"The objective was to evaluate the utility of cryo-preserved human amniotic membrane (HAM) as a support for repairing human articular cartilage injuries, which have a very limited capacity for self-healing", Francisco J. Blanco, lead author of the study and a researcher at the Institute of Biomedical Research of La Coruna (INIBIC), tells SINC.
The results, which have been published in the journal Cell and Tissue Banking, show that cryo-preserved HAM is useful as a scaffold for growing human chondrocytes in cell therapy and for repairing human cartilage injuries. "It provides a more regular surface and fills in the cavities and fissures", explains Blanco.
The authors cultivated the chondrocytes (cells that form part of the cartilaginous tissue), isolated from human articular cartilage, on the amniotic membrane over a period of three and four weeks. The amniotic membranes were used to develop 44 repair models of arthritic human articular cartilage in vitro, which was assessed between four and 16 weeks later.
The HAM also bonds well with the native cartilage. "In some models, we could not differentiate between where the native tissue stopped and the neo-synthesised tissue began", says the expert. This tissue had a fibrous appearance and high cellular density (cellularity), which in some cases was greater than that of the actual native cartilage.
The use of differentiated chondrocytes is a useful therapeutic option for repairing articular cartilage injuries. However, there are limitations to implanting these cells, since many patients will be ruled out due to their lack of healthy chondrocytes, and this technique also causes additional damage to the joint.
"Transplanting chondrocytes cultivated on different natural or synthetic 'scaffolds' is used today in cell tissue engineering. The HAM has sparked great interest over recent years, above all in the field of regenerative medicine", concludes Blanco.
Clinical solutions to osteoarthritis
Osteoarthritis (OA) is a major articular pathology that is characterised by alteration of the cartilage and the bone that supports it, the subchondral bone. As the current pharmacological and surgical treatments have only palliative effects, cell therapy is a new clinical approach for repairing damaged or destroyed tissues.
HAM has many clinical advantages as a support - it is an anti-microbial, anti-angiogenic, anti-tumour tissue, which reduces inflammation and pain and improves scarring. In addition, the amnios of the HAM has no immune response, meaning there are no risks associated with transplanting it, and it contains many of the components of natural cartilage.
References: Silvia D?az-Prado; M?? Esther Rendal-V??zquez; Emma Mui?±os-L??pez; Tamara Hermida-G??mez; Margarita Rodr?guez-Cabarcos; Isaac Fuentes-Boquete; Francisco J. de Toro; Francisco J. Blanco. "Potential use of the human amniotic membrane as a scaffold in human articular cartilage repair". Cell Tissue Bank (2010) 11:183-195 DOI 10.1007/s10561-009-9144-1.
Source:
SINC
FECYT - Spanish Foundation for Science and Technology
вторник, 30 августа 2011 г.
суббота, 27 августа 2011 г.
Renowned Bone Health Experts To Lead Interactive Sessions At The World Congress On Osteoporosis 2010
The International Osteoporosis Foundation (IOF) and the European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) will hold a joint global congress, IOF WCO- ECCEO10, in Florence, Italy from May 5-8, 2010.
Complete programme information, online registration and abstract submission will be available on iofwco-ecceo10 .
IOF WCO-ECCEO10 will be an excellent forum for interaction and the exchange of ideas among researchers and clinicians as well as specialists from allied health fields. It will offer an overview of the most recent developments and cutting-edge research in the pathophysiology, diagnosis, prevention and treatment of osteoporosis and osteoarthritis, as well as policy related issues such as health economics.
Offering a broad global perspective, the scientific programme will provide a mix of stimulating plenary lectures on 'hot' topics in the field and more clinically-oriented meet-the-expert sessions led by world experts. There will also be poster presentations, late breaking news, satellite symposia, and a large exhibition area.
Meet-the-expert sessions to be led by world experts:
Each day specialists will lead exchanges on 20 key topics. Small groups, on a first come first served basis, will be encouraged to not only ask questions but to also provide feedback about their own experiences. The following topics and speakers are scheduled:
Assessing bone strength beyond DXA, C. Gl??er (Germany)
Optimal dose of vitamin D, B. Dawson-Hughes (USA)
Muscle and bone interaction, D. Felsenberg (Germany)
Practical approach of glucocorticoid-treated patients, J. Adachi (Canada)
Health economics and treatment selection, J-Y. Reginster (Belgium)
BMU balance: effects of anti-osteoporotic agents, Jpston (UK)
Premenopausal osteoporosis, E. Siris (USA)
Bone mass/structure measurements during growth, R. Rizzoli (Switzerland)
Bone disease in primary hyperparathyroidism, J.P. Bilezikian (USA)
Bisphosphonates in chronic renal failure, S. Papapoulos (NL)
Pharmaco-genomics, M.L. Brandi (Italy)
Vertebro/kyphoplasty, S. Boonen (Belgium)
Issues in designing and conducting clinical trials, S. Cummings (USA)
Osteoporosis in men, E. Seeman (Australia)
Post-fracture management, K. Akesson (Sweden)
Fracture healing: can we influence it?, J. Goldhahn (Switzerland)
Genetics and osteoporosis: how to assess it?, S. Ferrari (Switzerland)
Side effects of anti fracture drugs, S. Adami (Italy)
Developmental origins of osteoporotic fracture, C. Cooper (UK)
Gait and falls, T. Masud (UK)
Don't miss the premiere global skeletal health meeting of 2010 - reserve May 5-8, 2010 on your calendar.
Notes:
Abstract submission deadline: February 4, 2010.
ABOUT IOF
The International Osteoporosis Foundation (IOF) is a nongovernmental umbrella organization dedicated to the worldwide fight against osteoporosis, the disease known as "the silent epidemic". IOF's members - committees of scientific researchers, patient, medical and research societies and industry representatives from around the world - share a common vision of a world without osteoporotic fractures. Launched in 1998 with the merger of the European Foundation for Osteoporosis (EFFO, founded in 1987) and the International Federation of Societies on Skeletal Diseases, IOF now represents 191 societies in 91 locations.
ABOUT ESCEO
The European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) is a non-profit organization, dedicated to a close interaction between clinical scientists dealing with rheumatic disorders, pharmaceutical industry developing new compounds in this field, regulators responsible for the registration of such drugs and health policy makers, to integrate the management of osteoporosis and osteoarthritis within the comprehensive perspective of health resources utilization. The objective of ESCEO is to provide practitioners with the latest clinical and economic information, allowing them to organize their daily practice, in an evidence-based medicine perspective, with a cost-conscious perception.
Source:
L. Misteli
International Osteoporosis Foundation
Complete programme information, online registration and abstract submission will be available on iofwco-ecceo10 .
IOF WCO-ECCEO10 will be an excellent forum for interaction and the exchange of ideas among researchers and clinicians as well as specialists from allied health fields. It will offer an overview of the most recent developments and cutting-edge research in the pathophysiology, diagnosis, prevention and treatment of osteoporosis and osteoarthritis, as well as policy related issues such as health economics.
Offering a broad global perspective, the scientific programme will provide a mix of stimulating plenary lectures on 'hot' topics in the field and more clinically-oriented meet-the-expert sessions led by world experts. There will also be poster presentations, late breaking news, satellite symposia, and a large exhibition area.
Meet-the-expert sessions to be led by world experts:
Each day specialists will lead exchanges on 20 key topics. Small groups, on a first come first served basis, will be encouraged to not only ask questions but to also provide feedback about their own experiences. The following topics and speakers are scheduled:
Assessing bone strength beyond DXA, C. Gl??er (Germany)
Optimal dose of vitamin D, B. Dawson-Hughes (USA)
Muscle and bone interaction, D. Felsenberg (Germany)
Practical approach of glucocorticoid-treated patients, J. Adachi (Canada)
Health economics and treatment selection, J-Y. Reginster (Belgium)
BMU balance: effects of anti-osteoporotic agents, Jpston (UK)
Premenopausal osteoporosis, E. Siris (USA)
Bone mass/structure measurements during growth, R. Rizzoli (Switzerland)
Bone disease in primary hyperparathyroidism, J.P. Bilezikian (USA)
Bisphosphonates in chronic renal failure, S. Papapoulos (NL)
Pharmaco-genomics, M.L. Brandi (Italy)
Vertebro/kyphoplasty, S. Boonen (Belgium)
Issues in designing and conducting clinical trials, S. Cummings (USA)
Osteoporosis in men, E. Seeman (Australia)
Post-fracture management, K. Akesson (Sweden)
Fracture healing: can we influence it?, J. Goldhahn (Switzerland)
Genetics and osteoporosis: how to assess it?, S. Ferrari (Switzerland)
Side effects of anti fracture drugs, S. Adami (Italy)
Developmental origins of osteoporotic fracture, C. Cooper (UK)
Gait and falls, T. Masud (UK)
Don't miss the premiere global skeletal health meeting of 2010 - reserve May 5-8, 2010 on your calendar.
Notes:
Abstract submission deadline: February 4, 2010.
ABOUT IOF
The International Osteoporosis Foundation (IOF) is a nongovernmental umbrella organization dedicated to the worldwide fight against osteoporosis, the disease known as "the silent epidemic". IOF's members - committees of scientific researchers, patient, medical and research societies and industry representatives from around the world - share a common vision of a world without osteoporotic fractures. Launched in 1998 with the merger of the European Foundation for Osteoporosis (EFFO, founded in 1987) and the International Federation of Societies on Skeletal Diseases, IOF now represents 191 societies in 91 locations.
