551 |
The Effect of Refractive Error and Light Exposure on Red and Blue Light-Driven Pupil ResponsesOrr, Danielle Jean 28 July 2017 (has links)
No description available.
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552 |
Variation of Ocular Parameters in Young Normal EyesPosvar, Winston Blair 30 August 2017 (has links)
No description available.
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553 |
An Analysis of Heat Shock Protein Production in Human Retinal Pigment Epithelial Cells After Different Stress-Induced StatesKrainz, Thomas Edward January 2018 (has links)
No description available.
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554 |
Computational Study of Stimulus-Induced Synchrony in the Cat RetinaAfghan, Muhammad K.N. January 2004 (has links)
No description available.
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555 |
Induction of vascular endothelial growth factor-A165a in human retinal and endothelial cells in response to glyoxalMorawietz, Henning, Frenzel, Annika, Mieting, Alic, Goettsch, Winfried, Valtink, Monika, Roehlecke, Cora, Jászai, József, Funk, Richard H. W., Becker, Klio A., Engelmann, Katrin 22 May 2024 (has links)
Low-density lipoprotein (LDL) apheresis is effective and safe for patients with diabetes, proteinuria, and dyslipidemia. Diabetes mellitus is accompanied by ocular microvascular complications like retinal neovascularization or diabetic macular edema. These are leading causes of blindness and can be mediated by abnormal vessel growth and increased vascular permeability due to elevated levels of vascular endothelial growth factor (VEGF) in diabetic patients. In this study, we established methods to study the expression of different VEGF isoforms in human retinal and endothelial cells. The VEGF-A165a isoform is much higher expressed in retinal cells, compared to endothelial cells. Stimulation with glyoxal as a model of oxidative stress under diabetic conditions lead to a pronounced induction of VEGF-A165a in human retinal and endothelial cells. These data suggest that diabetes and oxidative stress induce VEGF-A isoforms which could be relevant in regulating the ingrowths of novel blood vessels into the retina in diabetic patients.
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Novel molecular mechanisms of neuronal and vascular protection in experimental glaucomaAlmasieh, Mohammadali 04 1900 (has links)
Le glaucome est la deuxième cause de cécité irréversible dans le monde. La perte
de vision qui se produit lors du glaucome s’explique par une dégénérescence du nerf
optique et une mort progressive et sélective des cellules ganglionnaires de la rétine
(CRG). L'hypertension oculaire est un facteur de risque majeur dans le glaucome, mais
des défauts du champ visuel continuent à se développer chez un contingent de patients
malgré l'administration de médicaments qui abaissent la pression intraoculaire (PIO). Par
conséquent, bien que la PIO représente le seul facteur de risque modifiable dans le
développement du glaucome, son contrôle ne suffit pas à protéger les CRGs et préserver
la fonction visuelle chez de nombreux patients. Dans ce contexte, j'ai avancé l'hypothèse
centrale voulant que les stratégies de traitement du glaucome visant à promouvoir la
protection structurale et fonctionnelle des CRGs doivent agir sur les mécanismes
moléculaires qui conduisent à la mort des ces neurones.
Dans la première partie de ma thèse, j'ai caractérisé l'effet neuroprotecteur de la
galantamine, un inhibiteur de l'acétylcholinestérase qui est utilisé cliniquement dans le
traitement de la maladie d'Alzheimer. Cette étude s’est basée sur l'hypothèse que la
galantamine, en modulant l'activité du récepteur de l'acétylcholine, puisse améliorer la
survie des CRGs lors du glaucome. Nous avons utilisé un modèle expérimental bien
caractérisé d'hypertension oculaire induite par l’administration d'une solution saline
hypertonique dans une veine épisclérale de rats Brown Norway. Les résultats de cette
étude (Almasieh et al. Cell Death and Disease, 2010) ont démontré que l'administration
quotidienne de galantamine améliore de manière significative la survie des corps
cellulaires et des axones CRGs. La protection structurelle des CRGs s’accompagne d’une
préservation remarquable de la fonction visuelle, évaluée par l'enregistrement des
potentiels évoqués visuels (PEV) dans le collicule supérieur, la cible principale des CRGs
chez le rongeur. Une autre constatation intéressante de cette étude est la perte
substantielle de capillaires rétiniens et la réduction du débit sanguin associé à la perte des
CRGs dans le glaucome expérimental. Il est très intéressant que la galantamine ait
également favorisé la protection de la microvascularisation et amélioré le débit sanguin
rétinien des animaux glaucomateux (Almasieh et al. en préparation). J'ai notamment
démontré que les neuro-et vasoprotections médiées par la galantamine se produisent par
iv
l'activation des récepteurs muscariniques de l'acétylcholine.
