BreakThrough Digest Medical News |
- Green tea compound shows promise for tackling cancer
- Targeting inflammation to prevent, treat cancers
- Clinical trial seeks to cure advanced Crohn’s disease using bone marrow transplant
- Study offers new clue on how brain processes visual information
- Cell research opens new avenues in combating neurodegenerative diseases
- Scripps Research scientists show potent new compound virtually eliminates HIV in cell culture
- New studies show spinal cord injury and ALS respond to cell transplantation
- Moffitt Cancer Center researchers find potential key to new treatment for mantle cell lymphoma
- New technology improves heart rhythm treatment
- Drug shown to improve memory in those with Down syndrome
- Experimental drug may extend therapeutic window for stroke
- Gene therapy treatment extends lives of mice with fatal disease, MU study finds
- Real-life spider men using protein found in venom to develop muscular dystrophy treatment
- SIgN scientists discover dendritic cells key to activating human immune responses
- Platelet-rich plasma therapy a safe option for cartilage damage, new study finds
| Green tea compound shows promise for tackling cancer Posted: 21 Aug 2012 09:00 PM PDT
A compound found in green tea could be a weapon in treatments for tackling cancer, according to newly-published research at the University of Strathclyde in Glasgow, Scotland. The extract, known as epigallocatechin gallate, has been known to have preventative anti-cancer properties but fails to reach tumours when delivered by conventional intravenous administration.
However, in initial laboratory tests at the Universities of Strathclyde and Glasgow, researchers used an approach which allowed the treatment to be delivered specifically to the tumours after intravenous administration. Nearly two-thirds of the tumours it was delivered to either shrank or disappeared within one month and the treatment displayed no side effects to normal tissues. The tests are thought to be the first time that this type of treatment has made cancerous tumours shrink or vanish. In the tests, on two different types of skin cancer, 40% of both types of tumour vanished, while 30% of one and 20% of another shrank. A further 10% of one of the types were stabilised. The researchers encapsulated the green tea extract in vesicles that also carried transferrin, a plasma protein which transports iron through the blood. Receptors for transferrin are found in large amounts in many cancers. Dr Christine Dufès, a senior lecturer at the Strathclyde Institute of Pharmacy and Biomedical Sciences, led the research. She said: “These are very encouraging results which we hope could pave the way for new and effective cancer treatments. “When we used our method, the green tea extract reduced the size of many of the tumours every day, in some cases removing them altogether. By contrast, the extract had no effect at all when it was delivered by other means, as every one of these tumours continued to grow. “This research could open doors to new treatments for what is still one of the biggest killer diseases in many countries.” The research paper has been published in the journal Nanomedicine. Imaging equipment used in the research was funded by a grant from the Wellcome Trust. ### The research links to Advanced Science and Technology, one of the research themes at Strathclyde’s Technology and Innovation Centre, a world-class facility uniting academic and industrial partners in seeking innovative research solutions, job creation and business development. Contact: Paul Gallagher |
| Targeting inflammation to prevent, treat cancers Posted: 21 Aug 2012 09:00 PM PDT Researchers at the Georgia Health Sciences University Cancer Center have identified a gene that disrupts the inflammatory process implicated in liver cancer.
The study, published in Cancer Research, a journal for the American Association for Cancer Research, could lead to drug therapies to target TREM-1, said Dr. Anatolij Horuzsko, an immunologist at the GHSU Cancer Center and principal investigator on the study. “We have long suspected that chronic inflammation is a very powerful tool in the initiation of cancer, and also in the progression or metastasis of cancer,” said Horuzsko. “We [looked] at the molecules that control inflammatory responses to gain a better understanding of how this process works. One important triggering receptor for inflammation is TREM-1.” TREM-1′s role in promoting inflammation is useful in cases such as battling viral or bacterial infections and in maintaining normal tissue function. But as Horuzsko’s team discovered, in abnormal conditions?such as liver damage due to alcohol abuse or other irritants?production of TREM-1 goes haywire. A chronic, low-level state of inflammation is produced as TREM-1 leads to the development of other inflammatory agents, which causes more damage, increases cell production and creates mutated cells. These mutated cells then reproduce?planting the seeds that can lead to cancer. During the 14-month study, Horuzsko and his team used mouse studies to gather data on the effect of TREM-1 in the liver cells and identify potential sources for therapies. Because a mouse’s life span is about three years, the length of the study mimicked a similar 20- to 30-year cancer progression of liver cancer in humans. Two sets of mice?one with the TREM-1 gene removed?were exposed to the cancer-causing agent diethylnitrosamine, or DEN, which is present in tobacco smoke, chemicals and other products. Within just 48 hours of DEN injection, the control mice were already showing signs of liver cell injury and death and high levels of TREM-1 expression in the liver’s Kupffer cells. These specialized liver cells normally destroy bacteria and worn-out red blood cells. Eight months later, these mice also showed massive liver tumors. But the mice with the gene removed remained healthy, showing very few changes?and very small, if any, tumors after eight months. The only difference between the two groups was the appearance of TREM-1 in the Kupffer cells. Horuzko’s team hopes the findings?and their potential in TREM-1-related cancer treatment?will be applicable to other cancers as well. “TREM-1 could be a target for any inflammation-associated cancer,” said Horuzsko. “In the future, we could use a drug to target TREM-1 in the body. We are already working in this direction.” Horuzsko’s team also identified another potential target for drug therapy during the study?a product of liver cell injury and death called HMGB1. HMGB1 is a previously unknown activating ligand, or agent, that stimulates Kupffer cells to produce the TREM-1 protein and start the inflammatory process. “Advanced drug therapies for cancer are a growing field of research, and immune therapies are an important part of our mission,” said Dr. Samir N. Khleif, Director of the GHSU Cancer Center. “Studies like Dr. Horuzsko’s are leading the way to identify targeted therapies that will become our future standards of care. As we open the door to new scientific discoveries, this enables us to provide better care to patients and families with cancer. ” ### The GHSU Cancer Center is the region’s only dedicated clinical cancer and cancer research center, offering Phase 1 clinical trials. The center is also working to become Georgia’s second National Cancer Institute-designated cancer center. The Cancer and Inflammation Program at the National Cancer Institute also provided work on this study, which was funded by National Institutes of Health grants. Contact: Christen Carter |
| Clinical trial seeks to cure advanced Crohn’s disease using bone marrow transplant Posted: 22 Jul 2012 09:00 PM PDT Researchers at Fred Hutchinson Cancer Research Center have opened a clinical trial to test the theory that giving a patient a new immune system can cure severe cases of Crohn’s disease, a chronic inflammatory condition of the gastrointestinal tract.