ABOUT ESCEO
The European Society for Clinical and Economic Aspects of Osteoporosis and Osteoarthritis (ESCEO) is a non-profit organization, dedicated to a close interaction between clinical scientists dealing with rheumatic disorders, pharmaceutical industry developing new compounds in this field, regulators responsible for the registration of such drugs and health policy makers, to integrate the management of osteoporosis and osteoarthritis within the comprehensive perspective of health resources utilization. The objective of ESCEO is to provide practitioners with the latest clinical and economic information, allowing them to organize their daily practice, in an evidence-based medicine perspective, with a cost-conscious perception.
Source:
L. Misteli
International Osteoporosis Foundation
среда, 24 августа 2011 г.
New Way To Block Destructive Rush Of Immune Cells
Researchers have found a way to selectively block the ability of white blood cells to "crawl" toward the sites of injury and infection when such mobility drives disease, according to a study published in The Journal of Experimental Medicine. The results suggest a new treatment approach for autoimmune diseases like rheumatoid arthritis, lupus and multiple sclerosis, and for conditions made worse by misplaced inflammation, like atherosclerosis, stroke and transplant rejection, researchers said.
Where a single-celled amoeba moves to find food, human cells migrate as part of complex bodily functions like immunity. Disease-fighting cells for instance move toward bacteria and cells infected with viruses, which they target for destruction. Unfortunately, the same cells can mistakenly attack the body's own cells or drive inflammation too far, worsening the problem they rushed in to solve.
A team of researchers at the University of Rochester Medical Center has been studying proteins called integrins that enable T cells, a major subset of immune cells, to migrate. The integrin-related mechanisms described for the first time in the current paper suggest a way to shut down only those T cells currently in the act of disease-related migration, while leaving in place reserves needed in the likely event that another infection occurs during treatment. Making the mechanistic discoveries possible was a successful effort by the team to capture on video the first detailed images of fast-migrating T cells and the behavior of key proteins related to migration, which had been tagged with fluorescence. Twelve videos of T cells, and their key migration proteins, in action are part of the publication and are available online.
"There are many cases where it would be incredibly useful to precisely block integrin activation, and thus T cell migration," said Minsoo Kim, Ph.D., assistant professor of Microbiology and Immunology within the David H. Smith Center for Vaccine Biology and Immunology at the Medical Center, and lead author of the article. "Good examples include when our immune system attacks our own cells, or rejects a lifesaving transplant or clogs our blood vessels by mistake. The problem is that past, system-wide attempts that block all integrin activation, like the multiple sclerosis drug Tysabri, shut down not only unwanted inflammation in one locale, but also vital immune defenses elsewhere, leaving patients vulnerable to infection."
The Great Migration
Two mechanisms make cell migration, or programmed directional movement, possible. The first, called chemotaxis, tells the cell which direction to move in. Cell surface proteins sense and follow chemicals and molecules they are attracted to toward wherever those attractants are most concentrated. T cells, named after the thymus (T) where they mature, move toward the byproducts of bacteria and viruses.
The second migratory mechanism is propulsion. In between infections and injuries, inactive T cells ride along with the bloodstream. T cells "realize" when they pass by part of a blood vessel wall close to the site of an injury or infection. Integrins on their surfaces unfold and grab onto key proteins on the surface of blood vessel wall cells (e.g. ICAM), resisting the surrounding blood flow. The T cells then pass through the vessel wall, and once outside the bloodstream, crawl along the tissue scaffolding toward the site of injury.
In a T cell at rest, integrins are distributed evenly over the entire surface of the T cell. When the cell gets ready to move, however, activated integrins cluster on the leading edge of the cell in the direction the cell wants to move in. They bind to their counterpart adhesion proteins like ICAM on the surface that the T cell is moving across. The T cell then contracts using its cell skeleton to pull itself over the leading edge integrins. Finally, the integrins on the trailing edge of the cell let go. Without precise changes that enable the front end to gain traction, and the tail to let go, the cell cannot migrate.
Kim's team found that a subset of integrins, including lymphocyte function???"associated antigen-1 (LFA-1), control whether or not the tail end of the T cell can "let go" (de- adhesion). Data revealed for the first time that a protein called non-muscle myosin heavy chain-IIA (MyH9) is recruited to LFA-1 at the trailing end of migrating T lymphocytes. Experiments that interfered with the association between MyH9 and the LFA-1 integrin were found to prevent the trailing edge of the crawling T cell from letting go, dramatically reducing the ability of T cells to move. Myosins are motor proteins that expend energy to enable cell skeletons to contract. That contraction creates force that is used in many cases to move muscle fibers, but in the case of MyH9, to rip the trailing end of a migrating T cell foot away from the surface it is migrating across by breaking integrin-ICAM bonds. The results provide the first evidentiary support of the longstanding theory that cell skeleton contractile force is used to drive T cell migration, with MyH9 as the mechanical link. Captured images show fluorescently tagged actin (which partners with LFA-1 to grip the surface) gathering at the front end of the cell, and fluorescently tagged MyH9 gathering at the tail end in cycles, each time the cell takes a "step."
The study was a joint effort by the Department of Surgery at Rhode Island Hospital, Brown Medical School, the Department of Physics at Brown University, the CBR Institute for Biomedical Research at Harvard Medical School and the departments of Chemical Engineering, Biomedical Engineering and Department of Microbiology and Immunology at the University of Rochester. The project was supported by the American Heart Association, the Rhode Island Foundation, the National Institutes of Health, the National Science Foundation and the Brown University Seed Grant.
In the next phase, the team will seek to develop better-targeted, anti-integrin therapies, with MyH9 among the rational targets for new classes of drugs. Toward that end, experiments currently underway are designed to determine which molecules regulate MyH9 activity during T cell migration.
"Initial clinical studies on T cell migration focused on overall blocking of migration, but general inhibition is a blunt tool," said Tim Mosmann, Ph.D., director of the David H. Smith Center for Vaccine Biology and Immunology. "As studies such as Dr. Kim's help us to understand the process more precisely, we should be able to design much more precise methods to block migration in the selected circumstances that cause problems, without crippling the essential immune responses to infections."
Source: Greg Williams
University of Rochester Medical Center
View drug information on Tysabri.
Where a single-celled amoeba moves to find food, human cells migrate as part of complex bodily functions like immunity. Disease-fighting cells for instance move toward bacteria and cells infected with viruses, which they target for destruction. Unfortunately, the same cells can mistakenly attack the body's own cells or drive inflammation too far, worsening the problem they rushed in to solve.
A team of researchers at the University of Rochester Medical Center has been studying proteins called integrins that enable T cells, a major subset of immune cells, to migrate. The integrin-related mechanisms described for the first time in the current paper suggest a way to shut down only those T cells currently in the act of disease-related migration, while leaving in place reserves needed in the likely event that another infection occurs during treatment. Making the mechanistic discoveries possible was a successful effort by the team to capture on video the first detailed images of fast-migrating T cells and the behavior of key proteins related to migration, which had been tagged with fluorescence. Twelve videos of T cells, and their key migration proteins, in action are part of the publication and are available online.
"There are many cases where it would be incredibly useful to precisely block integrin activation, and thus T cell migration," said Minsoo Kim, Ph.D., assistant professor of Microbiology and Immunology within the David H. Smith Center for Vaccine Biology and Immunology at the Medical Center, and lead author of the article. "Good examples include when our immune system attacks our own cells, or rejects a lifesaving transplant or clogs our blood vessels by mistake. The problem is that past, system-wide attempts that block all integrin activation, like the multiple sclerosis drug Tysabri, shut down not only unwanted inflammation in one locale, but also vital immune defenses elsewhere, leaving patients vulnerable to infection."
The Great Migration
Two mechanisms make cell migration, or programmed directional movement, possible. The first, called chemotaxis, tells the cell which direction to move in. Cell surface proteins sense and follow chemicals and molecules they are attracted to toward wherever those attractants are most concentrated. T cells, named after the thymus (T) where they mature, move toward the byproducts of bacteria and viruses.
The second migratory mechanism is propulsion. In between infections and injuries, inactive T cells ride along with the bloodstream. T cells "realize" when they pass by part of a blood vessel wall close to the site of an injury or infection. Integrins on their surfaces unfold and grab onto key proteins on the surface of blood vessel wall cells (e.g. ICAM), resisting the surrounding blood flow. The T cells then pass through the vessel wall, and once outside the bloodstream, crawl along the tissue scaffolding toward the site of injury.
In a T cell at rest, integrins are distributed evenly over the entire surface of the T cell. When the cell gets ready to move, however, activated integrins cluster on the leading edge of the cell in the direction the cell wants to move in. They bind to their counterpart adhesion proteins like ICAM on the surface that the T cell is moving across. The T cell then contracts using its cell skeleton to pull itself over the leading edge integrins. Finally, the integrins on the trailing edge of the cell let go. Without precise changes that enable the front end to gain traction, and the tail to let go, the cell cannot migrate.
Kim's team found that a subset of integrins, including lymphocyte function???"associated antigen-1 (LFA-1), control whether or not the tail end of the T cell can "let go" (de- adhesion). Data revealed for the first time that a protein called non-muscle myosin heavy chain-IIA (MyH9) is recruited to LFA-1 at the trailing end of migrating T lymphocytes. Experiments that interfered with the association between MyH9 and the LFA-1 integrin were found to prevent the trailing edge of the crawling T cell from letting go, dramatically reducing the ability of T cells to move. Myosins are motor proteins that expend energy to enable cell skeletons to contract. That contraction creates force that is used in many cases to move muscle fibers, but in the case of MyH9, to rip the trailing end of a migrating T cell foot away from the surface it is migrating across by breaking integrin-ICAM bonds. The results provide the first evidentiary support of the longstanding theory that cell skeleton contractile force is used to drive T cell migration, with MyH9 as the mechanical link. Captured images show fluorescently tagged actin (which partners with LFA-1 to grip the surface) gathering at the front end of the cell, and fluorescently tagged MyH9 gathering at the tail end in cycles, each time the cell takes a "step."
