Dissertations / Theses on the topic 'The crystalline lens'
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Wang, Kai. "Involvement of O-glcnacylation in lens development and cataract formation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2010r/wang.pdf.
Full textKumar, Bharat. "The Mechanobiology of the Crystalline Lens." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1587649113548924.
Full textJones, Catherine Elizabeth. "Studies of the crystalline lens using magnetic resonance imaging." Queensland University of Technology, 2004. http://eprints.qut.edu.au/15950/.
Full textWilson, Cynthia Nicole. "A Fully Customizable Anatomically Correct Model of the Crystalline Lens." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20130.
Full textHott, John Lester. "Photochemical alterations of ocular lens proteins." Diss., Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/30087.
Full textO'Leary, Christine Marie. "Expression of the Ets family in the lens." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 2.78 Mb., 100 p, 2005. http://wwwlib.umi.com/dissertations/fullcit/1428194.
Full textRabie, E. P. "Biometry of the crystalline lens during accommodation." Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.378316.
Full textChen, Wen-Lung. "Raman spectroscopic/imaging studies of eye lenses and lens proteins." Diss., Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/30431.
Full textWalker, Marlon LeBrone. "Light scattering and light transmission studies of uv-induced protein crosslinking in separated lens crystallins and whole lenses." Diss., Georgia Institute of Technology, 1988. http://hdl.handle.net/1853/26245.
Full textWalker, Heather Mhairi. "Investigating the role of the lens in the growth and development of the vertebrate eye." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=225773.
Full textWang, Zaiqi. "Lens calcium homeostasis and selenite cataract." Diss., This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-05042006-164509/.
Full textBanks, Eric A. "Connexin 45.6 in lens development : a dissertation /." San Antonio : UTHSC, 2007. http://proquest.umi.com/pqdweb?did=1400957401&sid=1&Fmt=2&clientId=70986&RQT=309&VName=PQD.
Full textLi, Dongyun. "The effect of UV-laser radiation on lenses and lens proteins." Thesis, Georgia Institute of Technology, 1989. http://hdl.handle.net/1853/27271.
Full textHook, Darren W. A. "Protection of enzymes by the molecular chaperone #alpha#-Crystalline." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300133.
Full textTaube, Jennifer Remington. "Regulation of beta-B1 crystallin expression." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file 8.90 Mb., 227 p, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3200530.
Full textNeveling, Lauren Leigh. "Probing the kinetics of unfolding and aggregation of human gamma-D crystallin at low PH using Fourier transform infrared spectroscopy /." Connect to online version, 2007. http://ada.mtholyoke.edu/setr/websrc/pdfs/www/2007/212.pdf.
Full textHawse, John R. "Identification and functional characterization of cataract-specific gene expression changes reveals important pathways for human lens maintenance, aging and disease." Morgantown, W. Va. : [West Virginia University Libraries], 2004. https://etd.wvu.edu/etd/controller.jsp?moduleName=documentdata&jsp%5FetdId=3365.
Full textTitle from document title page. Document formatted into pages; contains x, 201 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 185-201).
Bergbauer, Katrina L. "Laser raman spectroscopic studies of ocular lens aging and cataractogenesis." Diss., Georgia Institute of Technology, 1991. http://hdl.handle.net/1853/30031.
Full textSchultz, Kristin E. "Accommodative microfluctuations, crystalline lens tension, ciliary body thickness, and refractive error in children." Columbus, Ohio : Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1240445960.
Full textGrant, Edwin Arthur. "Immuno-Labeling of Yes-associated Protein in the Crystalline Lens." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1460499774.
Full textTravers, Margaret J. "Structural correlates of shape change in the primate crystalline lens." Thesis, City University London, 1990. http://openaccess.city.ac.uk/7669/.
Full textBeck, Claire. "The characterisation of fluorescent proteins in the diabetic crystalline lens." Thesis, University of Warwick, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404870.
