimer’s patients have found lower levels of BDNF in the brain. In bench assays using living nerve cells to monitor new neuron connections, Prof. Harding and his colleagues found Dihexa to be seven orders of magnitude more powerful than BDNF, which has yet to be effectively developed for therapeutic use. In other words, it would take 10 million times as much BDNF to get as much new synapse formation as Dihexa.

RNA-based therapy could cure deadly blood cancer

Mantle cell lymphoma (MCL) is a devastating form of blood cancer with a median survival span of only 5-7 years. One of the characteristics of MCL is the heightened activity in the gene CCND1, which leads to the aggressive over-production of Cyclin D1, a protein that controls the proliferation of cells, explains Prof. Dan Peer from the Department of Cell Research and Immunology of Tel Aviv University, Israel. In MCL, Cyclin D1 production spins out of control, producing a 3,000-5,000 fold increase.

Now, in an international collaboration between the academia the and industry, Prof. Peer has developed a new class of drugs based on RNA interference (RNAi), which can repair or destroy faulty proteins and reprogramme the cells to act normally. The drugs have the ability to terminate the mutated protein to stop the over-proliferation of cells. In MCL, Cyclin D1 is the exclusive cause of the over-production of B lymphocytes, cells responsible for generating antibodies, explains Prof. Peer. This makes the protein a perfect target for RNAi. The RNAi that the researchers have developed targets the faulty Cyclin D1 within the cancerous cells. When the cells are inhibited from proliferating, they sense they are being targeted and begin to “commit suicide,” Prof. Peer says.

In the lab, the researchers have successfully used RNAi in human cells, a crucial step towards proving that Cyclin D1 can be targeted through right interventions. “Ultimately, we want to be able to cure this disease, and I think we are on the way,” explains Prof. Peer. He hopes that the results might cause scientists to reconsider previous and unproductive results on the effectiveness of treating MCL by addressing all aberrations of this protein.

New drug to destroy tumour cells

A new drug created at the University of Minnesota (UM), the United States, may hold the answer to defeating pancreatic cancer. The research is based on successful outcomes in a mouse model, and researchers expect to repeat them in human trials scheduled for 2013. The drug, Minnelide, is an injectable chemotherapy designed to target tumour cells. It works by inhibiting HSP 70, a heat shock protein that has been proven to aid the growth of tumour cells. By stopping HSP 70 from working, Minnelide disperses the cells integral to the tumour’s growth and the cancer disintegrates.

In 2007, Dr. Ashok Saluja, Professor and Vice Chair of Research in the UM Medical School’s Department of Surgery, and colleagues had discovered that pancreatic cancer cells have too much HSP 70, which protects cells from dying and thus make them difficult to target with drugs. The researchers then found that triptolide, a compound derived from certain plants in China, worked to halt the development of HSP 70 in tumour cells. However, because triptolide is not water-soluble, it was difficult to administer to patients. Dr. Saluja and his collaborators then worked to develop Minnelide – a water-soluble version of triptolide.

Tweaked immune system fights melanoma

Loyola University Medical Centre, the United States, has launched the first clinical trial in the Midwest of an experimental melanoma treatment that genetically engineers a patient’s immune system to fight the deadly cancer. A batch of the immune system’s killer T-cells will be removed from the patient and genetically modified (GM) by inserting two genes into them so that the T-cells will recognize tumour cells as abnormal. The patient will undergo high-dose chemotherapy to kill most of his or her remaining T-cells, and the GM T-cells will then be put back in the patient. The modified T-cells, it is hoped, will recognize the tumour cells as abnormal and kill them.

The Phase 1 trial will determine the optimum dose and whether the treatment is safe. Four doses will be tested, with the highest dose consisting of about 5 billion GM T-cells. If Phase 1 demonstrates the treatment to be safe, investigators will proceed to Phase 2, which will determine whether the treatment is effective. The experimental immune system therapy was developed by Dr. Michael I. Nishimura, Director of Immunotherapeutics Programme at Loyola’s Cardinal Bernardin Cancer Centre. The cells will be prepared in the Robert R. McCormick Foundation Centre for Cellular Therapy in the Bernardin Cancer Centre, the United States.