Dans la deuxième partie de ma thèse, j'ai étudié le rôle du stress oxydatif ainsi que
l'utilisation de composés réducteurs pour tester l'hypothèse que le blocage d'une
augmentation de superoxyde puisse retarder la mort des CRG lors du glaucome
expérimental. J'ai profité d'un composé novateur, un antioxydant à base de phosphineborane
(PB1), pour tester sur son effet neuroprotecteur et examiner son mécanisme
d'action dans le glaucome expérimental. Les données démontrent que l'administration
intraoculaire de PB1 entraîne une protection significative des corps cellulaire et axones
des CRGs. Les voies moléculaires conduisant à la survie neuronale médiée par PB1 ont
été explorées en déterminant la cascade de signalisation apoptotique en cause. Les
résultats démontrent que la survie des CRGs médiée par PB1 ne dépend pas d’une
inhibition de signalisation de protéines kinases activées par le stress, y compris ASK1,
JNK ou p38. Par contre, PB1 induit une augmentation marquée des niveaux rétiniens de
BDNF et une activation en aval de la voie de survie des ERK1 / 2 (Almasieh et al.
Journal of Neurochemistry, 2011).
En conclusion, les résultats présentés dans cette thèse contribuent à une meilleure
compréhension des mécanismes pathologiques qui conduisent à la perte de CRGs dans le
glaucome et pourraient fournir des pistes pour la conception de nouvelles stratégies
neuroprotectrices et vasoprotectrices pour le traitement et la gestion de cette maladie. / Glaucoma is the second cause of irreversible blindness worldwide. Loss of vision
in glaucoma is accompanied by progressive optic nerve degeneration and selective loss of
retinal ganglion cells (RGCs). Ocular hypertension is a major risk factor in glaucoma, but
visual field defects continue to progress in a large group of patients despite the use of
drugs that lower intraocular pressure (IOP). Therefore, although IOP is the sole
modifiable risk factor in the development of glaucoma, its regulation is not sufficient to
protect RGCs and preserve visual function in many affected patients. To address this
issue, I put forward the central hypothesis that effective therapeutic strategies for
glaucoma must interfere with molecular mechanisms that lead to RGC death to
successfully promote structural and functional protection of these neurons.
In the first part of my thesis, I characterized the neuroprotective effect of
galantamine, an acetylcholinesterase inhibitor that is clinically used for the treatment of
Alzheimer’s disease. The specific hypothesis of this study was that galantamine, by
modulating acetylcholine receptor activity, can improve the survival of injured RGCs in
glaucoma. A well characterized experimental model of ocular hypertension induced by
administration of a hypertonic saline into an episcleral vein of Brown Norway rats was
used. The results of this study (Almasieh et al. Cell Death and Disease, 2010)
demonstrated that daily administration of galantamine significantly improved the survival
of RGC soma and axons in this model. Structural protection of RGCs correlated with
substantial preservation of visual function, assessed by recording visual evoked potentials
(VEPs) from the superior colliculus, the primary target of RGCs in the rodent brain. An
interesting finding during the course of my thesis was that there is a substantial loss of
retinal capillaries and a reduction in retinal blood that correlates with RGC loss in
experimental glaucoma. Interestingly, galantamine also promoted the protection of the
microvasculature and improved retinal blood flow in ocular hypertensive animals
(Almasieh et al. in preparation). Importantly, I demonstrated that galantamine-mediated
neuro- and vasoprotection occur through activation of muscarinic acetylcholine receptors.
