Academic literature on the topic 'Growth plate injury'
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Journal articles on the topic "Growth plate injury"
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Hansen, Pamela. "Growth Plate Injury Prevention." Strategies 16, no. 4 (March 2003): 23–24. http://dx.doi.org/10.1080/08924562.2003.10591027.
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Caine, Dennis J. "Growth Plate Injury and Bone Growth: An Update." Pediatric Exercise Science 2, no. 3 (August 1990): 209–29. http://dx.doi.org/10.1123/pes.2.3.209.
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This literature review reveals an accumulating body of evidence indicating that growth disturbance associated with both chronic and acute growth plate injury occurs in young athletes and may be more prevalent than formerly believed. Skeletal complications resulting from these injuries may include progressive bone shortening, progressive deformity, joint incongruity, and arthritic sequelae. Against this background an increased concern for the welfare of young athletes is recommended. It is emphasized that back pain or pain around a joint in young athletes may be the symptom of significant growth plate changes that require accurate diagnosis, adequate treatment, and specific recommendations about return to activity. Suggestions are given for further research and prevention of growth plate injuries.
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Anton, Christopher, and Daniel J. Podberesky. "Little League shoulder: a growth plate injury." Pediatric Radiology 40, S1 (October 23, 2010): 54. http://dx.doi.org/10.1007/s00247-010-1868-3.
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Chung, Rosa. "Injury responses and repair mechanisms of the injured growth plate." Frontiers in Bioscience S3, no. 1 (2011): 117–25. http://dx.doi.org/10.2741/s137.
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Chung, Rosa, Bruce K. Foster, and Cory J. Xian. "The potential role of VEGF-induced vascularisation in the bony repair of injured growth plate cartilage." Journal of Endocrinology 221, no. 1 (January 24, 2014): 63–75. http://dx.doi.org/10.1530/joe-13-0539.
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Growth plate injuries often result in undesirable bony repair causing bone growth defects, for which the underlying mechanisms are unclear. Whilst the key importance of pro-angiogenic vascular endothelial growth factor (VEGF) is well-known in bone development and fracture repair, its role during growth plate bony repair remains unexplored. Using a rat tibial growth plate injury repair model with anti-VEGF antibody, Bevacizumab, as a single i.p. injection (2.5 mg/kg) after injury, this study examined the roles of VEGF-driven angiogenesis during growth plate bony repair. Histology analyses observed isolectin-B4-positive endothelial cells and blood vessel-like structures within the injury site on days 6 and 14, with anti-VEGF treatment significantly decreasing blood-vessel-like structures within the injury site (P<0.05). Compared with untreated controls, anti-VEGF treatment resulted in an increase in undifferentiated mesenchymal repair tissue, but decreased bony tissue at the injury site at day 14 (P<0.01). Consistently, microcomputed tomography analysis of the injury site showed significantly decreased bony repair tissue after treatment (P<0.01). RT-PCR analyses revealed a significant decrease in osteocalcin (P<0.01) and a decreasing trend in Runx2 expression at the injury site following treatment. Furthermore, growth plate injury-induced reduced tibial lengthening was more pronounced in anti-VEGF-treated injured rats on day 60, consistent with the observation of a significantly increased height of the hypertrophic zone adjacent to the growth plate injury site (P<0.05). These results indicate that VEGF is important for angiogenesis and formation of bony repair tissue at the growth plate injury site as well as for endochondral bone lengthening function of the uninjured growth plate.
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Chung, Rosa, and Cory J. Xian. "RECENT RESEARCH ON THE GROWTH PLATE: Mechanisms for growth plate injury repair and potential cell-based therapies for regeneration." Journal of Molecular Endocrinology 53, no. 1 (August 2014): T45—T61. http://dx.doi.org/10.1530/jme-14-0062.
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Injuries to the growth plate cartilage often lead to bony repair, resulting in bone growth defects such as limb length discrepancy and angulation deformity in children. Currently utilised corrective surgeries are highly invasive and limited in their effectiveness, and there are no known biological therapies to induce cartilage regeneration and prevent the undesirable bony repair. In the last 2 decades, studies have investigated the cellular and molecular events that lead to bony repair at the injured growth plate including the identification of the four phases of injury repair responses (inflammatory, fibrogenic, osteogenic and remodelling), the important role of inflammatory cytokine tumour necrosis factor alpha in regulating downstream repair responses, the role of chemotactic and mitogenic platelet-derived growth factor in the fibrogenic response, the involvement and roles of bone morphogenic protein and Wnt/B-catenin signalling pathways, as well as vascular endothelial growth factor-based angiogenesis during the osteogenic response. These new findings could potentially lead to identification of new targets for developing a future biological therapy. In addition, recent advances in cartilage tissue engineering highlight the promising potential for utilising multipotent mesenchymal stem cells (MSCs) for inducing regeneration of injured growth plate cartilage. This review aims to summarise current understanding of the mechanisms for growth plate injury repair and discuss some progress, potential and challenges of MSC-based therapies to induce growth plate cartilage regeneration in combination with chemotactic and chondrogenic growth factors and supporting scaffolds.