Full textKnight, Grady C. "The molecular chaperone α-crystallin protects proteins from UV-induced aggregation." Diss., Georgia Institute of Technology, 1999. http://hdl.handle.net/1853/30486.
Full textBarron, Brent Christian. "Characterization of normal aging and cataractous processes in the eye lens by laser raman spectroscopy." Diss., Georgia Institute of Technology, 1988. http://hdl.handle.net/1853/30052.
Full textLehman, Bret M. "Validation of Optical Coherence Tomography-Based Crystalline Lens Thickness Measurements in Children." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1242248244.
Full textKoivula, Annemari. "Long-term results of phakic refractive lenses for correction of myopia and hyperopia /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-424-2/.
Full textTuten, William Scott. "Anterior Segment Optical Coherence Tomography-Based Phakometry Measurements in Children." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1243629782.
Full textNisa, Georgette. "The prevalenceof anterior segment and crystalline lens changes in a Nicaraguan population." Thesis, Linnéuniversitetet, Institutionen för medicin och optometri (MEO), 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-54213.
Full textEckes, Melissa. "Shroom3 Localization and Apical Constriction during the Development of the Crystalline Lens in Mouse Embryos." The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492728223255337.
Full textNankivil, Derek. "A Second Generation Ex-Vivo Accommodation Simulator: Design and Calibration." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_theses/161.
Full textLi, Yi. "Cell proliferation as a biomarker of aging and effect of caloric restriction in mouse lens /." Thesis, Connect to this title online; UW restricted, 1997. http://hdl.handle.net/1773/6328.
Full textBorja, David. "Dynamic Optical Model of the Primate Crystalline Lens and Implications for the Restoration of Accommodation." Scholarly Repository, 2008. http://scholarlyrepository.miami.edu/oa_dissertations/355.
Full textParker, Nicole Renee. "The role of kynurenine and UV light in lens protein modification." Access electronically, 2005. http://www.library.uow.edu.au/adt-NWU/public/adt-NWU20060720.111305/index.html.
Full textTypescript. EMBARGOED - This thesis is subject to a 12 month embargo (07/03/06 to 07/03/07) and may only be viewed and copied with the permission of the author. For further information please Contact the Archivist. Includes bibliographical references: leaf 236-266.
Cheng, Man-hei. "The novel mouse [gamma]A-crystallin mutation leads to misfolded protein aggregate and cataract." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43572108.
Full textMichael, Ralph. "Development and repair of cataract induced by ultraviolet radiation /." Basel ; Stockholm : Karger, 2000. http://diss.kib.ki.se/2000/3-8055-7044-9/.
Full textChiu, Kin. "Immune modulation on retinal ganglion cell survival in experimental glaucoma." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40987693.
Full textMizdrak, Jasminka. "Human lens chemistry: UV filters and age-related nuclear cataract." Australia : Macquarie University, 2007. http://hdl.handle.net/1959.14/16855.
Full textThesis (PhD) -- Macquarie University, Division of Environmental and Life Sciences, Dept. of Chemistry and Biomolecular Sciences, 2007.
Bibliography: p. 243-277.
Introduction -- A convenient synthesis of 30HKG -- Facile synthesis of the UV filter compounds 30HKyn and AHBG -- Synthesis, identification and quantification of novel human lens metabolites -- Modification of bovine lens protein with UV filters and related metabolites -- Effect of UV light on UV filter-treated lens proteins -- Conclusions and future directions.
