Research Focus 2010:

The Southwest Association for Education in Biomedical Research members and other researchers are continually furthering research. This section will be to highlight ongoing research.

Caffeine and painkillers could be the most effective cure for a hangover headache, suggests new research on rats. Researchers directly linked the chemical acetate to hangover headaches in rats. Caffeine, known to counteract the effects of acetate, was found to relieve the effects of alcohol. Headaches were induced in rats using a small dose of ethanol - about the equivalent of a single alcoholic drink. Four to six hours later the rats were found to suffer headaches. The extent of the headache was judged by the sensitivity of the skin around the rats' eyes. An 'inflammatory soup' had previously been administered to the rats' brains. This made the rats sensitive to headaches when given only a small quantity of alcohol, enabling researchers to study alcohol-induced headaches without the complications of intoxication. Ethanol is converted into a chemical called acetaldehyde in the body, which is then quickly turned into another chemical called acetate. It was thought that a build up of acetaldehyde caused hangover headaches. However, the new research suggests that it is actually acetate that is responsible. Rats injected with acetate were found to suffer more severe headaches. Further, when given caffeine, which can combat the effects of acetate, headaches were reduced in the rats. Anti-inflammatory drugs, from the same family as ibuprofen, were found to have a similar effect. The rats were not dehydrated, suggesting that alcohol-induced headaches cannot simply be fixed by drinking water. - PloS One, 10.1371/journal.pone.0015963, 31 Dec 11

Nerve cells that are unable to communicate effectively may be responsible for autism spectrum disorders (ASDs), according to new research on mice. The findings could lead to new therapies for ASDs. Previous research had found that a mutation in a gene called SHANK3 is associated with delayed language abilities, learning disabilities and ASDs. However, the underlying mechanism was unknown. To explore this mechanism, researchers bred mice that were genetically modified to lack one copy of the SHANK3 gene. This is similar to ASD patients, who have a mutation in one copy of this gene. Communication between nerve cells in mice lacking SHANK3 was found to be impaired. Also nerve cells and their contact points, called synapses, did not show cellular properties associated with normal learning. The researchers found reduce male-female social interactions in the modified mice. This is similar to behavioral problems seen in suffers of ASDs. Current treatments target the symptoms of ASDs, such as anxiety or aggression. However, the findings may lead to new therapies that aim to improve nerve cell communication instead. - Molecular Autism, 10.1186/2040-2392-1-15, 17 Dec 10

Experiments on zebrafish larvae have revealed how cancer cells harness the immune system to quicken the spread of the disease. Researchers found that cancer cells are less likely to spread if white blood cells, the body's immune cells, are prevented from contacting the cancer cells. Cancer cells are renowned for their ability to avoid being destroyed by the body's immune system. It now seems that cancer cells also co-opt the body's immune system to help them grow. Researchers activated cancer in skin pigment cells, called melanocytes, by introducing a cancer-promoting gene, called an oncogene. The cancer cells were also tagged using a fluorescent protein so that they could be tracked as they moved through the zebrafish. As zebrafish are completely translucent it is easy to see cells as they move around the fish and grow. Cancer cells were found to actively attract immune cells. Researchers discovered the chemical hydrogen peroxide was the attractant: hydrogen peroxide is a natural by-product of the body's energy producing processes. To test this further, the researchers reduced the production of hydrogen peroxide in the zebrafish. They found that white blood cells did not move to the cancer site and fewer cancer cells formed. This also happened when the development of the zebrafish's immune cells was blocked. As well as attracting white blood cells, researchers observed tethers linking together white blood cells and cancer cells. In some cases, when white blood cells started to leave the area they appeared to be held back by cancer cells. The results were the same when using a different type of cancer cell and when the cancer cells were injected into mucus secreting cells instead of skin pigment cells. Cancer growth in zebrafish resembles that in mammals, making it likely that the findings are applicable to human cancer growth. The research could lead to new therapies for early-stage cancer in humans. - PLoS Biology, 10.1371/journal.pbio.1001004, 14 Dec 10

Exposure to bacteria or viruses as child could reduce your chances of contracting asthma, according to new research on mice. Baby mice infected with influenza virus were protected from induced symptoms of asthma. However, there was no protection against asthma if mice were infected with flu as adults. The researchers linked the findings to effect of immune system cells called natural killer T-cells (NKT). It is thought that NKT cells help control the immune system response and so prevent extreme allergic reactions, such as those seen in asthma. NKT cells were found to increase in baby mice with flu, but not in adult mice with flu. This suggests that NKT cells prime the immune system in babies infected with flu and so stop it over-reacting later in life. Influenza virus is not the only agent that protects against asthma. The researchers also showed that infecting baby mice with a stomach ulcer causing bacteria called Helicobacter pylori had a similar effect. General childhood viral and bacteria infections may help to prime the body's immune response. This research supports the 'hygiene hypothesis', which suggests the recent surge in asthma rates in developed countries is caused in part by reduced exposure to bacteria and viruses as a child. - Journal of Clinical Investigation, 10.1172/JCI44845, 14 Dec 10

Memory loss has been reversed in Alzheimer's mice by boosting levels of a memory related protein. Researchers administered the protein called CBP to the mice using a harmless virus. They then measured the mice's memory using a water maze learning test. The mice had to find an exit platform hidden in a basin of milky liquid. Alzheimer's mice given the protein performed as well as normal mice and significantly better than Alzheimer's mice not given the protein. Alzheimer's is associated with the buildup of a protein called beta amyloid. The appearance of clumps of this protein, called amyloid plaques, is one of the first signs of the disease. Beta amyloid is thought to control the signaling between nerve cells in the brain, preventing nerve firing from getting out of control. Too much beta amyloid, however, will shut down nerves and eventually cause cell death. The researchers found that excess beta amyloid also interferes with the activity of a protein called CREB, important in the development of long term memory. CBP restores the function of CREB and so counters the effects of excess beta-amyloid. This research may lead to new medicines that help express the CBP protein. - PNAS, 10.1073/pnas.1012851108, 13 Dec 10

