In a first-of-its kind procedure, physicians have used stem cells taken from the fat tissue of a 14-year-old boy and combined them with growth protein and donor tissue to grow viable cheek bones in the teen.
The new procedure dramatically improves the options surgeons have for repairing bone deficiencies caused by traumatic injuries such as those from car accidents or soldiers wounded in battle or by disease and genetic conditions, according to Jesse Taylor, M.D., a surgeon and researcher in the Division of Craniofacial and Pediatric Plastic Surgery at Cincinnati Children's Hospital Medical Center. An estimated 7 million people in the United States have defects in bone continuity so severe that repair is difficult.
"We think this will benefit millions of people who, through traumatic injury or disease, have significant bone defects," Dr. Taylor explained. "The current methods we have like borrowing bone from another part of the body, or implanting cadaver bone or something artificial are reasonable alternatives, but far less than perfect."
Because the body rejects or absorbs implanted donor material, many reconstructive surgeries can have high failure rates. In procedures where bone is borrowed from one part of the body to replace another, the corrective surgery itself can be disfiguring to the person doctors are trying to help.
The new procedure avoids these problems because it uses the patient's own cells, Dr. Taylor explained. His team developed the procedure based in part on scientific research conducted in pigs at Cincinnati Children's. The operation is the first to blend and refine several techniques used or under study in surgical practice for repairing bone deficiencies.
The teenage recipient of the surgery, performed on May 28, has a rare genetic condition known as Treacher Collins syndrome, which includes underdeveloped or missing cheek bones. In this case the teenage patient, Brad Guilkey of Cincinnati, did not have developed zygomatic bones on either side of his face. The zygomatic bones form the prominence of the cheek and part of the outer rim of the eye socket.
The missing bones affected the active teenager's appearance, but more importantly put his eyes at increased risk of injury, Dr. Taylor said. The bones are supposed to surround most of the lower and side areas of the eye sockets, with a portion protruding toward the ear at the cranial base.
"This bone is critical structurally and acts as a shock absorber for the face, protecting the eyes and other critical structures in the event of facial impact," explained Dr. Taylor. "This young man is extremely active, he loves to play basketball and baseball, and growing new bone in this area of his craniofacial structure is critically important for him."
Dr. Taylor said the procedure has been successful and, more than four months after the surgery, computer tomography (CT) scans show the teenager's cheek bones have filled in normally with viable bone. The new bone structure enhances his appearance and improves protection for his eyes. Additional touchup surgery to the teenager's eye lids is under consideration to address a slight downward slant, also characteristic of Treacher Collins syndrome.
During the day-long operation, surgeons used a section of donor bone to craft what essentially were mineral-based scaffolding implants (known as allografts), which also served as a growth guide for the new bone. Surgeons drilled holes in the allografts, which then were filled with mesenchymal stem cells taken from the patient's abdominal fat. Also injected into the allografts was a growth protein called bone morphogenic protein-2 (BMP-2) that instructs the stem cells to become bone cells called osteoblasts.
One of nature's roles for mesenchymal stem cells is to become cell types for a variety of different tissues in the body - including connective tissue and bone - giving the body a ready reserve of replacement cells as older cells die. In the surgery, and in the earlier lab experiments involving pigs, the doctors used BMP-2 to jumpstart nature's normal process of transforming these malleable stem cells.
"We only need to use a fairly small amount of bone morphogenic protein to serve as a cue to tell the mesenchymal stem cells that they're going to become bone," explained Donna Jones, Ph.D., a researcher at Cincinnati Children's and part of the scientific team that conducted experiments leading to the procedure. "The actual molecular mechanisms BMP-2 uses to do this are not well understood, but once we use BMP-2 to start the process, the body's own biological processes take over and it produces its own BMP-2 to continue the transformation."
Particularly critical to that process is wrapping the donor allograft bone in a thin membrane of tissue that coats bone surfaces called periosteum. The periosteum used in this surgery was taken from the patient's thigh. Periosteum is important to the body's normal production of BMP-2, and just as vital to providing a blood supply to nourish new bone formation.
Drs. Taylor, Jones and their fellow researchers are conducting ongoing studies into growing mandible bones in pigs. In a research paper being prepared for peer-review journal publication, they explain the use of the procedure to grow viable, dense bone in the animals and the duplication of results numerous times. The researchers worked with pigs because the porcine immune system is very similar to that of humans, making the animals a good model for simulating engineered bone growth in people.
Peer-review presentations of results from aspects of the study results have occurred at national re-constructive surgery conferences including the American Association of Plastic Surgeons and the Plastic Surgery Research Council and received with great enthusiasm, said Christopher Runyan, M.D., Ph.D., a member of the research team at Cincinnati Children's.
The team also plans additional research projects to test the procedure's ability to engineer bones of different lengths and sizes. Drs. Taylor and Jones said the technology may have the potential to grow almost any bone in the human body. As for Brad, now 15, and his mother, Christine, they're just happy Brad can play sports and participate in other activities without having to worry about a lack of facial bone making him more susceptible to serious eye injury.
"Until we had the CT scans before surgery, we had no idea that Brad was missing the bones that protect his eyes, and that's very dangerous," said Christine. "I was nervous about the procedure, but we're glad we did it and amazed with the results. The people at Cincinnati Children's do a great job of explaining things to you and we have a lot of trust in the doctors and staff."
About Cincinnati Children's
Cincinnati Children's Hospital Medical Center is one of 10 children's hospitals in the United States to make the Honor Roll in U.S. News and World Reports 2009-10 America's Best Children's Hospitals issue. It is #1 ranked for digestive disorders and is also highly ranked for its expertise in respiratory diseases, cancer, neonatal care, heart care, neurosurgery, diabetes, orthopedics, kidney disorders and urology. One of the three largest children's hospitals in the U.S., Cincinnati Children's is affiliated with the University of Cincinnati College of Medicine and is one of the top two recipients of pediatric research grants from the National Institutes of Health.
President Barack Obama in June 2009 cited Cincinnati Children's as an "island of excellence" in health care. For its achievements in transforming health care, Cincinnati Children's is one of six U.S. hospitals since 2002 to be awarded the American Hospital Association-McKesson Quest for Quality Prize for leadership and innovation in quality, safety and commitment to patient care. The hospital is a national and international referral center for complex cases.
Source: Cincinnati Children's Hospital Medical Center
воскресенье, 31 июля 2011 г.
четверг, 28 июля 2011 г.
Bone May Be Repaired By Turning On Adult Stem Cells
The use of a drug to activate stem cells that differentiate into bone appears to cause regeneration of bone tissue and be may be a potential treatment strategy for osteoporosis, according to a report in the February 2008 Journal of Clinical Investigation. The study - led by researchers from Massachusetts General Hospital (MGH) and the Harvard Stem Cell Institute (HSCI) - found that treatment with a medication used to treat bone marrow cancer improved bone density in a mouse model of osteoporosis, apparently through its effect on the mesenchymal stem cells (MSCs) that differentiate into several types of tissues.
"Stem cell therapies are often thought of as putting new cells into the body, but this study suggests that medications can turn on existing stem cells that reside in the body's tissues, acting as regenerative medicines to enhance the body's own repair mechanisms," says David Scadden, MD, director of the MGH Center for Regenerative Medicine and HSCI co-director. "Drugs that direct immature cells to become a particular cell type, like in this study, could potentially be very useful."
The study was designed to examine whether the drug bortezamib (Bzb), which can alleviate bone destruction associated with the cancer multiple myeloma, could also regenerate bone damaged by non-cancerous conditions. In their first experiments, the researchers showed that treating mice with Bzb increased several factors associated with bone formation. Similar results were seen when cultured MSCs were treated with Bzb, but not when the drug was applied to cells that were committed to become particular cell types. Found in the bone marrow, MSCs have the potential to develop into the bone-building osteoblasts and several other types of cells - including cartilage, fat, skin and muscle.
Subsequent experiments supported the hypothesis that Bzb increases osteoblast activity and bone formation by acting on MSCs but not on more differentiated osteoblast precursors. Use of Bzb to treat a mouse model of menopausal osteoporosis produced significant improvements in bone formation and density. Since current treatments for osteoporosis - which target differentiated cells like osteoblasts and the osteoclasts that break down bone - have limitations, the ability to direct differentiation of MSCs could be a promising approach to treating osteoporosis and cancer-associated bone loss, the researchers note.
"If the paradigm displayed in this study holds true for other tissues, we may have options for repairing and regenerating sites affected by injury or disease with medications - that would be pretty exciting." says Scadden, who is the Gerald and Darlene Jordan Professor of Medicine at Harvard Medical School.
Siddhartha Mukherjee, MD, of the MGH Center for Regenerative Medicine (CRM) and HSCI is lead author of the study, which was supported by grants from the National Institutes of Health. Additional co-authors are Jesse Schoonmaker, David Seo, Joshua Aronson, and Louise Purton, PhD, MGH-CRM; Noopur Raje, MD, MB, MGH Cancer Center; Julie Liu, Jane Lian, PhD, and Gary Stein, PhD, University of Massachusetts Medical School; Teru Hideshima, MD, PhD, Sonia Vallet, MD, Samantha Pozzi, Shweta Chhetry, Mariateresa Fulciniti and Kenneth Anderson, MD, Dana-Farber Cancer Institute; Marc Wein, Dallas Jone, PhD, and Laurie Glimcher, MD, Harvard School of Public Health; and Mary Bouxsein, PhD, Beth Israel Deaconess Medical Center.
