Relevant bibliographies by topics / Degeneration (Pathology)

Contents

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

Academic literature on the topic 'Degeneration (Pathology)'

Author: Grafiati
Published: 4 June 2021
Last updated: 28 July 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Degeneration (Pathology).'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Degeneration (Pathology)"

1

Murali, Aishwarya, Subramanian Krishnakumar, Anuradha Subramanian, and Sowmya Parameswaran. "Bruch’s membrane pathology: A mechanistic perspective." European Journal of Ophthalmology 30, no. 6 (April 28, 2020): 1195–206. http://dx.doi.org/10.1177/1120672120919337.

Full text
Abstract:
Bruch’s membrane, an extracellular matrix located between the retinal pigment epithelium and the choroid, plays a vital role as structural and functional support to the retinal pigment epithelium. Dysfunction of Bruch’s membrane in both age-related macular degeneration and other ocular diseases is caused mostly by extracellular matrix degeneration, deposit formation, and angiogenesis. Although these factors are dealt in greater detail with respect to the cells that are degenerated such as the retinal pigment epithelium and the endothelial cells, the pathology involving the Bruch’s membrane is often underrated. Since in most of the macular degenerations early degenerative changes are also observed in the Bruch’s membrane, addressing only the cellular component without the underlying membrane will not yield an ideal clinical benefit. This review aims to discuss the factors and the mechanisms affecting the integrity of the Bruch’s membrane, which would aid in developing an effective therapy for these pathologies.
APA, Harvard, Vancouver, ISO, and other styles
2

Ikeda, Kenji. "Basic pathology of corticobasal degeneration." Neuropathology 17, no. 2 (June 1997): 127–33. http://dx.doi.org/10.1111/j.1440-1789.1997.tb00026.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Behzadi, Fardad, Peter J. Fiester, and Dinesh Rao. "Bilateral Hypertrophic Olivary Degeneration Following Brainstem Insult: A Retrospective Review and Examination of Causative Pathology." Neuroscience Insights 16 (January 2021): 263310552110074. http://dx.doi.org/10.1177/26331055211007445.

Full text
Abstract:
Hypertrophic olivary degeneration is a rare condition caused by a lesion in the Guillain-Mollaret triangle which leads to trans-synaptic degeneration resulting in the degenerative hypertrophy of the inferior olivary nucleus. This condition presents clinically with palatal tremor but can also produce ocular myoclonus or cerebellar signs. While any lesion that occurs within the Guillian-Mollaret triangle and results in the deafferentation of the inferior olive can lead to hypertrophic olivary degeneration, the most common etiologies include ischemic and hemorrhagic stroke, vascular malformation, neoplasm, and iatrogenic injury related to surgery. We report a series of 7 patients who presented with this condition bilaterally on MRI imaging, including 1 case which represents the first report of toxoplasmosis leading to the development of bilateral hypertrophic olivary degeneration and only the third reported case, unilateral or bilateral, related to an infectious etiology.
APA, Harvard, Vancouver, ISO, and other styles
4

Hales, Chadwick M., and William T. Hu. "From frontotemporal lobar degeneration pathology to frontotemporal lobar degeneration biomarkers." International Review of Psychiatry 25, no. 2 (April 2013): 210–20. http://dx.doi.org/10.3109/09540261.2013.776522.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Bohnert, Kathryn L., Mary K. Hastings, David R. Sinacore, Jeffrey E. Johnson, Sandra E. Klein, Jeremy J. McCormick, Paul Gontarz, and Gretchen A. Meyer. "Skeletal Muscle Regeneration in Advanced Diabetic Peripheral Neuropathy." Foot & Ankle International 41, no. 5 (February 14, 2020): 536–48. http://dx.doi.org/10.1177/1071100720907035.

Full text
Abstract:
Background: Decreased lean muscle mass in the lower extremity in diabetic peripheral neuropathy (DPN) is thought to contribute to altered joint loading, immobility, and disability. However, the mechanism behind this loss is unknown and could derive from a reduction in size of myofibers (atrophy), destruction of myofibers (degeneration), or both. Degenerative changes require participation of muscle stem (satellite) cells to regenerate lost myofibers and restore lean mass. Determining the degenerative state and residual regenerative capacity of DPN muscle will inform the utility of regeneration-targeted therapeutic strategies. Methods: Biopsies were acquired from 2 muscles in 12 individuals with and without diabetic neuropathy undergoing below-knee amputation surgery. Biopsies were subdivided for histological analysis, transcriptional profiling, and satellite cell isolation and culture. Results: Histological analysis revealed evidence of ongoing degeneration and regeneration in DPN muscles. Transcriptional profiling supports these findings, indicating significant upregulation of regeneration-related pathways. However, regeneration appeared to be limited in samples exhibiting the most severe structural pathology as only extremely small, immature regenerated myofibers were found. Immunostaining for satellite cells revealed a significant decrease in their relative frequency only in the subset with severe pathology. Similarly, a reduction in fusion in cultured satellite cells in this group suggests impairment in regenerative capacity in severe DPN pathology. Conclusion: DPN muscle exhibited features of degeneration with attempted regeneration. In the most severely pathological muscle samples, regeneration appeared to be stymied and our data suggest that this may be partly due to intrinsic dysfunction of the satellite cell pool in addition to extrinsic structural pathology (eg, nerve damage). Clinical Relevance: Restoration of DPN muscle function for improved mobility and physical activity is a goal of surgical and rehabilitation clinicians. Identifying myofiber degeneration and compromised regeneration as contributors to dysfunction suggests that adjuvant cell-based therapies may improve clinical outcomes.
APA, Harvard, Vancouver, ISO, and other styles
6

Mimuro, Maya, and Yasushi Iwasaki. "Age-Related Pathology in Corticobasal Degeneration." International Journal of Molecular Sciences 25, no. 5 (February 27, 2024): 2740. http://dx.doi.org/10.3390/ijms25052740.

