Academic literature on the topic 'Growth plate Diseases'

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Journal articles on the topic "Growth plate Diseases"

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Xie, Yangli, Siru Zhou, Hangang Chen, Xiaolan Du, and Lin Chen. "RECENT RESEARCH ON THE GROWTH PLATE: Advances in fibroblast growth factor signaling in growth plate development and disorders." Journal of Molecular Endocrinology 53, no. 1 (August 2014): T11—T34. http://dx.doi.org/10.1530/jme-14-0012.

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Skeletons are formed through two distinct developmental actions, intramembranous ossification and endochondral ossification. During embryonic development, most bone is formed by endochondral ossification. The growth plate is the developmental center for endochondral ossification. Multiple signaling pathways participate in the regulation of endochondral ossification. Fibroblast growth factor (FGF)/FGF receptor (FGFR) signaling has been found to play a vital role in the development and maintenance of growth plates. Missense mutations inFGFsandFGFRscan cause multiple genetic skeletal diseases with disordered endochondral ossification. Clarifying the molecular mechanisms of FGFs/FGFRs signaling in skeletal development and genetic skeletal diseases will have implications for the development of therapies for FGF-signaling-related skeletal dysplasias and growth plate injuries. In this review, we summarize the recent advances in elucidating the role of FGFs/FGFRs signaling in growth plate development, genetic skeletal disorders, and the promising therapies for those genetic skeletal diseases resulting from FGFs/FGFRs dysfunction. Finally, we also examine the potential important research in this field in the future.
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Holzer, Tatjana, Kristina Probst, Julia Etich, Markus Auler, Veronika S. Georgieva, Björn Bluhm, Christian Frie, et al. "Respiratory chain inactivation links cartilage-mediated growth retardation to mitochondrial diseases." Journal of Cell Biology 218, no. 6 (May 13, 2019): 1853–70. http://dx.doi.org/10.1083/jcb.201809056.

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In childhood, skeletal growth is driven by transient expansion of cartilage in the growth plate. The common belief is that energy production in this hypoxic tissue mainly relies on anaerobic glycolysis and not on mitochondrial respiratory chain (RC) activity. However, children with mitochondrial diseases causing RC dysfunction often present with short stature, which indicates that RC activity may be essential for cartilage-mediated skeletal growth. To elucidate the role of the mitochondrial RC in cartilage growth and pathology, we generated mice with impaired RC function in cartilage. These mice develop normally until birth, but their later growth is retarded. A detailed molecular analysis revealed that metabolic signaling and extracellular matrix formation is disturbed and induces cell death at the cartilage–bone junction to cause a chondrodysplasia-like phenotype. Hence, the results demonstrate the overall importance of the metabolic switch from fetal glycolysis to postnatal RC activation in growth plate cartilage and explain why RC dysfunction can cause short stature in children with mitochondrial diseases.
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Gersing, Alexandra S., Klaus Woertler, Pia M. Jungmann, Christine Bollwein, and Benedikt J. Schwaiger. "Vertebrae, Vertebral End Plates, and Disks: Concepts and Specific Pathologies." Seminars in Musculoskeletal Radiology 23, no. 05 (September 25, 2019): 489–96. http://dx.doi.org/10.1055/s-0039-1693976.

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AbstractVertebral end plates cover the osseous vertebral body. The integrity of the cartilaginous end plates is of great importance for the entire vertebral segment because the vascularized end plate provides the nutrition for the avascular disk. Yet several pathologies may occur at these end plates at the embryonic stage, in childhood to adolescence (e.g., ossification and segmentation disorders of the spine, persistent notochord, slippage of the growth plate), as well as in the mature spine of an adult (degenerative disk disease), that may impact the integrity of the cartilaginous end plate and therefore lead to severe diseases of the spine. This article reviews specific congenital, developmental, and degenerative disorders of the vertebral end plate as well as both established and newly introduced imaging techniques, such as ultrashort echo time imaging based on magnetic resonance imaging, that are suitable for imaging of the end plate.
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Sederquist, Bettina, Paola Fernandez-Vojvodich, Farasat Zaman, and Lars Sävendahl. "RECENT RESEARCH ON THE GROWTH PLATE: Impact of inflammatory cytokines on longitudinal bone growth." Journal of Molecular Endocrinology 53, no. 1 (April 7, 2014): T35—T44. http://dx.doi.org/10.1530/jme-14-0006.