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Carter and MJ Aldridge. "Stress injury of the distal radial growth plate." Journal of Bone and Joint Surgery. British volume 70-B, no. 5 (November 1988): 834–36. http://dx.doi.org/10.1302/0301-620x.70b5.3192589.
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LEET, ARABELLA I., WILLIAM G. MACKENZIE, GEORGE SZOKE, and H. THEODORE HARCKE. "Injury to the Growth Plate After Pemberton Osteotomy*." Journal of Bone & Joint Surgery 81, no. 2 (February 1999): 169–76. http://dx.doi.org/10.2106/00004623-199902000-00004.
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Tobita, Masatoshi, Mitsuo Ochi, Yuji Uchio, Ryuji Mori, Junji Iwasa, Kenichi Katsube, and Tetsuhisa Motomura. "Treatment of growth plate injury with autogenous chondrocytes." Acta Orthopaedica Scandinavica 73, no. 3 (January 2002): 352–58. http://dx.doi.org/10.1080/000164702320155383.
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Lee, Eun Woo, Eui Chan Jang, Ki Seong Kim, Ho Rim Choi, and Jun Han Lee. "Chronic injury to the distal ulnar growth plate." Journal of the Korean Orthopaedic Association 28, no. 3 (1993): 1079. http://dx.doi.org/10.4055/jkoa.1993.28.3.1079.
Full textDissertations / Theses on the topic "Growth plate injury"
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Arasapam, Ganesan. "Roles of COX-2 and iNOS in the bony repair of the injured growth plate cartilage /." Title page and abstract only, 2005. http://web4.library.adelaide.edu.au/theses/09SB/09sba6629.pdf.
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Chung, Rosa. "Cellular and molecular mechanisms involved in bony tissue repair of injured growth plate cartilage in rats." Thesis, 2011. http://hdl.handle.net/2440/69319.
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Being cartilage, the growth plate is often injury prone. This remains to be a significant problem particularly in children where, due to the dynamic nature of their skeletal growth, injury to the growth plate can result in orthopaedic problems including limb-length discrepancy and angulation deformity. Previous studies have identified these problems as a direct result of formation of bony repair tissue at the injury site. Although the sequential post-injury responses (namely the inflammatory, fibrogenic, osteogenic and remodelling phases) have been previously well documented histologically, the
molecular and cellular events underlying the bony repair remain unclear. Using a well established rat growth plate injury model, this PhD project characterised presence of possible stromal progenitor cells within the mesenchymal infiltrate, roles of chemotactic growth factor PDGF-BB and protein kinase-D (PKD) in the fibrogenic response and subsequent bony repair events. Immunohistochemical analysis of tibial growth plates at different time points post-injury revealed cells immunopositive for alphasmooth muscle-actin (αSMA) or Activin-A Receptor Type II-like kinase- 3 (ALK-3) within the mesenchymal infiltrate, suggesting the potential presence of mesenchymal stem cell (MSC)-like cells. In addition, positive immunostaining of MSC-negative but endothelial cell-positive marker, von Willebrand Factor (vWF), also indicated that not all the cells within the infiltrate were MSC-like cells. Further analysis revealed that a portion of cells were immunopositive for osteogenic transcription factor core-binding factor-alpha 1 (cbf-α1) or chondrogenesis marker collagen-IIa, suggesting osteogenic and chondrogenic progenitors may also exist, respectively. Further studies are required for confirmation of MSC-like and progenitor cell existence within the infiltrate and their involvement in the bony repair. While the importance of the fibrogenic phase of repair is evident, the factors responsible for this cell influx are poorly studied. Previous studies have shown upregulation of the known key chemoattractant, PDGF-BB just prior to and during fibrogenic response. Studies in this project revealed that inhibition of PDGF signalling resulted in a significant delay in the healing responses in rats. Also in vitro studies found that PDGF-BB increased bone marrow stromal cell migration into an artificial “wound” site (P<0.005), which can be suppressed by the PDGF receptor inhibitor. These results suggest that PDGF signalling contributes to growth plate injury repair by promoting mesenchymal progenitor cell infiltration and subsequent tissue repair. Fibrogenic cells within the injury site can differentiate into bone or cartilage cells. However, what signals/ factors underlie these cell differentiation processes and bony repair remain unexplored. While osterix is one known important transcriptional factor for osteoblast maturation, and PKD is known to be involved in transcription of osterix, their potential roles in growth plate bony repair are unknown and were investigated in this project. Micro-CT and histology analysis of injury sites in rats treated with PKD inhibitor revealed significantly lower amount of bone formed after inhibiting PKD
signalling (P<0.05). Consistently, inhibitor-treated animals showed decreased mRNA expression of bone-related genes (osterix and osteocalcin) and increased levels of cartilage-related genes
(collagen-IIa and Sox9). In support, in vitro experiments showed that addition of PKD inhibitor during chondrogenic differentiation of rat primary bone marrow stromal progenitor cells resulted in a significant increase in collagen-IIa expression (P<0.05). These results suggest that PKD is an important factor for growth plate bony repair and blocking PKD activity after growth plate injury may result in partial suppression of osterix, less bone formation and potentially more desirable cartilage repair.Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2011
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Macsai, Carmen Elizabeth. "Cellular and molecular mechanisms involved in the repair of the injured growth plate in young rats." Thesis, 2012. http://hdl.handle.net/2440/77097.
