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Samuel Veres

Assistant Professor, School of Biomedical Engineering

sam veres



Samuel Veres, PhD
Email: sam.veres@smu.ca
Web: http://smu-facweb.smu.ca/~sveres

Our Group

My laboratory specializes in investigating interactions between structure and function in the load-bearing tissues of the human body, and how these relationships change in health and disease. We take a hierarchical approach to tissue damage assessment. At the macro level, we examine the mechanical response of whole tissues like tendons and ligaments. Damage to collagen fibres and the connection between collagen fibres and bone is explored using light microscopy. Damage to individual collagen fibrils is examined using nanoscale microscopy techniques, such as scanning electron microscopy and atomic force microscopy. At the molecular level, we explore damage to collagen molecules using tools such as hydrothermal isometric tension testing (shown above) and differential scanning calorimetry. As part of the Tissue Development, Damage, & Repair Collaborative, we work closely with several collaborators in SBME.


Overload Damage: Because the tensile strengths of tendons and ligaments are provided by collagen fibrils, overload damage to these tissues means overload damage to collagen fibrils. By looking at the nanoscale structure of collagen fibrils within tendons before and after overload, we have identified a new collagen fibril failure mode called discrete plasticity. Discrete plasticity is characterized by fibrils that develop longitudinally repeating zones of plastic deformation (i.e., structural changes that persist after unloading). We are continuing to investigate whether discrete plasticity occurs in all tendons and ligaments when they are overloaded, whether cells are able to distinguish these fibrils from normal fibrils, and if and how fibrils with discrete plasticity are repaired.
Fatigue Damage: Overuse of tendons and ligaments without proper training may eventually lead to tendon or ligament damage, or even rupture. But how does cyclic loading actually damage tendons and ligaments? Are individual collagen fibrils damaged by repetitive loading, even when applied forces are low? Can the collagen molecules within fibrils experience fatigue damage? Why are some people susceptible to overuse injury, while others are not? Can proper physical training prevent overuse injury, and if so how does this work? By investigating the nanoscale structure of tendons and ligaments both before and after fatigue loading, we are working to answer important questions about the development of overuse injuries that cost our healthcare system millions of dollars annually.
Spinal Research: The spinal column is composed of vertebrae, intervertebral discs, and ligaments. Working together, these structures support the weight of your upper body, while allowing your torso a large range of motion. Between adjacent vertebrae in the spine lie the intervertebral discs. Intervertebral discs support load in a similar fashion to car tires. When the spine is loaded in compression, pressure is generated within the central, gelatinous region of each disc. The gel-filled centre, called the nucleus, is equivalent to the air in a tire. Pressure generated within the nucleus is supported by tensile forces developed in the surrounding ligament that circumferentially joins the adjacent vertebrae. This ligamentous ring, called the annulus, withholds the nucleus, just like the rubber of a car tire withholds the air inside. Both the annulus of intervertebral discs and the ligaments that run along the back of the spinal column are composed of collagen fibrils, which, as we know from our work with tendons, can sustain longitudinally distributed overload damage. Similar fibril-level damage in the spine could play a role in a range of low back pathologies.
Disk Herniation: Nanoscale damage to collagen fibrils may play a role in a range of low back pathologies, including: non-specific low back pain, internal disc disruption, intervertebral disc degeneration, and intervertebral disc herniation. The most dramatic of these mechanically-driven injuries is herniation, which occurs when a disc's nucleus ruptures through the surrounding, ligamentous annulus. Because the posterior aspect of the annulus is thinnest, ruptures most often occur here. Unfortunately, the posterior annulus is located adjacent to the spinal cord. Consequently, herniated discs can mechanically compress or chemically irritate the spinal cord, causing pain. Often, disc herniations need to be corrected by surgically excising the herniated mass. In order to better understand the development of spinal pathologies, we mechanically disrupt spinal ligaments and intervertebral discs, and then study the damage created at both the micro- and nano scales. Shown here is an optical micrograph of the posterior annulus of a disc herniation that was created in the laboratory.


Recent Publications

Macrophage‐like U937 cells recognize collagen fibrils with strain‐induced discrete plasticity damage. SP Veres, EP Brennan‐Pierce, JM Lee
Journal of Biomedical Materials Research Part A (2014).
Mechanically overloading collagen fibrils uncoils collagen molecules, placing them in a stable, denatured state. SP Veres, JM Harrison, JM Lee. Matrix Biology (2014) 33:54-59.
Cross‐link stabilization does not affect the response of collagen molecules, fibrils, or tendons to tensile overload. SP Veres, JM Harrison, JM Lee. Journal of Orthopaedic Research (2013) 31(12), 1907-1913.
Accurate Nano-Mechanical Mapping of Collagen I Fibrils. S Baldwin, S Veres, M Lee, L Kreplak. Microscopy and Microanalysis (2013) 19(S2), 34-35.
Repeated subrupture overload causes progression of nanoscaled discrete plasticity damage in tendon collagen fibrils. SP Veres, JM Harrison, JM Lee. Journal of Orthopaedic Research (2013) 31(5), 731-737.
Designed to Fail: A Novel Mode of Collagen Fibril Disruption and Its Relevance to Tissue Toughness. SP Veres, JM Lee. Biophysical Journal (2012) 102(12), 2876-2884.