Research on the genetic defect that causes myotonic muscular dystrophy has revealed that the mutation disrupts an array of metabolic pathways in muscle cells through its effects on two key proteins. A study published in Nature Structural & Molecular Biology shows that the loss of a single protein accounts for most of the molecular abnormalities associated with the disease, while loss of a second protein also seems to play an important role.

Each of the affected proteins interacts with an array of genes that are active in muscle cells and other tissues, said coauthor Manuel Ares, professor of molecular, cell, and developmental biology at the University of California, Santa Cruz. The study reveals a cascading sequence of molecular events in which a mutation in one gene ends up affecting hundreds of other genes and the physiological processes that depend on them.

“This is a genetic disease in which there isn’t just one gene that is affected,” Ares said. “Our hope is that by chasing down more of the affected genes we might be able to figure out how to address more of the symptoms.”

Myotonic dystrophy involves difficulty relaxing muscles (myotonia) and, as in other muscular dystrophies, progressive muscle weakness and wasting. The most common type of myotonic dystrophy (type 1) is caused by changes in a gene that has a repeating sequence of three DNA building blocks. This sequence is repeated five to 35 times in the normal gene, but an excessive number of repeats (50 to 5,000) leads to disease. When the defective gene is transcribed into a messenger RNA molecule, the expanded repeat section causes the RNA to bind tightly to certain proteins, forming clumps within the muscle cells.

“Previous studies have shown that two proteins called Mbnl1 and Mbnl2 are bound up by the repeat RNA and create an aggregate inside the nucleus of the muscle cell,” Ares said.

By binding these proteins in clumps, the abnormal RNA prevents them from carrying out their normal functions in the cell. Mbnl1 is involved in a process called RNA splicing, in which the messenger RNA copied from a gene gets “edited” before it can direct the synthesis of proteins.

“When a gene is turned on, its DNA sequence gets copied into a messenger RNA molecule. But that direct copy needs to be processed to make a functional message that can be translated into a protein,” Ares said. “Splicing factors like Mbnl1 tell the splicing machinery where to do the cutting and pasting. Without Mbnl1, incorrect splicing can affect lots of different genes.”

Ares has pioneered the use of microarray technology to detect changes in RNA splicing caused by genetic mutations and other perturbations. UCSC graduate student Hongqing Du, the first author of the paper, earned her M.D. from Harbin Medical University in China and was eager to apply this technology to a human disease. So Ares and Du teamed up with leading investigators of mytonic dystrophy who had developed animal models of the disease.

Charles Thornton’s lab at the University of Rochester School of Medicine developed a mouse strain that expresses large amounts of the abnormal repeat RNA in muscle cells. Maurice Swanson’s lab at the University of Florida College of Medicine developed a mouse strain that is unable to make the Mbnl1 protein. Both strains of mice show symptoms similar to myotonic dystrophy.

Ares’s lab used splicing-sensitive microarrays developed in collaboration with Affymetrix to show that the RNA splicing defects in muscle cells from these two mouse strains are nearly the same. This indicates that the vast majority of the splicing problems are due to the loss of the Mbnl1 protein as a result of binding to the abnormal repeat RNA. Earlier studies had associated several splicing defects with the disease, but the microarrays revealed effects on a much larger number of genes.

“Our microarray methods detected hundreds of splicing events that were being affected, giving us a broader picture of what’s going on in cells as the disease is taking hold,” Ares said.

Tests for some of the newly identified splicing defects in human patients with myotonic dystrophy confirmed that the same changes occur in both mouse and human cells. More extensive testing in humans will enable the researchers to identify which RNA splicing changes might be clinically useful for diagnosing or monitoring the disease, Ares said.

The researchers also found another set of changes that were seen only in the mouse strain that makes the abnormal repeat RNA and not in the mice lacking Mbnl1. These effects were not splicing errors, but changes in gene expression detected by microarrays that measured the amounts of messenger RNA being transcribed from different genes.

“We suspect that the loss of Mbnl2 is responsible for those gene expression defects,” Ares said.

Many of the genes with altered expression levels are involved in making the extracellular matrix, a protein coat that binds muscle cells together and enables muscle tissue to generate a coherent force when it contracts.