Funded by an infrastructure grant from The Eli and Edythe Broad Foundation, the initial goal of the Crohn’s Allogeneic Transplant Study (CATS) is to treat a small number of patients with treatment-resistant Crohn’s disease by transplanting matched bone marrow cells from a sibling or unrelated donor. Such a bone marrow transplant replaces a diseased or abnormal immune system with a healthy one. The idea of swapping out the immune system is based on evidence that Crohn’s is related to an abnormal immune response to intestinal bacteria and a loss of immune tolerance. There is strong evidence that genetic abnormalities in the immune regulatory system are linked to the disease, according to CATS principal investigator George McDonald, M.D., a transplant researcher and gastroenterologist in the Hutchinson Center’s Clinical Research Division. Although the CATS clinical trial represents a new direction for bone marrow transplantation, the procedure has precedent. The Hutchinson Center, which pioneered bone marrow and hematopoietic cell transplantation to treat blood cancers, has used allogeneic transplants to cure patients who suffered from both leukemia and Crohn’s, with subsequent disappearance of the signs and symptoms of Crohn’s. Similar experiences have been reported from studies done in Germany. While autologous stem cell transplants ? in which the patient’s own hematopoietic cells are removed and then returned after high-dose chemotherapy is given to suppress the immune system ? have been used to treat Crohn’s patients, the benefits have not always been permanent, probably because the risk genes for Crohn’s are still present. “Autologous transplantation following chemotherapy beats the disease down but the Crohn’s tends to come back,” McDonald said. More information about CATS can be found on the website www.cats-fhcrc.org, which includes a patient-eligibility questionnaire. In general, patients must be 18 to 60 years of age and have failed all existing conventional treatments but be healthy enough to undergo a bone marrow transplant. A matched donor of bone marrow must be found from either a sibling or an unrelated person who has volunteered to donate marrow. Private insurance must cover the cost of the transplant and related medical expenses. Crohn’s disease is usually discovered in adolescents and young adults but can occur from early childhood to older age. The incidence of Crohn’s disease varies in different parts of the world with rates of four to nine persons per 100,000 people in North America. According to the Crohn’s and Colitis Foundation of America, a leading advocacy organization, Crohn’s may affect more than 700,000 Americans. Of those affected by Crohn’s, about 10 percent suffer from the most severe form for which no treatment is completely effective. Symptoms of Crohn’s may include pain, fever, diarrhea and weight loss. Substantial progress has been made in medical treatment of Crohn’s disease over the last 15 years. However, even with the best immunosuppressive therapy, less than half of patients with moderate to severe Crohn’s achieve long-term relief. When patients stop taking their medicines, their intestinal inflammation returns. Some severe infections have been seen in patients who took prolonged courses of medicines that suppress the immune system. “The burden of this disease lays heavily on those who don’t respond to any therapy,” McDonald said. The CATS investigator team includes transplant physicians, gastroenterologists, pathologists and nurses from the Hutchinson Center, University of Washington, Seattle Children’s and the Benaroya Research Institute. The bone marrow transplant procedures will be conducted at the Seattle Cancer Care Alliance, the University of Washington Medical Center, and Seattle Children’s Hospital. ### At Fred Hutchinson Cancer Research Center, our interdisciplinary teams of world-renowned scientists and humanitarians work together to prevent, diagnose and treat cancer, HIV/AIDS and other diseases. Our researchers, including three Nobel laureates, bring a relentless pursuit and passion for health, knowledge and hope to their work and to the world. For more information, please visit fhcrc.org Contact: Dean Forbes
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| Study offers new clue on how brain processes visual information Posted: 21 Jul 2012 09:00 PM PDT Ever wonder how the human brain, which is constantly bombarded with millions of pieces of visual information, can filter out what’s unimportant and focus on what’s most useful? The process is known as selective attention and scientists have long debated how it works. But now, researchers at Wake Forest Baptist Medical Center have discovered an important clue. Evidence from an animal study, published in the July 22 online edition of the journal Nature Neuroscience, shows that the prefrontal cortex is involved in a previously unknown way.
Two types of attention are utilized in the selective attention process ? bottom up and top down. Bottom-up attention is automatically guided to images that stand out from a background by virtue of color, shape or motion, such as a billboard on a highway. Top-down attention occurs when one’s focus is consciously shifted to look for a known target in a visual scene, as when searching for a relative in a crowd. Traditionally, scientists have believed that separate areas of the brain controlled these two processes, with bottom-up attention occurring in the posterior parietal cortex and top-down attention occurring in the prefrontal cortex. “Our findings provide insights on the neural mechanisms behind the guidance of attention,” said Christos Constantinidis, Ph.D., associate professor of neurobiology and anatomy at Wake Forest Baptist and senior author of the study. “This has implications for conditions such as attention deficit hyperactivity disorder (ADHD), which affects millions of people worldwide. People with ADHD have difficulty filtering information and focusing attention. Our findings suggest that both the ability to focus attention intentionally and shifting attention to eye-catching but sometimes unimportant stimuli depend on the prefrontal cortex.” In the Wake Forest Baptist study, two monkeys were trained to detect images on a computer screen while activity in both areas of the brain was recorded. The visual display was designed to let one image “pop out” due to its color difference from the background, such as a red circle surrounded by green. To trigger bottom-up attention, neither the identity nor the location of the pop-out image could be predicted before it appeared. The monkeys indicated that they detected the pop-out image by pushing a lever. The neural activity associated with identifying the pop-out images occurred in the prefrontal cortex at the same time as in the posterior parietal cortex. This unexpected finding indicates early involvement of the prefrontal cortex in bottom-up attention, in addition to its known role in top-down attention, and provides new insights into the neural mechanisms of attention. “We hope that our findings will guide future work targeting attention deficits,” Constantinidis said. ### The research was supported by the National Eye Institute contract ROI EY016773 and the Tab Williams Family Endowment. Fumi Katsuki, Ph.D., a post-doctoral fellow at Wake Forest Baptist, co-authored the study. Contact: Marguerite Beck |
| Cell research opens new avenues in combating neurodegenerative diseases Posted: 19 Jul 2012 09:00 PM PDT
Scientists at the University of Manchester have uncovered how the internal mechanisms in nerve cells wire the brain. The findings open up new avenues in the investigation of neurodegenerative diseases by analysing the cellular processes underlying these conditions.