Mice have been genetically modified to grow stronger hearts. The changes to the heart mimic those usually seen after strenuous exercise, even though in this case the mice were relatively inactive. The research may lead to new treatments for heart damage in humans. Altering the expression of a single gene in the mice caused heart muscle cells to replicate and grow larger. The effects were the same as in mice that were endurance trained for two weeks. Adult mice were made to swim for up to three hours a day. After two weeks the mice hearts were found to be enlarged. The effect is similar to the enlarged 'athlete's heart' caused by strenuous exercise in humans. Researchers compared mice that had exercised to those that were inactive for differences in their transcription factors. A transcription factor is a protein that turns up or down the expression of a gene. They found differences in a pair of transcription factors called C/EPB-beta and CITED4. In the exercised mice C/EPB-beta activity was reduced, while CITED4 activity was increased. Researchers then genetically modified mice to artificially change the activity of these transcription factors. They found that turning down C/EPB-beta in mice increased the activity of CITED4. This caused heart cells to divide and grow in size even though the mice didn't exercise. The genetic alteration also improved the maximum exercise capacity of the mice. The enlarged mouse hearts were more resistant to cardiac stress, caused by heart disease and high blood pressure. The finding could lead to new treatments to protect against heart failure in humans. Although the same gene alteration can not be made in humans, the research raises the possibility of exploring similar molecular pathways in humans. These pathways could then be manipulated through specific exercise regimes or medicines. - Cell, 10.1016/j.cell.2010.11.036, 23 Dec 10

A new mouse model of muscular dystrophy has found that stem cells play an important role in this genetic disease. Sufferers of Duchenne muscular dystrophy, the most common form of muscular dystrophy, have severe muscle wasting and often die in their 20s or 30s. Laboratory mice with a similar genetic fault, however, only show slight muscle weakness because they relapse and recover. The researchers discovered that human muscle stem cells were not able to keep up with the muscle damage caused by the disease. But in mice the stem cells are able to keep replicating for longer, and so repair the muscle damage. The DNA in cells is stored in strands called chromosomes with protective caps on the end called telomeres. Telomeres ensure that the DNA is correctly copied each time a cell divides. But telomeres also get shorter each time a cell divides. When they are too short the cell is no longer able to replicate. The researchers found that mouse telomeres are four times as long as human telomeres. This suggests the mice's longer protective caps enable muscle stem cells to replicate a greater number of times and so continue to repair damaged muscle. To test this, researchers created a mouse model of Duchenne muscular dystrophy that more closely mimics the human disease. These mice exhibit severe muscle weakness and have reduced life span, as in humans. In the Duchenne muscular dystrophy mice the telomerase enzyme had stopped functioning. This caused cell telomeres to shorten more quickly than normal so reducing the number of times that each cell could replicate and repair muscle damage. This is the first time that muscular dystrophy has been shown to be a stem-cell-based disorder, suggesting new treatments take into account stem cells and not just focus on therapies aimed at protecting muscle fibers. The new research also suggests that any treatment should begin early, before the stem cell pool is reduced. - Cell, 10.1016/j.cell.2010.11.039, 9 Dec 10

Confused memories rather than memory loss may be the cause of 'forgetfulness' in dementia patients, according to new research. Memory problems were thought to be the result of losing memories of previously encountered items or events. But the new research suggests that dementia patients don't lose memories. Instead they form incomplete memories that are more easily confused. Researchers allowed rats to look briefly at an object. After an hour, the rats were given a memory test in which they were shown either the same object or a new object. Normal rats spent more time exploring the new object, indicating they had an existing memory of the old object. However, rats suffering from amnesia, one of the symptoms of dementia, spent an equal amount of time exploring the old and new object. The results suggest that the amnesic rat brains were not able to form complete memories of the original object. To explore this further, researchers did the same experiment but placed the rats in a dark quiet space before the memory test. This stopped the formation of other memories of the surrounding environment that could confuse the brain. In this case, amnesic rats that previously had no recollection of the object performed as well as the normal rats. The findings provide a new understanding of how memory is impaired in amnesia and dementia. The results could lead to new treatments, such as medicines that enhance the detailed representation of objects and events needed to separate memories. - Science, 10.1126/science.1194780,3 Dec 10

Light sensing cells (photosensitive ganglion cells) in the eye, which contain the pigment melanopsin, set the body's biological clock. They also play an important role in our perception of brightness, according to recent research in mice. Treatments for blindness could result from modifying the cells that contain melanopsin. Researchers used mice to trace melanopsin messenger cells from the eye into the brain. They found they extended all the way to the brain's visual processing center. This suggests that melanopsin may play a role in our perception of light. To test this further, researchers then exposed mice lacking rods and cones to light. Even though these mice were technically blind, they still showed activity in the 'sight-region' of the brain. Until now melanopsin's main function was thought to be that of regulating our biological clock. By detecting changes in ambient light levels throughout the day, melanopsin synchronizes the body's daily rhythms. This process is subconscious, but the newly discovered function of melanopsin affects conscious visual perception - the experience of sight. A common cause of blindness in humans is the loss of rods and cones. Despite this, these people are still able to perceive some light. It was previously thought this was because the loss of road and cones was incomplete. However, the new research suggests this is could be due to melanopsin containing cells. As melanopsin containing cells are not normally destroyed with rods and cones, it is hoped that they could be used to treat blindness. Melanopsin cells have worse resolution than rods and cones and so only forms a blurry picture of our surroundings. Researchers hope to engineer melanopsin to be produced in a greater number of cells. This may increase resolution and so be used to improve the sight of blind people. - PLoS Biology, 10.1371/journal.pbio.1000558, 7 Dec 10

An enzyme responsible for making pain last after nerve injury has been discovered in mice. The finding could lead to new treatments for chronic pain in humans. Raised levels of the enzyme, called protein kinase M zeta, were found in the brains of injured mice. The researchers then knocked out the gene responsible for producing the enzyme. These GM mice experience less or no chronic pain after nerve injury. Many painkillers are ineffective for treating chronic pain. The research may allow new medicines to be designed that block this enzyme. - Science, 10.1126/science.1191792, 3 Dec 10

By removing a protein that muscles use to convert fuel into energy, the researchers produced a mouse with normal body weight but which did not have enough energy to exercise. The mice had no difficulty walking but could not run on a treadmill. The results could explain the difficulties of some obese individuals experience when exercising. The protein, called PGC-1, is normally boosted when people exercise. This turns on genes that increase fuel storage in the muscle cells. But in obesity sufferers it is thought PGC-1 levels fall. This makes it harder for the cell's 'batteries' (called mitochondria) to convert fuel into energy. Hard work depletes the cells fuel stores and so obese people quickly become tired. The research also provided unexpected insights into diabetes. The couch potato mice responded normally to insulin, a hormone used to regulate blood sugar levels. Even though they didn't exercise, the mice were not at greater risk of developing diabetes. It was believed that problems with cell mitochondria caused diabetes, but the new research suggests it may be the other way around: mitochondrial problems may actually be a result of diabetes. The researchers are now investigating what happens when PGC-1 is given in short bursts to replicate what happens when people exercise. - Cell Metabolism, 10.1016/j.cmet.2010.11.008, 1 Dec 10