Full text
Abstract:
Elderly human brains are vulnerable to multiple proteinopathies, although each protein has a different transmission pathway. Tau-immunoreactive astrocytes are well-known in elderly brains. In contrast, astrocytic plaques, a hallmark in corticobasal degeneration (CBD), rarely occur in aging and neurodegenerative disease other than CBD. To elucidate the clinicopathological correlation of aging-related pathology in CBD, we examined 21 pathologically proven CBD cases in our institute (12 males and 9 females, with a mean age of death 70.6 years). All CBD cases showed grains and neurofibrillary tangles (NFTs). Fifteen cases (71.4%) showed beta-amyloid deposition such as senile plaques or cerebral amyloid angiopathy. Three cases (14.3%) had Lewy body pathology. One case was classified as amygdala-predominant Lewy body disease, although no cases met the pathological criteria for Alzheimer’s disease. Five cases (23.8%) displayed Limbic-predominant and age-related TDP-43 encephalopathy (LATE). NFTs, grains, and TDP-43-positive neuronal inclusions were widely distributed throughout the limbic system of CBD patients, but their densities were low. CBD might a have similar cell vulnerability and transmission pathway to that of multiple proteinopathy in aging brains.
APA, Harvard, Vancouver, ISO, and other styles
7

TAN, CELIA I. C., SWITHIN SONG, STEPHEN J. EDMONDSTON, and KEVIN P. SINGER. "PATTERNS OF THORACIC DISC DEGENERATION FROM MRI: AGE, GENDER AND SPINAL LEVEL INFLUENCES." Journal of Musculoskeletal Research 05, no. 04 (December 2001): 269–78. http://dx.doi.org/10.1142/s0218957701000635.

Full text
Abstract:
The present retrospective study reviewed and examined the prevalence of thoracic disc degeneration, end-plate lesions and osteophytes in the thoracic spine using T2-weighted sagittal magnetic resonance images (MRI). The sample comprised 216 thoracic spine cases (101 males and 115 females), aged from 1 to 85 years (mean age = 42±19.7 years). Nuclear and anular degeneration, end-plate lesions and osteophytes were graded using a 3-point scale. The prevalence of degeneration was highest in the nucleus (86%) and lowest in the end-plates (63%). Males had a higher prevalence of degeneration in the nucleus, anulus and end-plates, and a lower prevalence of osteophytes compared to females. Increasing cranio-caudal trends in the prevalence of degeneration in the nucleus, anulus and end-plates were observed, and these trends were statistically significant (p<0.01). Vertebral body osteophytes were most prevalent in the mid thoracic region. Osteophytes and degenerative changes in the nucleus and anulus increased significantly with age (p<0.05). These regional and age-related degenerative trends may influence the interpretation of thoracic spine pathology from MRI investigations.
APA, Harvard, Vancouver, ISO, and other styles
8

Ashinsky, B., HE Smith, RL Mauck, and SE Gullbrand. "Intervertebral disc degeneration and regeneration: a motion segment perspective." European Cells and Materials 41 (March 24, 2021): 370–87. http://dx.doi.org/10.22203/ecm.v041a24.

Full text
Abstract:
Back and neck pain have become primary reasons for disability and healthcare spending globally. While the causes of back pain are multifactorial, intervertebral disc degeneration is frequently cited as a primary source of pain. The annulus fibrosus (AF) and nucleus pulposus (NP) subcomponents of the disc are common targets for regenerative therapeutics. However, disc degeneration is also associated with degenerative changes to adjacent spinal tissues, and successful regenerative therapies will likely need to consider and address the pathology of adjacent spinal structures beyond solely the disc subcomponents. This review summarises the current state of knowledge in the field regarding associations between back pain, disc degeneration, and degeneration of the cartilaginous and bony endplates, the AF-vertebral body interface, the facet joints and spinal muscles, in addition to a discussion of regenerative strategies for treating pain and degeneration from a whole motion segment perspective.
APA, Harvard, Vancouver, ISO, and other styles
9

Tfayli, Yehia, Joseph E. Nassar, Ahmad Salaheddine Naja, and Muhyeddine Al-Taki. "Arthroscopic Meniscus Trephination: A Novel Technique for the Treatment of Symptomatic Meniscal Degeneration: Surgical Technique and Literature Review." Journal of Orthopaedic Case Reports 13, no. 10 (2023): 141–44. http://dx.doi.org/10.13107/jocr.2023.v13.i10.3968.

Full text
Abstract:
Introduction: Meniscal pathology constitutes a major reason for a vast number of patients suffering from knee pain. It is, in general, attributed either to meniscal tearing or degeneration. Debridement and partial meniscectomy, or repair, when possible, is the mainstay surgical approach for refractory knee pain from meniscal degeneration or tears. Sometimes, the patient has clinical symptoms of meniscal pathology, but despite those highly suggestive clinical symptoms, the patient turns out, during knee arthroscopy, to have meniscal degeneration and hardening of the meniscus without frank tearing of the meniscus Surgical Technique: To initiate meniscal trephination, we first conduct a diagnostic knee arthroscopy to examine the suprapatellar space, the gutters, and the anterior knee space for any pathologies. Following this, both menisci are inspected for any signs of tearing or hardening. For the purposes of our study, the medial meniscus is considered pathological if it shows signs of degeneration or hardening, which then justifies our intervention. An 18-gauge spinal needle, manually bent for the procedure, is inserted through the portal to perform trephination on the hardened menisci. Care is taken to adequately space the needle insertion points to prevent accidental tearing. Our trephination technique aims to soften the meniscus, facilitating its ability to compact and compress when patients ambulate. Additionally, the needle insertion points help attract blood flow to the meniscus, thereby enriching it with growth factors and stem cells that may aid in improving the degenerative condition. Conclusion: Meniscal trephination is benign and effective for meniscal degenerative pathologies. The procedure allows for a healthier meniscus, free from degeneration, that would otherwise disable patients. The intervention does not have long-term adverse effects. To this end, more comparative trials are required to confirm the effectiveness of the technique and to ensure minimal to no associated side effects. Keywords: Trephination, Meniscus, Knee, Degeneration
APA, Harvard, Vancouver, ISO, and other styles
10

Zhang, Chao, Sigurd H. Berven, Maryse Fortin, and Michael H. Weber. "Adjacent Segment Degeneration Versus Disease After Lumbar Spine Fusion for Degenerative Pathology." Clinical Spine Surgery 29, no. 1 (February 2016): 21–29. http://dx.doi.org/10.1097/bsd.0000000000000328.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Degeneration (Pathology)"

1

Berg, N. J. "Characterisation of axon degeneration in a model of Tau pathology." Thesis, University of Cambridge, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596584.

