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Relevant bibliographies by topics / Degeneration in art

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Academic literature on the topic 'Degeneration in art'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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Journal articles on the topic "Degeneration in art"

1

Chu, Constance R., Ashley Williams, David Tolliver, C. Kent Kwoh, Stephen Bruno, and James J. Irrgang. "Clinical optical coherence tomography of early articular cartilage degeneration in patients with degenerative meniscal tears." Arthritis & Rheumatism 62, no. 5 (March 8, 2010): 1412–20. http://dx.doi.org/10.1002/art.27378.

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Bendele, A. M., and J. F. Hulman. "Spontaneous cartilage degeneration in guinea pigs." Arthritis & Rheumatism 31, no. 4 (April 1988): 561–65. http://dx.doi.org/10.1002/art.1780310416.

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MATICH, OLGA. "THREE RUSSIAN DANCERS: DECADENCE, ART NOUVEAU, DEGENERATION." Experiment 10, no. 1 (2004): 115–32. http://dx.doi.org/10.1163/2211730x04x00091.

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Aigner, T., and H. A. Kim. "Apoptosis and cellular vitality: Issues in osteoarthritic cartilage degeneration." Arthritis & Rheumatism 46, no. 8 (August 2002): 1986–96. http://dx.doi.org/10.1002/art.10554.

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Van de Sande, Michiel A. J., Jurriaan H. De Groot, and Piet M. Rozing. "Clinical implications of rotator cuff degeneration in the rheumatic shoulder." Arthritis & Rheumatism 59, no. 3 (2008): 317–24. http://dx.doi.org/10.1002/art.23330.

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Bae, Won C., Michele M. Temple, David Amiel, Richard D. Coutts, Gabriele G. Niederauer, and Robert L. Sah. "Indentation testing of human cartilage: Sensitivity to articular surface degeneration." Arthritis & Rheumatism 48, no. 12 (December 2003): 3382–94. http://dx.doi.org/10.1002/art.11347.

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Cheung, Kenneth M. C., Dino Samartzis, Jaro Karppinen, Florence P. S. Mok, Daniel W. H. Ho, Daniel Y. T. Fong, and Keith D. K. Luk. "Intervertebral disc degeneration: New insights based on “skipped” level disc pathology." Arthritis & Rheumatism 62, no. 8 (April 19, 2010): 2392–400. http://dx.doi.org/10.1002/art.27523.

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Yudoh, Kazuo, Kiyoshi Shishido, Hideki Murayama, Mitsunobu Yano, Kenji Matsubayashi, Hiroya Takada, Hiroshi Nakamura, Kayo Masuko, Tomohiro Kato, and Kusuki Nishioka. "Water-soluble C60 fullerene prevents degeneration of articular cartilage in osteoarthritis via down-regulation of chondrocyte catabolic activity and inhibition of cartilage degeneration during disease development." Arthritis & Rheumatism 56, no. 10 (2007): 3307–18. http://dx.doi.org/10.1002/art.22917.

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Cohen, Miriam H., Amelia M. Carton, Christopher J. Hardy, Hannah L. Golden, Camilla N. Clark, Phillip D. Fletcher, Kankamol Jaisin, et al. "Processing emotion from abstract art in frontotemporal lobar degeneration." Neuropsychologia 81 (January 2016): 245–54. http://dx.doi.org/10.1016/j.neuropsychologia.2015.12.031.

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Cheung, Herman S., John D. Sallis, Konstantino D. Demadis, and Andrzej Wierzbicki. "Phosphocitrate blocks calcification-induced articular joint degeneration in a guinea pig model." Arthritis & Rheumatism 54, no. 8 (2006): 2452–61. http://dx.doi.org/10.1002/art.22017.

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Dissertations / Theses on the topic "Degeneration in art"

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Ostrander, Edward Frank. "Decline, Decay, And Degeneration: Channeling A Capacity To Discover Truth In Destruction." Columbus, Ohio : Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1245263805.

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TAVARES, Márcio Júnior Montelo. "CRÍTICA ROUSSEAUNIANA DA IMITAÇÃO TEATRAL: da recusa do teatro de classe francês ao consentimento da festa." Universidade Federal do Maranhão, 2017. http://tedebc.ufma.br:8080/jspui/handle/tede/1758.