The study was a joint effort by the Department of Surgery at Rhode Island Hospital, Brown Medical School, the Department of Physics at Brown University, the CBR Institute for Biomedical Research at Harvard Medical School and the departments of Chemical Engineering, Biomedical Engineering and Department of Microbiology and Immunology at the University of Rochester. The project was supported by the American Heart Association, the Rhode Island Foundation, the National Institutes of Health, the National Science Foundation and the Brown University Seed Grant.
In the next phase, the team will seek to develop better-targeted, anti-integrin therapies, with MyH9 among the rational targets for new classes of drugs. Toward that end, experiments currently underway are designed to determine which molecules regulate MyH9 activity during T cell migration.
"Initial clinical studies on T cell migration focused on overall blocking of migration, but general inhibition is a blunt tool," said Tim Mosmann, Ph.D., director of the David H. Smith Center for Vaccine Biology and Immunology. "As studies such as Dr. Kim's help us to understand the process more precisely, we should be able to design much more precise methods to block migration in the selected circumstances that cause problems, without crippling the essential immune responses to infections."
Source: Greg Williams
University of Rochester Medical Center
View drug information on Tysabri.
воскресенье, 21 августа 2011 г.
Arthritis Advisory Committee Recommends FDA Approval Of Febuxostat For The Treatment Of Hyperuricemia In Patients With Gout
Takeda Pharmaceutical Company Limited and its wholly-owned
subsidiary, Takeda Global Research & Development Center, Inc., U.S.,
announced today that the Arthritis Advisory Committee of the U.S.
Food and Drug Administration (FDA) recommended that the FDA approve
febuxostat for the treatment of hyperuricemia in patients with gout.
The vote was 12 to zero in favor of approval, with one panel member
abstaining. The vote followed presentations by Takeda Global Research
& Development Center, Inc., the FDA, and invited guest speakers. If
approved in the United States by the FDA, febuxostat will be the
first new treatment for the management of hyperuricemia associated
with gout in more than 40 years.
The FDA will review the current new drug application for febuxostat
and make its approval decision. The FDA's decision may or may not
follow the Committee's recommendation.
"Today's vote by the Arthritis Advisory Committee, recommending
approval of febuxostat for the treatment of hyperuricemia in patients
with gout, is a positive step in bringing this new treatment to
market," said Nancy Joseph-Ridge, MD, president, Takeda Global
Research & Development, Inc., U.S. "Takeda is committed to developing
innovative therapies that fulfill unmet treatment needs, and we
believe febuxostat will represent an important new option for
patients who suffer the debilitating effects of gout. In the coming
months, we will work with the FDA to complete their review, including
the design of post-marketing studies."
Febuxostat is a potent non-purine, selective inhibitor of xanthine
oxidase, which was studied for its ability to lower levels of serum
uric acid in patients with hyperuricemia associated with gout.
Hyperuricemia, elevated uric acid levels in the body, is associated
with gout, a painful type of arthritis. In clinical trials,
febuxostat 40 mg and 80 mg were shown to be effective treatments for
the management of hyperuricemia associated with gout. Both doses were
well tolerated and required no dose adjustments in patients with
renal impairment. The most commonly reported adverse events were
upper respiratory tract infections, musculoskeletal and connective
tissue signs and symptoms, and diarrhea.
About Gout and Uric Acid
Uric acid is an end-product created when the body breaks down
naturally occurring substances called purines. Hyperuricemia occurs
when this process results in elevated uric acid levels, either
through overproduction or underexcretion of uric acid or a
combination of the two. Hyperuricemia is a precursor to gout; the
higher a person's urate level, the greater the risk for developing
gout.
Gout is the most common inflammatory arthritis in men over age 40.
According to the National Health and Nutrition Examination Survey III
1988-1994, an estimated 5.1 million Americans suffer from gout. It is
a chronic condition characterized by attacks, or "flares," marked by
intense pain, redness, swelling, and heat in the affected joint. These
symptoms are the result of an acute inflammatory response to the
presence of crystallized uric acid in the joint(s). As the disease
progresses, these attacks may become more frequent and patients may
develop large deposits of crystallized uric acid visible under the
skin, known as tophi, that can eventually lead to complications
including pain, soft tissue damage and deformity, as well as joint
destruction and nerve compression syndromes such as carpal tunnel
syndrome.
Takeda Pharmaceutical Company Limited
Takeda, located in Osaka, Japan, is a research-based global company
with its main focus on pharmaceuticals. As the largest pharmaceutical
company in Japan, and one of the global leaders of the industry,
Takeda is committed to striving toward better health for individuals
and progress in medicine by developing superior pharmaceutical
products. Additional information about Takeda is available through
its corporate website, takeda.
Takeda Pharmaceuticals North America, Inc. and Takeda Global Research
& Development Center, Inc.
Based in Deerfield, Ill., Takeda Pharmaceuticals North America, Inc.
and Takeda Global Research & Development Center, Inc. are subsidiaries
of Takeda Pharmaceutical Company Limited, the largest pharmaceutical
company in Japan. The respective companies currently market oral
diabetes, insomnia and gastroenterology treatments and seek to bring
innovative products to patients through a pipeline that includes
compounds in development for diabetes, cardiovascular disease,
oncology, gastroenterology, neurology, rheumatology and other
conditions. Takeda is committed to striving toward better health for
individuals and progress in medicine by developing superior
pharmaceutical products. To learn more about these Takeda companies,
visit tpna.
Takeda Pharmaceuticals
subsidiary, Takeda Global Research & Development Center, Inc., U.S.,
announced today that the Arthritis Advisory Committee of the U.S.
Food and Drug Administration (FDA) recommended that the FDA approve
febuxostat for the treatment of hyperuricemia in patients with gout.
The vote was 12 to zero in favor of approval, with one panel member
abstaining. The vote followed presentations by Takeda Global Research
& Development Center, Inc., the FDA, and invited guest speakers. If
approved in the United States by the FDA, febuxostat will be the
first new treatment for the management of hyperuricemia associated
with gout in more than 40 years.
The FDA will review the current new drug application for febuxostat
and make its approval decision. The FDA's decision may or may not
follow the Committee's recommendation.
"Today's vote by the Arthritis Advisory Committee, recommending
approval of febuxostat for the treatment of hyperuricemia in patients
with gout, is a positive step in bringing this new treatment to
market," said Nancy Joseph-Ridge, MD, president, Takeda Global
Research & Development, Inc., U.S. "Takeda is committed to developing
innovative therapies that fulfill unmet treatment needs, and we
believe febuxostat will represent an important new option for
patients who suffer the debilitating effects of gout. In the coming
months, we will work with the FDA to complete their review, including
the design of post-marketing studies."
Febuxostat is a potent non-purine, selective inhibitor of xanthine
oxidase, which was studied for its ability to lower levels of serum
uric acid in patients with hyperuricemia associated with gout.
Hyperuricemia, elevated uric acid levels in the body, is associated
with gout, a painful type of arthritis. In clinical trials,
febuxostat 40 mg and 80 mg were shown to be effective treatments for
the management of hyperuricemia associated with gout. Both doses were
well tolerated and required no dose adjustments in patients with
renal impairment. The most commonly reported adverse events were
upper respiratory tract infections, musculoskeletal and connective
tissue signs and symptoms, and diarrhea.
About Gout and Uric Acid
Uric acid is an end-product created when the body breaks down
naturally occurring substances called purines. Hyperuricemia occurs
when this process results in elevated uric acid levels, either
through overproduction or underexcretion of uric acid or a
combination of the two. Hyperuricemia is a precursor to gout; the
higher a person's urate level, the greater the risk for developing
gout.
Gout is the most common inflammatory arthritis in men over age 40.
According to the National Health and Nutrition Examination Survey III
1988-1994, an estimated 5.1 million Americans suffer from gout. It is
a chronic condition characterized by attacks, or "flares," marked by
intense pain, redness, swelling, and heat in the affected joint. These
symptoms are the result of an acute inflammatory response to the
presence of crystallized uric acid in the joint(s). As the disease
progresses, these attacks may become more frequent and patients may
develop large deposits of crystallized uric acid visible under the
skin, known as tophi, that can eventually lead to complications
including pain, soft tissue damage and deformity, as well as joint
destruction and nerve compression syndromes such as carpal tunnel
syndrome.
Takeda Pharmaceutical Company Limited
Takeda, located in Osaka, Japan, is a research-based global company
with its main focus on pharmaceuticals. As the largest pharmaceutical
company in Japan, and one of the global leaders of the industry,
Takeda is committed to striving toward better health for individuals
and progress in medicine by developing superior pharmaceutical
products. Additional information about Takeda is available through
its corporate website, takeda.
Takeda Pharmaceuticals North America, Inc. and Takeda Global Research
& Development Center, Inc.