Premature ageing can be reversed in mice, hinting at the possibility of anti-aging treatments for humans. Scientists were able to rejuvenate GM mice using an enzyme called telomerase that prevents DNA damage. Our DNA is contained in long strands called chromosomes. These are protected by other DNA strands called telomeres, acting much like the caps on the end of shoe laces. Each time cells divide telomeres get shorter. Eventually cell division ceases and the animal dies. Telomerase stops this process by lengthening telomeres. Researchers engineered mice to lack telomerase. These GM mice died much quicker than normal mice and suffered from age-related conditions such as osteoporosis and neuro-degeneration. However, when the enzyme was switched back on, the aged mice regenerated. New neurons were produced and degenerated organs, such as the liver and intestines, were repaired. Neuron production also improved the mice's survival behavior. The aged mice has lost the ability to smell unpleasant odors associated with predators, but the regenerated mice regained this skill. The research suggests that some early-aging disorders could be treated by boosting telomerase in cells in which the enzyme has stopped working. Telomerase may also be used to restore organ function. However, the results won't necessarily be the same in humans. Mice produce telomerase throughout their lives, but in humans the enzyme is switched off in adults. This prevents cells growing out of control and becoming cancerous. It is suggested that using telomerase as a treatment for aging-disorders in humans would come at the cost of an increase in cancer. - Nature, 10.1038/nature09603, 28 Nov 10

A new compound has been designed that controls weight and blood sugar in mice, raising the prospect of a treatment for sufferers of obesity and diabetes. Researchers injected the compound, called GO-CoA-Tat, into the stomachs of live mice. Taking blood samples the next day, they found that the levels of the hormone known to cause weight gain, acyl-ghrelin, had gone down. It is thought the new compound works by disrupting the production of an enzyme called GOAT. GOAT is known to boost the production of acyl-ghrelin. Researchers tested this idea using GM mice which had been modified not to produce the GOAT enzyme. The new compound had no effect on the GM mice, whereas the blood sugar levels of non-GM mice were almost halved. This suggests that the new compound depends on the GOAT enzyme to work. Finally, researchers investigated the effects of the compound on weight. In a month-long experiment, mice were injected with the new compound daily. After a month, the fat mass of the treated mice was a third lower than the untreated mice. The blood sugar levels of the treated mice were also lower than the untreated mice. It is hoped that the compound could be developed into medicine to treat overweight patients and sufferers of type 2 diabetes. - Science, 10.1126/science.1196154,18 Nov 10

Scientists have found that the onset of labor is controlled by tiny molecules called microRNA. The discovery may lead to new medicines designed to prevent premature labor. Researchers used pregnant mice to measure microRNA levels in the wombs of mice mid-pregnancy and near labor. The amount of a specific group of microRNA was found to greatly increase just before labor. The increase was also seen when researchers artificially caused premature labor in the mice. This led researchers to a chain reaction that explains how the hormone progesterone stops the womb from contracting during most of pregnancy. It was found that progesterone controls this group of microRNA molecules. As progesterone levels decrease towards the end of pregnancy this allows the microRNA to multiply which initiates a chain of events that end in labor. Cultured cells from a human womb were found to act in the same way as the cells from pregnant mice. The research raises the possibility of using these microRNAs to stop premature labor. However, researchers stress that the same microRNAs are known to play a role in cancer which may restrict opportunities for developing medicines based on microRNA. - Proceedings of the National Academy of Sciences,10.1073/pnas.1008301107, 15 Nov 10

A ‘fat gene' has been found to cause overeating in GM mice. The research may lead to an anti-obesity medicine that dampens appetite by reducing the activity of this gene. Researchers bred mice with extra copies of the gene, called FTO, and observed their eating behavior over 20 weeks. Mice with two extra copies of the gene were found to consume more food, causing female mice to become one fifth heavier and male mice to become a tenth heavier than normal. However, the effects on humans will not necessarily be so dramatic. The FTO gene was first linked to obesity in 2007 when it was found that people with two copies of this genetic type (around one eighth of Europeans) were on average 3kg heavier than those without. In order to develop an anti-obesity medicine, researchers say they must now understand exactly how the gene increases appetite. It is unclear whether the gene increases appetite by influencing our brain or by altering the messages to the body from fat stored in the body. Almost 1 in 3 people in the UK are overweight or obese, predisposing them to diseases such as diabetes, heart disease and cancer. The estimated cost of obesity to the NHS is approximately £1 billion a year. - Nature Genetics, 10.1038/ng.713, 14 Nov 10

Cancer tumors somehow escape the body's immune system, even when that immune system is primed by a vaccine designed to specifically target the cancer. Recent work with a GM strain of mice helps explain why. Many 'normal' cancers are made up of a mixture of cell-types including a small proportion of cells that produce a protein called FAP (fibroblast activation protein). FAP is usually produced in normal cells that heal wounds. By producing FAP, cancer fools the body into thinking the cancer is a wound. FAP not only stops rejection, it also encourages the production of blood vessels that nourish the cancer. The evidence was seen in GM mice that developed cancers and could also have their FAP production altered. When FAP production was turned off in these mice, the mouse immune system was able to attack and reduce the volume of the cancers. Because of FAP's role in normal wound healing, it is unlikely that FAP could be the basis of a vaccine against cancer. Instead, a treatment based on the new understanding of FAP's role in cancer may be possible. - Science, 10.1126/science.1195300, 5 Nov 10

The dementia associated with Alzheimer's and Parkinson's diseases is commonly associated with abnormal clumps of a protein (B-synuclein) in the brain. But it has not been clear whether these aggregates were a cause of the disease or merely a by-product. Now work with a GM mouse with mutated B-synuclein gene mutation shows that the protein clumps cause the brain damage that leads to dementia. These findings establish B-synuclein's links to Parkinson's disease and related disorders, making it a new target for potential therapies. Beta-synuclein is closely related to alpha-synuclein, a protein that can cause Parkinson's disease when it is mutated or over-expressed. - Nature Communications, 10.1038/ncomms1101, 2 Nov 10

Mice treated with a brain enzyme inhibitor performed better in memory tests than untreated mice. Spatial memory is key to being able to function independently, whether navigating your way around a shopping complex or finding your way around your kitchen. The inhibitor reduced the activity of a brain enzyme that damages the hippocampus and reduces spatial memory. Mice that had been treated performed better in mazes than untreated mice. Loss of spatial memory is associated with a number of degenerative conditions of old age, such as Alzheimer's disease, so any treatment that can diminish this loss would be extremely useful to the third of us who will suffer memory loss with ageing. As no side-effects from the treatment have been detected so far, the treatment is expected go into human trials in the near future. - The Journal of Neuroscience, 10.1523/JNEUROSCI.2783-10.2010, 13 Oct 10

