Relevant bibliographies by topics / Degeneration and regeneration

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Degeneration and regeneration'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Degeneration and regeneration"

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Berki, Sándor, Tamás Klára, György Szőke, Tibor Németh, Miklós Dunay, and Károly Pap. "A rabbit model for studying degeneration and regeneration properties of young striated muscle at different distraction rates." Acta Veterinaria Hungarica 60, no. 2 (June 1, 2012): 223–32. http://dx.doi.org/10.1556/avet.2012.019.

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The present study evaluated the histological changes in the muscle tissue after limb lengthening in skeletally immature rabbits and assessed the effect of different lengthening rates on the regeneration and degeneration properties of striated muscle. Thirteen different lengthening protocols were applied on a total of 16 male domestic white rabbits divided into four groups. The histopathological changes were analysed by a semiquantitative method according to the scoring system of Lee et al. (1993). After evaluation of the five main degenerative parameters (muscle atrophy, internalisation of muscle nuclei, degeneration of the muscle fibre, perimysial and endomysial fibrosis, haematomas), it is evident that rabbits subjected to limb lengthening at a rate of 3.2 mm/day showed more degenerative changes than those limb-lengthened at 0.8 or 1.6 mm/day. Our study showed that the regenerative mechanisms were not endless. If the daily lengthening rate reached the 3.2 mm/day limit, the regenerating ability of the muscle decreased, and signs of degeneration increased significantly.
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Bohnert, Kathryn L., Mary K. Hastings, David R. Sinacore, Jeffrey E. Johnson, Sandra E. Klein, Jeremy J. McCormick, Paul Gontarz, and Gretchen A. Meyer. "Skeletal Muscle Regeneration in Advanced Diabetic Peripheral Neuropathy." Foot & Ankle International 41, no. 5 (February 14, 2020): 536–48. http://dx.doi.org/10.1177/1071100720907035.

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Background: Decreased lean muscle mass in the lower extremity in diabetic peripheral neuropathy (DPN) is thought to contribute to altered joint loading, immobility, and disability. However, the mechanism behind this loss is unknown and could derive from a reduction in size of myofibers (atrophy), destruction of myofibers (degeneration), or both. Degenerative changes require participation of muscle stem (satellite) cells to regenerate lost myofibers and restore lean mass. Determining the degenerative state and residual regenerative capacity of DPN muscle will inform the utility of regeneration-targeted therapeutic strategies. Methods: Biopsies were acquired from 2 muscles in 12 individuals with and without diabetic neuropathy undergoing below-knee amputation surgery. Biopsies were subdivided for histological analysis, transcriptional profiling, and satellite cell isolation and culture. Results: Histological analysis revealed evidence of ongoing degeneration and regeneration in DPN muscles. Transcriptional profiling supports these findings, indicating significant upregulation of regeneration-related pathways. However, regeneration appeared to be limited in samples exhibiting the most severe structural pathology as only extremely small, immature regenerated myofibers were found. Immunostaining for satellite cells revealed a significant decrease in their relative frequency only in the subset with severe pathology. Similarly, a reduction in fusion in cultured satellite cells in this group suggests impairment in regenerative capacity in severe DPN pathology. Conclusion: DPN muscle exhibited features of degeneration with attempted regeneration. In the most severely pathological muscle samples, regeneration appeared to be stymied and our data suggest that this may be partly due to intrinsic dysfunction of the satellite cell pool in addition to extrinsic structural pathology (eg, nerve damage). Clinical Relevance: Restoration of DPN muscle function for improved mobility and physical activity is a goal of surgical and rehabilitation clinicians. Identifying myofiber degeneration and compromised regeneration as contributors to dysfunction suggests that adjuvant cell-based therapies may improve clinical outcomes.
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Yamada, Katsuhisa, Norimasa Iwasaki, and Hideki Sudo. "Biomaterials and Cell-Based Regenerative Therapies for Intervertebral Disc Degeneration with a Focus on Biological and Biomechanical Functional Repair: Targeting Treatments for Disc Herniation." Cells 11, no. 4 (February 9, 2022): 602. http://dx.doi.org/10.3390/cells11040602.

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Intervertebral disc (IVD) degeneration is a common cause of low back pain and most spinal disorders. As IVD degeneration is a major obstacle to the healthy life of so many individuals, it is a major issue that needs to be overcome. Currently, there is no clinical treatment for the regeneration of degenerated IVDs. However, recent advances in regenerative medicine and tissue engineering suggest the potential of cell-based and/or biomaterial-based IVD regeneration therapies. These treatments may be indicated for patients with IVDs in the intermediate degenerative stage, a point where the number of viable cells decreases, and the structural integrity of the disc begins to collapse. However, there are many biological, biomechanical, and clinical challenges that must be overcome before the clinical application of these IVD regeneration therapies can be realized. This review summarizes the basic research and clinical trials literature on cell-based and biomaterial-based IVD regenerative therapies and outlines the important role of these strategies in regenerative treatment for IVD degenerative diseases, especially disc herniation.
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Chau, Monica J., Jorge E. Quintero, Eric Blalock, Stephanie Byrum, Samuel G. Mackintosh, Christopher Samaan, Greg A. Gerhardt, and Craig G. van Horne. "Transection injury differentially alters the proteome of the human sural nerve." PLOS ONE 17, no. 11 (November 23, 2022): e0260998. http://dx.doi.org/10.1371/journal.pone.0260998.