“We’re excited by this finding because the group of genes affected is rich in these structural components operating outside the cell to hold the tissue together, and that might explain some aspects of the disease,” Ares said. “Some of the genes in this class have been implicated in other kinds of genetically inherited muscular dystrophy and connective tissue diseases, revealing unanticipated links with the myotonic form of muscular dystrophy.”

A recent grant from the Muscular Dystrophy Association will enable Ares and his collaborators to investigate how these findings might be used to help patients with myotonic dystrophy. The researchers may be able to develop methods for early detection of the disease or for predicting how the disease will progress in individual patients. Further research could also yield molecular markers of the disease for use in developing and evaluating new treatments.

“Right now we have a bewildering list of splicing events that are going wrong, as well as gene expression defects, and we have a lot of work to do to figure out which are the key events that might be used as reliable markers of the disease,” Ares said.

In addition to Ares, Du, Swanson, and Thornton, the coauthors of the paper include Melissa Cline, John Paul Donohue, Megan Hall, and Lily Shiue of UC Santa Cruz; Robert Osborne of the University of Rochester School of Medicine; Daniel Tuttle of the University of Florida College of Medicine; and Tyson Clark of Affymetrix. This research was supported by grants from the National Institute of General Medical Sciences, National Institute of Arthritis and Musculoskeletal and Skin Diseases, and the National Institute of Neurological Disorders and Stroke.

Source:
Tim Stephens
University of California – Santa Cruz Continue reading →

UCB’s new treatment for epilepsy, has today been accepted for use in Scotland by the Scottish Medicines Consortium (SMC) for adults with partial onset seizures, as an add-on to patients’ current therapy. All NHS health boards in Scotland will now consider the SMC’s advice and ensure that this new treatment is made available where there is a clinical need. The SMC advise use in patients with refractory epilepsy.

The efficacy of VIMPAT® as adjunctive therapy at recommended doses (200 mg/day, 400 mg/day) was established in 3 multicentre, randomised, placebo-controlled clinical trials with a 12-week maintenance period. Overall the proportion of patients with a 50% reduction in seizure frequency was 23%, 34%, and 40% for placebo, Vimpat 200 mg/day and 400 mg/day, respectively. In addition, results from an open-label extension study demonstrate long-term retention; of the 370 patients enrolled, 77% were still taking Vimpat after one year.

Between, 20,000 ??” 40,000 adults in Scotland have epilepsy. In the UK, it is estimated that around a third of people with epilepsy still experience seizures despite treatment with these medications. Epilepsy can have a huge impact on the work, social and personal lives of those with the illness, as well as their family and friends. Commenting on the SMC approval, Dr. John Paul Leach, Southern General Hospital, Glasgow said, “This acceptance by the SMC means that specialists have another therapeutic choice to offer those patients in Scotland not achieving adequate seizure control.”

References

1. VIMPAT® Summary of Product Characteristics
2. Scottish Intercollegiate Guidelines Network, Royal College Physicians. Diagnosis and Management of Epilepsy in Adults. April 2003
3. Scottish Intercollegiate Guidelines Network, Royal College Physicians. Diagnosis and Management of Epilepsies in Children and Young People.March 2005
4. Rosenfeld W et al Lacosamide: An Interim Evaluation of Long-term Safety and Efficacy as Oral Adjunctive Therapy in Subjects with Partial Onset Seizures. 61st Annual American Epilepsy Meeting 30 Nov ??” 4 Dec 2007
5. Shorvan, S. Handbook of Epilepsy Treatment. Second Edition. Blackwell Publishing 2005

VIMPAT (lacosamide) is a new antiepileptic drug approved in the UK as adjunctive therapy in the treatment of partial-onset seizures with or without secondary generalisation in patients with epilepsy aged 16 years and older.

The recommended VIMPAT doses are 200 mg/day and 400 mg/day. The maximum recommended dose for VIMPAT is 400 mg/day.

- The key clinical trials, involving 1308 patients with a history of an average of 23 years of partial-onset seizures, were designed to evaluate the efficacy and safety of lacosamide when administered concomitantly with 1 3 antiepileptic drugs in patients with uncontrolled partial-onset seizures with or without secondary generalisation.

- Strong enzyme inducers such as rifampicin or St John??s wort (Hypericum perforatum) may moderately reduce the systemic exposure of lacosamide. Therefore, starting or ending treatment with these enzyme inducers should be done with caution

- Based on the analysis of pooled placebo-controlled clinical trials in 1,308 patients with partial-onset seizures, a total of 61.9% of patients randomized to lacosamide and 35.2% of patients randomized to placebo reported at least 1 adverse reaction.