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Children with inflammatory diseases usually display abnormal growth patterns as well as delayed puberty. This is a result of several factors related to the disease itself, such as malnutrition, hypercortisolism, and elevated levels of pro-inflammatory cytokines. These factors in combination with glucocorticoid treatment contribute to growth retardation during chronic inflammation by systemically affecting the major regulator of growth, the GH/IGF1 axis. However, recent studies have also shown evidence of a direct effect of these factors at the growth plate level. In conditions of chronic inflammation, pro-inflammatory cytokines are upregulated and released into the circulation. The most abundant of these, tumor necrosis factor α, interleukin 1β (IL1β), and IL6, are all known to directly act on growth plate cartilage to induce apoptosis and thereby suppress bone growth. Both clinical and experimental studies have shown that growth retardation can partly be rescued when these cytokines are blocked. Therefore, therapy modulating the local actions of these cytokines may be effective for preventing growth failure in patients with chronic inflammatory disorders. In this review, we report the current knowledge of inflammatory cytokines and their role in regulating bone growth.
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Guevara-Morales, Johana M., Michael Frohbergh, Hector Castro-Abril, Juan J. Vaca-González, Luis A. Barrera, Diego A. Garzón-Alvarado, Edward Schuchman, and Calogera Simonaro. "Growth Plate Pathology in the Mucopolysaccharidosis Type VI Rat Model—An Experimental and Computational Approach." Diagnostics 10, no. 6 (May 31, 2020): 360. http://dx.doi.org/10.3390/diagnostics10060360.

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Background: Mucopolysaccharidoses (MPS) are a group of inherited metabolic diseases caused by impaired function or absence of lysosomal enzymes involved in degradation of glycosaminoglycans. Clinically, MPS are skeletal dysplasias, characterized by cartilage abnormalities and disturbances in the process of endochondral ossification. Histologic abnormalities of growth cartilage have been reported at advanced stages of the disease, but information regarding growth plate pathology progression either in humans or in animal models, as well as its pathophysiology, is limited. Methods: Histological analyses of distal femur growth plates of wild type (WT) and mucopolysaccharidosis type VI (MPS VI) rats at different stages of development were performed, including quantitative data. Experimental findings were then analyzed in a theoretical scenario. Results: Histological evaluation showed a progressive loss of histological architecture within the growth plate. Furthermore, in silico simulation suggest the abnormal cell distribution in the tissue may lead to alterations in biochemical gradients, which may be one of the factors contributing to the growth plate abnormalities observed, highlighting aspects that must be the focus of future experimental works. Conclusion: The results presented shed some light on the progression of growth plate alterations observed in MPS VI and evidence the potentiality of combined theoretical and experimental approaches to better understand pathological scenarios, which is a necessary step to improve the search for novel therapeutic approaches.
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Kosowska-Shick, Klaudia, Lois M. Ednie, Pamela McGhee, Kathy Smith, Cynthia D. Todd, Amanda Wehler, and Peter C. Appelbaum. "Incidence and Characteristics of Vancomycin Nonsusceptible Strains of Methicillin-Resistant Staphylococcus aureus at Hershey Medical Center." Antimicrobial Agents and Chemotherapy 52, no. 12 (October 6, 2008): 4510–13. http://dx.doi.org/10.1128/aac.01073-08.

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ABSTRACT All 982 methicillin-resistant Staphylococcus aureus strains collected from August 2006 to December 2007 were tested for vancomycin susceptibility by using 3-μg/ml vancomycin brain heart infusion screening plates, a vancomycin Etest, and a vancomycin/teicoplanin macro Etest. Three vancomycin-intermediate Staphylococcus aureus (VISA) (0.3%) and two heterogeneous VISA (0.2%) isolates were identified. The screening method yielded 895 cases of ≤1 colony and 87 positive results (with growth of >1 colony after 48 h); further Etests showed 82/87 isolates with growth on screening plates to be false positive. Repeat testing showed a false-positivity rate of only 15 of the original 87 isolates by plate screening.
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Evans, K. D., L. E. Sheppard, D. I. Grossman, S. H. Rao, R. B. Martin, and A. M. Oberbauer. "Long Term Cyclic Pamidronate Reduces Bone Growth by Inhibiting Osteoclast Mediated Cartilage-to-Bone Turnover in the Mouse." Open Orthopaedics Journal 2, no. 1 (July 14, 2008): 121–25. http://dx.doi.org/10.2174/1874325000802010121.

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Bisphosphonates, used to treat diseases exhibiting increased osteoclast activity, reduce longitudinal bone growth through an as yet undefined mechanism. Pamidronate, an aminobisphosphonate, was given weekly to mice at 0, 1.25, or 2.50 mg/kg/wk beginning at 4 weeks of age. At 12 weeks of age, humeral length, growth plate area, regional chondrocyte cell numbers, chondrocyte apoptosis, TRAP stained osteoclast number, and osteoclast function assessed by cathepsin K immunohistochemistry were quantified. Humeral length was decreased in pamidronate treated mice compared to vehicle control mice, and correlated with greater growth plate areas reflecting greater proliferative and hypertrophic chondrocyte cell numbers with fewer hypertrophic cells undergoing apoptosis. Pamidronate treatment increased TRAP stained osteoclast numbers yet decreased cathepsin K indicating that pamidronate repressed osteoclast maturation and function. The data suggest that long term cyclic pamidronate treatment impairs bone growth by inhibition of osteoclast maturation thereby reducing cartilage-to-bone turnover within the growth plate.
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Jeremic, Svetlana, Vladimir Radosavljevic, and Dobrila Jakic-Dimic. "Current bacterial diseases of fresh water fishes." Biotehnologija u stocarstvu 21, no. 3-4 (2005): 141–51. http://dx.doi.org/10.2298/bah0504141j.

