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Dissertations / Theses on the topic 'Choroidea'

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Published: 4 June 2021
Last updated: 1 February 2022

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1

Stumpf, Carmen. "Vergleichende Evaluation eines Weitwinkel Scanning-Laser-Verfahrens (Optomap) zur Darstellung pigmentierter Tumoren der Choroidea." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-172546.

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2

Stumpf, Carmen [Verfasser], and Aljoscha [Akademischer Betreuer] Neubauer. "Vergleichende Evaluation eines Weitwinkel Scanning-Laser-Verfahrens (Optomap) zur Darstellung pigmentierter Tumoren der Choroidea / Carmen Stumpf. Betreuer: Aljoscha Neubauer." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1055907718/34.

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3

Richert, Elisabeth [Verfasser]. "Wirkung schonender Laserverfahren auf den Komplex aus retinalem Pigmentepithel, Bruch´scher Membran und Choroidea - mögliche Therapieoption der frühen altersabhängigen Makuladegeneration / Elisabeth Richert." Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/1133074014/34.

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4

Hartmann, Daniel Michael. "Einsatz eines superfundierten Retina-RPE-Choroidea Präparats vom Haushuhn (Gallus domesticus) zur Untersuchung pharmakologischer Wirkungen mittels in vitro elektroretinographischer Erfassung (ERG und EOG) von okulären Funktionen." [S.l. : s.n.], 2004. http://www.bsz-bw.de/cgi-bin/xvms.cgi?SWB11679860.

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5

Hartmann, Daniel Michael [Verfasser]. "Einsatz eines superfundierten Retina-RPE-Choroidea-Präparats vom Haushuhn (Gallus domesticus) zur Untersuchung pharmakologischer Wirkungen mittels in-vitro-elektroretinographischer Erfassung (ERG und EOG) von okulären Funktionen / vorgelegt von Daniel Michael Hartmann." Tübingen, Stöcklestr. 22 : D. M. Hartmann, 2004. http://d-nb.info/973244127/34.

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6

JEANNEAU, PHILIPPE. "Les metastases choroidiennes : a propos de 18 cas." Toulouse 3, 1989. http://www.theses.fr/1989TOU31021.

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7

WEISSLINGER, JEAN-MARIE. "Contribution a l'etude des metastases choroidiennes : etude de 28 cas personnels." Lille 2, 1992. http://www.theses.fr/1992LIL2M177.

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8

TAVERNIER, LEMAN ANNICK. "Les membranes neovasculaires choroidiennes chez l'enfant." Lille 2, 1990. http://www.theses.fr/1990LIL2M036.

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9

Berglin, Lennart. "Choroidal neovascularization (CNV) : clinical and experimental aspects /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-284-1/.

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10

Balaggan, K. S. "Development of gene therapy for choroidal neovascularisation." Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1335615/.

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Exudative age-related macular degeneration, characterised by choroidal neovascularisation (CNV), is the leading cause of severe visual impairment in developed societies. Until recently, established treatments were of limited efficacy, and associated with other disadvantages including being inherently destructive therapies. Although novel anti-VEGF pharmacotherapy has since revolutionised the management and prognosis of many patients, current treatment regimens have distinct limitations, particularly in terms of the probable requirement for life-long, frequent invasive dosing, and associated cumulative medical, financial and logistical consequences. Furthermore, many patients respond suboptimally despite frequent administration. Continued development of superior therapies, therefore remains essential. Targeted angiostatic gene delivery may achieve many of the characteristics required of an ideal treatment modality. Work is presented which further expands the possibility of safe and efficacious retinal gene therapy by viral methods, for the ultimate intention of controlling human CNV. Proof of principle is demonstrated for in vivo intraocular expression from equine infectious anaemia virus-based vectors and non-integrating HIV-1-based vectors, which both represent significant advances in biosafety. The angiostatic efficacies of sFlt-1, endostatin, angiostatin and Pedf are then evaluated in an established murine laser model of CNV. This model is further optimised to quantify CNV-associated hyperpermeability in addition to CNV area. Lentiviral transfer of sFlt-1, endostatin or angiostatin, and Pedf upregulation by bespoke zinc finger transcription factors delivered by adeno-associated viral vectors potently inhibited angiogenesis, with sFlt-1, endostatin and angiostatin additionally inhibiting CNV-associated hyperpermeability. Finally, a novel angiogenic role of sonic hedgehog signalling in experimental CNV is identified, and its pharmacological inhibition demonstrated to be angiostatic. These results complement the current body of experimental evidence, which coupled with the demonstration of efficacious molecular targeting of angiogenic pathways in humans, support the further development of this technology to provide novel treatments which may be used as adjuncts or as superior alternatives to existing therapies.
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11

