James H. Beaty, M.D.: New Chair at University of Tennessee-Campbell Clinic
James H. Beaty, M.D., a former president of the American Academy of Orthopaedic Surgeons, is the new department chairman and Harold B. Boyd, M.D. Professor in the University of Tennessee-Campbell Clinic Department of Orthopaedic Surgery and Biomedical Engineering.
The editor of 7 textbooks, author of 58 book chapters, and nearly 70 peer-reviewed scientific articles, Dr. Beaty has served as president of the American Board of Orthopaedic Surgery, the Pediatric Orthopaedic Society of North America, the Mid-America Orthopaedic Association, and the Tennessee Orthopaedic Society.
Dr. Beaty earned his undergraduate degree at Washington & Lee University in 1973, then attended medical school at the University of Tennessee (UT) College of Medicine. After completing a residency at UT-Campbell Clinic in 1981, Dr. Beaty undertook a pediatric fellowship at the A.I. DuPont Institute in Wilmington, Delaware. He joined the staff of Campbell Clinic in 1982 as a specialist in pediatric orthopedics and pediatric trauma. Dr. Beaty has done both an American Orthopaedic Association North American Traveling Fellowship (1984) and an American Orthopaedic Association ABC-Traveling Fellowship (1991). He served as chief of staff at Campbell Clinic from 2001-2010.
Regarding his new role, Dr. Beaty told OTW, “My initial goal is to continue our progress in building both translational and basic research in our department. We continue to add to the body of knowledge and science in the orthopaedic community.”
Cell Phone Sensor Measures Frailty in 20 Seconds!
With so many elderly orthopedic patients these days, it is critical to know who is frail, at risk of falling, and who stands a good chance of recovering well from surgery. Now, researchers from Baylor College of Medicine, Houston, and University of Arizona, Tucson, say that with just a 20-second upper arm extension test (called upper extremity frailty: UEF system), they can get solid information on things such as slowness of motion, weakness, and exhaustion.
Study author Bijan Najafi, Ph.D., professor of surgery and director of the Interdisciplinary Consortium on Advanced Motion Performance at Baylor College of Medicine, told OTW, “Using sensors found in cell phones in community-dwelling older adults, we administered the Trauma-Specific Frailty Index questionnaire to 101 patients, 65 years and older, who had been admitted to the hospital due to traumatic falls. Patients then performed the 20-second arm extension test while wearing the UEF system.”
“We found that we can obtain similar results as gait assessment by testing the kinematic and kinetic of the upper arm and elbow flexion extension. This finding is very valuable because gait assessment is often not practical in a busy hospital setting.”
Dr. Najafi commented to OTW, “I believe when we are providing care to older adults including orthopedic surgery, assessment of frailty could be highly beneficial for personalized decision making about care management as well as appropriately informing patients and their family about potential risks and expected outcomes. Until now, many of such decisions were based on subjective modalities mainly due to the fact that conventional objective methods were often impractical for routine care. In particular those methods based on gait assessment are often unsuitable due to space constraint for administrating the test as well as confounders which may influence the accuracy of the test (e.g., joint pain, fracture, or simply inability to safely walk).”
“The proposed test is an alternative test to gait, which takes just 20 seconds, while patient is sitting or laying down and could provide valuable objective information about level of slowness (gait speed), weakness (grip force), flexibility (joint range of motion), and exhaustion. These parameters are markers of frailty and are well established to be predictors of surgical outcomes and potential adverse events. For the first time, we have demonstrated that we could extract these biomarkers of frailty without a walking test and using a test which could be more practical for patients irrespective of setting.”
The researchers recently received a National Institutes of Health grant to continue this study in a larger hospital population.
Muscles “Driving” Rare Neurodegenerative Disease?
Spinal-bulbar muscular atrophy (SBMA)…ever heard of it? A devastating condition that, according to the National Institutes of Health (NIH), is “characterized by wasting of the proximal muscles (those closer to the trunk) and bulbar muscles (those of the face and throat).” According to a May 6, 2016 news release, Michigan State University researchers were motivated to think differently about the condition by Youfen Xu, senior research associate in MSU’s Neuroscience Program. Xu hypothesized that if motor dysfunction is not caused by loss of motorneurons, then perhaps synaptic drive at the neuromuscular junction fails.
As indicated in the May 6, 2016 news release, SBMA is a “late-onset neurodegenerative disease that robs men of the capacity to walk, run, chew and swallow.”
“…By studying recordings from muscle fibers, the researchers listened in on how disease affects the function of neuromuscular synapses in three different mouse models of SBMA.”
“When I joined Cindy Jordan’s research project to study the electrophysiological features of neuromuscular transmission in SBMA mouse models, I was surprised to find that no one in the field had yet looked to see whether the function of neuromuscular synapses was affected, and I was equally surprised to find that virtually all aspects of their function are disrupted. The fact that we find pretty much the same kind of dysfunction across three quite different mouse models of SBMA makes me suspect that we have stumbled on to core attributes of the disease in humans.”
Youfen Xu told OTW, “It is hard to study diseased muscles and synapses. Historically the androgen-dependent loss of motor function in SBMA has long been attributed to the degeneration of motor neurons. But, several SBMA mouse models show motor dysfunction without motor neuron death, raising questions about the origin of motor dysfunction. Recent evidences show skeletal muscles likely trigger the disease. One possibility is that disease signals which originate in muscle retrogradely perturb the function of neuromuscular junctions or directly originate in neuromuscular junctions, ultimately triggering motor neuronal degeneration and death. However, there was no data in the research field of SBMA to show whether or not the function of neuromuscular synapses was affected. We found that neuromuscular transmission was defective in several ways in our mouse models of SBMA which resulted from both deficits in presynaptic transmitter release and postsynaptic changes in signal transduction and muscle excitability.”
“While physical exercise might represent a promising approach for alleviating symptoms, the benefits of exercise are not yet clear. A recently completed clinical trial run at NIH showed very minimal benefits for improving motor function of SBMA patients although there is some hint that exercise early in the disease process may actually be beneficial. Muscle cramping is one of the earliest symptoms of SBMA and might be controlled simply be drinking lots of water and perhaps Gatorade when a person sweats. Clearly, we still have lots to learn, including whether muscles of SBMA patients show the same changes in ion channels as we have found in our mouse models of SBMA.”
