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Journal articles on the topic 'Ocular pathogenesis'

To see the other types of publications on this topic, follow the link: Ocular pathogenesis.

Author: Grafiati

Published: 10 December 2022

Last updated: 29 January 2023

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1

Zhang, Jun, Jingsheng Tuo, Zhongfeng Wang, Aiqin Zhu, Anna Machalińska, and Qin Long. "Pathogenesis of Common Ocular Diseases." Journal of Ophthalmology 2015 (2015): 1–2. http://dx.doi.org/10.1155/2015/734527.

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2

Deepthi, KrishnanNair Geetha, and Solai Ramatchandirane Prabagaran. "Ocular bacterial infections: Pathogenesis and diagnosis." Microbial Pathogenesis 145 (August 2020): 104206. http://dx.doi.org/10.1016/j.micpath.2020.104206.

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3

Pavesio, C. E., and S. Lightman. "Toxoplasma gondii and ocular toxoplasmosis: pathogenesis." British Journal of Ophthalmology 80, no. 12 (December 1, 1996): 1099–107. http://dx.doi.org/10.1136/bjo.80.12.1099.

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4

Holland, Gary N. "Reconsidering the pathogenesis of ocular toxoplasmosis." American Journal of Ophthalmology 128, no. 4 (October 1999): 502–5. http://dx.doi.org/10.1016/s0002-9394(99)00263-9.

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5

Ponzoni, M., R. Dolcetti, S. Magnino, F. Bertoni, M. Milco D'Elios, S. Govi, E. Guerini, C. Doglioni, and A. J. M. Ferreri. "3 Pathogenesis of ocular adnexal lymphoma." European Journal of Cancer Supplements 8, no. 4 (April 2010): 3. http://dx.doi.org/10.1016/s1359-6349(10)70674-1.

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6

Pierce, Eric A., and Donald J. D'amico. "Ocular Toxoplasmosis: Pathogenesis, Diagnosis, and Management." Seminars in Ophthalmology 8, no. 1 (January 1993): 40–52. http://dx.doi.org/10.3109/08820539309060209.

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7

Vitaly, V. Potemkin, Olga A. Marchenko, Elena V. Ageeva, and Yuliya I. Malakhova. "Ocular cicatricial pemphigoid." Ophthalmology journal 10, no. 1 (March 15, 2017): 102–6. http://dx.doi.org/10.17816/ov101102-106.

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8

Calugaru, Dan. "Etiology, pathogenesis, and diagnosis of neovascular glaucoma." International Journal of Ophthalmology 15, no. 6 (June 18, 2022): 1005–10. http://dx.doi.org/10.18240/ijo.2022.06.20.

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Neovascular glaucoma is defined as iris and/or anterior chamber angle neovascularization associated with increased intraocular pressure. It is a secondary glaucoma that is most frequently caused by severe retinal ischemia. The most common diseases responsible for the development of neovascular glaucoma are diabetic retinopathy, ischemic central retinal vein occlusion, and ocular ischemic syndrome. Uncommon causes include ocular radiation, ocular tumors, uveitis and other miscellaneous conditions. Vascular endothelial growth factor is an important and likely predominant agent involved in the pathogenesis of intraocular neovascularization and neovascular glaucoma. The evolution of clinical and histopathological changes from predisposing conditions to the occurrence of rubeosis iridis and neovascular glaucoma is divided into four stages: prerubeosis, preglaucoma, open angle glaucoma, and angle-closure glaucoma.

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9

Egwuagu, C. E., L. Sun, S. H. Kim, and I. M. Dambuza. "Ocular Inflammatory Diseases: Molecular Pathogenesis and Immunotherapy." Current Molecular Medicine 15, no. 6 (August 19, 2015): 517–28. http://dx.doi.org/10.2174/1566524015666150731095426.