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Made available in DSpace on 2017-07-25T12:00:41Z (GMT). No. of bitstreams: 1 Márcio Júnior.pdf: 700191 bytes, checksum: b80202af09892b899af3e4bd760c67dd (MD5) Previous issue date: 2017-05-26
In the present bibliographical research, the theater is analyzed, under a critical perspective, as an imitation of the social representation in the writings of JeanJacques Rousseau, taking as a parameter the criticism elaborated by the philosopher genebrino on the French theater, especially in what concerns The comedy of customs advocated by thinkers such as Voltaire and D'Alembert, as well as his negative response to the question about the contribution of the sciences and the arts to the moral improvement of man, presented in his First Discourse. In this panorama, Rousseau disproves most of the philosophers of his time, showing that art, instead of elevating man to a higher moral level, corrupts it by making it vile and attached to frivolities and luxuries unnecessary to a society Virtuous Indeed, unlike ordinary Enlightenment thought, the Geneva philosopher did not assert that this society and that historical moment in which he was inserted represented the pinnacle of moral progress in the history of human civilization, but rather preached that the man had entered a dangerous Process of moral degeneration, of narcissism, from which the other is taken as a mere projection of itself. In this way, we are dealing with the French theater considerations of some Enlightenment philosophers, as well as the answer given by Rousseau to D'Alembert in the famous missive on the Geneva entry in Diderot's Encyclopaedia. It is concluded that, while recognizing the importance of the sciences and the arts for humanity, Rousseau viewed such dimensions of knowledge as harmful insofar as they served distorted purposes, especially when used as a form of distinction between men. The theater, conceived in this perspective, had the function of being simple distraction for the masses, being mere caricature of the daily life.
Na presente pesquisa de cunho bibliográfico, analisa-se o teatro, sob uma ótica crítica, como imitação da representação social nos escritos de Jean-Jacques Rousseau, tomando como parâmetro a crítica elaborada pelo filósofo genebrino sobre o teatro francês, em especial no que tange a comédia de costumes defendida por pensadores como Voltaire e D‟Alembert, bem como sua resposta negativa à questão acerca da contribuição das ciências e das artes para o aprimoramento moral do homem, apresentada no seu Primeiro Discurso. Neste panorama, Rousseau destoa de grande parte dos filósofos de seu tempo, mostrando que a arte, em vez de elevar o homem a um patamar moral superior, acaba corrompendo-o, tornando-o vil e apegado a frivolidades e luxos desnecessários a uma sociedade virtuosa. Aliás, diferente do pensamento iluminista corrente, o filósofo genebrino não asseverou que aquela sociedade e aquele momento histórico nos quais ele estava inserido representavam o auge do progresso moral da história da civilização humana, mas, antes, preconizou que o homem tinha entrado em um perigoso processo de degeneração moral, de narcisismo, a partir do qual o outro é tomado como mera projeção de si mesmo. Aborda-se, assim, as considerações sobre o teatro francês tecidas por alguns filósofos iluministas, bem como a resposta dada por Rousseau a D‟Alembert na célebre missiva a respeito do verbete Genebra contido na Enciclopédia de Diderot. Conclui-se que, mesmo reconhecendo a importância das ciências e das artes para a humanidade, Rousseau via tais dimensões do conhecimento como danosas na medida em que serviam a propósitos distorcidos, em especial quando utilizadas como forma de distinção entre os homens. O teatro, concebido nesta perspectiva, tinha como função ser simples distração para as massas, sendo mera caricatura da vida cotidiana.

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Fowler, Benjamin J. "NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS ARE ANTI-INFLAMMATORY AND TARGET DRY AGE-RELATED MACULAR DEGENERATION." UKnowledge, 2014. http://uknowledge.uky.edu/physiology_etds/17.

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Age-related macular degeneration (AMD) is a principal cause of blindness in the United States and other industrialized nations. An estimated 10 million Americans are afflicted with AMD, which is comparable in scope to the 12 million living with cancer, or the 5 million with Alzheimer’s disease. The prevalence of AMD steadily increases with age, affecting 2% of the population at age 40, and one in four people by age 80. For reasons that are not fully understood, AMD is more common in lightly-pigmented and female populations. Treatment of AMD is largely an unmet need: There are no FDA approved therapies except for a small percentage of individuals with end-stage disease. This dissertation investigates the mechanisms of AMD pathogenesis and offers insight into novel therapeutic strategies for this disease.

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Akagi, Yumiko. "MMP20 and ARMS2/HTRA1 are Associated with Neovascular Lesion Size in Age-Related Macular Degeneration." Kyoto University, 2016. http://hdl.handle.net/2433/204581.

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Boegman, Leon. "The degeneration of internal waves in lakes with sloping topography." University of Western Australia. Centre for Water Research, 2004. http://theses.library.uwa.edu.au/adt-WU2005.0043.

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[Truncated abstract] Observations are presented from Lake Biwa (Japan) and Lake Kinneret (Israel) showing the ubiquitous and often periodic nature of high-frequency internal waves in large stratified lakes. In both lakes, high-frequency wave events were observed within two distinct categories: (1) Vertical mode one solitary waves with wavelength ˜100-500 m and frequency near 103 Hz and (2) sinusoidal vertical mode one waves with wavelength ˜5-30 m and frequency just below the local maximum buoyancy frequency near 102 Hz. The sinusoidal waves were associated with shear instability and were shown to dissipate their energy sporadically within the lake interior. Conversely, the solitary waves were found to be capable of propagating to the lake perimeter where they may break upon sloping topography, each releasing ˜1% of the total basin-scale internal wave energy to the benthic boundary layer.