Based in Deerfield, Ill., Takeda Pharmaceuticals North America, Inc.
and Takeda Global Research & Development Center, Inc. are subsidiaries
of Takeda Pharmaceutical Company Limited, the largest pharmaceutical
company in Japan. The respective companies currently market oral
diabetes, insomnia and gastroenterology treatments and seek to bring
innovative products to patients through a pipeline that includes
compounds in development for diabetes, cardiovascular disease,
oncology, gastroenterology, neurology, rheumatology and other
conditions. Takeda is committed to striving toward better health for
individuals and progress in medicine by developing superior
pharmaceutical products. To learn more about these Takeda companies,
visit tpna.
Takeda Pharmaceuticals
четверг, 18 августа 2011 г.
Ultraviolet Light Therapy Is As Beneficial For Darker Skin As Lighter Skin
An analysis of more than 100 patients has confirmed for the first time that darker-skinned patients benefit as those with lighter skin when given light therapy for morphea and related diseases, UT Southwestern Medical Center researchers show.
Phototherapy is the use of ultraviolet light to treat skin disorders, ranging from common problems such as acne and psoriasis to rarer conditions such as scleroderma and morphea, a hardening of the skin.
Some clinical observations have suggested that darker skin may not respond as well to light therapy, but the new data indicate that skin type does not significantly influence the effectiveness of UVA1 phototherapy, said Dr. Heidi Jacobe, assistant professor of dermatology at UT Southwestern and lead author of the study appearing in the June edition of the British Journal of Dermatology.
"This study is good news, indicating that UVA1 phototherapy should be considered as a therapeutic option for more darkly pigmented patients," noted Dr. Jacobe, who heads UT Southwestern's phototherapy clinic, one of a select few UVA1 phototherapy units in the Southwest.
Patients with diseases such as morphea respond better when treated earlier in the course of the disease, so it's important to know whether a particular treatment such as light therapy is useful.
Researchers reviewed 101 cases treated at UT Southwestern's phototherapy clinic over a three-year period ending in 2007, noting demographic and diagnostic data, skin type and clinical outcome, using standard improvement scales.
Researchers noted that the cumulative dose used did not vary significantly between skin types, and there was little or no correlation between skin type and clinical improvement scores.
The majority of patients treated at the center were diagnosed with either morphea or scleroderma. The maladies often cause discolorations of the thickened skin, usually red or purple in color, and therefore can be disfiguring. The discoloration may initially appear similar to a bruise that doesn't go away. The cause remains a mystery, and there is no known cure.
Dr. Jacobe has helped pioneer an experimental treatment that uses a highly specific range of ultraviolet light (UVA1) for some patients. Other treatments may include topical corticosteroids, antimalarials, systemic immunosuppressive medications and physical therapy.
In 2007, Dr. Jacobe launched the nation's first and only DNA repository for adults and children with morphea. Information is also available at utsouthwestern/.
Researchers are collecting blood and skin samples to investigate genes and blood markers associated with morphea. Other information is used to identify and clarify its prevalence, its demographic distribution among race, gender and age, and recurrence rates. Currently, more women are diagnosed with the disease, but other factors aren't known. UT Southwestern dermatologists also hope to identify associated health problems that may be common for those with morphea, particularly rheumatic diseases such as lupus and rheumatoid arthritis.
Other UT Southwestern researchers involved in the study are Dr. Rachael Cayce, who has a clinical research fellowship from the Doris Duke Charitable Foundation, and medical student Julie Nguyen.
Visit utsouthwestern/dermatology to learn more about UT Southwestern's clinical services in dermatology.
Dr. Heidi Jacobe utsouthwestern/findfac/professional/0,2356,54629,00.html
Source: Russell Rian
UT Southwestern Medical Center
Phototherapy is the use of ultraviolet light to treat skin disorders, ranging from common problems such as acne and psoriasis to rarer conditions such as scleroderma and morphea, a hardening of the skin.
Some clinical observations have suggested that darker skin may not respond as well to light therapy, but the new data indicate that skin type does not significantly influence the effectiveness of UVA1 phototherapy, said Dr. Heidi Jacobe, assistant professor of dermatology at UT Southwestern and lead author of the study appearing in the June edition of the British Journal of Dermatology.
"This study is good news, indicating that UVA1 phototherapy should be considered as a therapeutic option for more darkly pigmented patients," noted Dr. Jacobe, who heads UT Southwestern's phototherapy clinic, one of a select few UVA1 phototherapy units in the Southwest.
Patients with diseases such as morphea respond better when treated earlier in the course of the disease, so it's important to know whether a particular treatment such as light therapy is useful.
Researchers reviewed 101 cases treated at UT Southwestern's phototherapy clinic over a three-year period ending in 2007, noting demographic and diagnostic data, skin type and clinical outcome, using standard improvement scales.
Researchers noted that the cumulative dose used did not vary significantly between skin types, and there was little or no correlation between skin type and clinical improvement scores.
The majority of patients treated at the center were diagnosed with either morphea or scleroderma. The maladies often cause discolorations of the thickened skin, usually red or purple in color, and therefore can be disfiguring. The discoloration may initially appear similar to a bruise that doesn't go away. The cause remains a mystery, and there is no known cure.
Dr. Jacobe has helped pioneer an experimental treatment that uses a highly specific range of ultraviolet light (UVA1) for some patients. Other treatments may include topical corticosteroids, antimalarials, systemic immunosuppressive medications and physical therapy.
In 2007, Dr. Jacobe launched the nation's first and only DNA repository for adults and children with morphea. Information is also available at utsouthwestern/.
Researchers are collecting blood and skin samples to investigate genes and blood markers associated with morphea. Other information is used to identify and clarify its prevalence, its demographic distribution among race, gender and age, and recurrence rates. Currently, more women are diagnosed with the disease, but other factors aren't known. UT Southwestern dermatologists also hope to identify associated health problems that may be common for those with morphea, particularly rheumatic diseases such as lupus and rheumatoid arthritis.
Other UT Southwestern researchers involved in the study are Dr. Rachael Cayce, who has a clinical research fellowship from the Doris Duke Charitable Foundation, and medical student Julie Nguyen.
Visit utsouthwestern/dermatology to learn more about UT Southwestern's clinical services in dermatology.
Dr. Heidi Jacobe utsouthwestern/findfac/professional/0,2356,54629,00.html
Source: Russell Rian
UT Southwestern Medical Center
понедельник, 15 августа 2011 г.
Merrimack Pharmaceuticals Completes Enrollment In A Phase 2 Study Of MM-093 In Patients With Rheumatoid Arthritis
Merrimack Pharmaceuticals,
Inc. announced that enrollment has been completed in a Phase 2 trial
of 100 patients that evaluates the safety and efficacy of its lead product,
MM-093, in patients suffering from rheumatoid arthritis (RA). MM-093 is a
recombinant version of human alpha-fetoprotein (AFP).
The randomized, double-blind, placebo-controlled, Phase 2 study is
being conducted at 20 centers throughout the United States. The objective
of this study is to examine the safety and efficacy of MM-093 in patients
with moderate to severe, active RA despite treatment with stable doses of
methotrexate. Each patient receives 60mg of MM-093 per week or placebo for
12 weeks and will then be followed for a period of 4 weeks. In addition to
evaluating the safety of MM-093, patients will be assessed for changes in
the signs and symptoms of their disease using standard clinical outcome
measurements for RA, such as ACR20 and DAS28 scores. Patients who complete
the study are eligible to participate in an ongoing Open-Label Extension
study, which has enrolled over 35 patients to date.
"We are pleased to have completed enrollment and are thankful for the
enthusiasm of the investigators who have worked diligently to enroll
patients," said Dr. William Slichenmyer, Senior Vice President and Chief
Medical Officer at Merrimack. "We believe MM-093 represents a promising and
novel approach to the treatment of a broad range of autoimmune diseases. We
look forward to completing the study and communicating the results later
this year."
In addition to the ongoing studies in RA, MM-093 is currently being
tested in a pilot study for patients with certain types of autoimmune
uveitis, an inflammatory disorder of the eye.
Merrimack controls a strong intellectual property estate around MM-093
including 15 issued patents and a number of pending applications, both in
the U.S. and internationally, which cover composition of matter, production
methods and therapeutic uses of the drug.
Merrimack Pharmaceuticals, Inc., is a biotechnology company focused on
the discovery and development of novel treatments for diseases in the areas
of autoimmunity and cancer. Its lead compound, MM-093, is currently in
clinical development to treat patients with rheumatoid arthritis or with
autoimmune uveitis. MM-093 is an investigational drug and has not been
approved by the U.S. Food and Drug Administration or any international
regulatory agency. The company's proprietary Network Biology discovery
platform, developed with the help of leading scientists from MIT and
Harvard, enables the high throughput profiling of protein networks as a
basis for improved validation, lead identification and speed in the
development of innovative, effective and safe therapeutics. Merrimack is a
privately-held company based in Cambridge, Massachusetts. For additional
information, please visit merrimackpharma.
Merrimack Pharmaceuticals, Inc.
merrimackpharma
Inc. announced that enrollment has been completed in a Phase 2 trial
of 100 patients that evaluates the safety and efficacy of its lead product,
MM-093, in patients suffering from rheumatoid arthritis (RA). MM-093 is a
recombinant version of human alpha-fetoprotein (AFP).
The randomized, double-blind, placebo-controlled, Phase 2 study is
being conducted at 20 centers throughout the United States. The objective
of this study is to examine the safety and efficacy of MM-093 in patients
with moderate to severe, active RA despite treatment with stable doses of
methotrexate. Each patient receives 60mg of MM-093 per week or placebo for
12 weeks and will then be followed for a period of 4 weeks. In addition to
evaluating the safety of MM-093, patients will be assessed for changes in
the signs and symptoms of their disease using standard clinical outcome
measurements for RA, such as ACR20 and DAS28 scores. Patients who complete
the study are eligible to participate in an ongoing Open-Label Extension
study, which has enrolled over 35 patients to date.
