Relevant bibliographies by topics / Degeneration

Academic literature on the topic 'Degeneration'

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

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Journal articles on the topic "Degeneration"

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Ahluwalia, Kabir, Juan-Carlos Martinez-Camarillo, Biju B. Thomas, Aditya Naik, Alejandra Gonzalez-Calle, Dimitrios Pollalis, Jane Lebkowski, et al. "Polarized RPE Secretome Preserves Photoreceptors in Retinal Dystrophic RCS Rats." Cells 12, no. 13 (June 22, 2023): 1689. http://dx.doi.org/10.3390/cells12131689.

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Retinal degenerative diseases, including age-related macular degeneration (AMD) and retinitis pigmentosa, lack effective therapies. Conventional monotherapeutic approaches fail to target the multiple affected pathways in retinal degeneration. However, the retinal pigment epithelium (RPE) secretes several neurotrophic factors addressing diverse cellular pathways, potentially preserving photoreceptors. This study explored human embryonic stem cell-derived, polarized RPE soluble factors (PRPE-SF) as a combination treatment for retinal degeneration. PRPE-SF promoted retinal progenitor cell survival, reduced oxidative stress in ARPE-19 cells, and demonstrated critical antioxidant and anti-inflammatory effects for preventing retinal degeneration in the Royal College of Surgeons (RCS) rat model. Importantly, PRPE-SF treatment preserved retinal structure and scotopic b-wave amplitudes, suggesting therapeutic potential for delaying retinal degeneration. PRPE-SF is uniquely produced using biomimetic membranes for RPE polarization and maturation, promoting a protective RPE secretome phenotype. Additionally, PRPE-SF is produced without animal serum to avoid immunogenicity in future clinical development. Lastly, PRPE-SF is a combination of neurotrophic factors, potentially ameliorating multiple dysfunctions in retinal degenerations. In conclusion, PRPE-SF offers a promising therapeutic candidate for retinal degenerative diseases, advancing the development of effective therapeutic strategies for these debilitating conditions.
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Chen, Xiaofeng, Weijun Guo, Hao Li, Xi Li, Zhuangxun Han, Xueyuan Chu, Zehui Lao, Junxian Xie, and Dongling Cai. "Evaluation of Cartilaginous Endplate Degeneration Based on Magnetic Resonance Imaging." Journal of Healthcare Engineering 2021 (March 23, 2021): 1–12. http://dx.doi.org/10.1155/2021/5534227.

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In order to carry out the evaluation of cartilaginous endplate degeneration based on magnetic resonance imaging (MRI), this paper retrospectively analyzed the MRI data from 120 cases of patients who were diagnosed as lumbar intervertebral disc degeneration and underwent MRI examinations in the designated hospital of this study from June 2018 to June 2020. All cases underwent conventional sagittal and transverse T1WI and T2WI scans, and some cases were added with sagittal fat-suppression T2WI scans; then, the number of degenerative cartilaginous endplates and its ratio to degenerative lumbar intervertebral discs were counted and calculated, and the T1WI and T2WI signal characteristics of each degenerative cartilage endplate and its correlation with cartilaginous endplate degeneration were summarized, compared, and analyzed to evaluate the cartilaginous endplate degeneration by those magnetic resonance information. The study results show that there were 33 cases of cartilaginous endplate degeneration, accounting for 27.50% of all those 120 patients with lumbar intervertebral disc degeneration (54 degenerative endplates in total), including 9 cases with low T1WI and high T2WI signals, 5 cases with high T1WI and low T2WI signals, 12 cases with high and low mixed T1WI and high or mixed T2WI signals, and 4 cases with both low T1WI and T2WI signals. Therefore, MRI scanning can clearly present the abnormal signals of lumbar intervertebral disc and cartilaginous endplate degeneration, accurately identity their lesion locations, and type their degenerative characteristics, which may be best inspection method for the evaluation of cartilaginous endplate degeneration in the early diagnosis of intervertebral disc degeneration. The study results of this paper provide a reference for further researches on the evaluation of cartilaginous endplate degeneration based on magnetic resonance imaging.
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Zhang, Ting, Yajing Zuo, Yantao Wei, Wenbin Huang, Xuezhi Zhou, Rongjiao Liu, Lili Zhong, Manjuan Peng, and Shaochong Zhang. "The Prevalence and Associations of Peripheral Retinopathy: Baseline Study of Guangzhou Office Computer Workers." Journal of Ophthalmology 2018 (June 20, 2018): 1–6. http://dx.doi.org/10.1155/2018/2358690.