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Regeneration after severe peripheral nerve injury is often poor. Knowledge of human nerve regeneration and the growth microenvironment is greatly lacking. We aimed to identify the regenerative proteins in human peripheral nerve by comparing the proteome before and after a transection injury. In a unique study design, we collected closely matched samples of naïve and injured sural nerve. Naïve and injured (two weeks after injury) samples were analyzed using mass spectrometry and immunoassays. We found significantly altered levels following the nerve injury. Mass spectrometry revealed that injury samples had 568 proteins significantly upregulated and 471 significantly downregulated compared to naïve samples (q-value ≤ 0.05 and Z ≥ |2| (log2)). We used Gene Ontology (GO) pathway overrepresentation analysis to highlight groups of proteins that were significantly upregulated or downregulated with injury-induced degeneration and regeneration. Significant protein changes in key pathways were identified including growth factor levels, Schwann cell de-differentiation, myelination downregulation, epithelial-mesenchymal transition (EMT), and axonal regeneration pathways. The proteomes of the uninjured nerve compared to the degenerating/regenerating nerve may reveal biomarkers to aid in the development of repair strategies such as infusing supplemental trophic factors and in monitoring neural tissue regeneration.
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PELETTI-FIGUEIRÓ, MANUELA, ISRAEL SILVEIRA DE AGUIAR, SUELEN PAESI, DENISE CANTARELLI MACHADO, SERGIO ECHEVERRIGARAY, MARIANA ROESCH-ELY, ASDRUBAL FALAVIGNA, and JOÃO ANTONIO PÊGAS HENRIQUES. "HISTOLOGICAL MARKERS OF DEGENERATION AND REGENERATION OF THE HUMAN INTERVERTEBRAL DISK." Coluna/Columna 16, no. 1 (January 2017): 42–47. http://dx.doi.org/10.1590/s1808-185120171601170833.

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ABSTRACT Objective: To define histological scores for intervertebral disc degeneration that would enable the definition of morphological characteristics of disease, besides improving knowledge of the lumbar degenerative disc disease by means of immunohistochemical markers. Methods: Hematoxylin and Eosin, Alcian/PAS, Masson Trichrome and Safranin O/FCF staining was used on the intervertebral disc degeneration sections of patients with lumbar degenerative disc disease. The protein markers defined in immunohistochemistry were cell proliferation (Ki-67) and apoptosis (p53). Results: The study data enabled the determination of Safranin O/FCF stain as the most effective one for evaluating parameters such as area, diameter, and number of chondrocyte clusters. The importance of using stains in association, such as Safranin O/FCF, Masson Trichrome, Alcian/PAS and Hematoxylin and Eosin, was also determined, as they are complementary for the histopathological verification of intervertebral disc degeneration. By expressing proteins using the immunohistochemistry technique, it was possible to consider two stages of disc degeneration: cell proliferation with chondrocyte cluster formation, and induction of apoptosis. Conclusion: This study enabled the histological and immunohistochemical characterization to be determined for lumbar degenerative disc disease, and its degrees of evolution, by determining new disc degeneration scores.
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Molinos, Maria, Catarina R. Almeida, Joana Caldeira, Carla Cunha, Raquel M. Gonçalves, and Mário A. Barbosa. "Inflammation in intervertebral disc degeneration and regeneration." Journal of The Royal Society Interface 12, no. 104 (March 2015): 20141191. http://dx.doi.org/10.1098/rsif.2014.1191.

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Intervertebral disc (IVD) degeneration is one of the major causes of low back pain, a problem with a heavy economic burden, which has been increasing in prevalence as populations age. Deeper knowledge of the complex spatial and temporal orchestration of cellular interactions and extracellular matrix remodelling is critical to improve current IVD therapies, which have so far proved unsatisfactory. Inflammation has been correlated with degenerative disc disease but its role in discogenic pain and hernia regression remains controversial. The inflammatory response may be involved in the onset of disease, but it is also crucial in maintaining tissue homeostasis. Furthermore, if properly balanced it may contribute to tissue repair/regeneration as has already been demonstrated in other tissues. In this review, we focus on how inflammation has been associated with IVD degeneration by describing observational and in vitro studies as well as in vivo animal models. Finally, we provide an overview of IVD regenerative therapies that target key inflammatory players.
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Gulati, Adarshk. "Pattern of skeletal muscle regeneration after reautotransplantation of regenerated muscle." Development 92, no. 1 (March 1, 1986): 1–10. http://dx.doi.org/10.1242/dev.92.1.1.

