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Pro-Test: standing up for science
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18/08/10

Permalink 02:53:44 pm, by Tom, 1426 words, 2224 views   English (UK)
Categories: Information

Mice, rats, and the secrets of the genome.

It’s just over a decade since the completion of the first working draft of the human genome was announced, and seven years since the publication of the complete sequence, but in that short time the impact of this new knowledge on all areas medical research has been immense. Sequencing the human genome was a huge achievement, but having got the sequence an even greater task confronts scientists - working out what it all means. To do this scientists have studied the natural variations that exist between individuals, and have also sequenced the genomes of a wide variety of species, some closely related to us, others separated from us by hundreds of millions of years of evolution. Scientists can analyze the similarities and differences between the genes of different species, and examine how changes to the structure or regulation of these genes are reflected in physiology. In many cases it is also possible to use genetic modification to study the function of conserved genes in other species in ways that are just not possible, for technical and/or ethical reasons, in humans. A study published a couple of weeks ago in the scientific journal Nature provides an excellent example of how animal research contributes to our understanding of the human genome.

As the cost of technology such as DNA microarrays has fallen genome-wide association studies (GWAS) have become an increasingly popular way of examining the relationship between genetic differences between individuals and particular diseases. In a GWAS the whole genome of many individuals is screened for variations, and then any association between those variations and particular phenotypes or diseases is determined. Tanya M. Teslovich and colleagues (1) analysed the genomes of over 100,000 people who had been enrolled in 46 separate clinical studies, and identified 95 genes that have variants associated with increases in blood lipid (fat and cholesterol) levels. One of the problems with GWAS studies is that while they are often good at identifying genes that are associated with a disease, they are not so good at identifying which genetic variations actually cause disease, or explaining how the genetic variations contribute to disease. This is where Tanya Teslovich and colleagues scored highly; they were able to show that 14 of the 95 lipid-associated genes were also associated with the development of coronary artery disease, supporting the proposition that elevated blood lipids contribute to coronary artery disease. They also found that overall the effect of the variants was additive, the more risk variants of these 95 genes you have the greater your chance of having elevated blood lipids.

So that established that the gene variants were associated with elevated blood lipids, but to use that information to develop new treatments you need to know how the particular gene affects lipid levels. As you might expect many of the 95 genes identified were already known from previous studies to be involved in the regulation of blood lipids, and in several cases their precise role has been thoroughly studied. However, several of the genes had not been implicated in regulating blood lipids before, and the team decided to use genetically modified mice to investigate their function. They injected viral vectors into the liver of the mice that contained either an extra copy of the gene being studied, to increase expression of the gene, or a short-hairpin RNA, to target the gene for knockdown via RNAi. This allowed them to discover that one gene, GALNT2, decreases levels of high-density lipoprotein cholesterol (HDLC), the so-called “good cholesterol”, while two other genes, Ttc39b and Ppp1r3b, increase HDLC.

Another associated paper (2) in the same issue of Nature takes the analysis even further. Several studies, including the GWAS performed by Tanya M. Teslovich and colleagues, had demonstrated that variations in a particular region of chromosome 1 known as 1p13 were associated with high levels of Low-density lipoprotein “bad” cholesterol (LDLC) in the blood and heart disease, but that these variations were not within the coding sequence of any genes, so they would not affect the structure of any proteins. They first show through genetic studies of human subjects and human liver tissue culture that variations at 1p13 affect the expression of several genes – and hence the amount of protein produced by those genes - and that one particular variation creates a binding site for the transcription factor C/EBP. Transcription factors are proteins that regulate the expression of genes, and this particular site altered the levels of a gene named SORT1. But what does SORT1 do? To answer this they again turned to GM mice, using virus vectors that specifically reduced or increased the levels of SORT1 in the mouse liver. Reducing or eliminating SORT1 expression in the mouse liver led to a reduction in the levels of LDLC in the blood, and that this was found to be due to SORT1 regulating the production of very-low-density lipoprotein (VLDL), a precursor to low-density lipoprotein, in the liver. As a result of this work a whole new pathway for the regulation of blood lipids has been uncovered, one that may offer new opportunities to scientists developing treatments for hypercholesterolemia.