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10

Ahmed, Muna, Ghassan Zein, Faizullah Khawaja, and C. Stephen Foster. "Ocular cicatricial pemphigoid: pathogenesis, diagnosis and treatment." Progress in Retinal and Eye Research 23, no. 6 (November 2004): 579–92. http://dx.doi.org/10.1016/j.preteyeres.2004.05.005.

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11

Li, Yu-jie, Qin Jiang, Guo-fan Cao, Jin Yao, and Biao Yan. "Repertoires of Autophagy in the Pathogenesis of Ocular Diseases." Cellular Physiology and Biochemistry 35, no. 5 (2015): 1663–76. http://dx.doi.org/10.1159/000373980.

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Autophagy is an important intracellular degradative process that delivers cytoplasmic proteins to lysosome for degradation. Dysfunction of autophagy is implicated in several human diseases, such as neurodegenerative diseases, infectious diseases, and cancers. Autophagy-related proteins are constitutively expressed in the eye. Increasing studies have revealed that abnormal autophagy is an important pathological feature of several ocular diseases. Pharmacological manipulation of autophagy may provide an alternative therapeutic target for some ocular diseases. In this manuscript, we reviewed the relevant progress about the role of autophagy in the pathogenesis of ocular diseases.

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12

Lu, Fangli, Shiguang Huang, and Lloyd H. Kasper. "CD4+ T Cells in the Pathogenesis of Murine Ocular Toxoplasmosis." Infection and Immunity 72, no. 9 (September 2004): 4966–72. http://dx.doi.org/10.1128/iai.72.9.4966-4972.2004.

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ABSTRACT The role of CD4+ T cells in the pathogenesis of ocular toxoplasmosis was investigated in murine models utilizing inbred C57BL/6 mice deficient either in CD4+, CD8+, or B cells (μMT). Severe necrosis and inflammation with replicating parasites were observed in the eyes of control mice after primary ocular infection, and near-normal histology with few tachyzoites was observed in the eyes of mice immunized intraperitoneally with the avirulent ts-4 strain followed by intraocular challenge with the RH strain of Toxoplasma gondii. In contrast, mild inflammation without evidence of necrosis associated with increased parasite burdens were observed in the eyes of CD4 knockout (KO) mice after both primary ocular infection and challenge with RH tachyzoites. CD8 KO mice, as well as μMT mice, demonstrated increased ocular necrosis in response to either primary ocular infection or challenge. The parasite burden was increased in the eyes of both CD8 KO and μMT mice in which the parasite load was even higher. As expected, there were no increases in the levels of immunoglobulin G in serum or aqueous humor in μMT mice, and there was no increase in the levels of gamma interferon and tumor necrosis factor alpha in the sera of CD4 KO mice after both infection and challenge. These results suggest that the ocular inflammatory response to the parasite is mediated primarily by the CD4+-T-cell response. CD8+ T cells and B cells may play an important role in limiting tachyzoite proliferation in the eyes. Mice deficient in CD8+ CD4+ T cells or B cells exhibit diminished vaccine-induced resistance and increased ocular parasite burden after challenge.

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13

Memar, Omeed. "Ocular manifestations of atopic dermatitis." Journal of Dermatology & Cosmetology 3, no. 2 (2019): 36–40. http://dx.doi.org/10.15406/jdc.2019.03.00112.

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Purpose: A review of the published literature on the history, pathogenesis, and treatment of atopic dermatitis (AD) and its ocular involvement. Methods: Literature searches were conducted in MEDLINE (Ovid) and Google scholar for AD and ocular AD. Results: AD is an inflammatory dermatosis that has classic presentations on the skin at different age points. The primary immunological profile is a Th2 profile, releasing an abundance of IL4 and IL10 both systemically and locally. AD can involve the eye and have devastating consequences. Here we review the latest understanding of AD pathogenesis and treatments vis-à-vis the ocular surface. Conclusion: Ocular AD is a common manifestation of AD. The newest drugs for systemic AD might be deleterious for ocular AD.

