Journal articles on the topic 'Degeneration'
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1
Ahluwalia, Kabir, Juan-Carlos Martinez-Camarillo, Biju B. Thomas, Aditya Naik, Alejandra Gonzalez-Calle, Dimitrios Pollalis, Jane Lebkowski, et al. "Polarized RPE Secretome Preserves Photoreceptors in Retinal Dystrophic RCS Rats." Cells 12, no. 13 (June 22, 2023): 1689. http://dx.doi.org/10.3390/cells12131689.
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Retinal degenerative diseases, including age-related macular degeneration (AMD) and retinitis pigmentosa, lack effective therapies. Conventional monotherapeutic approaches fail to target the multiple affected pathways in retinal degeneration. However, the retinal pigment epithelium (RPE) secretes several neurotrophic factors addressing diverse cellular pathways, potentially preserving photoreceptors. This study explored human embryonic stem cell-derived, polarized RPE soluble factors (PRPE-SF) as a combination treatment for retinal degeneration. PRPE-SF promoted retinal progenitor cell survival, reduced oxidative stress in ARPE-19 cells, and demonstrated critical antioxidant and anti-inflammatory effects for preventing retinal degeneration in the Royal College of Surgeons (RCS) rat model. Importantly, PRPE-SF treatment preserved retinal structure and scotopic b-wave amplitudes, suggesting therapeutic potential for delaying retinal degeneration. PRPE-SF is uniquely produced using biomimetic membranes for RPE polarization and maturation, promoting a protective RPE secretome phenotype. Additionally, PRPE-SF is produced without animal serum to avoid immunogenicity in future clinical development. Lastly, PRPE-SF is a combination of neurotrophic factors, potentially ameliorating multiple dysfunctions in retinal degenerations. In conclusion, PRPE-SF offers a promising therapeutic candidate for retinal degenerative diseases, advancing the development of effective therapeutic strategies for these debilitating conditions.
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Chen, Xiaofeng, Weijun Guo, Hao Li, Xi Li, Zhuangxun Han, Xueyuan Chu, Zehui Lao, Junxian Xie, and Dongling Cai. "Evaluation of Cartilaginous Endplate Degeneration Based on Magnetic Resonance Imaging." Journal of Healthcare Engineering 2021 (March 23, 2021): 1–12. http://dx.doi.org/10.1155/2021/5534227.
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In order to carry out the evaluation of cartilaginous endplate degeneration based on magnetic resonance imaging (MRI), this paper retrospectively analyzed the MRI data from 120 cases of patients who were diagnosed as lumbar intervertebral disc degeneration and underwent MRI examinations in the designated hospital of this study from June 2018 to June 2020. All cases underwent conventional sagittal and transverse T1WI and T2WI scans, and some cases were added with sagittal fat-suppression T2WI scans; then, the number of degenerative cartilaginous endplates and its ratio to degenerative lumbar intervertebral discs were counted and calculated, and the T1WI and T2WI signal characteristics of each degenerative cartilage endplate and its correlation with cartilaginous endplate degeneration were summarized, compared, and analyzed to evaluate the cartilaginous endplate degeneration by those magnetic resonance information. The study results show that there were 33 cases of cartilaginous endplate degeneration, accounting for 27.50% of all those 120 patients with lumbar intervertebral disc degeneration (54 degenerative endplates in total), including 9 cases with low T1WI and high T2WI signals, 5 cases with high T1WI and low T2WI signals, 12 cases with high and low mixed T1WI and high or mixed T2WI signals, and 4 cases with both low T1WI and T2WI signals. Therefore, MRI scanning can clearly present the abnormal signals of lumbar intervertebral disc and cartilaginous endplate degeneration, accurately identity their lesion locations, and type their degenerative characteristics, which may be best inspection method for the evaluation of cartilaginous endplate degeneration in the early diagnosis of intervertebral disc degeneration. The study results of this paper provide a reference for further researches on the evaluation of cartilaginous endplate degeneration based on magnetic resonance imaging.
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Zhang, Ting, Yajing Zuo, Yantao Wei, Wenbin Huang, Xuezhi Zhou, Rongjiao Liu, Lili Zhong, Manjuan Peng, and Shaochong Zhang. "The Prevalence and Associations of Peripheral Retinopathy: Baseline Study of Guangzhou Office Computer Workers." Journal of Ophthalmology 2018 (June 20, 2018): 1–6. http://dx.doi.org/10.1155/2018/2358690.
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Purpose. To determine the prevalence of peripheral retinopathy and its associated risk factors among a sample of Guangzhou office computer workers. Methods. A cross-sectional study of Guangzhou Chinese computer workstations and operators in different departments and units of the Guangzhou Power Supply Bureau, China, in 2016. Peripheral retinopathy was recorded and analyzed using a scanning laser ophthalmoscope (SLO; Optos, Daytona, United Kingdom) and slit-lamp microscopy combined with a three-mirror contact lens. Results. The 1934 eyes of 967 subjects (513 females and 454 males) were included in this study. In total, 79.1% of the eyes were myopic in workers aged 20–29 years, 72.9% in workers aged 30–39 years, 62.2% in workers aged 40–49 years, and 43.4% in workers aged 50–59 years (p<0.001). Most eyes had optic nerve crescents (81.3%). Various peripheral degenerations were found: 7 eyes (0.4%) had microcystoid degeneration, 40 (2.1%) had peripheral pigmentary degeneration, 87 (4.5%) had lattice degeneration, and 4 (0.2%) had snail-track degeneration. Nineteen (1.0%) eyes had paving-stone degeneration, 11 (0.6%) eyes had a retinal hole or tear, and 16 (0.8%) eyes had chorioretinal degeneration. Multivariate regression confirmed that greater axial length (OR: 1.18 (1.03, 1.35), p=0.012) and more serious spherical equivalent (OR: 0.82 (0.77, 0.88), p<0.001) were significant risk factors for peripheral retinal changes. Conclusion. Peripheral retinal degenerative changes were found in a larger proportion of younger computer workers than older ones. Myopia is occurring in younger and younger people, accompanied by peripheral retinal degeneration.
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Voigt, Andrew P., Elaine Binkley, Miles J. Flamme-Wiese, Shemin Zeng, Adam P. DeLuca, Todd E. Scheetz, Budd A. Tucker, Robert F. Mullins, and Edwin M. Stone. "Single-Cell RNA Sequencing in Human Retinal Degeneration Reveals Distinct Glial Cell Populations." Cells 9, no. 2 (February 13, 2020): 438. http://dx.doi.org/10.3390/cells9020438.
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Degenerative diseases affecting retinal photoreceptor cells have numerous etiologies and clinical presentations. We clinically and molecularly studied the retina of a 70-year-old patient with retinal degeneration attributed to autoimmune retinopathy. The patient was followed for 19 years for progressive peripheral visual field loss and pigmentary changes. Single-cell RNA sequencing was performed on foveal and peripheral retina from this patient and four control patients, and cell-specific gene expression differences were identified between healthy and degenerating retina. Distinct populations of glial cells, including astrocytes and Müller cells, were identified in the tissue from the retinal degeneration patient. The glial cell populations demonstrated an expression profile consistent with reactive gliosis. This report provides evidence that glial cells have a distinct transcriptome in the setting of human retinal degeneration and represents a complementary clinical and molecular investigation of a case of progressive retinal disease.
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Börner, W., and P. Schneider. "The Impact of Degenerative Spinal Changes on the Correlation of Peripheral and Axial Bone Density." Nuklearmedizin 33, no. 04 (1994): 138–43. http://dx.doi.org/10.1055/s-0038-1629808.
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SummaryResults of bone density measurements by quantitative computed tomography of the peripheral skeleton (pQCT) were compared with those of measurements at the axial skeleton with a view to study the effects of degenerative spinal changes on the validity of bone densitometry of the lumbar spine. 556 consecutive patients were examined by dual-energy x-ray absorptiometry (DXA) of the spine and by peripheral quantitative computed tomography (pQCT) of the distal radius. There were significant differences between the bone mineral values at the distal radius and those at the spine, depending on the degree of spinal degeneration. As expected, spinal degenerations showed a highly significant age dependence. With increasing degeneration the correlations between the radius total bone mineral concentration and the bone density of the lumbar spine decreased from r = 0.45 to 0.23 in women and from r = 0.64 to 0.28 in men. We conclude that the value of spinal DXA is reduced in patients with degenerative spinal disease, compared to the pQCT at the peripheral skeleton.
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Marques, Christine, Thibaut Burg, Jelena Scekic-Zahirovic, Mathieu Fischer, and Caroline Rouaux. "Upper and Lower Motor Neuron Degenerations Are Somatotopically Related and Temporally Ordered in the Sod1 Mouse Model of Amyotrophic Lateral Sclerosis." Brain Sciences 11, no. 3 (March 13, 2021): 369. http://dx.doi.org/10.3390/brainsci11030369.