Dr Andreas Prokop and his team at the Faculty of Life Sciences have been studying the growth of axons, the thin cable-like extensions of nerve cells that wire the brain. If axons don’t develop properly this can lead to birth disorders, mental and physical impairments and the gradual decay of brain capacity during aging. Axon growth is directed by the hand shaped growth cone which sits in the tip of the axon. It is well documented how growth cones perceive signals from the outside to follow pathways to specific targets, but very little is known about the internal machinery that dictates their behaviour. Dr Prokop has been studying the key driver of growth cone movements, the cytoskeleton. The cytoskeleton helps to maintain a cell’s shape and is made up of the protein filaments, actin and microtubules. Microtubules are the key driving force of axon growth whilst actin helps to regulate the direction the axon grows. Dr Prokop and his team used fruit flies to analyse how actin and microtubule proteins combine in the cytoskeleton to coordinate axon growth. They focussed on the multifunctional proteins called spectraplakins which are essential for axonal growth and have known roles in neurodegeneration and wound healing of the skin. What the team demonstrate in this recent paper is that spectraplakins link microtubules to actin to help them extend in the direction the axon is growing. If this link is missing then microtubule networks show disorganised criss-crossed arrangements instead of parallel bundles and axon growth is hampered. By understanding the molecular detail of these interactions the team made a second important finding. Spectraplakins collect not only at the tip of microtubules but also along the shaft, which helps to stabilise them and ensure they act as a stable structure within the axon. This additional function of spectraplakins relates them to a class of microtubule-binding proteins including Tau. Tau is an important player in neurodegenerative diseases, such as Alzheimer’s, which is still little understood. In support of the author’s findings, another publication has just shown that the human spectraplakin, Dystonin, causes neurodegeneration when affected in its linkage to microtubules. Talking about his research Dr Prokop said: “Understanding cytoskeletal machinery at the cell level is a holy grail of current cell research that will have powerful clinical applications. Thus, cytoskeleton is crucially involved in virtually all aspects of a cell’s life, including cell shape changes, cell division, cell movement, contacts and signalling between cells, and dynamic transport events within cells. Accordingly, the cytoskeleton lies at the root of many brain disorders. Therefore, deciphering the principles of cytoskeletal machinery during the fundamental process of axon growth will essentially help research into the causes of a broad spectrum of diseases. Spectraplakins like at the heart of this machinery and our research opens up new avenues for its investigation” What Dr Prokop’s paper in the Journal of Neuroscience also demonstrates is the successful research technique using the fruit fly Drosophila. The team was able to replicate its findings regarding axon growth in mice which in turn means the findings can be translated to humans. Dr Prokop points out fruit flies provide ideal means to make sense of these findings and essentially help to unravel the many mysteries of neurodegeneration. Dr Prokop continues: “Understanding how spectraplakins perform their cellular functions has important implications for basic as well as biomedical research. Thus, besides their roles during axon growth, spectraplakins of mice and humans are clinically important for a number of conditions and processes including skin blistering, neuro-degeneration, wound healing, synapse formation and neuron migration during brain development. Understanding spectraplakins in one biological process will instruct research on the other clinically relevant roles of these proteins.” The recently published paper represents six years of work by Dr Prokop and his dedicated team. ### Notes to Editors:
The paper is entitled “Spectraplakins Promote Microtubule-Mediated Axonal Growth by Functioning As Structural Microtubule – Associated Proteins and EB1-Dependent +TIPs (Tip Interacting Proteins) It was published on July 4 2012 in The Journal of Neuroscience. Images for this story are available from the press office and Dr Andreas Prokop is available for interviews. Please contactContact: Morwenna Grills
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| Scripps Research scientists show potent new compound virtually eliminates HIV in cell culture Posted: 18 Jul 2012 09:00 PM PDT
A new study by scientists on the Florida campus of The Scripps Research Institute shows, in cell culture, a natural compound can virtually eliminate human immunodeficiency virus (HIV) in infected cells. The compound defines a novel class of HIV anti-viral drugs endowed with the capacity to repress viral replication in acutely and chronically infected cells.
The HIV/AIDS pandemic continues to affect 34 million individuals worldwide, including more than 3 million children, according to the World Health Organization. Current treatment involves the use of several antiretroviral drugs, termed Highly Active Antiretroviral Therapy (HAART), which can extend the life expectancy of HIV-positive individuals and decrease viral load without, however, eradicating the virus. “We know that there are reservoirs of HIV that aren’t being eliminated by current treatment and that keep replenishing the infection,” said Susana Valente, a Scripps Research biologist who led the study. “Viral production from these cellular reservoirs that harbor an integrated viral genome is not affected by current antiretroviral drugs, which only stop novel rounds of infection. The compound in the current study virtually eliminates all viral replication from already-infected cells where HIV hides.” The new study, published in the July 20, 2012 issue of the journal Cell Host and Microbe, focused on a medically promising compound known as Cortistatin A. This natural product was isolated in 2006 from a marine sponge, Corticium simplex, discovered more than 100 years ago. In 2008, Scripps Research chemist Phil Baran and his team won the global race to synthesize the compound, presenting an efficient and economical method. In the new study, Valente and her colleagues collaborated with the Baran lab, using a synthetic version of the compound, didehydro-Cortistatin A, to study the compound’s effect on two strains of HIV. The strains were HIV-1, the most common form of the virus, and HIV-2, which is concentrated in West Africa and some parts of Europe. The results showed that the compound reduced viral production by 99.7 percent from primary CD4+T cells (a type of immune cell) isolated from patients without levels of the virus in their bloodstream and who had been under HAART treatment for a long period of time. When the compound was added to other antiviral treatments, it further reduced by 20 percent viral replication from CD4+T cells isolated from patients with detectable amounts of virus in their bloodstreams. The inhibitor works by binding tightly to the viral protein known as Tat, a potent activator of HIV gene expression, effectively preventing the virus from replicating even at miniscule concentrations?making it the most potent anti-Tat inhibitor described to date, Valente said. Another interesting feature of this compound is that withdrawal of the drug from cell culture does not result in virus rebound, which is normally observed with other antiretrovirals. While most antiretroviral compounds block only new infections, didehydro-Cortistatin A reduces viral replication from already-infected cells, potentially limiting cell-to-cell transmission. The new inhibitor already has a drug-like structure, is effective at very low concentrations, and has no toxicity associated with it, at least at the cellular level, the study noted. ### The first author of the study “Potent Suppression of Tat-dependent HIV Transcription by didehydro-Cortistatin A” is Guillaume Mousseau of Scripps Research. In addition to Valente and Baran, other authors include Mark A. Clementz, Wendy N. Bakeman, Nisha Nagarsheth, Michael Cameron, and Jun Shi of Scripps Research; and Rémi Fromentin and Nicolas Chomont of the Vaccine and Gene Therapy Institute. The study was supported by the National Institutes of Health’s National Institute of Allergy and Infectious Diseases (NIAID) and the Landenberger Foundation. Contact: Eric Sauter |
| New studies show spinal cord injury and ALS respond to cell transplantation Posted: 17 Jul 2012 09:00 PM PDT
Two studies published in a recent issue of Cell Medicine [2(2)] report on the therapeutic efficacy of stem cell transplantation in animal models of amyotrophic lateral sclerosis (ALS) and spinal cord injury (SCI). Cell Medicine is freely available on-line at http://www.ingentaconnect.com/content/cog/cm.