- Adverse Reactions: the most frequently reported adverse reactions with Vimpat treatment were dizziness, headache, nausea and diplopia (double vision). They were usually mild to moderate in intensity and some were dose-related and could be alleviated by reducing the dose. Incidence and severity of CNS and gastrointestinal (GI) adverse reactions decreased over time.

About UCB

UCB, Brussels, Belgium is a global leader in the biopharmaceutical industry dedicated to the research, development and commercialisation of innovative medicines with focus on the fields of central nervous system and immunology disorders. Employing around 12 000 people in over 40 countries, UCB achieved revenue of 3.6 billion euro in 2007. UCB is listed on Euronext Brussels (symbol: UCB). ucb

Forward looking statement

This press release contains forward-looking statements based on current plans, estimates and beliefs of management. Such statements are subject to risks and uncertainties that may cause actual results to be materially different from those that may be implied by such forward-looking statements contained in this press release. Important factors that could result in such differences include: changes in general economic, business and competitive conditions, effects of future judicial decisions, changes in regulation, exchange rate fluctuations and hiring and retention of its employees.

UCB, Brussels

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Many people struggle to maintain a regular exercise schedule on their own, but do better when they exercise with friends. In rats, exercising in groups is better for the brain as well, reports a study in the April issue of Nature Neuroscience.

Elizabeth Gould and colleagues study the effects of running on the generation of new neurons (neurogenesis) in the brains of adult rats housed in groups and in isolation. The authors report that running increases neurogenesis only when rats were housed in groups. However, in rats that run in social isolation, neurogenesis is suppressed.

Running caused similar elevations of the stress hormone corticosterone in isolated or group-housed rats, but only animals that ran alone were vulnerable to the negative influence of corticosterone on neurogenesis.

Moreover, individually housed runners showed higher levels of corticosterone in response to additional stress when compared to group-housed runners. Preventing the elevation in corticosterone levels in individually housed runners stimulated neurogenesis.

These results suggest that without social interaction, a normally beneficial experience can have negative effects on the brain.

Author:
Elizabeth Gould (Princeton University, Princeton, NJ, USA)

NATURE NEUROSCIENCE
www.nature/natureneuroscience
DOI: 10.1038/nn1668

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The Guardian today looks into concerns raised by the MS Society about the promotion and sale of Aimspro – a treatment derived from goat serum that is currently available on a specials licence to people with MS who are prepared to pay for it.

Today’s Guardian story, ‘On sale in the UK: unproven goats’ blood treatment for MS patients’ focuses on the ways in which the drug has continued to be promoted and sold to people affected by MS, despite a lack of any trial data supporting its safety and efficacy.

MS Society chief executive Simon Gillespie said: “The MS Society has been calling on Daval International, who make Aimspro, to put it through proper trials for more than two years. During that period, hundreds of people with MS have been paying to use the treatment.

“The safety of this product for human use has not been proven, and there is a distinct lack of evidence for its effectiveness. Without rigorous proof of safety in clinical trials, no drug can be approved for sale by the regulators. The need to prove safety and efficay in clinical trials before bringing a drug to market has been circumvented and Aimspro is being sold direct to hundreds of people with MS as a safe and effective drug.

“We are particularly concerned that people with severe MS – who have few or no alternative options – are being urged to run up debt to pay for something that has not been proven to work. This is simply not acceptable.”

A charity, Proventus, has been holding ‘roadshows’ throughout this time advocating the use of the drug. MS Society members have attended a number of these and raised concerns with the Society about the tone and content, which were borne out when our research team attended sessions to see for themselves.

The Medicines and Healthcare Products Regulatory Agency (MHRA) has been aware of the MS Society’s concerns for two years and has confirmed that Daval are under investigation, but has so far not taken any action.

Simon added: “We would like to see the regulator take some action.”

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Toddlers who are overweight or obese are much more likely to become overweight/obese 12-year-olds when compared to toddlers of normal weight, say American researchers who monitored children from 2 to 12 years of age.

You can read about this study in the journal Pediatrics September 2006 issue.

Duane Alexander, M.D., Director of NIH’s National Institute of Child Health and Human Development, said “These findings underscore the need to maintain a healthy weight beginning in early childhood. Contrary to popular belief, young children who are overweight or obese typically won’t lose the extra weight simply as a result of getting older.” The NIH funded the study.