As a BBC news report indicates, the identification of these genes and the elucidation of their function may aid the development of better diagnostic tools to identify those at risk of heart disease, and ultimately the development of better treatments.

These studies illustrate how important animal models, particularly GM mice, are to efforts to decode the human genome. As the biosciences move towards a more systems based approach to biology, one where knowledge of how networks of genes interact to produce a particular physiological or clinical outcome is applied to areas such as toxicology, the information that studies of GM animals can yield will become increasingly important. This importance has not gone unrecognized by the wider scientific community, the 2007 Nobel Prize in Medicine was awarded to Mario Capecchi, Sir Martin Evans, and Oliver Smithies for their discoveries of " principles for introducing specific gene modifications in mice by the use of embryonic stem cells".

With this in mind let’s turn briefly to another GM animal that’s been in the news lately - the rat. While GM mice have become a mainstay of modern scientific research the rat has lagged behind, which is a shame since the larger size, longer lifespan, and more complex behavior of rats make them more effective animal models than mice for studying many human diseases, particularly neurological conditions. The lack of GM rats was due to the difficulty in growing rat embryonic stem cells (ESCs) in culture, a necessary first step in the most common methods of producing GM animals. Last year Matthew Evans wrote an article for the Pro-Test blog discussing how scientists at the University of Cambridge and the University of Southern California had developed a method for growing rat ESCs in culture, and how this achievement paved the way for the production of transgenic rats. Last week the same group of scientists announced that they had employed this method to produce GM rats whose p53 gene, a key tumor suppressor that is defective in several cancers, was deleted.

This is not the first time GM rats have been produced, as for the past few years scientists have been able to use zinc finger nucleases to knock-out rat genes. Zinc fingers, so called because one or more zinc ions stabilizes the finger like structure, are found in many proteins, allowing them to bind specifically to a structure within a cell, such as a particular DNA sequence. Scientists found that they could produce artificial zinc fingers that recognize particular genes, and then join a nuclease to that zinc finger so that it cuts out the target gene. This method, discussed in more detail in this excellent article by Elie Dolgin, allows scientists to knock-out genes in rat embryos. The downside of the zinc finger nuclease technique can only be used to knock-out genes, whereas the ESC method is more flexible – it can also be used to add extra copies of a gene, or to delete genes in specific tissues or stages of development.

It is now clear that the rat is joining the mouse at the forefront of the GM revolution in medicine, and that has to be great news for medical science and the patients that depend on it.

Paul Browne

1) Teslovich T.M. et al. "Biological, clinical and population relevance of 95 loci for blood lipids" Nature Volume 466, Pages 707-713 (2010) DOI:10.1038/nature09270

2) Musunuru K. et al. "From noncoding variant to phenotype via SORT1 at the 1p13 cholesterol locus" Nature Volume 466, Pages 714–719 (2010) DOI:10.1038/nature09266

22/07/10

Permalink 03:32:09 pm, by Tom, 842 words, 23371 views   English (UK)
Categories: News

Great news from HIV microbicide trial - thank the monkeys!

There was exciting news on Monday when it was announced at an international AIDS conference in Vienna that microbicide gel had dramatically reduced the transmission of HIV in a Phase 2 clinical trial involving 889 women in South Africa. If confirmed by larger phase 3 trials this gel will offer millions of women a way to protect themselves against this dread disease that blights communities around the world.

Dr Abdool Karim explains how to use a microbicide gel applicator. Image courtesy of CAPRISA.

Unlike previous microbicide gels that failed to offer significant protection against HIV infection this gel included the anti-retroviral drug tenofovir. Tenofovir was one of several anti-retroviral drugs discussed in an article on the role of non-human primate research in developing HIV prophylaxis by virologist Dr. Koen Van Rompay that was posted on the Speaking of Research blog last year. Dr. Van Rompay’s article looked at the use of oral tenofovir in pre- and post-exposure prophylaxis rather than its use in a microbicide gel.

