Rick Lieber | |
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Born | Richard L. Lieber Walnut Creek, California |
Alma mater | University of California, Davis (BS, Ph.D) University of California, San Diego (Postdoc, MBA) |
Scientific career | |
Fields | Physiology, Anatomy, Biology, Biomedical Engineering |
Institutions | Shirley Ryan AbilityLab Northwestern University |
Website | https://www.sralab.org/researchers/richard-lieber-phd |
Richard (Rick) L. Lieber (born December 14, 1956) is an American scientist in the field of muscle physiology. [1] Lieber is Chief Scientific Officer and Senior Vice-president at Shirley Ryan AbilityLab, [1] Professor of Physiology, Biomedical Engineering & Physical Medicine & Rehabilitation at Northwestern University's Feinberg School of Medicine, [2] [3] and Senior Research Career Scientist at the Edward Hines Jr. Veterans Administration Hospital. [4] He is internationally recognized as an expert in skeletal muscle structure and function. [5] [6] [7] His research focuses on skeletal muscle properties in individuals with neurological disorders such as spinal cord injury or cerebral palsy. [8] [9] [10] [11] [12]
Dr. Lieber was born in Walnut Creek, California, the son of a big band musician and hospital administrator. After graduation from Las Lomas High School in Walnut Creek, he completed a B.S. in physiology in 1978 at University of California, Davis. [13] In 1983, he earned his Ph.D. in biophysics from University of California, Davis, applied a theory of light diffraction to study mechanical properties of muscle cells [14] and was one of the first to use the Intel 8080 microprocessor to control a biological system in real-time. [15] He received his M.B.A. in 2013 from Rady School of Management, University of California, San Diego.
Lieber was hired as an assistant professor at UC San Diego in 1985, promoted to associate professor in 1990, and promoted to Professor in 1994. He was also a Biomedical Engineer at the Veterans Administration Medical Center in San Diego from 1983 to 2000. He was recruited as the Chief Scientific Officer at Shirley Ryan AbilityLab (formerly the Rehabilitation Institute of Chicago) in 2014 to lead the research enterprise in this new translational rehabilitation research hospital.
Lieber has published over 350 articles in peer-reviewed scientific journals ranging from basic science such as The Journal of Cell Biology [16] to clinical research such as The Journal of Hand Surgery . [17] [18] [19] He is an established expert in using biological approaches to understand muscle contractures in neurological conditions such as cerebral palsy, stroke and spinal cord injury. Lieber's work includes the development of pharmacological and surgical interventions to improve muscle function in individuals with neurological conditions. [20] [21] [22] He has made significant contributions to the field of muscle physiology, especially in the area of in vivo muscle measurements, [23] [24] and he is frequently referenced by colleagues. [25] His most often cited paper is "Functional and clinical significance of skeletal muscle architecture" in the peer-reviewed journal Muscle & Nerve with 1447 citations. His work has over 34,000 citations in the scientific community and his h-index is 91. [26] In addition to his publications in peer-reviewed journals, he authored the textbook, "Skeletal Muscle Structure, Function, and Plasticity," which explores basic and applied physiological properties of skeletal muscle. [27]
Lieber's career is marked by significant professional collaborations with international colleagues and organizations, including Jan Fridén, M.D., Ph.D. at Gothenburg University, [28] [29] Eva Pontén at the Karolinska Institute, [30] and Allistair Rothwell at Christ Church, New Zealand. [31]
Lieber also serves as a member of the scientific advisory board of the NFL [32] and has six patents on surgical techniques, methods to measure muscle fibers, and methods to administer stimulation to skeletal muscles [33]
Lieber has received a number of awards and honors throughout his career. These include:
Elsass Foundation Research Prize, June 2023 [34] [35]
Paul B. Magnuson Award, Rehabilitation Research and Development, Department of Veterans Affairs, March 2023 [36] [37]
Goel Award for Translational Biomechanics, North American Congress on Biomechanics (NACOB), American Society for Biomechanics, August 2022, Ottawa, Ontario, Canada. [38]
Lifetime Achievement Award, American Academy of Cerebral Palsy and Developmental Medicine, [39] [40] 2021
Fellow, Orthopaedic Research Society (ORS), November 2020 [41] [42]
Fellow, American Institute of Medical and Biological Engineering (AIMBE), March 2019 [43]
Hay Award in Sport Biomechanics, American Society of Biomechanics, August 2017 [38] [44]