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Autotransplantation of rat extensor digitorum longus muscle results in initial myofibre degeneration and subsequent regeneration from precursor myosatellite cells. To determine what effect a reinjury would have on the regenerative response, in the present,study, once transplanted and regenerated muscles were reinjured by reautotransplantion. In rats, four weeks after initial transplantation, when the regeneration was complete, the extensor digitorum longus muscle was transplanted again and the pattern of regeneration in reautotransplanted and once auto transplanted muscles was compared. Muscles were analysed 2, 4, 7, 14 and 30 days after autotransplantation and reautotransplantation. Both autotransplanted and reautotransplanted muscles underwent degeneration and regeneration; however, the pattern of regeneration in these two transplants was quite different. In autotransplants, a thin myogenic zone, marked by activated myoblasts, was first seen at 4 days. By 7 days the width of myogenic zone increased but still many degenerating myofibres were present in the central region of the muscle. By 14 days the muscle was filled with regenerated myotubes and myofibres. The reautotransplanted muscles underwent similar regenerative events; however, the rate of regeneration was considerably faster. The myogenic zone was apparent as early as 2 days and was much larger at 4 days, and by 7 days the entire muscle was filled with regenerated myotubes and myofibres which matured at later time intervals. Furthermore, the decrease in muscle weight in reautotransplanted muscles was not as much as that seen after autotransplantation. These findings reveal that not only is skeletal muscle capable of regeneration after a second injury, but the rate of this regeneration is much faster. This increased rate and recovery may be due to a conditioning effect of the first injury.
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Ashinsky, B., HE Smith, RL Mauck, and SE Gullbrand. "Intervertebral disc degeneration and regeneration: a motion segment perspective." European Cells and Materials 41 (March 24, 2021): 370–87. http://dx.doi.org/10.22203/ecm.v041a24.

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Back and neck pain have become primary reasons for disability and healthcare spending globally. While the causes of back pain are multifactorial, intervertebral disc degeneration is frequently cited as a primary source of pain. The annulus fibrosus (AF) and nucleus pulposus (NP) subcomponents of the disc are common targets for regenerative therapeutics. However, disc degeneration is also associated with degenerative changes to adjacent spinal tissues, and successful regenerative therapies will likely need to consider and address the pathology of adjacent spinal structures beyond solely the disc subcomponents. This review summarises the current state of knowledge in the field regarding associations between back pain, disc degeneration, and degeneration of the cartilaginous and bony endplates, the AF-vertebral body interface, the facet joints and spinal muscles, in addition to a discussion of regenerative strategies for treating pain and degeneration from a whole motion segment perspective.
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Kastenschmidt, Jenna. "A role for group 2 innate lymphoid cells in muscular dystrophy." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 183.20. http://dx.doi.org/10.4049/jimmunol.202.supp.183.20.

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Abstract Duchenne muscular dystrophy (DMD) is a genetic neuromuscular disorder characterized by progressive myofiber degeneration and chronic inflammation. Asynchronous and continuous bouts of injury dysregulate the immune response to injured myofibers, exacerbating muscle degeneration and impairing regeneration. In contrast, activation of type 2 immunity during acute injury is required for efficient muscle regeneration. Evidence in the literature suggests a similar type 2 immune response is activated in dystrophic muscle, but is dysregulated by competing degenerative inflammatory responses. However, the regulation of type 2 immunity in dystrophic muscle is largely unknown. A recently identified subset of immune cells, group 2 innate lymphoid cells (ILC2), were shown to potently regulate type 2 immunity and promote tissue repair. In this study, we found that muscle ILC2s were increased in number and expressed higher levels of interleukin-5 (IL-5) in mdx mice compared to wildtype controls, indicating that muscle degeneration activates ILC2s. In vivo expansion of ILC2s using IL-2/anti-IL-2 complex (IL-2c) and IL-33 enhanced type 2 cytokine expression in mdx skeletal muscle and increased the cross-sectional area of regenerating myofibers, suggesting that ILC2s enhance muscle regeneration through the upregulation of type 2 cytokines. In addition, loss-and gain-of-function experiments demonstrated that ILC2s promote the skeletal muscle recruitment of eosinophils, an innate immune cell population previously shown to promote muscle regeneration. Collectively our data support a working model in which ILC2s promote skeletal muscle regeneration by enhancing type 2 immunity (i.e. eosinophilia and increased type 2 cytokines).
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Lu, Fangfang, Lyndsay L. Leach, and Jeffrey M. Gross. "mTOR activity is essential for retinal pigment epithelium regeneration in zebrafish." PLOS Genetics 18, no. 3 (March 10, 2022): e1009628. http://dx.doi.org/10.1371/journal.pgen.1009628.

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The retinal pigment epithelium (RPE) plays numerous critical roles in maintaining vision and this is underscored by the prevalence of degenerative blinding diseases like age-related macular degeneration (AMD), in which visual impairment is caused by progressive loss of RPE cells. In contrast to mammals, zebrafish possess the ability to intrinsically regenerate a functional RPE layer after severe injury. The molecular underpinnings of this regenerative process remain largely unknown yet hold tremendous potential for developing treatment strategies to stimulate endogenous regeneration in the human eye. In this study, we demonstrate that the mTOR pathway is activated in RPE cells post-genetic ablation. Pharmacological and genetic inhibition of mTOR activity impaired RPE regeneration, while mTOR activation enhanced RPE recovery post-injury, demonstrating that mTOR activity is essential for RPE regeneration in zebrafish. RNA-seq of RPE isolated from mTOR-inhibited larvae identified a number of genes and pathways dependent on mTOR activity at early and late stages of regeneration; amongst these were components of the immune system, which is emerging as a key regulator of regenerative responses across various tissue and model systems. Our results identify crosstalk between macrophages/microglia and the RPE, wherein mTOR activity is required for recruitment of macrophages/microglia to the RPE injury site. Macrophages/microglia then reinforce mTOR activity in regenerating RPE cells. Interestingly, the function of macrophages/microglia in maintaining mTOR activity in the RPE appeared to be inflammation-independent. Taken together, these data identify mTOR activity as a key regulator of RPE regeneration and link the mTOR pathway to immune responses in facilitating RPE regeneration.
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Dissertations / Theses on the topic "Degeneration and regeneration"

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Wernicke, Catrin V. [Verfasser]. "Degeneration, Protektion und Regeneration dopaminerger Neurone / Catrin V. Wernicke." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2011. http://d-nb.info/1025239318/34.