So did the research on preventing SIV transmission in monkeys influence the decision to use tenofovir in this microbicide gel? You betcha! In the first report of a Phase 1 trial of this tenofovir-containing microbicide gel published in 2006 (1) the authors state that the success of tenofovir in preventing SIV infection on monkeys – the same research discussed by Dr. Van Rompay – was a deciding factor when they took this gel into clinical trials.

"Tenofovir gel, 9-[(R)-9-(2-phosphonylmethoxyprophyl) propyl]adenine monohydrate, a nucleotide reverse transcriptase inhibitor, has demonstrated ability to inhibit retroviral replication in animals and humans, and it has been well tolerated when used orally, as tenofovir disoproxil fumarate, (tenofovir DF; Viread) [16–20]. Tenofovir DF has been approved for treatment of HIV-1 infection and is increasingly used as part of therapeutic regimens for HIV-positive individuals [21]. Tenofovir has been proven to be effective in blocking the transmission of SIV in animal models when given as pre- or postexposure prophylaxis systemically or when applied as an intravaginal gel [22–25]. Tenofovir bisphosphate, the active intracellular moiety, has a very long intracellular half-life (> 72 h), which could allow for more convenient, coitally independent intravaginal use [26]. Given the data showing animal protection with tenofovir gel, and the extensive human safety data with oral tenofovir in HIV-positive patients, the HIV Prevention Trials Network (HPTN) decided to assess the safety and tolerability of tenofovir gel in HIV-negative and HIV-positive women and their male sexual partners (HPTN 050)."

The above passage also mentions that they tested whether the microbicide gel containing tenofovir could prevent vaginal SIV transmission in monkeys*, and the finding that it could drove their subsequent decision to take the gel into clinical trials. This was an important decision, a review of HIV microbicide gels published in the journal Science (2) two years ago pointed out the failure to evaluate other microbicide gels in monkey models of HIV transmission allowed these gels to proceed into clinical trials where they subsequently failed. It is notable that the microbicide PRO 2000, also evaluated in monkeys, is the only other microbicide to demonstrate an ability (albeit less dramatic) to prevent HIV infection in clinical trials.

So what now? Well the tenofovir containing gel will go on into larger phase 3 trials to further evaluate its ability to prevent HIV infection in women. In the meantime following a study showing that it can prevent the transmission of rectal SIV transmission in macaques (3) this gel is now in phase 1 safety trials in men.

This is welcome news after years of disappointment, and further evidence that where HIV is concerned there can be no shortcuts; all therapies whether microbicide gels or vaccines must be thoroughly evaluated in stringent animal models before being taken to human clinical trials. Perhaps now we can start to turn realism into optimism.

In other good news, Mel Broughton, former spokesperson for the animal rights group SPEAK that waged an often vicious (though occasionally bizarre) campaign against the new biosciences laboratory at Oxford, was jailed for 10 years last week for conspiracy to commit arson.

The unanimous verdict highlights once again how closely so-called "above ground" extremist campaings such as SPEAK and SHAC are connected to the criminality of those who operate under the banner of the ALF. Hopefully this verdict and sentence, along with the failure of Broughton's campaign to prevent the completion of the new laboratory, will help to dissuade other activists from resorting to such terror tactics.

* Unfortunately this study was never published in the scientific literature, this is something that sometimes happens with pre-clinical studies performed by biotechnology and pharmaceutical companies…usually because they wish to keep the work confidential for commercial reasons…and is a source of great frustration to people like me who write about this work!

Paul Browne

1) Mayer K.H. et al. “Safety and tolerability of tenofovir vaginal gel in abstinent and sexually active HIV-infected and uninfected women.” AIDS. volume 20(4), pages 543-551 (2006), DOI:10.1097/01.aids.0000210608.70762.c3.