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Amyotrophic lateral sclerosis (ALS) is a devastating and fatal neurodegenerative disease arising from the combined degeneration of upper motor neurons (UMN) in the motor cortex, and lower motor neurons (LMN) in the brainstem and spinal cord. This dual impairment raises two major questions: (i) are the degenerations of these two neuronal populations somatotopically related? and if yes (ii), where does neurodegeneration start? If studies carried out on ALS patients clearly demonstrated the somatotopic relationship between UMN and LMN degenerations, their temporal relationship remained an unanswered question. In the present study, we took advantage of the well-described Sod1G86R model of ALS to interrogate the somatotopic and temporal relationships between UMN and LMN degenerations in ALS. Using retrograde labelling from the cervical or lumbar spinal cord of Sod1G86R mice and controls to identify UMN, along with electrophysiology and histology to assess LMN degeneration, we applied rigorous sampling, counting, and statistical analyses, and show that UMN and LMN degenerations are somatotopically related and that UMN depletion precedes LMN degeneration. Together, the data indicate that UMN degeneration is a particularly early and thus relevant event in ALS, in accordance with a possible cortical origin of the disease, and emphasize the need to further elucidate the molecular mechanisms behind UMN degeneration, towards new therapeutic avenues.
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Alkhasawneh, Mahmoud H., Asma’a Al-Mnayyis, and Yazeed Bagain. "Spinal Degeneration and Degenerative Disc Disease correlation identified with Magnetic Resonance Imaging." Biomedical and Pharmacology Journal 14, no. 1 (March 30, 2021): 491–96. http://dx.doi.org/10.13005/bpj/2149.
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Magnetic resonance imaging (MRI) is the golden standard technique for spine disc disease diagnosis. Vertebral body endplate signal intensity on MRI is confirming lumber spine degenerative disc disease.The study aimed to record the lumbar spine degenerative relation between disc and diseaseusing magnetic resonance imaging. Our prospective and double blind investigation included 142 participants,having lumbar spine degenerativedisease confirmed by MRI. Pfirrmann score was used to record the relation between lumbar spine disc degeneration and lumbar spine degenerative disease. Modic modifications with the Pfirrmann and modified Pfirrmann scores of disc degeneration were assessed.Lumbar spine MRI was done for all participants using sagittal T1 and T2 WI. Modic was scored (0-III) The Pfirrmann scored I-V for disc degeneration. Lumbar disc degeneration was evaluated by modified Pfirrmann scoring from 1-8 according to signal intensity of the nucleus pulposus and inner annulus.Modic was recorded in 41.5%, 24.6%, 32.4% and 1.4% of participants with scores 0, I, II and III, respectively. Pfirrmann score was 13.4%, 73.9% and 12.7% of disc degeneration with scores III, IV and V, respectively, while,the modified Pfirrmann score was 2.1%, 15.5%, 38.7%, 26.8% and 16.9% of disc degeneration with scores of 4, 5, 6, 7 and 8, respectively. The modified Pfirrmann score showed notableinconsistencyin participants with Modic 0, I and II, but no difference between Modic I and II.There was significant relation between Modicand lumbar spine disc degeneration. In conclusion, there is a relation between Modic, Pfirrmann and modified Pfirrmann scores of lumbar spine disc degeneration in participants with lumbar spine degenerative disease.
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Baker, Brent A., Robert R. Mercer, Ken B. Geronilla, Michael L. Kashon, G. R. Miller, and Robert G. Cutlip. "Stereological analysis of muscle morphology following exposure to repetitive stretch-shortening cycles in a rat model." Applied Physiology, Nutrition, and Metabolism 31, no. 2 (April 1, 2006): 167–79. http://dx.doi.org/10.1139/h05-009.
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Repetitive motion is one risk factor associated with contraction-induced muscle injury, which leads to skeletal muscle degeneration, inflammation, and dysfunction. Since current methods are unable to quantify the acute degenerative and inflammatory responses of muscle tissue concurrently, the purpose of this study was to quantify the temporal myofiber response after exposure to injurious stretch-shortening cycles (SSCs) using a standardized stereological technique. Functional testing was performed on the ankle dorsiflexor muscles of Sprague-Dawley rats in vivo. Rats were anesthetized and exposed to 15 sets of 10 SSCs. Control rats were exposed to 15 sets of single isometric contractions of the same stimulation duration. Changes in muscle morphometry were assessed at 0.5, 24, 48, 72, and 240 h post-exposure to quantify the degree of myofiber degeneration and inflammation in the tibialis anterior muscle from each group. There was an increase in the volume density and average thickness of degenerating myofibers over time in the muscle collected from rats exposed to SSCs (p < 0.0001) that was significantly greater than in muscle exposed to isometric contractions at 24, 48, and 72 h post-exposure (p = 0.003). The volume density of degenerative myofibers was associated with functional deficits at 48 h. Stereological quantification of degenerative myofibers and interstitial space changes were associated with functional defects 48-72 h after SSC-induced injury, thus demonstrating stereology is an accurate measure of SSC-induced skeletal muscle injury.Key words: stereology, morphometry, myofiber degeneration, interstitial space, stretch-shortening cycles.
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Feinberg, Konstantin, Adelaida Kolaj, Chen Wu, Natalie Grinshtein, Jonathan R. Krieger, Michael F. Moran, Lee L. Rubin, Freda D. Miller, and David R. Kaplan. "A neuroprotective agent that inactivates prodegenerative TrkA and preserves mitochondria." Journal of Cell Biology 216, no. 11 (September 6, 2017): 3655–75. http://dx.doi.org/10.1083/jcb.201705085.
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Axon degeneration is an early event and pathological in neurodegenerative conditions and nerve injuries. To discover agents that suppress neuronal death and axonal degeneration, we performed drug screens on primary rodent neurons and identified the pan-kinase inhibitor foretinib, which potently rescued sympathetic, sensory, and motor wt and SOD1 mutant neurons from trophic factor withdrawal-induced degeneration. By using primary sympathetic neurons grown in mass cultures and Campenot chambers, we show that foretinib protected neurons by suppressing both known degenerative pathways and a new pathway involving unliganded TrkA and transcriptional regulation of the proapoptotic BH3 family members BimEL, Harakiri,and Puma, culminating in preservation of mitochondria in the degenerative setting. Foretinib delayed chemotherapy-induced and Wallerian axonal degeneration in culture by preventing axotomy-induced local energy deficit and preserving mitochondria, and peripheral Wallerian degeneration in vivo. These findings identify a new axon degeneration pathway and a potentially clinically useful therapeutic drug.
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Musarella, Maria A., and Ian M. MacDonald. "Current Concepts in the Treatment of Retinitis Pigmentosa." Journal of Ophthalmology 2011 (2011): 1–8. http://dx.doi.org/10.1155/2011/753547.
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Inherited retinal degenerations, including retinitis pigmentosa (RP) and Leber congenital amaurosis (LCA), affect 1 in 4000 individuals in the general population. A majority of the genes which are mutated in these conditions are expressed in either photoreceptors or the retinal pigment epithelium (RPE). There is considerable variation in the clinical severity of these conditions; the most severe being autosomal recessive LCA, a heterogeneous retinal degenerative disease and the commonest cause of congenital blindness in children. Here, we discuss all the potential treatments that are now available for retinal degeneration. A number of therapeutic avenues are being explored based on our knowledge of the pathophysiology of retinal degeneration derived from research on animal models, including: gene therapy, antiapoptosis agents, neurotrophic factors, and dietary supplementation. Technological advances in retinal implant devices continue to provide the promise of vision for patients with end-stage disease.
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Bano, Shehar, Usman Tahir, Fatima Khalid, Nauman Ahmed, Amina Bibi, and Muhammad Imran. "Young Pakistani Individuals are Genetically Predisposed to Lumbar Degenerative Disc Degeneration." Pakistan Journal of Medical and Health Sciences 16, no. 1 (January 31, 2022): 1479–81. http://dx.doi.org/10.53350/pjmhs221611479.
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Aim: Even though the specific processes that cause degenerative disc degeneration are unknown, a major hereditary effect has indeed been discovered. Concentrating on DDD in emerging adults can help determine the precise role of genetic susceptibility to DDD. Methods: MRI imaging (1.6 Tesla) was used to analyses individuals (41 years old) having lumbar disc degeneration, and genome wide association testing was made for 58 single nucleotide polymorphisms in 38 potential genes. Pfirrman's grading had been used to classify disc degeneration in specific lumbar spine discs from L1 to S1. The participants have been divided into 2 sets based on their Total Disc Degenerative Score. DDD intensity has been rated as mild or severe depending on TDDS. Results: MRI imaging (1.6 Tesla) was used to analyze individuals (41 years old) having lumbar disc degeneration, and genome wide association testing was made for 58 single nucleotide polymorphisms in 38 potential genes. Pfirrman's grading had been used to classify disc degradation in specific lumbar spine discs from L1 to S1. The participants have been divided into 2 sets grounded on their Total Disc Degenerative Score. DDD intensity has been rated as moderately severe depending on TDDS. Conclusion: The researchers discovered significant SNP correlations of five genes in young people with serious lumbar disc degeneration. Those five genes have various roles in matrix metabolism, intracellular transmission, and the inflammatory cascade. The current demonstrates that disc degeneration is very complicated illness characterized by the intricate interaction of several genetic variations. Keywords: Lumbar Degenerative Disc, Degeneration, Predisposed.