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Evans, Alyssa. "The Effect of Mechanical Load on Biomarkers of Knee Joint Inflammation for Individuals Who Are Predisposed to Knee Cartilage Degeneration: An Exploratory Study." BYU ScholarsArchive, 2018. https://scholarsarchive.byu.edu/etd/7560.

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Objective: Physical exercise decreases disability and pain associated with chronic articular cartilage degradation. However, understanding of the pathology is lacking. In this study, the levels of 17 biomarkers of inflammation and cartilage degradation were measured in synovial fluid (SF) before and after a 30-minute run in able-bodied and previously-injured individuals. Materials & Methods: Four able-bodied recreational runners (3 men and 1 woman: 24 ± 2 years, 68 ± 7 kg, and 173 ± 9 cm) and 4 recreational runners who had undergone a unilateral anterior cruciate ligament reconstruction (ACLr) (2 men and 2 women: 23 ± 1 years, 71 ± 6 kg, and 175 ± 4 cm) were recruited to participate in this study. Using a saline-assisted method, SF was aspirated before and after both a 30-minute unloading and 30-minute exercise session. Samples were corrected for blood contamination and analyzed for 15 cytokines and 2 matrix metalloproteinases (MMPs). Mixed model analyses were used to determine the main effects of session, case/control status, pre/post aspirations, and the interactions between case/control status and pre/post aspirations. Results: Blood protein contamination was calculated and accounted for in 15 of 32 synovial fluid samples. Granulocyte colony stimulating factor (GCSF) was the only detectable cytokine of the 15 analyzed. No statistical differences were found in GCSF concentrations between pretreatment and posttreatment aspirations (p = 0.45), ACLr and able-bodied control groups (p = 0.60), or unloading and exercise sessions (p = 0.96). MMP-13 was undetectable. No statistical differences were found in MMP-3 between pretreatment and posttreatment aspirations (p = 0.15), ACLr and able-bodied control groups (p = 0.85), or unloading and exercise sessions (p = 0.14).Conclusions: Two (GCSF and MMP-3) of the 17 measured biomarkers were detectable. There were no significant differences in either GCSF or MMP-3 due to a 30-minute run or 30-minute unloading period in either the able-bodied or ACLr participants. Further, there were no significant differences between biomarker concentrations and case-control status. A novel method of controlling for blood contamination in synovial fluid samples was implemented.

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Tan, Celia I. C. "A radiological and biochemical perspective on ageing and degeneration of the human thoracic intervertebral disc." University of Western Australia. School of Surgery and Pathology, 2004. http://theses.library.uwa.edu.au/adt-WU2004.0059.

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Disc degenerative changes are directly or indirectly associated with spinal pain and disability. Literature revealed a high prevalence of disc degeneration in the thoracic region, however thoracic MRI degeneration trends and information on disc biochemical matrix constituents are limited for thoracic discs compared to lumbar and cervical discs. The objective of this thesis was to use MRI to investigate the prevalence of disc degenerative changes affecting the human thoracic spine, and to determine the factors affecting spinal disc biochemical matrix. A 3-point subjective MRI grading scale was used to grade the films. The feasibility of using archived formalin-fixed cadaver material was investigated to analyse collagen and elastin crosslinks. The prevalence of degenerative changes in human thoracic discs and vertebrae (T1 to T12) was determined retrospectively from an audit of 216 MRI cases, using sagittal T1- and T2-weighted MR images. In a subsequent series of ex-vivo studies, human thoracic discs and LF from 26 formalin-fixed and two fresh spines, involving all thoracic levels, were examined macroscopically to determine the degeneration status. Subsequently, disc and ligament tissues were analysed biochemically for collagen (pyridinoline and deoxypyridinoline) and elastin (desmosine and isodesmosine) crosslinks. These crosslinks were extracted from hydrolysed samples by cellulose partition chromatography, and analysed by reverse-phase HPLC. Collagen content was determined using its hydroxyproline content, and proteoglycan content was assayed using a modified DMB assay for chondroitin sulphate. Finally the MRI and macroscopic assessments of thoracic discs, were compared with the biochemical data from two fresh cadaver thoracic spines. The 3-point MRI grading scale had a high inter- (k = 0.57 to 0.78) and intra-rater (k = 0.71 to 0.87) reliability. There were no significant differences in the collagen and elastin content and extent of collagen crosslinks between formalin fixed and unfixed ligament and disc tissues, after 25 weeks of formalin fixation. From the in-vivo MRI series of investigations (n = 216 MRI films), the prevalence of thoracic disc degenerative and vertebral morphological changes revealed significant age, gender and spinal level trends (p < 0.05).Generally, males had a higher propensity for disc degeneration in contrast to females, especially older females, where the trend showed a higher prevalence of osteophytes and vertebral body changes. In particular, the mid and lower thoracic levels have a higher prevalence of degenerative changes, except for osteophytes and anterior vertebral wedging. With increased age, there was a concomitant increase in anterior wedging and bi-concavity and disc degenerative changes except for end-plates. The biochemical investigations on the ex-vivo series of formalin-fixed thoracic discs (n = 303) also revealed significant changes in the disc matrix due to degeneration status, age, gender and spinal regional factors. With increased age, normal disc matrices have significantly lower collagen content and extent of pyridinoline (p < 0.001). In contrast, the degenerated disc matrix revealed significantly higher collagen content and extent of deoxypyridinoline (p < 0.05). These findings suggest that an altered matrix existed in normal ageing discs, which render the disc prone to injury and degeneration over the life span. The higher collagen and deoxypyridinoline in degenerated disc matrices reflects an increase in chondrocyte synthesis, and is also a novel finding, suggesting that they may be used as markers of ageing and degeneration processes. The biochemical investigations on another series of ex-vivo spinal LF tissues (n = 364), revealed that this had a lower collagen and pyridinoline, but significantly higher elastin and deoxypyridinoline compared to spinal discs (p < 0.05). Elastin crosslinks however were difficult to detect in spinal discs, being present in negligible amounts in a few lumbar discs. The elastin crosslinks in the LF were not significantly affected by age, but were significantly higher in calcified, and female ligamentum tissues, and also in the lumbar region (p < 0.05). These MRI prevalence findings enhanced our knowledge of vertebral body and disc degeneration trends in the thoracic region and contributed to the interpretation of MR images for pathology in the human thoracic spine. Information on the associated collagenous and elastic changes in the disc and ligamentum matrices provide original data and insight on the pathogenesis of degeneration in the disc matrix from a biochemical perspective, highlighting gender, age and spinal level influences on the matrix tensile strength and cellular synthetic activities.