Massachusetts General Hospital (massgeneral/), established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $500 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, systems biology, transplantation biology and photomedicine.
Source: Sue McGreevey
Massachusetts General Hospital
"Stem cell therapies are often thought of as putting new cells into the body, but this study suggests that medications can turn on existing stem cells that reside in the body's tissues, acting as regenerative medicines to enhance the body's own repair mechanisms," says David Scadden, MD, director of the MGH Center for Regenerative Medicine and HSCI co-director. "Drugs that direct immature cells to become a particular cell type, like in this study, could potentially be very useful."
The study was designed to examine whether the drug bortezamib (Bzb), which can alleviate bone destruction associated with the cancer multiple myeloma, could also regenerate bone damaged by non-cancerous conditions. In their first experiments, the researchers showed that treating mice with Bzb increased several factors associated with bone formation. Similar results were seen when cultured MSCs were treated with Bzb, but not when the drug was applied to cells that were committed to become particular cell types. Found in the bone marrow, MSCs have the potential to develop into the bone-building osteoblasts and several other types of cells - including cartilage, fat, skin and muscle.
Subsequent experiments supported the hypothesis that Bzb increases osteoblast activity and bone formation by acting on MSCs but not on more differentiated osteoblast precursors. Use of Bzb to treat a mouse model of menopausal osteoporosis produced significant improvements in bone formation and density. Since current treatments for osteoporosis - which target differentiated cells like osteoblasts and the osteoclasts that break down bone - have limitations, the ability to direct differentiation of MSCs could be a promising approach to treating osteoporosis and cancer-associated bone loss, the researchers note.
"If the paradigm displayed in this study holds true for other tissues, we may have options for repairing and regenerating sites affected by injury or disease with medications - that would be pretty exciting." says Scadden, who is the Gerald and Darlene Jordan Professor of Medicine at Harvard Medical School.
Siddhartha Mukherjee, MD, of the MGH Center for Regenerative Medicine (CRM) and HSCI is lead author of the study, which was supported by grants from the National Institutes of Health. Additional co-authors are Jesse Schoonmaker, David Seo, Joshua Aronson, and Louise Purton, PhD, MGH-CRM; Noopur Raje, MD, MB, MGH Cancer Center; Julie Liu, Jane Lian, PhD, and Gary Stein, PhD, University of Massachusetts Medical School; Teru Hideshima, MD, PhD, Sonia Vallet, MD, Samantha Pozzi, Shweta Chhetry, Mariateresa Fulciniti and Kenneth Anderson, MD, Dana-Farber Cancer Institute; Marc Wein, Dallas Jone, PhD, and Laurie Glimcher, MD, Harvard School of Public Health; and Mary Bouxsein, PhD, Beth Israel Deaconess Medical Center.
Massachusetts General Hospital (massgeneral/), established in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $500 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, systems biology, transplantation biology and photomedicine.
Source: Sue McGreevey
Massachusetts General Hospital
понедельник, 25 июля 2011 г.
New Type Of Genetic Change Identified In Inherited Cancer
Duke University Medical Center and National Cancer Institute scientists have discovered that a novel genetic alteration - a second copy of an entire gene - is a cause of familial chordoma, an uncommon form of cancer arising in bones and frequently affecting the nervous system.
Inherited differences in gene copy number, known as copy number variation (CNV), have been implicated in some hereditary diseases but none of the previously discovered familial cancer genes has had CNV as the genetic change.
"This alteration is unlike anything we have ever seen before in families that tend to develop the same kind of cancers," says Michael Kelley, M.D., an associate professor at Duke University Medical Center and senior author of the study appearing in Nature Genetics. "We are not talking about a mutation in a single gene, but the duplication of an entire gene. This discovery is a classic example of where science answers one question but raises many, many more."
Chordoma is rare, striking only one in every million people. But it is a devastating diagnosis. People who have the disorder typically develop tumors at the base of the skull, in the pelvis, or along the spinal column. The growths are thought to arise from remnants of the notochord, an embryonic precursor to spinal column. There are few treatments and no cure for chordoma; most who have the disease usually die within 10 years.
Kelley, chief of hematology and oncology at the Durham Veterans Affairs Medical Center, has been studying chordoma for years after a collaborator at the National Cancer Institute, Dilys Parry, a co-author of the study, discovered a family with a history of the disease spanning several generations. They concluded that there had to be some sort of inherited genetic defect at work. Parry conducted clinical studies that eventually identified six additional families with multiple relatives with chordoma.
Initial work focused on possible defects on chromosome 7, but no defect was found that was shared by all of those affected. Researchers conducted linkage studies that revealed six new areas in the genome where potential mutations were likely. But it wasn't until they used a technique called array comparative genomic hybridization, a method that allowed them to see structural changes in the genome in exquisite detail, that they were able to pinpoint the source of the culprit. They identified it as the T (Brachyury) gene on chromosome 6.
"Brachyury is a transcription factor that helps regulate the development of the notochord and we know the gene is overly active in the tumor tissue in many people with chordoma," says Kelley, "so we were pretty sure we were on to something."
Investigators screened 65 individuals (21 with chordoma) in seven families with a history of the disease, specifically looking for any alterations in the T gene. They discovered that all the patients with chordoma in four of the seven families had a second copy of the T gene. The duplication did not appear among members of the three other families, nor did it appear in 100 healthy, normal controls.
Kelley says investigators do not understand what Brachyury does to cause chordoma. Brachyury expression was found in tissue from chordomas not only in patients who had inherited the duplication but also in those who did not have the duplication.
"It is likely that other genes are at work here, or that some other mechanism we do not yet understand is in play. Based on our research, however, we do feel that it may be worthwhile to screen for complex genomic rearragements when trying to find the cause of familial cancers. It may be a more productive route than traditional gene-mapping methods."
Xiaohong Yang of the National Cancer Institute wrote the first draft of the paper, and along with David Ng, also of the NCI, analyzed the data. Ng, Sufeng Li, Kelly and David Alcorta, all of Duke, performed the laboratory studies including genotyping, sequencing and breakpoint evaluation. Parry, Ng, Eamonn Sheridan of St. James Hospital in Leeds, UK, and Norbert Liebsch, from Massachusetts General Hospital, identified and evaluated the chordoma families. Yang, Ng, Kelley, Parry and Alisa Goldstein planned the work and interpreted the results.
The study was funded by the U.S. Department of Veterans Affairs, the National Cancer Institute and the Chordoma Foundation.
Source:
Michelle Gailiun
Duke University Medical Center
Inherited differences in gene copy number, known as copy number variation (CNV), have been implicated in some hereditary diseases but none of the previously discovered familial cancer genes has had CNV as the genetic change.
"This alteration is unlike anything we have ever seen before in families that tend to develop the same kind of cancers," says Michael Kelley, M.D., an associate professor at Duke University Medical Center and senior author of the study appearing in Nature Genetics. "We are not talking about a mutation in a single gene, but the duplication of an entire gene. This discovery is a classic example of where science answers one question but raises many, many more."
Chordoma is rare, striking only one in every million people. But it is a devastating diagnosis. People who have the disorder typically develop tumors at the base of the skull, in the pelvis, or along the spinal column. The growths are thought to arise from remnants of the notochord, an embryonic precursor to spinal column. There are few treatments and no cure for chordoma; most who have the disease usually die within 10 years.
Kelley, chief of hematology and oncology at the Durham Veterans Affairs Medical Center, has been studying chordoma for years after a collaborator at the National Cancer Institute, Dilys Parry, a co-author of the study, discovered a family with a history of the disease spanning several generations. They concluded that there had to be some sort of inherited genetic defect at work. Parry conducted clinical studies that eventually identified six additional families with multiple relatives with chordoma.
Initial work focused on possible defects on chromosome 7, but no defect was found that was shared by all of those affected. Researchers conducted linkage studies that revealed six new areas in the genome where potential mutations were likely. But it wasn't until they used a technique called array comparative genomic hybridization, a method that allowed them to see structural changes in the genome in exquisite detail, that they were able to pinpoint the source of the culprit. They identified it as the T (Brachyury) gene on chromosome 6.
"Brachyury is a transcription factor that helps regulate the development of the notochord and we know the gene is overly active in the tumor tissue in many people with chordoma," says Kelley, "so we were pretty sure we were on to something."
Investigators screened 65 individuals (21 with chordoma) in seven families with a history of the disease, specifically looking for any alterations in the T gene. They discovered that all the patients with chordoma in four of the seven families had a second copy of the T gene. The duplication did not appear among members of the three other families, nor did it appear in 100 healthy, normal controls.
Kelley says investigators do not understand what Brachyury does to cause chordoma. Brachyury expression was found in tissue from chordomas not only in patients who had inherited the duplication but also in those who did not have the duplication.
"It is likely that other genes are at work here, or that some other mechanism we do not yet understand is in play. Based on our research, however, we do feel that it may be worthwhile to screen for complex genomic rearragements when trying to find the cause of familial cancers. It may be a more productive route than traditional gene-mapping methods."