FASTRE, JEAN-CHRISTOPHE. "Angiome choroidien diffus : a propos d'un cas." Toulouse 3, 1991. http://www.theses.fr/1991TOU31006.

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12

Gardner, Dustin J. "Investigation of Myopic Periphery Affecting Choroidal Thickness." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1366286421.

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13

TISSERAND, GILLES. "Traitement des melanomes malins de la choroide par les protons : resultats sur les premiers patients traites a nice." Nice, 1993. http://www.theses.fr/1993NICE6511.

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14

LAFFON, DE MAZIERES MONTAUT FRANCOISE. "Metastases hepatiques des melanomes de l'uvee posterieure : a propos d'un cas de revelation tardive." Toulouse 3, 1989. http://www.theses.fr/1989TOU31085.

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15

ORTEGA, NICOLE. "Metastases viscerales tardives des melanomes choroidiens." Toulouse 3, 1989. http://www.theses.fr/1989TOU31237.

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16

COURET, BOUTONNET FRANCOISE. "Interet de la mesure de l'epaississement choroidien dans le devenir des globes oculaires traumatises." Toulouse 3, 1988. http://www.theses.fr/1988TOU31035.

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17

BERRIER, BONNET BERNADETTE. "Formes pseudo-tumorales des manifestations choroidiennes de la sarcoidose : a propos de deux observations personnelles, revue de la litterature." Lille 2, 1988. http://www.theses.fr/1988LIL2M270.

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18

PROUST, HELENE. "Etude experimentale sur les nouveaux lasers monochromatiques." Aix-Marseille 2, 1990. http://www.theses.fr/1990AIX20701.

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19

Panijel, Karine. "Les facteurs du pronostic vital du melanome choroidien apres enucleation." Université Louis Pasteur (Strasbourg) (1971-2008), 1989. http://www.theses.fr/1989STR1M038.

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20

Mäkitie, Teemu. "Prognostic indicators in choroidal and ciliary body melanoma." Helsinki : University of Helsinki, 2001. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/makitie/.

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21

Boonarpha, N. "Choroidal structure and function in chronic retinal diseases." Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3001786/.