Mensenchymal stem cell transplantation in spinal cord injured rats promotes functional recovery
Transplantation of mesenchymal stem cells (MSCs), multipotent stem cells with the ability to differentiate into a variety of cell types with renewal capacities, has been found to enhance laboratory animal function after induced spinal cord injury. However, the biological mechanism of the functional enhancement has not been clearly defined. In an attempt to gain a clearer picture of the mechanism, a team of Korean researchers transplanted MSCs derived from human umbilical cord blood into the tail veins of laboratory rats immediately after spinal cord injury. The intravenous route was selected because the researchers felt that injection into the damaged site could further traumatize the injured spinal cord, although intravenously injected MSCs risk being eliminated by the host immune system. “We found that MSCs express immunomodulatory effects during the acute phase following SCI,” said study corresponding author Dr. Sung-Rae Cho of the Yonsei University College of Medicine in Seoul, Korea. “In our study, MSCs suppressed activated micoglia and inflammatory cytokines, increased anti-inflammatory cytokines and, consequently, promoted functional recovery in SCI rats.” They reported “modest but significant improvement” in a number of functional test scores in the rats subjected to transplantation when compared with control group animals not subjected to cell transplantation. The researchers suggested that their study not only confirmed the established link between microglial activation and inflammatory cytokines, but also demonstrated that functional recovery might be attributed to immunomodulatory effects rather than cell replacement. They also recommended that autologous (self-donated) MSCs, rather than human-derived MSCs, should be used in subsequent studies to “suppress undesirable immune response.” Contact: Dr. Sung-Rae Cho, Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, Seoul, Korea 120-752 Citation: Seo, J. H.; Jang, I. K.; Kim, H.; Yang, M. S.; Lee, J. E.; Kim, H. E.; Eom, Y-W.; Lee, D-H.; Yu, J. H.; Kim, J. Y.; Kim, H. O.; Cho, S-R. Early immunomodulation by intravenously transplanted mesenchymal stem cells promotes functional recovery in spinal cord injured rats. Cell Med. 2(2):55-67; 2011. Bone marrow cell transplantation coupled with stimulating factor offers neuroprotective and angiogenic effects in ALS animal models
In this the first report showing the effects of bone marrow cell transplantation (BMT) combined with granulocyte colony-stimulating factor (GCSF) in mouse models of ALS, researchers from Okayama University, Japan demonstrated that the co-treatment potentially confers neuroprotective and angiogenic (blood vessel growth) effects on the test mice. “Combined treatment with BMT and GCSF delayed disease progression and prolonged the survival of G93A mice while BMT or GCSF treatment alone did not,” said corresponding author professor Koji Abe of the Department of Neurology in the Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences. “In addition, the mice treated with BMT and GCSF also showed a reduction in motor neuron loss, induced neuronal precursor cell proliferation, and the increased expression of several neurotrophic factors.” Since ALS is a progressive, fatal disease characterized by the loss of motor neurons, motor neuron preservation is critical. According to the researchers, the combination treatment of BMT and GCSF had a greater impact via significant neuroprotective and neuroregenerative effects than when compared to BMT alone. GCSF was administered to not only provide a neuroprotective effect, but also to stimulate the proliferation of bone marrow cells,” said Dr. Abe. Contact: Prof. Koji Abe, Department of Neurology, Citation: Ohta, Y.; Nagai, M.; Miyazaki, K.; Tanaka, N.; Kawai, H.; Mimoto, T.; Morimoto, N.; Kurata, T.; Ikeda, Y.; Matsuura T.; Abe, K. Neuroprotective and Angiogenic Effects of Bone Marrow Transplantation Combined With Granulocyte Colony-Stimulating Factor in a Mouse Model of Amyotrophic Lateral Sclerosis. Cell Med. 2(2):69-83; 2011 ### The editorial offices for Cell Medicine are at the Center of Excellence for Aging and Brain Repair, College of Medicine, the University of South Florida. Contact, David Eve, PhD. at cellmedicinect@gmail.com News Release by Florida Science Communications www.scienscribe.net |
| Moffitt Cancer Center researchers find potential key to new treatment for mantle cell lymphoma Posted: 17 Jul 2012 09:00 PM PDT
Researchers at Moffitt Cancer Center and colleagues have demonstrated that the inhibition of signal transducer and activator of transcription 3 (STAT3) in mouse models of mantle cell lymphoma (MCL), an aggressive and incurable subtype of B-cell non-Hodgkin lymphoma that becomes resistant to treatment, can harness the immune system to eradicate residual malignant cells responsible for disease relapse.