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Purpose. To determine the prevalence of peripheral retinopathy and its associated risk factors among a sample of Guangzhou office computer workers. Methods. A cross-sectional study of Guangzhou Chinese computer workstations and operators in different departments and units of the Guangzhou Power Supply Bureau, China, in 2016. Peripheral retinopathy was recorded and analyzed using a scanning laser ophthalmoscope (SLO; Optos, Daytona, United Kingdom) and slit-lamp microscopy combined with a three-mirror contact lens. Results. The 1934 eyes of 967 subjects (513 females and 454 males) were included in this study. In total, 79.1% of the eyes were myopic in workers aged 20–29 years, 72.9% in workers aged 30–39 years, 62.2% in workers aged 40–49 years, and 43.4% in workers aged 50–59 years (p<0.001). Most eyes had optic nerve crescents (81.3%). Various peripheral degenerations were found: 7 eyes (0.4%) had microcystoid degeneration, 40 (2.1%) had peripheral pigmentary degeneration, 87 (4.5%) had lattice degeneration, and 4 (0.2%) had snail-track degeneration. Nineteen (1.0%) eyes had paving-stone degeneration, 11 (0.6%) eyes had a retinal hole or tear, and 16 (0.8%) eyes had chorioretinal degeneration. Multivariate regression confirmed that greater axial length (OR: 1.18 (1.03, 1.35), p=0.012) and more serious spherical equivalent (OR: 0.82 (0.77, 0.88), p<0.001) were significant risk factors for peripheral retinal changes. Conclusion. Peripheral retinal degenerative changes were found in a larger proportion of younger computer workers than older ones. Myopia is occurring in younger and younger people, accompanied by peripheral retinal degeneration.
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Voigt, Andrew P., Elaine Binkley, Miles J. Flamme-Wiese, Shemin Zeng, Adam P. DeLuca, Todd E. Scheetz, Budd A. Tucker, Robert F. Mullins, and Edwin M. Stone. "Single-Cell RNA Sequencing in Human Retinal Degeneration Reveals Distinct Glial Cell Populations." Cells 9, no. 2 (February 13, 2020): 438. http://dx.doi.org/10.3390/cells9020438.

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Degenerative diseases affecting retinal photoreceptor cells have numerous etiologies and clinical presentations. We clinically and molecularly studied the retina of a 70-year-old patient with retinal degeneration attributed to autoimmune retinopathy. The patient was followed for 19 years for progressive peripheral visual field loss and pigmentary changes. Single-cell RNA sequencing was performed on foveal and peripheral retina from this patient and four control patients, and cell-specific gene expression differences were identified between healthy and degenerating retina. Distinct populations of glial cells, including astrocytes and Müller cells, were identified in the tissue from the retinal degeneration patient. The glial cell populations demonstrated an expression profile consistent with reactive gliosis. This report provides evidence that glial cells have a distinct transcriptome in the setting of human retinal degeneration and represents a complementary clinical and molecular investigation of a case of progressive retinal disease.
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Börner, W., and P. Schneider. "The Impact of Degenerative Spinal Changes on the Correlation of Peripheral and Axial Bone Density." Nuklearmedizin 33, no. 04 (1994): 138–43. http://dx.doi.org/10.1055/s-0038-1629808.

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SummaryResults of bone density measurements by quantitative computed tomography of the peripheral skeleton (pQCT) were compared with those of measurements at the axial skeleton with a view to study the effects of degenerative spinal changes on the validity of bone densitometry of the lumbar spine. 556 consecutive patients were examined by dual-energy x-ray absorptiometry (DXA) of the spine and by peripheral quantitative computed tomography (pQCT) of the distal radius. There were significant differences between the bone mineral values at the distal radius and those at the spine, depending on the degree of spinal degeneration. As expected, spinal degenerations showed a highly significant age dependence. With increasing degeneration the correlations between the radius total bone mineral concentration and the bone density of the lumbar spine decreased from r = 0.45 to 0.23 in women and from r = 0.64 to 0.28 in men. We conclude that the value of spinal DXA is reduced in patients with degenerative spinal disease, compared to the pQCT at the peripheral skeleton.
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Marques, Christine, Thibaut Burg, Jelena Scekic-Zahirovic, Mathieu Fischer, and Caroline Rouaux. "Upper and Lower Motor Neuron Degenerations Are Somatotopically Related and Temporally Ordered in the Sod1 Mouse Model of Amyotrophic Lateral Sclerosis." Brain Sciences 11, no. 3 (March 13, 2021): 369. http://dx.doi.org/10.3390/brainsci11030369.