Xiaohong Yang of the National Cancer Institute wrote the first draft of the paper, and along with David Ng, also of the NCI, analyzed the data. Ng, Sufeng Li, Kelly and David Alcorta, all of Duke, performed the laboratory studies including genotyping, sequencing and breakpoint evaluation. Parry, Ng, Eamonn Sheridan of St. James Hospital in Leeds, UK, and Norbert Liebsch, from Massachusetts General Hospital, identified and evaluated the chordoma families. Yang, Ng, Kelley, Parry and Alisa Goldstein planned the work and interpreted the results.
The study was funded by the U.S. Department of Veterans Affairs, the National Cancer Institute and the Chordoma Foundation.
Source:
Michelle Gailiun
Duke University Medical Center
пятница, 22 июля 2011 г.
Leptin-Serotonin Pathway Offers New Clues For Obesity And Osteoporosis Prevention
New research from Columbia University Medical Center has illuminated a previously unknown leptin-serotonin pathway in the brain that simultaneously promotes appetite and bone mass accrual. The research, which explains how leptin - well-known appetite-suppressing hormone - acts in the brain, is published in the Sept. 4 issue of Cell.
When the leptin-serotonin pathway is turned on in mice, the researchers found, appetite increases, the animals eat more, gain weight, and their bone mass increases. When the pathway is turned off, mice eat less, lose weight, and their bones weaken. Furthermore, leptin was found to not act in the hypothalamus as previously thought, but in the brain stem acting on serotonin, a hormone that in the brain acts to control appetite, mood and anger.
The identification of this pathway helps explain why, as doctors have long known, obese people tend to have a significantly lower prevalence of osteoporosis, says the study's senior author, Gerard Karsenty, M.D., Ph.D., chair of the Department of Genetics & Development at Columbia University's College of Physician and Surgeons. Though obese people produce high levels of leptin, they are resistant, or unresponsive, to its signals - instead, they operate in a false state of leptin deficiency, which increases serotonin - and thereby, appetite and bone mass. Dr. Karsenty points out that these current findings may have more influence on developing a new way to reduce appetite and obesity than preventing osteoporosis.
"It will be difficult to turn on the pathway to strengthen bone without increasing appetite at the same time," Dr. Karsenty said. "But this finding shows that it is feasible to alter parts of the leptin-serotonin pathway to decrease appetite without weakening bone."
HORMONE LEPTIN SUPRESSES BONE FORMATION BY SHUTTING OFF SEROTONIN
Dr. Karsenty and his colleagues discovered this pathway after first noticing the powerful effect of leptin - known for suppressing appetite - on bone mass accrual. Dr. Karsenty previously discovered that leptin is the most powerful inhibitor of bone formation in the body. This new study reveals that high levels of leptin suppress bone formation by shutting off the synthesis of serotonin in certain neurons in the brainstem.
Dr. Karsenty and his colleagues were surprised to observe that increased serotonin in the brainstem also increased appetite in mice. "We previously thought that leptin's modes of action on appetite and bone mass accrual were distinct," Dr. Karsenty said. "But we found instead that they behave more like twins - taking the same pathway through the brainstem. This correlates strikingly with the fact that leptin appears during evolution of bone cells when bone is first formed in the body."
Dr. Karsenty's team found that the appetite and bone pathways diverge once serotonin is released: one set of serotonin receptors turns on appetite, while a second increases bone mass accrual.
The findings may open the door for weight loss drugs that have no side effects on bone density.
"Theoretically, one can imagine that a drug that blocks only the appetite receptors, but not the bone receptors, could help people lose weight without losing bone mass," Dr. Karsenty said.
Dr. Karsenty explained the surprising link between appetite and the skeleton by noting that the pathway monitors the amount of energy available to maintain bone.
"Our bones are constantly broken down and rebuilt during our lifetimes, and those renovations require an enormous and daily supply of energy," he said.
DISCOVERY CLARIFIES PREVIOUS RESEARCH; ADDS TO WORK ON BONE
In November 2008, Dr. Karsenty published a paper in Cell, which describes how serotonin released from the gut controls bone formation. Unlike the brain's serotonin, an increase in gut serotonin impairs bone formation. (A press release about the Nov. 2008 finding is available at: cumc.columbia/news/press_releases/Karsenty-cell-serotonin-lrp5.html.)
Dr. Karsenty's new research shows that while both derivations of serotonin influence bone mass, the brain's serotonin dominates the effect of serotonin from the gut.
LEPTIN-SEROTONIN PATHWAY MAY ALSO EXPLAIN OSTEOPOROSIS/ANTI-DEPRESSANT LINK
In some studies, selective serotonin reuptake inhibitors (SSRIs), which are commonly used to treat depression, have been associated with osteoporosis in some patients.
SSRIs enhance the action of serotonin, and depending on the person, that may lead to weakened, or strengthened bones, says study co-author J. John Mann, M.D., Ph.D., professor of translational neuroscience (in psychiatry and in radiology) and vice chair for Research in the Department of Psychiatry at Columbia University Medical Center and the New York State Psychiatric Institute.
"SSRIs work in the brain and in the gut, but in some people they may work more strongly in the gut," Dr. Mann said. "In that case, SSRIs could lead to a decrease in bone growth and osteoporosis."
The hope is that these research findings will help explain this phenomena and lead to potential treatment for this side effect.
Source:
Elizabeth Streich
Columbia University Medical Center
When the leptin-serotonin pathway is turned on in mice, the researchers found, appetite increases, the animals eat more, gain weight, and their bone mass increases. When the pathway is turned off, mice eat less, lose weight, and their bones weaken. Furthermore, leptin was found to not act in the hypothalamus as previously thought, but in the brain stem acting on serotonin, a hormone that in the brain acts to control appetite, mood and anger.
The identification of this pathway helps explain why, as doctors have long known, obese people tend to have a significantly lower prevalence of osteoporosis, says the study's senior author, Gerard Karsenty, M.D., Ph.D., chair of the Department of Genetics & Development at Columbia University's College of Physician and Surgeons. Though obese people produce high levels of leptin, they are resistant, or unresponsive, to its signals - instead, they operate in a false state of leptin deficiency, which increases serotonin - and thereby, appetite and bone mass. Dr. Karsenty points out that these current findings may have more influence on developing a new way to reduce appetite and obesity than preventing osteoporosis.
"It will be difficult to turn on the pathway to strengthen bone without increasing appetite at the same time," Dr. Karsenty said. "But this finding shows that it is feasible to alter parts of the leptin-serotonin pathway to decrease appetite without weakening bone."
HORMONE LEPTIN SUPRESSES BONE FORMATION BY SHUTTING OFF SEROTONIN
Dr. Karsenty and his colleagues discovered this pathway after first noticing the powerful effect of leptin - known for suppressing appetite - on bone mass accrual. Dr. Karsenty previously discovered that leptin is the most powerful inhibitor of bone formation in the body. This new study reveals that high levels of leptin suppress bone formation by shutting off the synthesis of serotonin in certain neurons in the brainstem.
Dr. Karsenty and his colleagues were surprised to observe that increased serotonin in the brainstem also increased appetite in mice. "We previously thought that leptin's modes of action on appetite and bone mass accrual were distinct," Dr. Karsenty said. "But we found instead that they behave more like twins - taking the same pathway through the brainstem. This correlates strikingly with the fact that leptin appears during evolution of bone cells when bone is first formed in the body."
Dr. Karsenty's team found that the appetite and bone pathways diverge once serotonin is released: one set of serotonin receptors turns on appetite, while a second increases bone mass accrual.
The findings may open the door for weight loss drugs that have no side effects on bone density.
"Theoretically, one can imagine that a drug that blocks only the appetite receptors, but not the bone receptors, could help people lose weight without losing bone mass," Dr. Karsenty said.
Dr. Karsenty explained the surprising link between appetite and the skeleton by noting that the pathway monitors the amount of energy available to maintain bone.
"Our bones are constantly broken down and rebuilt during our lifetimes, and those renovations require an enormous and daily supply of energy," he said.
DISCOVERY CLARIFIES PREVIOUS RESEARCH; ADDS TO WORK ON BONE
In November 2008, Dr. Karsenty published a paper in Cell, which describes how serotonin released from the gut controls bone formation. Unlike the brain's serotonin, an increase in gut serotonin impairs bone formation. (A press release about the Nov. 2008 finding is available at: cumc.columbia/news/press_releases/Karsenty-cell-serotonin-lrp5.html.)
Dr. Karsenty's new research shows that while both derivations of serotonin influence bone mass, the brain's serotonin dominates the effect of serotonin from the gut.
LEPTIN-SEROTONIN PATHWAY MAY ALSO EXPLAIN OSTEOPOROSIS/ANTI-DEPRESSANT LINK
In some studies, selective serotonin reuptake inhibitors (SSRIs), which are commonly used to treat depression, have been associated with osteoporosis in some patients.
SSRIs enhance the action of serotonin, and depending on the person, that may lead to weakened, or strengthened bones, says study co-author J. John Mann, M.D., Ph.D., professor of translational neuroscience (in psychiatry and in radiology) and vice chair for Research in the Department of Psychiatry at Columbia University Medical Center and the New York State Psychiatric Institute.
"SSRIs work in the brain and in the gut, but in some people they may work more strongly in the gut," Dr. Mann said. "In that case, SSRIs could lead to a decrease in bone growth and osteoporosis."
The hope is that these research findings will help explain this phenomena and lead to potential treatment for this side effect.