"We are pleased to have completed enrollment and are thankful for the
enthusiasm of the investigators who have worked diligently to enroll
patients," said Dr. William Slichenmyer, Senior Vice President and Chief
Medical Officer at Merrimack. "We believe MM-093 represents a promising and
novel approach to the treatment of a broad range of autoimmune diseases. We
look forward to completing the study and communicating the results later
this year."
In addition to the ongoing studies in RA, MM-093 is currently being
tested in a pilot study for patients with certain types of autoimmune
uveitis, an inflammatory disorder of the eye.
Merrimack controls a strong intellectual property estate around MM-093
including 15 issued patents and a number of pending applications, both in
the U.S. and internationally, which cover composition of matter, production
methods and therapeutic uses of the drug.
Merrimack Pharmaceuticals, Inc., is a biotechnology company focused on
the discovery and development of novel treatments for diseases in the areas
of autoimmunity and cancer. Its lead compound, MM-093, is currently in
clinical development to treat patients with rheumatoid arthritis or with
autoimmune uveitis. MM-093 is an investigational drug and has not been
approved by the U.S. Food and Drug Administration or any international
regulatory agency. The company's proprietary Network Biology discovery
platform, developed with the help of leading scientists from MIT and
Harvard, enables the high throughput profiling of protein networks as a
basis for improved validation, lead identification and speed in the
development of innovative, effective and safe therapeutics. Merrimack is a
privately-held company based in Cambridge, Massachusetts. For additional
information, please visit merrimackpharma.
Merrimack Pharmaceuticals, Inc.
merrimackpharma
пятница, 12 августа 2011 г.
Better Interaction And Education Between Rheumatoid Arthritis Patients And Care Providers Needed, New Study Indicates
UCB announced today findings from large-scale rheumatoid arthritis (RA) surveys collectively called the DESIGN study that showed patients rating themselves as having substantially less knowledge of RA therapies than their physicians and nurses believed. The survey also showed disagreement between physicians and nurses over who should be charged with patient education, as well a high level of patient dissatisfaction with the level of pain they suffer from RA. These surveys, designed to assess the attitudes of RA patients and their healthcare providers, were presented at the American College of Rheumatology (ACR) Annual Scientific Meeting.
In the global study of more than 3,300 patients, nurses and physicians, 87 percent of physicians and 90 percent of nurses believed their patients had a high level of knowledge of current RA treatments. But when asked, only 50 percent of RA patients rated their knowledge as high.
The survey also asked doctors and nurses about who should be responsible for educating patients to monitor for side effects of therapies. Only 14 percent of physicians believed that nurses should educate patients, while 68 percent of nurses thought they were best able to handle this aspect of patient care. Despite these differences, nurses, physicians and patients were aligned in terms of RA treatment goals.
"These findings help pinpoint areas for additional attention where we can better work together to improve the patient understanding of this complex disease," said Nicole Furfaro, A.R.N.P., M.S.N., study investigator at Seattle Rheumatology Associates. "Patients clearly can benefit from more interaction and education from their care providers to help bridge the gaps in knowledge and manage expectations of RA therapy."
The study also assessed RA-associated pain in U.S. and European Union (EU) patients. The survey found that 34 percent of EU and 37 percent of U.S. patients were either extremely dissatisfied or dissatisfied with their level of pain from RA. Only 12 percent of EU and 9 percent of U.S. patients were extremely satisfied or satisfied.
"This survey indicates that, despite treatment, RA patients' levels of arthritis pain remain high in both the EU and the U.S. and effective pain management remains an extensive unmet need," Furfaro said.
Patients reported dissatisfaction within the 30 days prior to the survey and most patients reported moderate to severe pain in the past two months. Not surprisingly, there was a significant correlation between arthritis pain and mood and tension levels.
"It is understandable that arthritis pain would significantly affect quality of life for patients," said Arthur Kavanaugh, M.D., study investigator at the University of California, San Diego School of Medicine. "With recent advances in treatment and continuing understanding of the pathophysiology of RA, the goals of treatment have been elevated. Even though a number of patients can do extremely well with current agents, there is still room for improvement in the therapies offered to manage RA symptoms and achieve the highest levels of disease control."
Forty-four percent of U.S. patients rated pain relief as the top benefit wanted from their RA medication, and they were satisfied with a biologic therapy if pain reduction was provided. Most EU respondents were satisfied with their biologic therapy, although pain relief was not cited as the leading reason for their satisfaction.
The DESIGN study was sponsored by UCB. Additional findings will be presented or published at a later date.
About DESIGN Study
The international DESIGN (DEveloping SuperIor understandinG of RA patients' Needs) study is one of the largest international Rheumatoid Arthritis (RA) surveys to explore the attitudes and behaviors of RA patients and their physicians regarding RA and its treatment, and assess emotional, informational, and clinical needs. The goal of the study is to highlight the burden of RA on the patient and create awareness around the importance of strong relationships between the patient and their treating rheumatologist.
Quantitative data was collected via a 45-minute phone or internet surveys fielded to 2,795 RA patients (18+ years of age; US = 2,039 RA patients; EU = 756 RA patients), 500 rheumatologists and 101 RA nurses between February and March 2008. The surveys were conducted by the bioStrategies Group. Survey questions covered disease status, disease knowledge and severity, rheumatologist visits and relationships to providers, RA treatments, as well as emotions, attitudes, and behaviors related to RA. Patient demographics and results of the EU and U.S. survey:
Mean age (y) EU (n=756) 60 - U.S. (n=2,039) 54
% females EU (n=756) 76 - U.S. (n=2,039) 79
Mean disease duration (y) EU (n=756) 12 - U.S. (n=2,039) 8
% moderate to severe RA EU (n=756) 77 - U.S. (n=2,039) 83
% taking prescription RA medication EU (n=756) 98 - U.S. (n=2,039) 92
% currently taking a biologic EU (n=756) 24 - U.S. (n=2,039) 34
Extremely dissatisfied/dissatisfied EU (n=756) 34 - U.S. (n=2,039) 37
Extremely satisfied/satisfied EU (n=756) 12 - U.S. (n=2,039) 9
Experienced moderate to severe pain in past 2 months (%) EU (n=756) 75 - U.S. (n=2,039) 82
Feel their life will be filled with pain (agree/strongly agree, %) EU (n=756) 31 - U.S. (n=2,039) 39
Worried medicine will not be strong enough to control pain (agree/strongly agree, %) EU (n=756) 37 - U.S. (n=2,039) 52
About Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a progressive autoimmune disease that causes chronic inflammation of the joints. It is estimated that five million people suffer from RA globally, with 0.3 percent to 1 percent of the population in industrialized countries suffering from RA. It is estimated that, approximately 1.3 million people in the United States have RA. Women are three times more likely to be affected than men. Although it can affect people of all ages, the onset of RA usually occurs between the ages of 35-55.
Symptoms of RA include joint stiffness, joint pain, inflammation of the affected areas and an associated reduction in mobility. These symptoms can be intermittent and vary in severity from patient to patient. In more severe cases RA can eventually lead to disability. RA patients are also at a higher risk of developing other conditions, in particular heart disease, stroke, infections, lung problems and osteoporosis.
As there is currently no cure for RA, treatment goals center on disease management and controlling symptoms. Treatment is aimed at controlling disease progression, providing pain relief and reducing swelling, preventing joint damage and deformity and maintaining function of the affected joints to prevent disability.
Traditional treatments for RA include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids and disease-modifying antirheumatic drugs (DMARDs), with biological therapies a more recent addition. Anti-TNF (TNF-alpha; Tumor Necrosis Factor) therapies are specific types of biological therapies which have been used in patients with RA. They may be given alone but are usually given in combination with methotrexate or another immunosuppressant. They work by inhibiting the action of TNF-alpha, an inflammatory mediator, either directly or indirectly responsible for damaging the joint.
About UCB
UCB, Brussels, Belgium (ucb-group) is a global leader in the biopharmaceutical industry dedicated to the research, development and commercialization of innovative medicines with a focus on the fields of central nervous system and immunology disorders. Employing around 12 000 people in over 40 countries, UCB achieved revenue of 3.6 billion euro in 2007. UCB is listed on Euronext Brussels (symbol: UCB). UCB's North American headquarters is located in Atlanta, Ga. ucb-group/
Forward-looking statement
This press release contains forward-looking statements based on current plans, estimates and beliefs of management. Such statements are subject to risks and uncertainties that may cause actual results to be materially different from those that may be implied by such forward-looking statements contained in this press release. Important factors that could result in such differences include: changes in general economic, business and competitive conditions, effects of future judicial decisions, changes in regulation, exchange rate fluctuations and hiring and retention of its employees.
UCB
In the global study of more than 3,300 patients, nurses and physicians, 87 percent of physicians and 90 percent of nurses believed their patients had a high level of knowledge of current RA treatments. But when asked, only 50 percent of RA patients rated their knowledge as high.
The survey also asked doctors and nurses about who should be responsible for educating patients to monitor for side effects of therapies. Only 14 percent of physicians believed that nurses should educate patients, while 68 percent of nurses thought they were best able to handle this aspect of patient care. Despite these differences, nurses, physicians and patients were aligned in terms of RA treatment goals.