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The growth plate cartilage, which is located at the ends of children’s long bones, is responsible for longitudinal growth of the skeleton. However, due to its cartilaginous composition and its location, the growth plate is commonly injured, mostly through fractures. An undesirable outcome to growth plate fracture is the bony repair of the injured cartilage at the fractured area. Consequently, children often incur skeletal angular deformities and growth arrest. Current corrective surgical treatments for these outcomes are highly invasive, and therapeutic interventions are not possible as little is known about the mechanisms and pathways that lead to bone bridge formation. Using a rat model, previous studies have shown sequential inflammatory, fibrogenic, osteogenic and bone maturation responses involved in the bony repair of the injured growth plate. However, structural changes in the growth plate, at both the injury site and at the non-injured area, have not been closely examined previously, and little is known about the molecular mechanisms underlying the bony repair. Therefore, this PhD study, using a rat tibial growth plate injury model, aimed to examine the effects of growth plate injury on the structure and composition of the injured growth plate in a longitudinal study using micro-CT and histology. Microarray analysis of the injury site only, collected using laser capture microdissection was used to identify potential cellular and molecular mechanisms involved in bone bridge formation. In addition, Real Time RT-PCR on adjacent uninjured growth plate was used to examine potential cellular/molecular changes at the uninjured area and on whole growth plate scrapes to examine the potential involvement of Wnt signalling in bone bridge formation. Micro-CT analysis revealed a significant increase in bone material within the injury site (when compared to normal) at 14 and 60 days post-injury, where 12% and 40% of the injury site was replaced by bone, respectively. Interestingly, although there were no changes in growth plate thickness between injured and normal rats at either day 14 or 60, at day 60, many small bone tethers formed at the adjacent growth plate outside the injury site but none were found in normal aged-matched control rats. Histological studies revealed dereased proliferation but increased apoptosis of chondrocytes at the adjacent growth plate cartilage, and RT-PCR analysis revealed differential expression of apoptosis-regulatory genes Bcl-2 and FasL (compared to normal), confirming the increase in apoptosis in the adjacent uninjured growth plate. Down-regulation of Sox-9 and IGF-1 on days 7 and 14 suggests that growth plate injury may slow down the rate of longitudinal growth by decreasing chondrocyte proliferation and/or differentiaiton soon after injury. Lastly, bone matrix protein osteocalcin was increased on day 60, suggesting degeneration and bone formation at the adjacent uninjured area. Microarray analysis identified changes in several key BMP and Wnt signalling components across the time-course of bone bridge formation, including BMP-2, BMP-6, BMP-7, chordin, chordin-like 2, and Id-1, and β-catenin, Csnk2a1, SFRP-1 and SFRP-4, respectively, in early stages of bone bridge formation (day 4 and day 8). Osteocalcin expression was also prominent at day 8, supportive of osteoblast development and bone formation. During later stages (day 14), active bone formation and remodelling was prominent and was largely regulated by the BMP signalling pathway (increased BMP-1 and BMP-6 but decreased inhibitor chordin), as well as by Traf6, Fgfr1, osteopontin, Mmp9 and Wnt signalling, where several genes were up and down-regulated. Expression levels of Wnt signalling inhibitors (SFRP-1, SFRP-4 and Wisp1) were increased at days 8 and 14 and may be negatively regulating bone formation during the osteogenic phases of the repair of the growth plate injury site. Findings were also suggestive of an overall increase in the canonical Wnt signalling pathway at days 4 and14, supported by increased expression of β-catenin and drecreased expression of Wnt inhibitors, and decreased expression of Fzd1 and Fzd2 and increased Lef1 expression, respectively. Overall, this study found a complex balance between the canonical and non-canonical Wnt pathways as well as an association with BMP signalling over the time-course of bone bridge formation. Lastly, Real-Time PCR on Wnt signalling components revealed significant changes in gene expression of Wnt genes, receptors and inhibitors, but were inconclusive as the method of tissue isolation was not specific enough to represent true changes in gene expression.Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2012
Books on the topic "Growth plate injury"
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Wilson-MacDonald, James, and Colin Nnadi. Fractures of the spine in children. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199550647.003.014003.