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From the beginning of fish cultivation, diseases have appeared as a serious problem in this branch of agriculture. In recent years, by the intensifying of production, fish diseases have become even more significant and complex field. Bacterial diseases are constant threat for fish farming, and because of rapid course and severity of clinical manifestations the represent significant part of fish pathology, and also have great economical importance. Harmful effects of bacterial diseases on fishes are: increased morbidity and mortality rate, decreased feed conversion efficiency, decreased growth rates, weakening of fishes, and reproduction problems. In order to examine epizootiological situation and occurrence of bacterial diseases among cultured fish in Serbia, three year research was carried out in 7 carp farms and 3 rainbow trout farms. Also, regular systematic examinations were conducted. Samples of internal organs, skin and gills were inoculated with streak-plate technique on standard and differential culture media plates. Inoculated plates were incubated for 24-48 hours at 20?C and 30?C. After incubation period, colonies were examined, and determination was done on the basis of following characteristics of colonies: form, color, mucosity granulation, roughness and hemolytic properties. Determination of bacterial isolates was done by using API 20E, API rapid. API Coryne systems, and by agglutination method with hyper immune aera. The most frequent diseases among the farmed carp and rainbow trout populations in the examined fish farms were: Bacterial gill disease, Columnaris disease. Yersiniosis Renibacteriosis, Erythrodermatitis. Motile Aeromonas and Pseudomonas infections. Based on the obtained results, modern diagnostic methods were implemented and proper prevention and successful therapy was taken.
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Martsyniak, S. M., and S. S. Strafun. "Surgical treatment of multidimensional deformities of lower limbs before closure of the growth plate in children with rachitic diseases." TRAUMA 21, no. 2 (March 1, 2020): 17–23. http://dx.doi.org/10.22141/1608-1706.2.21.2020.202229.

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Haseeb, Abdul, Ranjan Kc, Marco Angelozzi, Charles de Charleroy, Danielle Rux, Robert J. Tower, Lutian Yao, et al. "SOX9 keeps growth plates and articular cartilage healthy by inhibiting chondrocyte dedifferentiation/osteoblastic redifferentiation." Proceedings of the National Academy of Sciences 118, no. 8 (February 17, 2021): e2019152118. http://dx.doi.org/10.1073/pnas.2019152118.

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Cartilage is essential throughout vertebrate life. It starts developing in embryos when osteochondroprogenitor cells commit to chondrogenesis, activate a pancartilaginous program to form cartilaginous skeletal primordia, and also embrace a growth-plate program to drive skeletal growth or an articular program to build permanent joint cartilage. Various forms of cartilage malformation and degeneration diseases afflict humans, but underlying mechanisms are still incompletely understood and treatment options suboptimal. The transcription factor SOX9 is required for embryonic chondrogenesis, but its postnatal roles remain unclear, despite evidence that it is down-regulated in osteoarthritis and heterozygously inactivated in campomelic dysplasia, a severe skeletal dysplasia characterized postnatally by small stature and kyphoscoliosis. Using conditional knockout mice and high-throughput sequencing assays, we show here that SOX9 is required postnatally to prevent growth-plate closure and preosteoarthritic deterioration of articular cartilage. Its deficiency prompts growth-plate chondrocytes at all stages to swiftly reach a terminal/dedifferentiated stage marked by expression of chondrocyte-specific (Mgp) and progenitor-specific (Nt5e and Sox4) genes. Up-regulation of osteogenic genes (Runx2, Sp7, and Postn) and overt osteoblastogenesis quickly ensue. SOX9 deficiency does not perturb the articular program, except in load-bearing regions, where it also provokes chondrocyte-to-osteoblast conversion via a progenitor stage. Pathway analyses support roles for SOX9 in controlling TGFβ and BMP signaling activities during this cell lineage transition. Altogether, these findings deepen our current understanding of the cellular and molecular mechanisms that specifically ensure lifelong growth-plate and articular cartilage vigor by identifying osteogenic plasticity of growth-plate and articular chondrocytes and a SOX9-countered chondrocyte dedifferentiation/osteoblast redifferentiation process.
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Dissertations / Theses on the topic "Growth plate Diseases"

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Foster, Bruce Kristian. "Epiphyseal plate repair using fat interposition to reverse physeal deformity : an experimental study." Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09MD/09mdf754.pdf.