2) Grant R.M. “Whither or wither microbicides?” Science. Volume 321(5888), pages 532-534 (2008), PubMed Central:PMC2835691.

3) Cranage M. et al. “Prevention of SIV Rectal Transmission and Priming of T Cell Responses in Macaques after Local Pre-exposure Application of Tenofovir Gel” PLoS Med. Volume 5(8):e157(2008) DOI:10.1371/journal.pmed.0050157

07/06/10

Permalink 02:29:04 pm, by Tom, 886 words, 2425 views   English (UK)
Categories: Information

Septic shock: Mice show way to a new treatment

When we think of the immune system we usually think of the adaptive immune system - the B-cells and T-cells that recognize and destroy specific pathogens – which isn’t surprising since this is the arm of the immune system that vaccines are designed to stimulate. However working alongside the adaptive immune system is the innate immune system which protects us form infection in a non-specific fashion. Key to this system are phagocytes, a diverse set of cells whose primary characteristic is their ability to consume and digest invading microorganisms and secrete a range of chemical messengers known as the proinflammatory cytokines which stimulate other components of the immune system. This usually a useful part of the immune response, but sometimes there is an excessive release of cytokines which causes the patient to enter a condition known as septic shock where the immune system over-reacts and causes serious tissue damage, eventually leading multiple organ failure. As a consequence of the increase in complicated surgery, implantable medical devices, elderly patients and patients with weakened immune systems, there has been an increase in the incidence of septic shock in recent years, and with around half of septic shock cases proving fatal it is now the number one cause of death in intensive care units.

This week a multinational team of scientists based in Bern, Frankfurt, Glasgow and Singapore, and led by University of Glasgow physician Professor Alirio Melendeza, have published a paper in Science (1) announcing an important development in the struggle to reduce the death rate from septic shock.

They had previously used in vitro cell culture techniques to identify an enzyme called sphingosine kinase 1 (SphK1) in human phagocytes and demonstrated using both RNAi and a specific inhibitor of SphK1 called 5c that SphK1 was involved in stimulating the cellular signaling pathways that promote release of proinflammatory cytokines. In this study they began by examining phagocytes isolated from 30 septic shock patients, finding that SphK1 levels were higher in these patients than in a control group. They next found that treating the phagocytes from septic shock patients with the inhibitor 5c blocked the production of proinflammatory cytokines by these cells in response to exposure to bacterial lipopolysaccharide, a molecule found on the exterior of some bacteria that usually provokes a strong inflammatory response.

The ability of 5c to block SphK1 dependent inflammation in-vitro was impressive but would the same happen in a whole organism where other pathways might promote inflammation? The team led by Professor Melendez next examined if 5c or RNAi could protect mice which were injected with an otherwise lethal dose of lipopolysaccharide, and they found that both methods of blocking the action of SphK1 did indeed provide complete protection against septic shock.

This was a very exciting result but acute, one-off exposure to lipopolysaccharide in vitro or in vivo is not the same as bacterial infection, where bacteria are multiplying and constantly interacting with the immune system to induce inflammation. Of course it is also vital that when turning down the inflammatory response the treatment doesn’t also compromise the immune system’s ability to fight the infection. The team therefore assessed whether pre-treatment with 5c or RNAi could prevent systemic inflammation and mortality from septic shock in a mouse model that simulates microbial infection in humans following surgery or injury, and not only was the immune system’s ability to combat the infection not compromised but the infection was cleared more quickly.

Pre-treatment is all very well but in the clinic treatment almost always starts after sepsis develops, so it was cheering to note that the inhibitor 5c reduced mortality when given up to 12 hours after infection it reduced mortality from septic shock, though it was most effective when given within 6 hours. This was as effective as the broad-spectrum the antibiotic co-amoxiclav, a standard treatment for sepsis, and when co-amoxiclav was administered along with 5c the combination was observed to be considerably more effective than either treatment used alone.