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♦ Spinal injuries in children are rare♦ Pseudosubluxation above C4 is common in healthy children so the sign needs careful interpretation♦ Epiphyseal plates and a high incidence of skeletal variability make the interpretation of spinal x-rays in children difficult. Anterior wedging is also normal as is interpedicular widening♦ Spinal cord injury without radiographic abnormality (SCIWORA) may occur for up to one-third of spinal injuries in children♦ Deformity secondary to trauma tends to deteriorate with growth.
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Schielke, Hugo J., Bethany L. Brand, and Ruth A. Lanius. The Finding Solid Ground Program Workbook. Oxford University Press, 2022. http://dx.doi.org/10.1093/med-psych/9780197629031.001.0001.
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You can heal, recover from trauma, and grow, and this workbook can guide you through this important, meaningful work, step by step, at a pace that feels safe for you. If you’ve experienced trauma, life may sometimes feel hopeless, full of feeling too much or too little. You may feel that the world is a terrifying and dangerous place. You may even feel like you don’t deserve anything positive, especially if you have been hurt by people you needed, loved, or relied on. To escape the pain, you may have been disconnecting from yourself and the world, including in risky or unsafe ways. In this workbook, the expert authors guide you step by step along the path of healing from trauma and offer specific exercises to practice daily that will help you feel safer and develop a grounded, worthy sense of self. This book includes the information sheets and exercises that are the foundation for the Finding Solid Ground program. The companion book, Finding Solid Ground: Overcoming Obstacles in Trauma Treatment, provides the theoretical, clinical, and research rationale for the program. This workbook breaks recovery into practical manageable steps that can be immediately implemented. Participation in the Finding Solid Ground program in the Treatment of Patients with Dissociative Disorder (TOP DD) Network study was associated with increased ability to manage emotions in healthy ways and reduced dissociation, posttraumatic stress symptoms, and self-injury. Join the international community of people who have used this program to find solid ground!
Book chapters on the topic "Growth plate injury"
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Adhikari, Sapana P. "Orthopedics." In Diagnosketch, 73–94. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/med/9780197636954.003.0006.
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Abstract This chapter includes various images that pertain to the orthopedic system. The first images depict different types of broken bones followed by an image that depict growth plate injury. The next images depict compression fracture, arthiritis, bursitis, rib fracture, pneumothorax, back pain, sacroiliitis, sciatica, cervical strain, motor vehicle accident, osteoarthritis, knee strain, joint diseases like gout and septic joint, Baker’s cyst, ankle pain, carpal tunnel syndrome and plantar fasciitis.
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Semple-Hess, Janet. "Pediatric Orthopedic Emergencies." In Pediatric Emergencies, 410–42. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190073879.003.0037.
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Children’s bones, due to their continual maturity during childhood and into late adolescence and their unique features such as growth plates, can present a challenge to the emergency physician. Interpretation of radiographs when looking for fractures in growing children, as well as deciding on treatment and determining whether to employ surgical versus nonsurgical management, requires knowledge of the patterns of injury in children. This chapter discusses these injuries as well as fractures related to child abuse, overuse injuries, back pain in children, radial head subluxation, slipped capital femoral epiphyses, avulsion fractures of the pelvis, Perthes disease, and infectious diseases (osteomyelitis and septic arthritis).
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Yung, Siyi Zhang, Kimberly Cheong, and James Heaysung Lee. "Preventive General Pediatrics." In General Pediatrics Board Review, 1–43. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190848712.003.0001.
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The preventive care chapter of this book examines aspects of a pediatric patient’s well-child care that may be relevant to the general primary care pediatrician in an outpatient setting. It reviews normal growth and nutrition, developmental milestones and how to conduct surveillance and screening, and routine vaccinations, as well as the precautions and special considerations for specific immunizations and diseases. It also reviews common anticipatory guidance and key injury prevention and safety discussions that should take place at each well-child check interval according to the American Academy of Pediatrics recommendations for preventive pediatric healthcare. This chapter is written for pediatric residents who are still in training as well as for the practicing pediatrician who wishes to study and refresh his or her knowledge of updated evidence-based guidelines in primary care pediatrics.