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Bibliography: leaves 169-197. Hypothesises that the physis has an internal mechanism of repair to restore physeal function. Aims to establish a defined degree of deformity by partial growth plate excision, then to examine different methods of reversal of such deformity to observe the process of growth plate repair. A secondary aim was to define the percentage of physis that could be resected yet still enable reversal of deformity.
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Rutt, Julianne Eileen. "Molecular Analysis Of The Epiphyseal Growth Plate In Rachitic Broilers: Evidence For The Etilogy Of The Condition." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1223319403.

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Taïeb, Mahdia. "Investigation des mécanismes moléculaires impliqués dans les anomalies du développement ostéoarticulaire chez la souris invalidée pour le gène de la Xylosyltransférase I." Thesis, Université de Lorraine, 2019. http://www.theses.fr/2019LORR0032/document.

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Les protéoglycanes (PGs) jouent un rôle essentiel dans plusieurs processus physiologiques majeurs tels que la signalisation cellulaire, la prolifération et la migration ; ceci grâce aux interactions entre leurs chaînes de glycosaminoglycanes (GAGs) avec des médiateurs solubles et leurs récepteurs. L'initiation de la synthèse des chaînes de GAGs des PGs est catalysée par la xylosyltransferase I (XT-I). Récemment plusieurs études ont montré différentes mutations au niveau du gène de la XT-I associées au syndrome Desbuquois de type II, caractérisée des anomalies ostéoarticulaires. Afin d’étudier le rôle de la XT-I dans le développement ostéoarticulaire, nous avons généré des souris invalidées pour le gène de la XT-I (XT-I KO). L'analyse morphologique des embryons montre que les souris XT-I KO présentent un nanisme prononcé et une hypoplasie frontonasale apparente, indiquant des anomalies du développement ostéoarticulaire. L'évaluation du contenu en PGs a révélé une forte diminution de la synthèse des PGs chez les souris XT-I KO. L'examen des différentes zones chondrocytaires au niveau de la plaque de croissance des os longs a révélé la perte de l’organisation en colonne des chondrocytes prolifératifs et une réduction importante de la zone hypertrophique. Afin d'identifier les mécanismes et les facteurs à l’origine des anomalies squelettiques chez les souris XT-I KO, l'expression de plusieurs gènes impliqués dans le développement du squelette et dans la régulation de la chondrogenèse a été analysée par hybridation in situ à l'aide de la technique RNAscope. Les résultats ont montré une forte expression des marqueurs de l’hypertrophie chondrocytaires suggérant ainsi une maturation précoce des chondrocytes chez les souris XT-I KO. Les embryons XT-I KO montrent également une formation précoce du centre d'ossification secondaire, indiquant une ossification précoce qui participerait aux anomalies de croissance observées chez les souris XT-I KO. L’étude des voies de signalisation impliquées dans la différenciation et la maturation chondrocytaire a révélé une surexpression du récepteur FGFR3 et une activation importante de la signalisation sous-jacente, suggérant ainsi des perturbations de la signalisation du FGF. Compte tenu du rôle important du FGFR3 dans la régulation de la chondrogenèse et de l’ossification endochondrale, ces résultats suggèrent fortement l’implication de la voie de FGF dans le développement des anomalies squelettiques chez les souris XT-I KO et ouvrent la voie pour le développement de de nouvelles thérapeutiques pour le traitement des patients atteints du syndrome Desbuquois de type II
Proteoglycans (PGs) play an essential role in several major physiological processes such as cell signaling, proliferation and migration; this is mainly due to the interactions between their glycosaminoglycan chains (GAGs) with soluble mediators and their receptors. The initiation of the synthesis of GAG chains of PGs is catalyzed by Xylosyltransferase I (XT-I). Recently several studies have shown that mutations in XT-I gene are associated with Desbuquois syndrome type II which is characterized by skeletal abnormalities. To study the role of XT-I in skeletal development, we generated knockout mice for the XT-I gene (XT-I KO). XT-I KO mice show pronounced dwarfism and apparent frontonasal hypoplasia reflecting abnormalities in skeletal development. Evaluation of PG content revealed a strong decrease in PG synthesis in XT-I KO mice. Analysis of the different chondrocyte zones in the growth plate revealed a loss of columnar organization of proliferative chondrocyte and a significant reduction of the hypertrophic zone. To identify the mechanisms and factors underlying skeletal abnormalities in XT-I KO mice, the expression of several genes involved in skeletal development and in the regulation of chondrogenesis were analyzed by in situ hybridization using RNAscope technique. The results showed a strong expression of markers of chondrocyte hypertrophy thus suggesting early maturation of chondrocytes in XT-I KO mice. The XT-I KO embryos show also a premature formation of the secondary ossification center, indicating a precocious ossification which ultimately leads to the growth abnormalities showed in XT-I KO mice. The study of the signaling pathways involved in differentiation and chondrocyte maturation revealed an overexpression of the FGFR3 receptor and a significant activation of the downstream signaling pathways, thus suggesting disturbances of FGF signaling. Given the important role of FGFR3 in the regulation of chondrogenesis and endochondral ossification, these results strongly suggest the involvement of the FGF pathway in the development of skeletal abnormalities in XT-I KO mice and pave the way for the development of new therapeutics for the treatment of patients with Desbuquois syndrome type II
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Bercetche, Joëlle. "Effets rhizogenes exerces par a. Rhizogenes chez le pois : aspects morphogenetiques, cellulaires et hormonaux." Paris 6, 1987. http://www.theses.fr/1987PA066145.