"These findings help pinpoint areas for additional attention where we can better work together to improve the patient understanding of this complex disease," said Nicole Furfaro, A.R.N.P., M.S.N., study investigator at Seattle Rheumatology Associates. "Patients clearly can benefit from more interaction and education from their care providers to help bridge the gaps in knowledge and manage expectations of RA therapy."
The study also assessed RA-associated pain in U.S. and European Union (EU) patients. The survey found that 34 percent of EU and 37 percent of U.S. patients were either extremely dissatisfied or dissatisfied with their level of pain from RA. Only 12 percent of EU and 9 percent of U.S. patients were extremely satisfied or satisfied.
"This survey indicates that, despite treatment, RA patients' levels of arthritis pain remain high in both the EU and the U.S. and effective pain management remains an extensive unmet need," Furfaro said.
Patients reported dissatisfaction within the 30 days prior to the survey and most patients reported moderate to severe pain in the past two months. Not surprisingly, there was a significant correlation between arthritis pain and mood and tension levels.
"It is understandable that arthritis pain would significantly affect quality of life for patients," said Arthur Kavanaugh, M.D., study investigator at the University of California, San Diego School of Medicine. "With recent advances in treatment and continuing understanding of the pathophysiology of RA, the goals of treatment have been elevated. Even though a number of patients can do extremely well with current agents, there is still room for improvement in the therapies offered to manage RA symptoms and achieve the highest levels of disease control."
Forty-four percent of U.S. patients rated pain relief as the top benefit wanted from their RA medication, and they were satisfied with a biologic therapy if pain reduction was provided. Most EU respondents were satisfied with their biologic therapy, although pain relief was not cited as the leading reason for their satisfaction.
The DESIGN study was sponsored by UCB. Additional findings will be presented or published at a later date.
About DESIGN Study
The international DESIGN (DEveloping SuperIor understandinG of RA patients' Needs) study is one of the largest international Rheumatoid Arthritis (RA) surveys to explore the attitudes and behaviors of RA patients and their physicians regarding RA and its treatment, and assess emotional, informational, and clinical needs. The goal of the study is to highlight the burden of RA on the patient and create awareness around the importance of strong relationships between the patient and their treating rheumatologist.
Quantitative data was collected via a 45-minute phone or internet surveys fielded to 2,795 RA patients (18+ years of age; US = 2,039 RA patients; EU = 756 RA patients), 500 rheumatologists and 101 RA nurses between February and March 2008. The surveys were conducted by the bioStrategies Group. Survey questions covered disease status, disease knowledge and severity, rheumatologist visits and relationships to providers, RA treatments, as well as emotions, attitudes, and behaviors related to RA. Patient demographics and results of the EU and U.S. survey:
Mean age (y) EU (n=756) 60 - U.S. (n=2,039) 54
% females EU (n=756) 76 - U.S. (n=2,039) 79
Mean disease duration (y) EU (n=756) 12 - U.S. (n=2,039) 8
% moderate to severe RA EU (n=756) 77 - U.S. (n=2,039) 83
% taking prescription RA medication EU (n=756) 98 - U.S. (n=2,039) 92
% currently taking a biologic EU (n=756) 24 - U.S. (n=2,039) 34
Extremely dissatisfied/dissatisfied EU (n=756) 34 - U.S. (n=2,039) 37
Extremely satisfied/satisfied EU (n=756) 12 - U.S. (n=2,039) 9
Experienced moderate to severe pain in past 2 months (%) EU (n=756) 75 - U.S. (n=2,039) 82
Feel their life will be filled with pain (agree/strongly agree, %) EU (n=756) 31 - U.S. (n=2,039) 39
Worried medicine will not be strong enough to control pain (agree/strongly agree, %) EU (n=756) 37 - U.S. (n=2,039) 52
About Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a progressive autoimmune disease that causes chronic inflammation of the joints. It is estimated that five million people suffer from RA globally, with 0.3 percent to 1 percent of the population in industrialized countries suffering from RA. It is estimated that, approximately 1.3 million people in the United States have RA. Women are three times more likely to be affected than men. Although it can affect people of all ages, the onset of RA usually occurs between the ages of 35-55.
Symptoms of RA include joint stiffness, joint pain, inflammation of the affected areas and an associated reduction in mobility. These symptoms can be intermittent and vary in severity from patient to patient. In more severe cases RA can eventually lead to disability. RA patients are also at a higher risk of developing other conditions, in particular heart disease, stroke, infections, lung problems and osteoporosis.
As there is currently no cure for RA, treatment goals center on disease management and controlling symptoms. Treatment is aimed at controlling disease progression, providing pain relief and reducing swelling, preventing joint damage and deformity and maintaining function of the affected joints to prevent disability.
Traditional treatments for RA include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids and disease-modifying antirheumatic drugs (DMARDs), with biological therapies a more recent addition. Anti-TNF (TNF-alpha; Tumor Necrosis Factor) therapies are specific types of biological therapies which have been used in patients with RA. They may be given alone but are usually given in combination with methotrexate or another immunosuppressant. They work by inhibiting the action of TNF-alpha, an inflammatory mediator, either directly or indirectly responsible for damaging the joint.
About UCB
UCB, Brussels, Belgium (ucb-group) is a global leader in the biopharmaceutical industry dedicated to the research, development and commercialization of innovative medicines with a focus on the fields of central nervous system and immunology disorders. Employing around 12 000 people in over 40 countries, UCB achieved revenue of 3.6 billion euro in 2007. UCB is listed on Euronext Brussels (symbol: UCB). UCB's North American headquarters is located in Atlanta, Ga. ucb-group/
Forward-looking statement
This press release contains forward-looking statements based on current plans, estimates and beliefs of management. Such statements are subject to risks and uncertainties that may cause actual results to be materially different from those that may be implied by such forward-looking statements contained in this press release. Important factors that could result in such differences include: changes in general economic, business and competitive conditions, effects of future judicial decisions, changes in regulation, exchange rate fluctuations and hiring and retention of its employees.
UCB
вторник, 9 августа 2011 г.
Editorial urges 'black-box' warning for Bextra and Celebrex
Physicians should avoid prescribing Bextra altogether, or use it only as a drug of last resort, says a researcher from
Wake Forest University Baptist Medical Center and colleagues in an editorial published on-line Jan. 17 in Circulation, a
publication of the American Heart Association.
Curt D. Furberg, M.D., Ph.D., professor of public health sciences, and colleagues describe an analysis of two studies
revealed that patients treated with Bextra after heart bypass surgery tripled their risk of heart attack and stroke compared
to patients who received a placebo, or "dummy" drug. The data is a followup to information reported at the American Heart
Association meeting in November.
"These data raise questions about the safety of the drug in other patients who have heart conditions, but who aren't having
surgery," said Furberg. "In the absence of evidence of safety, it is prudent to avoid the use of Bextra altogether or use it
only as a drug of last resort," says the editorial. Furberg's co-authors are Bruce M. Psaty, M.D., Ph.D., from the University
of Washington in Seattle, and Garret A. FitzGerald, M.D., from the University of Pennsylvania.
The researchers say the Bextra results, combined with studies showing cardiovascular hazards with Celebrex and Vioxx,
"provide compelling evidence that these adverse coronary and cerebrovascular events represent a class effect…" The drugs are
all part of a class called COX-2 inhibitors.
"A black-box warning that alerts practitioners to the potential cardiovascular hazards, especially in patients at moderate to
high risk, seems timely for all COX-2 inhibitors," said Psaty.
Furberg supports the advice of the Food and Drug Administration, which issued a Public Health Advisory on COX-2 inhibitors
and other non-steroidal anti-inflammatory drug products urging physicians to weigh the benefits against the risk for
individual patients.
In the editorial, the authors support research to learn whether the drugs can be safely given for extended periods to
patients at low risk of cardiovascular disease.
"It is currently unclear to what degree the risk extends to patients treated with lower doses for arthritis because studies
of sufficient size and duration have not been reported," Furberg said.
FitzGerald, who has been studying COX-2 inhibitors for more than six years, says that plans by Pfizer to study potential
cardiovascular benefits of Celebrex are ill-advised.
In a separate article in Circulation, FitzGerald and colleagues report on evidence from mice showing that the combination of
aspirin and a COX-2 inhibitor could make plaque in the arteries more likely to rupture and cause clotting, resulting in heart
attack or stroke.
"These results have disturbing implications for patients at high cardiovascular risk treated with aspirin and a COX
inhibitor," writes FitzGerald.
Media Contacts: Karen Richardson, krchrdsnwfubmc; Shannon Koontz, shkoontzwfubmc; at 336-716-4587
About Wake Forest University Baptist Medical Center:
Wake Forest Baptist is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University
Health Sciences, which operates the university's School of Medicine. The system comprises 1,282 acute care, psychiatric,
rehabilitation and long-term care beds.
Karen Richardson
krchrdsnwfubmc
Wake Forest University Baptist Medical Center
View drug information on Bextra; Vioxx.
Wake Forest University Baptist Medical Center and colleagues in an editorial published on-line Jan. 17 in Circulation, a
publication of the American Heart Association.
Curt D. Furberg, M.D., Ph.D., professor of public health sciences, and colleagues describe an analysis of two studies
revealed that patients treated with Bextra after heart bypass surgery tripled their risk of heart attack and stroke compared
to patients who received a placebo, or "dummy" drug. The data is a followup to information reported at the American Heart
Association meeting in November.
