- Browse by Author
Browsing by Author "Surowiec, Rachel"
Now showing 1 - 3 of 3
Results Per Page
Sort Options
Item Am I big boned? Bone length scaled reference data for HRpQCT measures of the radial and tibial diaphysis in White adults(Elsevier, 2024-01-06) Warden, Stuart J.; Fuchs, Robyn K.; Liu, Ziyue; Toloday, Katelynn R.; Surowiec, Rachel; Moe, Sharon M.; Physical Therapy, School of Health and Human SciencesCross-sectional size of a long bone shaft influences its mechanical properties. We recently used high-resolution peripheral quantitative computed tomography (HRpQCT) to create reference data for size measures of the radial and tibial diaphyses. However, data did not take into account the impact of bone length. Human bone exhibits relatively isometric allometry whereby cross-sectional area increases proportionally with bone length. The consequence is that taller than average individuals will generally have larger z-scores for bone size outcomes when length is not considered. The goal of the current work was to develop a means of determining whether an individual's cross-sectional bone size is suitable for their bone length. HRpQCT scans performed at 30 % of bone length proximal from the distal end of the radius and tibia were acquired from 1034 White females (age = 18.0 to 85.3 y) and 392 White males (age = 18.4 to 83.6 y). Positive relationships were confirmed between bone length and cross-sectional areas and estimated mechanical properties. Scaling factors were calculated and used to scale HRpQCT outcomes to bone length. Centile curves were generated for both raw and bone length scaled HRpQCT data using the LMS approach. Excel-based calculators are provided to facilitate calculation of z-scores for both raw and bone length scaled HRpQCT outcomes. The raw z-scores indicate the magnitude that an individual's HRpQCT outcomes differ relative to expected sex- and age-specific values, with the scaled z-scores also considering bone length. The latter enables it to be determined whether an individual or population of interest has normal sized bones for their length, which may have implications for injury risk. In addition to providing a means of expressing HRpQCT bone size outcomes relative to bone length, the current study also provides centile curves for outcomes previously without reference data, including tissue mineral density and moments of inertia.Item Characterization of Biomimetic Spinal Cord Stimulations for Restoration of Sensory Feedback(2024-05) Zeiser, Sidnee L.; Yadav, Amol; Yoshida, Ken; Berbari, Edward; Sangha, Susan; Surowiec, RachelSensory feedback is a critical component for controlling neuroprosthetic devices and brain-machine interfaces (BMIs). A lack of sensory pathways can result in slow, coarse movements when using either of these technologies and, in addition, the user is unable to fully interact with the environment around them. Spinal cord stimulation (SCS) has shown potential for restoring these pathways, but traditional stimulation patterns with constant parameters fail to reproduce the complex neural firing necessary for conveying sensory information. Recent studies have proposed various biomimetic stimulation patterns as a more effective means of evoking naturalistic neural activity and, in turn, communicating meaningful sensory information to the brain. Unlike conventional patterns, biomimetic waveforms vary in frequency, amplitude, or pulse-width over the duration of the stimulation. To better understand the role of these parameters in sensory perception, this thesis worked to investigate the effects of SCS patterns utilizing stochastic frequency modulation, linear frequency modulation, and linear amplitude modulation. By calculating sensory detection thresholds and just-noticeable differences, the null hypothesis for stochastically-varied frequency and linear amplitude modulation techniques was rejected.Item Targeting Bone Quality in Murine Models of Osteogenesis Imperfecta, Diabetes, and Chronic Kidney Disease(2024-05) Kohler, Rachel; Wallace, Joseph; Allen, Matthew; Bidwell, Joseph; Surowiec, RachelSkeletal fragility can be caused by a wide array of diseases and disorders, but the most difficult etiologies to clinically circumvent are those in which the body loses not just bone mass but the ability to create healthy bone tissue. While in conditions such as osteoporosis (the most prevalent cause of age-related skeletal fragility in which elevated resorption without compensatory elevated formation leads to bone loss), interventions can target bone remodeling pathways to protect and increase bone mass, many other diseases are characterized by genetic and metabolic crippling of the remodeling process, rendering those same mass-based interventions less effective at reducing fracture risk. Osteogenesis imperfecta (OI) is a class of genetic disorders in which gene mutations affect the formation of collagen, a crucial building block of bone tissue that makes up 90% of its organic matrix, leading to lost bone mass and quality. As the main genetic causes of OI cannot currently be directly treated, therapeutic OI treatments are needed that improve tissue-level material properties. Similarly, metabolic conditions such as diabetes, a disorder in which the body cannot properly regulate blood sugar due to loss of insulin production and/or efficacy, can have multi-organ impacts including increased risk of developing chronic kidney disease and skeletal fragility. Type 2 diabetes is especially notorious for increasing fracture risk despite maintained or even increased apparent bone mass, which is strong evidence that intrinsic bone material properties are impaired by the disease state. A possible solution to the bone quality problem may be treatments that increase bone water content, as amplifying the water content of bone can improve multi-scale material properties such as collagen fibril elasticity and whole-bone toughness. Therefore, increasing bone hydration could be a way of improving tissue-level material properties, despite being unable to eradicate the genetic or metabolic disorders that alter how collagen is produced and incorporated into the bone matrix. To that end, this dissertation presents several studies that characterize models of osteogenesis imperfecta and diabetic kidney disease in mice and investigate methods of rescuing skeletal fragility in these animals through treatments that target both bone mass and bone quality with ties to tissue hydration.