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La sequence ontogenetique de la rhizogenese transformee et les effets cellulaires induits par trois souches d'a. Rhizogenes (1855, 2659 et 8196) chez l'epicotyle de pois sont recherches. Apres inoculation par la souche 1855, on enregistre une large gamme de symptomes comparables a ceux produits par des auxines exogenes. Il s'agit de symptomes comparables a ceux produits par des auxines exogenes. Il s'agit de symptomes cytophysiologiques (hyperhydrie, synthese d'adn, fragmentations nucleaires), histologiques (cambiogenese, tracheogenese) et morphogenetiques (rhizogenese transformee aux points d'inoculation et non transformee dans les regions sous-jacentes aux inoculations). La sequence morphogenetique de la mise en place des racines transformees a ete etablie
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LE, COZ SERGE. "La rhizomanie de la betterave sucriere : multiplication du virus et aspects agronomiques de la maladie." Paris 6, 1986. http://www.theses.fr/1986PA066644.

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Les chloroplastes des feuilles de betteraves rhizomaniees sont appauvries en pigments, en proteines, en liquides polaires et leur activite photosynthetique est reduite. Dans les cellules virosees, l'etude ultrastructure montre une association des amas de virus avec le reticulum endoplasmique granuleux. Un protocole pour la preparation de suspensions enrichies en cytosores isoles de polymyxa betae est propose. Le champignon est retrouve a tous les niveaux du sol de quatre parcelles rhizomaniees ou saines de la region de pithiviers. Une terre rhizomaniee reste infectieuse aprese un an et demi de lagune en bassin
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Foster, Bruce K. "Epiphyseal plate repair using fat interposition to reverse physeal deformity : an experimental study / thesis submitted in March 1989 for the degree of Doctor of Medicine in the University of Adelaide by Bruce Kristian Foster." 1989. http://hdl.handle.net/2440/38304.

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Bibliography: leaves 169-197.
xiv, 197 leaves :
Title page, contents and abstract only. The complete thesis in print form is available from the University Library.
Hypothesises that the physis has an internal mechanism of repair to restore physeal function. Aims to establish a defined degree of deformity by partial growth plate excision, then to examine different methods of reversal of such deformity to observe the process of growth plate repair. A secondary aim was to define the percentage of physis that could be resected yet still enable reversal of deformity.
Thesis (Ph.D.)--University of Adelaide, Dept. of Pathology, 1989
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Lapointe, Marie. "Les facteurs écologiques influençant la dynamique d'une espèce exotique envahissante, Acer platanoides, et d'un congénère indigène, A. saccharum, dans une forêt urbaine du sud du Québec." Thèse, 2009. http://hdl.handle.net/1866/8136.

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Books on the topic "Growth plate Diseases"

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M, Shapiro Irving, Boyan Barbara, and Anderson H. Clarke, eds. The growth plate. Amsterdam: IOS Press, 2002.

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Organisation, International Labour, ed. HIV and AIDS in the informal workplaces: Pilot project research report : creating an enabling environment in the market place for business growath and sustainability. Lusaka: International Labour Organisation, 2007.

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1925-, Uhthoff Hans K., Wiley James J, University of Ottawa. Division of Orthopedic Surgery., and Pediatric Orthopaedic Society of North America., eds. Behavior of the growth plate. New York: Raven Press, 1988.

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(Editor), Irving M. Shapiro, Barbara Boyan (Editor), and H. Clarke Anderson (Editor), eds. The Growth Plate (Biomedical and Health Research, 54). Ios Pr Inc, 2002.

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Joshi, Mahesh K., and J. R. Klein. Australia—The Hidden Jewel. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198827481.003.0012.

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The twenty-first century is being touted as the Asian century. With its stable economy, good governance, education system, and above all the abundant natural resources, will Australia to take its place in the global economy by becoming more entrepreneurial and accelerating its rate of growth, or will it get infected with the so-called Dutch disease? It has been successful in managing trade ties with fast-developing economies like China and India as well as developed countries like the United States. It has participated in the growth of China by providing iron ore and coal. Because it is a low-risk country, it has enabled inflow of large foreign capital investments. A lot will depend on its capability and willingness to invest the capital available in entrepreneurial ventures, its ability to capture the full value chain of natural resources, and to export the finished products instead of raw materials, while building a robust manufacturing sector.
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Medforth, Janet, Linda Ball, Angela Walker, Sue Battersby, and Sarah Stables. Antenatal care. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198754787.003.0004.