Previous studies have indicated that early teenagers who are overweight/obese are much more likely to become overweight/obese adults than early teenagers of normal weight. One could extrapolate from this study that an overweight/obese toddler is much more likely to become an overweight/obese adult, compared to a toddler of normal weight.

In this study, the researchers wanted to assist clinicians by estimating a toddler’s risk of overweight and obesity during middle childhood and early adolescent years by monitoring his/her BMI status. They monitored the development of 1,042 children from ten locations in the USA – they were all enrolled in the study at birth, in 1991. They used data collected as part of the NICHD Study of Eatly Child Care and Youth Development. The children came from a wide range of socioeconomic levels. 80% of them were brought up in households where two parents were present.

The researchers collected data on the childrens’ height and weight when they were 2, 3, 4, 6, 7, 9, 11 and 12 years old. Children were classed as overweight if their BMI (Body Mass Index) was above the 85th percentile (compared to national statistics for kids of their age).

They found that:

– If a child was overweight at least once, aged 2-4, he/she was 5 times more likely to be overweight at 12, compared to a child who was never overweight aged 2-4.

– A child who was overweight once while at elementary school was 25 times more likely to be overweight at 12, compared to a child who was never overweight while at elementary school.

– A child who was overweight twice while at elementary school was 159 times more likely to be overweight at 12, compared to a child who was never overweight while at elementary school.

– A child who was overweight three times while at elementary school was 374 times more likely to be overweight at 12, compared to a child who was never overweight while at elementary school.

“Identifying Risk for Obesity in Early Childhood”
Philip R. Nader, M, Marion O’Brien, PhD, Renate Houts, PhD, Robert Bradley, PhD, Jay Belsky, PhD, Robert Crosnoe, PhD, Sarah Friedman, PhD, Zuguo Mei, MD, Elizabeth J. Susman, PhD for the National Institute of Child Health and Human Development Early Child Care Research Network
PEDIATRICS Vol. 118 No. 3 September 2006, pp. e594-e601
(doi:10.1542/peds.2005-2801)
Click Here To View Abstract

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The evidence is accumulating on how bad stress is for health. Chronic stress can intensify inflammation and increase a person’s risk for developing central nervous system infections, neurodegenerative diseases, like multiple sclerosis (MS), and other inflammatory diseases, say researchers presenting at the 115th Annual Convention of the American Psychological Association (APA). These researchers have demonstrated for the first time that stress related increases in central nervous system inflammation are behind the adverse effects of stress in an animal model of MS.

Researchers from Texas A & M University used mice to show what role social stress plays in the immune process to influence the course of an MS like disease. They proposed that stress induced increases of pro inflammatory cytokines, which are proteins that regulate immune and inflammatory functions, inhibit the clearing of a virus and allow the inflammatory process to run amok. Stress, say the authors, may interact with viral infections to increase vulnerability

to diseases such as MS. Meta-analysis of studies investigating the impact of stressful events in patients with MS show an increased risk of worsening symptoms of the disease.

In a series of experiments on mice, the authors showed that increases in a particular cytokine interleukin-6 (IL-6), which is released during stress and regulates the part of the immune system that fights infection can make socially stressed mice vulnerable to MS-like illnesses.

The researchers used a social disruption model (SDR) to simulate social stress for mice and then infected the mice with Theiler’s murine encephalomyelitis (TMEV). Infection with TMEV results in an acute infection of the central nervous system followed by a chronic autoimmune disease similar to that seen in humans with MS. Their laboratory has previously shown that exposure to social stress prior to infection exacerbates both the early viral infection and the later autoimmune demyelinating MS-like phase of the disease.

To create a stressful environment, researchers housed three young male mice together for several weeks. After the mice established a stable social hierarchy, researchers introduced an older aggressive male into the residence for a couple of hours. The intruder exhibits aggressive behavior posturing, fighting, wounding, pursuit that results in submissive behaviors and social defeat in the younger resident mice. This procedure was repeated for three consecutive nightly two-hour sessions with one night off, followed by an additional three nightly sessions. To keep the mice from getting used to the intruder, a new intruder was introduced for each session.

What they found was this stress appears to elevate levels of IL-6, which subsequently increases the severity of the MS-like illness. Furthermore, using specific IL-6 neutralizing antibody treatments during the stress exposure can prevent the stress-related worsening of the disease, said the authors.