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Li, Yan, and n/a. "In vitro and in vivo studies on the absorption of mitoquinone." University of Otago. School of Pharmacy, 2007. http://adt.otago.ac.nz./public/adt-NZDU20070615.135534.

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Mitoquinone (MitoQ₁₀ mesylate) is a mitochondria-targeted antioxidant for the treatment of neurodegenerative diseases. As the oral bioavailability of mitoquinone is low in rat, it is necessary to better understand the mechanisms of its absorption in rat and in human. The aims of this thesis were 1) to investigate oral absorption mechanisms of mitoquinone in Caco-2 cell monolayers and in a rat intestinal tissue model; 2) to investigate the correlation between chemical structure and permeability of mitoquinone analogues in Caco-2 cell monolayers; and 3) to explore the hypothesis that active transport and/or drug metabolism contribute to the pharmacokinetics of oral mitoquinone in rat. In Caco-2 studies, transport of mitoquinone was polarized with the apparent permeability (P[app]) from basolateral (BL) to apical (AP) (P[appBL to AP]) being >2.5-fold the P[app] from AP to BL (P[appAP to BL]). The P[appBL to AP] value decreased by 26%, 31% and 61% by P-glycoprotein (P-gp) inhibitors verapamil 100 [mu]M, cyclosporine A (CsA) 10 [mu]M and CsA 30 [mu]M, respectively, whereas the P[appAP to BL] increased 71% by CsA 30 [mu]M. Some of the intracellular mitoquinone was reduced to mitoquinol and subsequently metabolized to glucuronide and sulfate conjugates. Apical effluxes of mitoquinol sulfate and mitoquinol glucuronide conjugates were significantly decreased by cyclosporine A 30 [mu]M and the breast cancer receptor protein (BCRP) inhibitor, reserpine 25 [mu]M, respectively. In the presence of 4% bovine serum albumin on the BL side, the P[appAP to BL] was 4.52 � 0.92 x 10⁶ cm/s. Based on a absorption-disposition model, F[a] value of mitoquinone in human is estimated to be 56%. A bellshaped relationship exists between the Caco-2 permeability of mitoquinone analogues and their lipophilicity. Permeability of mitoquinone analogues initially increases as lipophilicity increase, reaches a maximum, and then decreases due to significant cellular accumulation and active efflux. The physicochemical parameters of mitoquinone and its analogues (such as log P or polar surface area) alone do not predict their permeability across the cell membranes. The bidirectional transport of mitoquinone displays polarity across rat ileal mucosa. The P[app] from s to m (P[app s to m) of mitoquinone decreased and P[app m to s] increased but not significantly by P-gp inhibitor CsA 30 [mu]M. The tissue accumulation of mitoquinone was ~16% of the total amount of mitoquinone added. In addition, several phase I and one phase II metabolites generated by rat ileum tissue were detected. Results from pharmacokinetic studies indicate that mitoquinone was poorly (~24%) but rapidly absorbed and conjugated after oral administration. It was quickly excreted as unchanged drug and as its glucuronides (the major metabolites in rat) into intestine where it was reabsorbed. P-gp inhibition studies in rat indicate that inhibition of P-gp may increase the intestinal absorption of mitoquinone, but cannot change its oral bioavailability due to increased first-pass phase II metabolism and decreased enterohepatic recycling. In conclusion, mitoquinone is poorly absorbed in rat but may be well absorbed in human. The barrier functions of intracellular metabolism and the action of P-gp to oral absorption of mitoquinone in human may be less significant, whereas P-gp play an important role in the absorption and disposition of mitoquinone in rat in vivo. These results, together with those from its analogues, demonstrate that the actual absorption profile of a compound depends on its intrinsic membrane permeability, transporter affinity, metabolizing enzyme affinity and plasma protein binding affinity.