Scientists have discovered a virus linked to genital cancer in horses. The finding could lead to a vaccination that prevents the disease, similar to that used against human cervical cancer. Genital cancer in horses affects both sexes, is difficult to treat and often results in the horse's death. Cervical cancer in humans is caused by a type of virus called papilloma virus. As horse genital cancers are similar to human genital cancers, researchers thought horse genital cancer may also be caused by a papilloma virus. Researchers looked for papilloma virus DNA in tissue samples from horses with genital cancer. They found a new type of papilloma virus which they have called Equus caballus papilloma virus-2, or EcPV-2 for short. EcPV-2 was found in all but one of the horses with genital cancer sampled. The virus has not been found in samples from horses without genital cancer, or in horses with other types of cancer. When researchers sequenced the genome of EcPV-2. they found the virus to be closely related to the viruses that cause genital cancer in humans. The problem of cervical cancer in humans has been significantly reduced by the recent introduction of a vaccine. The findings may lead to the development of a similar vaccine to protect horses against - Equine Veterinary Journal, 10.1111/j.2042-3306.2010.00311.x, 8 Oct 10

Nerve cells made from a person's own skin suggest a novel way to treat spinal injury. Spinal cord damage in rats and dogs has previously been treated using a specific type of nerve cell stem called OEC. OECs were only thought to be produced in the lining of the nose and the smell-sense region of the brain. This makes it difficult and dangerous to extract the large number of these cells needed for spinal damage treatment. But researchers have now found the OECs can be produced from a different type of nerve cell called neural crest cells. Using growing chicken and mice embryos they found that these neural crest cells change into OECs. They were able to visually track the changing cells by genetically modifying the embryos so that these cells glowed green in UV light. As neural crest cells are also found in human skin cells, OECs for spinal injury treatment could be grown from a patient's own skin. Scientist now face the challenge of growing enough of these OEC's from human skin. - Proceedings of the National Academy of Sciences, 10.1073/pnas.1012248107, 7 Oct 10

For the first time, researchers have discovered a therapy that can treat the invariably lethal terminal stages of cancer in animals. The new monoclonal antibody is effective in mice against colon and breast cancers and melanoma and does not appear to have any toxic effects. Currently, the end stages of metastatic cancer - secondary cancers that have already spread to other parts of the body from original locations - are untreatable. Many patients die because of the progressively debilitating, organ-destroying qualities of secondary cancer. In this research scientists created a monoclonal antibody that specifically blocks an adhesion molecule called PECAM-1. The researchers found treatment with the antibody effectively treats the terminal stages of cancer, with tumors shrinking and treated animals gaining weight. The anti-PECAM-1 antibody binds to a cell-surface protein. This protein appears to control the secretion of critical growth factors, which regulate the growth of advanced tumors. While this current round of research was done in mice, the researchers say they hope to be able to begin testing this approach in people within two years. - Proceedings of the National Academy of Sciences, 10.1073/pnas.1004654107,

6 Oct 10

Supplementing the diet of healthy middle-aged mice with a mixture of amino-acids - the building blocks of proteins - extended their average lifespan by over one tenth. The treated mice also had more stamina and improved muscle co-ordination. The dietary supplement comprised branch-chained amino-acids leucine, isoleucine and valine added to the mouse drinking water. It increased the production of mitochondria within cells, especially in heart and skeletal muscle cells. Mitochondria are the power plants of cells. The mice also showed an increased activity of SIRT1, a known longevity gene. Last year scientists showed that the same amino acids could extend the lifespan of single-celled yeast. - Cell Metabolism, 10.1016/j.cmet.2010.08.016, 6 Oct 10

How do you re-animate paralyzed limbs? A new approach being trialed on genetically modified mice uses flashes of light. The modified mice contain a protein from green algae (ChR2) that attaches to the surface of nerve cells. When the sciatic nerve of anaesthetized mice was stimulated with a flash of light the Achilles tendon contracted. Previously electrical stimulation has been used to artificially activate muscles, but electricity only stimulates fast fibers in muscles. This causes jerky movements and the muscle quickly tires. In this case the light-stimulated contractions were much more similar to normal muscle activity with the experimenters able to activate just slow fibers by altering the intensity of light. - Nature medicine, 10.1038/nm.2228, 26 Sep 10

Mice with a disabled RGS14 gene are able to remember objects and learn to navigate mazes better than normal mice. RGS14 is primarily turned on in the CA2 region of the hippocampus, a region of the brain involved in consolidating new learning and forming new memories. RGS14, which is also found in humans, has been previously shown to regulate several molecules involved in processing different types of signals in the brain that are known to be important for learning and memory. Mice were raised with the RGS gene knocked to explore this process of regulation and with the expectation that these mice would demonstrate learning deficiencies, making the actual research findings all the more unexpected. - PNAS, 10.1073/pnas.1005362107, 21 Sep 10

New research shows female mice, monkeys and humans appear to metabolize the oestrogen-like chemical bisphenol A (BPA) in similar ways. Consequently, the data from mice on the bioaccumulation and health effects of BPA are relevant to predicting the effects of BPA on humans. Huge quantities of BPA are used in the manufacture of plastics such as polycarbonates and concerns have been raised about the health consequences of BPA leaching out of plastic containers into food and drink. In particular there have been concerns about the impact of BPA on the development of the foetus, infants and young children. Bisphenol A is an endocrine disruptor, which can mimic the body's own hormones. Regulatory bodies have determined safety levels for humans, but those safety levels are currently being questioned or under review. - Environmental Health Perspectives, 10.1289/ehp.1002514, 20 Sep 10

Retinal cells, necessary for color vision, have been successfully transplanted into blind mice. The mice were engineered to mimic a form of childhood blindness called Leber's congenital amaurosis. Cells for the transplant were extracted from the eyes of newborn mice. Then 200,000 cells were injected into each eye at the rear of the retina. Within 21 days the transplanted cells grew into rod and cone cells - the cells responsible for detecting light/dark, and determining color. It has still to be demonstrated that the cells become functional and restore any sight, however the fact that they became established and grew into the correct cell types is promising. The ultimate aim of the work is to provide a treatment for the one in 3,000 people affected by incurable genetically inherited retinal disease. - Human Molecular Genetics, 10.1093/hmg/ddq378, 19 Oct 10

As a normal mammalian body grows, hundreds of motor neurons grow from the spinal cord to the muscles they will control. During development of mice with a single mutation in the gene Hoxc9, thoracic motor neurons were transformed into limb motor neurons. This study shows that the gene acts as a global organizer of motor neurons and their connections, helping to explain how the nervous system develops to control movements such as breathing and walking. Humans have 39 hox genes, of which 21 have a role in coordinating motor neurons in the spinal cord. Understanding motor neuron development can contribute to the ultimate goal of finding mechanisms to repair spinal injury. - Cell, 10.1016/j.neuron.2010.08.008, 9 Sep 10