Source:
Elizabeth Streich
Columbia University Medical Center
вторник, 19 июля 2011 г.
Aging Motorcyclists Hit The Road, But At Greater Risk Of Injury, Death
Motorcycle riders across the country are growing older, and the impact of this trend is evident in emergency rooms daily. Doctors are finding that these aging road warriors are more likely to be injured or die as a result of a motorcycle mishap compared to their younger counterparts.
While the typical injured motorcyclist has long been thought of as a young, otherwise healthy victim of sudden injury, a study from the University of Rochester Medical Center suggests otherwise. Between 1996 and 2005, researchers found the average age of motorcyclists involved in crashes increased from approximately 34 to 39 years, and the proportion of injured riders above the age of 40 increased from around 28 percent to close to 50 percent. Of all injured riders included in the study, 50- to 59-year-olds represented the fastest growing group, while 20- to 29-year-olds were the most rapidly declining.
"We made the clinical observation that older patients - people in their 50's, 60's and even 70's - were being injured on motorcycles with increasing frequency," said Mark Gestring, M.D., director of the trauma program at the University of Rochester Medical Center. "We wanted to see if this observation was true on a national level and we found that it was."
For riders above the age of 40, injury severity, length of stay in the hospital or intensive care unit, and mortality were higher compared to riders below the age of 40. The risk of dying was one-and-a-half to two times more likely in riders over 40, based on the severity of the original injury. The study also found that older riders are more likely to die from less severe injuries than younger riders, to spend at least 24 hours in the intensive care unit, and to have more pre-existing co-morbidities and complications, such as heart attack and infections, that contribute to longer hospital stays.
"Treating a 60-year-old who has been in a motorcycle accident is very different from treating a 21-year-old who has been in a similar accident - 60-year-olds bring a lot more medical baggage with them, and this can adversely impact outcomes following injury," said Gestring. "As people start to dust off their motorcycles this spring, older riders should take an extra measure of caution; if an accident happens they'll often pay a higher price than younger riders."
The increase in injury severity for older riders may be related to the reduced capacity to withstand injury as the body ages. Age-related changes, such as decreases in bone strength and brain size, may make older riders more susceptible to injury. Other factors associated with aging, such as impaired vision, delayed reaction time, and altered balance contribute to motorcycle crashes in this population, explaining in part the researchers' finding that older riders crashed more often as a result of loss of control than younger riders.
In the study, which was published in the March issue of the American Surgeon, researchers using the National Trauma Databank reviewed the records of 61,689 motorcyclists aged 17 to 89 years involved in a motorcycle crash between 1996 and 2005. The average age of motorcyclists involved in crashes steadily increased over the study period, which is consistent with published statistics from the Motorcycle Industry Council which report that the average age of motorcycle ownership rose from 33 years in 1998 to 40 years in 2003.
Injury patterns remained stable over the study period, with extremity fractures, such as broken arms and legs, being the most common injuries, occurring in approximately 25 to 40 percent of motorcyclists studied. The majority of severe injuries were chest and head injuries, and researchers found significantly higher proportions of older riders sustained these types of injuries compared to younger riders.
The younger and older riders did have two things in common: helmet use and alcohol use. Overall helmet use was around 73 percent for both groups, and alcohol use was seen in approximately one third of injured motorcyclists, with no significant difference between the older and younger riders.
Alcohol use and helmet use have been linked in prior reports, with intoxicated drivers less likely to be wearing a helmet and therefore at greater risk for injury and death. It is not surprising that the researchers at the University of Rochester found that riders who tested positive for alcohol use were two-and-a-half times more likely to not be wearing a helmet at the time of injury. Despite abundant evidence that helmets reduce mortality, brain injury, length of hospital stay and economic burden, only 20 states have universal helmet laws.
Motorcycle crashes are a significant cause of injury and death on our nation's roadways, despite the fact that motorcycles are responsible for only a small fraction of the total miles traveled annually in the United States. The authors say that the study provides justification for expanding the scope of motorcycle safety research, education and training initiatives to specifically target the older motorcyclist.
"At the University of Rochester, we are looking at the development of prevention programs targeting motorcycle safety for older individuals, possibly in partnership with local motorcycle clubs and other interested groups," said Gestring.
In addition to Gestring, Joshua B. Brown, Paul E. Bankey, M.D., Ph.D., John T. Gorczyca, M.D., Julius D. Cheng, M.D., and Nicole A. Stassen, M.D., from the departments of Surgery and Orthopaedics and the Strong Regional Trauma Center at the University of Rochester Medical Center also contributed to the study.
Source:
Emily Butler
University of Rochester Medical Center
While the typical injured motorcyclist has long been thought of as a young, otherwise healthy victim of sudden injury, a study from the University of Rochester Medical Center suggests otherwise. Between 1996 and 2005, researchers found the average age of motorcyclists involved in crashes increased from approximately 34 to 39 years, and the proportion of injured riders above the age of 40 increased from around 28 percent to close to 50 percent. Of all injured riders included in the study, 50- to 59-year-olds represented the fastest growing group, while 20- to 29-year-olds were the most rapidly declining.
"We made the clinical observation that older patients - people in their 50's, 60's and even 70's - were being injured on motorcycles with increasing frequency," said Mark Gestring, M.D., director of the trauma program at the University of Rochester Medical Center. "We wanted to see if this observation was true on a national level and we found that it was."
For riders above the age of 40, injury severity, length of stay in the hospital or intensive care unit, and mortality were higher compared to riders below the age of 40. The risk of dying was one-and-a-half to two times more likely in riders over 40, based on the severity of the original injury. The study also found that older riders are more likely to die from less severe injuries than younger riders, to spend at least 24 hours in the intensive care unit, and to have more pre-existing co-morbidities and complications, such as heart attack and infections, that contribute to longer hospital stays.
"Treating a 60-year-old who has been in a motorcycle accident is very different from treating a 21-year-old who has been in a similar accident - 60-year-olds bring a lot more medical baggage with them, and this can adversely impact outcomes following injury," said Gestring. "As people start to dust off their motorcycles this spring, older riders should take an extra measure of caution; if an accident happens they'll often pay a higher price than younger riders."
The increase in injury severity for older riders may be related to the reduced capacity to withstand injury as the body ages. Age-related changes, such as decreases in bone strength and brain size, may make older riders more susceptible to injury. Other factors associated with aging, such as impaired vision, delayed reaction time, and altered balance contribute to motorcycle crashes in this population, explaining in part the researchers' finding that older riders crashed more often as a result of loss of control than younger riders.
In the study, which was published in the March issue of the American Surgeon, researchers using the National Trauma Databank reviewed the records of 61,689 motorcyclists aged 17 to 89 years involved in a motorcycle crash between 1996 and 2005. The average age of motorcyclists involved in crashes steadily increased over the study period, which is consistent with published statistics from the Motorcycle Industry Council which report that the average age of motorcycle ownership rose from 33 years in 1998 to 40 years in 2003.
Injury patterns remained stable over the study period, with extremity fractures, such as broken arms and legs, being the most common injuries, occurring in approximately 25 to 40 percent of motorcyclists studied. The majority of severe injuries were chest and head injuries, and researchers found significantly higher proportions of older riders sustained these types of injuries compared to younger riders.
The younger and older riders did have two things in common: helmet use and alcohol use. Overall helmet use was around 73 percent for both groups, and alcohol use was seen in approximately one third of injured motorcyclists, with no significant difference between the older and younger riders.
Alcohol use and helmet use have been linked in prior reports, with intoxicated drivers less likely to be wearing a helmet and therefore at greater risk for injury and death. It is not surprising that the researchers at the University of Rochester found that riders who tested positive for alcohol use were two-and-a-half times more likely to not be wearing a helmet at the time of injury. Despite abundant evidence that helmets reduce mortality, brain injury, length of hospital stay and economic burden, only 20 states have universal helmet laws.
Motorcycle crashes are a significant cause of injury and death on our nation's roadways, despite the fact that motorcycles are responsible for only a small fraction of the total miles traveled annually in the United States. The authors say that the study provides justification for expanding the scope of motorcycle safety research, education and training initiatives to specifically target the older motorcyclist.
"At the University of Rochester, we are looking at the development of prevention programs targeting motorcycle safety for older individuals, possibly in partnership with local motorcycle clubs and other interested groups," said Gestring.
In addition to Gestring, Joshua B. Brown, Paul E. Bankey, M.D., Ph.D., John T. Gorczyca, M.D., Julius D. Cheng, M.D., and Nicole A. Stassen, M.D., from the departments of Surgery and Orthopaedics and the Strong Regional Trauma Center at the University of Rochester Medical Center also contributed to the study.
Source:
Emily Butler
University of Rochester Medical Center
суббота, 16 июля 2011 г.
Dietary Calcium Could Possibly Prevent The Spread Of Breast Cancer To Bone
A strong skeleton is less likely to be penetrated by metastasizing cancer cells, so a fortified glass of milk might be the way to block cancer's spread, according to researchers at the ANZAC Research Institute in Concord, Australia. Using a mouse model of breast cancer metastasis, the researchers found that a calcium deficiency may increase the tendency of advanced breast cancer to target bone. Dietary calcium, they reason, might help prevent the spread of breast cancer to bone and serve as an adjuvant treatment during therapy.