Honorary Member, American Physical Therapy Association, February 2015 [45]
Founders Award, American College of Sports Medicine (Southwest Chapter), October 2014. [44] [46]
Gayle G. Arnold Award, American Academy of Cerebral Palsy and Developmental Medicine, October 2013 [39]
Kappa Delta Award, American Academy of Orthopaedic Surgeons, February 2013, Chicago, IL. [47] [48]
Fellow, American Society for Biomechanics, July 2012 [49]
Outstanding Research Award, International Society for the Study of the Lumbar Spine (ISSLS), Göteborg, Sweden. June 2011. [50]
Giovanni Borelli Award, American Society of Biomechanics, August, 2007. [51]
The Göteborg University Medal, Sahlgrenska University Hospital, June 2007. [52] [7]
Fulbright Scholarship (Sweden), 2007 [53]
Nicolas Andry Award, American Bone and Joint Surgeons, Vancouver, British Columbia, Canada, May 2002 [54] [55]
Fellow, American College of Sports Medicine, March, 1994. [1]
Kappa Delta Young Investigator Award, American Academy of Orthopaedic Surgeons, February 1994. [47]
Selected publications [3]
Pelizaeus–Merzbacher disease is an X-linked neurological disorder that damages oligodendrocytes in the central nervous system. It is caused by mutations in proteolipid protein 1 (PLP1), a major myelin protein. It is characterized by a decrease in the amount of insulating myelin surrounding the nerves (hypomyelination) and belongs to a group of genetic diseases referred to as leukodystrophies.
The muscular system is an organ system consisting of skeletal, smooth, and cardiac muscle. It permits movement of the body, maintains posture, and circulates blood throughout the body. The muscular systems in vertebrates are controlled through the nervous system although some muscles can be completely autonomous. Together with the skeletal system in the human, it forms the musculoskeletal system, which is responsible for the movement of the body.
Skeletal muscle is one of the three types of vertebrate muscle tissue, the other being cardiac muscle and smooth muscle. They are part of the voluntary muscular system and typically are attached by tendons to bones of a skeleton. The skeletal muscle cells are much longer than in the other types of muscle tissue, and are also known as muscle fibers. The tissue of a skeletal muscle is striated – having a striped appearance due to the arrangement of the sarcomeres.
A sarcomere is the smallest functional unit of striated muscle tissue. It is the repeating unit between two Z-lines. Skeletal muscles are composed of tubular muscle cells which are formed during embryonic myogenesis. Muscle fibers contain numerous tubular myofibrils. Myofibrils are composed of repeating sections of sarcomeres, which appear under the microscope as alternating dark and light bands. Sarcomeres are composed of long, fibrous proteins as filaments that slide past each other when a muscle contracts or relaxes. The costamere is a different component that connects the sarcomere to the sarcolemma.
A muscle cell, also known as a myocyte, is a mature contractile cell in the muscle of an animal. In humans and other vertebrates there are three types: skeletal, smooth, and cardiac (cardiomyocytes). A skeletal muscle cell is long and threadlike with many nuclei and is called a muscle fiber. Muscle cells develop from embryonic precursor cells called myoblasts.
The Frank–Starling law of the heart represents the relationship between stroke volume and end diastolic volume. The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction, when all other factors remain constant. As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, leading to an increase in the force of contraction. The Frank-Starling mechanism allows the cardiac output to be synchronized with the venous return, arterial blood supply and humoral length, without depending upon external regulation to make alterations. The physiological importance of the mechanism lies mainly in maintaining left and right ventricular output equality.
Striated muscle tissue is a muscle tissue that features repeating functional units called sarcomeres. The presence of sarcomeres manifests as a series of bands visible along the muscle fibers, which is responsible for the striated appearance observed in microscopic images of this tissue. There are two types of striated muscle:
Muscle contraction is the activation of tension-generating sites within muscle cells. In physiology, muscle contraction does not necessarily mean muscle shortening because muscle tension can be produced without changes in muscle length, such as when holding something heavy in the same position. The termination of muscle contraction is followed by muscle relaxation, which is a return of the muscle fibers to their low tension-generating state.