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Amyotrophic lateral sclerosis (ALS) is a devastating and fatal neurodegenerative disease arising from the combined degeneration of upper motor neurons (UMN) in the motor cortex, and lower motor neurons (LMN) in the brainstem and spinal cord. This dual impairment raises two major questions: (i) are the degenerations of these two neuronal populations somatotopically related? and if yes (ii), where does neurodegeneration start? If studies carried out on ALS patients clearly demonstrated the somatotopic relationship between UMN and LMN degenerations, their temporal relationship remained an unanswered question. In the present study, we took advantage of the well-described Sod1G86R model of ALS to interrogate the somatotopic and temporal relationships between UMN and LMN degenerations in ALS. Using retrograde labelling from the cervical or lumbar spinal cord of Sod1G86R mice and controls to identify UMN, along with electrophysiology and histology to assess LMN degeneration, we applied rigorous sampling, counting, and statistical analyses, and show that UMN and LMN degenerations are somatotopically related and that UMN depletion precedes LMN degeneration. Together, the data indicate that UMN degeneration is a particularly early and thus relevant event in ALS, in accordance with a possible cortical origin of the disease, and emphasize the need to further elucidate the molecular mechanisms behind UMN degeneration, towards new therapeutic avenues.
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Alkhasawneh, Mahmoud H., Asma’a Al-Mnayyis, and Yazeed Bagain. "Spinal Degeneration and Degenerative Disc Disease correlation identified with Magnetic Resonance Imaging." Biomedical and Pharmacology Journal 14, no. 1 (March 30, 2021): 491–96. http://dx.doi.org/10.13005/bpj/2149.

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Magnetic resonance imaging (MRI) is the golden standard technique for spine disc disease diagnosis. Vertebral body endplate signal intensity on MRI is confirming lumber spine degenerative disc disease.The study aimed to record the lumbar spine degenerative relation between disc and diseaseusing magnetic resonance imaging. Our prospective and double blind investigation included 142 participants,having lumbar spine degenerativedisease confirmed by MRI. Pfirrmann score was used to record the relation between lumbar spine disc degeneration and lumbar spine degenerative disease. Modic modifications with the Pfirrmann and modified Pfirrmann scores of disc degeneration were assessed.Lumbar spine MRI was done for all participants using sagittal T1 and T2 WI. Modic was scored (0-III) The Pfirrmann scored I-V for disc degeneration. Lumbar disc degeneration was evaluated by modified Pfirrmann scoring from 1-8 according to signal intensity of the nucleus pulposus and inner annulus.Modic was recorded in 41.5%, 24.6%, 32.4% and 1.4% of participants with scores 0, I, II and III, respectively. Pfirrmann score was 13.4%, 73.9% and 12.7% of disc degeneration with scores III, IV and V, respectively, while,the modified Pfirrmann score was 2.1%, 15.5%, 38.7%, 26.8% and 16.9% of disc degeneration with scores of 4, 5, 6, 7 and 8, respectively. The modified Pfirrmann score showed notableinconsistencyin participants with Modic 0, I and II, but no difference between Modic I and II.There was significant relation between Modicand lumbar spine disc degeneration. In conclusion, there is a relation between Modic, Pfirrmann and modified Pfirrmann scores of lumbar spine disc degeneration in participants with lumbar spine degenerative disease.
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Baker, Brent A., Robert R. Mercer, Ken B. Geronilla, Michael L. Kashon, G. R. Miller, and Robert G. Cutlip. "Stereological analysis of muscle morphology following exposure to repetitive stretch-shortening cycles in a rat model." Applied Physiology, Nutrition, and Metabolism 31, no. 2 (April 1, 2006): 167–79. http://dx.doi.org/10.1139/h05-009.

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Repetitive motion is one risk factor associated with contraction-induced muscle injury, which leads to skeletal muscle degeneration, inflammation, and dysfunction. Since current methods are unable to quantify the acute degenerative and inflammatory responses of muscle tissue concurrently, the purpose of this study was to quantify the temporal myofiber response after exposure to injurious stretch-shortening cycles (SSCs) using a standardized stereological technique. Functional testing was performed on the ankle dorsiflexor muscles of Sprague-Dawley rats in vivo. Rats were anesthetized and exposed to 15 sets of 10 SSCs. Control rats were exposed to 15 sets of single isometric contractions of the same stimulation duration. Changes in muscle morphometry were assessed at 0.5, 24, 48, 72, and 240 h post-exposure to quantify the degree of myofiber degeneration and inflammation in the tibialis anterior muscle from each group. There was an increase in the volume density and average thickness of degenerating myofibers over time in the muscle collected from rats exposed to SSCs (p < 0.0001) that was significantly greater than in muscle exposed to isometric contractions at 24, 48, and 72 h post-exposure (p = 0.003). The volume density of degenerative myofibers was associated with functional deficits at 48 h. Stereological quantification of degenerative myofibers and interstitial space changes were associated with functional defects 48-72 h after SSC-induced injury, thus demonstrating stereology is an accurate measure of SSC-induced skeletal muscle injury.Key words: stereology, morphometry, myofiber degeneration, interstitial space, stretch-shortening cycles.
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Feinberg, Konstantin, Adelaida Kolaj, Chen Wu, Natalie Grinshtein, Jonathan R. Krieger, Michael F. Moran, Lee L. Rubin, Freda D. Miller, and David R. Kaplan. "A neuroprotective agent that inactivates prodegenerative TrkA and preserves mitochondria." Journal of Cell Biology 216, no. 11 (September 6, 2017): 3655–75. http://dx.doi.org/10.1083/jcb.201705085.