Their findings are presented in the Oct. 1 issue of Cancer Research, a journal of the American Association for Cancer Research.
According to the researchers, about 70 percent of patients who develop advanced breast cancer will have secondary tumors in the bone. The spread of cancer to bones leads to cellular processes that physically break down existing bone, leading to further pain and illness. In fact, the breakdown of bone and subsequent bone re-growth forms what senior author Colin R. Dunstan, Ph.D., terms a "vicious cycle" that turns bone into an environment conducive to cancer growth.
To better understand the role of bone turnover in the spread of cancer, Dunstan and his team compared the effects of a low- and high-calcium diet in mice. They found that dietary calcium deficiency independent of the chemical factors that control turnover was related to a significantly higher increase in cancer cell proliferation and the total proportion of bone that had been penetrated.
"These results could have implications for patients with breast cancer bone metastases or who are at high risk for developing metastatic disease," Dunstan said. "Many older women in our community are known to be calcium deficient due to low calcium dietary intake or due to vitamin D deficiency. These women could be at increased risk for the devastating effects of bone metastases."
According to Dunstan, his results call for further, directed clinical trials "to investigate how calcium and vitamin D status influence progression to metastatic disease, and to determine if corrections of calcium and vitamin D deficiencies are important in breast cancer patients."
The ANZAC Research Institute study was funded by the National Health and Medical Research Council of Australia and the New South Wales Government
The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes nearly 26,000 basic, translational, and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 70 other countries. AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants. The AACR Annual Meeting attracts more than 17,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment, and patient care. AACR publishes five major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. Its most recent publication, CR, is a magazine for cancer survivors, patient advocates, their families, physicians, and scientists. It provides a forum for sharing essential, evidence-based information and perspectives on progress in cancer research, survivorship, and advocacy.
American Association for Cancer Research (AACR)
615 Chestnut Street, 17th Floor
Philadelphia, PA 19106
United States
aacr
Their findings are presented in the Oct. 1 issue of Cancer Research, a journal of the American Association for Cancer Research.
According to the researchers, about 70 percent of patients who develop advanced breast cancer will have secondary tumors in the bone. The spread of cancer to bones leads to cellular processes that physically break down existing bone, leading to further pain and illness. In fact, the breakdown of bone and subsequent bone re-growth forms what senior author Colin R. Dunstan, Ph.D., terms a "vicious cycle" that turns bone into an environment conducive to cancer growth.
To better understand the role of bone turnover in the spread of cancer, Dunstan and his team compared the effects of a low- and high-calcium diet in mice. They found that dietary calcium deficiency independent of the chemical factors that control turnover was related to a significantly higher increase in cancer cell proliferation and the total proportion of bone that had been penetrated.
"These results could have implications for patients with breast cancer bone metastases or who are at high risk for developing metastatic disease," Dunstan said. "Many older women in our community are known to be calcium deficient due to low calcium dietary intake or due to vitamin D deficiency. These women could be at increased risk for the devastating effects of bone metastases."
According to Dunstan, his results call for further, directed clinical trials "to investigate how calcium and vitamin D status influence progression to metastatic disease, and to determine if corrections of calcium and vitamin D deficiencies are important in breast cancer patients."
The ANZAC Research Institute study was funded by the National Health and Medical Research Council of Australia and the New South Wales Government
The mission of the American Association for Cancer Research is to prevent and cure cancer. Founded in 1907, AACR is the world's oldest and largest professional organization dedicated to advancing cancer research. The membership includes nearly 26,000 basic, translational, and clinical researchers; health care professionals; and cancer survivors and advocates in the United States and more than 70 other countries. AACR marshals the full spectrum of expertise from the cancer community to accelerate progress in the prevention, diagnosis and treatment of cancer through high-quality scientific and educational programs. It funds innovative, meritorious research grants. The AACR Annual Meeting attracts more than 17,000 participants who share the latest discoveries and developments in the field. Special Conferences throughout the year present novel data across a wide variety of topics in cancer research, treatment, and patient care. AACR publishes five major peer-reviewed journals: Cancer Research; Clinical Cancer Research; Molecular Cancer Therapeutics; Molecular Cancer Research; and Cancer Epidemiology, Biomarkers & Prevention. Its most recent publication, CR, is a magazine for cancer survivors, patient advocates, their families, physicians, and scientists. It provides a forum for sharing essential, evidence-based information and perspectives on progress in cancer research, survivorship, and advocacy.
American Association for Cancer Research (AACR)
615 Chestnut Street, 17th Floor
Philadelphia, PA 19106
United States
aacr
среда, 13 июля 2011 г.
Bone Up On Calcium-Rich Foods To Prevent Osteoporosis
Osteoporosis, a disease
characterized by low bone mass that often leads to fractures of the hip,
spine and wrist, affects more than 5 million Californians, most of whom are
women.(1) In observation of World Osteoporosis Day on October 20, Dairy
Council of California offers tips to help women and their families reduce
their risk of osteoporosis throughout their lifetimes by eating a healthy
diet rich in calcium and other bone-building nutrients, and participating
in weight-bearing cardiovascular activities.
An estimated 55,000 osteoporosis-related fractures occur annually in
California, and treatment costs for these incidents exceed $2.4 billion.(2)
Although its effects are not realized until later in life, inadequate
calcium intake and lack of physical activity during childhood and
adolescence are among the factors that significantly increase the risk of
developing osteoporosis. There is no known cure for osteoporosis, but
evidence shows that prevention, early diagnosis and treatment can address
the prevalence and debilitating effects of this disease.(3) By using a
whole-family approach to bone-building foods and activities, younger
children will benefit by building peak bone mass while they are young and
adults may reduce the rate of bone density loss later in life.
"Parents have total control over what their child eats, drinks and does
from the time they are born until they start school, so early childhood is
the best time to make milk, dairy products and activity part of the family
lifestyle," said Laura K. Bachrach, M.D., professor of pediatrics at
Stanford Medical Center. "I think parents give up on dairy too quickly.
They may not realize the impact that this decision could have on their
children's health later in life."
Meals Matter (mealsmatter), Dairy Council of California's
online consumer meal planning and nutrition resource, features an
interactive Calcium Quiz to determine whether daily food choices provide
adequate calcium. The tool can be individualized for each member of the
family, as calcium needs change based on factors like age, gender and
supplement use. An important window of opportunity for building a lifetime
of strong bones occurs from roughly age 9 to 14, when the body is growing
and can most rapidly gain bone-building minerals. Peak bone mass, the
strongest the bones will ever be, is reached by mid to late 20s. During
this window, children and adolescents need three to four servings of dairy
a day for optimal bone-building gains. Because adolescence is typically
when teens forgo milk and dairy products for sodas and other snack foods,
early family reinforcement and lifestyle adoption is very important.
"Without a doubt, milk and dairy products are the best sources of
calcium and vitamin D in the American diet, so parents need to be creative
in their efforts to put dairy into their children's diets," said Bachrach.
"Focus on real foods like milk, cheese, yogurt or pudding before turning to
supplements."
Beyond providing calcium and vitamin D, milk and dairy products are
also high in essential vitamins and nutrients like potassium, phosphorus,
magnesium and protein. Try pairing dairy products with other foods
containing calcium like broccoli, almonds, beans, kale and
calcium-fortified foods. For instance, a side dish of broccoli with melted
cheese and sliced almonds is a bone-building bonanza.
"Exercise is the other piece of the bone-building puzzle," explains
Bachrach. "Turn off the T.V., head to the park and get those growing bones
moving!"
Exercise and exposure to sunlight are also important bone-building
factors. At least 30 minutes of weight-bearing exercise like playing tag or
hide-and-seek, walking, jumping rope, tennis or yoga most days of the week
will help strengthen bones, and exercising outdoors can double the
bone-building benefits. Sunlight allows the body to produce vitamin D,
which the body needs to absorb calcium. Vitamin D also protects against
soft, misshapen bones called rickets in children and osteomalacia in
adults.
In addition to the Calcium Quiz, Meals Matter (mealsmatter)
offers many quick and delicious recipes to bone up on calcium-rich foods.
About Dairy Council of California
Dairy Council of California develops nutrition education programs that
are easy to use and designed to be personally relevant to each user. This
customization allows consumers to make decisions considering their unique
needs, resulting in healthy food choices and contributing to optimal
health.
Sweet Apricots and Roasted Chicken in Pasta
From the California Apricot Advisory Board
Ingredients
1 (19 ounce) package bow tie noodles
1 1/2 cups low-fat milk
2 chicken breast halves; boned, skinned, roasted and sliced
1 (17 ounce) can California apricot halves, drained and quartered
1/3 cup chopped green onions
2 tablespoons butter
salt and pepper to taste
Preparation
Cook noodles according to package directions; drain. In medium
saucepan, simmer milk for 4 minutes. Add chicken, apricots, onions and
butter; continue simmering for 2 minutes. Pour over pasta in large bowl;
toss gently to coat. Season with salt and pepper to taste and serve
immediately.
(1) California Osteoporosis Prevention and Education Program Home Page. Chief,
M.P.H. Alongi, Jeanne. California Osteoporosis Prevention and Education
Program. 15 Oct. 2006.
dhs.ca/CDIC/cdcb/Medicine/Gerontology/OAUnit/html/COPE.htm.