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This chapter comprises confirming the pregnancy, the signs and symptoms of pregnancy, pregnancy testing and how to go about it, pregnancy adaptation, how the body changes in response to the pregnancy, the booking interview, and where, when, how, and why it takes place. Pregnancy screening and risk assessment, based on the medical, social, and obstetric history, is outlined. Blood group and the rhesus factor, their importance in terms of preventing haemolytic disease in the newborn, and anti-D prophylaxis are explained. Down’s syndrome risk screening protocols, gaining consent, and the testing options are presented, as well as antenatal examination and how and when this is carried out, the abdominal examination procedure, and the significance of findings and how this relates to fetal well-being. Monitoring fetal growth and well-being by a variety of clinical and technical measures is also included, explaining the procedure for measuring growth and plotting the results on a customized chart.
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Fox, Dov. Birth Rights and Wrongs. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780190675721.001.0001.

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Today, tens of millions of Americans rely on reproductive advances to help them carry out decisions more personal and far-reaching than almost any other they will ever make: They use birth control or abortion to delay or avoid having children; surrogacy or tissue donation to start or grow a family; and genetic diagnosis or embryo selection to have offspring who survive and flourish. This is no less than the medicine of miracles: It fills empty cradles; frees families from debilitating disease; and empowers them to plan a life that doesn’t include parenthood. But accidents happen: Embryologists miss ailments; egg vendors switch donors; obstetricians tell pregnant women their healthy fetuses will be stillborn. The aftermaths can last a lifetime, yet political and economic forces conspire against regulation to prevent negligence from happening in the first place. After the fact, social stigma and lawyers’ fees stave off lawsuits, and legal relief is a long shot: Judges and juries are reluctant to designate reproductive losses as worthy of redress when mix-ups foist parenthood on patients who didn’t want it, or childlessness on those who did. Some courts insist that babies are blessings, planned or not; others shrug over the fact that infertile couples weren’t assured offspring anyway. The result is a society that lets badly behaving specialists off the hook and leaves broken victims to pick up the pieces. Failed abortions, switched donors, and lost embryos may be First World problems—but these aren’t innocent lapses or harmless errors: They’re wrongs in need of rights.
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Book chapters on the topic "Growth plate Diseases"

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Meßler, H., W. Rüther, J. Kühr, and K. J. Münzenberg. "The Influence of Magnesium and Calcium Antagonists on the Epiphyseal Growth Plate — A Comparison." In Generalized Bone Diseases, 313–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73346-8_28.

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Karbowski, A., J. Herwig, H. H. Matthiaß, and E. Buddecke. "Effects of Mechanical Factors on Structure and Function of the Growth Plate of Long Bones." In Generalized Bone Diseases, 337–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73346-8_31.

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Quint, P., J. Althoff, I. Harmeyer, K. D. Richter, and H. J. Höhling. "Concentration Profiles of Zinc and Lead Along the Epiphyseal Growth Plate of Normal and Rachitic Piglets as Related to Activities of Esterases." In Generalized Bone Diseases, 181–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-73346-8_18.

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Srinivas, Vickram, and Irving M. Shapiro. "The Epiphyseal Growth Plate: The Engine That Drives Bone Elongation." In Handbook of Growth and Growth Monitoring in Health and Disease, 1331–49. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1795-9_80.

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Salvatore, Seminara, Stagi Stefano, and Nanni Laura. "Thyroid Function During Catch-Up Growth: A Focus on the Growth Plate." In Handbook of Growth and Growth Monitoring in Health and Disease, 905–16. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1795-9_54.

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Gat-Yablonski, Galia, and Moshe Phillip. "Nutritional-Induced Longitudinal Catch-Up Growth: A Focus on the Growth Plate, Growth-Related Genes, Autophagy, mTOR, and microRNAs." In Handbook of Growth and Growth Monitoring in Health and Disease, 1029–43. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-1795-9_61.

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Lui, Julian C., and Jeffrey Baron. "Effects of Glucocorticoids on the Growth Plate." In Pediatric Adrenal Diseases, 187–93. S. Karger AG, 2010. http://dx.doi.org/10.1159/000321244.

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Da Rin de Lorenzo, Ferdinando. "Specific Bacterial Immunotherapy in Treating Chronic Osteomyelitis." In Infectious Diseases and Sepsis [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98751.