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Dowbor, Piotr, and Adam Hajduk. "A Comparison of Various Types of Degenerations for Algebras." Algebra Colloquium 14, no. 03 (September 2007): 361–88. http://dx.doi.org/10.1142/s1005386707000351.
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Three different notions of geometric degeneration for finite dimensional algebras are compared. It is proved that for algebras A0 and A1 of same dimension, if A0 is a CB-degeneration of A1, then A0 is a degeneration of A1 in the classical sense; moreover, if additionally A0 and A1 are basic, then A0 is a CB-degeneration of A1 if and only if A0 is a rigid degeneration of A1. It is also shown that CB-degenerations along affine lines in the different dimension case do not differ so much from those in the equal dimension case.
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Lee, K. P., and L. A. Kinney. "The infrastructure and Reversibility of Testicular Atrophy Induced by Ethylene Glycol Monomethyl Ether (EGME) in the Rat." Toxicologic Pathology 17, no. 4_part_2 (April 1989): 759–73. http://dx.doi.org/10.1177/0192623389017004204.
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Inhalation exposure to 300 ppm ethylene glycol monomethyl ether (EGME) for 3 days produced degenerative changes in spermatocytes of pachytene and meiotic division at spermatogenic stage XIV in rats. However, a wide range of germ cell types including spermatogonia was affected and the stage-specific damage was not discernible after 2 weeks exposure to 300 ppm EGME. The stage-specific damage was related to exposure concentration-time course. In early stages, degenerating spermatocytes showed nuclear chromatin clumping around synaptonemal complexes, cytoplasmic vesiculation with electron-dense material deposition, and disruption of the plasma membrane. Chromosomal microtubules in the meiotic division of spermatocytes were discontinued with deposition of electron-dense chromatin material. Sertoli cells showed cytoplasmic vacuolization, contact loss to germ cells, and cytoplasmic processes fragmentation with disrupted microtubules. Degenerative pachytene or meiotic spermatocytes were associated with disrupted Sertoli-germ cell relationship, chromosomal microtubules, and synaptonemal complexes. Spermatid degeneration and giant cell formation were observed after spermatocyte degeneration. Spermatid degeneration appeared to be a secondary change resulting from disrupted Sertoli-to-germ cell association. After 14 days post-exposure (PE) following 2 weeks exposure, some tubules were lined with regenerating spermatocytes with or without round spermatids. By 42 days PE, many tubules regained normal germinal epithelium, but some tubules were still atrophic even after 84 days PE. Reversibility of testicular atrophy was inversely proportional to severity of damaged stem cells.
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Vanhoenacker, Filip M., Michiel Eyselbergs, and Anne Cotten. "“Spinal degeneration: beyond degenerative disc disease”: how to discriminate degeneration from spondylarthropathies?" Neuroradiology 53, S1 (August 24, 2011): 175–79. http://dx.doi.org/10.1007/s00234-011-0936-1.
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Fairbank, J. "COMPARISON OF DEGENERATIVE MRI FEATURES OF THE INTERVERTEBRAL DISC BETWEEN THOSE WITH AND WITHOUT CHRONIC LOW BACK PAIN: AN EXPLORATORY STUDY OF TWO LARGE FEMALE POPULATIONS USING AUTOMATED ANNOTATION." Orthopaedic Proceedings 106-B, SUPP_2 (January 2, 2024): 52. http://dx.doi.org/10.1302/1358-992x.2024.2.052.
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The relationship of degeneration to symptoms has been questioned. MRI detects apparently similar disc degeneration and degenerative changes in subjects both with and without back pain. We aimed to overcome these problems by re-annotating MRIs from asymptomatic and symptomatic groups onto the same grading system.We analysed disc degeneration in pre-existing large MRI datasets. Their MRIs were all originally annotated on different scales. We re-annotated all MRIs independent of their initial grading system, using a verified, rapid automated MRI annotation system (SpineNet) which reported degeneration on the Pfirrmann (1-5) scale, and other degenerative features (herniation, endplate defects, marrow signs, spinal stenosis) as binary present/absent. We compared prevalence of degenerative features between symptomatics and asymptomatics.Pfirrmann degeneration grades in relation to age and spinal level were very similar for the two independent groups of symptomatics over all ages and spinal levels. Severe degenerative changes were significantly more prevalent in discs of symptomatics than asymptomatics in the caudal but not the rostral lumbar discs in subjects < 60 years. We found high co-existence of degenerative features in both populations. Degeneration was minimal in around 30% of symptomatics < 50 years.We confirmed age and disc level are significant in determining imaging differences between asymptomatic and symptomatic populations and should not be ignored. Automated analysis, by rapidly combining and comparing data from existing groups with MRIs and information on LBP, provides a way in which epidemiological and ‘big data’ analysis could be advanced without the expense of collecting new groups.
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Fang, X., E. Feigin, G. Fourier, and I. Makhlin. "Weighted PBW degenerations and tropical flag varieties." Communications in Contemporary Mathematics 21, no. 01 (January 28, 2019): 1850016. http://dx.doi.org/10.1142/s0219199718500165.
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We study algebraic, combinatorial and geometric aspects of weighted Poincaré–Birkhoff–Witt (PBW)-type degenerations of (partial) flag varieties in type [Formula: see text]. These degenerations are labeled by degree functions lying in an explicitly defined polyhedral cone, which can be identified with a maximal cone in the tropical flag variety. Varying the degree function in the cone, we recover, for example, the classical flag variety, its abelian PBW degeneration, some of its linear degenerations and a particular toric degeneration.
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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.
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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.
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Herrmann, Kelsey A., Yizhou Liu, Arnau Llobet-Rosell, Colleen N. McLaughlin, Lukas J. Neukomm, Jaeda C. Coutinho-Budd, and Heather T. Broihier. "Divergent signaling requirements of dSARM in injury-induced degeneration and developmental glial phagocytosis." PLOS Genetics 18, no. 6 (June 23, 2022): e1010257. http://dx.doi.org/10.1371/journal.pgen.1010257.
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Elucidating signal transduction mechanisms of innate immune pathways is essential to defining how they elicit distinct cellular responses. Toll-like receptors (TLR) signal through their cytoplasmic TIR domains which bind other TIR domain-containing adaptors. dSARM/SARM1 is one such TIR domain adaptor best known for its role as the central axon degeneration trigger after injury. In degeneration, SARM1’s domains have been assigned unique functions: the ARM domain is auto-inhibitory, SAM-SAM domain interactions mediate multimerization, and the TIR domain has intrinsic NAD+ hydrolase activity that precipitates axonal demise. Whether and how these distinct functions contribute to TLR signaling is unknown. Here we show divergent signaling requirements for dSARM in injury-induced axon degeneration and TLR-mediated developmental glial phagocytosis through analysis of new knock-in domain and point mutations. We demonstrate intragenic complementation between reciprocal pairs of domain mutants during development, providing evidence for separability of dSARM functional domains in TLR signaling. Surprisingly, dSARM’s NAD+ hydrolase activity is strictly required for both degenerative and developmental signaling, demonstrating that TLR signal transduction requires dSARM’s enzymatic activity. In contrast, while SAM domain-mediated dSARM multimerization is important for axon degeneration, it is dispensable for TLR signaling. Finally, dSARM functions in a linear genetic pathway with the MAP3K Ask1 during development but not in degenerating axons. Thus, we propose that dSARM exists in distinct signaling states in developmental and pathological contexts.
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Sekirnjak, Chris, Clare Hulse, Lauren H. Jepson, Pawel Hottowy, Alexander Sher, Wladyslaw Dabrowski, A. M. Litke, and E. J. Chichilnisky. "Loss of Responses to Visual But Not Electrical Stimulation in Ganglion Cells of Rats With Severe Photoreceptor Degeneration." Journal of Neurophysiology 102, no. 6 (December 2009): 3260–69. http://dx.doi.org/10.1152/jn.00663.2009.
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Retinal implants are intended to help patients with degenerative conditions by electrically stimulating surviving cells to produce artificial vision. However, little is known about how individual retinal ganglion cells respond to direct electrical stimulation in degenerating retina. Here we used a transgenic rat model to characterize ganglion cell responses to light and electrical stimulation during photoreceptor degeneration. Retinas from pigmented P23H-1 rats were compared with wild-type retinas between ages P37 and P752. During degeneration, retinal thickness declined by 50%, largely as a consequence of photoreceptor loss. Spontaneous electrical activity in retinal ganglion cells initially increased two- to threefold, but returned to nearly normal levels around P600. A profound decrease in the number of light-responsive ganglion cells was observed during degeneration, culminating in retinas without detectable light responses by P550. Ganglion cells from transgenic and wild-type animals were targeted for focal electrical stimulation using multielectrode arrays with electrode diameters of ∼10 microns. Ganglion cells were stimulated directly and the success rate of stimulation in both groups was 60–70% at all ages. Surprisingly, thresholds (∼0.05 mC/cm2) and latencies (∼0.25 ms) in P23H rat ganglion cells were comparable to those in wild-type ganglion cells at all ages and showed no change over time. Thus ganglion cells in P23H rats respond normally to direct electrical stimulation despite severe photoreceptor degeneration and complete loss of light responses. These findings suggest that high-resolution epiretinal prosthetic devices may be effective in treating vision loss resulting from photoreceptor degeneration.