The omega-3 fatty acids DHA and EPA found in oily fish reduce inflammation, which in turn reduces the symptoms of arthritis and reduces the risk of heart attacks and strokes. Inflammation pathways also contribute to insulin resistance, a step on the path to diabetes. Scientists have now shown how these fatty acids reduce inflammation in mice. They act specifically on a cell-receptor (GPR 120) in white blood cells to switch-off a chemical pathway that causes inflammation. So the scientists produced a colony of mice that lacked the GPR 120 receptor. They then fed this colony and a control group of normal mice a high fat diet, either with or without a supplement of DHA and EPA fatty acids. All the mice became obese and all mice without the fatty acid supplement became insulin insensitive. The fatty acids had no effect on the mice lacking the receptor but normal mice fed the fatty acids maintained sensitivity to insulin, clarifying the health benefits of these fatty acids in reducing inflammation. - Cell, 10.1016/j.cell.2010.07.041, 8 Sep 10

An ultimate goal of regenerative medicine is the generation of organs derived from a patient's stem cells. In new research scientists were able to provide a pancreas deficient mouse with a fully functioning pancreas derived from rat stem cells. The research was in two stages. Firstly the team created mouse-rat chimeras, the first time this has been achieved. To do this, mouse stem cells were injected into a rat blastocyst (very early embryo). This gave rise to a rat-like chimera. Conversely, rat stem cells injected into a mouse blastocyst gave rise to a mouse-like chimera. Next, the team injected rat stem cells into mouse blastocysts from a pancreas deficient strain of mice. In the resulting chimera, the ‘mouse' had a fully functioning pancreas made up entirely of rat cells. The scientists have proved, at least in principle, that donor cells of one species can rescue a defect in organ development in a different species. However, the legal and ethical barriers to producing human-animal chimeras makes it unlikely this will become a route to organ replacement in humans. - Cell, 10.1016/j.cell.2010.07.039, 3 Sep 10

As women get older the chances of infertility, birth defects and developmental disabilities go up. These risks often relate to errors in chromosomes in the egg. By examining the eggs from mice at different ages, scientists showed that weakened chromosome cohesion in older mice caused eggs to divide abnormally, leading to extra or missing chromosomes in the daughter cells. Older mice had far less of a protein called cohesin that helps form a cell body called the centromere. This ensures chromosomes align and separate during cell division. In the mice, weakened centromere cohesion explained 90% of age-related chromosomal abnormalities. As the cohesin proteins are laid down in the human egg before birth, it is possible that the birth defects and infertility associated with human maternal age are also due to falling levels of cohesin. - Cell, 10.1016/j.cub.2010.06.069, 3 Sep 10

Increasing resistance to anti-malarials, such as those based on Artemisinin, have prompted a need for new treatments. The new medicine, NIT609, has a different mechanism of action and is effective against two of the most common malarial parasites including the most dangerous species, Plasmodium falciparum. The new medicine appears safe, offers the potential of a cure with a single oral dose and is also relatively easy to manufacture. The drug killed the blood stages of Plasmodium falciparum and Plasmodium vivax at low nanomolar concentrations by inhibiting protein synthesis. - Science,10.1126/science.1193225, 3 Sep 10

Lupus is a chronic disease where the body's own immune system attacks healthy tissue, causing inflammation, pain and damage in organs, particularly the kidneys. Using mice with lupus, scientists found that if they removed blood platelets by using an anti-clotting medicine, inflammation was significantly decreased. The treated mice had less kidney damage than untreated lupus mice and lived for an extra three months. There is no cure for lupus, although its symptoms can be managed to some extent with a range of different medicines. Infections and kidney failure are the most common causes of death in people with the disease. Clinical trials using a similar treatment on humans are being planned. - Science Translational Medicine, 10.1126/scitranslmed.3001001, 1 Sep 10

A medicine previously used to treat high blood pressure could now be applied to Alzheimer's disease following tests on GM mice. Research found that the medicine diazoxide slowed the development of Alzheimer like symptoms in GM mice. Mice given the medicine performed better in memory tests and analysis of brain tissue showed fewer of the changes associated with Alzheimer’s. The Alzheimer's mice were given diazoxide in their drinking water for eight months. In standard tests of learning and memory these mice outperformed those given normal drinking water. Brain tissue analysis showed the medicine prevented the accumulation of two proteins, beta-amyloid and tau, which are hallmarks of Alzheimer's. In addition there was increased cerebral blood flow in the treated mice. These beneficial effects were seen with low doses of diazoxide, increasing the possibility that diazoxide could be safe to use as these doses would be low enough to avoid a major decrease in blood pressure. - Journal of Alzheimer’s Disease, 10.3233/JAD-2010-101017, 30 Aug 10

Researchers have successfully used a chemical to reset and restart the natural 24-hour body clock in mice. This opens up the possibility of treatments for human mental illnesses such as bipolar disorder, as well as curing jet lag and some of the negative effects of shift-work, all of which are linked to abnormalities of, or disruptions to, the body clock. Many organisms have an internal body timing system called the circadian clock. Light, and the day and night cycle, are very important for resetting the clock and fine adjustments are made by several enzymes. One of these enzymes, called casein kinase 1, was at the center of this study. Mice whose daily cycle had been disrupted by either genetic modification or by living under constant light returned to a normal 24-hour activity cycle during treatment with a casein kinase 1 inhibitor. The normal cycle persisted throughout treatment. - PNAS, 10.1073/pnas.1005101107, 24 Aug 10

Monkeys treated with a therapy that targets specific viral genes survived deadly Ebola and Marbug infections, a new study reports. Both Ebola and Marbug viruses cause high fevers and hemorrhaging which frequently lead to death. Currently there are no vaccines or medicines licensed to counter infections with these viruses. Scientists working with 'antisense' compounds developed a therapy which was 90% successful in guinea pigs and mice whether it was administered before or after exposure to the Ebola virus. It is believed that the antisense compound enters host cells and prevents the pathogen from replicating. This gives time for the host to build an effective immune response. As the therapy was successful in mice and guinea pigs the team then went on to conduct trials in rhesus monkeys. Of the eight monkeys exposed to the virus, five survived when the antisense medicine was delivered 30-60 minutes after infection. The Marbug virus was studied in a similar way. Researchers developed an antisense therapy known as AVI-6003 which had at least 90% success rate in trials on guinea pigs and mice. 13 Cynomolgus monkeys all survived when treated between 30-60 minutes after exposure to the virus. The US Food and Drugs Administration has now granted permission for both antisense treatments to proceed to clinical trials. - Nature Medicine, 10.1038/nm.2202, 22 Aug 10