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Charge, Sophie Barbara Pauline. "Skeletal muscle hypertrophy : its regulation and effect on muscle regeneration." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340500.

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Saini, Amarjit. "The molecular and cellular aspects of muscle degeneration and regeneration." Thesis, Manchester Metropolitan University, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.585529.

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The concept of skeletal muscle homeostasis - often viewed as the net balance between two separate processes, namely protein degradation and protein synthesis - are not occurring independently of each other, but are finely co-ordinated by a web of intricate signalling networks (Nader, 2005). Such signalling networks are in charge of executing environmental and cellular cues that ultimately determine whether muscle proteins are synthesised or degraded. Prolonged elevations of proinflammatory cytokines are closely associated with muscle wasting that occurs during the sarcopenia of ageing and in cachectic AIDS and cancer patients (Strle et a/. 2007). These clinical disorders occur along with a decline in IGF-I anabolic activity, which is consistent with in vitro findings in muscle progenitor cells (Strle et a/. 2007). Very low concentrations ofTNF-a (0.01-1 ng.ml") inhibit IGF-I-induced protein synthesis (Broussard et a/. 2003; Strle et al. 2004) and expression of the critical muscle differentiation factors, MyoD (Strle et a/., 2004) and myogenin (Broussard et al. 2003; Strle et a/. 2004). Potential treatments that might overcome TNF-a-induced hormone resistance in myoblasts are unknown. Increased activation of the IGF/insulin pathway is an attractive target for combating many of the cachectic conditions associated with muscle wasting. Using rodent skeletal muscle cell lines we have investigated TNF-a/IGF-I interactions, in an attempt to mimic and understand mechanisms underlying the wasting process. We hypothesised that treatment of mouse myoblasts with TNF-a at specific doses ranging from high (20 ng.ml') to low (1.25 ng.ml") would result in dose-dependent block of differentiation and induction of apoptosis and that subsequent IGF-I co-incubations would stimulate myoblast survival and myotube formation. Objectives were to ascertain signalling pathways underpinning these outcomes. In contrast to our hypothesis, a novel role of IGF-I has been identified whereby eo-incubation of skeletal muscle C2 cells with IGF-I (1.5 ng.ml') and a non- apoptotic dose of TNF-a (1.25 ng.ml"; sufficient to block differentiation) unexpectedly were shown to facilitate a significant four-fold increase in myoblast death (P < 0.05). Specificity of the apoptotic potential of this growth factor was confirmed when neither bFGF-2 nor PDGF-BB (10 or 30 ng.ml' and 1.25 or 5 ng.rnl", respectively) were able to reveal the apoptotic potential of low dose TNF-a. By contrast, but in line with our II hypothesis, dosing with 10 ng.ml" TNF-a resulted in a block of differentiation and initiation of apoptosis, which was rescued by IGF-1. Preliminary signalling studies suggest that MAPK activation rather than the caspases are involved in the induction of death associated with low dose TNF-a (1.25 ng.mrl)/IGF-I incubation and therefore blocking the caspases would be without effect in this circumstance. The PI(3)K pathway is involved in the survival effects of high TNF-a (10 ng.mrl)/IGF co-incubations. Importantly, the rescue of death (regardless of the means required) did not facilitate differentiation and did not rescue the block of expression of IGF-ll or IGFBP-5 (produced by skeletal myoblasts as early events in their terminal differentiation and associated with preventing cell death) in our models. Using array technology we further established potential insulin survival and apoptotic genes that were upregulated in the above conditions and confirmed their expression with qRT-PCR. Of these genes three were selected to conduct gene silencing experiments. The gene silencing studies were effective in reducing expression of Adrald, Birc2 and Sirtl. Our findings suggest that inhibition of Adrald leads to an increase in myoblast death in conditions that are associated with myoblast survival and include basal conditions. This novel finding indicates Adrald expression to be essential for the general maintenance of myoblasts. This may be due to the multiple signalling pathways which the al-ARs regulate which include the PI(3)K-Akt pathway that is associated with growth and anti-apoptosis. Birc2 expression, which is upregulated in our cell model under conditions of myotoxic stress showed no significant effect on myoblast survival when suppressed. Associated with inhibition of apoptosis, it was hypothesised that inhibition of Birc2 would result in an increase in myoblast death however levels of damage were comparable to control myoblasts. Recent articles have stated that Birc, only when overexpressed above physiological levels, is associated with anti-apoptosis and consequently have proposed an alternative nomenclature that names the family after its distinctive structural feature, the BIR, rather than by inhibitor of apoptosis proteins lAPs (Silke & Vaux, 200 l; for review Srinivasula & Ashwell, 2008). Finally Sirtl, similar to Birc2 was highly expressed in conditions that induced the greatest incidence of myoblast death. Subsequent inhibition resulted in further increase in death which was not observed under basal conditions where myoblasts received DM alone. Unlike Adrald, this implicates Sirtl expression as a III survival mechanism which is specific for conditions associated with myotoxic stress. The mammalian Sirtl deacetylase was originally shown to modulate life-span in various species. However, the molecular mechanisms by which Sirtl increases longevity and with regard to the present study, survival, are largely unknown. In mammalian cells, Sirtl appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors. The FOXO family members are negatively regulated by the PI(3)K-Akt signalling pathway. Mammalian FOXOs control various biological functions, including cell cycle arrest, differentiation, repair of damaged DNA and apoptosis. Because the ability to regulate apoptosis and repair damage is correlated with increased organismal longevity and survival in many species these particular functions of FOXO transcription factors may be relevant to Sirtl ability to control longevity These experiments in myoblasts show that IGF-I (Lcng.ml') can facilitate apoptosis in the presence of non-a pop to tic doses ofTNF-a (1.25ng.mr\ which appears to depend not only on the upregulation of specific apoptosis genes (potentially downstream of MAPK) but also on the suppression of survival factors IGF-ll and IGFBP-5 which may also lie downstream of MAPK. These studies highlight the complex regulation of cell survival and cell death at the signalling level, as a consequence of interactions of one cytokine, TNF-a, and one growth factor, IGF-I. More information regarding the pathways involved in regulating their expression and activity will be necessary to fully understand the action of these molecules.
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Lunn, Elizabeth Ruth. "Studies on the degeneration and regeneration of neurons to skeletal muscle." Thesis, University of Oxford, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292675.