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PELETTI-FIGUEIRÓ, MANUELA, ISRAEL SILVEIRA DE AGUIAR, SUELEN PAESI, DENISE CANTARELLI MACHADO, SERGIO ECHEVERRIGARAY, MARIANA ROESCH-ELY, ASDRUBAL FALAVIGNA, and JOÃO ANTONIO PÊGAS HENRIQUES. "HISTOLOGICAL MARKERS OF DEGENERATION AND REGENERATION OF THE HUMAN INTERVERTEBRAL DISK." Coluna/Columna 16, no. 1 (January 2017): 42–47. http://dx.doi.org/10.1590/s1808-185120171601170833.
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ABSTRACT Objective: To define histological scores for intervertebral disc degeneration that would enable the definition of morphological characteristics of disease, besides improving knowledge of the lumbar degenerative disc disease by means of immunohistochemical markers. Methods: Hematoxylin and Eosin, Alcian/PAS, Masson Trichrome and Safranin O/FCF staining was used on the intervertebral disc degeneration sections of patients with lumbar degenerative disc disease. The protein markers defined in immunohistochemistry were cell proliferation (Ki-67) and apoptosis (p53). Results: The study data enabled the determination of Safranin O/FCF stain as the most effective one for evaluating parameters such as area, diameter, and number of chondrocyte clusters. The importance of using stains in association, such as Safranin O/FCF, Masson Trichrome, Alcian/PAS and Hematoxylin and Eosin, was also determined, as they are complementary for the histopathological verification of intervertebral disc degeneration. By expressing proteins using the immunohistochemistry technique, it was possible to consider two stages of disc degeneration: cell proliferation with chondrocyte cluster formation, and induction of apoptosis. Conclusion: This study enabled the histological and immunohistochemical characterization to be determined for lumbar degenerative disc disease, and its degrees of evolution, by determining new disc degeneration scores.
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Muellner, Maximilian, Virginie Kreutzinger, Luis Becker, Torsten Diekhoff, Matthias Pumberger, Friederike Schömig, Mark Heyland, and Katharina Ziegeler. "Unexpected Sex Differences in the Relationship of Sacroiliac Joint and Lumbar Spine Degeneration." Diagnostics 12, no. 2 (January 21, 2022): 275. http://dx.doi.org/10.3390/diagnostics12020275.
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The relationship between degenerative changes of the sacroiliac joints and the lumbar spine on CT has not been studied yet. The aim of this analysis is to determine the nature of their association as well as the influence of fixed anatomical spinopelvic parameters on sacroiliac joint degeneration. For this institutional review-board-approved investigation, imaging datasets as well as electronic medical records of 719 patients without back pain from the clinical routine of our department of radiology were included. Age, sex, weight category (slim, normal, obese), parity in women and indication for imaging were noted for all patients. The presence of degenerative lesions of the lumbar spine (disc degeneration, endplate degeneration, spondylophytes, and facet joint osteoarthritis) was noted separately at each lumbar segment (L1 to L5). Sacroiliac joints were assessed for sclerosis and osteophytes. Fixed anatomical spinopelvic parameters were measured: pelvic radius = PR; pelvic incidence = PI; sacral table angle = STA. Correlation as well as regression analyses were performed; data were analyzed for males and females separately. PI increased significantly with age in both women and men, while STA decreased and PR remained constant; neither of them was associated with SIJ degeneration. SIJ degeneration correlated with disc degeneration (tau = 0.331; p < 0.001), spondylophytes (tau = 0.397; p < 0.001), and facet joint degeneration (tau = 0.310; p < 0.001) in men, but with no parameter of spinal degeneration in women. Lumbar spinal degeneration increased the risk of sacroiliac joint degeneration in men significantly (OR 7.2; 95%CI 2.8–19.0), but it was not a significant covariable in women. Fixed spinopelvic parameters have little impact on sacroiliac joint degeneration. The degeneration of the sacroiliac joints and the lumbar spine appear to be parallel processes in men, but are largely unrelated in women.
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Chen, Qile. "The degeneration formula for logarithmic expanded degenerations." Journal of Algebraic Geometry 23, no. 2 (November 15, 2013): 341–92. http://dx.doi.org/10.1090/s1056-3911-2013-00614-1.
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RAEDER, Mariana Trombetta de Lima, Eduardo Pontes REIS, Brunno Machado CAMPOS, Igor Aloísio Garcez ZAMILUTE, Marcondes Cavalcante FRANÇA JÚNIOR, and Fabiano REIS. "Transaxonal degenerations of cerebellar connections: the value of anatomical knowledge." Arquivos de Neuro-Psiquiatria 78, no. 5 (May 2020): 301–6. http://dx.doi.org/10.1590/0004-282x20200021.
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ABSTRACT Transaxonal degenerations result from neuronal death or the interruption of synaptic connections among neuronal structures. These degenerations are not common but may be recognized by conventional magnetic resonance imaging. Objective: The learning objectives of this review include recognition of the imaging characteristics of transaxonal degenerations involving cerebellar connections, the identification of potential encephalic lesions that can lead to these degenerations and correlation of the clinical manifestations with imaging findings that reflect this involvement. Methods: In this report, we review the neuroanatomical knowledge that provides a basis for identifying potential lesions that can result in these degenerations involving cerebellar structures. Results: Hypertrophic olivary degeneration results from an injury that interrupts any of the components of the Guillain-Mollaret triangle. In this work, we describe cases of lesions in the dentate nucleus and central tegmental tract. The crossed cerebellar diaschisis presents specific imaging findings and clinical correlations associated with its acute and chronic phases. The Wallerian degeneration of the middle cerebellar peduncle is illustrated by fiber injury of the pontine cerebellar tracts. A T2-hyperintensity in the dentate nucleus due to a thalamic acute lesion (in ventral lateral nuclei) is also described. Each condition described here is documented by MRI images and is accompanied by teaching points and an anatomical review of the pathways involved. Conclusion: Neurologists and radiologists need to become familiar with the diagnosis of these conditions since their presentations are peculiar and often subtle, and can easily be misdiagnosed as ischemic events, degenerative disease, demyelinating disease or even tumors.
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Taher, Fadi, David Essig, Darren R. Lebl, Alexander P. Hughes, Andrew A. Sama, Frank P. Cammisa, and Federico P. Girardi. "Lumbar Degenerative Disc Disease: Current and Future Concepts of Diagnosis and Management." Advances in Orthopedics 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/970752.
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Low back pain as a result of degenerative disc disease imparts a large socioeconomic impact on the health care system. Traditional concepts for treatment of lumbar disc degeneration have aimed at symptomatic relief by limiting motion in the lumbar spine, but novel treatment strategies involving stem cells, growth factors, and gene therapy have the theoretical potential to prevent, slow, or even reverse disc degeneration. Understanding the pathophysiological basis of disc degeneration is essential for the development of treatment strategies that target the underlying mechanisms of disc degeneration rather than the downstream symptom of pain. Such strategies ideally aim to induce disc regeneration or to replace the degenerated disc. However, at present, treatment options for degenerative disc disease remain suboptimal, and development and outcomes of novel treatment options currently have to be considered unpredictable.
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Aswad Layikh, Haider. "Estimation of Peripheral Retinal degenerations in myopia." AL-QADISIYAH MEDICAL JOURNAL 12, no. 22 (September 25, 2017): 42–48. http://dx.doi.org/10.28922/qmj.2016.12.22.42-48.
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Purpose: The purpose of this study is to estimate the peripheral retinal degenerations rate in myopic subjects, and compare the results between different degrees of myopia.Methods: subjects with different degrees of myopia who attended the consultations in Al-Diwaniya teaching hospital during the period from 1st Dec. 2014 to 1st of March 2015 got involved in this study, they were examined and peripheral retinal degeneration assessed and recorded.Results: The study included 237 patients with a mean age of 41.93 ±13.16 years and an age range of 18-65 years. Male patients accounted for 131 (55.3%) whereas female patients accounted for 106 (44.7%) with a male to female ratio of 1.24: 1. Mean refraction was -4.72 ± -3.05 D and ranged from -18.1 to -1.1 D. lattice degeneration was found in 64 patients (27.0%), while snail track degeneration was found in 11 patients (4.6%), results showed no significant relation between age, gender with the incidence of peripheral retinal degenerations while its clearly increasing in incidence with increasing degree of myopia .Conclusion: The incidence of peripheral retinal degeneration is more in high myopia subjects , although Low& moderate myopic subject still have considerable rate of peripheral retinal degeneration
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Martin, Michael D., Christopher M. Boxell, and David G. Malone. "Pathophysiology of lumbar disc degeneration: a review of the literature." Neurosurgical Focus 13, no. 2 (August 2002): 1–6. http://dx.doi.org/10.3171/foc.2002.13.2.2.