Professor Melendeza and his colleagues have identified an exciting new approach to reducing the toll from septic shock, hopefully work is already underway to translate this promising study from the bench to the bedside.

In other news the 2010 Kavli Prize in Neuroscience has gone to three scientists, Richard H. Scheller, Thomas C. Südhof, and James E. Rothman, who have “used a creative multidisciplinary set of approaches to elucidate the key molecular events of neurotransmitter release”. Their work, which involved the study of tissues from a variety of species including rats and marine rays and studies of knockout mice, has made a huge contribution to our understanding of how the release of the molecules that carry messages between the cells of the immune system work. This research may sit squarely in the realm of basic science, but the understanding of nerve cell communication that these three scientists have provided is now informing the development of new therapies for a wide range of psychiatric and neurological disorders.

Both these news items may at first seem unrelated, but what they have in common is animal research at the heart of a multidisclipinary approach that is increasingly typical of how biomedical science is done in the 21st century.
Paul Browne

1) Puneet P. et al. "SphK1 Regulates Proinflammatory Responses Associated with Endotoxin and Polymicrobial Sepsis" Science Volume 328(5983), pages 1290 - 1294 (2010) DOI:10.1126/science.1188635

20/05/10

Permalink 04:56:32 pm, by Tom, 1255 words, 2398 views   English (UK)
Categories: Information

Finding animal research in medical news

One of the things that often strikes me when reading about medical advances or clinical trials is how variable the reporting of basic and applied research, including animal research, that underpins the clinical research is. In some cases it is discussed in some depth, but far too often it is either skimmed over or not mentioned at all. This is a shame since it makes it more difficult for readers to make the connection between what is happening in the clinic and animal research that may have begun years earlier. A few recent stories in the news illustrate this variability very nicely.

I’ll start with an excellent report by Miriam Falco on CNN entitled “Stem cell treatment goes from lab to operating room” which describes a clinical trial of fetal stem cells in the treatment of Amylotrophic Lateral Sclerosis (Lou Gehrig’s disease), a progressive neurodegenerative disease affecting the motor neurons that leads to severe muscle weakness and eventually death as the muscles that control breathing fail. As the CNN report points out research on rats was vital to the identification of the correct type of cells for this transplant, and Dr. Eva Feldman demonstrated that injecting fetal stem cells into rats with ALS preserved the large motor neurons and muscle strength.

'Lead researcher Dr. Eva Feldman, a neurologist at the University of Michigan, designed the trial just four years ago. After a lot of animal testing, her team determined that using fetal nerve stems rather than human embryonic or adult stem cells (such as bone marrow stem cells) was most effective, she says.

Stem cells have the ability to turn into different cells in the body. However, human embryonic stem cells, which come from 4- or 5-day-old embryos, also been found to sometimes turn into cancer cells. Fetal stem cells, such as those used in this trial, are a few weeks older and have already taken on a specific identity — in this case nerve cells.'

'Feldman says the fetal stem cells used in this trial did not become any of the unwanted cell types. “That’s very, very important,” she says.'

Basic animal research showed the potential of this therapy, but applied research also played an important part in making this clinical trial possible. Through studies on pigs Dr. Nicholas Boulis developed an apparatus that allows the stem cells to be injected at precise locations in the spine, and then practice the technique before attempting to use it on a human patient.

'Animal testing also proved very useful when it came to figuring out how to actually inject the stem cells. Emory University’s neurosurgeon Dr. Nicholas Boulis invented the device that holds the needle that injects the stem cells. The goal is to inject the cells without injuring the spine and causing even more paralysis. He practiced on 100 pigs before attempting the procedure on a human.'

Our second report is from the LA Times, and in an article entitled “A personal fight against a lethal childhood illness” reports on the work being done at the Centre for Duchenne Muscular Dystrophy at UCLA. It’s a nice report which shows how passionate scientists like Stan Nelson and Carrie Miceli are about finding effective treatments and cures for serious diseases. While the report does refer to experimental therapies such as exon-skipping and gene therapy it unfortunately does not discuss them or the research that led to their development in any depth.