Their study appears in a recent issue of Cancer Research, published by the American Association for Cancer Research. “Despite good initial response to first-line treatment with chemotherapy and monoclonal antibodies, almost all patients with MCL will eventually relapse,” said Eduardo M. Sotomayor, M.D., a senior member at Moffitt and the Susan and John Sykes Endowed Chair for Hematologic Malignancies. “MCL has one of the worst prognoses among all B-cell non-Hodgkin lymphomas.” Moffitt researchers and colleagues have exploited evidence that suggests the manipulation of the patient’s own immune system might prove a good therapeutic strategy for patients with therapy-resistant MCL. In a study using mouse models of MCL, the researchers hypothesized that targeting and inhibiting STAT3 ? a “negative regulator” of inflammatory responses in a variety of immune cells ? might “unleash an effective anti-lymphoma immune response.” According to Sotomayor, much of their work is in seeking new immunotherapeutic strategies capable of breaking tolerance to tumor antigens ? that is finding ways to defeat lymphoma cells’ ability to resist treatment. In this study, the researchers found that the inhibition of STAT3 in malignant B-cells, either by genetic manipulation or by using drugs (CPA-7 provided by Said M. Sebti, Ph.D., chair of the Drug Discovery Program at Moffitt and co-author of this study), render these cells “more visible” to specific immune cells (T-cells), which in turn can eradicate mantle cell lymphoma in murine models. “The unique property of STAT3 inhibition to influence the inflammatory status of both malignant B-cells, as well as the antigen-presenting cells (as previously demonstrated by our group and others), points to pharmacologic inhibition of this signaling pathway as an appealing strategy to overcome tolerance to tumor antigens to elicit a strong anti-tumor immunity,” concluded Sotomayor and his colleagues. There have been other, similar attempts to induce an immune response, the authors noted. But these attempts offered effects that were “transient and not strong enough to fully eradicate systemic lymphoma.” The authors speculated that the past limited success came from targeting either the malignant B-cell or the antigen-presenting cell, but not targeting both. “It would be desirable to find approaches with the dual ability of enhancing the antigen-presenting function of malignant B-cells and inducing inflammatory antigen-presenting cells,” Sotomayor said. “The inhibition of STAT3 signaling can do both. Therefore, STAT3 inhibition is an effective strategy in mouse models of MCL and provides a framework for future use of STAT3 inhibitors in combination with drugs that are capable of repairing defective immune responses in lymphoma patients.” ### Research for this study was supported by grants CA134807 and CA087583 from the National Cancer Institute and grant support from the Susan and John Sykes Lymphoma Foundation. About Moffitt Cancer Center Media release by Florida Science Communications Contact: Kim Polacek |
| New technology improves heart rhythm treatment Posted: 17 Jul 2012 09:00 PM PDT
Researchers from UC San Diego, the University of California Los Angeles and Indiana University report having found, for the first time, that atrial fibrillation or irregular heart rhythms is caused by small electrical sources within the heart, in the form of electrical spinning tops (“rotors”) or focal beats. Importantly, they found a way of detecting these key sources, then precisely targeting them for therapy that can shut them down in minutes with long lasting results.
The team, which included cardiologists, physicists and bioengineers, report the findings in the July issue of the Journal of the American College of Cardiology as the CONFIRM trial (Conventional Ablation for Atrial Fibrillation?With or Without Focal Impulse and Rotor Modulation). Currently, many patients treated for atrial fibrillation with standard therapies will experience a recurrence due to the difficulty of finding the source of the arrhythmia. The new findings will help cardiologists better target and treat arrhythmias. The CONFIRM study examined 107 patients with atrial fibrillation referred for a non-surgical catheter ablation procedure. During this procedure, doctors thread a wire with a metal-tipped catheter inside the body, from a vein in the groin, to apply heat to the area of the heart that is producing the arrhythmia to stop it. In one group of patients, the team used the new technique to help perform precise burns, called Focal Impulse and Rotor Modulation (FIRM) that were aimed directly at the fundamental source of the arrhythmia ? tiny electrical disturbances in the heart called rotors or focal sources that look like mini tornadoes or spinning tops. Remarkably, this new procedure shut down atrial fibrillation or very significantly slowed it in 86 percent of patients in an average of only 2.5 minutes. In comparison, conventional catheter procedures were performed in a second group of patients. Since this approach is less targeted, it involved hours of treatment over larger regions in the heart and often did not shut down the atrial fibrillation. To track outcomes, patients received an implanted ECG monitor that very accurately assessed their heart rhythms over time. Researchers found that after two years, the FIRM-guided group had an 82.4 percent freedom from atrial fibrillation episodes, compared to only 44.9 percent freedom in the group that received standard therapy. The new targeted method demonstrated an 86 percent improvement over the conventional method in the study. “We are very excited by this trial, which for the first time shows that atrial fibrillation is maintained by small electrical hotspots, where brief FIRM guided ablation can shut down the arrhythmia and bring the heart back to a normal rhythm after only minutes of ablation,” said lead author Sanjiv Narayan, MD, PhD, professor of medicine at UC San Diego Sulpizio Cardiovascular Center, director of Electrophysiology at the San Diego Veterans Affairs Medical Center and visiting professor at the UCLA Cardiac Arrhythmia Center. “The results of this trial, with an 80 percent ablation success rate after a single procedure, are very gratifying. This is the dawn of a new phase of managing this common arrhythmia that is mechanism-based,” said Kalyanam Shivkumar, MD, PhD, director of the UCLA Cardiac Arrhythmia Center, and professor of medicine and radiological sciences at UCLA. ### This study also represents a successful example of technology transfer from U.S. researchers supported by U.S. research funding to a small U.S. enterprise. The science behind this work was funded by grants to Narayan from the National Institutes of Health, including a grant awarded as part of the American Recovery and Reinvestment Act, and by the Doris Duke Charitable Foundation. These discoveries, owned by the Regents of the University of California, were then licensed to a local startup company, Topera Medical, which has recently obtained FDA clearance for the mapping system it developed (RhythmViewTM) from this early science. Narayan is a co-founder with equity interest in Topera. Wouter-Jan Rappel, PhD, holds equity interest in Topera. John Miller, MD, has received modest honoraria from Topera. Shivkumar is an unpaid advisor to Topera, and the other authors report no relationship with Topera. Other authors included John Miller, MD, chief of electrophysiology at Indiana University; David Krummen, MD, associate professor of medicine with UC San Diego Sulpizio Cardiovascular Center and associate director of electrophysiology at the San Diego Veterans Affairs Medical Center; Wouter-Jan Rappel, PhD, University of California San Diego Department of Theoretical Biological Physics; and Paul Clopton from the San Diego Veterans Affairs Medical Center Department of Statistics. Contact: Kim Edwards |
| Drug shown to improve memory in those with Down syndrome Posted: 16 Jul 2012 09:00 PM PDT
Researchers at the University of Colorado School of Medicine have found a drug that boosts memory function in those with Down syndrome, a major milestone in the treatment of this genetic disorder that could significantly improve quality of life.