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Lumbar disc degeneration occurs because of a variety of factors and results in a multitude of conditions. Alterations in the vertebral endplate cause loss of disc nutrition and disc degeneration. Aging, apoptosis, abnormalities in collagen, vascular ingrowth, loads placed on the disc, and abnormal proteoglycan all contribute to disc degeneration. Some forms of disc degeneration lead to loss of height of the motion segment with concomitant changes in biomechanics of the segment. Disc herniation with radiculopathy and chronic discogenic pain are the result of this degenerative process.
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Protsakh, Nataliya. "Mixed problem for degenerate nonlinear ultraparabolic equation." Tatra Mountains Mathematical Publications 43, no. 1 (December 1, 2009): 203–14. http://dx.doi.org/10.2478/v10127-009-0038-1.
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Abstract This paper describes the solvability of mixed problem for nonlinear ultraparabolic equation with degeneration. The result is obtained in the cases of the weak and the strong degenerations. The conditions of solvability depend on the relations between the coefficients of the equation and the parameter of degeneration.
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Johansson, Kjell, and Camilla Mohlin. "Microglia in Cultured Porcine Retina: Qualitative Immunohistochemical Analyses of Reactive Microglia in the Outer Retina." International Journal of Molecular Sciences 24, no. 1 (January 3, 2023): 871. http://dx.doi.org/10.3390/ijms24010871.
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A late stage of several retinal disorders is retinal detachment, a complication that results in rapid photoreceptor degeneration and synaptic damages. Experimental retinal detachment in vivo is an invasive and complicated method performed on anesthetized animals. As retinal detachment may result in visual impairment and blindness, research is of fundamental importance for understanding degenerative processes. Both morphological and ethical issues make the porcine retina a favorable organotypic model for studies of the degenerative processes that follow retinal detachment. In the cultured retina, photoreceptor degeneration and synaptic injuries develop rapidly and correlate with resident microglial cells’ transition into a reactive phenotype. In this immunohistochemical study, we have begun to analyze the transition of subsets of reactive microglia which are known to localize close to the outer plexiform layer (OPL) in degenerating in vivo and in vitro retina. Biomarkers for reactive microglia included P2Ry12, CD63 and CD68 and the general microglial markers were CD11b, Iba1 and isolectin B4 (IB4). The reactive microglia markers labeled microglia subpopulations, suggesting that protective or harmful reactive microglia may be present simultaneously in the injured retina. Our findings support the usage of porcine retina cultures for studies of photoreceptor injuries related to retinal detachment.
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Draghi, Ferdinando, Chandra Bortolotto, Davide Renato Coscia, Mario Canepari, and Salvatore Gitto. "Magnetic resonance imaging of degenerative changes of the posterior cruciate ligament." Acta Radiologica 58, no. 3 (July 20, 2016): 338–43. http://dx.doi.org/10.1177/0284185116653280.
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Background Mucoid degeneration and ganglia reflect a continuum of degenerative changes within the posterior cruciate ligament (PCL). Purpose To assess the prevalence of and radiologists’ familiarity with PCL mucoid degeneration and ganglia. Material and Methods Knee magnetic resonance imaging (MRI) from July 2013 to June 2015, excluding patients who had a preceding trauma or MRI findings indicative of a prior injury, were retrospectively reviewed, with the specific request to assess degenerative changes of the PCL, by the same musculoskeletal radiologists who previously reported these examinations, and one fellow. Results A total of 692 patients entered this study. The radiologists and the fellow together identified mucoid degeneration in 34 patients (4.9%), ganglia in 14 patients (2.0%), and both in four patients (0.6%). Several patterns of PCL mucoid degeneration were identified: diffuse thickening in seven patients, partial thickening in 16 (four associated with a ganglion), longitudinal intraligamentous PCL signal-intensity abnormalities resembling a “tram track” in 15. In all cases there was increased signal intensity on fluid-sensitive sequences. In the previous reports, only three cases of PCL mucoid degeneration out of 38 (7.9%) were described, with intraligamentous PCL signal-intensity abnormalities. In the reports of the patients with degeneration and ganglia, only ganglia were described. In the previous reports, ganglia were correctly diagnosed. Conclusion Mucoid degeneration of the PCL is much more common than previously assumed and is underestimated by radiologists.
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Kitab, Sameer, Ghaith Habboub, Salam B. Abdulkareem, Muthanna B. Alimidhatti, and Edward Benzel. "Redefining lumbar spinal stenosis as a developmental syndrome: does age matter?" Journal of Neurosurgery: Spine 31, no. 3 (September 2019): 357–65. http://dx.doi.org/10.3171/2019.2.spine181383.
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OBJECTIVEAge is commonly thought to be a risk factor in defining lumbar spinal stenosis (LSS) degenerative or developmental subtypes. This article is a follow-up to a previous article (“Redefining Lumbar Spinal Stenosis as a Developmental Syndrome: An MRI-Based Multivariate Analysis of Findings in 709 Patients Throughout the 16- to 82-Year Age Spectrum”) that describes the radiological differences between developmental and degenerative types of LSS. MRI-based analysis of “degeneration” variables and spinal canal morphometric characteristics of LSS segments have been thought to correlate with age at presentation.METHODSThe authors performed a re-analysis of data from their previously reported prospective MRI-based study, stratifying data from the 709 cases into 3 age categories of equal size (instead of the original < 60 vs ≥ 60 years). Relative spinal canal dimensions, as well as radiological degenerative variables from L1 to S1, were analyzed across age groups in a multivariate mode. The total degenerative scale score (TDSS) for each lumbar segment from L1 to S1 was calculated for each patient. The relationships between age and qualitative stenosis grades, TDSS, disc degeneration, and facet degeneration were analyzed using Pearson’s product-moment correlation and multiple regression.RESULTSMultivariate analysis of TDSS and spinal canal dimensions revealed highly significant differences across the 3 age groups at L2–3 and L3–4 and a weaker, but still significant, association with changes at L5–S1. Age helped to explain only 9.6% and 12.2% of the variance in TDSS at L1–2 and L2–3, respectively, with a moderate positive correlation, and 7.8%, 1.2%, and 1.9% of the variance in TDSS at L3–4, L4–5, and L5–S1, respectively, with weak positive correlation. Age explained 24%, 26%, and 18.4% of the variance in lumbar intervertebral disc (LID) degeneration at L1–2, L2–3, and L3–4, respectively, while it explained only 6.2% and 7.2% of the variance of LID degeneration at L4–5 and L5–S1, respectively. Age explained only 2.5%, 4.0%, 1.2%, 0.8%, and 0.8% of the variance in facet degeneration at L1–2, L2–3, L3–4, L4–5, and L5–S1, respectively.CONCLUSIONSAge at presentation correlated weakly with degeneration variables and spinal canal morphometries in LSS segments. Age correlated with upper lumbar segment (L1–4) degeneration more than with lower segment (L4–S1) degeneration. The actual chronological age of the patients did not significantly correlate with the extent of degenerative pathology of the lumbar stenosis segments. These study results lend support for a developmental contribution to LSS.
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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.
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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.
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García-Ayuso, Diego, Johnny Di Pierdomenico, Manuel Vidal-Sanz, and María P. Villegas-Pérez. "Retinal Ganglion Cell Death as a Late Remodeling Effect of Photoreceptor Degeneration." International Journal of Molecular Sciences 20, no. 18 (September 19, 2019): 4649. http://dx.doi.org/10.3390/ijms20184649.
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Inherited or acquired photoreceptor degenerations, one of the leading causes of irreversible blindness in the world, are a group of retinal disorders that initially affect rods and cones, situated in the outer retina. For many years it was assumed that these diseases did not spread to the inner retina. However, it is now known that photoreceptor loss leads to an unavoidable chain of events that cause neurovascular changes in the retina including migration of retinal pigment epithelium cells, formation of “subretinal vascular complexes”, vessel displacement, retinal ganglion cell (RGC) axonal strangulation by retinal vessels, axonal transport alteration and, ultimately, RGC death. These events are common to all photoreceptor degenerations regardless of the initial trigger and thus threaten the outcome of photoreceptor substitution as a therapeutic approach, because with a degenerating inner retina, the photoreceptor signal will not reach the brain. In conclusion, therapies should be applied early in the course of photoreceptor degeneration, before the remodeling process reaches the inner retina.
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Zou, Jun. "Selection of the Optimal Puncture Needle for Induction of a Rat Intervertebral Disc Degeneration Model." Pain Physician 4, no. 22;4 (July 11, 2019): 353–60. http://dx.doi.org/10.36076/ppj/2019.22.353.