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Axon degeneration is an early event and pathological in neurodegenerative conditions and nerve injuries. To discover agents that suppress neuronal death and axonal degeneration, we performed drug screens on primary rodent neurons and identified the pan-kinase inhibitor foretinib, which potently rescued sympathetic, sensory, and motor wt and SOD1 mutant neurons from trophic factor withdrawal-induced degeneration. By using primary sympathetic neurons grown in mass cultures and Campenot chambers, we show that foretinib protected neurons by suppressing both known degenerative pathways and a new pathway involving unliganded TrkA and transcriptional regulation of the proapoptotic BH3 family members BimEL, Harakiri,and Puma, culminating in preservation of mitochondria in the degenerative setting. Foretinib delayed chemotherapy-induced and Wallerian axonal degeneration in culture by preventing axotomy-induced local energy deficit and preserving mitochondria, and peripheral Wallerian degeneration in vivo. These findings identify a new axon degeneration pathway and a potentially clinically useful therapeutic drug.
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Musarella, Maria A., and Ian M. MacDonald. "Current Concepts in the Treatment of Retinitis Pigmentosa." Journal of Ophthalmology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/753547.

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Inherited retinal degenerations, including retinitis pigmentosa (RP) and Leber congenital amaurosis (LCA), affect 1 in 4000 individuals in the general population. A majority of the genes which are mutated in these conditions are expressed in either photoreceptors or the retinal pigment epithelium (RPE). There is considerable variation in the clinical severity of these conditions; the most severe being autosomal recessive LCA, a heterogeneous retinal degenerative disease and the commonest cause of congenital blindness in children. Here, we discuss all the potential treatments that are now available for retinal degeneration. A number of therapeutic avenues are being explored based on our knowledge of the pathophysiology of retinal degeneration derived from research on animal models, including: gene therapy, antiapoptosis agents, neurotrophic factors, and dietary supplementation. Technological advances in retinal implant devices continue to provide the promise of vision for patients with end-stage disease.
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Dissertations / Theses on the topic "Degeneration"

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Axell, Tim. "Degeneration av varumärken." Thesis, Örebro universitet, Institutionen för juridik, psykologi och socialt arbete, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-92939.

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Rooney, Timothy M. "Genes Required for Wallerian Degeneration Also Govern Dendrite Degeneration: A Dissertation." eScholarship@UMMS, 2015. https://escholarship.umassmed.edu/gsbs_diss/775.

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Neurons comprise the main information processing cells of the nervous system. To integrate and transmit information, neurons elaborate dendritic structures to receive input and axons to relay that information to other cells. Due to their intricate structures, dendrites and axons are susceptible to damage whether by physical means or via disease mechanisms. Studying responses to axon injury, called Wallerian degeneration, in the neuronal processes of Drosophila melanogaster has allowed the identification of genes that are required for injury responses. Screens in Drosophila have identified dsarm and highwire as two genes required for axon degeneration; when these genes are mutated axons fail to degenerate after injury, even when completely cut off from the neuronal cell body. We found that these genes are also required for dendrite degeneration after injury in vivo. Further, we reveal differences between axon and dendrite injury responses using in vivo timelapse recordings and GCaMP indicators of intracellular and mitochondrial calcium transients. These data provide insights into the neuronal responses to injury, and better define novel targets for the treatment of neurodegenerative diseases.
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Rooney, Timothy M. "Genes Required for Wallerian Degeneration Also Govern Dendrite Degeneration: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/775.

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Neurons comprise the main information processing cells of the nervous system. To integrate and transmit information, neurons elaborate dendritic structures to receive input and axons to relay that information to other cells. Due to their intricate structures, dendrites and axons are susceptible to damage whether by physical means or via disease mechanisms. Studying responses to axon injury, called Wallerian degeneration, in the neuronal processes of Drosophila melanogaster has allowed the identification of genes that are required for injury responses. Screens in Drosophila have identified dsarm and highwire as two genes required for axon degeneration; when these genes are mutated axons fail to degenerate after injury, even when completely cut off from the neuronal cell body. We found that these genes are also required for dendrite degeneration after injury in vivo. Further, we reveal differences between axon and dendrite injury responses using in vivo timelapse recordings and GCaMP indicators of intracellular and mitochondrial calcium transients. These data provide insights into the neuronal responses to injury, and better define novel targets for the treatment of neurodegenerative diseases.
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Goldsmith, P. "Zebrafish models of retinal degeneration." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.599478.