The kynurenine-based UV filters are unstable under physiological conditions and undergo side chain deamination, resulting in α,β-unsaturated carbonyl compounds. These compounds can react with free or protein bound nucleophiles in the lens via Michael addition. The key sites of the UV filters kynurenine (Kyn) and 3-hydroxykynurenine (3OHKyn) modification in human lenses include cysteine (Cys), and to a lesser extent, lysine (Lys) and histidine (His) residues. Recent in vivo studies have revealed that 3-hydroxykynurenine-O-β-D-glucoside (3OHKG) binds to Cys residues of lens crystallins in older normal human lenses. As a result of this binding, human lens proteins become progressively modified by UV filters in an age-dependent manner, contributing to changes that occur with the development of age-related nuclear (ARN) cataract. Upon exposure to UV light, free UV filters are poor photosensitisers, however the role of protein-bound species is less clear. It has been recently demonstrated that Kyn, when bound to lens proteins, becomes more susceptible to photo-oxidation by UV light. Therefore, the investigation of 3OHKG binding to lens proteins, and the effect of UV light on proteins modified with 3OHKG and 3OHKyn, were major aims of this study. As a result of the role of these compounds as UV filters and their possible involvement in ARN cataract formation, it is crucial to understand the nature, concentration and modes of action of the UV filters and their metabolites present in the human lenses. Therefore, an additional aim was to investigate human lenses for the presence of novel kynurenine-based human lens metabolites and examine their reactivity.--As 3OHKG is not commercially available, to conduct protein binding studies, an initial aim of this study was to synthesise 3OHKG (Chapter 2). Through the expansion and optimisation of a literature procedure, 3OHKG was successfully synthesised using commercially available and inexpensive reagents, and applying green chemistry principles, where toxic and corrosive reagents were replaced with benign reagents and solvent-free and microwave chemistry was used. A detailed investigation of different reaction conditions was also conducted, resulting in either the improvement of reaction yields or reaction time compared to the literature method. Applying the same synthetic strategy, and using key precursors from the synthesis of 3OHKG, the UV filters 3OHKyn and 4-(2-amino-3-hydroxyphenyl)-4-oxobutanoic acid-O-β-D-glucoside (AHBG), were also successfully synthesised (Chapter 3).
Chapter 4 describes the investigation of both normal and cataractous human lenses in an attempt to identify novel human lens metabolites derived from deaminated Kyn and 3OHKyn (Chapter 4, Part A). Initially, 4-(2-aminophenyl)-4-oxobutanoic acid (AHA), glutathionyl-kynurenine (GSH-Kyn), kynurenine yellow (Kyn yellow), 4-(2-amino-3-hydroxyphenyl)-4-oxobutanoic acid (AHB), glutathionyl-3-hydroxykynurenine (GSH-3OHKyn) and 3-hydroxykynurenine yellow (3OHKyn yellow) were synthesised and human lenses were examined for their presence. AHA and AHB were synthesised from similar precursors to those used in the synthesis of 3OHKG, while the GSH adducts and yellow compounds were synthesised from Kyn and 3OHKyn via base induced deamination. Following isolation and structural elucidation, AHA, AHB and GSH-Kyn were confirmed as novel human lens metabolites. They were quantified in low pmol/mg lens (dry mass) levels in normal and cataractous lenses of all ages, while GSH-3OHKyn, Kyn yellow and 3OHKyn yellow were not detected. In contrast to AHA, the lens metabolites AHB, GSH-Kyn and GSH-3OHKyn were found to be unstable at physiological pH. The spectral properties of these compounds suggest that they may act as UV filters. --Chapter 4 (Part B) also describes the identification and characterisation of a novel human lens UV filter, cysteinyl-3-hydroxykynurenine -O-β-D-glucoside (Cys-3OHKG). An authentic standard was synthesised via Michael addition of cysteine to deaminated 3OHKG. Cys-3OHKG was detected in low pmol/mg lens (dry mass) levels in normal lenses only after the 5th decade of life and was absent in cataractous lenses. Cys-3OHKG showed rapid decomposition at physiological pH.