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Costa, Júlio, Pedro Figueiredo, Fábio Y. Nakamura, and João Brito. "The Importance of Sleep in Athletes." In Exercise Physiology [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102535.
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Sleep is an essential component for athletes’ recovery from fatigue, due especially to its physiological and psychological restorative effects. Moreover, sleep is extremely important for numerous biological functions, and sleep deprivation can have significant effects on athletic performance in short-, medium-, and long term. For example, and considering the physiology of sleep for athletes, some hormonal responses that take place in the lead up to and during sleep (e.g., growth hormone—important role in muscle growth and repair) may be affected following exercise (i.e., training and competition), especially when compared with non-athlete’s populations. Thus, monitoring sleep is also crucial to understand responses to training and readiness, enabling appropriate planning. Importantly, sleep monitoring also intends to reduce the risk of injury, illness, and nonfunctional overreaching. Moreover, an “individual approach” in athletes monitoring could help in better prescribe training contents and more adequately manage fatigue, as well as recommend pertinent post-match recovery strategies, such as sleep hygiene interventions. Overall, for understanding the athlete’s sleep patterns/responses and to optimize the recovery strategies, it is crucial for comprehensive monitoring of his/her health, performance, fitness, and fatigue status.
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Becker, Richard C., and Frederick A. Spencer. "Historical Perspectives in Hemostasis, Coagulation, and Fibrinolysis: A Foundation for Understanding Thrombotic Disorders and Developing Effective Treatment." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0005.
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Hemostasis, the prompt cessation of bleeding at a site of vascular injury, is among the most fundamental physiologic and teleologically vital defense mechanisms in nature. Without a functionally intact hemostatic mechanism, death could ensue rapidly even after minor traumas associated with everyday life. In mammalian blood coagulation, regulated by a complex network of integrated biochemical events, five protease factors (f ) (fIIa [thrombin], fVIIa, fIXa, fXa, and protein C) interact with five cofactors (tissue factor, f VIIIa, fVa, thrombomodulin, and protein S) to regulate the generation of fibrin (Davidson et al., 2003). Although each component of the mammalian coagulation network has unique functional properties, available data based on gene organizations, protein structure, and sequence analysis suggest that it may have resulted from the reduplication and diversification of two gene structures over 400 million years ago. A vitamin K–dependent serine protease is composed of a γ-carboxylated glutamic acid (GLA) epidermal growth factor-like (EGF) 1–EGF 2-serine protease domain structure common to fVII, fIX, fX, and protein C, and the A1-A2-B-AB-C1-C2 domain structure common to fV and fVIII. Prothrombin is also a vitamin K–dependent serine protease; however, it contains kringle domains rather than EGF domains (suggesting a replacement during gene duplication and shuffling). Analyses of active site function amino acid residues reveal distinguishing characteristics of thrombin from other serine proteases, supporting its position as the ancestral blood enzyme (Krem and Cera, 2002; McLysaght et al., 2002). The rapid transformation of fluid blood to a gel-like substance (clot) has been a topic of great interest to scientists, physicians, and philosophers since the days of Plato and Aristotle ( Jewett, 1892; Lee, 1952). However, it was not until the beginning of the 18th century that blood clotting (coagulation) was appreciated as a means to stem blood loss from wounds (hemostasis) (Petit, 1731). As with other areas of science, the microscope played a pivotal role in the understanding of coagulation. In the mid-17th century, Marcello Malpighi separated the individual components of a blood clot into fibers, cells, and serum (Forester, 1956).
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Schatz, Jeffrey, and Eve S. Puffer. "Neuropsychological Aspects of Sickle Cell Disease." In Comprehensive Handbook of Childhood Cancer and Sickle Cell Disease. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195169850.003.0033.
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The purpose of this chapter is to summarize current knowledge about the brain bases of the psychological effects of sickle cell disease (SCD). For the purpose of this chapter, we categorize two broad approaches commonly used to identify the behavioral correlates of brain function. Psychological or behavioral models are used that have been developed independent of the study of the nervous system. A common example of this approach is psychoeducational assessment, which focuses on constructs relevant to functional outcomes such as IQ scores and academic skills. Psychological models are also used for assessments that have been derived more directly from neuroscience. This approach typically involves assessing specific neurocognitive domains derived from theories of brain organization, such as language, visual-spatial, and executive functions. SCD offers a challenge to neuropsychologists because of the multiple factors to consider for understanding brain function. Because SCD is a genetic condition present from birth, the disease is likely to interact with developmental factors in infancy or early childhood. Because of social-historical factors, individuals with SCD are more likely than the general population to grow up in difficult social and economic conditions that place them at higher risk for some adverse brain effects. The disease itself also has specific effects on the brain that may lead to acquired brain injury during childhood or later in life. This context creates a challenge; there are multiple potential routes for brain effects that could have an impact on psychological functioning throughout the life span. We discuss research to date on a number of these factors, including pregnancy and birth risks, social and environmental factors in early childhood, and more direct effects of the disease on the brain. These factors are discussed in their likely order of impact based on current research, with direct effects of SCD on the brain having the most robust and well-established effects on neuropsychological functioning. An overview is presented in table 24-1. Mothers of children born with SCD either have SCD or trait. Data on pregnancy outcomes of mothers with SCD or trait indicate that most of these pregnancies are successful and without serious complications (Koshy, 1995; Sun, Wilburn, Raynor, & Jamieson, 2001).