Full text
Abstract:
In disorders known as ‘dying-back’ neuropathies, the distal nerves appear to degenerate first and this form of degeneration has many similarities to Wallerian degeneration. In the slow Wallerian degeneration (Wlds) mouse there is a 85kb tandem triplication resulting in the expression of a chimeric protein, consisting of the first 70 amino acids of Ube4B and the full sequence of the Nmnat1 protein. In the Wlds mouse Wallerian degeneration appears to be slowed approximately ten fold. The aim of the present study was to determine whether the Wlds gene has a protective effect in neurodegeneration caused by tau pathology. In order to visualise in vivo axonal degeneration and a possible protective effect of the Wlds gene, P301S tau transgenic mice were crossed with TFP-H mice expressing yellow fluorescent protein in a subset of neurons. First it was determined whether the expression of YFP is harmful to axons, and then YFP expression was used to follow the progression of axonal pathology in the P301S mouse. The results indicate that expression of the YFP protein leads to an increase in axonal swellings in some brain regions of aged mice, older than the P301S tau used in this study. YFP expression allows visualisation of abundant broken and abnormal axons in the peripheral and central nervous systems of P301S tau transgenic, but not control mice. The Wlds gene does not rescue the axonal degeneration observed in P301S tau transgenic mice. These results indicate that YFP expression can be used for investigation in young mice, but possible pathological effects can be present in aged mice. Furthermore, the apparent lack of protection of the Wlds gene on P301S axonal pathology suggests that Wallerian degeneration is not a major player in tau-related neurodegeneration.
APA, Harvard, Vancouver, ISO, and other styles
2

Huseynova, Gunel. "Novel autophagy regulators that affect polyglutamine pathology in Drosophila." Thesis, University of Cambridge, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.709531.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Granner, Tamara. "Investigation of anti-angiogenic effects of 3,4 dihydroxyphenyl ethanol in macular degeneration." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114432.

