August 12, 2012 § Leave a comment
A serious injury can have lasting effects on victims of violent incidents such as car accidents, stabbings, and gunshot wounds, specifically in their nervous systems. Nerves and blood vessels can be split, bones can be broken, and cells can be damaged in such a way that, while wounds may heal and scars fade, the body never forgets.
The ruined debris from these injuries is often spread throughout the body like a wreckage site, making it extremely tricky to rectify. Highland Hospital neurosurgeon Jason Huang, M.D., who worked with Iraqi soldiers injured on the battlefield, is well aware that nerve damage is among the most difficult to treat.
Huang, now back at his University of Rochester Medical Center laboratory, is working with a team to increase the success of methods by which doctors can repair nerve damage. In the journal PLoS One, Huang and his colleagues published a report that there may be a specific group of cells useful in nerve transplantation.
Huang determines that, “Our long-term goal is to grow living nerves in the laboratory, then transplant them into patients and cut down the amount of time it takes for those nerves to work.” He explains that for a damaged nerve to repair itself, the two disengaged parts of the nerve must somehow reunite through a complicated labyrinth of tissues and cellular structures, then reconnect. For a small wound such as a scrape or a paper-cut, this occurs fairly easily, but for more destructive injuries, the nerve cannot repair itself without some kind of intercession.
Typically, the transplantation of nerve tissues from elsewhere in the patient’s body serves to scaffold for the repairs, like a rough sketch, that new nerves can fill in to bridge the gaps. The fact that these tissues come from the patient’s own body ensure that the immune system does not attack it.
Unfortunately in the case of severely injured patients, there is no healthy nerve tissue available from their own bodies. They must seek alternatives. Other options include nerve transplantation from human cadavers or animals, but this substitute involves lifelong dependency on extremely potent immunosuppressant drugs that come with a host of side effects.
The technology established by Huang and his team is called NeuraGen Nerve Guide. It includes a hollow, absorbable collagen tube that nerve fibers can grow and travel through to find each other. It is used to mend nerve damage over distances of less than half an inch long.
The team performed experiments on rats and found that dorsal root ganglion neurons (DRG cells) help to produce solid, healthy nerves, without inciting an undesirable reaction from the immune system. The team compared several methods to bridge half an inch nerve damage gaps in rats. They performed transplantations between rats combined with NeuraGen technology, comparing results of pairing NeuraGen with DRG cells, Schwann cells, and on its own. After four months, the tubes equipped with the DRG or Schwann cells were found to produce healthier nerves. Compared with each other, DRG cells incited the least amount of attention from the immune system, while Schwann cells attracted twice as many macrophages and more immune interferon gamma.
Schwann cells are currently more often preferred as potential partners in nerve transplantation, even though they cause problems due to the immune system’s reaction to them. Huang says, “The conventional wisdom has been that Schwann cells play a critical role in the regenerative process. While we know this is true, we have shown that DRG cells can play an important role also. We think DRG cells could be a rich resource for nerve regeneration.” This is great news for the yearly 350,000 patients in the United States who experience severe injuries to their peripheral nerves.
Huang’s laboratory is just one of many medical technology institutions geared towards the improvement of treatment methods for nerve damage. The team is currently collaborating with Douglas H. Smith’s team at the University of Pennsylvania to create DRG cells in the laboratory by stretching them. Stretching them encourages growth at the rate of one whole inch every three weeks. Instead of leaving it up to the nerves to travel and find each other inside the body, the team endeavors to grow the nerves externally in preparation for transplantation. This speeds the process of nerve repair.
“A Step Forward In Effort to Regenerate Damaged Nerves”. (February 21, 2012). Neuroscience News. March 2, 2012. http://neurosciencenews.com/regenerate-damaged-nerves-dorsal-root-ganglion/.
August 12, 2012 § Leave a comment
A study published the week of January 30th in the journal Nature reports that a major genetic breakthrough was made by an international research team, led by the Research Institute of the McGill University Health Centre (RI MUHC), which could possibly change the way pediatricians understand and treat child brain cancer.
Glioblastoma is a fatal brain cancer that is unresponsive to both chemotherapy and radiation therapy. The research team identified two genetic mutations that are responsible for up to 40% of Glioblastomas in children. The two mutations were discovered to be responsible for DNA regulation. Researchers suggest this may explain why Glioblastoma is resistant to traditional therapies.
Researchers from the team from McGill University and Génome Québec Innovation Centre identified the two mutations in the gene histone H3.3. The gene is very important, as it guards genetic heritage and is the key to modulating the expression of genes. The mutation apparently prevents cells from differentiating normally and helps to protect the genetic information of the cancerous cells.