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This project has explored whether zebrafish can model human neurological disease, using retinal degeneration as the prototype. The retinal degenerations are a major cause of morbidity, being the commonest cause of blindness in the Western world. Age-related macular degeneration, the commonest retinal degeneration, affects 1 in 20 of the population, and is not treatable. The project began with an F2 mutagenesis screen for candidate blind fish, using an optokinetic assay. Blind fish were characterised using a variety of histological techniques and transplantation studies. Two strains of fish were then selected for more detailed genetic analysis, as they appeared to have a photoreceptor degeneration resembling human retinal degenerations. This involved further mapping of the genes responsible for the phenotype in these two mutants and candidate gene selection.
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Hetherington, Leonard. "Reparative strategies for retinal degeneration." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425592.

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Chong, Ngai Hang Victor. "Retinal degeneration : model and therapies." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.268911.

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Treppo, Steven. "Physical diagnostics of cartilage degeneration." Thesis, Massachusetts Institute of Technology, 1999. http://hdl.handle.net/1721.1/85263.

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Thesis (Ph.D.)--Harvard--Massachusetts Institute of Technology Division of Health Sciences and Technology, February 1999.
"January 1999."
Includes bibliographical references (leaves 219-239).
by Steven Treppo.
Ph.D.
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Hughes, Edward Howard. "Microglial behaviour during photoreceptor degeneration." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446879/.

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Inherited photoreceptor dystrophies are a leading cause of blindness and have no effective treatment. Despite advances in our understanding of the genetic mechanisms underlying this diverse group of conditions, the sequence of events leading from genetic miscoding to photoreceptor death by apoptosis are still unknown, although influences from other cells within the retina have been implicated. Microglia, the macrophages of the central nervous system, have previously been shown to increase in number and migrate to the photoreceptor layer to phagocytose apoptotic cell debris. However increasing awareness of the cytotoxic potential of microglia, has led me to undertake this work with the primary remit of investigating the possible involvement of microglia in photoreceptor apoptosis using the rds mouse model of inherited photoreceptor degeneration. Using immunohistochemical and immunofluorescent methods I have demonstrated increased microglial numbers in the degenerating rds retina, resulting from both in situ proliferation and recruitment from the blood, with migration to the outer retinal layers and sub-retinal space. However, by closely scrutinising the period of greatest disease activity we have demonstrated that the peak rate of photoreceptor apoptosis precedes the peak in microglial numbers by approximately five days, suggesting that microglia respond to, rather than cause photoreceptor death. In addition, evidence of oxidative damage (a major mechanism of microglial cytotoxicity) is absent and depletion of retinal microglia using macrophage-depleting clodronate liposomes did not lead to a reduction in the rate of photoreceptor death, providing further evidence that microglia are not involved in causing photoreceptor apoptosis. Additional studies with the neuroprotective tetracycline antibiotic, minocycline showed that this drug was able to delay the onset of photoreceptor apoptosis in the rds mouse, possibly through a direct inhibitory effect on apoptosis and the caspase cascade. Delayed apoptosis was associated with a corresponding delay in microglial migration to the outer retina.
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Schindler, Emily Isaak. "Genetics of inherited retinal degeneration." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/1075.

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Heritable retinal degenerations dramatically affect individuals across the lifespan. Heritable degenerations with onset in childhood or young adulthood, such as the ABCA4- associated maculopathies, generally obey Mendelian segregation and are attributable to mutations within a single gene. Retinal degenerations with onset in late adulthood, such as age-related macular degeneration, are usually influenced by a complex constellation of genetic and environmental factors. This thesis applies several complementary, high-throughput genotyping platforms to identify relationships between specific heritable retinal phenotypes and genetic variation. This findings of this thesis will aid in the development of guidelines for inclusion in retinal gene therapy trials and help physicians refine their prognoses based on genetic information.
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Fornasin, Nelvis [Verfasser], Sebastian [Akademischer Betreuer] Goette, and Katrin [Akademischer Betreuer] Wendland. "[eta] invariants under degeneration to cone-edge singularities = η invariants under degeneration to cone-edge singularities." Freiburg : Universität, 2019. http://d-nb.info/1203804326/34.

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Books on the topic "Degeneration"

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Simon, Nordau Max. Degeneration. Lincoln: University of Nebraska Press, 1993.

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Weber, Bernhard H. F., and THOMAS LANGMANN, eds. Retinal Degeneration. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-080-9.

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Babetto, Elisabetta, ed. Axon Degeneration. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0585-1.

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Hollyfield, Joe G., Robert E. Anderson, and Matthew M. LaVail, eds. Retinal Degeneration. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2974-3.

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Weber, Bernhard H. F., and Thomas Langmann, eds. Retinal Degeneration. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-8669-9.

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Penfold, Philip L., and Jan M. Provis, eds. Macular Degeneration. Berlin, Heidelberg: Springer Berlin Heidelberg, 2005. http://dx.doi.org/10.1007/b138399.

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Milner, Fothergill J., and Morgan John Edward, eds. Degeneration amongst Londoners. New York: Garland Pub., 1985.