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Striedinger, Katharine. "Degeneration and regeneration of the retina after trauma: emphasis on gap junctions." [S.l.] : [s.n.], 2004. http://deposit.ddb.de/cgi-bin/dokserv?idn=973201126.

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Vargas, Mauricio Enrique. "Control of axon regeneration and wallerian degeneration by the humoral immune system /." May be available electronically:, 2008. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Colavincenzo, Justin. "Myelin debris clearance along the goldfish visual paths during Wallerian degeneration." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=21529.

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This study aimed to better understand the clearance of myelin debris during Wallerian degeneration in the goldfish visual paths. Myelin debris was first examined immunohistochemically in the presence or absence of regenerating axons. From these preliminary experiments it was apparent that the clearance of myelin debris was not affected by regenerating axons and that the debris was removed in a differential pattern along the visual pathway. Specifically, in the distal stump of the nerve as well as in the optic tract, myelin debris had been effectively cleared by one-month postoperative, while in the cranial segment of the nerve debris persisted for at least 6 weeks after injury. The differential pattern of myelin debris in the optic nerve and tract was then analyzed qualitatively and quantitatively using thick and thin plastic sections at various time points during regeneration. The results suggested that highly activated peripheral macrophages were responsible for the effective clearance of myelin in the distal nerve stump. In the optic tract a number of cellular properties, including their unique population of astrocytes may have enhanced the rate of debris clearance. By contrast, in the cranial segment of the nerve persistent debris was found both intracellularly in phagosomes and extracellularly, suggesting that the resident phagocytes were deficient in effecting both phagocytosis and emigration. Deficient phagocytosis may be a result of the production of anti-inflammatory cytokines in this region, while the failure to emigrate is most likely due to the rigid network of astrocytes in the nerve.
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Julian, Victoria L. "TIR-1/SARM1 Inhibits Axon Regeneration." eScholarship@UMMS, 2021. https://escholarship.umassmed.edu/gsbs_diss/1155.

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The inability to repair axonal damage is a feature of neurological impairment after injury and in neurodegenerative diseases. Axonal repair after injury depends in part on intrinsic factors. Several genes cell-autonomously regulate both axon regeneration and degeneration in response to injury. Recently, Sarm1 has emerged as a key regulator of neurodegeneration. Whether Sarm1 plays a role in axon regeneration is unknown. In this thesis, I identified a role for the C. elegans homolog of Sarm1, tir-1, as a negative regulator of axon regeneration. Investigating the genes which regulate axon regeneration and degeneration has been hindered by technical difficulties in visualizing and manipulating both of these processes in vivo simultaneously. To circumvent this challenge, I developed a new model of axon injury, where both axon regeneration and degeneration can be monitored in vivo with single neuron resolution in C. elegans. I found that the C. elegans homolog of Sarm1, tir-1, strongly inhibits axon regeneration in response to injury. I found that TIR-1 functions cell-intrinsically and that its subcellular localization is dynamically regulated in response to injury. To regulate both axon regeneration and degeneration after injury, I found that TIR-1 function is determined by interaction with two distinct genetic pathways. Together, this work reveals a novel role for tir-1/Sarm1 in axon regeneration, increases our understanding of the injury response, provides new avenues of investigation for studies of TIR-1/SARM1, and inspires candidate approaches to repair the injured nervous system.
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Vater, Ruth. "The fate of myofibrillar and cytoskeletal proteins during degeneration and regeneration of skeletal muscle." Thesis, University of Newcastle Upon Tyne, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.334746.

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Acosta-Saltos, F. C. "The effects of inflammation on the regeneration and degeneration of axons in the CNS." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1466480/.