“Before now there had never been any positive results in attempts to improve cognitive abilities in persons with Down syndrome through medication,” said Alberto Costa, MD, Ph.D., who led the four- year study at the CU School of Medicine. “This is the first time we have been able to move the needle at all and that means improvement is possible.” The study was published today in the journal Translational Psychiatry. Costa, an associate professor of medicine, and his colleagues studied 38 adolescents and young adults with Down syndrome. Half took the drug memantine, used to treat Alzheimer’s disease, and the others took a placebo. Costa’s research team hypothesized that memantine, which improved memory in mice with Down syndrome, could increase test scores of young adults with the disorder in the area of spatial and episodic memory, functions associated with the hippocampus region of the brain. Participants underwent a 16-week course of either memantine or a placebo while scientists compared the adaptive and cognitive function of the two groups. While they found no major difference between the groups in adaptive and most measures of cognitive ability, researchers discovered that those taking memantine showed significant improvement in verbal episodic memory. One of the lowest functioning individuals in the study saw a ten-fold increase in memory skills. “People who took the medicine and memorized long lists of words did significantly better than those who took the placebo,” said Costa, a neuroscientist specializing in Down syndrome research. “This is a first step in a longer quest to see how we can improve the quality of life for those with Down syndrome.” Currently, there are drugs that treat the symptoms of medical conditions associated with Down syndrome but nothing to improve brain function. But in 2007 Costa demonstrated that memantine could improve memory in mice with Down syndrome. He then set out to replicate those findings in a human trial of the drug. “This is an excellent example of translational science,” he said. “We took a drug that worked well in mice and we tested it in humans with positive results.” Although the trial was small, the results could have far-reaching implications. Costa said a follow-up study was needed using a larger group of people with Down syndrome. Another important step will be to pursue studies with younger, school-age participants with Down syndrome. They would have more rapidly developing brains and, since they are in school, would be routinely tested so the effects of the drug could be closely monitored. That could take as little as five years. Researchers also want to know if memantine can ward off the onset of Alzheimer’s disease in those with Down syndrome. The two conditions show striking similarities and researchers are actively exploring how they may be linked. Babies born with Down syndrome, for example, often carry the biological markers for Alzheimer’s disease. “Everyone with Down syndrome will develop Alzheimer’s disease pathology by their mid-30s,” Costa said. “We would like to know if this drug can slow down or even halt the development of that disease in adults with Down syndrome.” Memantine works by normalizing the function of a glutamate receptor in the brain known as the N-methyl-D-aspartate or the NMDA receptor. “This receptor plays a central role in memory and learning,” Costa said. Given the small size of the study and the need for more research, Costa stressed that people should not start taking memantine for Down syndrome. Although it has proven safe and well-tolerated by the study participants, researchers urge caution, saying more work needs to be done to determine if this is a viable treatment option. “Our study is a significant and hopeful sign that certain drugs can enhance the intellectual capacity of those with Down syndrome,” he said. “For more than 30 years we have been unable to impact cognition in Down syndrome. Now it appears that we may be able to.” Costa has a major stake in improving the lives of those with Down syndrome, the most common cause of intellectual disability. He has a 17-year-old daughter with the condition. “For me this research is not merely academic,” he said. “It’s personal.” The CU School of Medicine’s work on Down syndrome has resulted in it being chosen as one of nine national testing centers for a new drug manufactured by F. Hoffmann-La Roche LTD aimed at improving memory in adults with Down syndrome. Costa is the principal investigator of the Colorado center. He will give a lecture about his latest research July 20 in Washington D.C. at the 2012 Annual Meeting & Clinical Symposium of the Down Syndrome Medical Interest Group – USA. The conference is being held from 1 p.m. to 9 p.m. at the Marriott Wardman Park, 2660 Woodley Rd. NW. The other researchers in the study included Richard Boada, Ph.D., Christa Hutaff-Lee, Ph.D., David Weitzenkamp, Ph.D., Timothy A. Benke, MD, Ph.D. and Edward J. Goldson, MD. The trial was funded by Forest Research Institute Investigator Initiated Grant NAM-58. During the course of this study, Costa was also supported in part by grants from the Eunice Kennedy Shriver National Institute of Child Health and Human Development. “I also am grateful to the Anna and John J. Sie Foundation, the Linda Crnic Institute and the Coleman Institute for Cognitive Disabilities for believing in my research all these years. This work would not have been possible without their support in these harsh economic times,” Costa said. ### About the University of Colorado School of Medicine Faculty at the University of Colorado School of Medicine work to advance science and improve care. These faculty members include physicians, educators and scientists at University of Colorado Hospital, Children’s Hospital Colorado, Denver Health, National Jewish Health, and the Denver Veterans Affairs Medical Center. Degrees offered by the CU Denver School of Medicine include doctor of medicine, doctor of physical therapy, and masters of physician assistant studies. The School is located on the University of Colorado’s Anschutz Medical Campus, one of four campuses in the University of Colorado system. For additional news and information, please visit the CU Denver newsroom online. Contact: Jacque Montgomery |
| Experimental drug may extend therapeutic window for stroke Posted: 16 Jul 2012 09:00 PM PDT
A team led by a physician-scientist at the University of Southern California (USC) has created an experimental drug that reduces brain damage and improves motor skills among stroke-afflicted rodents when given with federally approved clot-busting therapy.
Clinical trials to test the safety of the drug in people are expected to start later this summer. Stroke, which occurs when blood flow to a part of the brain stops, is the No. 4 cause of death and the leading cause of adult disability in the United States. According to the American Stroke Association, the Food and Drug Administration-approved tPA (tissue plasminogen activator) is the best treatment for stroke caused by a blocked artery, but to be effective, it must be administered within three hours after symptoms start. If given outside that three-hour window, tPA has shown serious side effects in animal and human brains, including bleeding and breakdown of the brain’s protective barrier. Generally, according to the American Stroke Association, only 3 to 5 percent of those who suffer a stroke reach the hospital in time to be considered for tPA treatment. “What tPA does best is to break down clots in the blood vessel and restore blood flow, but it is a powerful enzyme,” said Berislav V. Zlokovic, M.D., Ph.D., director of the Zilkha Neurogenetic Institute at the Keck School of Medicine of USC and the study’s lead investigator. “After three hours, tPA also damages the blood vessel and causes intracerebral bleeding. We have developed something that not only counteracts the bleeding but also reduces brain damage and significantly improves behavior after stroke. I feel very strongly that this approach will extend the therapeutic window for tPA.” Zlokovic is the scientific founder of ZZ Biotech, a Houston-based biotechnology company he co-founded with USC benefactor Selim Zilkha to develop biological treatments for stroke and other neurological ailments. The company’s 3K3A-APC is a genetically engineered variant of the naturally occurring activated protein C (APC), which plays a role in the regulation of blood clotting and inflammation. APC has cell-protecting, anti-inflammatory and anti-coagulant properties; 3K3A-APC has reduced anti-coagulant ability, which minimizes the risk of bleeding induced by normal APC. The protective effect of 3K3A-APC on the lining of blood vessels in the brain further helps prevent bleeding caused by tPA. In collaboration with the University of Rochester Medical Center, Henry Ford Health Sciences Center, University of Arizona College of Medicine and The Scripps Research Institute, Zlokovic and his team gave tPA ? alone and in combination with 3K3A-APC ? to mice and rats four hours after stroke. They also gave 3K3A-APC for three consecutive days after stroke. They measured the amount of brain damage, bleeding and motor ability of the rodents up to seven days afterward. The researchers found that, under those conditions, tPA therapy alone caused bleeding in the brain and did not reduce brain damage or improve motor ability when compared to the control. The combination of tPA and 3K3A-APC, however, reduced brain damage by more than half, eliminated tPA-induced bleeding and significantly improved motor ability. “Dr. Zlokovic’s study really demonstrates the promise of the drug and we are eager to show the same results in human clinical trials,” said Kent Pryor, Ph.D., M.B.A., ZZ Biotech’s chief operating officer. Previous research suggests that the experimental drug may also protect against other neurological maladies such as amyotrophic lateral sclerosis and traumatic brain injury as a standalone therapy. “We are encouraged by these results,” said Joe Romano, CEO and president of ZZ Biotech. “In terms of improving treatment for stroke and other neurological diseases, this could be really exciting.” ### The research was supported by ZZ Biotech and grants from the National Heart, Lung and Blood Institute of the National Institutes of Health (R01-HL063290-14, R01-HL052246-18). Results of the study, “An activated protein C analog with reduced anticoagulant activity extends the therapeutic window of tissue plasminogen activator for ischemic stroke in rodents,” are available online in the journal Stroke, published by the American Heart Association. Contact: Alison Trinidad |
| Gene therapy treatment extends lives of mice with fatal disease, MU study finds Posted: 15 Jul 2012 09:00 PM PDT
A team of University of Missouri researchers has found that introducing a missing gene into the central nervous system could help extend the lives of patients with Spinal Muscular Atrophy (SMA) ? the leading genetic cause of infantile death in the world.