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Chew, Emily Y., and Anand Swaroop, eds. Age-related Macular Degeneration. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-66014-7.

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Holz, Frank G., Daniel Pauleikhoff, Richard F. Spaide, and Alan C. Bird, eds. Age-related Macular Degeneration. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-22107-1.

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Wykoff, Charles, Mariam Hussain, T. Ashwini Kini, and Bayan Al Othman. Age-Related Macular Degeneration. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-36973-6.

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Book chapters on the topic "Degeneration"

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Van den Wyngaert, Tim. "Degenerative Spine: Uncovertebral Joint Degeneration." In Clinical Atlas of Bone SPECT/CT, 125–27. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-26449-8_100.

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Van den Wyngaert, Tim. "Degenerative Spine: Uncovertebral Joint Degeneration." In Clinical Atlas of Bone SPECT/CT, 1–3. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-030-32256-4_100-1.

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Bährle-Rapp, Marina. "Degeneration." In Springer Lexikon Kosmetik und Körperpflege, 144. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-71095-0_2704.

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Tedesco, Salvatore. "Degeneration." In Lecture Notes in Morphogenesis, 103–5. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-51324-5_21.

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Brush, Stephen G. "Degeneration." In Die Temperatur der Geschichte, 122–42. Wiesbaden: Vieweg+Teubner Verlag, 1987. http://dx.doi.org/10.1007/978-3-322-88803-7_7.

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Price, George McCready. "Degeneration." In Selected Works of George McCready Price, 70–73. London: Routledge, 2021. http://dx.doi.org/10.4324/9781003003601-14.

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Trotter, David. "Degeneration." In The English Novel in History 1895–1920, 111–27. London: Routledge, 2022. http://dx.doi.org/10.4324/9781315002088-9.

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Van den Wyngaert, Tim. "Degenerative Spine Disease – Atlanto-Occipital Degeneration." In Clinical Atlas of Bone SPECT/CT, 1–3. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-32256-4_98-1.

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Van den Wyngaert, Tim. "Degenerative Spine Disease: Atlanto-occipital Degeneration." In Clinical Atlas of Bone SPECT/CT, 121–23. Cham: Springer International Publishing, 2023. http://dx.doi.org/10.1007/978-3-031-26449-8_98.

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Falup-Pecurariu, Cristian, and Dafin Fior Mureşanu. "Corticobasal Degeneration." In Movement Disorders Curricula, 203–10. Vienna: Springer Vienna, 2017. http://dx.doi.org/10.1007/978-3-7091-1628-9_19.

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Conference papers on the topic "Degeneration"

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Hussain, Mozammil. "Application of Manual Traction Forces on the Cervical Discs With Degenerative Annular Fibers: A Finite Element Model Analysis." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80091.

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Degeneration in intervertebral discs is a complex multifactorial process. Studies have speculated the biomechanical and biochemical reasons factoring the degenerative disc pathology. Disc degeneration begins in inner nucleus pulposus (NP) that has high fluid content. As degeneration advances over time, the load is shifted from inner NP to outer annulus fibrosus (AF) that is more fibrous in nature. In addition to morphological changes in the discs that occur with degeneration in the form of tears and delamination, tissue compositional variations are also noted. These degenerative changes have not only been seen in the disc tissue matrix, but they are also quite apparent in the fibers of AF in the form of incompleteness and laxity [1]. These tensile fibers in AF have a critical functionality in maintaining the mechanical strength of the disc segments, and any form of degenerative impairment in these fibers may lead to abnormal physiology, both in the AF and NP. Despite past research have reported the annular and nucleus stresses in degenerative discs, area that still unclear is the relative contributions of degenerative properties in annular fibers — incompleteness and slackness — to the overall degenerative disc response. Typically, degeneration related neck pain that involve abnormal disc pressures has been shown to be temporarily relieved by the therapeutical application of manual traction forces. The objective of the present study is to understand the pattern of stresses in the AF and NP due to degenerative AF fibers when the manual traction forces are applied on the degenerated discs.
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2

Natarajan, Raghu N., Jigar Gorasia, and Gunnar Andersson. "Generation of Grade Specific Finite Element Model of Lumbar Spines." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14123.

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The anatomy and biomechanics of the intervertebral motion segments is complex, and the development of degenerative motion segment disorders, which occur frequently, is poorly understood. When disc degeneration occurs at one level, whether treated or not, degeneration frequently develops at mobile segments above or below the degenerated or treated segments. After surgical treatment the process is referred to adjacent segment disc disease (ASDD), and the condition clinically called transition syndrome. We do not know at this time if the ASDD is caused by the neighboring degenerated disc or if they represent the natural progression of the lumbar degenerative processes. The development of ASDD is clinically problematic because it can cause pain and necessitate further surgical intervention. The development and severity of ASDD in disc degeneration is broadly believed to depend on a number of variables such as the severity of degeneration, the number of levels that are degenerated and the location of the degenerative disc. Thus it is important to understand how ASDD develops and progresses and how different variables that cause ASDD compare with reference to normal disc biomechanics. It is proposed to address this clinically relevant problem using poroelastic finite element models.
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Dyment, Nathaniel A., Jason T. Shearn, Marc T. Galloway, R. Michael Greiwe, Keith Kenter, Samer S. Hasan, David L. Butler, and Gregory P. Boivin. "Comparative Histological and Biomechanical Effects of Prostaglandin-E2 and Bacterial Collagenase on the Rabbit Patellar Tendon." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192395.