Scientists have created a ‘knockout rat' that can be used to model certain diseases in the same way as mice. Researchers made knockout rats by extracting embryonic stem cells (ESCs) from rat embryos, then genetically engineered the cells so that a specific gene no longer functions. The altered ESCs were then injected into early stage rat embryos. The resulting mixture of embryonic cells was implanted into the womb of a rat foster mother. This creates offspring that are chimeras, born containing tissue from both the normal embryo and the altered ESC. When the rats' germline cells (sperm and eggs) are derived from the manipulated cells, the rats pass those genetic changes onto their offspring resulting in new strains of pure breeding knockout rats. Rats have long been a popular model system for many aspects of biomedical research. Their liver enzyme systems and nervous systems are surprisingly similar to humans and, as rats are more socially sophisticated than mice, they could provide better models for studying psychiatric disorders. This powerful technique, already widely used in mice, provides greater control than previous methods used to create GM rats. - Nature, 10.1038/nature09368, 11 Aug 10

The barrier between blood vessels and the brain may no longer limit the delivery of medicines to tumors, research on rats shows. The blood-brain barrier protects the brain from viruses and other types of infection but also limits the delivery of medicines to treat brain tumors. Now scientists have found a new way to overcome this problem by combining two earlier approaches to produce a more effective treatment. Ultrasound waves were used to temporarily disrupt the blood-brain barrier. While the barrier was open a strong magnetic field attracted medicine coated, magnetically charged nanoparticles towards the tumor, targeting the medicine to where it is needed. The team tested the procedure on rats. One group was treated using the new procedure while the other received a normal injection into the bloodstream. Results showed tumor regions in the first group to have 20 times the concentration of medicine compared to rodents that did not receive the treatment. Scientists hope that this technique could be used to treat all brain based diseases, such as Parkinson's and Alzheimer's disease. However, they will first need to see if it is possible to safely translate the study to humans, because disrupting the blood brain barrier can be dangerous. - PNAS, 10.1073/pnas.1003388107, 9 Aug 10

A study on mice suggests that cell suicide may encourage tumors to grow instead of destroying them. Damaged DNA causes cell death – a process triggered by the protein PUMA. Previous studies had shown that another protein, p53, activates PUMA. It was thought that mice with mutated p53 developed tumors and PUMA was subsequently triggered to induce cell death in an attempt to control the damage. However, the new study suggests PUMA may not be as beneficial as once thought. Scientists studied genetically modified mice without the protein and exposed them to high doses of radiation. Without PUMA, it was predicted that cell death would not occur and tumor growth would expand at a faster rate causing the mice to succumb to cancer sooner. Yet the results showed the opposite, with mice lacking PUMA faring far better. The team suggests this may be due to cell death clearing the way for more damaged cells to grow. Stem cells, which may have sustained some damage from earlier radiation, are forced to rapidly fill the areas where injured cells have died, creating an area of potentially cancerous cells. Researchers stress that the results are not applicable to humans and are useful for only a small subset of cancers. Still, the study raises questions about current anti-cancer medicines designed to mimic PUMA. - Genes and Development, 10.1101/gad.1940110, 1 Aug 10

The body's own cells could be used to aid the repair of joints, a pioneering rabbit study has revealed. Scientists made computer-designed shoulder joint scaffolds out of biodegradable polymer and added growth factors, which attracted stem cells. In total 23 rabbits were used, of which 20 had bioscaffold replacements after the removal of their shoulder joint. The remaining three rabbits did not receive the bioscaffold. Half the 20 rabbits also had their scaffolds coated in the growth factor TGFß3. The team then studied the rabbits' ability to walk and took bone and cartilage samples. Within a month of surgery all rabbits with the growth factor were better able to bear weight than those without. The rabbits without the scaffold were not able to move as well. Scaffolds with the growth factor were covered fully in the cartilage which naturally lines the joints. Rabbits without the growth factor had limited cartilage formation. The researchers are still unsure as to where the stem cells came from. They suggest the growth factor can attract different cell types for limb growth. More research is needed to work out how specific cell populations could be made to promote the growth of more complex tissues. But this work paves the way for a future of naturally grown joints that would last longer than current artificial joint replacements. - The Lancet, 10.1016/S0140-6736(10)60668-X, 29 Jul 10

For the first time scientists will be able to study the development of human testes in mice. These mice will be used to look at the origins of a type of testicular cancer that is quite common in young men. It was already known that TGCC testicular cancer originates from the abnormal development of cells in fetuses. But how and why this happens has been impossible to explore before now, because researchers were unable to study testicular development in fetuses during pregnancy. Human types of TGCC do not occur in laboratory animals and the tissue cannot be studied in the test tube as it does not survive or develop normally. So researchers applied for approval to take testicular tissue from aborted human fetuses. The fetuses used had been aborted at nine weeks and between 14—18 weeks and only from women who had given consent. None of the terminations were related to fetal abnormalities. Following approval, the team grafted the tissue into mouse models with compromised immune systems so they could accept the transplant. They were able to watch the testicular grafts developing normally over a six-week period. The mice should be useful for determining the causes of testicular cancer and disorders of sexual development (DSDs) known to be caused by abnormal testicular development. For instance, it should be possible to work out the role, if any, of exposure to environmental chemicals during pregnancy. - Human Reproduction, 10.1093/humrep/deq183, 3 Aug 10

Capsaicin, a compound found in chili peppers, has been found to reduce high blood pressure in rats. Earlier research on capsaicin-like molecules showed that they are involved in activating a pain pathway. This study is the first to investigate the long-term effects of capsaicin on blood pressure in animals. Researchers studied the compound in rats with high blood pressure over seven months. They found that activation of a pore in cell membranes called the ‘TRPV1 channel’ reduced blood pressure. The channel is found in the lining of blood vessels, and once switched on it increases the production of nitric oxide – a gas known to protect blood vessels against inflammation. Studies will be needed to see if the same effect happens in people. Scientists would need to work out the exact quantity of chili a person would need to consume each day to lower blood pressure. These studies highlight the need for more research into the function and potential uses of chili compounds in medicine. - Cell Metabolism, 10.1016/j.cmet.2010.05.015, 4 Aug 10