Full text
Abstract:
Age Related Macular Degeneration (AMD) is the most common cause of vision loss among the elderly in developed countries. It occurs primarily in individuals over the age of 50. Currently, 1.75 million people in the US suffer from the advanced form of AMD. AMD is characterised as an abnormality of retinal pigment epithelium (RPE) and/or choroid leading to photoreceptor degeneration of central retina (macula). There are two forms of AMD: Dry AMD (characterized by the build-up of drusen between the choroid and RPE layer resulting in RPE and photoreceptor cell death) and Wet AMD (characterized by abnormal blood vessel growth from the choroid into the retinal pigment epithelium). Current pharmacotherapies in AMD include anti-angiogenics (anti-VEGF) such as Macugen, Avastin, and Lucentis. Thus current research is focusing on trying to form combination therapies (such as anti-VEGF and other agents) to achieve better clinical efficacy. We will be investigating the compound 3,4 dihydroxyphenyl ethanol (DPE), which is a polyphenol present in virgin olive oil known to have antioxidant, anti-angiogenic, anti-inflammatory, and antithrombotic properties. Previous studies have investigated DPE and its ability to prevent cardiovascular diseases and treat different types of cancer. We believe that DPE can reduce angiogenic signalling in the macula. Our objective is to assess the potential utility of DPE as a therapeutic agent in combination with anti-VEGF drugs. ARPE-19 cells were treated with 0.25 mg/ml bevacizumab to study the effects of bevacizumab on the secretion of pro-angiogenic cytokines. The cells were then treated with 100M DPE for 24 hours in culture in both normoxic and CoCl₂-simulated hypoxic conditions. RPE cells were also treated with the combination of DPE and bevacizumab in order to determine the effectiveness of the combination therapy on RPE cells. Media was then harvested after 24 hours for sandwich ELISA-based angiogenesis arrays. The secretion of the following 10 pro-angiogenic cytokines was measured: Angiogenin, ANG-2, EGF, bFGF, HB-EGF, PDGF-BB, Leptin, PlGF, HGF, and VEGF-A. The secretion of three (Angiogenin, ANG-2, and EGF) was increased following treatment with bevacizumab, however only Angiogenin was significant. Angiogenin and VEGF-A were secreted under normoxia, and significantly increased under CoCl₂-simulated hypoxia, whereas ANG-2, HB-EGF, and PlGF were increased under hypoxia. Following treatment with DPE, levels of Angiogenin and VEGF-A were significantly reduced under normoxia, whereas secretion of all 5 secreted cytokines were significantly decreased under hypoxia. The combination of DPE and bevacizumab significantly reduced the secretion of Angiogenin under both normoxic and hypoxic conditions compared to bevacizumab alone. Considering the implications of angiogenesis in AMD, these studies could provide the framework for future studies to further investigate a potential therapeutic role for DPE. DPE may reduce the secretion of pro-angiogenic cytokines, such as Angiogenin, that are up-regulated following treatment with bevacizumab as a possible compensatory mechanism. Therefore, the combination of DPE and bevacizumab may represent a valuable therapeutic option for the wet form of AMD.
La dégénérescence maculaire liée à l'âge (DMLA) est la cause la plus fréquente de la perte de la vision chez les personnes âgées dans les pays développés. Il survient principalement chez les personnes âgées de plus de 50 ans. Actuellement, 1,75 millions de personnes aux États-Unis souffrent de la forme avancée de la DMLA. La DMLA se caractérise par une anomalie de l'épithélium pigmentaire rétinien (EPR) et / ou de la choroïde, conduisant à la dégénérescence des photorécepteurs de la rétine centrale (macula). Il existe deux formes de DMLA: la DMLA de type sèche (caractérisée par l'accumulation de petites taches blanches sous la rétine (drusen) entre la choroïde et l'EPR résultant en la mort des cellules photoréceptrices) et la DMLA de type humide (caractérisée par une croissance anormale de néovaisseaux choroïdiens (NVC) sous l'épithélium pigmentaire de la rétine). Les pharmacothérapies actuelles pour traiter la DMLA comprennent les anti-angiogéniques (anti-VEGF), tels que Macugen, Avastin et Lucentis. Ainsi la recherche actuelle se concentre à essayer de former des combinaisons thérapeutiques (tels que des agents anti-VEGF et d'autres) pour parvenir à une meilleure efficacité clinique. Nous examinerons le 3,4 dihydroxyphenyl ethanol (DPE), qui est un polyphénol présent dans l'huile d'olive vierge connu pour avoir des propriétés antioxydantes, anti-angiogéniques, anti-inflammatoire, et des propriétés antithrombotiques. Des études antérieures sur le DPE ont démontré sa capacité à prévenir les maladies cardio-vasculaires et traiter les différents types de cancer. Nous croyons que le DPE peut réduire la signalisation angiogénique dans la macula. Notre objectif est d'évaluer la potentielle utilité de DPE comme agent thérapeutique en combinaison avec des médicaments anti-VEGF. Les cellules ARPE-19 ont été traitées avec 0,25 mg/ml de bevacizumab pour étudier les effets du bevacizumab sur la sécrétion de cytokines pro-angiogéniques. Ces cellules ont ensuite été traitées avec 100µM de DPE en culture pendant 24 heures à la fois dans des conditions normoxiques et des conditions simulé hypoxiques (CoCl₂). Les cellules de l'EPR ont également été traitées avec la combinaison de DPE et de bevacizumab en vue de déterminer l'efficacité de la thérapie avec cette combinaison sur les cellules de l'EPR. Le milieu de culture a ensuite été récolté après 24 heures pour proceder au sandwich ELISA pour tester l'angiogenèse. La sécrétion des 10 suivants cytokines pro-angiogéniques a été mesurée: Angiogenin, ANG-2, EGF, bFGF, HB-EGF, PDGF-BB, Leptin, PlGF, HGF, and VEGF-A. La sécrétion de trois d'entre eux (Angiogenin, ANG-2, et EGF) a été augmentée à la suite du traitement par bevacizumab, mais seulement celle de l'Angiogenin a été significative. L'Angiogenin et le VEGF-A ont été sécrétés sous normoxie, et ont considérablement augmenté en vertu de l'hypoxie simulée par CoCl₂, alors que le ANG-2, le HB-EGF et le PlGF ont été augmentée en vertu de l'hypoxie. Après le traitement avec DPE, les niveaux de Angiogenin et le VEGF-A ont été considérablement réduits en normoxie, tandis que la sécrétion de toutes les 5 cytokines sécrétées a été significativement diminuée sous l'hypoxie. La combinaison de la DPE et du bevacizumab a considérablement réduit la sécrétion de l'Angiogenin dans des conditions à la fois normoxiques et hypoxiques en comparaison avec le bevacizumab utilisé seul. Considérant les implications de l'angiogenèse dans la DMLA, ces études pourraient servir de base pour de futures études pour pousuivre les recherches sur le rôle thérapeutique potentiel du DPE. Le DPE peut réduire la sécrétion de cytokines pro-angiogéniques, comme celle de l'Angiogenin, qui augmentent après un traitement par le bevacizumab comme un possible mécanisme compensatoire. Par conséquent, la combinaison du DPE et du bevacizumab peut représenter une option thérapeutique valable pour la forme humide de la DMLA.
APA, Harvard, Vancouver, ISO, and other styles
4

Shih, Ann Yu-Jung. "Wallerian Degeneration Slow mutation does not alter the amyloid pathology of Alzheimer's disease." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2008. http://wwwlib.umi.com/cr/ucsd/fullcit?p1453673.

Full text
Abstract:
Thesis (M.S.)--University of California, San Diego, 2008.
Title from first page of PDF file (viewed July 25, 2008). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 43-45).
APA, Harvard, Vancouver, ISO, and other styles
5

Schofield, Emma Medical Sciences Faculty of Medicine UNSW. "Characterisation of cortical pathology and clinicopathological correlates in progressive supranuclear palsy." Awarded by:University of New South Wales. School of Medical Sciences, 2006. http://handle.unsw.edu.au/1959.4/27326.