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Microglia have neurotoxic and neuroprotective effects. The aim of the current project was to investigate the effects of perineuronal microglial activation on axonal regeneration in adult rats and the effects of prolonged neuroinflammation on foetal mouse brain. In contrast to the PNS, the CNS only displays limited axonal regeneration after injury and little perineuronal inflammation. Inflammation around the cell bodies of axotomised neurons has been demonstrated to promote CNS regeneration. Polyinosinic:polycytidylic acid (Poly I:C) is an inflammatory agent. Following delivery of Poly I:C into the motor cortex and a concomitant C4 dorsal corticospinal tract (CST) injury, rats exhibited more CST axons in the cervical spinal cord and less retraction from the injury site than controls. Following facial nerve axotomy, Poly I:C injections adjacent to the facial nucleus accelerated functional recovery. Viral vectors carrying Granulocyte Macrophage Colony Stimulating Factor (GM-CSF) were injected into motor cortex. GM-CSF virus reduced retraction of corticospinal axons from a spinal cord injury site. Behavioural studies of forelimb movements showed that C4 injury had a greater impact on fine distal movements, particularly reaching and grasping, which are known to be controlled by the CST. Treating rats with GM-CSF virus showed a trend towards improved forelimb sub-movements and significantly aided the reaching function recovery. Perinatal activation of periventricular phagocytes has been suggested to result in white matter damage, causing persistent motor disabilities. Transuterine injections of control or GM-CSF virus targeting the lateral ventricles of mice at gestational day 14, resulted in a widespread virally-transduced cells. Greater numbers of phagocytic and activated microglia were present in the areas of viral transduction. There was increased inflammation in the periventricular white matter. Although, the level of transduction remained relatively constant with increasing time, inflammation decreased, suggesting that GM-CSF toxicity is high before or around birth.
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Books on the topic "Degeneration and regeneration"

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Dziegielewska, K. M., Anatomy Physiology, and Physiology. Degeneration and Regeneration in the Nervous System. Edited by N. R. Saunders. Abingdon, UK: Taylor & Francis, 1991. http://dx.doi.org/10.4324/9780203304488.

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1938-, Saunders Norman, and Dziegielewska Katarzyna M. 1949-, eds. Degeneration and regeneration in the nervous system. Australia: Harwood Academic, 2000.

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International Summer School in Brain Reseach (20th 1997 Royal Netherlands Academy of Arts and Sciences). Neuronal degeneration and regeneration: From basic mechanisms to prospects for therapy : proceedings of the 20th International Summer School of Brain Research, held at the Royal Netherlands Academy of Sciences, Amsterdam, The Netherlands from 25 to 29 August 1997. Amsterdam: Elsevier, 1998.

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E, Ribak Charles, ed. From development to degeneration and regeneration of the nervous system. New York: Oxford University Press, 2009.

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K, Chichinadze N., and Al. Natʻišvilis saxelobis ekʻsperimentuli morpʻologiis instituti., eds. Obshchie zakonomernosti morfogeneza i regenerat͡s︡ii. Tbilisi: "Met͡s︡niereba", 1988.

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Degeneration and regeneration in neurons. Kerala, India: Research Signpost, 2006.

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DeFelipe, Javier. Degeneration and Regeneration of the Nervous System. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190842833.003.0011.

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Saunders, Norman, and Katarzyna Dziegielewska. Degeneration and Regeneration in the Nervous System. Taylor & Francis Group, 2000.

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Saunders, Norman, Katarzyna M. Dziegielewska, and Katarzyna Dziegielewska. Degeneration and Regeneration in the Nervous System. Taylor & Francis Group, 2003.

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Saunders, Norman, and Katarzyna Dziegielewska. Degeneration and Regeneration in the Nervous System. Taylor & Francis Group, 2000.

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Book chapters on the topic "Degeneration and regeneration"

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Chu, Genglei, Chen Shi, Jun Lin, Shenghao Wang, Huan Wang, Tao Liu, Huilin Yang, and Bin Li. "Biomechanics in Annulus Fibrosus Degeneration and Regeneration." In Advances in Experimental Medicine and Biology, 409–20. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-0950-2_21.

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Brook, Gary A., Dorothee Hodde, and Thomas Kretschmer. "Grundlegendes zu Degeneration und Regeneration von Nerven." In Nervenchirurgie, 1–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-45894-5_1.

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Reier, Paul J., and Michael A. Lane. "Degeneration, Regeneration, and Plasticity in the Nervous System." In Neuroscience in Medicine, 691–727. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-455-5_46.

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Jo, Junghyo, Deborah A. Striegel, Manami Hara, and Vipul Periwal. "Mathematical Modeling of Islet Generation, Degeneration and Regeneration." In Pancreatic Islet Biology, 65–81. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-45307-1_3.

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Brown, N. "Degeneration versus regeneration — logging in tropical rain forests." In Tropical Rain Forest: A Wider Perspective, 43–73. Dordrecht: Springer Netherlands, 1998. http://dx.doi.org/10.1007/978-94-011-4912-9_3.

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Reier, Paul J., and Margaret J. Velardo. "Degeneration, Regeneration, and Plasticity in the Nervous System." In Neuroscience in Medicine, 663–701. Totowa, NJ: Humana Press, 2003. http://dx.doi.org/10.1007/978-1-59259-371-2_32.

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Fleurot, Magali. "Decadence and Regeneration: Oscar Wilde’s Fairy Tales as a Tool for Social Change." In Decadence, Degeneration, and the End, 67–82. New York: Palgrave Macmillan US, 2014. http://dx.doi.org/10.1057/9781137470867_5.

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Laorden, Natalia Santamaría. "A Regenerative Decadence or a Decadent Regeneration: Challenges to Darwinian Determinism by French, Spanish, and Latin American Writers in the Fin de Siècle." In Decadence, Degeneration, and the End, 35–47. New York: Palgrave Macmillan US, 2014. http://dx.doi.org/10.1057/9781137470867_3.