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Clarkson, Andrew N., and n/a. "Lasting neuroprotection with clomethiazole following hypoxia-ischaemia-induced neurodegeneration : a mechanistic study." University of Otago. Department of Pharmacology & Toxicology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070424.120005.

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Subsequent to an hypoxic-ischaemic (HI)-insult a multi-faceted complex cascade of events occurs that ultimately results in cellular and neurological impairments within cortical and sub-cortical central nervous system (CNS) regions. In the present studies a modified �Levine� rat-pup model of HI (left carotid artery ligation + 1 hour global hypoxia on post-natal day (PND) 26) was employed to assess the neuroprotective properties of clomethiazole (CMZ; a γ-aminobutyric acid (GABA)A receptor agonist). In this study, histological and electrophysiological paradigms were used to assess the long-term neuroprotective properties of CMZ (414mg/kg/day via mini-pumps). Key enzymes involved in inflammation, namely nitric oxide synthase (NOS) and arginase, were also examined to assess other potential CMZ mechanisms. Assessments were carried out 3- and 90-days post-HI, with extensive ipsilateral CNS lesions evident at a gross histological level, at both the early and long-term stages, with CMZ significantly decreasing the lesion size at 3- and 90-days (P<0.01; P<0.05). Evoked field potential analyses were used to assess hippocampal CA1 neuronal activity ex vivo. Electrophysiological measurements contralateral to the occlusion revealed impaired neuronal function following HI relative to short- and long-term controls (P<0.001, 3- and 14-days; P<0.01, 90-days), with CMZ providing near complete protection (P<0.001 at 3- and 14-days; P<0.01 at 90-days). Both inducible NOS (iNOS) and arginase activities were significantly increased at 3-days (P<0.01), with arginase activity remaining elevated at 90-days post-HI (P<0.05) ipsilaterally. CMZ suppressed the HI-induced increase in iNOS and arginase activities (P<0.001; P<0.05). These data provide evidence of long-term functional neuroprotection afforded by CMZ in a model of HI-induced neurodegeneration. In addition, under conditions of HI, functional deficits were not restricted to the ipsilateral hemisphere and were due, at least in part, to changes in the activity of NOS and arginase. Underlying mitochondrial dysfunction is eminently present in many neuropathological conditions. The full extent of mitochondrial dysfunction in cortical, hippocampal and cerebellar tissues was assessed following HI. Assessment of mitochondrial FAD-linked respiration at both 1- and 3-days post-HI revealed a significant decrease in activity from ipsilateral cortical and hippocampal regions (P<0.001). In addition, significant changes in respiratory function were also evident in contralateral regions and cerebellum, 3-days post-HI (P<0.05). Assessment of the mitochondrial electron transport chain (complexes I-V) and mitochondrial markers of integrity (citrate synthase) and oxidative stress (aconitase) confirmed ipsilateral mitochondrial impairment following HI. Complexes I, II-III, V and citrate synthase were also impaired, in contralateral regions and cerebellum, 3-days post-HI. CMZ treatment provided significant protection to all mitochondrial aspects of neuronal tissue assessed. This study provides evidence of the full extent of mitochondrial damage following an HI-insult and may contribute, in part, to the impairment seen contralaterally. In addition, protection afforded by CMZ extends to preservation of mitochondrial function and integrity. Cerebral ischaemia-induced angiogenesis has been shown within and around infarcted regions and may contribute to a more favourable neurological outcome. The level of angiogenesis was examined using platelet endothelial cell adhesion molecule-1 (PECAM-1 / CD31). CD31 immunolabelling 7-days post-HI revealed a significant increase in angiogenesis compared with non-intervention controls (P<0.001). Treatment with CMZ decreased the level of angiogenesis compared to HI + saline (P<0.001) back to non-intervention control levels. Conversely, N[omega]-nitro-L-arginine methyl ester (L-NAME) treatment (5mg/kg/day) exacerbated the ischaemic lesion (P<0.001) and resulted in a marked decrease in angiogenesis compared to non-intervention controls (P<0.001). The extent of cerebral infarction in these studies is dependent on the level of NOS activity with CMZ increasing total NOS levels compared to HI + saline, while L-NAME halted the HI-induce increase in total NOS activity (P<0.001). These results show for the first time, that angiogenesis may be used as an assessment of neurodegeneration / neuroprotection in pathologies of cerebral ischaemia and are directly correlated with changes in NOS activity. These studies have therefore shown that following HI, damage also occurs contralateral to the occlusion, and is not restricted to the ipsilateral hemisphere. In addition, the neuroprotective effects of CMZ have been shown to extend out to 90-days post-HI, whereby significant protection to CA1 neuronal activity was seen. These studies also provide in vivo evidence that CMZ may also afford neuroprotection via anti-inflammatory pathways, as evidenced by a decrease in iNOS and arginase activities. Furthermore, these studies have also show evidence that angiogenesis (CD31) can be used as a diagnostic tool to assess neuroprotection / neurodegeneration.