In one experiment, they showed that mice exposed to social disruption had elevated central and peripheral levels of IL-6. However, infusing the neutralizing antibody into the brain prevented this stress-induced increase in IL-6. This demonstrated that the antibody could effectively reverse the stress-related increases in IL-6 in brain and in circulating blood.

Results from a second experiment showed that administering the IL-6 neutralizing antibody during the stress exposure prevented worsening of the TMEV infection. By blocking the stress-induced elevation of IL-6, TMEV infection was weakened, which lessened some of the disease symptoms, such as motor impairment, inflammation in the brain and spinal cord, and the viral level in the central nervous system. Based on these findings, Dr. Mary Meagher, the lead researcher, proposes that the adverse effects of stress-induced IL-6 on TMEV infection are enough to create a pro-inflammatory environment that interferes with the immune response to infection. Because the early immune response shapes the later specific immune response to infection, impairment of the early response could account for the increased viral level, prolonged viral infection, increased CNS inflammation, and the subsequent exacerbation of the chronic autoimmune disease.

There is a growing body of evidence in both animal and human studies that suggests that exposure to stress can increase and sustain the release of pro-in?¬‚ammatory cytokines following an assault on the immune system. Thus, the present findings might help scientists unravel which biobehavioral mechanisms offset the adverse health effects of chronic social stress in humans. “Similar to mice exposed to repeated social defeat by an aggressive intruder, people exposed to chronic social conflict experience high levels of stress and consequent dysregulation of the immune system, thereby increasing vulnerability to infectious and autoimmune disease,” said Meagher. “The cytokine response during chronic stress appears to play a key role in exacerbating the acute CNS infection and the development of subsequent autoimmune responses.”

Furthermore, interventions that prevented or reversed the stress-induced increases in IL-6 in the mouse model may have implications for humans, said Meagher. It is possible that the adverse effects of social conflict on people who are vulnerable to certain inflammatory diseases may be prevented or reversed by treatments aimed at blocking increases in this cytokine. Recent evidence suggests that some potential interventions include certain anti-inflammatory drugs, exercise, antidepressant medication, omega-3 fatty acids, and mindfulness relaxation training. However, human clinical trials are needed to fully evaluate this issue.

Presentation: “Severe or Traumatic Stress and Inflammation in Multiple Sclerosis,” Mary W. Meagher, PhD, Texas A&M University

Session 1157 Symposium: Traumatic Stress, Cardiovascular Disease, Metabolic Syndrome, and Neurodegenerative Disease, 11:00 11:50 AM, Friday, August 17, Moscone Center, Second Floor-West Building, Room 2020

The American Psychological Association (APA), in Washington, DC, is the largest scientific and professional organization representing psychology in the United States and is the world’s largest association of psychologists. APA’s membership includes more than 148,000 researchers, educators, clinicians, consultants and students. Through its divisions in 54 subfields of psychology and affiliations with 60 state, territorial and Canadian provincial associations, APA works to advance psychology as a science, as a profession and as a means of promoting health, education and human welfare.

American Psychological Association (APA)
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University of Pennsylvania School of Medicine researchers have answered long-running questions about the way that anesthetics act on the body, by showing that the cellular pathway for emerging from anesthesia is different from the one that drugs take to put patients to sleep during operations. The findings will be published in Proceedings of the National Academy of Sciences.

The research focuses on orexins, the small, specialized fraction of the brain’s 100 billion neurons that play a key role in regulating the body’s wakeful state. Studying mice whose orexin systems had been genetically destroyed – a state similar to humans suffering from narcolepsy, a neurological condition that causes unusual daytime sleepiness – Max B. Kelz, MD, PhD, an assistant professor in Penn’s Department of Anesthesiology and Critical Care and the Mahoney Institute of Neurological Sciences, found that these mice took much longer to emerge from general anesthesia than those with normal orexin signaling systems. However, the mice with faulty orexin systems did not appear to fall asleep faster during anesthesia, which suggests that different processes are at play when transitioning to and from the anesthetized stated.

“The modern expectation is that anesthesiologists can simply flip a consciousness switch as easily as we might turn the room lights on or off,” says lead author Max B. Kelz, MD, PhD, an assistant professor in Penn’s Department of Anesthesiology and Critical Care and the Mahoney Institute of Neurological Sciences. “However, what patients do not realize is that despite 160 years of widespread clinical use, the mechanisms through which the state of anesthesia arises and dissipates remain unknown.”

