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Brenda J. Tripathi

Bio: Brenda J. Tripathi is an academic researcher from University of South Carolina. The author has contributed to research in topics: Trabecular meshwork & Glaucoma. The author has an hindex of 36, co-authored 102 publications receiving 4858 citations. Previous affiliations of Brenda J. Tripathi include Moorfields Eye Hospital & University of Chicago.


Papers
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Journal ArticleDOI
TL;DR: The present findings support the concept of the intraocular derivation of this cytokine and hypothesize that the increased level of TGF-β2 in the aqueous humor of POAG patients causes a decrease in the cellularity of the trabecular meshwork and promotes the buildup of excessive amounts of ECM materials that are characteristic of this disease and contribute to the increased resistance to aQueous outflow.

511 citations

Book
01 Jun 1997
TL;DR: Bony orbit and paranasal sinuses Ocular appendages Orbital and cerebral vessels Extraocular muscles and ocular movements Innervation and nerves of the orbit The eyeball and its dimensions Cornea and sclera Anterior chamber and drainage angle The iris Posterior chamber and ciliary body Choroid and uveal vessels Lens and zonules The vitreous The retina Visual pathway Autonomic aminergic, peptidergic and nitrergic innervation of the human eye as mentioned in this paper.
Abstract: Bony orbit and paranasal sinuses Ocular appendages Orbital and cerebral vessels Extraocular muscles and ocular movements Innervation and nerves of the orbit The eyeball and its dimensions Cornea and sclera Anterior chamber and drainage angle The iris Posterior chamber and ciliary body Choroid and uveal vessels Lens and zonules The vitreous The retina Visual pathway Autonomic aminergic, peptidergic and nitrergic innervation of the eye Development of the human eye References and further reading.

508 citations

Journal ArticleDOI
TL;DR: Several hypotheses regarding the pathogenesis of Fuchs' dystrophy are discussed, including the possible influences of aberrant embryogenesis, hormones, and injury on the development of the disease.

295 citations

Journal ArticleDOI
TL;DR: The authors' findings show that patients with NVG had a significantly increased level of VEGF in the aqueous humor and implicate V EGF as an important factor in the pathogenesis of intraocular neovascularization in these patients.

269 citations

Journal ArticleDOI
TL;DR: The proposed mechanism of corticosteroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork system and is similar to the pathogenesis of POAG.
Abstract: Corticosteroids (glucocorticoids), used frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure (IOP) when administered exogenously (topically, periocularly or systemically) and in certain conditions of increased endogenous production (e.g. Cushing's syndrome). Approximately 18 to 36% of the general population are corticosteroid responders. This response is increased to 46 to 92% in patients with primary open-angle glaucoma (POAG). Patients over 40 years of age and with certain systemic diseases (e.g. diabetes mellitus, high myopia) as well as relatives of patients with POAG are more vulnerable to corticosteroid-induced glaucoma. The association of corticosteroid-induced ocular hypertension in other conditions which are considered as risk factors for glaucoma (racial origins, hypertension, migraine, vasospasm) is likely but not fully established. The proposed mechanism of corticosteroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork system and is similar to the pathogenesis of POAG. Trabecular cells exposed to corticosteroids in vitro show endoreplication of nuclei, an increase in cell size and excessive production of an approximately 56kD glycoprotein, identified as myocilin and transcribed by the GLC1A gene. Induction of ocular hypertension after corticosteroid administration depends on the specific drug, the dose, the frequency of administration and the corticosteroid responsiveness of the patient. The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medical practitioners. New treatment modalities include modified steroids and nonsteroidal anti-inflammatory agents that will have less effect on the elevation of IOP.

195 citations


Cited by
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Journal ArticleDOI
TL;DR: This review summarizes the current knowledge of the most important GC-mediated side effects from a clinical to a molecular perspective and should be helpful in predicting the potential advantages of selective GR agonists in comparison to classical GCs.

1,624 citations

01 Feb 2009
TL;DR: eMedicine创建于1996年,由近万名临床医师作为作者或编辑参与此临校医学知识库。
Abstract: eMedicine创建于1996年,由近万名临床医师作为作者或编辑参与此临床医学知识库的建设,其中编辑均是来自美国哈佛、耶鲁、斯坦福、芝加哥、德克萨斯、加州大学等各分校医学院的教授或副教授。

1,459 citations

Journal ArticleDOI
TL;DR: It seems that the thickening of the choroid may be mechanistically linked to the scleral synthesis of macromolecules, and thus may play an important role in the homeostatic control of eye growth, and, consequently, in the etiology of myopia and hyperopia.

1,356 citations

Journal ArticleDOI
TL;DR: The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease, finding the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation to be important.
Abstract: The TFOS DEWS II Pathophysiology Subcommittee reviewed the mechanisms involved in the initiation and perpetuation of dry eye disease. Its central mechanism is evaporative water loss leading to hyperosmolar tissue damage. Research in human disease and in animal models has shown that this, either directly or by inducing inflammation, causes a loss of both epithelial and goblet cells. The consequent decrease in surface wettability leads to early tear film breakup and amplifies hyperosmolarity via a Vicious Circle. Pain in dry eye is caused by tear hyperosmolarity, loss of lubrication, inflammatory mediators and neurosensory factors, while visual symptoms arise from tear and ocular surface irregularity. Increased friction targets damage to the lids and ocular surface, resulting in characteristic punctate epithelial keratitis, superior limbic keratoconjunctivitis, filamentary keratitis, lid parallel conjunctival folds, and lid wiper epitheliopathy. Hybrid dry eye disease, with features of both aqueous deficiency and increased evaporation, is common and efforts should be made to determine the relative contribution of each form to the total picture. To this end, practical methods are needed to measure tear evaporation in the clinic, and similarly, methods are needed to measure osmolarity at the tissue level across the ocular surface, to better determine the severity of dry eye. Areas for future research include the role of genetic mechanisms in non-Sjogren syndrome dry eye, the targeting of the terminal duct in meibomian gland disease and the influence of gaze dynamics and the closed eye state on tear stability and ocular surface inflammation.

994 citations

Journal ArticleDOI
TL;DR: Transgenic and knockout studies have provided important mechanistic insights into the development of choroidal neovascularization, the principal cause of vision loss in age-related macular degeneration, and this in turn has culminated in preclinical and clinical trials of directed molecular interventions.

932 citations