‘Humanized’ mice advance study of rheumatoid arthritis

At Northwestern University Feinberg School of Medicine in the United States, researchers have developed the first animal model that duplicates the human response in rheumatoid arthritis (RA), an important step that may enable scientists to discover better medicines to treat the disease. “This is the first time human stem cells have been transplanted into mice in order to find RA treatments,” said Dr. Harris Perlman, an associate professor of rheumatology.

Until now, scientists have relied on the common scientific method of using specially bred mice to develop drugs to control RA. However, as human and mouse immune systems differ dramatically, studying RA in these mice does not give an accurate representation of how the disease functions in humans. In some cases, RA drugs that had seemed promising based on results in mice have failed in human clinical trials.

The Northwestern team injected one day-old mice with human stem cells from umbilical cord blood, including white blood cells, which regulate immunity. Then, RA was introduced in the mice and suppressed with Enbrel®, a common first-line drug for joint inflammation in humans. This offered evidence that their immune systems were indeed replicating human defences. Earlier in 2012, Dr. Perlman had introduced a mouse model that develops RA and is predisposed to atherosclerosis, a common RA complication in humans.

Building a better drug for type 2 diabetes

Thiazolidinedione drugs (TZDs), which are used to treat type 2 diabetes, cause potentially severe side-effects such as heart failure, bone fracture and bladder cancer in certain patients. Professor Curt Sigmund, Head of pharmacology at the University of Iowa Carver College of Medicine, the United States, led a study that looked into how TZDs lower blood pressure, so that more specific drugs might be developed that retain the beneficial effect of TZDs but eliminate the detrimental side-effects.

TZD drugs activate a protein called PPAR-gamma. Genetic mutations in this protein disrupt the normal function of blood vessels, causing high blood pressure in people. Dr. Sigmund and his team genetically modified a mouse in which the protein expressed in the blood vessels was mutated. These mice developed high blood pressure. Using these mice, the researchers uncovered an important biological pathway – the Cullin-3 pathway – in blood vessels, which may be the key to the blood pressure-lowering effects of TZD drugs. Decreased activity of Cullin-3, through disruption of PPAR-gamma, leads to increased blood pressure.


Gene suppression reduces sweetening in potatoes

Preventing activity of a key enzyme in potatoes may help boost potato quality by putting an end to cold-induced sweetening, according to the United States Department of Agriculture (USDA) scientists. Cold-induced sweetening, which occurs when potatoes are put in long-term cold storage, changes flavour and causes unwanted dark colours in fried and roasted potatoes. Long-term cold storage is, however, required to ensure year-round supply of potatoes.

USDA scientists at Agricultural Research Service (ARS) Vegetable Crops Research Unit found that during cold storage, an enzyme called invertase causes changes in potato sugars – more sucrose accumulation and a corresponding increase in the amount of glucose and fructose in tubers stored at very low temperatures. Mr. Paul Bethke, a plant physiologist, and Ms. Shelley Jansky, a geneticist, and technician Mr. Andy Hamernik used a recently developed technology to show that decreasing the activity of invertase is sufficient to enable cold storage of potatoes without compromising the appearance of potato chips or the growth characteristics of the potato plants.

Mr. Bethke and his colleagues are using molecular tools to improve understanding of what is controlling the process of cold-induced sweetening. Potatoes are sensitive to their environment and highly sensitive to low temperatures, and respond to these temperatures by producing “reducing sugars”, primarily glucose and fructose. When chips or fries are made from these potatoes, they tend to be bitter and dark-coloured. However, invertase’s level of importance has never been clear because there are other biochemical steps that might also contribute, according to Mr. Bethke.