In the second part of my thesis, I investigated the role of oxidative stress and the
use of reducing compounds to test the hypothesis that blockade of a superoxide burst may
delay RGC death in experimental glaucoma. I took advantage of a novel phosphinevi
borane based antioxidant compound available to us (PB1) to investigate its
neuroprotective effect and mechanism of action in experimental glaucoma. The data
demonstrate that intraocular administration of PB1 resulted in significant protection of
RGC soma and axons. I also explored the molecular pathways leading to PB1-mediated
neuronal survival by analyzing the components of survival and apoptotic signaling
pathways involved in this response. My results show that PB1-mediated RGC survival
did not correlate with inhibition of stress-activated protein kinase signaling, including
ASK1, JNK or p38. Instead, PB1 led to a striking increase in retinal BDNF levels and
downstream activation of the pro-survival ERK1/2 pathway (Almasieh et al. Journal of
Neurochemistry, 2011).
In conclusion, the findings presented in this thesis contribute to a better
understanding of the pathological mechanisms underlying RGC loss in glaucoma and
might provide insights into the design of novel neuroprotective and vasoprotective
strategies for the treatment and management of this disease.
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The relationship between retinal nerve fiber layer, visual function and vision-specific quality of life in multiple sclerosisBachir, Vanessa 06 1900 (has links)
La sclérose en plaques est une maladie dégénérative qui peut affecter la vision ainsi que différentes structures du système visuel afférent. La partie de l'oeil plus souvent affectée par la sclérose en plaques est le nerf optique, sous forme de névrite optique. Une technologie, nommée TCO (tomographie par cohérence optique), permet de prendre une image du nerf optique et de ses fibres nerveuses qui s'étendent sur la rétine. Dans cette thèse, la TCO a permis d’obtenir une épaisseur des fibres nerveuses autour du nerf optique, ainsi qu’une épaisseur totale de la macula et de la couche de cellules ganglionnaires chez les patients atteints de sclérose en plaques, avec et sans histoire de nérite optique, et chez un groupe de patients contrôle. Les résultats démontrent que seule l’épaisseur de la couche de cellules ganglionnaires permet de différentier les patients avec sclérose en plaques sans histoire de névrite optique des patients contrôle. Une deuxième étude a évalué la qualité visuelle en mesurant la sensibilité aux contrastes ainsi que la qualité de vie reliée à la vision avec un questionnaire de qualité de vie. Les résultats démontrent qu’une nouvelle charte de sensibilité aux contrastes, plus facile à administrer en clinique, permet aussi de différentier les patients sans névrite optique du groupe contrôle. De plus, la qualité de vie des patients ayant eu un épisode de névrite optique semble significativement affectée, même si le pronostic est considéré très favorable et que l’acuité visuelle est « bonne » suite à une névrite optique. En conclusion, l’utilisation de l’OCT en plus de mesures sensibles de fonction visuelle, telle la sensibilité aux contrastes, et de qualité de vié peuvent contribuer à mieux détecter des dysfonctions oculo-visuelles subtiles, mais importantes chez les patients atteints de sclérose en plaques. / Multiple sclerosis (MS) is the most common neurological condition causing disability in working-age adults. The hallmark of MS related disability is axonal loss. Through new technologies, such as optical coherence tomography (OCT), the retinal nerve fibre layer (RNFL), composed of ganglion cell axons, can be visualized and studied non-invasively in cross-section. Furthermore, recent OCT advances allow precise retinal layer segmentation and macular imaging of the ganglion cell layer. In this thesis, these different OCT parameters were measured to see which layers would be most affected in MS patients without previous optic neuritis. Results show that macular ganglion cell layer thickness is the only OCT parameter that can differentiate this sub-group of patients from healthy controls. Visual function was then assessed using a newly available, easy to use contrast sensitivity chart that can be self-administered by patients. Results show that this chart is also capable of differentiating MS patients without optic neuritis from controls, but usually gives better contrast sensitivity scores than the Mars chart. Lastly, vision-specific quality of life was assessed and proved to be reduced in MS patients with prior optic neuritis, despite supposed favorable recovery and good visual acuity in patients with this diagnosis. In sum, the use of OCT imaging, as well as sensitive visual function and quality of life measures, could help detect subtle, yet important structural or functional visual changes in patients with MS. This could ultimately help better screen, manage and counsel this subset of patients.