"These data raise questions about the safety of the drug in other patients who have heart conditions, but who aren't having
surgery," said Furberg. "In the absence of evidence of safety, it is prudent to avoid the use of Bextra altogether or use it
only as a drug of last resort," says the editorial. Furberg's co-authors are Bruce M. Psaty, M.D., Ph.D., from the University
of Washington in Seattle, and Garret A. FitzGerald, M.D., from the University of Pennsylvania.
The researchers say the Bextra results, combined with studies showing cardiovascular hazards with Celebrex and Vioxx,
"provide compelling evidence that these adverse coronary and cerebrovascular events represent a class effect…" The drugs are
all part of a class called COX-2 inhibitors.
"A black-box warning that alerts practitioners to the potential cardiovascular hazards, especially in patients at moderate to
high risk, seems timely for all COX-2 inhibitors," said Psaty.
Furberg supports the advice of the Food and Drug Administration, which issued a Public Health Advisory on COX-2 inhibitors
and other non-steroidal anti-inflammatory drug products urging physicians to weigh the benefits against the risk for
individual patients.
In the editorial, the authors support research to learn whether the drugs can be safely given for extended periods to
patients at low risk of cardiovascular disease.
"It is currently unclear to what degree the risk extends to patients treated with lower doses for arthritis because studies
of sufficient size and duration have not been reported," Furberg said.
FitzGerald, who has been studying COX-2 inhibitors for more than six years, says that plans by Pfizer to study potential
cardiovascular benefits of Celebrex are ill-advised.
In a separate article in Circulation, FitzGerald and colleagues report on evidence from mice showing that the combination of
aspirin and a COX-2 inhibitor could make plaque in the arteries more likely to rupture and cause clotting, resulting in heart
attack or stroke.
"These results have disturbing implications for patients at high cardiovascular risk treated with aspirin and a COX
inhibitor," writes FitzGerald.
Media Contacts: Karen Richardson, krchrdsnwfubmc; Shannon Koontz, shkoontzwfubmc; at 336-716-4587
About Wake Forest University Baptist Medical Center:
Wake Forest Baptist is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University
Health Sciences, which operates the university's School of Medicine. The system comprises 1,282 acute care, psychiatric,
rehabilitation and long-term care beds.
Karen Richardson
krchrdsnwfubmc
Wake Forest University Baptist Medical Center
View drug information on Bextra; Vioxx.
суббота, 6 августа 2011 г.
New Study Links Inflammation To Plaque Buildup In The Arteries Of People With Rheumatoid Arthritis
New data presented this week at the American College of Rheumatology Annual Scientific Meeting in Atlanta show that systemic inflammation and rheumatoid arthritis disease activity may contribute to the progression of atherosclerosis in people with RA. The data also show that this progression may be modified favorably by TNF inhibitors and detrimentally by glucocorticoids.
"These data suggest that by limiting inflammation in RA patients, you can potentially limit the rapidity of accumulation of at least carotid atherosclerosis, which is what our study looked at," says Jon T. Giles, MD, MPH; assistant professor of medicine in the Division of Rheumatology at Johns Hopkins and lead investigator in the study. "And because carotid atherosclerosis tends to be correlated with coronary atherosclerosis, then potentially you would have fewer cardiovascular events like myocardial infarction and stroke in RA patients. These links with subclinical atherosclerosis make intuitive sense, but they haven't [previously] been shown in prospective studies."
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
Coronary and extra-coronary atherosclerosis the buildup of plaque in the artery walls are increased in people with RA, when compared to people without the disease. However, few studies have explored predictors of change in atherosclerosis in RA patients. In a study funded in part by the ACR Research and Education Foundation, researchers recently addressed this by following 158 people with RA who were already enrolled in a study of cardiovascular disease in RA.
They focused on monitoring intima-medial thickness the thickness of artery walls that is used in diagnosing atherosclerosis. Participants underwent an ultrasound of their common and internal carotid arteries (arteries that provide blood to the head and neck) at the first and third study visits, which were an average of 3.2 years apart. Through this, researchers found that the thickness of the common carotid artery walls increased over time in 82 percent of the participants and the thickness in the internal carotid artery walls increased in 70 percent of the participants.
When the researchers adjusted their data to consider demographics, cardiovascular risk factors, and the thickness of the carotid artery walls at the beginning of the study, they found that those participants who used anti-TNF treatment at the beginning of the study had a 37 percent lower rate of progression of the thickness of the common carotid artery walls than those who did not use anti-TNF treatment. They also noted that the adjusted average yearly change in the thickness of the common carotid artery walls was significantly higher for patients earlier in their RA when compared to those who had the disease longer.
When looking at thickness in the internal carotid artery walls, prednisone exposure was the only RA feature researchers associated with progression of atherosclerosis after adjusting the data to consider demographics, cardiovascular risk factors and thickness of the internal carotid artery walls at the beginning of the study. And, this rate was significantly lower in participants who were prescribed statins at the beginning of the study.
"There seem to be some medications used in RA that can either be protective or can promote atherosclerosis," Dr. Giles says. "Prednisone may be more associated with progression of atherosclerosis in some vascular beds, but medications like TNF inhibitors and statins that are taken to lower cholesterol may limit atherosclerosis in these patients."
Finally, researchers noted that those participants with a higher than average number of swollen joints and a higher than average c-reactive protein were independently and significantly associated with incidence of plaque.
The next step for researchers is to conduct interventional studies that randomize patients to receive one medication or another and determine the direct cause-and-effect relationship between the medications and the progression of atherosclerosis, either in coronary artery circulation or the carotid artery circulation.
"Those studies are in the planning stages," Dr. Giles says. "They are big studies and hard to organize, but they're really required to determine what the role of the medications are in terms of protection."
Source: American College of Rheumatology (ACR)
"These data suggest that by limiting inflammation in RA patients, you can potentially limit the rapidity of accumulation of at least carotid atherosclerosis, which is what our study looked at," says Jon T. Giles, MD, MPH; assistant professor of medicine in the Division of Rheumatology at Johns Hopkins and lead investigator in the study. "And because carotid atherosclerosis tends to be correlated with coronary atherosclerosis, then potentially you would have fewer cardiovascular events like myocardial infarction and stroke in RA patients. These links with subclinical atherosclerosis make intuitive sense, but they haven't [previously] been shown in prospective studies."
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
Coronary and extra-coronary atherosclerosis the buildup of plaque in the artery walls are increased in people with RA, when compared to people without the disease. However, few studies have explored predictors of change in atherosclerosis in RA patients. In a study funded in part by the ACR Research and Education Foundation, researchers recently addressed this by following 158 people with RA who were already enrolled in a study of cardiovascular disease in RA.
They focused on monitoring intima-medial thickness the thickness of artery walls that is used in diagnosing atherosclerosis. Participants underwent an ultrasound of their common and internal carotid arteries (arteries that provide blood to the head and neck) at the first and third study visits, which were an average of 3.2 years apart. Through this, researchers found that the thickness of the common carotid artery walls increased over time in 82 percent of the participants and the thickness in the internal carotid artery walls increased in 70 percent of the participants.
When the researchers adjusted their data to consider demographics, cardiovascular risk factors, and the thickness of the carotid artery walls at the beginning of the study, they found that those participants who used anti-TNF treatment at the beginning of the study had a 37 percent lower rate of progression of the thickness of the common carotid artery walls than those who did not use anti-TNF treatment. They also noted that the adjusted average yearly change in the thickness of the common carotid artery walls was significantly higher for patients earlier in their RA when compared to those who had the disease longer.
When looking at thickness in the internal carotid artery walls, prednisone exposure was the only RA feature researchers associated with progression of atherosclerosis after adjusting the data to consider demographics, cardiovascular risk factors and thickness of the internal carotid artery walls at the beginning of the study. And, this rate was significantly lower in participants who were prescribed statins at the beginning of the study.
"There seem to be some medications used in RA that can either be protective or can promote atherosclerosis," Dr. Giles says. "Prednisone may be more associated with progression of atherosclerosis in some vascular beds, but medications like TNF inhibitors and statins that are taken to lower cholesterol may limit atherosclerosis in these patients."
Finally, researchers noted that those participants with a higher than average number of swollen joints and a higher than average c-reactive protein were independently and significantly associated with incidence of plaque.
The next step for researchers is to conduct interventional studies that randomize patients to receive one medication or another and determine the direct cause-and-effect relationship between the medications and the progression of atherosclerosis, either in coronary artery circulation or the carotid artery circulation.
"Those studies are in the planning stages," Dr. Giles says. "They are big studies and hard to organize, but they're really required to determine what the role of the medications are in terms of protection."
Source: American College of Rheumatology (ACR)
среда, 3 августа 2011 г.
Anoles Key To Medically Applicable Regeneration?
Anolis lizards first entered Arizona State University biologist Kenro Kusumi's life in 1980 when, as a member of a junior curator program, he recorded in his field notebook that he had found an Anolis egg on a field trip. Kusumi still has those notes, along with other memorabilia that document the influence that both his early life and more recent experiences have had on his current pursuits in developmental biology. One such souvenir is a small Pueblo lizard sculpture that sits on a table in his office. With one missing leg and a tail, broken and repaired in two places, it is not particularly eye-catching, but it does symbolize Kusumi's current research model: a lizard which can "fix" or more accurately, regenerate, its broken tail.