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Background: The incidence of intervertebral disc (IVD) degeneration has increased in recent years. A simple, reliable, and reproducible animal model is critical for understanding the underlying mechanisms of IVD degeneration. The caudal discs of rats have been proposed as a common puncture model in which to induce IVD degeneration. However, there is still no consensus on the size of needle to be used. Objectives: The present study aimed to identify the appropriate needle size to establish an IVD degeneration model. Study Design: A randomized, experimental trial. Setting: Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, China. Methods: Validity was verified by magnetic resonance imaging (MRI) and histology. Results: From T2-weighted MRI imaging and histological examination, the IVD punctured by the 16-gauge needle degenerated acutely one week after the operation, whereas the 26-gauge needle puncture did no harm to the IVD. An 18-gauge needle showed a progressive degeneration in IVD. Limitations: The observation period was not very long (4 weeks). Conclusions: An 18-gauge needle can be used to induce IVD degeneration in rats. Therefore, an 18-gauge needle is the optimal selection to establish the degenerative IVD model on rats, whereas the 26-gauge needle failed to cause IVD degeneration. Thus, to study the prevention and treatment of IVD degeneration, a 26-gauge needle can be used for IVD injection of growth factors, plasmids, and drugs. A 16-gauge needle may be used to induce acute disc injury, but not IVD degeneration. Key words: Low back pain, degenerative intervertebral disc, animal model, puncture needle, rat model, optimal choice
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Song, Sang Jun, Kyoung Ho Yoon, and Cheol Hee Park. "Patellofemoral Cartilage Degeneration After Closed- and Open-Wedge High Tibial Osteotomy With Large Alignment Correction." American Journal of Sports Medicine 48, no. 11 (August 7, 2020): 2718–25. http://dx.doi.org/10.1177/0363546520943872.
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Background: Previous studies have reported patellofemoral cartilage degeneration and analyzed the factors affecting degeneration after open-wedge high tibial osteotomy (OWHTO). However, no studies have evaluated patellofemoral cartilage degeneration or examined the factors affecting degeneration after closed-wedge high tibial osteotomy (CWHTO). Purpose: To investigate and compare patellofemoral cartilage degeneration after CWHTO and OWHTO via arthroscopic evaluation and to analyze the factors affecting the degeneration. Study Design: Cohort study; Level of evidence, 3. Methods: A total of 54 CWHTOs and 50 OWHTOs were performed with first-look arthroscopy between 2013 and 2017 at one institution. Hardware removal and second-look arthroscopy were performed, on average, 30.2 months after CWHTO and 26.8 months after OWHTO ( P = .178). Patient characteristics did not differ significantly between the groups. Radiographically, the mechanical axis, posterior tibial slope, and modified Blackburne-Peel ratio were evaluated. Arthroscopically, the percentage of patient with patellofemoral cartilage degeneration was evaluated according to the International Cartilage Repair Society grading system. Logistic regression analysis was used to identify the factors affecting patellofemoral cartilage degeneration in terms of demographics and the change of mechanical axis (correction angle), tibial posterior slope angle, and modified Blackburne-Peel ratio. The Anterior Knee Pain Scale was used for clinical comparison between the patellofemoral degenerative and nondegenerative groups. Results: No significant differences were observed in pre- and postoperative radiographic results between the CWHTO and OWHTO groups, except that the postoperative modified Blackburne-Peel ratio was significantly smaller among the OWHTOs. The percentage of patients with patellofemoral cartilage degeneration were 29.6% in the CWHTO group and 44% in the OWHTO group ( P = .156) at second-look arthroscopy. The correction angle was the only significant factor affecting cartilage degeneration in the CWHTO group (odds ratio, 2.324; P = .013; cutoff value, 9.6°) and the OWHTO group (odds ratio, 1.440; P = .041; cutoff value, 10.1°). The postoperative Anterior Knee Pain Scale score was significantly lower in the patellofemoral degenerative group as compared with the nondegenerative group among the OWHTO group (81.6 vs 76.4; P = .039); among the CWHTO group, there was a lower tendency in the degenerative group, but this was without significance (81.1 vs 79.6; P = .367). Conclusion: Patellofemoral cartilage degeneration progressed after CWHTO and OWHTO with large alignment correction. High tibial osteotomy should be selected with careful consideration of the osteoarthritic status of the patellofemoral joint and required correction angle, regardless of applying a closed- or open-wedge technique.
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Ding, Jun-zhe, Chao Kong, Xiang-yu Li, Xiang-yao Sun, Shi-bao Lu, and Guo-gunag Zhao. "Different degeneration patterns of paraspinal muscles in degenerative lumbar diseases: a MRI analysis of 154 patients." European Spine Journal 31, no. 3 (January 3, 2022): 764–73. http://dx.doi.org/10.1007/s00586-021-07053-2.
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Abstract Study design A retrospective study. Objective To evaluate the different degeneration patterns of paraspinal muscles in degenerative lumbar diseases and their correlation with lumbar spine degeneration severity. Summary of background data The degeneration characteristics of different paraspinal muscles in degenerative lumbar diseases remain unclear. Methods 78 patients diagnosed with single-level degenerative lumbar spondylolisthesis (DLS) and 76 patients with degenerative lumbar kyphosis (DLK) were included as DLS and DLK groups. Paraspinal muscle parameters of psoas major (PS), erector spinae (ES) and multifidus muscle (MF) were measured, including fatty infiltration (FI) and relative cross-sectional area (rCSA), namely the ratio of the paraspinal muscle CSA to the CSA of the vertebrae of the same segment. Sagittal parameters including lumbar lordosis (LL) and sagittal vertical axis (SVA) were measured. The paraspinal muscle parameters and ES/MF rCSA ratio were compared between the two groups. Paraspinal muscles parameters including rCSA and FI were also compared between each segments from L1 to L5 in both DLS and DLK groups. In order to determine the influence of sagittal spinal alignment on paraspinal muscle parameters, correlation analysis was conducted between the MF, ES, PS rCSA and FI and the LL in DLS and DLK group. Result MF atrophy is more significant in DLS patients compared with DLK. Also, MF fatty infiltration in the lower lumbar spine of DLS patients was greater compared to DLK patients. DLK patients showed more significant atrophy of ES and heavier ES fatty infiltration. MF FI was significantly different between all adjacent segments in both DLS and DLK groups. In DLS group, ES FI was significantly different between L2/L3 to L3/L4 and L4/L5 to L5/S1, while in DLK group, the difference of ES FI between all adjacent segments was not significant, and ES FI was found negatively correlated with LL. Conclusions Paraspinal muscles show different degeneration patterns in degenerative lumbar diseases. MF degeneration is segmental in both DLS and DLK patients, while ES degenerated diffusely in DLK patients and correlated with the severity of kyphosis. MF degeneration is more significant in the DLS group, while ES degeneration is more significant in DLK patients. MF is the stabilizer of the lumbar spine segments, while the ES tends to maintain the spinal sagittal balance.
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Yang, Xiaoxu, Yongjin Sun, Xu Li, and Wenzhi Zhang. "Rac1 regulates nucleus pulposus cell degeneration by activating the Wnt/β-catenin signaling pathway and promotes the progression of intervertebral disc degeneration." American Journal of Physiology-Cell Physiology 322, no. 3 (March 1, 2022): C496—C507. http://dx.doi.org/10.1152/ajpcell.00355.2021.
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Nucleus pulposus cell (NPC) dysfunction is considered as an important event related to intervertebral disc degeneration (IVDD). In the present study, tandem mass spectrometry (TMT) was used to detect total protein expression of nucleus pulposus (NP) in patients with IVDD and healthy controls. Bioinformatic analysis was performed to identify differentially expressed proteins that may be involved in the degeneration of NP. The results show that Rac1 may be a key protein involved in the degeneration of NP via Wnt/β-catenin pathway activation. We investigated the influence of Rac1 on IVDD degeneration and associated mechanisms. Rac1 expression increased in interleukin (IL)-1β-stimulated human NPCs, consistent with the results of TMT. The Rac1 inhibitor NSC23766 alleviated the degeneration of NPCs in vitro. Furthermore, Rac1 activated Wnt/β-catenin signaling, and the inhibition of this pathway significantly ameliorated the Rac1-mediated degenerative phenotype. NSC23766 exerted protective effects on IVDD in a puncture rat model. Taken together, these data suggest that Rac1 inhibition can delay NPC degeneration, probably through the regulation of the Wnt/β-catenin pathway. This study has the potential to advance understanding of the mechanism of occurrence of degenerative NP tissues and to provide novel strategies for slowing IVDD progression.
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Song, Weihua, Ifeyinwa Asuzu, and Jocelyn Villanueva. "Parasitic Leiomyoma After Laparoscopic Total Hysterectomy and Bilateral Salpingo-Oophorectomy, a Mimicker of Pelvic Neoplasm." American Journal of Clinical Pathology 152, Supplement_1 (September 11, 2019): S53—S54. http://dx.doi.org/10.1093/ajcp/aqz113.041.