Full text
Abstract:
This thesis characterises the cortical pattern of degeneration in progressive supranuclear palsy (PSP) and its consequences. Global atrophy was first examined using a recently developed staging scheme in pathologically-proven PSP cases compared with other tauopathies: gross atrophy was not observed in PSP. Quantification of regional volume loss throughout the brain was then used to determine the magnitude of more focal tissue atrophy in PSP, cortical dysfunction was investigated by measuring cerebral blood flow (CBF) changes, and several cortical cellular pathologies were analysed. Any changes observed were related to each other and clinical assessments of motor, cognitive and behavioural abnormalities. At mid-stage PSP, frontal and subcortical atrophy related to decreased CBF in the frontal cortex and cognitive decline. Parietocerebellar CBF increases were also identified (related to frontal CBF deficits) and related to motor and non-motor deficits. By end-stage PSP, focal atrophy had advanced from frontal and subcortical structures to include atrophy in the parietal lobe. Parietal lobe atrophy related to behavioural abnormalities. Histopathological analysis at end-stage revealed that the cortical atrophy and cell loss does not relate to tau deposition. The focal cortical cell loss related exclusively to motor deficits whilst the more widespread cortical tau deposition related to cognitive and behavioural impairments. Both the tau deposition and these non-motor impairments increased in severity over time. The results show that frontal atrophy and dysfunction occurs rapidly and early in PSP and relate to increasing cognitive deficits. Such deficits appear to cause compensatory CBF enhancement in parietocerebellar regions which then also undergo rapid and severe neurodegeneration. These later changes occur in concert with the more classic PSP symptoms, such as oculomotor features. Throughout the disease, the progressive increase in frontotemporal tau deposition contributes to cognitive and behavioural deficits which become most marked late in the disease. The findings strongly suggest that progressive clinical dysfunction in PSP is directly related to progressive cortical degeneration. Cortical degeneration appears to occur in two independent functional networks. Increased CBF in PSP may be a useful early indicator for future neurodegeneration, although the cellular mechanism leading to cell death requires further investigation.
APA, Harvard, Vancouver, ISO, and other styles
6

Kouri, Naomi. "Advances in clinical, neuropathologic, and genetic features of corticobasal degeneration." Thesis, College of Medicine - Mayo Clinic, 2015. http://pqdtopen.proquest.com/#viewpdf?dispub=3702551.

Full text
Abstract:

This is a dissertation on the neurodegenerative tauopathy corticobasal degeneration (CBD). Because CBD is a rare disorder and has <50% antemortem diagnostic accuracy, we sought to learn as much as possible from our invaluable resource, having the largest, single neuropathologically-confirmed CBD cohort in the world. This is a culmination of several different projects, all focused on neuropathologic, genetic, and clinical features of CBD, with the overall intent being to help patients who will suffer from this devastating disorder. Each study/chapter had a specific hypothesis, aimed to elucidate various unanswered questions about CBD. Essentially, the only possible approach to further our understanding of CBD is what we have done here: use patient tissue and DNA samples who have donated their brains to research.

Richardson syndrome is one of the most common clinical presentations of CBD: Clinicopathologic assessment of CBD patients presenting with Richardson syndrome (CBD-RS) (i.e. patients misdiagnosed as progressive supranuclear palsy), identified neuropathologic and clinical signs and symptoms that were able to differentiate CBD-RS from PSP patients. Digital microscopy and image analysis were used to quantify tau pathology in multiple brain regions and found CBD-CBS (corticobasal syndrome) cases had greater peri-Rolandic tau burden and CBD-RS had greater hindbrain and limbic tau pathology. CBD-RS patients exhibited a frontal/dysexecutive syndrome and urinary incontinence more often than PSP patients. We also describe an unusual variant of CBD with olivopontocerebellar atrophy, of which two of the patients presented with Richardson syndrome and had greater hindbrain tau pathology than CBD-CBS, and interestingly had significant TDP-43 (protein inclusions found in FTLD and ALS) pathology in affected regions. Regarding TDP-43 pathology in CBD, we found that >25% of cases have TDP-43 immunoreactive neuronal and glial cytoplasmic inclusions and threads, and the greatest burden was in the basal ganglia. With these studies we were able to show that Richardson syndrome is one of the most common clinical presentations of CBD.

Identification of a novel MAPT mutation (p.N410H) in a CBD case that is neuropathologically indistinguishable from sporadic CBD: We screened our autopsy-confirmed CBD cohort for MAPT mutations and identified a novel mutation in MAPT exon 13 (p.N410H) in a case that is neuropathologically indistinguishable from sporadic CBD. This is not only the first MAPT mutation identified to cause CBD, but it is also the first mutation to cause CBD. Functional studies with this mutation showed that there was decreased ability for mutant tau to promote microtubule assembly and exhibited a marked increase in filament formation in vitro. In this study we also identified two rare variants in the 3' untranslated regulatory region of MAPT that associate with CBD, and one of these variants also associated with PSP. CBD and PSP have shared and unique genetic risk factors: Our last study as part of my dissertation, is the first ever CBD genome-wide association study. We performed a discovery stage, replication stage, and meta-analysis in 152 CBD cases versus 3,111 control individuals (discovery), with 67 CBD cases versus 457 controls (replication). This identified two genome genome-wide significant associations with CBD at MAPT and KIF13B/DUSP4. Using a candidate gene approach, we tested for CBD association with the top progressive supranuclear palsy GWAS SNPs. This identified strong associations at MOBP and MAPT H1c haplotype. Another novel genetic association for CBD patients was identified at SOS1. Expression/SNP associations were tested from ~400 brain samples of cerebellum and temporal cortex and found significant associations at MAPT, MOBP, and SOS1. The genome-wide significant association at KIF13B/DUSP4 with CBD will require additional studies to determine which gene is responsible for the association signal. In summary, these findings show for the first time, that CBD and PSP share common genetic variation, other than MAPT, at MOBP which confers disease risk. Together, warranting future studies to understand the mechanism by which MOBP contributes to the CBD and PSP disease processes.

APA, Harvard, Vancouver, ISO, and other styles
7

Al-Malki, Hussain D. "Synaptic degeneration : a morphological study in a mouse model of prion disease." Thesis, University of Southampton, 2012. https://eprints.soton.ac.uk/334054/.