Exon skipping is a particularly innovative approach to treating some cases of Duchenne Muscular Dystrophy (DMD) where the disease is due to a mutation in the dystrophin gene that stops translation from messenger RNA prematurely and prevents the production of the protein dystrophin. In exon-skippping a molecule known as an antisense oligonucleotide or morpholino acts to remove the portion of mRNA that contains the mutation and allows the translational machinery of the cell to read through and produce a working dystrophin protein. As I discussed in a post last year research in mice and dogs has been crucial to the development and refinement of exon-skipping and early versions of this therapy have already had promising results in clinical trials undertaken at Great Ormond Street Hospital in London and Royal Victoria Infirmary in Newcastle. Gene therapy, where the faulty dystrophin gene is replaced by a working version, is also being developed, though it has not yet entered human clinical trials. A recent review (1) available to read for free at PubMed Central discusses the progress that has been made in recent years, the challenges that remain before DMD can be cured, and the vital role played by animal models in overcoming these challenges. The review also covers stem cell therapy for DMD, another exciting approach to treating the disease that we have discussed previously.

The final news item is a BBC report on a successful clinical trial of stem cells to treat Multiple Sclerosis, this time using stem cells isolated from a patient’s own bone marrow. Multiple Sclerosis (MS) is an autoimmune disorder where the patient’s immune system turns on the myelin sheath that insulates the axons of nerve cells, leading to a range of often serious neurological problems. At present few effective treatments have been approved for MS, and several are currently being evaluated in clinical trials. While the improvements seen in the clinical trial were modest they do hold promise for longer and lager trials that are now being planned, and I suspect that as with other therapies the key might be to start treatment early to prevent damage as well as allowing damage to be repaired.

The trial at Frenchay Hospital in Bristol built on years of careful animal research, including research conducted by Professor Neil Scolding who lead this clinical trial. Interestingly the research, conducted in mice with experimental allergic encephalomyelitis that reproduces many of the features seen in autoimmune diseases that attack the myelin sheath, showed that rather than replacing the damaged cells that produce the myelin sheath or nerve cells the injected stem cells protected the myelin sheath and nerve cells by turning down the pathogenic immune response responsible for damaging the myelin sheath (2,3). This was important since it meant that it was not necessary to inject the stem cells directly into the site of the MS lesion, rather the cells could be as (if not more) effective if injected into the bloodstream so that migrate to tissues such as the lymph nodes where they can interact with cells of the immune system. This discovery paved the way for the clinical trial reported by the BBC.

There’s a lot of stories in the news that are relevant to animal research, the trouble is that it’s not always easy to see the connection. At Speaking of Research we believe that the onus is on scientists to make sure that when they talk to reporters they give the full picture of what their research involves, and what earlier studies it depended on. Only then can the public really begin to appreciate just how important animal research is to continued medical progress.

Paul Browne

1) Wang Z. et al. “Gene Therapy in Large Animal Models of Muscular Dystrophy” ILAR J. Volume 50(2), Pages 187-198 (2009). PMCID: PMC2765825

2) Matysiak M. et al “Stem cells ameliorate EAE via an indoleamine 2,3-dioxygenase (IDO) mechanism” J Neuroimmunol. Volume 193(1-2), Pages 12-23 (2008) DOI:10.1016/j.jneuroim.2007.07.025

3) Gordon D . et al “Human mesenchymal stem cells abrogate experimental allergic encephalomyelitis after intraperitoneal injection, and with sparse CNS infiltration.” Neurosci Lett. Volume 448(1), Pages 71-73 (2008) DOI:10.1016/j.neulet.2008.10.040

11/04/10

Permalink 12:26:59 am, by Tom, 721 words, 3821 views   English (UK)
Categories: News

Pro-Test for Science have success in LA

Read more about Pro-Test for Science

On a beautiful sunny day in Los Angeles, Pro-Test for Science (A US side project of Pro-Test) organisers arrived at the junction of Le Conte and Westwood, on the edge of the UCLA campus, with armfuls of placards in support of animal research. Within ten minutes every placard had found a new owner as hundreds of scientists, students and members of the public showed up to support the cause. Those gathering chatted together, sharing their reasons for attending the rally.