Chapter 5 describes the identification and quantification of amino acids involved in covalent binding of 3OHKG to lens proteins. Model studies with bovine lens proteins and 3OHKG at pH 7.2 and 9.5 were undertaken. The amino acid adducts were identified via total synthesis and spectral analysis, and subsequently quantified upon acid hydrolysis of the modified lens proteins. Under both pH conditions, 3OHKG was found to react with lens proteins predominantly via Cys residues with low levels of binding also detected at Lys residues. Comparative studies with Kyn (pH 9.5) and 3OHKyn (pH 7.2 and 9.5) resulted in modified lens proteins at Cys residues, with only minor modification at Lys residues at pH 9.5. The extent of modification was found to be significantly higher at pH 9.5 in all cases. His adducts were not identified. 3OHKG-, Kyn- and 3OHKyn-modified lens proteins were found to be coloured and fluorescent, resembling those of aged and ARN cataractous lenses. In contrast, AHB and AHA, which can not form α,β-unsaturated carbonyl compounds, resulted in non-covalent modification of lens proteins. AHB may contribute to lens colouration and fluorescence as further reactions of this material yielded species that have similar characteristics to those identified from 3OHKyn modification. These species are postulated to arise via auto-oxidation of the o-aminophenol moiety present in both 3OHKyn and AHB.--In Chapter 6, the potential roles of 3OHKG and 3OHKyn, and the related species AHA and AHB, in generating reactive oxygen species and protein damage following illumination with UV light was examined. The UV filter compounds were examined in both their free and protein-bound forms. Kyn-modified proteins were used as a positive control. Exposure of these compounds to UV light (λ 305-385 nm) has been shown to generate H2O2 and protein-bound peroxides in a time-dependent manner, with shorter wavelengths generating more peroxides. The yields of peroxides were observed to be highly dependent on the nature of the UV filter compound and whether these species were free or protein bound, with much higher levels being detected with the bound species. Thus, protein-bound 3OHKyn yielded higher levels of peroxide than 3OHKG, with these levels, in turn, higher than for the free UV filter compounds. AHB-treated lens proteins resulted in formation of low but statistically significant levels of peroxides, while AHA-treated lens proteins resulted in insignificant peroxide formation. The consequences of these photochemical reactions have been examined by quantifying protein-bound tyrosine oxidation products (3,4-dihydroxyphenylalanine [DOPA], di-tyrosine [di-Tyr]) and protein cross-linking. 3OHKG-modified proteins gave elevated levels of di-Tyr, but not DOPA, whereas 3OHKyn-modified protein gave the inverse. DOPA formation was observed to be independent of illumination and most likely arose via o-aminophenol auto-oxidation. AHB- and AHA-treated lens proteins resulted in statistically insignificant di-Tyr formation, while a light independent increase in DOPA was observed for both samples. Both reducible (disulfide) and non-reducible cross-links were detected in modified proteins following illumination. These linkages were present at lower levels in modified, but non-illuminated proteins, and absent from unmodified protein samples.
This work has provided an optimised synthetic procedure for 3OHKG and other lens metabolites (Chapters 2 and 3). Four novel lens metabolites have been identified and quantified in normal and cataractous human lenses (Chapter 4). Subsequent experiments, described in Chapter 5, identified the major covalent binding sites of 3OHKG to lens proteins, while AHA and AHB showed non-covalent binding. Further work described in Chapter 6 showed that protein-bound 3OHKG, Kyn and 3OHKyn were better photosensitisers of oxidative damage than in their unbound state. Together, this research has provided strong evidence that post-translational modifications of lens proteins by kynurenine-based metabolites and their interaction with UV light appear, at least in part, responsible for the age-dependent colouration of human lenses and an elevated level of oxidative stress in older lenses. These processes may contribute to the progression of ARN cataract.
Mode of access: World Wide Web.
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Ruggeri, Marco. "Extended Depth Optical Coherence Tomography for Anterior Segment and Accommodation Imaging in Real-Time." Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/686.
Full textChandler, Heather Lynn. "Epithelial-mesenchymal transition in the anterior segment of the eye." Columbus, Ohio : Ohio State University, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1154533588.
Full textWejde, Gisela. "Posterior capsule opacification and postoperative endophthalmitis following cataract surgery : predictive and protective factors /." Stockholm : Karolinska institutet, 2005. http://diss.kib.ki.se/2005/91-7140-291-8/.