(2) Ibid
(3) Ibid
Dairy Council of California
dairycouncilofca
characterized by low bone mass that often leads to fractures of the hip,
spine and wrist, affects more than 5 million Californians, most of whom are
women.(1) In observation of World Osteoporosis Day on October 20, Dairy
Council of California offers tips to help women and their families reduce
their risk of osteoporosis throughout their lifetimes by eating a healthy
diet rich in calcium and other bone-building nutrients, and participating
in weight-bearing cardiovascular activities.
An estimated 55,000 osteoporosis-related fractures occur annually in
California, and treatment costs for these incidents exceed $2.4 billion.(2)
Although its effects are not realized until later in life, inadequate
calcium intake and lack of physical activity during childhood and
adolescence are among the factors that significantly increase the risk of
developing osteoporosis. There is no known cure for osteoporosis, but
evidence shows that prevention, early diagnosis and treatment can address
the prevalence and debilitating effects of this disease.(3) By using a
whole-family approach to bone-building foods and activities, younger
children will benefit by building peak bone mass while they are young and
adults may reduce the rate of bone density loss later in life.
"Parents have total control over what their child eats, drinks and does
from the time they are born until they start school, so early childhood is
the best time to make milk, dairy products and activity part of the family
lifestyle," said Laura K. Bachrach, M.D., professor of pediatrics at
Stanford Medical Center. "I think parents give up on dairy too quickly.
They may not realize the impact that this decision could have on their
children's health later in life."
Meals Matter (mealsmatter), Dairy Council of California's
online consumer meal planning and nutrition resource, features an
interactive Calcium Quiz to determine whether daily food choices provide
adequate calcium. The tool can be individualized for each member of the
family, as calcium needs change based on factors like age, gender and
supplement use. An important window of opportunity for building a lifetime
of strong bones occurs from roughly age 9 to 14, when the body is growing
and can most rapidly gain bone-building minerals. Peak bone mass, the
strongest the bones will ever be, is reached by mid to late 20s. During
this window, children and adolescents need three to four servings of dairy
a day for optimal bone-building gains. Because adolescence is typically
when teens forgo milk and dairy products for sodas and other snack foods,
early family reinforcement and lifestyle adoption is very important.
"Without a doubt, milk and dairy products are the best sources of
calcium and vitamin D in the American diet, so parents need to be creative
in their efforts to put dairy into their children's diets," said Bachrach.
"Focus on real foods like milk, cheese, yogurt or pudding before turning to
supplements."
Beyond providing calcium and vitamin D, milk and dairy products are
also high in essential vitamins and nutrients like potassium, phosphorus,
magnesium and protein. Try pairing dairy products with other foods
containing calcium like broccoli, almonds, beans, kale and
calcium-fortified foods. For instance, a side dish of broccoli with melted
cheese and sliced almonds is a bone-building bonanza.
"Exercise is the other piece of the bone-building puzzle," explains
Bachrach. "Turn off the T.V., head to the park and get those growing bones
moving!"
Exercise and exposure to sunlight are also important bone-building
factors. At least 30 minutes of weight-bearing exercise like playing tag or
hide-and-seek, walking, jumping rope, tennis or yoga most days of the week
will help strengthen bones, and exercising outdoors can double the
bone-building benefits. Sunlight allows the body to produce vitamin D,
which the body needs to absorb calcium. Vitamin D also protects against
soft, misshapen bones called rickets in children and osteomalacia in
adults.
In addition to the Calcium Quiz, Meals Matter (mealsmatter)
offers many quick and delicious recipes to bone up on calcium-rich foods.
About Dairy Council of California
Dairy Council of California develops nutrition education programs that
are easy to use and designed to be personally relevant to each user. This
customization allows consumers to make decisions considering their unique
needs, resulting in healthy food choices and contributing to optimal
health.
Sweet Apricots and Roasted Chicken in Pasta
From the California Apricot Advisory Board
Ingredients
1 (19 ounce) package bow tie noodles
1 1/2 cups low-fat milk
2 chicken breast halves; boned, skinned, roasted and sliced
1 (17 ounce) can California apricot halves, drained and quartered
1/3 cup chopped green onions
2 tablespoons butter
salt and pepper to taste
Preparation
Cook noodles according to package directions; drain. In medium
saucepan, simmer milk for 4 minutes. Add chicken, apricots, onions and
butter; continue simmering for 2 minutes. Pour over pasta in large bowl;
toss gently to coat. Season with salt and pepper to taste and serve
immediately.
(1) California Osteoporosis Prevention and Education Program Home Page. Chief,
M.P.H. Alongi, Jeanne. California Osteoporosis Prevention and Education
Program. 15 Oct. 2006.
dhs.ca/CDIC/cdcb/Medicine/Gerontology/OAUnit/html/COPE.htm.
(2) Ibid
(3) Ibid
Dairy Council of California
dairycouncilofca
воскресенье, 10 июля 2011 г.
Once-yearly Reclast(R) Significantly Reduced Bone Fractures In Women With Postmenopausal Osteoporosis
A once-yearly treatment of
Reclast(R) (zoledronic acid) Injection significantly reduced the incidence
of all types of osteoporotic bone fractures over three years in women with
postmenopausal osteoporosis. This study, published today in The New England
Journal of Medicine, marks the first time that an osteoporosis treatment
significantly reduced all types of fractures in a single study.
Reclast is a bisphosphonate, a class of drugs used to treat
osteoporosis, the most common metabolic bone disease affecting more than 10
million people in the US(1). An estimated one out of every two women over
age 50 will suffer a broken bone in her lifetime (1).
Unlike other bisphosphonate treatments, where women take daily, weekly
or monthly doses for postmenopausal osteoporosis, Reclast is given as a
once- yearly 15-minute infusion. Reclast is currently under review by the
US Food and Drug Administration (FDA) for the treatment of postmenopausal
osteoporosis.
"Unfortunately, many patients who are prescribed oral therapies stop
treatment or take less than the full dose throughout a full year, which
leads to reduced fracture protection," said Dennis Black, Ph.D., the
study's lead author and professor of epidemiology and biostatistics at the
University of California, San Francisco. "A once-yearly infusion is an
exciting potential treatment option because it offers fracture protection
for a full year with one dose."
Results from the study show that Reclast reduced the frequency of
fractures among the areas of the body that are typically affected by
osteoporosis, including the hip, spine, and wrist. Specifically, a 70
percent reduction was achieved in spine fractures. In the same study, the
risk of hip fractures, which are associated with significant mortality (2),
was reduced by 41 percent. Additionally, the reduction in spine fractures
was sustained over three years (60 percent in year one, 71 percent in year
two, and 70 percent in year three).
"We believe Reclast is an innovative treatment approach for the
millions of women with osteoporosis and provides impressive fracture
reduction, the primary goal of osteoporosis treatment," said James Shannon,
MD, Global Head of Development at Novartis Pharma AG.
About the Pivotal Fracture Trial
The Pivotal Fracture Trial was a Phase III, multi-center, randomized,
placebo-controlled study examining the efficacy and safety of Reclast in
reducing the risk of bone fracture in women with postmenopausal
osteoporosis. The study enrolled more than 7,700 women between the ages of
65 and 89 with postmenopausal osteoporosis in 27 countries. The primary
endpoints of the study were new spine and hip fractures over three years
compared to placebo. Secondary endpoints included reducing the incidence of
non-spine fractures, evaluation of bone mineral density (BMD),
normalization of bone turnover markers, and overall safety.
In addition to reductions in spine and hip fractures, the study also
demonstrated that Reclast significantly reduced the risk of non-spine, all
clinical, and clinical spine fractures by 25 percent, 33 percent and 77
percent respectively.
Bone mineral density increased significantly in the spine by 6.7
percent and the hip by 6 percent in women on Reclast compared to placebo.
In the study, overall incidence of adverse events experienced with
Reclast was comparable to placebo. The most common post-dose adverse events
with Reclast were fever, muscle pain, flu-like symptoms, headache, and
joint pain, most of which occurred within the first three days following
Reclast administration. The majority of these symptoms resolved within
three days of the event onset. The incidence decreased markedly with
subsequent annual doses of Reclast.
Analysis of key safety parameters, including kidney and bone safety
(including osteonecrosis of the jaw), found Reclast to be comparable to
placebo. There was an increased number of cases of serious atrial
fibrillation observed in the women on Reclast compared to those on placebo
(1.3 percent vs. 0.5 percent). These findings have not been observed in
other clinical studies or in post-marketing experience from over 1.5
million patients treated with zoledronic acid for oncology indications.
Data from a large trial in men and women following hip fracture will
provide additional efficacy and safety data for Reclast. These results will
be available in the second half of 2007.
About Reclast
HORIZON, the ongoing clinical program of Reclast, is one of the most
comprehensive drug evaluation programs ever undertaken in the area of
metabolic bone diseases. Approximately 13,000 patients have participated in
the program in more than 400 centers worldwide. It is the first program to
study a once-yearly dosing regimen for the prevention and treatment of
postmenopausal osteoporosis. Other studies involved in the program include
prevention of fractures following a hip fracture in men and women,
treatment of corticosteroid-induced osteoporosis and male osteoporosis.
Reclast is currently approved by the FDA for the treatment of Paget's
disease of bone, the second most common metabolic bone disorder. Reclast is
the first and only single-dose infusion regimen approved to treat Paget's
disease. Zoledronic acid, under the brand names Reclast or Aclasta(R), is
now approved in more than 50 countries, including the US, Canada and the
countries of the EU.