Full text
Abstract:
Early synaptic degeneration in prion disease has developed into a subject of interest, because it is thought that it may allow therapeutic intervention to prevent the neuronal death which is often observed at the late stage of the disease. However, the events behind the synaptic degeneration in prion disease, that may ultimately lead to neuronal death, are still unclear. Studying the morphology of neuronal components, namely synaptic boutons, axons, spines, dendrites and cell bodies, of the population of origin may help in understanding the neuropathology of prion disease. Intrahippocampal injection of murine modified scrapie (ME7 homogenate) provides a model of prion disease in vivo. Animals injected with ME7 were compared to control animals (injected with normal brain homogenate, NBH) and both groups were killed at 13, 16 and 19 weeks. At each time point, Biotinylated Dextran Amine (BDA) tracer was injected into the CA3 area of the hippocampus to reveal the morphology of neurons and their components during the disease progression, using both light and electron microscopy. The results showed that at 13 weeks, the number of synaptic boutons, which are distributed along the axons in the CA1 stratum radiatum, was significantly reduced, while most of the remainder were hypertrophied. This correlated with an increase in both the synaptic spacing along the axonal segments and the presence of abnormal swellings on the axons throughout the stratum radiatum. At 13 weeks, electron microscopic studies revealed vacuole-like structures in the synaptic boutons, which differed from actual autophagic or spongiform vacuoles. The results also showed a significant reduction in the number of dendritic spines on CA3 neurons, associated with a reduction in dendritic arborizations and length. Abnormal swellings were also seen in dendrites and occasionally in the cell bodies. Changes in CA3 cell body size were not observed until 16 weeks, when the soma area had reduced. The results indicate that changes in the morphology of synaptic boutons and dendritic spines were observed at an early time point, 13 weeks the fist observation time, and progressed with time. These results showed for the first time that there is a correlation between both synaptic bouton and spine loss in the neuron of origin, which may suggest that there is continual, simultaneous degeneration between the efferent and afferent components of neuron, leading to an early impairment of the neuronal communication within the brain. This suggests the notion that the loss of communication of the neuron at the early stage may lead to neuronal dysfunction and degeneration at the late stage of the disease. The results also suggest that the synaptic vacuoles may play a crucial role in the hypertrophy or degeneration of the remaining synapses. Additionally, it has been shown for the first time that astrocytes in ME7-animals express features of pathology and degeneration, suggesting that the astrocytes may be another target of PrPSc in prion disease. The combination of these findings has opened new avenues in the field of prion studies. The possible mechanisms behind these results are discussed.
APA, Harvard, Vancouver, ISO, and other styles
8

Williams, J. F. "Enzyme and metabolic studies of growth and degenerative processes in animal systems with emphasis on pentose pathway reactions." Thesis, Canberra, ACT : The Australian National University, 1987. http://hdl.handle.net/1885/143755.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Aladin, Kaderbatcha Darwesh Mohideen. "A macro, nano level study to evaluate the impact of Trp2 allele in the [alpha] 2 chain of collagen IX on the biomechanics of human intervertebral discs and disc collagens." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/hkuto/record/B39634425.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Aladin, Kaderbatcha Darwesh Mohideen. "A macro, nano level study to evaluate the impact of Trp2 allele in theα 2 chain of collagen IX on the biomechanics of human intervertebraldiscs and disc collagens." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39634425.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Degeneration (Pathology)"

1

Heier, Jeffrey S. 100 questions & answers about macular degeneration. Sudbury, Mass: Jones and Bartlett Publishers, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Heier, Jeffrey S. 100 questions & answers about macular degeneration. Sudbury, Mass: Jones and Bartlett Publishers, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Icheku, Vincent. Degenerative diseases of ageing: Causes and preventions. London: William Jacob Pub., 2006.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Pritikin, Nathan. A review of medical literature on relationships of various degenerative diseases to diet and activity. Santa Barbara, Calif: Nathan and Ilene Pritikin Family Trust, 1988.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

E, Anderson Robert, LaVail Matthew M, Hollyfield Joe G, and International Symposium on Retinal Degenerations (12th : 2006 : San Carlos de Bariloche, Argentina), eds. Recent advances in retinal degeneration. [New York, NY: Springer, 2008.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

Gotthard, Schettler, Greten H, and Habenicht A. 1948-, eds. Cellular metabolism of the arterial wall and central nervous system: Selected aspects. Berlin: Springer-Verlag, 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

1941-, Rainsford K. D., ed. Copper and zinc in inflammatory and degenerative diseases. Dordrecht: Kluwer Academic Publishers, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Reeve, Amy Katherine. Mitochondrial Dysfunction in Neurodegenerative Disorders. London: Springer-Verlag London Limited, 2012.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Strand, Ray D. Bionutrition: Winning the war within. Charlottesville, VA: Hampton Roads Pub., 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Degeneration (Pathology)"

1

Fortuna, Aldo, Luigi Ferrante, and Pierpaolo Lunardi. "Pathology of disk degeneration." In Essential Illustrated Neurosurgery, 183–209. Milano: Springer Milan, 2001. http://dx.doi.org/10.1007/978-88-470-2908-8_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Laver, Nora M. V. "Pathology of Age-Related Macular Degeneration." In Age-Related Macular Degeneration, 15–29. Boca Raton: CRC Press, 2024. http://dx.doi.org/10.1201/9781003522553-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Olsen, E. G. J., and R. A. Florio. "Degeneration, Deposition and Diseases of Connective Tissue." In Atlas of Cardiovascular Pathology, 42–52. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3209-8_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Mackenzie, Ian R. A., and Manuela Neumann. "Frontotemporal Lobar Degeneration with TDP-43 Pathology." In Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders, 393–403. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341256.ch41.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Dickson, Dennis W., Jean-Jaques Hauw, Yves Agid, and Irene Litvan. "Progressive Supranuclear Palsy and Corticobasal Degeneration." In Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders, 135–55. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341256.ch15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Neumann, Manuela, and Ian R. A. Mackenzie. "Frontotemporal Lobar Degeneration with FUS Immunoreactive Inclusions." In Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders, 412–17. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341256.ch43.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Chan, Chi-Chao, and Daniel Ardeljan. "Molecular Pathology of Macrophages and Interleukin-17 in Age-Related Macular Degeneration." In Retinal Degenerative Diseases, 193–98. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-3209-8_25.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Sango, Kazunori, Masami Tsukamoto, Kazunori Utsunomiya, and Kazuhiko Watabe. "Spontaneously Immortalized Adult Rodent Schwann Cells as Valuable Tools for the Study of Peripheral Nerve Degeneration and Regeneration." In Schwann Cell Development and Pathology, 147–70. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54764-8_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Dickson, D. W., M. B. Feany, S. H. Yen, L. A. Mattiace, and P. Davies. "Cytoskeletal pathology in non-Alzheimer degenerative dementia: new lesions in Diffuse Lewy body disease, Pick’s disease, and Corticobasal Degeneration." In Journal of Neural Transmission Supplement, 31–46. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-6892-9_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Gross-Fengels, Walter, and Karl Friedrich Rudolf Neufang. "Spezielle angiographische Pathologie und Technik." In Degenerative Gefäßerkrankungen, 23–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77364-8_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Degeneration (Pathology)"