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Introduction: The choroid plays an important role in maintaining retinal homeostasis. Changes in choroidal structure and a failure of choroidal autoregulation (the ability of a vascular bed to maintain blood flow despite changes in perfusion pressure) may have a great consequence in the pathogenesis of several chronic chorioretinal diseases including diabetic retinopathy (DR) and central serous chorioretinopathy (CSCR). Aim: The main aim of this thesis is to study the structure and function of the choroid and determine its role in the pathogenesis of DR and CSCR using enhanced depth imaging optical coherence tomography (EDI OCT) and laser Doppler flowmetry (LDF). Methods: A protocol for standardising the choroidal thickness (ChT) measurement using topographical appearances of the choroidal posterior boundary was developed and validated on EDI OCT images from healthy volunteers and patients with DR. Extensive experiments were performed in order to validate the hardware and software of the LDF device. Two controlled prospective studies were designed and performed; 1) Diabetic Retinopathy: Functional and Structural Study (DREFUS Study), and 2) Liverpool Central Serous Chorioretinopathy study (Liverpool CSCR Study). The DREFUS study involved diabetic patients with/without DR and healthy volunteers. DR patients were grouped using the presence or absence of clinically significant macular oedema (CSMO). The Liverpool CSCR study included patients presented with CSCR and healthy volunteers. For both of the studies the ChT was measured using a single horizontal EDI OCT scan while the choroidal blood flow (ChBFlow) parameters (choroidal blood volume [ChBVolume] and velocity [ChBVelocity]) were measured by using LDF. Isometric exercise was used to test choroidal autoregulation function. Mean arterial BP (MAP), ocular perfusion pressure (OPP) and change in choroidal vascular resistance were calculated to evaluate the choroidal autoregulation. In addition, best corrected visual acuity (BCVA), blood pressure (BP), colour fundus photography, fluorescein angiography (FA), and OCT were performed. Other tests including indocyanine green angiography (ICG), volumetric EDI OCT scans, microperimetry, intraocular pressure, and axial length were only performed by the CSCR study. Statistical analyses (correlation, t-test, ANOVA, ANCOVA, intraclass correlation coefficient [ICC], Fisher exact test, Mann-Whitney test) were performed as appropriate. Results: The standardised protocol for ChT measurement was produced. ICC for interobserver and intraobserver agreements on ChT measurements using of the protocol were 0.96 and 0.99 respectively for healthy eyes (n = 12) and 0.97 and 0.99 respectively for eyes with DR (n = 46). The mean subfoveal ChT (SfChT) was 304 µm (95% confidence interval (CI): 282 – 326) for patients with DR (N = 61). There were no significant differences in ChT between healthy eyes (N = 41; 351 µm (95% CI: 321 – 381)), diabetic eyes (N = 12; 299.9 µm (95% CI: 248.7 - 351.2) and eyes with DR (P >0.05). A statistically significant increase in ChBVelocity by 8% was observed following an increase of MAP by 18% in DR with CSMO. The mean SfChT of CSCR patients (N = 45) was 468.5 µm (95% CI: 437.1 – 499.9), approximately 30% thicker than in healthy eyes (N = 25; 361.4 µm (95% CI: 319.8 – 402.2) (P < 0.05). Hypertension was identified as the main risk factor affecting ChT in CSCR, particularly during the active stage of CSCR (normotensive CSCR: SfChT = 431 µm (95% CI: 378 – 485) vs hypertensive CSCR: SfChT = 521 µm (95% CI: 468 – 574): P < 0.05). An increase in OPP by 40% caused the ChT to increase significantly in CSCR patient (435.3 µm (95% CI: 378.2 - 492.4) at baseline vs 446.3 µm (95% CI: 393.4 - 499.2) at the end of exercise; P < 0.05). An increase of OPP by 31% caused significant change in ChBVolume in CSCR patients compared to healthy eyes (P = 0.03). Changes in ChBVolume in CSCR patients were negatively correlated with changes in choroidal vascular resistance (r = -0.83, P < 0.05). Conclusions: In patients with diabetes, no significant changes in the ChT were observed in any group of DR patients. ChBVelocity regulation was impaired in patients with severe DR. These findings suggest that functional changes of the choroid may occur well before the structural changes in patients with DR. In CSCR patients, increases in ChT and choroidal volume were observed in all CSCR phenotypes and also related with hypertension and the area of choroidal vascular hyperpermeability seen on ICG. The disruption of the regulation of choroidal structure and function was observed during isometric exercise in CSCR patients. These findings highlight the significance of choroidal regulation in the pathogenesis of DR and CSCR.
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22

Caillaud, Anne. "Le melanome de la choroide juxta-papillaire dans sa forme nodulaire avec extension au nerf optique : a propos de deux observations." Clermont-Ferrand 1, 1993. http://www.theses.fr/1993CLF11002.

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23

Ceschia, Charles. "Mélanome malin choroi͏̈dien et traitements actuels." Montpellier 1, 1998. http://www.theses.fr/1998MON11056.

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24

Kuhne, Francois. "Tumeurs choroïdiennes et imagerie par résonance magnétique." Bordeaux 2, 1988. http://www.theses.fr/1988BOR25277.

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25

BLONDEAU, ARMELLE. "Microcephalie et lacunes chorioretiniennes." Lille 2, 1994. http://www.theses.fr/1994LIL2M091.

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26

Sérot, Jean-Marie Faure Gilbert. "Plexus choroides et maladie d'Alzheimer : Immunologie d'une interface épithéliale (Doctorat : neurosciences et comportement)." [S.l.] : [s.n.], 2000. http://www.scd.uhp-nancy.fr/docnum/SCD_T_2000_0307_SEROT.pdf.

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27

Skeie, Jessica Marie. "Choroidal endothelial cell activation in age-related macular degeneration." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/602.