The team’s head investigator Dr. Nada Jabado, a hematologist-oncologist at The Montreal Children’s Hospital of the McGill University Health Centre (MUHC), explains that this protective aspect makes it less sensitive to chemotherapy and radiotherapy. She says of previous child brain cancer research, “we’ve been failing to hit the right spot. … It is clear now that Glioblastoma in children is due to different molecular mechanisms than those in adults, and should not be treated in the same way.” She is optimistic about being able to know where to focus future efforts to treat the cancer.
Dr. Jabado also believes that this finding is only the beginning. Improper management of this gene, which protects genetic information, has also been observed in other cancers such as colon, pancreatic, lymphoma and leukemia. Future research could therefore uncover better treatments for these cancers as well. Dr. Jabado declares that, “This is the irrefutable proof that our genome, if modified, can lead to cancer and probably other diseases.”
Marc Le Page, President and CEO of Génome Québec, confirmed that, “The outstanding contribution of experts in genomics and new sequencing technologies, made by the McGill University and Génome Québec Innovation Centre and as part of Dr. Jabado’s project, is further proof that genomics has become essential for development and innovation in medical research.” Dr. Morag Park, Scientific Director of the CIHR Institute of Cancer Research, also congratulated Dr. Jabado and her team on the results of these findings, claiming that, “Through research advancements like this, there is now greater emphasis on using genetic information to make medical decisions.”
“Genetic Breakthrough for Brain Cancer in Children”. (January 30, 2012). Neuroscience News. February 18, 2012. http://neurosciencenews.com/genetic-breakthrough-brain-cancer-children-gene-brain-tumor/.
August 7, 2012 § Leave a comment
Scientists from the Florida campus of The Scripps Research Institute have published two findings in the online-before-print edition of Journal of the American Chemical Society and ACS Chemical Biology that are of great interest to those suffering from adult-onset muscular dystrophy. For the first time, researchers have developed a series of small molecules that act against the one RNA defect that is responsible for the most common form of the medical condition.
The small molecule compounds were found to drastically improve various biological defects associated with myotonic dystrophy type 1 (MD1) in both cell cultures and animal subjects. Matthew Disney, PhD, associate professor at Scripps Research Institute said, “Our compounds attack the root cause of the disease and they improve defects in animal models. This represents a significant advance in rational design of compounds targeting RNA. The work not only opens up potential therapies for this type of muscular dystrophy, but also paves the way for RNA-targeted therapeutics in general.”
MD1 is the result of an RNA defect called a “triplet repeat.” This is a sequence of three nucleotides, cytosine-uracil-guanine (CUG), in an individual’s genetic code that are repeated an abnormal and excess number of times. Repetition of these nucleotides in RNA initiates MD1 by binding to and deactivating MBNL1, a specific protein. The resulting abnormality is a continuous splicing of the proteins. This can affect the muscles, causing them to desecrate and waste away.
The researchers involved in the studies utilized data within the RNA motif-small molecule database that the group had been building to locate compounds that are hostile to the problem RNA implicated in the disease. They queried the database against the secondary structure of the triplet repeat that causes the disorder. The chief compound affecting this RNA was found with ease. Afterwards, these compounds were assembled in such a way as to target the increased repeat, or in some cases they were simply optimized. One of the compounds improved the protein-splicing defect by more than 40 percent in an animal subject.
As for the future of this research, Disney commented, “There are limitless RNA targets involved in disease; the question is how to find small molecules that bind to them. We’ve answered that question by rationally designing these compounds that target this RNA. There’s no reason that other bioactive small molecules targeting other RNAs couldn’t be developed using a similar approach.”
“Research Scientists Create Potent Molecules Aimed at Treating Muscular Dystrophy”. (February 22, 2010). Neuroscience News. March 2, 2012. http://neurosciencenews.com/myotonic-muscular-dystrophy-rna-targeted-therapy/.
July 18, 2012 § Leave a comment
A Yale University study, published in the February issue of the Journal of Neuroscience, has revealed a cellular system, stemming from the brain, that controls weight, energy levels, and how much we eat. This group of cells is located in the hypothalamus region of the brain, and they are able to regulate these weight and energy functions by instigating through the nervous system.
The hypothalamus has long been identified as the area of the brain responsible for controlling energy levels. Melanin-Concentrating Hormone (MCH) is a hypothalamic neuron that controls an organism’s food intake and determines energy levels. Scientists are still probing this neuron’s role in these functions. Previous tests on MCH have revealed that it causes test subjects to eat more, sleep more, and have generally less energy.