Full textCheng, Man-hei, and 鄭文熙. "The novel mouse [gamma]A-crystallin mutation leads to misfolded protein aggregate and cataract." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43572108.
Full textMeyer, David. "A critical appraisal of the etiology of adult human lenticular opacification and an investigation into the role of metabolic factors in its pathogenesis." Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52069.
Full textENGLISH ABSTRACT: The eye is that biological instrument which conveys the light of the external world into the inner world of the mind, wherein we receive the miraculous gift of vision. So precious is this gift, that Science must search for ways to keep this portal clear for the flow of light. Indeed, Science is called upon to “make war upon the bloody tyrant, Time.” (Shakespeare W. Sonnet No. 16). For, in the course of ageing, the lens grows cloudy and cataractous. In this battle between Science and Time, we are fortunate to live in an era in which Science is uncovering the molecular basis for the various obstacles to vision. The question arises, whether or not, the ruinous hand of time can be stayed. Due to unrelenting, progressive lens opacification, most of the elderly are destined to be subjected to loss of vision and with passage of time, even blindness. Globally the cataract surgery rate is inadequate to keep pace with the ever growing demand on financial and human resources created by the cataract problem. An immense challenge therefore is directed to primary eye care: “Can cataract be prevented or can its onset at least be postponed?” This laudable ultimate aim can only be achieved once the etiology of cataractogenesis is well understood. This dissertation seeks to examine two previously unrecognized etiological aspects that, if correctly understood and managed, have the potential to achieve preventive ophthalmological goals that may indeed help to stay the ‘ruinous hand of time’. The first aspect deals with the role of lipids and was examined using a study group of dyslipidemic subjects. The first part of the study concluded that dyslipidemic patients develop cortical lens opacities more frequently and at an earlier age than the normal population, and that cortical lens opacities should be regarded as one of the most reliable clinical signs of dyslipidemia. Furthermore, an extremely strong correlation was found to exist between low HDL Cholesterol levels and the development of opacities. Below a HDL-Cholesterol level of 1,5mmol/l, subjects had more than seven-fold higher risk of falling in the lens opacity subgroup than those with HDLCholesterol levels above 1,5mmol/l. An equally strong correlation was demonstrated between high (>5) LDLHDL ratios and the development of lens opacities. Subjects with a LDL:HDL-C ratio below 5 possessed a 2.35 times greater risk of having lenticular opacities than the group with a LDL:HDL-C ratio greater than 5. The prevention or retardation of dyslipidemia associated lens opacities is therefore possible, provided patients with a genetic predisposition are detected early and their blood lipids managed adequately. The second aspect deals with the relationship between age related cataracts and the acetylation status of the individual. This study compellingly submits that the slow acetylator pheno- and genotype may be regarded as a genetic indicator of risk for age related cataract. The ability accurately to classify a patient genotypically and phenotypically, may henceforth be useful in health counseling since, if an individual is identified as being a slow acetylator, additional preventative and precautionary measures may be taken, i.e. the prevention of UVexposure to the eye and caution with the ingestion of xenobiotics like caffeine, commercial dyes, food preservatives, and drugs. Furthermore, such a finding should be taken into account in the long term therapeutic management of glaucoma, with special regard to carbonic anhydrase inhibitors which are sulphonamide-related drugs and totally dependent on the N-acetyltransferase pathway for metabolism. These drugs may accumulate in the slow acetylator over time and exert toxic effects intra-ocularly, conceivably including cataractogenesis. The search for genetic and metabolic mechanisms that may contribute to human cataractogenesis should be pursued with great enthusiasm. This endeavour may help Science to achieve its primary objective, ablate the effects of Time and really aid in preventing cataracts in man.