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Age-related macular degeneration (AMD) is a devastating ocular disease affecting one third of the elderly population in the western world. Some cases of AMD develop neovascular membranes, which are characterized by the pathologic growth of new blood vessels into the retina. This pathology may be initiated by proteins capable of activating endothelial cells to become angiogenic or inflammatory, later causing them to grow abnormally. This investigation aimed to determine the causes of pathologic blood vessel growth in AMD. Human eyes with AMD have been shown by us and others to have abnormal activities of angiogenin, complement component C5 anaphylatoxin (C5a), and/or elastin fragments. We therefore employed methods including PCR, immunoblotting, immunohistochemistry, morphometrics, tissue culture, ultrastructural observations, and functional assays to determine the effects angiogenin, C5a, and elastin fragments on the angiogenic and inflammatory changes of choroidal endothelial cells in vitro and in vivo. It was shown that choroidal endothelial cells express the surface receptor for C5a. Also, these cells increase their expression of ICAM-1, a surface protein that mediates leukocyte trafficking, in response to elevated levels of C5a in organ culture. This indicates that increased levels of C5a associated with AMD increase the inflammatory behavior of choroidal endothelial cells. It was demonstrated that choroidal endothelial cells are able to internalize angiogenin, a potent inducer of angiogenesis. Although cells from the choroid did not increase their angiogenic responses to this protein, their ability to internalize it indicates that they may respond to it by a different mechanism. Elevated levels of elastin fragments, however, did increase the migratory response of choroidal endothelial cells in culture, which is a key event in angiogenesis. Elevated levels of elastin fragents also increased the amount of collagen IV deposition within Bruch's membrane in a mouse model. This is relevant to AMD pathology as deposits within Bruch's membrane are common manifestations associated with AMD. This body of work has provided new insights into the roles of angiogenin, C5a, and elastin fragments in activating choroidal endothelial cells to becoming inflammatory or angiogenic. These endothelial cell behaviors are common characteristics found in neovascular AMD. These new findings will help aid in the further understanding of the pathobiology of this disease in hopes to provide improved treatments in the future.
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28

Wolfe, Jeremy Dean. "Vessel Formation and Feeder Vessel Treatment in Choroidal Neovascularization." University of Toledo Health Science Campus / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=mco1095878383.

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29

PEZET, CORTIAL GHISLAINE. "Effets des radiations ionisantes sur le melanome malin de la choroide : a propos de trois yeux enuclees apres curitherapie." Clermont-Ferrand 1, 1988. http://www.theses.fr/1988CLF11048.

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30

BAUTE, BERNARD. "Complications du traitement conservateur des melanomes malins de la choroide par applicateurs scleraux de ruthenium et d'iridium : a propos de 84 cas." Lyon 1, 1988. http://www.theses.fr/1988LYO1M203.

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31

MOUTTE, AMICO MIREILLE. "Etude comparative de l'echographie et de la resonance magnetique nucleaire dans le diagnostic du melanome choroidien : a propos de 4 cas." Aix-Marseille 2, 1988. http://www.theses.fr/1988AIX20056.

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32

PLOEGAERTS, PHILIPPE. "Segment posterieur et radiations ionisantes : a propos de 36 cas de tumeur intra-oculaire traites par radiotherapie." Lille 2, 1991. http://www.theses.fr/1991LIL2M016.

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33

Tatar, Olcay. "Immunohistopathologic evaluation of choroidal neovascular membranes following verteporfin photodynamic therapy." München Verl. Dr. Hut, 2008. http://d-nb.info/988623897/04.

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34

Miyamoto, Hideki. "Effect of Focal X-ray Irradiation on Experimental Choroidal Neovascularization." Kyoto University, 1999. http://hdl.handle.net/2433/181752.

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35

Ivert, Lena. "Interactions between neural retina, retinal epithelium and choroid /." Stockholm : Section of ophthalmology and vision, Department of clinical neuroscience, Karolinska institutet, 2006. http://diss.kib.ki.se/2006/91-7140-797-9/.

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36

Duval, Pierre-André. "Apport de l'angiographie au vert d'indocyanine dans les chorioépithéliopathies non néovasculaires." Montpellier 1, 1996. http://www.theses.fr/1996MON11179.