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Krstić, Radivoj V. "Growth, Regeneration, Hyperplasia, Hypertrophy, Atrophy, Involution, Degeneration, and Necrosis." In General Histology of the Mammal, 8–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70420-8_4.

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Kosik, K. S. "The Neuritic Dystrophy of Alzheimer’s Disease: Degeneration or Regeneration?" In Growth Factors and Alzheimer’s Disease, 234–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-46722-6_20.

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Conference papers on the topic "Degeneration and regeneration"

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Yanik, Mehmet. "Femtosecond Laser Nanosurgery and Study of Nerve Regeneration and Degeneration." In 2006 IEEE LEOS Annual Meeting. IEEE, 2006. http://dx.doi.org/10.1109/leos.2006.279138.

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Applegate, Mark A. "Development of Tissue-Engineered Human Articular Cartilage." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2507.

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Abstract Disability due to joint pain is increasing as our society ages. This pain often results from cartilage degeneration in joints due to osteoarthritis or trauma. Cartilage damage from sports injuries is common and the normal repair response results in the formation of fibrous tissue that is inferior to normal cartilage in structure and function and eventually degenerates with time. As a result, tens of thousands of total knee replacements and other surgical procedures are performed each year to repair cartilage defects in the knee. A common clinical treatment for cartilage lesions is debridement of the damaged tissue followed by drilling into the subchondral bone to stimulate tissue regeneration. Although this procedure often provides pain relief, it does not restore long-term function and frequently hastens additional degeneration of the injured site. Alternative procedures for repair or regeneration of human articular cartilage are needed.
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Cleary, Heather, Thomas Barkley, Adam Goodman, Michael Payne, John Virtue, Jennifer Vernengo, and Jennifer Kadlowec. "Design of a Bioreactor for Mechanical Stimulation of Adipose Derived Stem Cells for Intervertebral Disc Tissue Engineering." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80745.

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Lower back pain is one of the most common medical problems in the world [1], affecting between 70% and 85% of the US population at some point during their lives [2]. Disc degeneration is caused by biological changes in the disc, which result in dehydration of the nucleus pulposus (NP). The long term goal of this project is to treat disc degeneration with a tissue engineering strategy for the regeneration of the nucleus pulposus using messechymal stem cells derived from adipose tissue. It has been established in cartilage regeneration studies that cyclic compressive loading of stem cells is beneficial for tissue formation compared to static culture [3–7]. In this work, a bioreactor is being developed that can subject cell-seeded polymeric tissue engineering scaffolds to dynamic compressive forces. Ultimately, the bioreactor will be used to study the effects of different loading parameters on the production of new nucleus pulposus tissue from adipose-derived stem cells.
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Francisco, Aubrey T., Robert J. Mancino, Claire G. Jeong, Isaac O. Karikari, Robby D. Bowles, Stephen L. Craig, and Lori A. Setton. "Injectable and Photocrosslinkable Laminin Functionalized Biomaterials for Intervertebral Disc Regeneration." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80660.

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Biological and anatomical changes of intervertebral disc (IVD) degeneration frequently occur in the nucleus pulposus (NP) [1]. Changes in NP matrix composition coincide with the loss of a distinct notochord derived cell population [2],[3], which may have the potential to generate or maintain a functional NP-like matrix. Immature NP cells reside in an environment rich in laminin and express specific laminin-binding receptors [4],[5]. Additionally, NP cells attach in higher numbers to laminins as compared to cells isolated from other regions of the IVD [6]. Our initial work demonstrated that matrix protein and stiffness modulate NP cell-cell interactions upon surfaces [7], with results that suggest soft, laminin-functionalized hydrogels may be useful for promoting an NP-like cell phenotype.
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Houseman, C., M. Scro, S. Belverud, D. Chen, P. Razzano, M. Levine, D. A. Grande, and N. O. Chahine. "Effect of TGF-β3 on the Gene Expression of Intervertebral Disc Cells in 3D Pellet Cultures." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19246.

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Intervertebral disc (IVD) degeneration typically involves changes in the multiple constitutive tissues of the IVD. Many tissue repair efforts have focused on the use of differentiated disc cells or stem cells for the regeneration of an IVD in vitro. Consequently, successful long term culture of human disc cells is pivotal for tissue regeneration of the IVD. The aim of this study is to establish a long-term in vitro culture system for the growth of disc cells that maintain their phenotype based on the anatomical origin (annulus fibrosus (AF), nucleus pulposus (NP), or the vertebral end-plates (EP)). This maintenance of phenotype is crucial for examination of treatment efficacy, which is typically designed to induce regeneration of a single tissue type (i.e. injection of growth factors into the NP or anti-inflammatory treatment of the EPs).
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Fournier, Adam, Suneil Hosmane, and K. T. Ramesh. "Thresholds for Embryonic CNS Axon Integrity, Degeneration, and Regrowth Using a Focal Compression Platform." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80331.

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Traumatic axonal injuries (TAI) are broadly defined as the focal or multi-focal damage of axons within white matter tracts of the central nervous system (CNS), and can occur in the setting of spinal cord injury (SCI) and traumatic brain injury (TBI). TAI can result from mechanical forces associated with the rapid deformation of white matter regions during trauma. Through combinations of compression, stretch, and shear, axon injury often results in an irreversible loss of functional neural connectivity, since the scope for axonal regeneration in the CNS is extremely limited.
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Morimoto, David, Kathleen M. Keehan, Paul E. Kilbride, and Norman P. Blair. "Retinal Reattachment of the Human Macula Assessed by Imaging Fundus Reflectometry." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1990. http://dx.doi.org/10.1364/navs.1990.tha4.