Contrarily, Thyrotropin-Releasing Hormone (TRH), another hypothalamic neuron, impels an organism to eat less, causing a reduction in body mass, as well as increasing physical activity levels. TRH is an excitatory neurotransmitter, but acts as an inhibitor to MCH. During the study, THR only seemed to inhibit MCH cells by increasing inhibitory synaptic signals. It had little to no effect on other types of neurons involved in appetite, energy, and sleep functions.
The Yale University study revealed that these two neurons work in opposition to maintain a balance in an organism. Therefore both of these neurons are imperative for a healthy balance of hormones. When these hormones are not in equilibrium, an organism is unable to maintain a healthy weight. The study’s senior author Anthony van den Pol, professor of neurosurgery at Yale School of Medicine said, “That these two types of neurons interact at the synaptic level gives us clues as to how the brain controls the amount of food we eat, and how much we sleep.”
This study bolsters previous findings so as to conclude that hormones play a principal role in regulating appetite, energy, fatigue, and, by extension, weight regulation.
“Molecular Duo Dictate Weight and Energy Levels”. (February 28, 2012). Neuroscience News. March 2, 2012. http://neurosciencenews.com/melanin-thyrotropin-hormones-weight-loss-energy-levels/
April 1, 2012 § Leave a comment
Scientists from the Monell Center reported online in Proceedings of the National Academy of Sciences USA that, due to the evolution of diet specialization, 12 related mammals of the sweet-blind species, which eats only meat, is losing its liking for sweet tastes.
The team’s previous study revealed that both domestic and wild cats are unable to taste sweet things because of a defect in the gene that manages the construction of the receptor for sweet tastes. This is odd since cats survive only on meat.
The Monell scientists next endeavored to solve whether other obligate carnivores have lost the sweet taste receptor. To do this they examined the sweet taste receptor genes of 12 related mammalian species with various dietary habits. The results confirmed a taste loss that is spread through many meat-eating species.
Gary Beauchamp, Ph.D., a behavioral biologist at Monell, senior author of the study said, “Sweet taste was thought to be nearly a universal trait in animals. That evolution has independently led to its loss in so many different species was quite unexpected.”
Veracity of the sweet taste receptor gene was directly linked to the animals’ diets. Species with the defective sweet receptor genes include sea lions, fur seals, Pacific harbor seals, Asian otters, spotted hyenas, fossas, and banded lingsangs, all species of which are exclusive meat eaters.
Those species found with the receptor genes in tact were the aardwolf, Canadian otter, spectacled bear, raccoon, and red wolf. These species are from both the obligate carnivorous and omnivorous diet groups.
Additional study disclosed that the defective portion of the sweet receptor gene is various among the seven species with defective receptors.
All of these findings suggest that the taste loss is diet-related, and that it has occurred repeatedly through an evolutionary series. This expresses the magnitude to which the structure and function of an animal’s sensory system is influenced by dietary niche.
The researchers wanted to further explore this finding. They wished to focus on the connection between feeding behavior and taste function. They examined the sweet and umami (savory) taste receptor genes in two mammals that have returned to the sea: the sea lion and the bottlenose dolphin. Both of these animals swallow their food whole, indicating that taste is not of high importance in their dietary range.
As the team had predicted, taste loss was present in these mammals. In both of them the sweet and umami receptor genes were not functional. The dolphin was also found to lack bitter taste receptor genes.
Beauchamp explains, “Different animals live in different sensory worlds and this particularly applies to their worlds of food. Our findings provide further evidence that what animals like to eat – and this includes humans – is dependent to a significant degree on their basic taste receptor biology.”
This research begs questions beyond diet choice because taste receptors are present in organs throughout the body, including the intestine, pancreas, nose, and lungs. These extra-oral taste receptors allegedly serve various functions.
Lead author and molecular biologist at Monell Peihua Jiang, Ph.D, says, “Our findings clearly show that the extra-oral taste receptors are not needed for survival in certain species. The animals we examined did not have functional sweet, umami, or bitter taste receptors, so it will be important to identify how their functions were replaced throughout the body.”
“Extensive Taste Loss in Mammals”. (March 12, 2012). Neuroscience News. March 18, 2012. http://neurosciencenews.com/extensive-taste-loss-in-mammals/.
March 31, 2012 § Leave a comment
Every year millions of people experience lower back pain and neck discomfort. Cornell University engineers in Ithaca and doctors at the Weill Cornell Medical College in New York City have created a biologically based spinal implant that could bring relief to those countless sufferers.