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37

Lotery, Andrew John. "A clinical and molecular genetic study of central areolar choroidal dystrophy." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394467.

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38

Kamizuru, Hiroshi. "Monoclonal antibody-mediated drug targeting to choroidal neovascularization in the rat." Kyoto University, 2003. http://hdl.handle.net/2433/148716.

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39

Tanemura, Mai. "The role of estrogen and estrogen receptor β in choroidal neovascularization". Kyoto University, 2005. http://hdl.handle.net/2433/144767.

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40

LAFFINEUR, OLIVIER. "Le syndrome microcornee dystrophie choroido-retino-vitreenne, glaucome et cataracte." Lille 2, 1989. http://www.theses.fr/1989LIL2M372.

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41

Lee, Edward Chin Wang. "Optical frequency domain imaging of human retina and choroid." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/38556.

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Thesis (S.M.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 2006.<br>Includes bibliographical references (p. 81-87).<br>Optical coherence tomography (OCT) has emerged as a practical noninvasive technology for imaging the microstructure of the human eye in vivo. Using optical interferometry to spatially-resolve backreflections from within tissue, this high-resolution technique provides cross-sectional images of the anterior and posterior eye segments that had previously only been possible with histology. Current commercially-available OCT systems suffer limitations in speed and sensitivity, preventing them from effective screening of the retina and having a larger impact on the clinical environment. While other technological advances have addressed this problem, they are inadequate for imaging the choroid, which can be useful for evaluating choroidal disorders as well as early stages of retinal diseases. The objective of this thesis was to develop a new ophthalmic imaging method, termed optical frequency domain imaging (OFDI), to overcome these limitations. Preliminary imaging of the posterior segment of human eyes in vivo was performed to evaluate the utility of this instrument for comprehensive ophthalmic examination.<br>(cont.) The 1050-nm OFDI system developed for this thesis comprised a novel wavelength-swept laser that delivered 2.7 mW of average power at a sweep rate of 18.8 kHz, representing a two-order-of-magnitude improvement in speed over previously-demonstrated lasers in the 1050-nm range and below. The system, with an optical exposure level of 550 gW, achieved resolution of 10 gm in tissue and sensitivity of >92 dB over a depth range of 2.4 mm. Two healthy volunteers were imaged with the OFDI system, with 200,000 A-lines over 10.6 seconds in each imaging session. In comparison to results from a state-of-the-art spectral-domain OCT system, the OFDI system provided deeper penetration into the choroid. This thesis demonstrates OFDI's capability for comprehensive imaging of the human retina, optic disc, and choroid in vivo. The deep penetration power of the system enabled the first simultaneous visualization of retinal and choroidal vasculature without the exogenous dyes required by angiography. The combined capability for imaging microstructure and vasculature using a single instrument may be a significant factor influencing clinical acceptance of ophthalmic OFDI technology.<br>by Edward Chin Wang Lee.<br>S.M.
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42

Lobas, Mark Albert. "Novel roles for y-Protocadherins in the choroid plexus." Diss., University of Iowa, 2013. https://ir.uiowa.edu/etd/5017.

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Γ-protocadherins (Γ-Pcdhs) are important for neuronal development and regular nervous system patterning. Much of this work is based on the assumption that this family of 22 cadherin-like adhesion molecules acts in the manner of Roger Sperry's hypothesized "molecular code", with homophilic adhesion allowing neurons to find their proper neuronal partners during development. Therefore, most research has focused on the expression and roles of these adhesion molecules in neurons and glia. Although these molecules have been almost exclusively studied in neurons, there is evidence that Γ-Pcdhs are also expressed and play important roles in other cells. The work done for this thesis focuses on the roles of Γ-Pcdhs in the choroid plexus (CP), a brain epithelial tissue that produces the cerebrospinal fluid, as well as potential roles in neuro-immune interactions. The importance of the CP for proper nervous system development, maintenance, function, and neuro-immunosurveillance has largely been overlooked in the past. Prior to this research, the presence, let alone the function of Γ-Pcdhs in the CP was not documented. Here, we show that each epithelial cell of the CP expresses a subset of Γ-Pcdhs at high levels, and that restricted disruption of this gene family in the CP and in the adjacent ependymal epithelia of mice results in reduced cerebroventricular volume. Furthermore, we show that CP-restricted mutant mice have altered gene expression in the CP, including groups of genes associated with immune function and with TGFΒ signaling pathways, suggesting novel roles for the Γ-Pcdhs. Finally, we present preliminary data indicating that expression of the Γ-Pcdhs is up-regulated in the CP following an immune challenge (experimental autoimmune encephalomyelitis, a mouse model for multiple sclerosis) and that they are expressed in other non-neuronal tissues, which, like the CP, play roles in immunosurveillance.
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RIFFLART, DERUYTER GHISLAINE. "Comparaison des champs visuels centraux avant et apres photocoagulation au laser krypton des membranes neo-vasculaires dans la degenerescence maculaire liee a l'age." Amiens, 1990. http://www.theses.fr/1990AMIEM031.