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The immunological experience is treating osteomyelitis chronic forms at the Istituto Putti in Cortina starts in 1963 by introducing immunotherapy, applied by the progressive administration in growing doses of a staphylococci pool, that had been collected from some patients with bone infections by the same germ and then inactivated in an aqueous solution suspension. This therapy is coadjutant of antibiotics, surgical and hyperbaric therapy and not substitutive of these. This study ascertained indeed a reduction of the phagocytic activity as a whole, and especially the opsonisation activity It has been thought therefore that in immunotherapy more factors are involved; their principal property is to reduce the allergising effect and therefore to desensitise vs. the germ proteins and to increase the phagocytic activity. This condition, neither whose entity nor its lasting may be defined, does not appear to be unlimited. Obviously this desensitisation can be obtained also by the right antibiotic choice that, as already said mainly in acute forms, may develop their bactericidal properties and sterilise the focus. In the chronic forms it is possible to provoke this mechanism by carrying out a surgical toilette that restores the vascularization and stimulation conditions needed for a correct antibiotic action. Checks upon immuno-stimulation treatment termination clearly showed corresponding results between laboratory deficit corrected and clinical conditions bettering. The casuistry is based on 50 patients with hematogenic osteomyelitis, all under the age of 16, age at which the growth plate is still active, and 117 post-traumatic septic non-union, where this term was adopted for cases that showed a lack of non-solidification at 6 months after trauma. We have expressly made a distinction between hematogenic and post-traumatic forms, since the relationships between bacterial counts vs. host response do differ.
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"Growth of tissues and organs." In Oxford Assess and Progress: Medical Sciences, edited by Jade Chow, John Patterson, Kathy Boursicot, and David Sales. Oxford University Press, 2012. http://dx.doi.org/10.1093/oso/9780199605071.003.0017.

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Many of the basic pathological processes that take place in cells, tissues, and organs are common, regardless of tissue types. These are due to aetiologies and pathogenetic mechanisms that lead to a common fate. Understanding these allows students to develop a logical approach to classifying diseases according to the underlying mechanism. In so doing, students should not have to memorize lists, and will be able to deal with new or unfamiliar clinical scenarios. An understanding of the underlying disease processes, including having precise definitions of these, allows doctors to describe the diseases accurately and to communicate more clearly. Unfortunately, many of the terms sound like each other, but fortunately, there are not too many terms. In recent years, the molecular mechanisms underlying many disease processes that may have been known for decades have been uncovered. It is important to know these as they may have implications for management, for example genetic counselling, or may lead to development of new therapies.
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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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Conference papers on the topic "Growth plate Diseases"

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Trachet, Bram, Daniel Devos, Julie De Backer, Anne De Paepe, Bart L. Loeys, and Patrick Segers. "Patient-Specific Modelling of Aortic Arch Wall Shear Stress Patterns in Patients With Marfan Syndrome." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206340.

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Marfan syndrome (MFS) is a genetic connective tissue disorder with a high prevalence of aortic aneurysm formation (a pathological dilatation of the aorta), typically at the aortic root. The disorder is caused by mutations in the gene encoding fibrillin-1 [1]. Recently, it has been shown in mouse models that selected manifestations of MFS, such as aortic aneurysm formation, can be explained by excessive signaling by the transforming growth factor–beta (TGF-beta) family of cytokines [2]. Although the footprint of the disease is clearly genetic, there is still a role for (computational) biomechanics and hemodynamics to elucidate why aneurysms develop preferentially at the level of the aortic root, since the genetic defect affects the entire (arterial) system. One of the most obvious parameters to study is the arterial wall shear stress (WSS). WSS plays an important role in the regulation of the vascular system and is considered a significant factor in the development and progression of cardiovascular disease in humans. Low and/or oscillating values of WSS have been associated with the formation of atherosclerotic lesions [3] and with the growth of aneurysms [4]. It is, however, hard to show a link between low WSS and aneurysm initiation, since in most cases the geometrical and physiological data are lacking during the first and most important stages of the aneurysm development. Furthermore follow-up studies in human patients are difficult, since aneurysms grow very slowly (only 0.9 mm/year in MFS patients treated with beta-blockers) and it will take several years before significant changes will have taken place. Therefore, in this study, we have computed the aortic flow field and WSS patterns for 5 different MFS patients with ages varying from 14 to 54 years old, in order to get an idea about the effect of age on the development of the disease.
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McClain, Jacob, Sara L. Tuell, and Susan N. Thomas. "Tumors Change the Elastic and Viscoelastic Properties of Draining Lymph Node Tissues." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14419.

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Changes in tissue mechanical properties are often the first indication of malignant disease, with the detection of a stiff lump by a patient. These changes include growth-induced solid stresses, increased matrix stiffness, high fluid pressure, and increased interstitial flow, which in turn enhance fluid flux away from the tumor to downstream lymph nodes (LNs). But in addition to changing the way a tumor feels to a patient, altered tumor tissue mechanics promote cancer cell invasion into lymphatic vessels, allowing their metastatic dissemination to draining LNs. LN swelling and stiffening is another common indicator of tumor growth, and the presence of metastatic cells in the sentinel LN, or tumor draining lymph node (TDLN), is used clinically to stage disease. Recent studies indicate the LN microenvironment determines whether metastatic cancers can spread to the sentinel LNs. Yet despite the known correlation of LN swelling and stiffening with tumorigenesis and the role of the LN microenvironment in metastasis, our understanding of how changes in LN mechanical properties relate to tumor progression, anti-tumor immune response and metastatic colonization of the LN is limited. This lack of a quantitative understanding limits functional analyses of the role of LN mechanics in determining cancer cell colonization of the TDLN, their influence on immune suppression taking place within the TDLN, as well as the development of strategies to mitigate these effects.
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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.