Kelz became interested in these questions after treating a narcoleptic patient who took more than six hours to regain consciousness after anesthesia, compared to the typical six minutes or so. By probing what’s different about the narcoleptic brain, the Penn study has established for the first time that the process of entry into and exit from the anesthetized state are not mirror images of one another.

Kelz and his colleagues, including Sigrid Veasey, MD, associate professor in the Department of Medicine’s Sleep Medicine division, hope that further research on the brain’s neural signaling systems will lead to novel ways to administer anesthesia and “jump start” a speedy, safe return to consciousness – particularly among patients who struggle to wake up or in patient groups that may be more prone to anesthesia side effects such as the elderly and patients with neurodegenerative disorders. The findings might also be used to create designer anesthetic agents that “hijack” the body’s natural sleep cycles to mimic a state closer to natural sleep than a chemically-induced coma, Kelz says.

###

PENN Medicine is a $3.5 billion enterprise dedicated to the related missions of medical education, biomedical research, and excellence in patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation’s first medical school) and the University of Pennsylvania Health System.

Penn’s School of Medicine is currently ranked #3 in the nation in U.S.News & World Report’s survey of top research-oriented medical schools; and, according to most recent data from the National Institutes of Health, received over $379 million in NIH research funds in the 2006 fiscal year. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.

The University of Pennsylvania Health System includes three hospitals – its flagship hospital, the Hospital of the University of Pennsylvania, rated one of the nation’s “Honor Roll” hospitals by U.S.News & World Report; Pennsylvania Hospital, the nation’s first hospital; and Penn Presbyterian Medical Center – a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice.

Source: Holly Auer

University of Pennsylvania School of Medicine Continue reading →

The number of hectares planted with biotech crops worldwide increased by 9.0 million hectares (22 million acres) in 2005. This is according to new figures published today by ISAAA (The International Service for the Acquisition of Agri-biotech Applications (1).

“More farmers are choosing to plant GM crops than ever before. This is testament to the real advantages and benefits farmers worldwide are getting out of biotech crops,” says Simon Barber, Director of the Plant Biotechnology Unit at EuropaBio – the European association for bioindustries (2). “It is very encouraging to see that among the growing number of countries adopting biotech crops, a number of them are now European – farmers in 5 EU member states planted GM crops in 2005.”

The advantages and benefits accruing to farmers using the technology are considerable. A recent study produced by PG Economics (3) showed that farmers using the technology increased their income by US$27 billion during the period 1996 to 2004 with significant, additional environmental benefits delivered; the accumulative economic benefits during the nine years to developing countries ($15 billion), exceeded benefits to industrial countries ($12 billion).

The benefits that can be achieved through biotechnology applied to agriculture have also prompted more than 3,400 international scientists to sign the AgBioWorld declaration of support for agricultural biotechnology to improve agriculture in the developing world. Signatories include 25 Nobel Prize winners.

In Europe, the European Council of March 2003 asked the Commission to support a European Technology Platform for “Plants for the Future” – a stakeholder forum on plant genomics and biotechnology. The platform has published a 20 year vision and a Strategic Research Agenda to set the scene for European agricultural development for the next two decades. The project is supported by the European Commission and the major public and private stakeholders, and is coordinated by EPSO and EuropaBio.

(1) ISAAA
The International Service for the Acquisition of Agri-biotech Applications (ISAAA) is a not-for-profit organization that delivers the benefits of new agricultural biotechnologies to the poor in developing countries. It aims to share these powerful technologies to those who stand to benefit from them and at the same time establish an enabling environment for their safe use.
isaaa

(2) EuropaBio
EuropaBio, the European Association for Bioindustries, has 50 direct members operating worldwide and 25 national biotechnology associations representing some 1500 small and medium sized enterprises involved in research and development, testing, manufacturing and distribution of biotechnology products.
europabio

(3) PG Economics
PG Economics Limited is a specialist provider of advisory and consultancy services to agriculture and other natural resource-based industries. Its specific areas of specialisation are plant biotechnology, agricultural production systems, agricultural markets and policy.
pgeconomics

(4) AgBioWorld
The AgBioWorld Foundation is a 501(c)(3) non-profit organization headquartered in Auburn, Alabama, and is run by Professor C.S. Prakash of Tuskegee University.
agbioworld

The Declaration – agbioworld/declaration/petition/petition.php

(5) European Technology Platform – Plants for the Future
epsoweb/Catalog/TP/index.htm Continue reading →

Sports personality Gary Lineker visited the Royal Free Hospital in London on 24th September to meet the country’s first Leukaemia CARE Clinical Nurse Specialist.