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44

Terry, Louise. "An in vivo investigation of choroidal vasculature in age-related macular degeneration." Thesis, Cardiff University, 2017. http://orca.cf.ac.uk/107459/.

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Age-related macular degeneration (AMD) is the leading cause of visual impairment in the developed world. Whilst the pathogenesis is complex and not fully understood, changes to the choroidal vasculature in AMD have been demonstrated using histology. Advances in imaging technology, particularly long-wavelength optical coherence tomography (OCT), allow in vivo visualisation and investigation of this structure. The aim of this work is to determine whether changes to the choroidal vasculature are detectable in AMD using in vivo imaging. This was achieved through the evaluation of parameters for quantifying the structure, and the application of a machine learning approach to automated disease severity classification, based on choroidal appearance. Participants with early AMD (n=25), neovascular AMD (nAMD; n=25), and healthy controls (n=25) underwent imaging with a non-commercial long-wavelength (λc=1040 nm) OCT device. Subfoveal choroidal thickness, choroidal area, and luminal area were significantly lower in the nAMD group than the healthy and early AMD groups, whilst vessel ratio was significantly greater (P < 0.05 in all cases). There was no significant difference in visible vessel diameter, choroidal vascularity index, luminal area ratio, or luminal perimeter ratio between the groups. No significant differences were found between the healthy and early AMD groups for any of the eight vascular parameters assessed. Classification of the disease groups based on choroidal OCT images was demonstrated using machine learning techniques. Textural features within the images were extracted using Gabor filters, and K-nearest neighbour, support vector machine, and random forest classifiers were assessed for this classification task. Textural changes were most pronounced in late-stage disease, although attribution to pathology or pharmacological intervention (anti-VEGF treatment) was not possible. Changes were also discernible in the early AMD group, suggesting sensitivity of this approach to detecting vascular involvement in early disease. In conclusion, structural changes to the choroidal vasculature in AMD are detectable in vivo using OCT imaging, demonstrated with both manual and automated analysis techniques. Whilst changes were most prominent in late-stage disease, subtle structural changes in early AMD were identified with texture analysis, warranting further investigation to improve our understanding of choroidal involvement in the pathogenesis of early AMD.
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Sandinha, Teresa. "Prognostic assessment of choroidal melanoma based on interphase cytogenetics and pathological features." Thesis, University of Glasgow, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.437993.

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46

Boassa, Daniela. "Functional properties of aquaporin-1 ion channels in choroid plexus." Diss., The University of Arizona, 2004. http://hdl.handle.net/10150/280588.