AFRIKAANSE OPSOMMING: Die wondergawe van visie word vir ons moontlik gemaak deur die oog wat as biologiese instrument die lig van die buitewereld inlaat na die binnewereld van die brein. So kosbaar is hierdie gawe dat die Wetenskap deurgaans moet poog om die poort oop te hou. Inteendeel, die Wetenskap word gemaan deur Shakespeare in sy Sonnet nommer 16 om “oorlog te maak teen die bloeddorstige tiran, Tyd”. Soos ‘n mens ouer word, word die lens dof en ‘n katarak mag vorm. Ten spyte van hierdie stryd tussen ‘Wetenskap’ en ‘Tyd’ leef ons in die gelukkige era waarin die Wetenskap meer en meer leer van die verskeie obstruksies tot visie. Die vraag ontstaan of die rinnewerende hand van ‘Tyd’ gestuit sal kan word. Vanwee ongenaakbare, progressiewe lensvertroebeling is die meeste bejaardes bestem om aan visie verlies, en met verloop van tyd selfs blindheid, te ly. Die wereldwye katarakchirurgie tempo is nie voldoende om by te hou by die immergroeiende finansiele en mannekrag eise wat deur die katarak probleem gestel word nie. Daar word dus ‘n reuse uitdaging aan primere oogsorg gestel naamlik: “Kan katarakte nie eerder voorkom of die aanvang daarvan ten minste uitgestel word nie?” Hierdie prysenswaardige doelwit kan nie bereik word alvorens die etiologie van kataraktogenese goed verstaan word nie. Hierdie tesis ondersoek twee voorheen onerkende etiologiese aspekte wat, indien hulle korrek verstaan en hanteer word, beslis die potensiaal het om die gemelde voorkomende doelwitte te bereik en sekerlik te kan bydrae om die rinnewerende hand van Tyd te stuit. Die eerste aspek spreek die rol van lipiede aan deur te kyk na 'n studiegroep van dislipidemiese persone. Die eerste deel van die studie kom tot die gevolgtrekking dat dislipidemiese pasiente kortikale lens opasiteite meer dikwels en op ‘n vroeer ouderdom ontwikkel as die normale populasie en dat sulke opasiteite beskou moet word as een van die mees betroubare kliniese tekens van dislipidemie. Daar is ook ‘n baie sterk korrelasie gevind tussen lae HDL cholesterol vlakke en die voorkoms van opasiteite. Persone in die studie met ‘n HDL cholesterol vlak laer as 1,5mmol/l het ‘n sewe keer hoer kans gehad om in die lensopasiteit subgroep te val as die met ‘n HDL cholesterol vlak laer as 1,5mmol/l. ‘n Sterk korrelasie tussen ‘n hoe (>5) LDLHDL verhouding en die voorkoms van lens opasiteite is ook gevind. Persone met ‘n LDLHDL verhouding >5 het ‘n 2.35 maal groter risiko gehad om lensopasiteite te he as die met ‘n LDL:HDL verhouding van <5. Die voorkoming of vertraging van dislipiedemie geassosieerde lens opasiteite is dus moontlik, solank persone met ‘n genetiese geneigdheid daartoe vroeg ontdek en hulle bloedlipiede voldoende beheer word. Die tweede deel van die tesis handel oor die verhouding tussen ouderdoms verwante katarakte en die asetilasie status van die individu. Met oortuiging kom hierdie studie tot die gevolgtrekking dat die stadige asetilator fenoen genotipe as 'n genetiese merker vir ouderdoms verwante katarakte beskou moet word. Die vermoe om ‘n individu beide genotipies en fenotipies akkuraat te klassifiseer mag voorts bruikbaar wees in gesondheidsraadgewing. Indien ‘n individu geTdentifiseer is as ‘n stadige asetileerder, kan addisionele voorsorg maatreels getref word soos bv. die voorkoming van blootstelling van die oog aan UV lig sowel as omsigtigheid met die inname van xenobiotika soos kaffei'ene, kleurstowwe, voedsel preserveermiddels en geneesmiddels. Hierdie bevinding moet ook in berekening gebring word in die langtermyn terapeutiese hantering van gloukoom. Die koolsuuranhidrase inhibitore, dikwels gebruik in die behandeling van gloukoom, is sulfonamied-agtige middels en dus totaal afhanklik van die N-asetieltransferase pad vir hulle metabolisme. Hierdie middels kan ophoop in die stadige asetileerder en gegewe genoeg tyd, bes moontlik toksiese intra-okulere effekte tot gevolg he. Die soeke na genetiese en metaboliese meganismes wat mag bydra tot menslike kataraktogenese behoort nagestreef te word met groot entoesiasme. Hierdie strewe mag dalk net vir die 'Wetenskap' bystaan om sy primere mikpunt te bereik, die effek van ‘Tyd’ te neutraliseer en te help om katarakte werklik te voorkom.