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

Elsner, Ann E., Henry H. Zenzie, Stephen A. Burns, and Peter F. Moulton. "Changes in fundus pathology measurements with wavelength in the near IR." In OSA Annual Meeting. Washington, D.C.: Optica Publishing Group, 1992. http://dx.doi.org/10.1364/oam.1992.tull3.

Full text
Abstract:
To determine the best method of screening for and monitoring degeneration in age-related macular degeneration, we compared images of the ocular fundus taken in near IR light with a scanning laser ophthalmoscope. We digitized images from 795 to 895 nm on five normal adults (two females, three males) and four patients with age-related macular degeneration (two females, two males). The IR light source was a Ti:sapphire laser (Titan cw, SEO), pumped by all lines of an argon laser (American Laser). Wavelength tuning was performed quickly, with a stepper motor under computer control. Two of the normal subjects and all of the patients have pathology visible as bright deposits with dark vessels. The contrast of deposits and subretinal vessels was enhanced as wavelength increased, with areas that appeared uniform at 795 nm having pathology and vessels readily visible at longer wavelengths.
APA, Harvard, Vancouver, ISO, and other styles
3

Ferreira, João Henrique Fregadolli, Amanda Maieski, Caio Disserol, and Helio Afonso Ghizoni Teive. "Corticobasal syndrome with Balint syndrome: a clue for Alzheimer disease pathology." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.712.

Full text
Abstract:
Context: Balint syndrome (BS), first described in 1909, has three core features: optic ataxia, oculomotor apraxia and simultanagnosia, and has been described after various conditions amongst vascular, infectious, demyelinating and degenerative diseases1 . It has already been reported concomitant with corticobasal syndrome (CBS)2 . Case report: 59 year-old male without history of previous diseases presented with behavior changes in the last two years. He had a previous diagnosis of “stroke” because frequent falls to the left side and difficulty in using his left hand for simple daily activities. After that, he gradually evolved with visual problems (bumped into objects inside his house), fear of walking or sitting, and required constant assistance for basic activities of daily living. On physical examination he presented with clear visuospatial dysfunction, characterized by simultanagnosia, oculomotor apraxia and optic ataxia. Bilateral asymmetric upper limb apraxia (worse on left side), dystonic posturing and stimulus-sensitive myoclonus in the left arm were also present. No signs of parkinsonism or language/speech disturbances were identified. Brain MRI showed severe asymmetric biparietal lobe atrophy (right more than left). DISCUSSION: The pathologic findings underlying CBS are variable, including Corticobasal Degeneration, Progressive Supranuclear Palsy, Frontotemporal Lobar Degeneration and Alzheimer Disease (AD). The association of BS and CBS favors the possibility of AD pathologic findings3 . Imaging methods like FDG-PET have recently been shown to be capable of distinguishing AD-related CBS from those associated with other pathologies4 . FDG-PET is not widely available in our country; than the presence of BS in CBS patients may individualize their treatment.
APA, Harvard, Vancouver, ISO, and other styles
4

Mitra, Sunanda. "Spatial Contrast Threshold Perimetry in Macular Degeneration*." In Noninvasive Assessment of Visual Function. Washington, D.C.: Optica Publishing Group, 1985. http://dx.doi.org/10.1364/navf.1985.tub8.

Full text
Abstract:
Visual field defects are often not effectively detected by conventional clinical perimetry despite the presence of extensive pathophysiology in the neuronal pathways.1-2 In the case of localized retinal lesions resulting from macular degeneration, an accurate assessment of visual dysfunction across the central visual field is even a more formidable task. These uncertainties in the evaluation of visual function stem from our lack of understanding of the basic mechanisms underlying not only the disease processes3, but also the neural signal transmission processes.4 Regardless of the exactness of the existing models of neural filtering4, the use of grating patches as test-stimuli reveals differential sampling ability of the neuronal units in the presence of a pathology that is undetected by clinical perimetry.5,6 However, the structural inhomogeneity of the retina imposes further constraints on specific spatio-temporal domain, and the size of the grating patch to be used in detecting visual dysfunction in the local regions of the visual field.
APA, Harvard, Vancouver, ISO, and other styles
5

Elsner, Ann E., Stephen A. Burns, Mark R. Kreitz, and John J. Weiter. "New Views of the Retina/ RPE Complex: Quantifying Sub-retinal Pathology." In Noninvasive Assessment of the Visual System. Washington, D.C.: Optica Publishing Group, 1991. http://dx.doi.org/10.1364/navs.1991.tua1.

Full text
Abstract:
The early stages of sub-retinal pathology are often difficult to observe and quantify in vivo. One important example is age-related macular degeneration (AMD), which is one of the chief causes of visual loss in the United States. Histopathological studies of human eyes indicate that there is a deposition of material in the layers beneath the retina, particularly in Bruch’s membrane prior to clinical detection of the disease. (Fig 1, as in Ref 1). These changes are not visible clinically when the deposits are diffuse or small (e.g. <25 urn). We are currently attempting to determine if these earliest changes can be detected by non-invasive techniques.
APA, Harvard, Vancouver, ISO, and other styles
6

Wang, Roy, and C. Ross Ethier. "Residual Deformations of Ocular Tissues." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14368.