‘Superweeds’ linked to rising herbicide use in GM crops

A study by Professor Charles Benbrook of Washington State University, the United States, has found that the use of herbicides in the production of three genetically modified (GM) herbicide-tolerant crops – cotton, soybeans and corn – has actually increased. This counterintuitive finding is based on an exhaustive analysis of data publicly available from the National Agriculture Statistics Service of the United States Department of Agriculture (USDA). Prof. Benbrook’s analysis is the first peer-reviewed, published estimate of the impacts of genetically engineered (GE) herbicide-resistant crops on pesticide use.

Prof. Benbrook says that the emergence and spread of glyphosate-resistant weeds are strongly correlated with the upward trajectory in herbicide use. Glyphosate, which is marketed as ‘Roundup’ and other trade names, is a broad-spectrum systemic weedicide. Approximately 95 per cent of soybean and cotton acres, and more than 85 per cent of corn, are planted to GE varieties that are herbicide resistant. “Resistant weeds have become a major problem for many farmers reliant on GE crops, and they are now driving up the volume of herbicide needed each year by about 25 per cent,” Prof. Benbrook said.

Herbicide-tolerant crops worked extremely well in the first few years of use, Prof. Benbrook’s analysis shows, but over-reliance may have led to shifts in weed communities and the spread of resistant weeds that force farmers to increase herbicide application rates (especially glyphosate), spray more often and employ new herbicides that work through an alternate mode of action into their spray programmes.

Modern DNA techniques applied to ancient potatoes

At University of Hertfordshire, the United Kingdom, researchers led by Professor Bruce Fitt, have used modern DNA techniques on late 19th century potatoes to show how the potato blight might have survived between cropping seasons after the Irish potato famine of the 1840s. Late potato blight is caused by the microorganism, Phytophthora infestans, which rapidly destroys the leaves of potato crops and was responsible for the infamous Irish potato famine of the 1840s. Late blight remains a serious disease problem in current potato production and has also emerged as a significant threat to the organic tomato industry.

Prof. Fitt and his colleagues extracted DNA from the Rothamsted potato samples that had been dried, ground and stored in glass bottles in the 19th century. The DNA was then analysed for the presence of the potato blight pathogen. “It was the foresight of two 19th century plant scientists to archive potato samples from their experiment that has enabled us to apply modern DNA techniques to better understand late potato blight and the implications for today’s food security. The analysis of these late 19th century potato samples is the earliest proof of how this disease survived between seasons in England,” Prof. Fitt said.

The research findings have proved that the DNA technique applied to the potato samples is a very useful tool in plant disease diagnosis to test seed potatoes or tomato transplants for the presence of the late blight pathogen. This technique can be developed further for testing for other diseases in different plants that affect food production. “Using modern DNA techniques to detect and quantify the pathogen in potatoes enables us to better understand the spread of potato late blight,” Prof. Fitt remarked.

Napiergrass: a potential biofuel crop

A grass fed to cattle throughout much of the tropics may become a biofuel crop that could help us meet our future energy needs, say researchers at the United States Department of Agriculture (USDA). Napiergrass (Pennisetum purpureum) is fairly drought-tolerant, grows well on marginal lands and filters nutrients out of run-off in riparian areas.

As part of a nationwide search for alternatives, Mr. William Anderson, a geneticist with the USDA Agricultural Research Service (ARS) Crop Genetics and Breeding Research Unit, and his colleagues compared napiergrass with several other candidate feedstocks in a study to see how they would fare in head-to-head competition. The research team grew energy cane, napiergrass, switchgrass and giant reed for four years and compared biomass yields and soil nutrient requirements. The findings of the research show that napiergrass could be a viable biofuel crop. It is not as cold-tolerant as switchgrass, but does offer advantages, such as continuing to produce biomass until the first frost.

The researchers are continuing to study napiergrass with an eye towards yield improvements, usable fibre content and disease resistance. They are also evaluating production systems that use chicken litter, synthetic fertilizer and winter cover crops, as well as different irrigation levels, harvest times and planting dates. Preliminary findings in those studies show yields are sufficient without irrigation, and that there is hardly any difference in yield when poultry litter is used instead of synthetic fertilizers.