The active ingredient in Reclast is zoledronic acid, which is also
available under the brand name Zometa(R) (zoledronic acid) Injection for
use in certain oncology indications.
Reclast is also under review by the FDA for the treatment of
postmenopausal osteoporosis. If approved, Reclast will be the first and
only once-yearly bisphosphonate indicated for the treatment of
postmenopausal osteoporosis.
Reclast is contraindicated in patients with hypocalcemia (low blood
calcium), hypersensitivity to zoledronic acid and in women who are pregnant
or are breastfeeding. Reclast contains the same active ingredient found in
Zometa. Patients already being treated with Zometa should not be treated
with Reclast. Hypocalcemia may occur with Reclast therapy. All patients
with Paget's disease should receive 1,500 mg of calcium in divided doses
and 800 IU of vitamin D daily, particularly in the two weeks following
Reclast administration. Reclast is not recommended for use in patients with
severe renal impairment (creatinine clearance
Reclast(R) (zoledronic acid) Injection significantly reduced the incidence
of all types of osteoporotic bone fractures over three years in women with
postmenopausal osteoporosis. This study, published today in The New England
Journal of Medicine, marks the first time that an osteoporosis treatment
significantly reduced all types of fractures in a single study.
Reclast is a bisphosphonate, a class of drugs used to treat
osteoporosis, the most common metabolic bone disease affecting more than 10
million people in the US(1). An estimated one out of every two women over
age 50 will suffer a broken bone in her lifetime (1).
Unlike other bisphosphonate treatments, where women take daily, weekly
or monthly doses for postmenopausal osteoporosis, Reclast is given as a
once- yearly 15-minute infusion. Reclast is currently under review by the
US Food and Drug Administration (FDA) for the treatment of postmenopausal
osteoporosis.
"Unfortunately, many patients who are prescribed oral therapies stop
treatment or take less than the full dose throughout a full year, which
leads to reduced fracture protection," said Dennis Black, Ph.D., the
study's lead author and professor of epidemiology and biostatistics at the
University of California, San Francisco. "A once-yearly infusion is an
exciting potential treatment option because it offers fracture protection
for a full year with one dose."
Results from the study show that Reclast reduced the frequency of
fractures among the areas of the body that are typically affected by
osteoporosis, including the hip, spine, and wrist. Specifically, a 70
percent reduction was achieved in spine fractures. In the same study, the
risk of hip fractures, which are associated with significant mortality (2),
was reduced by 41 percent. Additionally, the reduction in spine fractures
was sustained over three years (60 percent in year one, 71 percent in year
two, and 70 percent in year three).
"We believe Reclast is an innovative treatment approach for the
millions of women with osteoporosis and provides impressive fracture
reduction, the primary goal of osteoporosis treatment," said James Shannon,
MD, Global Head of Development at Novartis Pharma AG.
About the Pivotal Fracture Trial
The Pivotal Fracture Trial was a Phase III, multi-center, randomized,
placebo-controlled study examining the efficacy and safety of Reclast in
reducing the risk of bone fracture in women with postmenopausal
osteoporosis. The study enrolled more than 7,700 women between the ages of
65 and 89 with postmenopausal osteoporosis in 27 countries. The primary
endpoints of the study were new spine and hip fractures over three years
compared to placebo. Secondary endpoints included reducing the incidence of
non-spine fractures, evaluation of bone mineral density (BMD),
normalization of bone turnover markers, and overall safety.
In addition to reductions in spine and hip fractures, the study also
demonstrated that Reclast significantly reduced the risk of non-spine, all
clinical, and clinical spine fractures by 25 percent, 33 percent and 77
percent respectively.
Bone mineral density increased significantly in the spine by 6.7
percent and the hip by 6 percent in women on Reclast compared to placebo.
In the study, overall incidence of adverse events experienced with
Reclast was comparable to placebo. The most common post-dose adverse events
with Reclast were fever, muscle pain, flu-like symptoms, headache, and
joint pain, most of which occurred within the first three days following
Reclast administration. The majority of these symptoms resolved within
three days of the event onset. The incidence decreased markedly with
subsequent annual doses of Reclast.
Analysis of key safety parameters, including kidney and bone safety
(including osteonecrosis of the jaw), found Reclast to be comparable to
placebo. There was an increased number of cases of serious atrial
fibrillation observed in the women on Reclast compared to those on placebo
(1.3 percent vs. 0.5 percent). These findings have not been observed in
other clinical studies or in post-marketing experience from over 1.5
million patients treated with zoledronic acid for oncology indications.
Data from a large trial in men and women following hip fracture will
provide additional efficacy and safety data for Reclast. These results will
be available in the second half of 2007.
About Reclast
HORIZON, the ongoing clinical program of Reclast, is one of the most
comprehensive drug evaluation programs ever undertaken in the area of
metabolic bone diseases. Approximately 13,000 patients have participated in
the program in more than 400 centers worldwide. It is the first program to
study a once-yearly dosing regimen for the prevention and treatment of
postmenopausal osteoporosis. Other studies involved in the program include
prevention of fractures following a hip fracture in men and women,
treatment of corticosteroid-induced osteoporosis and male osteoporosis.
Reclast is currently approved by the FDA for the treatment of Paget's
disease of bone, the second most common metabolic bone disorder. Reclast is
the first and only single-dose infusion regimen approved to treat Paget's
disease. Zoledronic acid, under the brand names Reclast or Aclasta(R), is
now approved in more than 50 countries, including the US, Canada and the
countries of the EU.
The active ingredient in Reclast is zoledronic acid, which is also
available under the brand name Zometa(R) (zoledronic acid) Injection for
use in certain oncology indications.
Reclast is also under review by the FDA for the treatment of
postmenopausal osteoporosis. If approved, Reclast will be the first and
only once-yearly bisphosphonate indicated for the treatment of
postmenopausal osteoporosis.
Reclast is contraindicated in patients with hypocalcemia (low blood
calcium), hypersensitivity to zoledronic acid and in women who are pregnant
or are breastfeeding. Reclast contains the same active ingredient found in
Zometa. Patients already being treated with Zometa should not be treated
with Reclast. Hypocalcemia may occur with Reclast therapy. All patients
with Paget's disease should receive 1,500 mg of calcium in divided doses
and 800 IU of vitamin D daily, particularly in the two weeks following
Reclast administration. Reclast is not recommended for use in patients with
severe renal impairment (creatinine clearance
четверг, 7 июля 2011 г.
Women's Sports Injuries: It's Not Just The Hormones
The long-held belief that women have
more sports injuries than men because of the difference in hormones is just
not true. Hormones certainly play a role according to orthopaedic surgeon
Kimberly J. Templeton, MD, spokesperson for the American Academy of
Orthopaedic Surgeons and Associate Professor with the University of Kansas
Medical Center, Department of Orthopedics. "There is definitely input from
the hormones but there are other musculoskeletal differences between men
and women."
Dr. Templeton points out how men land differently than women after
taking that basketball shot. "Men flex their hips and knees when they land.
Women tend to land with their hips and knees straight -- causing increased
tension on the ACL. That's one of the reasons why women have more ACL
("anterior cruciate ligament') injuries than do men." Templeton points out
that these types of injuries can be "career enders" to young female
athletes and may lead to an increased risk of degenerative arthritis later
in life, so it is critically important for girls to understand what they
need to do to stay healthy. There are very specific neuromuscular training
programs that have been shown to reduce the incidence of serious knee
injuries. Templeton advises parents to work with their daughter's coaches
-- particularly ones who understand the differences in training for girls
vs. boys.
Neuromuscular training programs are now being introduced in the schools
so young female athletes can learn the right way to land, among other
things, and protect themselves from serious injury. According to a study
conducted by Timothy E. Hewett, Ph.D., comprehensive neuromuscular training
is effective in improving measures of both performance and lower extremity
biomechanics in adolescent female athletes.
Dr. Templeton also underscores the importance of girls understanding
bone health. There is a common misconception that a woman protects herself
from osteoporosis only by engaging in weight bearing exercise. Dr.
Templeton encourages her patients to participate in weight-bearing exercise
and to lift weights but cautions that exercise must be balanced with enough
calories and nutrition. She emphasizes that, "Engaging in weight bearing
exercise without adequate calories and nutrition doesn't do anything for
systemic bone mass."
Without a balanced diet with enough calories, including adequate
amounts of Vitamin D and calcium, girls and women run an increased risk of
injury. Templeton also helps her patients learn the right way to lift
weights for to gain maximum benefit and to minimize injuries.
At the 74th Annual Meeting of the American Academy of Orthopaedic
Surgeons (AAOS), being held February 14 to 18, 2007, at the San Diego
Convention Center, Kimberly Templeton, MD served as moderator for a media
briefing, "Gender Issues in Orthopaedic Care". Dr. Templeton was joined by
three other orthopaedic surgeons, Laura L. Tosi, MD, Naomi N. Shields, MD,
and Letha Y. Griffin who have extensive experience with these issues.
American Academy of Orthopaedic Surgeons
aaos
more sports injuries than men because of the difference in hormones is just
not true. Hormones certainly play a role according to orthopaedic surgeon
Kimberly J. Templeton, MD, spokesperson for the American Academy of
Orthopaedic Surgeons and Associate Professor with the University of Kansas
Medical Center, Department of Orthopedics. "There is definitely input from
the hormones but there are other musculoskeletal differences between men
and women."