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Rahman, Rosanna, and n/a. "Potential causes of the delayed neural damage observed post-stroke & the effects of epigallocatechin gallate administration." University of Otago. Department of Pharmacology & Toxicology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070508.122246.

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Stroke is the 3rd leading cause of death and the leading cause of major disability worldwide. Currently, there are no neuroprotective drugs approved for the acute treatment of ischaemic stroke. The vast majority of stroke therapeutics failed in clinical trials due to toxic side effects and/or a clinically irrelevant therapeutic window. This thesis is focused on exploiting the delayed neurodegeneration that occurs in the compromised penumbra, as these cells may be capable of being saved by therapeutic intervention in a clinically obtainable window. In order to investigate the ischaemic cascade and be able to draw conclusions that are applicable to humans, the international gold standard animal model for cerebral ischaemia, the filament insertion middle cerebral artery occlusion (MCAO) model, was established at the University of Otago. This model was validated under new laboratory conditions and employed adult male Sprague Dawley rats. After testing multiple occlusion lengths, it was concluded that a 2hr ischaemic period was sufficient to produce a consistent infarct of optimal size. It has been well documented that neuroinflammation contributes to much of the delayed progression of neural injury post-stroke. Therefore, the catechin (-)-epigallocatechin gallate (EGCG), which is an anti-inflammatory, anti-oxidant and free-radical scavenging agent was investigated in the MCAO model of stroke. 50mg/kg i.p. of EGCG or saline was administered immediately post-MCAO and animals were sacrificed at 72hr post-filament insertion. The results confirmed that treatment with EGCG was neuroprotective and non-toxic. However, EGCG also induced an over 50% increase in the risk of haemorrhagic conversions. The anti-platelet effects of EGCG and lack of toxicity suggests that the catechin may prove to be an efficacious prophylactic for stroke. The contrary findings for EGCG treatment led to the re-evaluation of the neuroinflammatory pathway for alternate mechanisms to target therapeutic interventions. The temporal profile of the primary inducible enzymes nitric oxide synthase (NOS), cyclooxygenase (COX) and arginase (and their isoforms) were quantified 0, 3 and 7 days post-stroke. In both hemispheres, total NOS activity exhibited a significant and sustained up-regulation to 7 days post-occlusion. In the ipsilateral hemisphere at least half of the total increase was accounted for by inducible NOS (iNOS) expression. Arginase, which competes with NOS for L-arginine, demonstrated a delayed but significant increase in activity by day 7 in the infarcted hemisphere, thereby correlating well with the downward slope of NOS activity (illustrating the switch in the conversion pathway). COX activity was observably increased in the ipsilateral hemisphere, but the up-regulation did not reach significance by day 7. Alternately, the contralateral hemisphere displayed a significant decrease in activity by day 3. These results give conclusive evidence that the contralateral hemisphere is NOT an appropriate internal control and imply that NOS and COX inhibitors may prove to be efficacious for a much longer therapeutic window than current treatments. However, the delayed induction of COX activity may also indicate that this enzyme has a finite therapeutic window, as it may also stimulate remodelling of surviving neural networks. The prolonged up-regulation of inflammatory mediators implies that there may be an induction of an autoimmune component to the response. Therefore, the thymus (T) lymphocyte activation was quantified up to 14 days post-stroke. Cluster of differentiation (CD) 3⁺ T lymphocytes (equally contributed to by CD4⁺ and CD8⁺ T cells) exhibited a significant and sustained up-regulation in the infarcted region from day 3 up to at least day 14 post-ischaemia. Quantitative analysis of all cells present post-stroke determined that immune cells make up an average of 73% of all cells present in the 'peak' ischaemic areas. The CD4⁺ T helper cell response was delineated by double immunohistochemical labelling. Interferon-γ positively labelled with CD4⁺ T cells at days 3, 7 and 14 post-insult detailing a Th1-driven pro-inflammatory response. This evidence indicates that the autoimmune response is critical post-ischaemia and that it may be highly susceptible to modification by anti-inflammatory therapeutic intervention. The primary downstream effect of the pro-inflammatory/immune cascade is apoptosis. The main organelle responsible for the 'go, no go' response to apoptotic factors is the mitochondria. In order to distinguish whether mitochondrial dysfunction was initiated shortly after ischaemia induction or if it was delayed, like the inflammatory/immune response, to a clinically relevant window, the temporal profile of mitochondrial complex inactivation was studied. It was found that mitochondrial membrane viability was impaired by day 3, followed by a significant decrease in respiratory complex activation and an increase in tissue injury by oxidative stress by 7 days post-ischaemia. These results indicate that targeting the early decrease in membrane viability or mitochondrial permeability transition pore opening combined with anti-apoptotic therapeutics, may attenuate the proceeding mitochondrial impairment in oxidative phosphorylation, reactive oxygen species generation and subsequent cell death cascades. The current investigations into the temporal profile and quantitative contributions of the inflammatory, immune and apoptotic mechanisms post-stroke highlight potential strategies for modulation by acute stroke therapeutics. Furthermore, the general knowledge amassed from these studies dictates the necessity of a new approach to therapeutic intervention. The acknowledgement of so many contributing systems suggests that in addition to a thrombolytic, a combination therapy involving multiple neuroprotectants should be employed to account for the multifaceted nature of the sequelae of ischaemic stroke.