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Novel molecular mechanisms of neuronal and vascular protection in experimental glaucomaAlmasieh, Mohammadali 04 1900 (has links)
No description available.
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559 |
Haemostatic markers and cardiovascular function in black and white South Africans : the SABPA study / Leandi LammertynLammertyn, Leandi January 2015 (has links)
Motivation
In the black population of South Africa, cardiovascular disease (CVD) is rapidly increasing due to
urbanisation. Stroke is usually accompanied by a prothrombotic haemostatic profile. Changing
lifestyle factors that accompany the urbanisation process could have a negative impact on the
haemostatic profile of black South Africans. Elevated levels of pro-coagulant factors, von
Willebrand factor (vWF), fibrinogen and fibrin D-dimer have been reported in the black population,
which could increase the black population’s susceptibility to CVD. However, low levels of
plasminogen activator inhibitor-1 (PAI-1) previously reported in the black population could
contribute towards a pro-fibrinolytic state, which may counteract the hypercoagulant state. This
may have a beneficial effect on the haemostatic profile of the black population. More investigation
into the haemostatic profile of black South Africans is therefore needed to determine if an altered
haemostatic profile exists in this group, and if so, to what extent these alterations may relate to
cardiovascular dysfunction. This study included markers of both the coagulation (vWF, fibrinogen,
fibrin D-dimer) and fibrinolytic (PAI-1, fibrin D-dimer and fibrinolytic potential) systems in an
attempt to investigate the haemostatic profile of the black population of South Africa, and for
comparison purposes that of the white population as well. The relationship of these markers’ with
selected markers of cardiovascular function was also examined to determine if they could possibly
contribute to an increase in cardiovascular risk, especially in the black population.
Aims
The aims of this study were to first compare coagulation and fibrinolysis markers in the black and
white populations of South Africa. Furthermore, to determine if associations exist between the
selected components of the haemostatic system and markers of cardiovascular function,
especially in the black population of South Africa, who tends to be at a higher cardiovascular risk
due to altered metabolic and haemostatic profiles.
Methodology
The Sympathetic activity and Ambulatory Blood Pressure in Africans (SABPA) study was a
prospective cohort study that consisted of 409 participants at baseline (2008-2009) that were
equally distributed according to both ethnicity (200 black; 209 white) and gender (black, 101 men,
99 women; white, 101 men, 108 women). At follow-up (2011/2012) the cohort totalled 359
participants (170 black, 88 men and 82 women; 189 white, 93 men and 96 women). Data from
baseline measurements were used for the first two manuscripts (chapters 2 and 3), while followup
data was used for the third manuscript (chapter 4). vWF, fibrinogen, PAI-1, fibrin D-dimer, CLT,
serum peroxides, glutathione, glutathione peroxidase and reductase activity were determined,
and ambulatory blood pressure and the retinal vessel calibres were measured. The groups were
stratified by ethnicity as specified by statistical interaction terms. T-tests and chi-square tests were
used to compare means and proportions, respectively. Pearson and partial regression analyses
were used to determine correlations between the components of the haemostatic system and
cardiovascular function markers. This was followed by multiple linear regression analyses to
investigate whether independent associations exist between the variables in both ethnic groups.
P-values ≤0.050 were deemed significant.