Lawrence Bonassar, Ph.D., associate professor of biomedical engineering and mechanical engineering, in collaboration with Roger Härtl, M.D., associate professor of neurosurgery at Weill Cornell Medical College, and chief of spinal surgery at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, have created bioengineered spinal discs that have been successfully implanted and tested in animals.
“We’ve engineered discs that have the same structural components and behave just like real discs,” says Bonassar. “The hope is that this promising research will lead to engineered discs that we can implant into patients with damaged discs.”
Every year, 40-60% of American adults endure chronic back or neck pain. Patients diagnosed with severe Degenerate Disc Disease (herniated discs) will often undergo a surgery, called a ‘Discectomy’ by neurosurgeons. This surgery involves the removal of the spinal disc followed by a fusion of the vertebrate bones to stabilize the spine. The surgery, although it prevents pain, may limit an individual’s mobility. It can prevent an active lifestyle or end a professional athlete’s career.
The Bonassar-Härtl research team initially engineered an artificial disc, made of two polymers, collagen – which makes up the outer side – and a hydrogel, alginate – which makes up the middle. The discs designed for humans look like a tire. The outer part, the annulus, is made of a stiff metal and the inner part, the nucleus, is made up of a gel that bears weight and pressure. The implants are seeded with cells to repopulate the structure with new tissue.
Over time, the discs have shown to improve as they mature in the body due to the growth of the seeded cells. The implants are specifically intended to treat Degenerate Disc Disease. Traditional implants such as bone, metal and plastic have shown to develop wear and tear over time, leaving debris that can cause problems. The new discs’ material may have a larger advantage, from a biological perspective, due to their successful integration and maturation in the human body. With this new material, surgery will be safer, less painful and implicate fewer long-term effects.
Chimes, A. (2011, August 5). Bioengineered Spinal Disc Could Relieve Back Pain. Retrieved from Voice of America: http://www.voanews.com/english/news/health/Bioengineered-Spinal-Disc-Could-Relieve-Back-Pain-126850208.html
Ju, A. (2011, August 1). In the Battle to Relieve Back Aches, Researchers Create Bioengineered Spinal Disc Implants. Retrieved from Sciencedaily.com: http://www.sciencedaily.com/releases/2011/08/110801160152.htm
Ju, A. (2011, August 2). To Relieve Back Aches, Cornell Researchers Create Bioengineered Spinal Disc Implants. Retrieved from NeuroScience News.com: http://neurosciencenews.com/back-aches-pain-bioengineered-spinal-disc-implants-tissue-engineered-intervertebral-discs/
March 30, 2012 § Leave a comment
Many arthritis sufferers experience pain in a very specific area. One of the most irksome localities for arthritis pain is the knee joint. For those who experience knee pain and are unresponsive to simple painkillers, exercise, or physiotherapy, an alternative called Hyalgan® has been developed.
Hyalgan is a solution of sodium hyaluronate, a hyaluronic acid derivative. Hyaluronate is a natural chemical found in the body. Hyalgan is injected directly into the affected knee joint. It replicates and restores the natural lubricating and cushioning elements of normal Synovial fluid (joint fluid), thus improving shock absorption. Because of these facts it is considered a therapy, not a drug. It is intended for the treatment of osteoarthritic knee pain that will not respond to more conservative nonpharmacologic therapies or to simple analgesics such as Acetaminophen.
Hyalgan is given in a succession of injections, each one week apart, for a total of three to five injections, depending upon the particular product (i.e. concentration). It is imperative that the patients receive each injection at the scheduled time. Patients may not experience relief until they have received several injections. The injection can be given at home, but a health care provider must instruct the administrator in how to use it.
Injections of Hyalgan have in some cases been reported to increase inflammation in the affected knee, but this is only fleeting. In a U.S. clinical trial of 495 patients, adverse side effects included gastrointestinal complaints, headache, local ecchymosis and rash, local joint pain and swelling, and local pruritus. Other possible side effects are back pain and mild bruising, heat, redness, swelling, or pain at the injection site. Also, pregnant or lactating women and those with allergies to bird proteins, feathers, or egg products should not use Hyalgan.
Fidia. (November 2011). Hyalgan®. Fidia Pharma USA Inc. http://www.hyalgan.com/hcp.
“Hyalgan”. (February 1, 2012). Drugs.com. Wolters Kluwer Health, Inc. February 12, 2012. http://www.drugs.com/cdi/hyalgan.html.