Researchers create potatoes with higher levels of carotenoids

Potatoes with higher levels of beneficial carotenoids are the result of the United States Department of Agriculture (USDA) studies to improve one of the nation’s most popular vegetables. Scientists with USDA Agricultural Research Service (ARS) bred yellow potatoes with carotenoid levels that are two to three times higher than those of the popular Yukon Gold yellow-fleshed potato variety.

ARS plant geneticist Ms. Kathy Haynes and nutritionist Ms. Beverly Clevidence found wild potatoes with intense yellow flesh that have about 23 times more carotenoids than white-flesh potatoes. They, by crossing these wild potatoes with cultivated types, developed the high-carotenoid potatoes. In 2007, Ms. Haynes and her colleagues introduced ‘Peter Wilcox’, a new potato that they developed. The potato comes with purple skin and yellow flesh. The overall carotenoid levels in this potato are more than 15 per cent higher than those in the Yukon Gold variety, according to Ms. Haynes. The carotenoids involved include lutein, neoxanthin, antheraxanthin, violaxanthin and zeaxanthin. Among these, lutein and zeaxanthin are of keen interest for eye health; they appear to protect against age-related macular degeneration and perhaps against cataract formation.

Growing corn to treat rare diseases

The seeds of greenhouse-grown corn could hold the key to treating lysosomal storage (LS) diseases – rare, but deadly childhood genetic diseases – according to researchers from Simon Fraser University, Canada. Currently, enzyme treatments are available for only six of the more than 70 diverse types of LS diseases. Biologist Ms. Allison Kermode and her colleagues have found that greenhouse-grown maize could become a platform for producing alpha-L-iduronidase enzyme used to treat the LS disease called mucopolysaccharidosis I.

The novel technology manipulates processes inside the maize seed that “traffic” messenger RNAs to some parts of the cell as a means to control the subsequent sugar processing of the therapeutic protein. The researchers have been able to produce the enzyme drug in maize seeds, and the product could ultimately be used as a therapeutic for the disease.


Biofuel Technologies: Recent Developments

In this book international experts present recent advances in biofuel research and related technologies. Topics include biomethane and biobutanol production, microbial fuel cells, biomass pre-treatment, enzyme hydrolysis, genetic manipulation of microbial cells and their application in the biofuels industry, bioreactor systems, and economical processing technologies for biofuel residues. The chapters provide concise information to help understand the technology-related implications of biofuels development. Recent updates on biofuel feedstocks, biofuel types, associated co-products and by-products and their applications are also highlighted. The book addresses the needs of postgraduate researchers and scientists across diverse disciplines and industrial sectors in which biofuel technologies and related research and experimentation are pursued.

Contact: Springer GmbH, Haberstrasse 7, 69126, Heidelberg, Germany. Tel: +49 (6221) 345 4301; Fax: +49 (6221) 345 4229; E-mail:

Enzyme Engineering: Methods and Protocols (Methods in Molecular Biology)

Engineering a novel biological catalyst is an enticing challenge. High-resolution protein structure analysis allows for rational alteration of enzyme function, yet many useful enzyme variants are the product of well-designed selection schemes or screening strategies. This publication provides guidance to investigators wishing to create enzyme variants with desired properties. It covers such topics as a simple method for generating site-specific mutations within bacterial chromosomes and engineering of endonucleases that show great potential in gene therapy applications. The chapters include introductions to their respective topics, lists of the necessary materials and reagents, readily reproducible protocols, and notes on troubleshooting and avoiding known pitfalls. This authoritative volume will be valuable for scientists with an interest in protein engineering as well as veterans looking for data on new developments.

Contact: Humana Press, 999 Riverview Drive, Suite 208, Totowa, NJ, 07512, United States of America. Tel: +1 (973) 2561 699; Fax: +1 (973) 2568 341; Website:


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