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Books on the topic "Degeneration in art"

1

David, Weir. Decadent culture in the United States: Art and literature against the American grain, 1890-1926. Albany: State University of New York Press, 2008.

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1942-, Kline T. Jefferson, and Schor Naomi, eds. Decadent subjects: The idea of decadence in art, literature, philosophy, and culture of the fin de siècle in Europe. Baltimore, Md: Johns Hopkins University Press, 2001.

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David, Weir. Decadent culture in the United States: Art and literature against the American grain, 1890-1926. Albany: State University of New York Press, 2008.

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La follia rappresentata: Matti, degenerati e idioti nella letteratura e nell'arte figurativa italiane dell'Ottocento. Firenze: Atheneum, 2001.

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Degeneration. Shanghai, China: OCT Contemporary Art Terminal Shanghai, 2013.

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The End Again: Degeneration and Visual Culture in Modern Spain. Penn State University Press, 2017.

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Seki, Kusuo. Hitora to taihai geijutsu: "Taihai geijutsu ten" to "Dai Doitsu geijutsu ten". Kawade Shobo Shinsha, 1992.

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Bernheimer, Charles. Decadent Subjects: The Idea of Decadence in Art, Literature, Philosophy, and Culture of the Fin de Siècle in Europe (Parallax: Re-visions of Culture and Society). The Johns Hopkins University Press, 2002.

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The Fourfold Path to Healing: Working with the Laws of Nutrition, Therapeutics, Movement and Meditation in the Art of Medicine. NewTrends Publishing, Inc., 2004.

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Schor, Naomi, Charles Bernheimer, and T. Jefferson Kline. Decadent Subjects: The Idea of Decadence in Art, Literature, Philosophy, and Culture of the Fin de Sihcle in Europe. Johns Hopkins University Press, 2003.

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Book chapters on the topic "Degeneration in art"

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Bade, Patrick. "10. Art and Degeneration: Visual Icons of Corruption." In Degeneration the Dark Side of Progress, edited by J. Edward Chamberlin and Sander L. Gilman, 220–40. New York Chichester, West Sussex: Columbia University Press, 1985. http://dx.doi.org/10.7312/cham90822-011.

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Del Porto, Giuseppe, Enzo M. Vingolo, Dezsö David, Katharina Steindl, Heike Wedemann, Renato Forte, Alessandro Iannaccone, Andreas Gal, and Mario R. Pannarale. "Clinical Features of Autosomal Dominant Retinitis Pigmentosa Associated with the GLY-188-ARG Mutation of the Rhodopsin Gene." In Retinal Degeneration, 91–101. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2974-3_9.

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Geller, Andrew M., and Paul A. Sieving. "How Many Cones are Required to “See?”: Lessons from Stargardt’s Macular Dystrophy and from Modeling with Degenerate Photoreceptor Arrays." In Retinal Degeneration, 25–34. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2974-3_3.

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Hurwitz, Richard L., Steven J. Pittler, Michael L. Suber, Ning Qin, Rehwa H. Lee, Cheryl M. Craft, Richard N. Lolley, and Wolfgang Baehr. "Nonsense Mutations in the ß Subunit Gene of the Rod cGMP Phosphodiesterase That are Associated with Inherited Retinal Degenerative Disease." In Retinal Degeneration, 251–58. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2974-3_25.

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Sasore, Temitope, Alison L. Reynolds, and Breandán N. Kennedy. "Targeting the PI3K/Akt/mTOR Pathway in Ocular Neovascularization." In Retinal Degenerative Diseases, 805–11. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-3209-8_101.

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Rajala, Raju V. S., and Ammaji Rajala. "Redundant and Nonredundant Functions of Akt Isoforms in the Retina." In Retinal Degenerative Diseases, 585–91. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_71.