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Glatt, Stephen J., Stephen V. Faraone, and Ming T. Tsuang. "Is Schizophrenia A Neurodevelopmental Disorder?" In Schizophrenia. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198813774.003.0014.
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The research we have discussed suggests that schizophrenia occurs when abnormal genes and environmental risk factors combine to cause brain dysfunction. In the past two decades, several researchers— notably Drs Daniel Weinberger, Larry Seidman, and Patricia Goldman- Rakic— have concluded that schizophrenia is a neurodevelopmental brain disorder. This suggests that schizophrenia emerges because of the way the brain is built early in life. To understand this concept, consider brain disorders that do not have a neurodevelopmental origin but instead, come about because of the way the brain breaks down after it is developed. We call these disorders neurodegenerative because the causes of the disease attack and degrade a normal brain. The senility of old age, which doctors call dementia, is a common example. When some people age, their brain is degraded by events such as many strokes or the ravages of Alzheimer’s disease. After a few years, a person who once functioned normally can no longer do simple tasks. Other examples are acquired brain syndromes, which occur after an injury to the head, and disorders due to the ingestion of toxic substances (e.g., drugs, lead paint). In each of these cases, some external agent has acted on a normal brain to make it abnormal. In neurodevelopmental disorders, the brain does not develop (i.e., grow) properly. In other words, it was never really normal to begin with. We know that genes contain the ‘blueprint’ for building the brain. For schizophrenia, this blueprint contains errors so that the brain is not ‘built’ correctly. Dr Patricia Goldman- Rakic suggested that certain brain cells in individuals with schizophrenia do not ‘migrate’ correctly during development. That is, normal brain development requires that cells locate themselves in the right spot and connect to one another in specific patterns. In schizophrenia, it may be that some cells are in the wrong place, some do not make necessary connections, and others make connections that should not be made. It is as if the blueprint for a home told the electrician to put the light switch for the kitchen in the living room.
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Bauder, Harald. "Discourse of Foreign Farmworkers." In Labor Movement. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195180879.003.0018.
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In 1995, the Ontario provincial government, under conservative premier Mike Harris, repealed legislation put in place the year before by the former central-left government of Bob Rae that protected Ontario’s agricultural workers under the province’s labor code. Migrant workers were also affected by this legislation. In late April 2001, Mexican workers staged a two-day strike in a Leamington greenhouse, and in May 2001, approximately 100 Mexican offshore farmworkers protested in Leamington against substandard working and living conditions, including the lack of safety protection against pesticides, overcrowded living spaces, long working hours, no overtime pay, insufficient medical care, unfair government paycheck deductions, and threats of deportation to their home countries. After these events, some of the protesters were dismissed from the offshore program and sent back to Mexico. The media reports on these protests varied widely. Reports were either sympathetic to the workers’ concerns, or they condemned the protests as unjustified nagging by a small minority of angry workers. Several of the newspaper reports that were sympathetic to the protesting workers (e.g., Kitchener-Waterloo [Ontario] Record 2001; St. Catharines [Ontario] Standard 2001) presented the same quote from an anonymous migrant worker who criticizes the unfair treatment of foreign migrant workers by Canadian employers: “What I’ve realized here in Canada is that employers don’t hire us as human beings. They think we’re animals. . . . The first threat that they always make is that if you don’t like it, you can go back to Mexico.” In a report about the same protests, the Windsor (Ontario) Star quoted farmworkers who articulated similar concerns: “‘Growers don’t care whether you’re injured or not, they only care when you’re healthy,’” and “[the grower] said, ‘If you don’t work faster, you’ll be sent back to Mexico’” (Welch 2001). Other articles gave the events a different spin. A fact-finding mission after the protests uncovered that only a few migrant workers filed formal complaints against their employers. The lack of complaints was interpreted as assurance that workers were satisfied with their employment circumstances.
Conference papers on the topic "Growth plate injury"
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Basile, Susan, and Xiaopeng Zhao. "Modeling and Analysis of Proximal Tibial Growth Plate Fractures in Adolescents." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203651.