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Visual recovery following retinal reattachment surgery may be limited by a number of factors. Detachment of the macula is the most important of these, often yielding poor visual acuity after an anatomic success. Gross morphologic changes giving a poor visual result include macular pucker, cellophane maculopathy, cystoid macular edema, and subretinal fibrosis. Some cases with a normal appearing macula by ophthalmoscopy have reduced visual acuity, and these have been attributed to misalignment of photoreceptors, faulty regeneration of photoreceptors, or RPE atrophy (4,5,6). Histologic animal studies have shown degeneration of photoreceptor outer segments following retinal detachment with gradual regeneration following reattachment (2,8). In this report we use fundus reflectometry in vivo to compare the spatial distribution of the visual pigments, contained in photoreceptor outer segments, in 3 patients following retinal reattachment surgery with 9 controls.
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Burns, Stephen A., Ann E. Elsner, John J. Weiter, and Mark R. Kreitz. "Cone Photopigment Density in Aging and AMD." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.wa3.

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Age-related Macular Degeneration (AMD) is the leading cause of vision loss in the elderly. Histopathologically AMD is characterized by diffuse changes in Bruch’s membrane and in many cases by the development of drusen. The pathogenesis of AMD is thought to derive from abnormalities of the Retinal Pigment Epithelium (RPE). The RPE is critically important for the nourishment and health of the photoreceptors. For this reason we are using a psychophysical measure of photoreceptor function to examine patients with AMD. The measure used is the change in the color-match with retinal illuminance which provides information on the optical density and regeneration of the cone photopigments.
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Bitenc Zore, Sara, Domen Vozel, and Saba Battelino. "Facial Nerve Reconstructive Surgery in Otorhinolaryngology and its Enhancement by Platelet- and Extracellular Vesicle-Rich Plasma Therapy." In Socratic Lectures 7. University of Lubljana Press, 2022. http://dx.doi.org/10.55295/psl.2022.d5.

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The facial nerve and its reconstructive surgical procedures are complex and challenging. The main function of facial nerve is namely motor innervation of facial muscles and its dysfunction presents as facial paralysis. Depending on the extent of facial nerve injury (neurapraxia, axonotmesis, neurotmesis) and consequently a physiological phenomenon of Wallerian degeneration, mechanism, location of the injury, time course of the paralysis and medical condition we decide about the type of the reconstructive surgery. Generally, possible surgical interventions to improve facial nerve functioning are mainly nerve decompression, neurorrhaphy/end-to-end anastomosis, interposition (cable) grafts and nerve rerouting. Moreover, most commonly nerves undergoing facial reconstruction are great auricular and sural nerves. In addition, nerve rehabilitation can be improved by using platelet-rich plasma (PRP/PVRP), applied directly to nerve. There are many roles of PVRP, described in the literature such as neuroprotective, neurogenic, neuroinflammatory, angiogenic role and improving hemostasis. Also, its neoplastic and proliferative effects were not reported. Considering all these features implementing PVRP in the facial nerve regenerative treatment has strong potential in the future. Keywords: Facial nerve; Reeconstructive surgery; Platelet and extracellular vesicle rich plasma; Nerve regeneration
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Orlansky, Amy S., John I. Boxberger, and Dawn M. Elliott. "The Dynamic Viscoelastic Properties of the Rat Lumbar Disc Are Decreased Following Nucleus Pulposus GAG Reduction." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192634.

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The intervertebral disc has the important biomechanical function of dissipating energy during spinal loading. With degeneration, the disc experiences, among other changes, a loss of mechanical function and degradation of its composition. Using a rat model of early disc degeneration by injection of Chondroitinase ABC (ChABC), glycosaminoglycan (GAG) content in the nucleus pulposus (NP) was reduced which altered neutral zone mechanical properties. The contribution of decreased NP GAG content to the dynamic viscoelastic properties has yet to be determined. The advantage of dynamic viscoelastic testing is that it provides both viscous and elastic stiffness values as a function of loading frequency. These methods have been employed previously in a rabbit disc regeneration model, in ligament under three modes of loading, and in NP under oscillatory shear and compression. Therefore, the objective of this study was to determine the viscoelastic behavior of a rat lumbar disc at several equilibrium strains and to quantify the impact of GAG reduction on this behavior. Our hypotheses were: 1) elastic stiffness would be greater, and viscous stiffness and loss angle would be lower with increased frequency, and 2) both elastic and viscous stiffness would be lower in the reduced GAG discs at all frequencies.
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Reports on the topic "Degeneration and regeneration"

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Muir, David F. Nerve Degeneration and Regeneration Associated with NF1 Tumors. Fort Belvoir, VA: Defense Technical Information Center, June 2012. http://dx.doi.org/10.21236/ada610038.

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Muir, David F. Nerve Degeneration and Regeneration Associated with NF1 Tumors. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada612926.

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Muir, David F., and Betty Diamond. Nerve Degeneration and Regeneration Associated with NF1 Tumors. Fort Belvoir, VA: Defense Technical Information Center, September 2014. http://dx.doi.org/10.21236/ada612927.

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