Results and conclusion of each manuscript
The first manuscript (chapter 2) compares the haemostatic profiles of the black and white
population to determine whether ambulatory blood pressure is related to components of the
haemostatic system. The black participants displayed a prothrombotic profile with significantly
higher vWF, fibrinogen, PAI-1, fibrin D-dimer and a longer CLT than their white counterparts.
Furthermore, partial and multiple linear regression analyses showed a positive association of
systolic and diastolic blood pressure with fibrin D-dimer in the black population, while a negative
association existed between ambulatory blood pressure and CLT in the white population. These
associations suggest that fibrin D-dimer may contribute, at least in part, to the high prevalence of
hypertension in the black population.
The second manuscript (chapter 3) determined associations between markers of the haemostatic
and oxidant-antioxidant systems in the black and white populations. In addition to the
prothrombotic profile that exists in the black population, this group also had significantly higher
serum peroxides (oxidative stress) and lower glutathione peroxidase activity (antioxidant) levels.
Multiple linear regression analyses indicated positive associations between fibrinogen and serum
peroxides in both populations. In the white population, an additional positive association was
found between serum peroxide and CLT. In the black population, vWF and CLT were negatively
associated with GPx activity. The results suggest that there are ethnic-specific relationships
between the haemostatic and oxidant-antioxidant systems.
The third manuscript (chapter 4) investigated the relationships between the retinal vessel calibres
and components of the haemostatic system in the black and white population. The investigation
focussed specifically on arteriolar diameters in the lower median, since a narrow arteriolar
diameter is known to be associated with elevated blood pressure. In both ethnic groups, a
narrower arteriolar calibre was accompanied by narrower venular calibres. Independent positive
associations were found between the central retinal vein equivalent (CRVE) and fibrinogen in the
black population, as well as vWF and CLT in the white population. In addition, independent
negative associations were found between the central retinal artery equivalent and CLT in the
black population and with vWF in the white population. The results suggest that haemostatic
alterations are linked to early vascular changes that may differ between ethnicities.
General conclusion
Ethnic-specific relationships between the components of the haemostatic system and measures
of cardiovascular function are evident. The prothrombotic profile that is observed in the black
population, together with the adverse associations of the haemostatic components with blood
pressure, a compromised oxidant-antioxidant profile, and retinal vessel calibres may contribute,
at least in part, to the high cardiovascular and cerebrovascular risk evident in this population
group. / PhD (Physiology), North-West University, Potchefstroom Campus, 2015
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560 |
Haemostatic markers and cardiovascular function in black and white South Africans : the SABPA study / Leandi LammertynLammertyn, Leandi January 2015 (has links)
Motivation
In the black population of South Africa, cardiovascular disease (CVD) is rapidly increasing due to
urbanisation. Stroke is usually accompanied by a prothrombotic haemostatic profile. Changing
lifestyle factors that accompany the urbanisation process could have a negative impact on the
haemostatic profile of black South Africans. Elevated levels of pro-coagulant factors, von
Willebrand factor (vWF), fibrinogen and fibrin D-dimer have been reported in the black population,
which could increase the black population’s susceptibility to CVD. However, low levels of
plasminogen activator inhibitor-1 (PAI-1) previously reported in the black population could
contribute towards a pro-fibrinolytic state, which may counteract the hypercoagulant state. This
may have a beneficial effect on the haemostatic profile of the black population. More investigation
into the haemostatic profile of black South Africans is therefore needed to determine if an altered
haemostatic profile exists in this group, and if so, to what extent these alterations may relate to
cardiovascular dysfunction. This study included markers of both the coagulation (vWF, fibrinogen,
fibrin D-dimer) and fibrinolytic (PAI-1, fibrin D-dimer and fibrinolytic potential) systems in an
attempt to investigate the haemostatic profile of the black population of South Africa, and for
comparison purposes that of the white population as well. The relationship of these markers’ with
selected markers of cardiovascular function was also examined to determine if they could possibly
contribute to an increase in cardiovascular risk, especially in the black population.