Human regeneration is mainly limited to small portions of liver tissue, bone, or muscle, yet understanding how regeneration occurs in other taxonomic groups may enable scientists to improve human regenerative abilities in the future. Kusumi is working to understand the molecular processes that enable some lizards to regenerate their tissues with fellow ASU School of Life Sciences faculty members Jeanne Wilson-Rawls, Allan Rawls, Rebecca Fisher and Dale DeNardo (collectively referred to as "JARKD" by their students). Lizards can regenerate facial bones, certain areas of the spinal cord, and, as is most commonly known, most lizards can regenerate their tail - including muscles, cartilage, and spinal cord. The regenerated tail does not contain bone, but instead is supported by a tube of hyaline cartilage - the same cartilage humans have lining many of their joints. With widespread medical problems such as arthritis and spinal cord injuries, the application of these regenerative abilities is of extreme interest to medical institutions.
"Members of my family have terrible osteoarthritis," Kusumi explains. "That means the cartilage at the joints has degenerated. These lizards can regenerate that kind of cartilage, and they have no problem doing so. How is it that we can't do this, but they can?" With the help of the Anolis model, Kusumi and the rest of the JARKD team are delving into this mystery, recently funded by a $412,606 grant from the National Institutes of Health and a $225,000 grant from the Arizona Biomedical Research Commission.
Many vertebrate and invertebrate species can regenerate tissues, but there are several kinds of regeneration. Lizards most likely use stem-cell mediated regeneration, where new cells involved in regrowth arise from tissue-specific progenitor cells. This type of regeneration is the best bet for a regenerative process compatible with the human system, Kusumi says. Now that the Anolis carolinensis genome is sequenced, rather than trying to solve the puzzle blind, the research team has a view of the bigger picture as a guide to work from.
Molecular methods have improved to the point that the JARKD team is focusing on this question at the perfect time. Kusumi mused, "the beauty is that now we know enough about development that we can actually have candidates for what cells are making this new tail - we can have guesses as to what might be right." Using this candidate approach, Wilson-Rawls and graduate student Rajani George have successfully identified and isolated lizard cells that can make new muscle. Meanwhile, the Kusumi lab is working to uncover what developmental control genes are being expressed in regenerating tails. Here, with collaborators from the Translational Genomics Research Institute (TGen), JARKD is using RNA-Seq, a next-generation technology that allows researchers to take a more unbiased approach, finding all the genes being expressed in a tissue at one point in time. When compared with embryonic development of the tail, which is being investigated by graduate student Walter Eckalbar, differences between initial tissue generation and regenerative processes can be identified. The genes involved in regeneration are likely conserved across various taxonomic classes, but the genetic switches for those genes may be turned off or down. "Once we understand the nuts and bolts of how this is happening, we can use available technologies to manipulate and change that," Kusumi explains, "then we will try to translate that to the mouse model."
A regenerating mouse tail is only one of the many images inspired by Kusumi's Anolis studies. In concert with colleagues at the Smithsonian Tropical Research Institute (STRI) in Panama and Elizabeth Hutchins, one of Kusumi's graduate students, the JARKD team is adopting an evolutionary perspective of various Anolis processes or adaptations. "Occasionally you have a very unique opportunity to look at a natural experiment where one species arrived on one island or was isolated in a region, which then led to the adaptive radiation of many species to fill a variety of niches," Kusumi says. Anolis has in fact been described by some scientists as the "Darwin's finch" of reptiles. This reference points to the number and range of ecomorphs in the Anolis genus, as species have arisen in different regions bearing highly similar behaviors and morphology (also known as convergent evolution). While anoles have been the focus of many evolutionary studies, the JARKD-STRI team is focusing on the intersection of evolution and development, where "you can look for the regulatory changes that drove a limb to be longer or muscles to be more robust."
With such a bright road ahead for both the regenerative and evolutionary undertakings, Kusumi hopes ASU will lead internationally, as a center for the Anolis work. The opportunity to create such an interdisciplinary research program attracted him in part to School of Life Sciences in ASU's College of Liberal Arts and Sciences, which Kusumi describes as a place that "breaks down the walls between disciplines. Of course, the realization of this vision depends on complex collaborations, which Kusumi jokes are growing so large that listing those not involved may be easier. Kusumi's Anolis collaborations go well beyond JARKD, STRI, TGen and ASU, and also include some of Kusumi's undergraduate mentees. Glenn Markov, a Barrett's Honors College undergraduate and member of the School of Life Sciences Undergraduate Research (SOLUR) program, has spent two years contributing to the ground work of the regeneration project. Much like the tissue-specific process of human progenitor cells, each member of the collaborative team - whether undergraduate, graduate student, or faculty - makes unique contributions to ensure the creation of a functional end product.
Mark Twain once stated "a man who carries a cat by the tail learns something he can learn in no other way." In a similar vein, Kusumi, with lizard tail in hand, may hold the most likely key to unlock the secrets of medically applicable regeneration.
Source:
Margaret Coulombe
Arizona State University
Human regeneration is mainly limited to small portions of liver tissue, bone, or muscle, yet understanding how regeneration occurs in other taxonomic groups may enable scientists to improve human regenerative abilities in the future. Kusumi is working to understand the molecular processes that enable some lizards to regenerate their tissues with fellow ASU School of Life Sciences faculty members Jeanne Wilson-Rawls, Allan Rawls, Rebecca Fisher and Dale DeNardo (collectively referred to as "JARKD" by their students). Lizards can regenerate facial bones, certain areas of the spinal cord, and, as is most commonly known, most lizards can regenerate their tail - including muscles, cartilage, and spinal cord. The regenerated tail does not contain bone, but instead is supported by a tube of hyaline cartilage - the same cartilage humans have lining many of their joints. With widespread medical problems such as arthritis and spinal cord injuries, the application of these regenerative abilities is of extreme interest to medical institutions.
"Members of my family have terrible osteoarthritis," Kusumi explains. "That means the cartilage at the joints has degenerated. These lizards can regenerate that kind of cartilage, and they have no problem doing so. How is it that we can't do this, but they can?" With the help of the Anolis model, Kusumi and the rest of the JARKD team are delving into this mystery, recently funded by a $412,606 grant from the National Institutes of Health and a $225,000 grant from the Arizona Biomedical Research Commission.
Many vertebrate and invertebrate species can regenerate tissues, but there are several kinds of regeneration. Lizards most likely use stem-cell mediated regeneration, where new cells involved in regrowth arise from tissue-specific progenitor cells. This type of regeneration is the best bet for a regenerative process compatible with the human system, Kusumi says. Now that the Anolis carolinensis genome is sequenced, rather than trying to solve the puzzle blind, the research team has a view of the bigger picture as a guide to work from.
Molecular methods have improved to the point that the JARKD team is focusing on this question at the perfect time. Kusumi mused, "the beauty is that now we know enough about development that we can actually have candidates for what cells are making this new tail - we can have guesses as to what might be right." Using this candidate approach, Wilson-Rawls and graduate student Rajani George have successfully identified and isolated lizard cells that can make new muscle. Meanwhile, the Kusumi lab is working to uncover what developmental control genes are being expressed in regenerating tails. Here, with collaborators from the Translational Genomics Research Institute (TGen), JARKD is using RNA-Seq, a next-generation technology that allows researchers to take a more unbiased approach, finding all the genes being expressed in a tissue at one point in time. When compared with embryonic development of the tail, which is being investigated by graduate student Walter Eckalbar, differences between initial tissue generation and regenerative processes can be identified. The genes involved in regeneration are likely conserved across various taxonomic classes, but the genetic switches for those genes may be turned off or down. "Once we understand the nuts and bolts of how this is happening, we can use available technologies to manipulate and change that," Kusumi explains, "then we will try to translate that to the mouse model."
A regenerating mouse tail is only one of the many images inspired by Kusumi's Anolis studies. In concert with colleagues at the Smithsonian Tropical Research Institute (STRI) in Panama and Elizabeth Hutchins, one of Kusumi's graduate students, the JARKD team is adopting an evolutionary perspective of various Anolis processes or adaptations. "Occasionally you have a very unique opportunity to look at a natural experiment where one species arrived on one island or was isolated in a region, which then led to the adaptive radiation of many species to fill a variety of niches," Kusumi says. Anolis has in fact been described by some scientists as the "Darwin's finch" of reptiles. This reference points to the number and range of ecomorphs in the Anolis genus, as species have arisen in different regions bearing highly similar behaviors and morphology (also known as convergent evolution). While anoles have been the focus of many evolutionary studies, the JARKD-STRI team is focusing on the intersection of evolution and development, where "you can look for the regulatory changes that drove a limb to be longer or muscles to be more robust."
With such a bright road ahead for both the regenerative and evolutionary undertakings, Kusumi hopes ASU will lead internationally, as a center for the Anolis work. The opportunity to create such an interdisciplinary research program attracted him in part to School of Life Sciences in ASU's College of Liberal Arts and Sciences, which Kusumi describes as a place that "breaks down the walls between disciplines. Of course, the realization of this vision depends on complex collaborations, which Kusumi jokes are growing so large that listing those not involved may be easier. Kusumi's Anolis collaborations go well beyond JARKD, STRI, TGen and ASU, and also include some of Kusumi's undergraduate mentees. Glenn Markov, a Barrett's Honors College undergraduate and member of the School of Life Sciences Undergraduate Research (SOLUR) program, has spent two years contributing to the ground work of the regeneration project. Much like the tissue-specific process of human progenitor cells, each member of the collaborative team - whether undergraduate, graduate student, or faculty - makes unique contributions to ensure the creation of a functional end product.
Mark Twain once stated "a man who carries a cat by the tail learns something he can learn in no other way." In a similar vein, Kusumi, with lizard tail in hand, may hold the most likely key to unlock the secrets of medically applicable regeneration.
Source:
Margaret Coulombe
Arizona State University
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