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Aquaporins (also known as water channels) are members of the Major Intrinsic Protein family. Ion channel function has been shown for several members of the aquaporin family and the related neurogenic gene product Big Brain. Aquaporin-1 (AQP1) is a transmembrane channel that mediates osmotically-driven water flux. Prior work demonstrated that AQP1 channels expressed in Xenopus oocytes mediate a cGMP-dependent cationic current. Based on amino acid sequence alignments with cyclic nucleotide-gated channels and cGMP-selective phosphodiesterases, I found that the efficacy of ion channel activation is decreased by mutations of AQP1 at conserved residues in the C-terminal domain (aspartate D237 and lysine K243). These data provide direct evidence for the involvement of the AQP1 carboxyl terminal domain in cGMP-mediated ion channel activation. Because the proportion of active AQP1 ion channels seen in heterologous expression systems is low, it was of fundamental importance to investigate the functional properties of this channel in a physiological context. Using rat choroid plexus, a brain tissue that secretes cerebral spinal fluid (CSF) and endogenously expresses abundant AQP1, I demonstrated the existence of native AQP1 ion channels that show properties similar to those described previously in the oocyte expression system. They mediate a cGMP-dependent cationic conductance, are blocked by cadmium, and show a single-channel conductance of 166 pS. Given the skull's rigidity, pathological increases in CSF secretion (tumors, hydrocephalus, stroke) can result in brain damage. In the choroid plexus several proteins work in concert to regulate CSF secretion. The findings presented in this dissertation are first to demonstrate that AQP1 mediates a cationic current in response to intracellular signals that regulate CSF secretion such as ANP signaling. Fluxes of water and Na⁺ across confluent choroid plexus cell monolayers showed a decreased flow rate following treatment with ANP, and Cd²⁺ reversed the inhibitory effect. These results suggest that activation and block of the AQP1-mediated ionic current may alter net fluid transport across the choroid plexus barrier, and therefore be physiologically relevant in the regulation of net fluid transport in choroid plexus. This places AQP1 as one of the important targets for clinical intervention in brain volume disorders.
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47

Patyal, Pankaj. "Expression of Aquaporins in Mouse Choroid Plexus and Ependymal Cells." Wright State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=wright1440892851.

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48

Hughes, Alexandra. "Mechanisms of volume regulation in murine choroid plexus epithelial cells." Thesis, University of Manchester, 2010. https://www.research.manchester.ac.uk/portal/en/theses/mechanisms-of-volume-regulation-in-murine-choroid-plexus-epithelial-cells(66cb068e-0e38-4773-83ca-a7867aaff66c).html.

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Abstract:
The choroid plexuses are largely responsible for cerebrospinal fluid (CSF) secretion and therefore play a fundamental role in brain homeostasis. The membrane proteins involved in CSF secretion are not fully known. Several electroneutral transporters have been identified by molecular methods in choroid plexus epithelial cells but there is a lack of functional data to support their expression making it impossible to elucidate their role in CSF secretion fully. The activity of many of these transporters can be observed in cell volume regulation. Thus, the main aim of the present study was to determine the ability of mammalian choroid plexus epithelial cells to regulate their volume in response to anisosmotic challenge and to investigate the transporters involved.Experiments were performed on cells isolated from the mouse fourth ventricle choroid plexus. Cells were isolated using a combination of manual perturbation, the enzyme dispase and a Ca2+ free incubation to disrupt tight junctions. Cell volume was measured using a video-imaging method. Cells used in this study were all of a similar morphology and had a mean volume of 0.71 pL.Cells exhibited a HCO3- dependent regulatory volume increase (RVI) in response to hypertonic challenge. Strong evidence is presented that the Na+/H+ exchanger (NHE1) and the Cl-/HCO3- exchanger (AE2) contribute to the RVI but the Na+K+2Cl- cotransporter (NKCC1) and the epithelial Na+ channel (ENaC) do not. Choroid plexus cells exhibit a HCO3- dependent regulatory volume decrease (RVD) in response to hypotonic challenge. The RVD was unaffected by DIOA (an inhibitor of KCC activity), the K+ channel inhibitors TEA+, Ba2+ or 4AP or the Cl- channel inhibitors DIDS or NPPB. However removal of extracellular Ca2+ completely abolished cell swelling in response to hypotonic challenge. This sensitivity of volume change to Ca2+ was specific to cell swelling as cell shrinkage in hypertonic artificial CSF was unaffected by removal of extracellular Ca2+.Thus functional evidence is presented to further elucidate the role of several proteins in the choroid plexus cell volume regulatory response to anisosmotic challenge.
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49

Worden, William Lamont. "Response of choroid and forehead blood flow to systemic phenylephrine infusion." [New Haven, Conn. : s.n.], 2007. http://ymtdl.med.yale.edu/theses/available/etd-08282007-153017/.

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50

Kieffer, Jean-Claude. "Le decollement de la choroide apres chirurgie chorio-retinienne : frequence, caracteres, pronostic, correlation avec la proliferation vitreo-retinienne." Université Louis Pasteur (Strasbourg) (1971-2008), 1986. http://www.theses.fr/1986STR1M187.

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