SMA is a rare genetic disease that is inherited by one in 6,000 children who often die young because there is no cure. Children who inherit SMA are missing a gene that produces a protein which directs nerves in the spine to give commands to muscles. The MU team, led by Christian Lorson, professor in the Department of Veterinary Pathobiology and the Department of Molecular Microbiology and Immunology, introduced the missing gene into mice born with SMA through two different methods: intravenously and directly into the mice’s central nervous systems. While both methods were effective in extending the lives of the mice, Lorson found that introducing the missing gene directly into the central nervous system extended the lives of the mice longer. “Typically, mice born with SMA only live five or six days, but by introducing the missing SMN gene into the mice’s central nervous systems, we were able to extend their lives 10-25 days longer than SMA mice who go untreated,” said Lorson, who works in the MU Bond Life Sciences Center and the College of Veterinary Medicine. “While this system is still not perfect, what our study did show is that the direct administration of the missing gene into the central nervous system provides some degree of rescue and a profound extension of survival.” There are several different types of SMA that appear in humans, depending on the age that symptoms begin to appear. Lorson believes that introducing the missing gene through the central nervous system is a way to potentially treat humans regardless of what SMA type they have. “This is a treatment method that is very close to being a reality for human patients,” Lorson said. “Clinical trials of SMA treatment using gene therapy are likely to begin in next 12-18 months, barring any unforeseen problems.” ### The study, “Direct central nervous system delivery provides enhanced protection following vector mediated gene replacement in a severe model of Spinal Muscular Atrophy”, was published in Biochemical and Biophysical Research Communications. Co-authors of the study include Jacqueline Glascock and Monir Shababi from MU College of Veterinary Medicine. Contact: Nathan Hurst |
| Real-life spider men using protein found in venom to develop muscular dystrophy treatment Posted: 15 Jul 2012 09:00 PM PDT
While Spider-Man is capturing the imagination of theatergoers, real-life spider men in Upstate New York are working intently to save a young boy’s life. It all began in 2009, when Jeff Harvey, a stockbroker from the Buffalo suburbs, discovered that his grandson, JB, had Duchenne muscular dystrophy. The disease is fatal. It strikes only boys, causing their muscles to waste away.
Hoping to help his grandson, Harvey searched Google for promising muscular dystrophy treatments and, in a moment of serendipity, stumbled upon University at Buffalo scientist Frederick Sachs, PhD. Sachs was a professor of physiology and biophysics who had been studying the medical benefits of venom. In the venom of the Chilean rose tarantula, he and his colleagues discovered a protein that held promise for keeping muscular dystrophy at bay. Specifically, the protein helped stop muscle cells from deteriorating. Within months of getting in touch, Harvey and Sachs co-founded Tonus Therapeutics, a pharmaceutical company devoted to developing the protein as a drug. Though the treatment has yet to be tested in humans, it has helped dystrophic mice gain strength in preliminary experiments. The therapy is not a cure. But if it works in humans, it could extend the lives of children like JB for years — maybe even decades. Success can’t come quickly enough. JB, now four, can’t walk down the stairs alone. When he runs, he waddles. He receives physical therapy and takes steroids as a treatment. While playing tee ball one recent day, he confided to his grandfather, “When I grow up, I want to be a baseball player.” It was a heartbreaking moment. “Oh, I would be thrilled if you could be a baseball player,” Harvey remembers replying. He’s doing everything he can to make sure that JB — and other boys like him — can live out their dreams. ### Contact: Charlotte Hsu |
| SIgN scientists discover dendritic cells key to activating human immune responses Posted: 15 Jul 2012 09:00 PM PDT Scientists at A*STAR’s Singapore Immunology Network (SIgN), in collaboration with Newcastle University, UK, the Singapore Institute of Clinical Sciences and clinicians from multiple hospitals in Singapore, have identified a new subset of dendritic cells (DCs%r9 in human peripheral tissue which have a critical role in activating our immune response against harmful pathogens. This research will have significant impact on the design of vaccines and other targeted immunotherapies. The scientists also showed for the first time that DC subsets are conserved between species, facilitating the translation of mouse functional DC studies to the human setting. These research findings were published in the July issue of the prestigious journal Immunity.