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Abstract Parasitic leiomyomas are rare occurrences that may mimic malignancy and thus present a diagnostic dilemma. They are thought to arise from a pedunculated subserosal leiomyoma that undergoes torsion and detaches from the uterus, surviving by revascularization from adjacent structures, or from iatrogenic implantation during surgery, more common with the clinical popularity of laparoscopic surgery and power morcellation. We report a case of parasitic leiomyoma with degenerative changes in a 57-year-old female who was initially found to have a 6.5-cm left adnexal mass and multiple submucosal and intramural masses consistent with leiomyoma by abdominal pelvic computerized tomography test (CT) 7 years prior to presentation. She experienced severe abdominal discomfort that persisted after total abdominal hysterectomy and a 7.8-cm mass was found in the left pelvic cavity on reevaluation. Grossly, the pelvic mass was a 6.5-cm tan-gray ovoid firm mass with a 4.0-cm cystic cavity. The cut surfaces of the solid areas/cyst wall were gray-white and firm with focal yellow streaks. Microscopically, there was central cystic degeneration, with cyst wall showing extensive granulation tissue. The solid portion also showed extensive hyaline degeneration, fibrosis, and perinodular hydropic degeneration. Smooth muscle differentiation was evident at the periphery of the mass, confirmed by strong staining with desmin and smooth muscle actin. This represents a parasitic leiomyoma left behind following the first procedure and it developed degenerative changes. In addition to the high index of suspicion for malignancy in assessing adnexal masses, degenerating parasitic leiomyomas should be included in the differential diagnosis of such mass lesions.
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Hayashi, Tetsuo, Michael D. Daubs, Akinobu Suzuki, Trevor P. Scott, Kevin H. Phan, Monchai Ruangchainikom, Shinji Takahashi, Keiichiro Shiba, and Jeffrey C. Wang. "Motion characteristics and related factors of Modic changes in the lumbar spine." Journal of Neurosurgery: Spine 22, no. 5 (May 2015): 511–17. http://dx.doi.org/10.3171/2014.10.spine14496.
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OBJECT Most studies of Modic changes (MCs) have focused on investigating the relationship between MCs and lowback pain, whereas the kinematic characteristics and degenerative disc disease associated with MCs are not well understood. To the authors' knowledge, no previous study has reported on the kinematics of MCs. The purpose of this study was to elucidate the relationship of MCs to segmental motion and degenerative disc disease. METHODS Four hundred fifty symptomatic patients underwent weight-bearing lumbar kinematic MRI in the neutral, flexion, and extension positions. Segmental displacement and intervertebral angles were measured in 3 positions using computer analysis software. Modic changes, disc degeneration, disc bulging, spondylolisthesis, angular motion, and translational motion were recorded, and the relationship of MCs to these factors was analyzed using a logistic regression model. To control the influence of disc degeneration on segmental motion, angular and translational motion were analyzed according to mild and severe disc degeneration stages. The motion characteristics and disc degeneration among types of MCs were also evaluated. RESULTS Multivariate analysis revealed that age, disc degeneration, angular motion, and translational motion were factors significantly related to MCs. In the severe disc degeneration stage, a significant decrease of angular motion and significant increase of translational motion were found in segments with MCs, indicating that a disorder of the endplate had an additional effect on segmental motion. Disc degeneration increased and angular motion decreased significantly and gradually as the type of MC increased. Translational motion was significantly increased with Type 2 MCs. CONCLUSIONS Age, disc degeneration, angular motion, and translational motion were significantly linked to MCs in the lumbar spine. The translational motion of lumbar segments increased with Type 2 MCs, whereas angular motion decreased as the type of MC increased, indicating that Type 2 MCs may have translational instability likely due to degenerative changes. A disorder of the endplates could play an important role in spinal instability.
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Yamashita, Haruhiro, Mark J. Hoenerhoff, Shyamal D. Peddada, Robert C. Sills, and Arun R. Pandiri. "Chemical Exacerbation of Light-induced Retinal Degeneration in F344/N Rats in National Toxicology Program Rodent Bioassays." Toxicologic Pathology 44, no. 6 (July 11, 2016): 892–903. http://dx.doi.org/10.1177/0192623316650050.
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Retinal degeneration due to chronic ambient light exposure is a common spontaneous age-related finding in albino rats, but it can also be related to exposures associated with environmental chemicals and drugs. Typically, light-induced retinal degeneration has a central/hemispherical localization whereas chemical-induced retinal degeneration has a diffuse localization. This study was conducted to identify and characterize treatment-related retinal degeneration in National Toxicology Program rodent bioassays. A total of 3 chronic bioassays in F344/N rats (but not in B6C3F1/N mice) were identified that had treatment-related increases in retinal degeneration (kava kava extract, acrylamide, and leucomalachite green). A retrospective light microscopic evaluation of the retinas from rats in these 3 studies showed a dose-related increase in the frequencies of retinal degeneration, beginning with the loss of photoreceptor cells, followed by the inner nuclear layer cells. These dose-related increased frequencies of degenerative retinal lesions localized within the central/hemispherical region are suggestive of exacerbation of light-induced retinal degeneration.
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Wang, Jing, Qiwei Zhai, Ying Chen, Estelle Lin, Wei Gu, Michael W. McBurney, and Zhigang He. "A local mechanism mediates NAD-dependent protection of axon degeneration." Journal of Cell Biology 170, no. 3 (July 25, 2005): 349–55. http://dx.doi.org/10.1083/jcb.200504028.
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Axon degeneration occurs frequently in neurodegenerative diseases and peripheral neuropathies. Important insight into the mechanisms of axon degeneration arose from findings that the degeneration of transected axons is delayed in Wallerian degeneration slow (Wlds) mice with the overexpression of a fusion protein with the nicotinamide adenine dinucleotide (NAD) synthetic enzyme, nicotinamide mononucleotide adenylyltransferase (Nmnat1). Although both Wlds and Nmnat1 themselves are functional in preventing axon degeneration in neuronal cultures, the underlying mechanism for Nmnat1- and NAD-mediated axon protection remains largely unclear. We demonstrate that NAD levels decrease in degenerating axons and that preventing this axonal NAD decline efficiently protects axons from degeneration. In support of a local protective mechanism, we show that the degeneration of axonal segments that have been separated from their soma could be prevented by the exogenous application of NAD or its precursor nicotinamide. Furthermore, we provide evidence that such Nmnat1/NAD-mediated protection is primarily mediated by their effects on local bioenergetics. Together, our results suggest a novel molecular pathway for axon degeneration.
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Al-Abbasi, Maan, Abdal-Jabbar Falih Al-Rubai, and Mohammed Hussein Assi. "Quantification of the Water Content of Human Intervertebral Discs in Various Regions and Conditions." Al-Rafidain Journal of Medical Sciences ( ISSN 2789-3219 ) 6, no. 2 (April 22, 2024): 43–47. http://dx.doi.org/10.54133/ajms.v6i2.715.
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Background: Intervertebral disc (IVD) water is a basic factor for modeling tissue growth and nutritional diffusion and its amount is directly related to the development of degenerative processes. Objective: direct assessment of human IVD water contents in different disc regions in correlation to age and disc degeneration processes. Methods: 103 IVD samples that were taken from 30 cadavers underwent a lyophilization process to assess their water contents. The results were tabulated and tested statistically in relation to different parameters, including gender, age, spinal level and degeneration grading. Results: This study reveals that the water content was significantly lower in the group whose age was more than the median age (83 years) when compared with the group whose age was less than the median age. Additionally, the study shows that the water content is dramatically and significantly reduced in individuals who have degenerative changes. Conclusions: The water content of the intervertebral disc directly correlates with age and the degeneration process, decreasing as age and degeneration progress.
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Caminos, Elena, Susana López-López, and Juan R. Martinez-Galan. "Selective Assembly of TRPC Channels in the Rat Retina during Photoreceptor Degeneration." International Journal of Molecular Sciences 25, no. 13 (June 30, 2024): 7251. http://dx.doi.org/10.3390/ijms25137251.
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Transient receptor potential canonical (TRPC) channels are calcium channels with diverse expression profiles and physiological implications in the retina. Neurons and glial cells of rat retinas with photoreceptor degeneration caused by retinitis pigmentosa (RP) exhibit basal calcium levels that are above those detected in healthy retinas. Inner retinal cells are the last to degenerate and are responsible for maintaining the activity of the visual cortex, even after complete loss of photoreceptors. We considered the possibility that TRPC1 and TRPC5 channels might be associated with both the high calcium levels and the delay in inner retinal degeneration. TRPC1 is known to mediate protective effects in neurodegenerative processes while TRPC5 promotes cell death. In order to comprehend the implications of these channels in RP, the co-localization and subsequent physical interaction between TRPC1 and TRPC5 in healthy retina (Sprague-Dawley rats) and degenerating (P23H-1, a model of RP) retina were detected by immunofluorescence and proximity ligation assays. There was an overlapping signal in the innermost retina of all animals where TRPC1 and TRPC5 physically interacted. This interaction increased significantly as photoreceptor loss progressed. Both channels function as TRPC1/5 heteromers in the healthy and damaged retina, with a marked function of TRPC1 in response to retinal degenerative mechanisms. Furthermore, our findings support that TRPC5 channels also function in partnership with STIM1 in Müller and retinal ganglion cells. These results suggest that an increase in TRPC1/5 heteromers may contribute to the slowing of the degeneration of the inner retina during the outer retinal degeneration.
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Koroth, Jinsha, Erick O. Buko, Rebecca Abbott, Casey P. Johnson, Brenda M. Ogle, Laura S. Stone, Arin M. Ellingson, and Elizabeth W. Bradley. "Macrophages and Intervertebral Disc Degeneration." International Journal of Molecular Sciences 24, no. 2 (January 10, 2023): 1367. http://dx.doi.org/10.3390/ijms24021367.