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Ninety-seven percent of tendon ruptures are found in areas of chronic tendon degeneration, which is thought to be a cell-mediated process involving increased extracellular matrix turnover and remodeling [1,2]. The degenerative aspects seen within regions of tendon degeneration include collagen matrix disorganization, collagen fibril thinning, cellular hyperplasia, and neovascularization [1–3]. The etiology of tendon degeneration is unclear at this point. One theory involves the introduction of multiple mechanical insults (mechanical overuse) that act to trigger a degenerative pathway of increased matrix degradation by matrix metalloproteinases (MMP). Inflammation is not seen within regions of degenerative tendon. However, inflammatory mediators such as prostaglandin-E2 (PGE2) may have a role as they have been shown to be upregulated by fibroblasts as a result of mechanical over-stimulation in culture [4]. Multiple injections of PGE2 within the midsubstance of the rabbit patellar tendon (PT) also produced collagen fibril disorganization and thinning [5].
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4

Nagel, Tina M., Victor H. Barocas, and David J. Nuckley. "Quantification of In Vivo Deformation of Healthy Lumbar Intervertebral Discs in Flexion." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80685.

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Intervertebral disc (IVD) degeneration is hypothesized to be the precursor to non-specific low back pain, which is a widespread problem [1]. However, before disc degeneration can be understood, a better understanding of healthy discs must be gained. The disc is a short thick-walled cylinder with a gelatinous center, the nucleus pulposus, and a largely concentric, layered collagenous ring, the annulus fibrosus, Figure 1. The layers are referred to as lamella. The IVD is integral to the strength and flexibility of the spine. Whole disc mechanics have been widely studied, but degeneration occurs at the fiber level [2]. To understand the mechanics of degeneration, testing needs to be performed at a finer level where degenerative / injury effects occur. These effects such as tears occur in the annular lamella.
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Cusick, Joseph F., Srirangam Kumaresan, Brian Bunch, Narayan Yoganandan, and Frank A. Pintar. "Biomechanics of Lumbar Spondylotic Degeneration." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2599.

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Abstract Human lumbar spinal columns exhibit different degrees of spondylotic degeneration. However, the biomechanical effects of these changes have not been fully studied. Understanding the potential patterns of such responses relative to the severity of degenerative changes assist in clarifying the influence on clinical and laboratory investigations. This study was conducted to obtain the three-dimensional biomechanical stability parameters of degenerated and non-degenerated spines. The degree of degeneration in disc and facet joints was graded individually for severity allowing evaluation of overall effects as well as individual component influences. Pure moment and complex loading were applied under flexion, extension, and left and right lateral bending modalities. The degenerated columns responded with greater variations in the moment-rotation (pure-moment loading) and force-deflection and moment-rotation (combined loading) than normal spinal columns. Furthermore, the response of the degenerated column depended not only on the overall quality of the spine, but also on the difference in severity and type of components affected. Complex loading showed increased sensitivity to variations in the biomechanical responses compared to pure moment loading. Disc degeneration showed increased changes in rotational stability, whereas facet alterations demonstrated greater effects on axial stiffness.
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Ling, Carrie H., Janice H. Lai, James F. Nishimuta, and Marc E. Levenston. "Dose-Dependent Effects of Interleukin-1Alpha on Functional Degradation of Lateral and Medial Menisci." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19523.

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Despite a growing recognition that meniscal degeneration often precedes cartilage degeneration in the development of knee osteoarthritis (OA), little is known about the role of meniscal degeneration in the onset and progression of knee OA. Even a mild degenerative lesion increases meniscal extrusion, implying changes in biomechanical function. Understanding the mechanisms of meniscal degeneration may enable the diagnosis and disease-modifying treatment of early knee OA, potentially preventing or slowing the progression of the disease. The roles of pro-inflammatory cytokines such as interleukin-1 (IL-1) in promoting cartilage matrix degradation and mediating inflammation in the progression of OA have been widely demonstrated [1,2]. Recent results from our group indicated that 20ng/ml hrIL-1α produced similar cell-mediated degradation and loss of mechanical properties in immature cartilage and meniscus, but progresses more rapidly in meniscus explants [3]. This study further explored the effects of IL-1α dosage and medial-lateral differences on the functional degradation of meniscal explants.
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7

Capart, Antoine, Roman Allais, Julien Wojak, Olivier Boiron, and Anabela Da Silva. "Reconstruction of the opto-mechanical properties of the intervertebral disc with photoacoutic imaging." In Optical Tomography and Spectroscopy. Washington, D.C.: Optica Publishing Group, 2024. http://dx.doi.org/10.1364/ots.2024.otu3d.3.