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Today, children and adolescents are participating heavily in organized athletics year-round. Each year, approximately one third of these children will experience a serious injury requiring a doctor’s or hospital visit. Physeal, or growth plate fractures, are one such type of overuse injury commonly seen in adolescents. At the knee joint, injuries in adolescents occur most often in the proximal region of the tibia as opposed to the middle or distal thirds of the tibia, or in the soft tissues of the joint, as seen in adults. While the exact reasons for this difference have not been directly and definitively quantified, several hypotheses have been suggested. They include differences in movement strategies, changes in limb inertial and material properties, and the timing of these changes in relation to one another. This work aims to compare the changes in and interaction of inertial properties of the lower leg and forces transmitted through the patellar tendon, along with tibiofemoral contact before, during, and after puberty. Forces were first determined using Kane’s method of dynamics in conjunction with an isometric knee extension study yielding separate adult and youth data. These results were then extended to a finite element analysis to load tibial models and investigate changes in stress and strain at the proximal tibia.
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Konz, Regina J., Vijay K. Goel, Leon J. Grobler, Nicole M. Grosland, Kevin F. Spratt, Jeffrey L. Scifert, and Koichi Sairyo. "The Pathomechanism of Spondylolytic Spondylolisthesis in Pediatric Lumbar Spines: In Vitro and Finite Element Assessments." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0008.
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Abstract Experimentally, it was determined that the weakest link for A-P shear force in the immature baboon lumbar spine with pars interarticularis defects was between the growth-plate and osseous end-plate, even with an injured disc. Immature baboon finite element models (FEM) as well as an immature human FEM were developed. Numerical results predicted that a thin pars will increase stresses at the pars, eventually leading to a pars defect. Furthermore, a fracture in the pars interarticularis results in substantially greater loads being carried by the growth-plates. Upon combination of the experimental and numerical aspects of this study, it is possible to predict the A-P shear force needed for spondylolisthesis to occur.
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Sakariassen, S. K., E. Fressinaud, D. Meyer, J. J. Sixma, and R. H. Baumgartner. "RHEOLOGY AND PLATELET-SURFACE ADHESION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643987.
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The process of platelet adhesion to sites of vascular injury is pivotal for the arrest of bleeding. The same process may, on the other hand, lead to formation of mural thrombi and may play a role in atherogenesis through the release of platelet-derived growth factor. The events of platelet-surface adhesion may be divided into initial attachment and the subsequent spreading on the surface. These interactions are mediated by a variety of factors, including glycoproteins (GP) in the platelet membrane, von Willebrand factor (vWF) in plasma, and the composition of the surface.However, in most instances their effects on adhesion are dependent on the shear rate.We have investigated the importance of some of these factors in flowing blood at shear rates ranging from those present in large arteries (≃ 200 sec-1) to those present in the microcirculation (≃2600 sec-1). We used annular- and parallel-plate-perfusion chambers with de-endothelial-ized human arteries and collagen-coated surfaces, respectively. A highly reactive surface, such as formed by collagen fibrils, triggers rapid platelet adhesion and thrombus growth on the upstream portion of the surface. This rapid consumption of platelets depletes the boundary layer of the blood flow of platelets, resulting in fewer platelets to adhere further downstream. This effect is most pronounced at shear rates below 650 sec-1, i.e., at conditions with low radial transport of platelets. This phenomenon, apparently physical in nature, we have termed "axial dependence."Deficiency of GPIb results in impaired initial attachment of platelets to subendothelium, a defect which virtually abolishes initial attachment at shear rates above 500 sec-1. However, inhibition of binding of ADP to its putative 100Kd GP receptor by the adenosine analogue 5'-p-fluoro-sulfonyl-adenosine completely prevents initial attachment of platelets. Conversely, deficiency of GPIIb/IIIa results in partially impaired platelet spreading (20-50%), but only at shear rates above 1000 sec-1; deficiency of GPIa results in no platelet spreading, independent of the shear rate. The importance of GPIb and GPIIb/IIIa in adhesion was further demonstrated by experiments using monoclonal antibodies to either GPIb or GPIIb/IIIa.Addition of these antibodies to blood from healthy subjects duplicates the effects found in the natural deficiency states. Furthermore, we used two monoclonal antibodies to vWF, which specifically inhibit either ristocetin-induced binding of vWF to GPIb or thrombin/ADP-induced binding of vWF to GPIIb/IIIa. Each of these antibodies inhibits ≃ 90% of adhesion at 2600 sec-1 shear rate, while no effect is seen at 650 sec-1. Inhibition of binding of vWF, fibronectin, and fibrinogen to GPIIb/IIIa by a dodecapeptide of the γ-carboxy terminus of fibrinogen inhibits ≃ 30% of adhesion in normal blood at 2600 sec-1 shear rate. No effect is present at 650 sec-1 shear rate.These experiments indicate that (1) ADP and/or its putative receptor and GPIb are involved in the early phase of adhesion, whereas (2) GPIa and GPIIb/IIIa are involved in the spreading reaction. It is also apparent that (3) GPIb and GPIIb/IIIa act as receptors for vWF in the process of bridging the platelet to sites of vascular injury, and that (4) vWF is required for both initial attachment and spreading. (5) The shear rate has an unambiguous role in these complex interactions and in the "axial dependence" phenomenon.