All immune responses against harmful pathogens are activated and regulated by DCs, which present antigens (protein components from micro-organisms, vaccines or tumours) to the T cells. Of the different T cells, the cytotoxic CD8+ T cells specialize in cell-killing response and are crucial for our body to eliminate cancer or infected cells. However, only a small subset of DCs is capable of presenting externally derived antigens to activate this cell-killing response throug( a process termed “cross-presentation”. The identity of this subset of DCs in human tissue has been a mystery but the SIgN scientists and collaborators have now identified the human cross-presenting DC subset. This discovery enables better exploitation of targeted vaccine strategies to treat cancer and infection. In this paper, Dr Florent Ginhoux, Principal Investigator at SIgN and his collaborators, identified in human tissues, including dermis, lung and liver, a new subset of DCs, called CD141hi DC and described its genetic signaturen They also showed for the first time that CD141hi DCs were superior at cross-presenting soluble antigens compared to other DCs to activate the killer T cells. The scientists also carried out a comparison of human and mouse DC subsets and demonstrated that there was close alignment of the DC subsets between species. Functional alignment of human and mouse DC subsets had previously been hampered by differences in surface marker expression and accessibility of equivalent sources. This detailed study now aligns the mouse and human DC networks, and will facilitate better translation of mouse DC studies to the human setting. Dr Ginhoux, said, “This was technically very challenging work as we only had limited quantities of human tissue samples and limited amount of cells to work with. But we managed to obtain the full gene expression profile of tissue DC, including for this new CD141hi DC subset. This knowledge will be fundamentally important in learning how to manipulate immune responses to tumors, viruses and vaccines. Importantly, we were very fortunate to have an incredible bioinformatics team in SIgN to perform the intra and interspecies analysis of DCs from human and mouse samples. Our findings will allow scientists to draw clear inferences between mouse and human DC biology.” Scientific Director of SIgN, Professor Paola Castagnoli said, “These findings will facilitate translation of basic research into clinical applications such as future rational vaccine design and targeted immunotherapies. This is a fine example of how scientists and clinicians collaborate to carry out impactful research and benefit people.” ### Notes for editor:
The research findings described in this media release can be found in the 12 July online issue of Immunity under the title, “Human tissues contain CD141hi dendritic cells with cross-presenting capacity and functional homology to mouse CD103+ non-lymphoid dendritic cells” by Muzlifah Haniffa1,2, Amanda Shin2,*, Venetia Bigley 1,*, Naomi McGovern1, Pearline Teo2, Peter See2, Pavandip Singh Wasan2, Xiao-Nong Wang1, Frano Malinarich2, Benoit Malleret2, Anis Larbi2, Pearlie Tan3, Helen Zhao2, Michael Poidinger2, Sarah Pagan1, Sharon Cookson1, Rachel Dickinson1, Ian Dimmick1, Ruth F. Jarrett4, Laurent Renia2, John Tam5,6, Colin Song3, John Connolly2, Jerry K.Y. Chan6,7,8, Adam Gehring9, Antonio Bertoletti9, Matthew Collin1,*,# and Florent Ginhoux2,*,# 1 Institute of Cellular Medicine, Newcastle University, UK 2 Singapore Immunology Network, Agency for Science, Technology and Research (A*STAR), Singapore 3 Singapore General Hospital, Singapore 4 University of Glasgow Centre for Virus Research, University of Glasgow, UK 5 National University Hospital, Singapore 6 Yong Loo Lin School of Medicine, National University of Singapore 7 KK Women’s and Children’s Hospital, Singapore 8 Duke-NUS Graduate Medical School, Singapore 9 Singapore Institute of Clinical Sciences, Agency for Science, Technology and Research (A*STAR), Singapore *Equal contribution with adjacent author Matthew Collin Florent Ginhoux, AGENCY FOR SCIENCE, TECHNOLOGY AND RESEARCH (A*STAR) Ong Siok Ming (Ms) About the Singapore Immunology Network (SIgN) The Singapore Immunology Network (SIgN), officially inaugurated on 15 January 2008, is a research consortium under the Agency for Science, Technology and Research (A*STAR)’s Biomedical Research Council. The mandate of SIgN is to advance human immunology research and participate in international efforts to combat major health problems. Since its launch, SIgN has grown rapidly and currently includes 200 scientists from 25 different countries around the world working under 20 renowned principal investigators. At SIgN, researchers investigate immunity during infection and various inflammatory conditions including cancer and are supported by cutting edge technological research platforms and core services. Through this, SIgN aims to build a strong platform in basic human immunology research for better translation of research findings into clinical applications. SIgN also sets out to establish productive links with local and international institutions, and encourage the exchange of ideas and expertise between academic, industrial and clinical partners and thus contribute to a vibrant research environment in Singapore. For more information about SIgN, please visit www.sign.a-star.edu.sg. About the Agency for Science, Technology and Research (A*STAR) The Agency for Science, Technology and Research (A*STAR) is the lead agency for fostering world-class scientific research and talent for a vibrant knowledge-based and innovation-driven Singapore. A*STAR oversees 14 biomedical sciences and physical sciences and engineering research institutes, and six consortia & centres, located in Biopolis and Fusionopolis as well as their immediate vicinity. A*STAR supports Singapore’s key economic clusters by providing intellectual, human and industrial capital to its partners in industry. It also supports extramural research in the universities, and with other local and international partners. For more information about A*STAR, please visit www.a-star.edu.sg. Contact: Siok Ming Ong |
| Platelet-rich plasma therapy a safe option for cartilage damage, new study finds Posted: 13 Jul 2012 09:00 PM PDT
When it comes to treating cartilage tears in athletes, Platelet Rich Plasma (PRP) therapy is a safe and effective method of treatment, according to research presented today at the American Orthopaedic Society for Sports Medicine’s (AOSSM) Annual Meeting in Baltimore.
“Using PRP therapy to repair cartilage is still relatively experimental, but studies like this show it’s not only safe but also offers a significant improvement in function and quality of life for patients,” said Elizaveta Kon, MD, lead author for the study and Director of Nano-Biotecnology Laboratory at the Rizzoli Orthopaedic Institute in Bologna, Italy. “None of the patients treated experienced complications like infection, deep vein thrombosis or fever.” During the study, 180 patients were treated for chronic pain or swelling of the knee with either PRP therapy or viscosupplementation, a more common hyaluronic acid-based treatment for cartilage damage. A total of 109 patients, with an average age of 56, reached a final evaluation. Both treatment groups demonstrated significant improvement based on higher post-treatment IKDC scores, which measure pain and basic function in follow-up interviews. “As athletic participation has grown,” Kon noted, “new problems like cartilage lesions, or tears, continue to emerge. Finding the right approach to treatment is difficult, but PRP has emerged as a viable option according to our research.” Kon also noted that long-term follow-ups for PRP treatments are needed to further evaluate the overall effectiveness of the therapy for future patients. ### The American Orthopaedic Society for Sports Medicine (AOSSM) is a world leader in sports medicine education, research, communication and fellowship, and includes national and international orthopaedic sports medicine leaders. The Society works closely with many other sports medicine specialists, including athletic trainers, physical therapists, family physicians, and others to improve the identification, prevention, treatment, and rehabilitation of sports injuries. AOSSM is also a founding partner of the STOP Sports Injuries campaign to prevent overuse and traumatic injuries in kids. Contact: Lisa Weisenberger |
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