Meyer, Linda Maren. "Cataract from ultraviolet radiation in the mouse /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-583-6/.
Full textChiu, Kin, and 趙健. "Immune modulation on retinal ganglion cell survival in experimental glaucoma." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40987693.
Full textOriowo, Olanrewaju Matthew. "A study of ultraviolet radiation effects on porcine crystalline lens and development of a new assay methodology for UV cataractogenesis investigation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0027/NQ51219.pdf.
Full textZhao, Haotian. "Exploring the role of fibroblast growth factor (FGF) signaling in mouse lens fiber differentiation through tissue-specific disruption of FGF receptor gene family." Connect to this title online, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1072722841.
Full textTitle from first page of PDF file. Document formatted into pages; contains xii, 203 p.; also includes graphics (some col.) Includes bibliographical references (p. 179-203). Available online via OhioLINK's ETD Center
Dong, Xiuqin. "Safety limit estimation for cataract induced by ultraviolet radiation /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-451-1/.
Full textSjödal, My. "Specification of the lens and olfactory placodes and dorsoventral patterning of the telencephalon /." Umeå : Univ, 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1347.
Full textD'Antin, Justin Christopher. "Lens capsule tissue culture for the investigation and prevention of posterior capsule opacification." Doctoral thesis, Universitat Autònoma de Barcelona, 2020. http://hdl.handle.net/10803/670465.
Full textLas cataratas son la principal causa de ceguera en el mundo y se deben a una opacificación progresiva del cristalino. Aunque las cataratas sean fáciles de tratar, en muchos casos la misma cirugía puede dar lugar a una segunda pérdida de la visión, conocida como opacificación de la cápsula posterior (OCP). La OCP se desarrolla debido a una combinación de la proliferación, migración y transdiferenciación de las células residuales que quedan en la cápsula del cristalino tras la cirugía de cataratas, lo que resulta en una pérdida progresiva de la visión. Hay muchos estudios sobre la prevención de la OCP, desde ajustes de las técnicas y materiales quirúrgicos, hasta tratamientos farmacológicos. Actualmente, la opción más efectiva es evitar mecánicamente que las células invadan el eje visual. A pesar de estos avances, la OCP y sigue siendo una complicación postquirúrgica que afecta a muchos pacientes. En esta tesis, hemos utilizado un modelo in vitro de tejido capsular para estudiar el desarrollo y la posible prevención de OCP. En nuestro primer estudio, simulamos la progresión natural de la OCP in vitro y posteriormente tratamos de prevenirla con diferentes sustancias. Sin embargo, a pesar de utilizar un tratamiento agresivo de peróxido de hidrógeno, se desarrolló OCP en la mitad de los casos. Esto destacó la impresionante resistencia de estas células y la dificultad de prevenir su desarrollo. En nuestro segundo estudio, muestras de OCP que se habían desarrollado in vivo, fueron comparadas con nuestras muestras in vitro anteriores para comprender mejor el desarrollo de la OCP. Concluimos que la OCP se debe al proceso fallido por parte de las células residuales de regenerar el cristalino. Esto nos hizo reevaluar nuestro enfoque sobre la prevención de la OCP. En lugar de estudiar distintas formas de prevenir el desarrollo de la OCP farmacológicamente, ahora pretendimos estudiar si las células pudieran regenerar un cristalino transparente. La idea de regenerar el cristalino no es nueva, pero solo se ha observado y estudiado en animales y bebés, nunca en humanos adultos. Con este nuevo objetivo en mente, primero queríamos estudiar si los casos avanzados de OCP desarrollan de forma natural tejido transparente, a pesar de parecer opaco cuando se observa clínicamente. Para hacer esto, extrajimos muestras avanzadas de OCP de tejido ocular de donantes ex vivo y las seccionamos gruesamente para analizarlas sagitalmente. Observamos que en la mayoría de los casos una porción significativa del tejido interno era transparente. Esto apoyó aún más nuestra