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The intervertebral disc undergoes degeneration, resulting in its dehydration and the development of degenerative diseases. This study introduces quantitative photoacoustic imaging as a method for assessing the state of the disc.
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Chan, D. D., and C. P. Neu. "Human Tibiofemoral Joint Displacements Determined by Displacement-Encoded MRI." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53498.

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Articular cartilage and surrounding soft tissues in the knee are important to normal joint function. Osteoarthritis (OA) is highly prevalent in the United States [1] and features precocious degeneration of articular cartilage. Effective OA treatments require the ability to detect early degeneration, including mechanical and biochemical changes. Magnetic resonance imaging has shown promise for the detection of early degenerative changes, including various quantitative MRI techniques [2]. Displacement-encoded MRI has the ability to detect changes in mechanical behavior, and such techniques have previously been used in cartilage explants [3] and intact juvenile animal joints [4]. However, the authors are aware of no studies with displacement-encoded MRI of human articular cartilage. Tissue-level displacement patterns could be key to revealing early degeneration in articular cartilage. This study demonstrates for the first time displacement encoding with stimulated echoes (DENSE) in an adult human tibiofemoral joint.
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Hussain, Mozammil, Raghu N. Natarajan, Gunnar B. J. Andersson, and Howard S. An. "Effect of a Degenerated C5-C6 Disc on the Biomechanics of Adjacent Levels: A Poroelastic Finite Element Investigation." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176621.

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Degenerative changes in the cervical spine due to aging are very common causes of neck pain in general population. Although many investigators have quantified the gross morphological changes in the disc with progressive degeneration, the biomechanical changes due to degenerative pathologies of the disc and its effect on the adjacent levels are not well understood. Despite many in vivo and in vitro techniques used to study such complex phenomena, the finite element (FE) method is still a powerful tool to investigate the internal mechanics and complex clinical situations under various physiological loadings particularly when large numbers of parameters are involved. The objective of the present study was to develop and validate a poroelastic FE model of a healthy C3-T1 segment of the cervical spine under physiologic moment loads. The model included the regional effect of change in the fixed charged density of proteoglycan concentration and change in the permeability and porosity due to change in the axial strain of disc tissues. The model was further modified to include various degrees of disc degeneration at the C5-C6 level. Outcomes of this study provided a better understanding on the progression of degeneration along the cervical spine by investigating the biomechanical response of the adjacent segments with an intermediate degenerated C5-C6 level.
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Wang, Shaobai, Michal Kozanek, Kirkham B. Wood, and Guoan Li. "Lumbar Degenerative Disc Disease Increases Deformations at Cephalad Adjacent Levels In Vivo." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19629.

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Low back pain, one of the most common causes of disability in working population is in the vast majority of cases attributed to degeneration of the lumbar intervertebral disc (IVD). It has been reported that in patients with degenerative disc diseases (DDD) at one level, the discs adjacent to the diseased level have a greater tendency to degenerate. Studies have also suggested altered biomechanics as causative factors [1, 2]. However, to date no data has been reported on the deformation of the disc in vivo in DDD patients. The purpose of this study was to evaluate the effect of lumbar IVD degeneration on the deformation of the discs at the adjacent levels during functional weightbearing postures.
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Reports on the topic "Degeneration"

1

Przedborski, Serge. Role of Inflammation in MPTP-Induced Dopaminergic Degeneration. Fort Belvoir, VA: Defense Technical Information Center, December 2005. http://dx.doi.org/10.21236/ada446427.

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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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Agrela, Fabiano de Abreu. Animes e o emburrecimento do cérebro Animes and brain degeneration. CPAH REDAÇÃO, February 2023. http://dx.doi.org/10.56238/cpahciencia-003.

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Przedborski, Serge E. Role of Nitric Oxide in MPTP-Induced Dopaminergic Neuron Degeneration. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada450371.

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Yurek, David N. Neurotrophic Response to CNS Degeneration or Injury: Effects of Aging. Fort Belvoir, VA: Defense Technical Information Center, October 2004. http://dx.doi.org/10.21236/ada428519.

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Przedborski, Serge. Role of Nitric Oxide in MPTP-Induced Dopaminergic Neuron Degeneration. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada416386.

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Przedborski, Serge, and Vernice Jackson-Lewis. Role of Nitric Oxide in MPTP-Induced Dopaminergic Neuron Degeneration. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada420096.

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Yurek, David M., and Kim B. Seroogy. Neurotrophic Response to CNS Degeneration or Injury: Effects of Aging. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada463998.

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