Marchers Gather

Those participating were not limited to the UCLA community. Faculty from University of Southern California, California Institute of Technology, and California State University - Los Angeles, all came out to demonstrate their support for lifesaving medical research using animals. Soon the chants began to ring out - "Penicillin? ANIMAL RESEARCH! Insulin? ANIMAL RESEARCH! Vaccines? ANIMAL RESEARCH! Anaesthetics? ANIMAL RESEARCH!" A short while later, when the crowd had swelled further, the rally set off towards the center of the UCLA campus.

The marchers begin to walk towards the center of the UCLA

The mood was one of excitement and passion. Those participating exchanged ideas for public outreach in the future - sharing the best of ways of explaining to the public the clear connection between animal research and medical benefits. The rally continued to snake along Westwood and up towards Wilson Plaza.
Those at the front were unable to see the back of the rally!

As the rally turned into Wilson Plaza, passing the top of Bruin Walk, hundreds of students turned their heads towards the march, many shouting words of encouragement or joining in the rally.

Eventually the tail end of the rally reached the destination (some time after the front end due to the length), and Tom Holder brought the crowd together for a picture perfect moment of solidarity before shouting "What do we need?". "Animal Research" replied the hundreds of voices in unison.

David Jentsch at the Pro-Test rally 2010

Holder then introduced the first speaker, Prof. David Jentsch - founder of Pro-Test for Science and member of the Speaking of Research committee - who took the microphone to rapturous applause. David spoke of the progress of Pro-Test for Science, and the struggle against animal rights extremists in UCLA. He took the time to thank each of the individuals who had made the 2010 rally possible eliciting a cheer from the crowd as each name was called. Jentsch then passed over to Tom Holder, founder of Speaking of Research.

Tom Holder at the Pro-Test for Science Rally

Holder thanked the crowd, insisting that UCLA were winning in their battle against extremists. However he warned the crowd against complacency - saying that public outreach was the only way to win this battle in the long run. Holder also announced the success of the Pro-Test Petition, which had gained 11,621 signatures over the previous year (including Nobel Prize Laureates, and every chancellor in the UC system, including UC President Mark Yudof). He finished by announcing the presentation of the signatures to Dr. Kevin Quinn, Dr. Michael Steinmetz.

Dr. Quinn, the Chief of Behavioural Science and Intergrative Neuroscience at the National Institute of Mental Health (NIMH), accepted one copy of the petition on behalf of NIMH. Quinn spoke of the important role that animal research has in our understanding of Mental Health problems:

"Animal research conducted in a humane, ethical and responsible manner is absolutely critical … to understand, treat and cure mental disorders"

Dr. Michael Steinmetz, program director of the National Eye Institute, talked of the medical breakthroughs in vision. He spoke particularly of Leber's congenital amaurosis, a form of blindess which affects thousands of people across the United States. Through research in mice and then dogs (Briards), scientists found a way of inserting a gene into the eye through a virus, which could corect the problem.

"The National Eye Institute supports strongly the use of appropriate animal models in research, not just for the big clinical advances but for the many, many years of basic science that it takes to discover the underlying biological principles"

Jentsch then returned to the stage to introduce UC Executive Vice-Chancellor, Scott Waugh. Waugh offered his continued support to researchers at UCLA, mentioning that the Pro-Test for Science movement has played an important role in bolstering support for research. He congratulated Jentsch and Ringach for organizing the February pabel debate, explaining that "violence, threats and other criminal activity are never a viable alternative to dialogue".

Jentsch and Holder finished the rally by talking of the importance of continued education and outreach.

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