idea de la regeneración del cristalino como una posible opción de tratamiento futuro. Finalmente, desarrollamos un nuevo modelo de cultivo in vitro que consideramos que favoreciera el desarrollo de células normales del cristalino en lugar de células fibróticas. Realizamos cambios en la preparación quirúrgica de las muestras para aumentaron el número inicial de células, reducir el estrés celular y mejorar el contacto entre las cápsulas anterior y posterior. Sin embargo, no logramos la regeneración del cristalino, pero disminuimos algunos factores relacionados con la OCP fibrótica. Esto resalta la complejidad de este nuevo enfoque. Esta tesis y la idea de la regeneración del cristalino como tratamiento abren muchas nuevas vías de estudio interesantes y tenemos toda la intención de continuar por este nuevo camino.
Cataracts are the world's leading cause of blindness and are due to a progressive opacification of the eye lens. Fortunately, cataracts are easy to treat, however in many cases surgery can lead to a secondary loss of vision, known as posterior capsule opacification (PCO). PCO develops due to a combination of the proliferation, migration, and transdifferentiation of residual lens cells left in the lens capsule, after cataract surgery, resulting in a progressive loss of vision. Many approaches for PCO prevention have been studied, from adjustments to surgical techniques and materials, to pharmacological treatment. Currently the most effective option is to mechanically prevent cells from invading the visual axis. Despite these advances, the development of PCO is still a common post-surgical complication that affects many patients. In this thesis, we used an in vitro lens capsule tissue model to study the development and possible prevention of PCO. In our first study, we simulated the natural progression of PCO in vitro and subsequently tried to prevent it with different substances. However, despite using an aggressive approach of hydrogen peroxide, PCO still developed in half of the cases. This highlighted the impressive resilience of these cells and why prevention is such a difficult task. In our second study, samples of PCO developed in vivo, were compared to our previous in vitro samples in order to better understand the development of PCO. We concluded that PCO is due to a failed attempt of the residual lens cells to regenerate the lens. This made us reevaluate our approach to PCO prevention. Instead of studying ways to prevent the development of PCO pharmacologically, we intended to study whether residual lens epithelial cells could regenerate a transparent lens. The idea of regenerating the lens isn't new, but it has only ever been observed and studied in animals and infants, never in human adults. With this new goal in mind, we first wanted to study whether advanced cases of PCO naturally developed any transparent tissue, despite appearing opaque when observed clinically. In order to do this, we extracted advanced PCO tissue samples from ex vivo donor eye globes and thickly sectioned them in order to analyze them sagittally. We observed that in most cases a significant portion of the inner tissue is transparent. This further supported our idea of adult lens regeneration as a possible future treatment option. Finally, we developed a new in vitro culture model that we believed would favor the development of normal lens cells instead of fibrotic cells. We made changes to the surgical preparation of the samples to increase residual lens cells, reduce the stress to these and improve the contact between the anterior and posterior capsules. However, lens regeneration was not achieved, but we did decrease some factors related to fibrotic PCO. This highlights the complexity of this new approach. This thesis and the idea of lens regeneration as a treatment option, opens up many new interesting avenues of study and we intend to continue along this new path.
Universitat Autònoma de Barcelona. Programa de Doctorat en Biologia Cel·lular
Long, Amy Carise. "Influence of environmental and chemical factors on cellular signaling in lens epithelial cells." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1186677862.
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