Primitive retinal cells, that were previously thought to have no role in image formation, can help blind mice see. These photosensitive cells, known as ipRGCs, respond to light so that we know when to sleep, for instance. But they were not thought to play any role in seeing patterns or shapes. The cells were studied in mice without the rod or cone cells which are normally required to form images. The blind mice were divided into two groups – one with the ipRGCs and one without. In vision tests, the mice with the photosensitive cells were able to follow the movements of a rotating drum, which assesses their capability of tracking moving objects. Another test involved a ‘Y’ shaped maze from which mice could leave after selecting a certain visual pattern. Mice that lacked the ipRGCs as well as rod and cone cells were unable to complete the tasks. But with the ipRGC cells they were able to see shapes and patterns. These results suggested that the special eye cells can help clarity of vision. Perhaps in the past ipRGCs aided vision, but their function has since been overtaken by rod and cone cells. Researchers hope this discovery could aid future treatments for people with severe visual impairment. People with poor vision might be trained to use their ipRGCs again to perform simple tasks that require some clarity of vision. - Neuron, 10.1016/j.neuron.2010.05.023, 15 Jul 10

Elevated levels of the protein CIB1 causes enlargement of the heart and subsequent heart failure, according to rodent research. Cardiac hypertrophy is a condition in which the heart muscles thicken, leading to an enlarged and weakened heart. The cells which increase in size, usually after a heart attack or from high blood pressure, are called cardiomyocytes. To identify the factors regulating cardiomyocyte growth, researchers examined neonatal rat heart cells genetically altered to become hypertrophic, which led to the discovery of elevated CIB1 levels. They also analyzed mouse and human heart cells with similar results. To deduce the function and interactions of CIB1 during hypertension they studied the protein in GM mice. One group of mice was designed to lack CIB1, the other to over-express it. The group with high blood pressure and excess CIB1 exhibited cardiac hypertrophy, but mice without CIB1 were protected. Scientists also discovered that the protein activated the enzyme calcineurin. Calcineurin is known to be important in the development and function of heart cells. Although more research is needed on CIB1 and calcineurin, the team suggests that both insights may be used to prevent heart failure. - Nature Medicine, 10.1038/nm.2181, 18 Jul 10

A vaccine in the form of a skin patch has proved more effective than a needle in mice. Scientists tested the patches on a group of mice, comparing the results with mice immunized using a traditional syringe. A month later both groups were infected with influenza and dealt with the virus well. But the mice with the patches were better able to cope with a second flu infection three months after vaccination. The vaccine is effective because there are important immune cells within the skin. These cells form a special network that immediately recognizes foreign particles (antigens) which are present in vaccines, making the skin a good site for inoculation. The patch is made of biodegradable microneedles, each about six times the thickness of a human hair. Every microneedle is coated with the flu vaccine and dissolves away within minutes after contact with the skin. The new patch vaccine builds on earlier skin vaccine technology developed in the mid 1990s and the testing of microneedle delivery using proteins, nanoparticles and other small molecules. Skin patches eliminate the need for trained healthcare workers to give the vaccine. Developing countries would not need a costly medical infrastructure. People could send off for the patch or obtain it at their nearest clinic and administer the vaccine themselves. It is cost effective, convenient and overcomes the biohazard of ‘dirty’ needles and medical waste. The microneedles are made of the plastic polyvinylpyrrolidone. This material is already being used in medical equipment without any side effects, but the team will need to complete further trials before the patch is tested in humans. - Nature Medicine, http://dx.doi.org/10.1038/nm.2182, 18 Jul 10

Some of the symptoms relating to Down syndrome have been linked to two genes on chromosome 21, a study on mice has shown. People with Down syndrome carry an extra copy of chromosome 21. But it has been unclear which genes within this chromosome are responsible for the disorder, which includes mental retardation, early onset Alzheimer's disease and other health problems. The Olig1 and Olig2 genes were found to be over-expressed in GM mice with a form of Down syndrome. Ts65Dn mice carry additional copies of some genes similar to those found on human chromosome 21. To uncover the effects of the two genes, scientists made them both less active. Reduced activity of the genes in mice corrected neurological problems such as abnormal brain activity. It is likely that other genes are also involved, but having identified them it may be possible to inhibit them using gene therapy, thereby alleviating Down syndrome health problems. An earlier mouse study suggested that the extra copy of chromosome 21 protects against cancer. Using targeted gene therapies to tackle mental retardation would avoid a potentially difficult trade-off. - Nature Neuroscience, 10.1038/nn.2600, 18 Jul 10

Diabetes can cause the death of nerves in the body's extremities, a condition known as diabetic peripheral neuropathy (DPN). The loss of feeling from DPN makes diabetics susceptible to wounds and infections which often lead to amputation, making DPN the second cause of amputation after injuries. A new compound (KU-32) given to diabetic mice stopped DPN and restored sensory nerve function in damaged tissues. KU-32 increases the concentration of a common chaperone protein, Hsp 70, which repairs proteins damaged by high levels of glucose. So far KU-32 appears to be nontoxic and easy to administer making it a candidate for clinical trials in people with diabetes. - ASN Neuro, 10.1042/AN20100015, 14 Jul 10

Shining a laser into the brain may ease the symptoms of Parkinson’s, a new study in mice has shown. Previous studies have suggested that movement is controlled by the careful regulation of ‘stop’ and ‘go’ pathways. The new work, in mice that display similar symptoms to people with Parkinson’s, reveals that these pathways can in turn be controlled by genetically altering them to be responsive to light. The team genetically engineered some brain cells in the mice to respond to light. They then inserted a fine fibre optic cable into the brain through which they could shine a laser and control the cells. When the light was off, the mice showed symptoms of Parkinson’s. Yet when the light was on, motor pathways were activated and the symptoms eased, so that the mice were only able to move around normally when the laser was on. This study has revealed more about the pathways involved in motor function and how dopamine, a chemical messenger which Parkinson’s patients cannot produce, is not needed to regain control of the motor pathways. Although more research is needed, scientists hope the results could also help in the study of Huntington’s disease and Tourette’s syndrome. - Nature, 10.1038/nature09159, 7 Jul 10

Mice with cancer living in enriched environments had smaller tumors, new research has revealed.Although normally housed in groups of five, scientists studied mice with cancer in social groups of up to 20. These large groups had an enriched environment with more space, toys and running wheels. Over six weeks, researchers found that the mice stopped releasing the tumor-feeding hormone leptin – resulting in smaller tumors or cancer remission. The team believe this is due to increased social activity and competitiveness. They observed dominance displays in the mice and more scurrying around, leading to the conclusion that it is not exercise alone that can reduce tumors. At the end of the study, tumors had shrunk by about three quarters and one in six of the mice had no visible tumors. The results reinforce the idea that an active and challenging lifestyle can be beneficial in maintaining good health. - Cell, 10.1016/j.cell.2010.05.029, 9 Jul 10