Full textAbstract:
The intervertebral disc (IVD) aids in motion and acts to absorb energy transmitted to the spine. With little inherent regenerative capacity, degeneration of the intervertebral disc results in intervertebral disc disease, which contributes to low back pain and significant disability in many individuals. Increasing evidence suggests that IVD degeneration is a disease of the whole joint that is associated with significant inflammation. Moreover, studies show elevated macrophage accumulation within the IVD with increasing levels of disease severity; however, we still need to understand the roles, be they causative or consequential, of macrophages during the degenerative process. In this narrative review, we discuss hallmarks of IVD degeneration, showcase evidence of macrophage involvement during disc degeneration, and explore burgeoning research aimed at understanding the molecular pathways regulating macrophage functions during intervertebral disc degeneration.
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Iskhakova, R. R., and F. R. Saifullina. "Ozone therapy in ophthalmology." Kazan medical journal 94, no. 4 (December 15, 2013): 510–16. http://dx.doi.org/10.17816/kmj1960.
Full textAbstract:
Currently, ozone therapy is a method of treatment used in various fields of medicine, e.g., in treatment of neuropathies, liver diseases, as well as in cosmetology, surgery, traumatology, obstetrics, gynecology, urology, cardiology, pulmonology, gastroenterology, neurology, dentistry, otorhinolaryngology, ophthalmology. Recently, ozone therapy is increasingly used clinically as a complement to the classical treatment, which is contributed by the low cost and relative safety of the method. Ozone therapy as a modern and effective method of treatment continues to evolve, finding new areas of application, mechanisms of its action are being clarified, new techniques and new indications are offered. The main properties of ozone therapy are the stimulation of the antioxidant defense system, hypoxia reduction and metabolism activation, including carbohydrate and lipid metabolism, and improving blood circulation. Currently papers devoted to the application of ozone in ophthalmology in treatment of age-related macular degeneration, viral conjunctivitis and keratitis, corneal degenerations, purulent corneal ulcer, pigmentary retinal degeneration, optic neuritis and atrophy, degenerative changes of the choroid, high myopia, hemophthalmia, rhegmatogenous retinal detachment, diabetic retinopathy are known.
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Daly, Chris, Peter Ghosh, Graham Jenkin, David Oehme, and Tony Goldschlager. "A Review of Animal Models of Intervertebral Disc Degeneration: Pathophysiology, Regeneration, and Translation to the Clinic." BioMed Research International 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/5952165.
Full textAbstract:
Lower back pain is the leading cause of disability worldwide. Discogenic pain secondary to intervertebral disc degeneration is a significant cause of low back pain. Disc degeneration is a complex multifactorial process. Animal models are essential to furthering understanding of the degenerative process and testing potential therapies. The adult human lumbar intervertebral disc is characterized by the loss of notochordal cells, relatively large size, essentially avascular nature, and exposure to biomechanical stresses influenced by bipedalism. Animal models are compared with regard to the above characteristics. Numerous methods of inducing disc degeneration are reported. Broadly these can be considered under the categories of spontaneous degeneration, mechanical and structural models. The purpose of such animal models is to further our understanding and, ultimately, improve treatment of disc degeneration. The role of animal models of disc degeneration in translational research leading to clinical trials of novel cellular therapies is explored.
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Wang, Jack T., Zachary A. Medress, and Ben A. Barres. "Axon degeneration: Molecular mechanisms of a self-destruction pathway." Journal of Cell Biology 196, no. 1 (January 9, 2012): 7–18. http://dx.doi.org/10.1083/jcb.201108111.
Full textAbstract:
Axon degeneration is a characteristic event in many neurodegenerative conditions including stroke, glaucoma, and motor neuropathies. However, the molecular pathways that regulate this process remain unclear. Axon loss in chronic neurodegenerative diseases share many morphological features with those in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerve degeneration in both events, indicating a common mechanism of axonal self-destruction in traumatic injuries and degenerative diseases. A proposed model of axon degeneration is that nerve insults lead to impaired delivery or expression of a local axonal survival factor, which results in increased intra-axonal calcium levels and calcium-dependent cytoskeletal breakdown.
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Bisson, DG, M. Mannarino, R. Racine, and L. Haglund. "For whom the disc tolls: intervertebral disc degeneration, back pain and toll-like receptors." European Cells and Materials 41 (March 19, 2021): 355–69. http://dx.doi.org/10.22203/ecm.v041a23.
Full textAbstract:
Intervertebral disc (IVD) degeneration is characterised by catabolic and inflammatory processes that contribute largely to tissue degradation and chronic back pain. The disc cells are responsible for the pathological production of pro-inflammatory cytokines and catabolic enzymes leading to degeneration. However, this phenotypical change is poorly understood. Growing evidence in animal and human studies implicates Toll-like receptors (TLR) and their activation through danger-associated alarmins, found increasingly in degenerating IVDs. TLR signalling results in the release of pro-inflammatory cytokines and proteolytic enzymes that can directly cause IVD degeneration and back pain. This review aims to summarise the current literature on TLR activation in IVD degeneration and discuss potential treatment modalities to alleviate the inflammatory phenotype of disc cells in order to arrest IVD degeneration and back pain.
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Kang, Eugene Yu-Chuan, Pei-Kang Liu, Yao-Tseng Wen, Peter M. J. Quinn, Sarah R. Levi, Nan-Kai Wang, and Rong-Kung Tsai. "Role of Oxidative Stress in Ocular Diseases Associated with Retinal Ganglion Cells Degeneration." Antioxidants 10, no. 12 (December 5, 2021): 1948. http://dx.doi.org/10.3390/antiox10121948.
Full textAbstract:
Ocular diseases associated with retinal ganglion cell (RGC) degeneration is the most common neurodegenerative disorder that causes irreversible blindness worldwide. It is characterized by visual field defects and progressive optic nerve atrophy. The underlying pathophysiology and mechanisms of RGC degeneration in several ocular diseases remain largely unknown. RGCs are a population of central nervous system neurons, with their soma located in the retina and long axons that extend through the optic nerve to form distal terminals and connections in the brain. Because of this unique cytoarchitecture and highly compartmentalized energy demand, RGCs are highly mitochondrial-dependent for adenosine triphosphate (ATP) production. Recently, oxidative stress and mitochondrial dysfunction have been found to be the principal mechanisms in RGC degeneration as well as in other neurodegenerative disorders. Here, we review the role of oxidative stress in several ocular diseases associated with RGC degenerations, including glaucoma, hereditary optic atrophy, inflammatory optic neuritis, ischemic optic neuropathy, traumatic optic neuropathy, and drug toxicity. We also review experimental approaches using cell and animal models for research on the underlying mechanisms of RGC degeneration. Lastly, we discuss the application of antioxidants as a potential future therapy for the ocular diseases associated with RGC degenerations.
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Bhattachan, Kabin, Aruna Karki, Ganesh Dangal, Hema Kumari Pradhan, and Ranjana Shrestha. "Pedunculated Fibroid Mimicking an Ovarian Cancer." Nepal Journal of Obstetrics and Gynaecology 14, no. 1 (December 9, 2019): 56–58. http://dx.doi.org/10.3126/njog.v14i1.26630.
Full textAbstract:
Large myoma may show various type of degenerative change and have alteration of radiological view. Subserosal or pedunculated fibroid with cystic degeneration may mimic complex ovarian mass on radiological imaging. A 34 year female, para one, with normal menstrual period presented with radiological diagnosis of complex adnexal mass and CA 125 value 100 u/ml. Postoperative finding revealed cystic degeneration of pedunculated subserosal fibroid receiving blood supply from adherent omentum.
Keywords: Cystic degeneration, pedunculated fibroid, complex ovarian mass.
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Kaur, Geetika, and Nikhlesh K. Singh. "The Role of Inflammation in Retinal Neurodegeneration and Degenerative Diseases." International Journal of Molecular Sciences 23, no. 1 (December 30, 2021): 386. http://dx.doi.org/10.3390/ijms23010386.
Full textAbstract:
Retinal neurodegeneration is predominantly reported as the apoptosis or impaired function of the photoreceptors. Retinal degeneration is a major causative factor of irreversible vision loss leading to blindness. In recent years, retinal degenerative diseases have been investigated and many genes and genetic defects have been elucidated by many of the causative factors. An enormous amount of research has been performed to determine the pathogenesis of retinal degenerative conditions and to formulate the treatment modalities that are the critical requirements in this current scenario. Encouraging results have been obtained using gene therapy. We provide a narrative review of the various studies performed to date on the role of inflammation in human retinal degenerative diseases such as age-related macular degeneration, inherited retinal dystrophies, retinitis pigmentosa, Stargardt macular dystrophy, and Leber congenital amaurosis. In addition, we have highlighted the pivotal role of various inflammatory mechanisms in the progress of retinal degeneration. This review also offers an assessment of various therapeutic approaches, including gene-therapies and stem-cell-based therapies, for degenerative retinal diseases.