The vastus medialis is an extensor muscle located medially in the thigh that extends the knee. The vastus medialis is part of the quadriceps muscle group.
Myofilaments are the three protein filaments of myofibrils in muscle cells. The main proteins involved are myosin, actin, and titin. Myosin and actin are the contractile proteins and titin is an elastic protein. The myofilaments act together in muscle contraction, and in order of size are a thick one of mostly myosin, a thin one of mostly actin, and a very thin one of mostly titin.
Nebulin is an actin-binding protein which is localized to the thin filament of the sarcomeres in skeletal muscle. Nebulin in humans is coded for by the gene NEB. It is a very large protein and binds as many as 200 actin monomers. Because its length is proportional to thin filament length, it is believed that nebulin acts as a thin filament "ruler" and regulates thin filament length during sarcomere assembly. Other functions of nebulin, such as a role in cell signaling, remain uncertain.
Muscle atrophy is the loss of skeletal muscle mass. It can be caused by immobility, aging, malnutrition, medications, or a wide range of injuries or diseases that impact the musculoskeletal or nervous system. Muscle atrophy leads to muscle weakness and causes disability.
Actinin is a microfilament protein. The functional protein is an anti-parallel dimer, which cross-links the thin filaments in adjacent sarcomeres, and therefore coordinates contractions between sarcomeres in the horizontal axis. Alpha-actinin is a part of the spectrin superfamily. This superfamily is made of spectrin, dystrophin, and their homologous and isoforms. In non-muscle cells, it is found by the actin filaments and at the adhesion sites.The lattice like arrangement provides stability to the muscle contractile apparatus. Specifically, it helps bind actin filaments to the cell membrane. There is a binding site at each end of the rod and with bundles of actin filaments.
The costamere is a structural-functional component of striated muscle cells which connects the sarcomere of the muscle to the cell membrane.
Muscle is a soft tissue, one of the four basic types of animal tissue. Muscle tissue gives skeletal muscles the ability to contract. Muscle is formed during embryonic development, in a process known as myogenesis. Muscle tissue contains special contractile proteins called actin and myosin which interact to cause movement. Among many other muscle proteins present are two regulatory proteins, troponin and tropomyosin.
Ankyrin Repeat, PEST sequence and Proline-rich region (ARPP), also known as Ankyrin repeat domain-containing protein 2 is a protein that in humans is encoded by the ANKRD2 gene. ARPP is a member of the muscle ankyrin repeat proteins (MARP), which also includes CARP and DARP, and is highly expressed in cardiac and skeletal muscle and in other tissues. Expression of ARPP has been shown to be altered in patients with dilated cardiomyopathy and amyotrophic lateral sclerosis. A role for Ankrd2 in tumor progression and metastases spreading has also been described.
In vitro muscle testing is a method used to characterize properties of living muscle tissue after removing it from an organism, which allows more extensive and precise quantification of its properties than in vivo testing. In vitro muscle testing has provided the bulk of scientific knowledge of muscle structure and physiology, and how both relate to organismal performance. Stem cell research relies on in vitro muscle testing to establish sole muscle cell function and its individual behavior apart from muscle cells in the presence of nonmuscle cells seen in in vitro studies.
Muscle architecture is the physical arrangement of muscle fibers at the macroscopic level that determines a muscle's mechanical function. There are several different muscle architecture types including: parallel, pennate and hydrostats. Force production and gearing vary depending on the different muscle parameters such as muscle length, fiber length, pennation angle, and the physiological cross-sectional area (PCSA).
Bernard H. Bressler FCAHS is a Professor in the Department of Cellular and Physiological Sciences and an Associate Member in the Department of Orthopedics at the University of British Columbia (UBC).
Diane Louise Damiano is an American biomedical scientist and physical therapist specializing in physical medicine and rehabilitation approaches in children with cerebral palsy. She is chief of the functional and applied biomechanics section at the National Institutes of Health Clinical Center. Damiano has served as president of the Clinical Gait and Movement Analysis Society and the American Academy for Cerebral Palsy and Developmental Medicine.