A new compound that may reverse Alzheimer’s in humans has proven successful in rats and mice. The compound, P7C3, had the most positive effect out of a thousand substances that were screened. Scientists administered it to ageing rats and noticed an improvement in their ability to swim through water mazes – a standard memory test. They then tested the compound in modified mice lacking a gene crucial to the survival of newly formed neurons. It normalized the stunted growth of neurons in these mice, helped the cells to proliferate and thickened the layer of neuronal cells by 40%. The team found that P7C3 had an ability to protect cell machinery. In addition, researchers found that the derivative of P7C3 – A20 – is even more effective. A20 is 300 times stronger than another Alzheimer’s medicine that is currently going through clinical trials. These compounds may be involved in the prevention of apoptosis (cell death) but more research is needed to confirm this. - Cell, 10.1016/j.cell.2010.06.018, 13 Jul 10

Armed and tagged immune cells can be watched attacking tumors in mice in real time. Lymphocyte cells were armed with T cell receptors which allowed them to detect and destroy melanoma skin cancers. The cells also included a tag called a reporter gene, which glowed during scanning. This helped researchers visualize the immune reaction, from point of entry into the bloodstream to arrival at the tumor sites. The team saw the melanomas of mice attacked and degraded by the armed lymphocytes, similar to a normal immune response to foreign cells in the body. One million genetically engineered lymphocytes were created and injected into mice and in 2–3 days were seen attacking the tumors. But the process could take longer in humans and approximately one billion the engineered lymphocytes would be needed. Earlier research on the arming of human lymphocytes was successful. Now that scientists can track how the system works in mice with an intact immune system, they hope to observe similar results in humans. Doctors would be able to watch lymphocytes attacking cancer in patients. The team are now searching for a suitable vector that would be safe for humans. If they find one which is ideal, human studies could begin in a year. - Proceedings of the National Academy of Sciences, 10.1073/pnas.1008300107, 12 Jul 10

Prostate cancer and hereditary breast cancer could be linked by the same gene, research on mice suggests. It is known that the gene BRCA2 plays a role in the development of breast cancer. Scientists decided to investigate BRCA2 in relation to prostate cancer as it can have a hereditary component like breast or ovarian cancer. Male mice were modified to knock out the gene in their prostate glands. After their first birthday the mice began to accumulate damaged DNA at a fast rate, more than could be repaired. Anti-tumor genes became damaged and could no longer suppress the cancerous cells. These findings suggest that BRCA2 plays the same role in prostate as in breast cancer, and its absence or damage could lead to prostate cancer. Researchers believe this result could lead to the use of similar medicines to treat patients with either type of cancer. - PLoS Genetics, 10.1371/journal.pgen.1000995, 24 Jun 10

A functional artificial lung on a chip, which mimics the behavior of mouse lungs, has been created. The artificial lung mimics the boundary between the lung’s air sacs – where gaseous exchange takes place – and tiny blood vessels called capillaries. Scientists designed the lung to have two layers of human cells divided by a porous barrier. The upper layer has air sacs – alveoli cells – while the bottom contains capillary cells to mimic the vessels which carry the oxygen rich blood away. Breathing by the lung chip is achieved by a change in air pressure and the elasticity of the cells in response to the change. Researchers found that the lung could breathe in real time like a real mouse lung. The team tested and compared the artificial lungs with mouse lungs. Using silica nano-particles, they found both types of lungs displayed an identical uptake response. As the lung on a chip is transparent it would be valuable for future studies on pathogen inhalation, to study inflammation. But it is not yet developed enough to replace animal lung studies altogether. Researchers need cells which are more similar to those taken from patients, than cells from lines which have been grown in the lab. - Science, 10.1126/science.1188302, 25 Jun 10

For the first time rats have been able to breathe using lab grown lungs, a new study reports. Scientists created the lungs using the same technique used to create liver grafts. Decellularization flushes out old cells to leave just the structure of the organ and new stem cells are introduced to replace them and seed the empty area. A team of researchers used a decellularized adult rat lungs reseeded with lung cells from newborn rats. After eight days the cells had multiplied and shifted into the right places to form functional lung tissue. The tissue was then tested by replacing rats’ lungs with the new lab grown versions. X-rays showed the lungs were inflating (but not to their full capacity), while blood tests revealed that exchange of oxygen and carbon dioxide was working at 95% of normal efficiency. After two hours blood clots began to form, forcing the lungs to stop functioning. Researchers will now try to find cells that would allow the lungs to function for longer and not provoke an immune attack after transplantation. - Science, DOI: 10.1126/science.1189345, 24 Jun 10

A new vaccine which successfully treated mice with leukemia will undergo the first human trials this year. Leukemia is a cancer of the blood or bone marrow. There are many different types of leukemia which are usually treated through chemotherapy or a bone marrow transplant. Scientists will be using the newly developed vaccine to help treat patients with acute myeloid leukemia, which occurs when there is an overproduction of immature white blood cells. The over-abundant immature cells fill up the bone marrow, reducing the space available to create normal blood cells. Sometimes the cells may be released into the blood circulatory system and are unable to function like normal blood cells, causing anemia and bruising. The vaccine does not prevent the disease but treats diagnosed patients and protects them against future problems. It has been created using the patients' own blood cells by adding two genes which help the immune system to recognize and destroy leukemia cells. As a result the vaccine helps prevent the disease recurring after traditional treatments. The trials on mice have been crucial in the development of the vaccine for use in humans. Mice injected with the vaccine had an extended life, equivalent to 25 years in humans. Almost half did not have a relapse. Scientists hope that if the first human trials are successful, the vaccine will be able to treat other forms of leukemia and cancer. - Cancer Immunology, Immunotherapy, DOI: 10.1007/s00262-009-0756-x, 6 Jan 10

Eating pork that contains a micronutrient could help a growing brain develop, according to a recent study on mice. Previous research has shown that the diet of a pregnant mother can greatly affect the health of the foetus. The nutrient choline has been suggested to help treat heart problems by administering it in large doses. Now scientists claim choline, found in bacon, sausages and eggs assists recall function in foetal brains. The team studied groups of pregnant mice with differing diets of choline. One group received a larger amount of choline than the other. In the groups with larger choline consumption there were noticeable genetic changes in the hippocampus part of the brain, which is responsible for memory. Specifically the genetic changes were found in cells which are vital for creating new brain cells. The researchers isolated a few of the changed cells, grew them in a culture and found they produced proteins involved in brain cell regulation. Although scientists warn that bacon can never be entirely healthy, they hope the results will help people reconsider "unhealthy" food. - Federation of American Societies for Experimental Biology, DOI: 10.1096/fj.09-140145, 5 Jan 10