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Galle, Beth, Hui Ouyang, Riyi Shi, and Eric A. Nauman. "A Compressible, Transversely Isotropic, Hyperelastic Constitutive Model of the Guinea Pig Spinal Cord White Matter." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176676.
Full textAbstract:
Slow compression spinal cord injuries occur when the spinal canal narrows, the consequence of degenerative, infective, or oncologic legion growth, and exerts pressure throughout the spinal cord. Transverse tissue compression results in an amalgamation of mechanical insults at the cellular level [1]. However, the mechanism of cellular injury has yet to be elucidated. We have recently developed a hyperelastic, isotropic plane strain finite element model (FEM) of the guinea pig spinal cord white matter response to transverse compression based on force-deformation curves measured in vitro. The strongest correlation with in vitro axonal injury density was the combination of the in-plane shear stress with the in- and out-of-plane normal stresses quantified using the FEM [2]. However, we hypothesize that the guinea pig spinal cord white matter is a transversely isotropic material. Material anisotropy must be incorporated into the FEM to achieve enhanced model accuracy, specifically, the prediction of axial stresses within the spinal cord parenchyma during transverse tissue compression. Therefore, the objective of the present study was to propose a compressible, transversely isotropic, hyperelastic constitutive model of the guinea pig spinal cord white matter.
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Higuita-Castro, Natalia, Yan Huang, Cosmin Mihai, Derek J. Hansford, and Samir N. Ghadiali. "Influence of Wall Compliance on Epithelial Cell Structure and Injury During Airway Reopening." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19568.
Full textAbstract:
The present work describes the implementation of an in-vitro model for the evaluation of the injury mechanisms of lung epithelial cells during simulated airway reopening events. Collagen-coated polyacrylamide substrates with different rigidities served as cell culture substrates, and a parallel plate perfusion chamber was used for simulating the reopening of fluid-filled airways. Human alveolar epithelial cell (A549) monolayers were grown to confluence on the different substrates and the cellular response was evaluated in terms of cytoskeletal distribution, proliferation rate, and cell stiffness. One and five reopening events were simulated, and cell response was characterized via live/dead fluorescence imaging. Cells cultured on stiffer substrates showed higher proliferation rate, as well as a more spread and tightly packed morphology. Airway reopening simulations showed that cells cultured on softer substrates are less susceptible to cell injury.
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Zhang, Bolun, Daniel Farley, Heidi-Lynn Ploeg, and Michael Zinn. "Validation of Feedback Control Approach for an Implantable Limb Lengthening Device." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3456.
Full textAbstract:
Lower limb length discrepancy (LLD), defined by unequal length of paired lower limbs, contributes to lower back pain, osteoarthritis of the hip, and stress fractures [1–3]. The Center for Disease Control and Prevention estimated that there were approximately 700 children born with LLD each year in US [4]. Patients may receive distraction osteogenesis treatment, in which an osteotomy is performed on the shorter limb, and mechanical force is applied to gradually distract the two halves of the bone during the healing process. This stretches the bone callus during healing to achieve desired limb length upon callus consolidation [5]. The current correction devices are external fixators that leave unsightly scars and are prone to infection [6]. While recently developed intramedullary devices address many of the persistent issues with external lengthening devices, size limitations and potential damage to the bone growth plates make them impractical for use in children [7, 8]. The proposed research addresses an unmet need by developing a novel implantable extramedullary device for LLD correction that is targeted for pediatric use. The device will be implantable, submuscular, and fixed to the outside surface of the bone (extramedullary), thus allowing for use in children without concern for injury to the growth plates. The device’s function will be similar to an external fixator; however, it will not require exposed hardware, which increases risk of infection, or muscle penetration from the pins, which causes pain. Additionally, the device incorporates real-time control of the distraction rate, reducing the risk of complications arising from fixed rate distraction such as premature consolidation and non-union of the callus. [9–11]. The investigators of this study have previously designed and constructed a distraction mechanism prototype and test frame [10]. The current study aims to validate the real-time controller of the prototype.