Dr. Templeton points out how men land differently than women after
taking that basketball shot. "Men flex their hips and knees when they land.
Women tend to land with their hips and knees straight -- causing increased
tension on the ACL. That's one of the reasons why women have more ACL
("anterior cruciate ligament') injuries than do men." Templeton points out
that these types of injuries can be "career enders" to young female
athletes and may lead to an increased risk of degenerative arthritis later
in life, so it is critically important for girls to understand what they
need to do to stay healthy. There are very specific neuromuscular training
programs that have been shown to reduce the incidence of serious knee
injuries. Templeton advises parents to work with their daughter's coaches
-- particularly ones who understand the differences in training for girls
vs. boys.
Neuromuscular training programs are now being introduced in the schools
so young female athletes can learn the right way to land, among other
things, and protect themselves from serious injury. According to a study
conducted by Timothy E. Hewett, Ph.D., comprehensive neuromuscular training
is effective in improving measures of both performance and lower extremity
biomechanics in adolescent female athletes.
Dr. Templeton also underscores the importance of girls understanding
bone health. There is a common misconception that a woman protects herself
from osteoporosis only by engaging in weight bearing exercise. Dr.
Templeton encourages her patients to participate in weight-bearing exercise
and to lift weights but cautions that exercise must be balanced with enough
calories and nutrition. She emphasizes that, "Engaging in weight bearing
exercise without adequate calories and nutrition doesn't do anything for
systemic bone mass."
Without a balanced diet with enough calories, including adequate
amounts of Vitamin D and calcium, girls and women run an increased risk of
injury. Templeton also helps her patients learn the right way to lift
weights for to gain maximum benefit and to minimize injuries.
At the 74th Annual Meeting of the American Academy of Orthopaedic
Surgeons (AAOS), being held February 14 to 18, 2007, at the San Diego
Convention Center, Kimberly Templeton, MD served as moderator for a media
briefing, "Gender Issues in Orthopaedic Care". Dr. Templeton was joined by
three other orthopaedic surgeons, Laura L. Tosi, MD, Naomi N. Shields, MD,
and Letha Y. Griffin who have extensive experience with these issues.
American Academy of Orthopaedic Surgeons
aaos
понедельник, 4 июля 2011 г.
Proton Pump Inhibitors Increase Risk Of Bone Fractures
Patients who use proton pump inhibitors for 7 or more years to treat reflux, peptic ulcers and other conditions are at greater risk of osteoporosis-related fractures, according to this large observational study, cmaj.ca/press/pg319.pdf, of 15,792 patients published in CMAJ.
There is specifically an increased risk of hip fracture after 5 years of continuous exposure and an increased risk of any fracture after 7 years continuous exposure. Short-term exposure did not appear to increase risk of fractures.
Proton pump inhibitors - a class of drugs commonly prescribed to control and prevent symptoms and complications of peptic ulcer disease and GERD (reflux) - are widely used by patients for many years.
The study looked at people aged 50 and older who had hip, spinal, or wrist fractures and were matched by a control group with no history of hip, spinal or wrist fractures.
The use of proton pump inhibitors has increased in recent years and use is often of indefinite duration.
"These factors may promote the long-term use of proton pump inhibitors, leaving patients at increased risk of osteoporosis-related fractures," write Dr. Laura Targownik and coauthors.
In a related commentary, cmaj.ca/press/pg306.pdf, Drs. Brent Richards and David Goltzman comment that three large administrative database studies have found proton pump inhibitors increase fracture risk. They caution that both the physician and patient should together weigh the risks and benefits of the long-term use of these drugs.
Source:
Monique Shaw
Canadian Medical Association Journal
There is specifically an increased risk of hip fracture after 5 years of continuous exposure and an increased risk of any fracture after 7 years continuous exposure. Short-term exposure did not appear to increase risk of fractures.
Proton pump inhibitors - a class of drugs commonly prescribed to control and prevent symptoms and complications of peptic ulcer disease and GERD (reflux) - are widely used by patients for many years.
The study looked at people aged 50 and older who had hip, spinal, or wrist fractures and were matched by a control group with no history of hip, spinal or wrist fractures.
The use of proton pump inhibitors has increased in recent years and use is often of indefinite duration.
"These factors may promote the long-term use of proton pump inhibitors, leaving patients at increased risk of osteoporosis-related fractures," write Dr. Laura Targownik and coauthors.
In a related commentary, cmaj.ca/press/pg306.pdf, Drs. Brent Richards and David Goltzman comment that three large administrative database studies have found proton pump inhibitors increase fracture risk. They caution that both the physician and patient should together weigh the risks and benefits of the long-term use of these drugs.
Source:
Monique Shaw
Canadian Medical Association Journal
пятница, 1 июля 2011 г.
Small Bone Innovations, Inc. Receives US FDA 510(k) Clearance For Radial Head (rHead™) Extended Stem
Small Bone Innovations, Inc. (SBi), an orthopedics company focused exclusively on serving patients and their physicians with technologies and treatments for joint repair (arthroplasty) and trauma reconstruction around the small bones & joints of the thumb, fingers, hand, wrist, elbow, toes and foot & ankle announced that it has received 510(k) pre-market clearance notification from the U.S. Food and Drug Administration (FDA) for the radial Head (rHead™) Extended Stem to be used in the correction of complex elbow instabilities and/or elbow reconstruction.
The rHead Extended Stem further expands SBi's upper limb product line. It is intended to be used in conjunction with SBi's Elbow Management System (EMS), which incorporates an algorithmic approach to provide surgeons an array of solutions for treating elbow fractures. Addition of the rHead Extended Stem to EMS increases treatment options for elbow fractures where fixation may be inadequate.
Anthony G. Viscogliosi, Chairman & CEO of SBi, said: "The rHead Extended Stem was designed to be easily integrated with the EMS and provides surgeons greater flexibility to treat complex elbow fractures. The addition of the extended stem to our product portfolio is another step towards creating the most attractive, anatomically-focused product portfolio dedicated to restoring form, function and motion while alleviating pain in upper limb joints. This also reinforces SBi's commitment to work with key opinion leaders to continue to provide product solutions that serve the full range of clinical needs of surgeons and their patients."
SBi has been attracting considerable attention in recent months in both the financial and the orthopedics sector. Out of nearly 5,200 companies considered, SBi was the only orthopedic company on the list of the top 50 U.S. VC-backed companies in the Wall Street Journal article "Sizing Up Promising Young Firms" on March 9, 2010. Additionally, SBi was the 7th highest ranked healthcare company and was 24th amongst all 50 companies highlighted.
SBi closed on $12 million in Series E funding from Olympus Corporation in March 2010. The company secured a $30mm debt facility from Fortress Investment Group to fund accelerated business expansion and refinance existing indebtedness in November 2009. The company in mid 2009 closed on $144 million in Series D and Series C funding from a host of investors including, Goldman, Sachs & Co., Khazanah Nasional Berhad (the investment firm of the Government of Malaysia), Malaysian Technology Development Corporation (MTDC), an integrated Malaysian-based venture capital company, The Family Office of Bahrain, Viscogliosi Brothers, LLC, Trevi Health Ventures, NGN Capital, 3i Group, and TGap Ventures, among others.
Source:
Small Bone Innovations, Inc.
The rHead Extended Stem further expands SBi's upper limb product line. It is intended to be used in conjunction with SBi's Elbow Management System (EMS), which incorporates an algorithmic approach to provide surgeons an array of solutions for treating elbow fractures. Addition of the rHead Extended Stem to EMS increases treatment options for elbow fractures where fixation may be inadequate.
Anthony G. Viscogliosi, Chairman & CEO of SBi, said: "The rHead Extended Stem was designed to be easily integrated with the EMS and provides surgeons greater flexibility to treat complex elbow fractures. The addition of the extended stem to our product portfolio is another step towards creating the most attractive, anatomically-focused product portfolio dedicated to restoring form, function and motion while alleviating pain in upper limb joints. This also reinforces SBi's commitment to work with key opinion leaders to continue to provide product solutions that serve the full range of clinical needs of surgeons and their patients."
SBi has been attracting considerable attention in recent months in both the financial and the orthopedics sector. Out of nearly 5,200 companies considered, SBi was the only orthopedic company on the list of the top 50 U.S. VC-backed companies in the Wall Street Journal article "Sizing Up Promising Young Firms" on March 9, 2010. Additionally, SBi was the 7th highest ranked healthcare company and was 24th amongst all 50 companies highlighted.
SBi closed on $12 million in Series E funding from Olympus Corporation in March 2010. The company secured a $30mm debt facility from Fortress Investment Group to fund accelerated business expansion and refinance existing indebtedness in November 2009. The company in mid 2009 closed on $144 million in Series D and Series C funding from a host of investors including, Goldman, Sachs & Co., Khazanah Nasional Berhad (the investment firm of the Government of Malaysia), Malaysian Technology Development Corporation (MTDC), an integrated Malaysian-based venture capital company, The Family Office of Bahrain, Viscogliosi Brothers, LLC, Trevi Health Ventures, NGN Capital, 3i Group, and TGap Ventures, among others.
Source:
Small Bone Innovations, Inc.
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