Full text
Abstract:
Biomechanics and mechanobiology play a potentially significant role in several ocular pathologies. Glaucoma is perhaps the best studied of these, but other ocular conditions where mechanics are important include retinal detachment and macular degeneration (1, 2). Knowledge of the mechanical properties of the relevant ocular tissues, including their constitutive relationships, is required to understand the biomechanical basis of pathology and also for developing biomechanically mediated therapies. Towards this end, it is necessary to understand the residual strain state of relevant ocular tissues prior to formulating accurate and predictive mechanical models (3).
APA, Harvard, Vancouver, ISO, and other styles
7

Peltz, Cathryn D., Jason E. Hsu, David L. Glaser, and Louis J. Soslowsky. "Biceps Tendon Changes Along Its Length, and With Altered Loading, in the Presence of Rotator Cuff Tears in a Rat Model." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19070.

Full text
Abstract:
Biceps tendon pathology is commonly seen in the presence of rotator cuff tears and is often identified as a source of shoulder pain. However, the contribution of the biceps tendon to shoulder function is controversial and therefore the etiology of this pathology and its optimal treatment are unknown. Degeneration, inflammation and altered loading have all been hypothesized as possible mechanisms for biceps tendon pathologies. A previous study began to investigate the contribution of altered loading to these pathologies and showed that 4 weeks of increased loading resulted in decreased mechanical properties along the entire length of the tendon while decreased loading resulted in increased stiffness at the insertion site but decreased properties elsewhere [1]. Building on this study, the objective of the present study was to determine the effects of a longer period of altered loading along the length of the biceps tendon in order to determine where biceps tendon pathology originates following rotator cuff tears in a rat model. We hypothesized that: 1) increased loading would result in decreased mechanical and histological properties and decreased loading would result in increased mechanical properties and organization and 2) modulus and organization would increase along the length of the biceps tendon.
APA, Harvard, Vancouver, ISO, and other styles
8

Lipscomb, Kristen E., and Nesrin Sarigul-Klijn. "Experimentally Validated Computational Simulation of Lumbar Spine Intervertebral Disc Puncture." In ASME 2011 International Mechanical Engineering Congress and Exposition. ASMEDC, 2011. http://dx.doi.org/10.1115/imece2011-62447.

Full text
Abstract:
Back pain is a debilitating medical condition, often with an unclear source. Over time, back pain can affect the work and lifestyle of an individual by reducing job productivity and time spent on enjoyable activities. Discography of the intervertebral disc (IVD) is often used to diagnose pathology of the disc and determine if it may be a source for chronic back pain. It has recently been suggested that discography may lead to IVD degeneration, and has been a cause of controversy among spine care physicians. Using the results from a cadaveric experimental model, a finite element model was first validated. Then, a study was conducted to better understand the changes caused by discography on human spine mechanics. An anatomically accurate L3-L5 lumbar spine model was developed using computed tomography scans. Discography was simulated in the model as an area in the disc affected by needle puncture. The material properties in the nucleus pulposus were adjusted to match experimental data both before and after puncture. The results show that puncture of the IVD leads to increased deformation as well as increased stresses in the disc. Pressure in the nucleus pulposus found to decrease after puncture, and was calculated in the course of this study. Puncturing the IVD changes disc mechanics and may lead to progressive spine issues in the future such as disc degeneration. While discography has been the gold standard to determine if the disc was a source of back pain in patients for many years, the potential long-term degenerative effects of the procedure are only now coming into light, and must be closely examined.
APA, Harvard, Vancouver, ISO, and other styles
9

Korecki, Casey L., Benjamin A. Walter, Karolyn E. Godburn, and James C. Iatridis. "Asymmetric Loading Promotes Early Signs of Intervertebral Disc Degeneration in Large Animal Organ Culture." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206491.

Full text
Abstract:
Intervertebral disc (IVD) degeneration is a complex pathology, involving alterations in mechanical and biological function. Mechanical injury to IVDs may contribute to the development of IVD degeneration, and can arise following excessive loading or repeated exposure to loading levels which are not instantaneously damaging. Lateral bending and flexion produced the highest maximum shear strains in human IVDs and are considered the motions that place the IVD at greatest risk of injury (1). The biological response of the IVD to combined bending and compression has been examined in vivo in rat and mouse tail bending models demonstrating structural disruption, apoptosis and remodeling (2,4). However, there are practical limitations to current in vivo studies, as it can be difficult to apply repeated bending loads to the disc in vivo, and few large animal models exist capable of tracking the early biological, structural and compositional changes from asymmetrical loading. IVD organ culture allows control over mechanical boundary conditions and investigation of cellular responses to loading while the IVD remains largely intact, and allows the use of large animal models which more closely mimic the nutritional and compositional nature of human IVDs.
APA, Harvard, Vancouver, ISO, and other styles
10

Peloquin, John M., Jonathon H. Yoder, Nathan T. Jacobs, Sung M. Moon, Alexander C. Wright, Edward J. Vresilovic, and Dawn M. Elliott. "Intervertebral Disc Shape Variation and its Relationship to Degeneration Using Principal Components Analysis of a Population of MR Images." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80645.

Full text
Abstract:
Degeneration of the intervertebral disc (IVD) is implicated in low back pain, which is a costly and prevalent disease. Since the IVD is a mechanically active organ, it is important to consider its mechanical behavior as one factor in the degenerate pathology. Strain can be measured directly by imaging methods, but the stress distribution within the disc must be calculated. The stress distribution for a particular strain state is dependent on the IVD’s material properties and its geometry. While the material properties of the tissues comprising IVD have been extensively studied, its three-dimensional geometry remains incompletely characterized. Prior whole-disc models have been constructed from single IVDs. While this approach ensures that the geometry has a physiological basis, it is uncertain the degree to which results from a single IVD shape can be generalized to the entire population.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Degeneration (Pathology)' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography