Honors & News
March 18, 2009
Ten scientists from the University of Rochester Medical Center (URMC) have been awarded more than $6.8 million by the Empire State Stem Cell Board. The grants are for a wide range of research programs in the fields of neurological disorders, cancer, musculoskeletal diseases, the blood system, and efforts to understand the fundamental mechanics of stem cell biology.
Stem cell research for tissue engineering and regenerative medicine is a rapidly evolving field that holds great promise for the 21st century. Drs. Hani Awad, Laura Calvi, Edward Puzas, Edward Schwarz, Xinping Zhang, Dirk Bohmann, James Palis, Richard Waugh and others have obtained funding for stem cell research to further their efforts in this area that include: understanding the molecular genetic characteristic of mesenchymal stem cells (MSCs), how to expand MSCs in vitro and in vivo, methods to impregnate matrices with MSCs to tissue engineer bone and cartilage, and how to image labeled MSCs.
January 27, 2009
Old technologies, bone cement and a well known antibiotic, may effectively fight an emerging infection in soldiers with compound bone fractures, according to a study published online today in the Journal of Orthopaedic Research. Not common in the United States and not potentially fatal, A. baumannii OM had been largely ignored until recently by physicians and the pharmaceutical industry, which focuses on life-threatening infections that affect millions, not hundreds. Then military outbreaks of the infection started among American soldiers returning from Iraq in 2003, with the number of A. baumannii OM infections seen in field hospitals, and in stateside facilities receiving injured soldiers, growing.
If you apply the findings from two small studies to the entire U.S. military, which is a leap, perhaps 2,000 soldiers come into field hospitals with compound fractures each year that become infected with A. baumannii,said Edward Schwarz, Ph.D., professor of Orthopaedics within the Center for Musculoskeletal Research at the University of Rochester Medical Center.
About a third of them go on to get a staph infection after they reach the hospital, with about a third of those, perhaps 200 soldiers, suffering infectious complications that could cost them a limb. Studies already underway in our lab seek to clarify how the initial infections could gradually be replaced by catastrophic MRSA, and to prove that we can save limbs by putting an established antibiotic into bone cement for the first time.
January 15, 2009
Researchers have unraveled crucial details of how aging causes broken bones to heal slowly, or not at all, according to study results published online today in the Journal of Bone and Mineral Research. The research team also successfully conducted preclinical tests on a potential new class of treatments designed to
rescuehealing capability lost to aging.
Along with Dr. Regis O'Keefe, the study effort was led by Amish Naik, Chao Xie, Michael Zuscik, Edward Schwarz, Hani Awad, J. Edward Puzas, Brendan Boyce and Xinping Zhang within the Center for Musculoskeletal Research, as well as by Paul Kingsley within the Department of Pediatrics, at the Medical Center.
August 22, 2008
Researchers have discovered key details of how rheumatoid arthritis (RA) destroys bone, according to a study published in the Aug. 22 edition of the Journal of Biological Chemistry. The findings are already guiding attempts to design new drugs to reverse RA-related bone loss and may also address more common forms of osteoporosis with a few adjustments.
The significance of our study is that it identifies SMURF1 as the signaling partner through which TNF does damage in RA-related bone loss,said Lianping Xing, Ph.D., assistant professor of Pathology and Laboratory Medicine at the University of Rochester Medical Center.
That has enabled researchers to begin designing small molecule drugs to shut down the action of SMURF1 and its relatives. Furthermore, since mice engineered to have less SMURF1 expression develop thicker bones, future drugs that shut down SMURF1 may be also useful against more common forms of osteoporosis simply by changing the dose. Of course, this is early-stage work with many obstacles ahead, but it is exciting nonetheless.
Along with Xing, the study was led by Ruolin Guo, Motozo Yamashita, Qian Zhang, Quan Zhou, Di Chen, David G. Reynolds, Hani Awad, Laura Yanoso, Lan Zhao, Edward Schwarz, Ying Zhang and Brendan Boyce within the Department of Pathology and Laboratory Medicine at University of Rochester.
January 8, 2008
Donated, freeze-dried tendon grafts loaded with gene therapy may soon offer effective repair of injured tendons, a goal that has eluded surgeons to date. According to study data published online today in the journal Molecular Therapy, a new graft technique may provide the first effective framework around which flexor tendon tissue can reorganize as it heals. Such tissue-engineering approaches could significantly improve repair of anterior cruciate ligaments and rotator cuffs as well, researchers said. The study was in a mouse model designed to resemble hard-to-repair flexor tendons in human hands, and the results should provide an impetus for future clinical trials.
Along with Dr. Hani Awad, study authors were Patrick Basile, M.D., Tulin Dadali, B.S., Justin Jacobson, M.D., Yasuhiko Nishio, Ph.D., M. Hicham Drissi, Ph.D., Howard Langstein, M.D., David Mitten, M.D., Regis J O'Keefe, M.D., Ph.D., and Edward Schwarz, Ph.D. from the University of Rochester Medical Center as well as Sys Hasslund, Michael Ulrich-Vinther and Kjeld Soballe from Aarhus University.
October 19, 2006
Researchers from the University of Rochester Medical Center have received a $7.8 million grant to speed the conversion of basic bone science into new treatments that prevent arthritis, improve fracture healing and save limbs. In one case, the research aims to confirm preliminary findings that a handful of patients, previously confined to wheelchairs by fractures that would not heal, were able to walk again after receiving a drug treatment that finally healed the bone.
One of the research areas, led by Edward M. Schwarz, Ph.D., professor of Orthopaedics, will test a new method for replacing large segments of bone that are too shattered to heal, or are simply missing, to prevent amputation. Bone loss is an urgent issue for car crash victims, bone cancer patients and troops injured in the Middle East. Dead bone donated from cadavers is currently used to replace large portions of missing bone in trauma patients.
April 24, 2006
An early study has demonstrated for the first time that laser light can target gene therapy right up to the edge of damaged cartilage, while leaving nearby healthy tissue untouched, according to the April edition of the Journal of Bone and Joint Surgery. True repair of injuries to articular cartilage would enable millions of patients, currently consigned to worsening arthritis and joint replacement, to return to athletic exercise.
For years researchers have been trying to turn on gene therapy precisely within areas of damaged tissue without harming surrounding healthy tissue,said Edward M. Schwarz, Ph.D., professor of Orthopaedics within the Center for Musculoskeletal Research at the University of Rochester Medical Center.
Our study shows that we can use our cellular defenses against, of all things, sunlight, to finally achieve safe, precise control over tissue repair.
February 17, 2005
Researchers have created a way to transform the dead bone of a transplanted skeletal graft into living tissue in an experiment involving mice. The advance, which uses gene therapy to stimulate the body into treating the foreign splint as living bone, is a promising development for the thousands of cancer and trauma patients each year who suffer with fragile and failing bone grafts.
The procedure, designed by a team led by Edward M. Schwarz, Ph.D., associate professor of orthopedics and of microbiology and immunology at the University of Rochester Medical Center, is intended to eventually aid people with various cancers or injuries whose treatment involves the replacement of large sections of bone.
April 9, 2003
Researchers at the University of Rochester Medical Center's Musculoskeletal Research Unit believe that by the year 2005, when the majority of the female baby boomer generation begins entering menopause, more women than ever thought possible will begin to suffer from osteoporosis at a younger age due to high levels of lead exposure in their childhood. The early data indicate that as much as 10 percent of low bone density, the primary symptom of the disease, may be explained by lead in the skeleton.
According to Edward Puzas, Ph.D., the Donald and Mary Clark Professor of Orthopaedics and director of the Musculoskeletal Research Unit, research studies over the past four decades have consistently found that high levels of lead in the bloodstream can have adverse effects on bone growth and development. He and his team are expanding on this finding by trying to uncover the mechanism that explains this phenomenon and its relationship to osteoporosis.
March 17, 2003
Scientists have discovered in unprecedented detail the molecular forces that conspire to damage bone in patients with psoriatic arthritis, a disease that affects an estimated 500,000 to 1 million people in the United States. New findings show that people with the disease are awash in a type of cell that specializes in dissolving bone, and their joints have high amounts of a protein that persuades those cells to settle into joints, where most damage is done. Discovery of the one-two punch helps doctors understand why patients are responding so well to new medicines, and it opens the door to new remedies – all for a disease that had no approved treatment little more than a year ago. Among those leading the research effort is Edward Schwarz, Ph.D., of the Center for Musculoskeletal Research.
- Validation of Power Doppler Versus Contrast Enhanced Magnetic Resonance Imaging Quantification of Joint Inflammation in Murine Inflammatory Arthritis. J Bone Miner Res. In press. (2014 Oct 31).
- Passive immunization with anti-glucosaminidase monoclonal antibodies protects mice from implant-associated osteomyelitis by mediating opsonophagocytosis of Staphylococcus aureus megaclusters. J Orthop Res. 32, 1389-96. (2014 Oct 01).
- TGF-beta1 Suppresses Plasmin and MMP Activity in Flexor Tendon Cells via PAI-1: Implications for Scarless Flexor Tendon Repair. J Cell Physiol. In press. (2014 Jun 24).