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Hanke-Gogokhia, Christin, Houbin Zhang, Jeanne M. Frederick, and Wolfgang Baehr. "The Function of Arf-like Proteins ARL2 and ARL3 in Photoreceptors." In Retinal Degenerative Diseases, 655–61. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_87.

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Downs, Louise M., and Gustavo D. Aguirre. "FAM161A and TTC8 are Differentially Expressed in Non-Allelelic Early Onset Retinal Degeneration." In Retinal Degenerative Diseases, 201–7. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_27.

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Rajala, Raju V. S., Yogita Kanan, and Robert E. Anderson. "Photoreceptor Neuroprotection: Regulation of Akt Activation Through Serine/Threonine Phosphatases, PHLPP and PHLPPL." In Retinal Degenerative Diseases, 419–24. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-17121-0_55.

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Koriyama, Yoshiki, Ayako Furukawa, Kayo Sugitani, Miwa Kubo, Kenichi Harada, and Yoshiyasu Fukuyama. "Talaumidin Promotes Neurite Outgrowth of Staurosporine-Differentiated RGC-5 Cells Through PI3K/Akt-Dependent Pathways." In Retinal Degenerative Diseases, 649–53. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-75402-4_79.

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Conference papers on the topic "Degeneration in art"

1

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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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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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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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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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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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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Schroeder, Y., S. Sivan, W. Wilson, J. M. Huyghe, A. Maroudas, and F. P. T. Baaijens. "Intra- and Extrafibrillar Fluid Exchange in the Disc." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176329.

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The mechanical properties of the intervertebral disc are regulated by its biochemical composition. With ageing and degeneration the water content of the disc decreases which highly influences the mechanical properties. The disc is subjected to a combination of elastic, viscous and osmotic forces. Osmotic forces are shown to have a major impact on crack opening and propagation [1] and on cellular responses [2]. In particular, osmosis provides an understanding on why fissures in the degenerating disc are so poorly related to external mechanical load [3].

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Wagner, Hallie, Dawn Lowe, and Victor Barocas. "Reduced Compliance in Patellar Tendons From a Mouse Model of Muscular Dystrophy." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80762.

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Muscular dystrophies are degenerative diseases that affect primarily skeletal muscles. Most studies of muscular dystrophy focus on muscles, but tendons are an important part of the musculotendon complex that transmits forces from muscles to bones. As the disease progresses, tendon shortening occurs, and some patients require tendon release or cord lengthening surgery to increase tendon length [1]. Despite the prevalence of these surgeries, very little is known about the mechanical properties of tendons in muscular dystrophy patients, or how they change as the tendon remodels or compensate in response to muscle degeneration.

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Ruberté, Lissette M., Raghu Natarajan, and Gunnar B. J. Andersson. "Biomechanical Effect of Lumbar Disc Degeneration Under Flexion/Extension: A Finite Element Model Study." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176190.

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Degenerative disc disease (DDD) is a progressive pathological condition observed in 60 to 80% of the population [1]. It involves changes in both the biochemistry and morphology of the intervertebral disc and is associated with chronic low back pain, sciatica and adult scoliosis [2,3]. The most accepted theory of the effects of DDD on the kinematics of the spine is that proposed by Kirkaldy-Willis and Farfan which states that the condition initiates as a temporary dysfunction, followed by instability and then re-stabilization as the disease progresses [4]. Although there is no clear relationship between disc degeneration and the mechanical behavior of the lumbar spine, abnormal motion patterns either in the form of increased motion or erratic motion have been reported from studies on human cadaveric motion segments [5,6]. To date however no study has looked at how disc degeneration affects the adjacent segment mechanics. IN vivo testing is difficult for these purposes given that specimens are generally obtained from people at the later stages of life and consequently often display multiple pathologies. A finite element model is a viable alternative to study the mechanics of the segments adjacent to the diseased disc. It is hypothesized that moderate degeneration at one level will alter the kinematics of the whole lumbar spine.

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Miller, R. Matthew, Daisuke Araki, Yoshimasa Fujimaki, Volker Musahl, and Richard E. Debski. "Correlation Between Age and Tendon Strength in Supraspinatus Tendon With Full-Thickness Tears." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14037.

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Degenerative tears of the rotator cuff tendons are a significant clinical problem, with an incidence of more than 30% in asymptomatic persons over the age of 60 [1]. As the population continues to age, the incidence of partial and full-thickness rotator cuff tears continues to increase [2], with previous studies finding that greater age also correlates with worse surgical outcomes and increased fatty degeneration in the tissue [3]. Although the relationship between age, rotator cuff injury, and poor treatment outcomes has been previously established, insufficient information exists on the biological and mechanical changes in the tissue due to aging.

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Reports on the topic "Degeneration in art"

1

Regular monthly and “as needed” injections for wet age-related macular degeneration are similar in effect. National Institute for Health Research, January 2016. http://dx.doi.org/10.3310/signal-000185.

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