Aims
The aims of this study were to first compare coagulation and fibrinolysis markers in the black and
white populations of South Africa. Furthermore, to determine if associations exist between the
selected components of the haemostatic system and markers of cardiovascular function,
especially in the black population of South Africa, who tends to be at a higher cardiovascular risk
due to altered metabolic and haemostatic profiles.
Methodology
The Sympathetic activity and Ambulatory Blood Pressure in Africans (SABPA) study was a
prospective cohort study that consisted of 409 participants at baseline (2008-2009) that were
equally distributed according to both ethnicity (200 black; 209 white) and gender (black, 101 men,
99 women; white, 101 men, 108 women). At follow-up (2011/2012) the cohort totalled 359
participants (170 black, 88 men and 82 women; 189 white, 93 men and 96 women). Data from
baseline measurements were used for the first two manuscripts (chapters 2 and 3), while followup
data was used for the third manuscript (chapter 4). vWF, fibrinogen, PAI-1, fibrin D-dimer, CLT,
serum peroxides, glutathione, glutathione peroxidase and reductase activity were determined,
and ambulatory blood pressure and the retinal vessel calibres were measured. The groups were
stratified by ethnicity as specified by statistical interaction terms. T-tests and chi-square tests were
used to compare means and proportions, respectively. Pearson and partial regression analyses
were used to determine correlations between the components of the haemostatic system and
cardiovascular function markers. This was followed by multiple linear regression analyses to
investigate whether independent associations exist between the variables in both ethnic groups.
P-values ≤0.050 were deemed significant.
Results and conclusion of each manuscript
The first manuscript (chapter 2) compares the haemostatic profiles of the black and white
population to determine whether ambulatory blood pressure is related to components of the
haemostatic system. The black participants displayed a prothrombotic profile with significantly
higher vWF, fibrinogen, PAI-1, fibrin D-dimer and a longer CLT than their white counterparts.
Furthermore, partial and multiple linear regression analyses showed a positive association of
systolic and diastolic blood pressure with fibrin D-dimer in the black population, while a negative
association existed between ambulatory blood pressure and CLT in the white population. These
associations suggest that fibrin D-dimer may contribute, at least in part, to the high prevalence of
hypertension in the black population.
The second manuscript (chapter 3) determined associations between markers of the haemostatic
and oxidant-antioxidant systems in the black and white populations. In addition to the
prothrombotic profile that exists in the black population, this group also had significantly higher
serum peroxides (oxidative stress) and lower glutathione peroxidase activity (antioxidant) levels.
Multiple linear regression analyses indicated positive associations between fibrinogen and serum
peroxides in both populations. In the white population, an additional positive association was
found between serum peroxide and CLT. In the black population, vWF and CLT were negatively
associated with GPx activity. The results suggest that there are ethnic-specific relationships
between the haemostatic and oxidant-antioxidant systems.
The third manuscript (chapter 4) investigated the relationships between the retinal vessel calibres
and components of the haemostatic system in the black and white population. The investigation
focussed specifically on arteriolar diameters in the lower median, since a narrow arteriolar
diameter is known to be associated with elevated blood pressure. In both ethnic groups, a
narrower arteriolar calibre was accompanied by narrower venular calibres. Independent positive
associations were found between the central retinal vein equivalent (CRVE) and fibrinogen in the
black population, as well as vWF and CLT in the white population. In addition, independent
negative associations were found between the central retinal artery equivalent and CLT in the
black population and with vWF in the white population. The results suggest that haemostatic
alterations are linked to early vascular changes that may differ between ethnicities.
General conclusion
Ethnic-specific relationships between the components of the haemostatic system and measures
of cardiovascular function are evident. The prothrombotic profile that is observed in the black
population, together with the adverse associations of the haemostatic components with blood
pressure, a compromised oxidant-antioxidant profile, and retinal vessel calibres may contribute,
at least in part, to the high cardiovascular and cerebrovascular risk evident in this population
group. / PhD (Physiology), North-West University, Potchefstroom Campus, 2015
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