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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.
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Ochie, Samuel, and Karen Ochie. "Design and Construction of an Air Quality Monitoring System to Mitigate Virus Spread." In SPE Nigeria Annual International Conference and Exhibition. SPE, 2021. http://dx.doi.org/10.2118/208263-ms.

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Abstract Air pollution is one of the most dangerous problems we face in the world today. It causes many illnesses and diseases that affect the immune system of humans and non-human animals and is also a means of propagating the novel COVID-19 or corona virus. Temperature, humidity, and the level of carbon dioxide characterize the air quality in an environment. In addition to abnormal temperatures and humidity causing direct problems to humans like headaches, heatstroke, hypothermia and hyperthermia, death and so on, it could also cause complicated problems like the acceleration of the growth and lifespan of harmful viruses like the corona virus especially in closed spaces like on a drilling rig or a processing facility. Multiple studies show that the influenza virus, coronavirus, and many others spread from host to host faster in areas with low humidity and high temperatures and upon infection, mortality rate is higher in low humidity regions. Inhalation of toxic levels of carbon dioxide has adverse effects ranging from drowsiness to coma and even death. Despite safety measures put in place in offshore facilities, there are still cases of corona virus outbreaks, hence this study aims to combat the facilitated spread of viruses and enhancement of good air quality via the design and construction of a device that measures the temperature, humidity, and carbon dioxide levels, using a DHT11 and MQ135 sensor. The temperature, humidity and carbon dioxide levels of the living area, bedroom, kitchen, and balcony in a facility was captured by the device to determine the quality of air and characterized. The values were then compared with the expected values from a trusted website to determine the accuracy of the device. The device showed a 99.8% accuracy and passed quality check making it a recommendation to enhance air quality in facilities, houses, or offices.
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Mendygarin, Yertay, Luis R. Rojas-Solórzano, Nurassyl Kussaiyn, Rakhim Supiyev, and Mansur Zhussupbekov. "Eulerian-Eulerian Multiphase Modeling of Blood Cells Segregation in Flow Through Microtubes." In ASME 2017 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/imece2017-70850.

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Cardiovascular Diseases, the common name for various Heart Diseases, are responsible for nearly 17.3 million deaths annually and remain the leading global cause of death in the world. It is estimated that this number will grow to more than 23.6 million by 2030, with almost 80% of all cases taking place in low and middle income countries. Surgical treatment of these diseases involves the use of blood-wetted devices, whose relatively recent development has given rise to numerous possibilities for design improvements. However, blood can be damaged when flowing through these devices due to the lack of biocompatibility of surrounding walls, thermal and osmotic effects and most prominently, due to the excessive exposure of blood cells to shear stress for prolonged periods of time. This extended exposure may lead to a rupture of membrane of red blood cells, resulting in a release of hemoglobin into the blood plasma, in a process called hemolysis. Moreover, exposure of platelets to high shear stresses can increase the likelihood of thrombosis. Therefore, regions of high shear stress and residence time of blood cells must be considered thoroughly during the design of blood-contacting devices. Though laboratory tests are vital for design improvements, in-vitro experiments have proven to be costly, time-intensive and ethically controversial. On the other hand, simulating blood behavior using Computational Fluid Dynamics (CFD) is considered to be an inexpensive and promising tool to help predicting blood damage in complex flows. Nevertheless, current state-of-the-art CFD models of blood flow to predict hemolysis are still far from being fully reliable and accurate for design purposes. Previous work have demonstrated that prediction of hemolysis can be dramatically improved when using a multiphase (i.e., phases are plasma, red blood cells and platelets) model of the blood instead of assuming the blood as a homogeneous mixture. Nonetheless, the accurate determination of how the cells segregate becomes the critical issue in reaching a truthful prediction of blood damage. Therefore, the attempt of this study is to develop and validate a numerical model based on Granular Kinetic Theory (GKT) for solid phases (i.e., cells treated as particles) that provides an improved prediction of blood cells segregation within the flow in a microtube. Simulations were based on finite volume method using Eulerian-Eulerian modeling for treatment of three-phase (liquid-red blood cells and platelets) flow including the GKT to deal with viscous properties of the solid phases. GKT proved to be a good model to predict particle concentration and pressure drop by taking into account the contribution of collisional, kinetic and frictional effects in the stress tensor of the segregated solid phases. Preliminary results show that the improved segregated model leads to a better prediction of spatial distribution of blood cells. Simulations were performed using ANSYS FLUENT platform.
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