Clara Patmore, who started in her new role at the Hampstead hospital this summer, is the first nurse in the UK to be funded by the charity Leukaemia CARE.

Among her duties, she acts as a continuous point of contact between the medical team and the leukaemia patient, provides information and support for patients and their families, goes through treatment plans with patients and visits inpatients.

Gary, who is Leukaemia CARE’s patron, was met by Pam Chesters, trust chairman, and Tony Gavin, the charity’s chief executive, and given a tour of the hospital’s oncology and chemotherapy suite by Dr Panos Kottaridis, leukaemia consultant. He also spoke to Kate Skupin, 52, from Wembley, and Christopher Frost, a 50-year-old driving instructor, from Barnet, who were both treated for leukaemia at the Royal Free.

After meeting staff and patients, Gary said: “With the launch of the first Leukaemia CARE nurse at the Royal Free Hospital, patients diagnosed with leukaemia will be looked after by a specialist nurse providing one-to-one support for anything they need. She will provide support for families during what I know is a very difficult time.

“It is thanks to Leukaemia CARE that this role has been made possible, and to the fantastic support of staff at the Royal Free Hospital.”

Clara qualified as a nurse in 2000 and has worked in the haematology department at the Royal Free since 2001.

She said: “I am grateful to Leukaemia CARE for funding my role, and delighted to work with such an expert haematology team at the Royal Free where we are involved in national and international trials. It is very rewarding to work in a hospital with such a good record in terms of clinical care and also in research.”

Dr Kottaridis said: “We are extremely grateful to Leukaemia CARE for choosing the Royal Free to support this special job.

“Clara has been a very successful nurse and junior sister at our hospital and she will be a very successful leukaemia nurse, providing a vital link between the patient and the medical team.”

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The Switch™ programme, ‘Switch what you Do, View, and Chew’, has been shown to be capable of promoting children’s fruit and vegetable consumption and lowering ‘screen time’. Researchers writing in the open access journal BMC Medicine tested the programme and report that it offers promise for use in youth obesity prevention.

Douglas Gentile, a psychology professor from Iowa State University, USA, worked with a team of researchers to evaluate the intervention in a group of 1,323 children and their parents from 10 schools. He said, “Reversing the pediatric obesity epidemic has been established as a critical priority. We tested Switch, a family-, school-, and community-based intervention aimed at changing the key behaviors of physical activity, television viewing/screen time, and nutrition”.

The Switch programme features three components, Community, School and Family. The Community component is designed to promote awareness of the importance of healthy lifestyles using paid advertising (such as billboards) and unpaid media (such as letters to the editors of print publications). The School component reinforces the Switch messages by providing teachers with materials and methods to integrate key health concepts into the school day. Finally in the Family component, participating families receive monthly packets containing behavioral tools to assist families in altering their health behaviors.

Gentile said, “Family components are critical for youth obesity prevention programs because parents directly and indirectly influence children’s activity and nutrition behaviors. Parents also influence the physical and social environments that are available to their children. The School and Community components are essential to integrate the programme into the places where families live, work and play”.

The intervention yielded encouraging results, with the experimental group showing significant differences from the control group in both screen time and fruit and vegetable consumption. According to Gentile, “Although modest, these results are not trivial. The effects remained significant at the 6-month follow-up evaluation, indicating maintenance of these differences over time. Such maintenance may contribute to reduced weight risks in the future”.

Notes:

Evaluation of a multiple ecological level child obesity prevention program: Switch what you Do, View, and Chew
Douglas A Gentile, Gregory Welk, Joey C Eisenmann, Rachel A Reimer, David A Walsh, Daniel W Russell, Randi Callahan, Monica Walsh, Sarah Strickland and Katie Fritz
BMC Medicine 2009, 7:49 doi:10.1186/1741-7015-7-49

biomedcentral/1741-7015/7/49/abstract

Source:
Graeme Baldwin

BioMed Central Continue reading →