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14

Ahn, Jeeyun, and Michael B. Gorin. "The Associations of Obstructive Sleep Apnea and Eye Disorders: Potential Insights into Pathogenesis and Treatment." Current Sleep Medicine Reports 7, no. 3 (July 23, 2021): 65–79. http://dx.doi.org/10.1007/s40675-021-00215-0.

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Abstract Purpose of Review Obstructive sleep apnea (OSA) patients are at significantly increased risks for cardiovascular and cerebrovascular morbidities. Recently, there has been heightened interest in the association of OSA with numerous ocular diseases and possible improvement of these conditions with the initiation of OSA treatment. We reviewed the current evidence with an emphasis on the overlapping pathogeneses of both diseases. Recent Findings Currently available literature points to a substantial association of OSA with ocular diseases, ranging from those involving the eyelid to optic neuropathies and retinal vascular diseases. Since the retina is one of the highest oxygen-consuming tissues in the body, the intermittent hypoxia and hypercapnia ensuing in OSA can have deleterious effects on ocular function and health. Tissue hypoxia, autonomic dysfunction, microvascular dysfunction, and inflammation all play important roles in the pathogenesis of both OSA and ocular diseases. Whether OSA treatment is capable of reversing the course of associated ocular diseases remains to be determined. It is anticipated that future therapeutic approaches will target the common underlying pathophysiologic mechanisms and promote favorable effects on the treatment of known associated ocular diseases. Summary Emerging evidence supports the association of ocular diseases with untreated OSA. Future studies focusing on whether therapeutic approaches targeting the common pathophysiologic mechanisms will be beneficial for the course of both diseases are warranted.

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15

Lu, Fangli, Shiguang Huang, and Lloyd H. Kasper. "Interleukin-10 and Pathogenesis of Murine Ocular Toxoplasmosis." Infection and Immunity 71, no. 12 (December 2003): 7159–63. http://dx.doi.org/10.1128/iai.71.12.7159-7163.2003.

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ABSTRACT To understand the role of interleukin-10 (IL-10) in ocular toxoplasmosis, we compared C57BL/6 (B6) and BALB/c background mice lacking a functional IL-10 gene (IL-10−/−) and B6 transgenic mice expressing IL-10 under the control of the IL-2 promoter. Increased cellular infiltration and necrosis were observed in the eye tissue of IL-10−/− mice of both the B6 and BALB/c backgrounds with associated changes in the levels of cytokines in serum. In contrast, there was no evidence of necrosis in the eye tissue from IL-10 transgenic mice following parasite exposure. Our results demonstrate that IL-10 is important in the regulation of inflammation during acute ocular toxoplasmosis.

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16

Labib, Bisant A., and DeGaulle I. Chigbu. "Pathogenesis and Manifestations of Zika Virus-Associated Ocular Diseases." Tropical Medicine and Infectious Disease 7, no. 6 (June 15, 2022): 106. http://dx.doi.org/10.3390/tropicalmed7060106.

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Zika virus (ZIKV) is mosquito-borne flavivirus that caused a significant public health concern in French Polynesia and South America. The two major complications that gained the most media attention during the ZIKV outbreak were Guillain–Barré syndrome (GBS) and microcephaly in newborn infants. The two modes of ZIKV transmission are the vector-borne and non-vector borne modes of transmission. Aedes aegypti and Aedes albopictus are the most important vectors of ZIKV. ZIKV binds to surface receptors on permissive cells that support infection and replication, such as neural progenitor cells, dendritic cells, dermal fibroblasts, retinal pigment epithelial cells, endothelial cells, macrophages, epidermal keratinocytes, and trophoblasts to cause infection. The innate immune response to ZIKV infection is mediated by interferons and natural killer cells, whereas the adaptive immune response is mediated by CD8+T cells, Th1 cells, and neutralizing antibodies. The non-structural proteins of ZIKV, such as non-structural protein 5, are involved in the evasion of the host’s immune defense mechanisms. Ocular manifestations of ZIKV arise from the virus’ ability to cross both the blood–brain barrier and blood-retinal barrier, as well as the blood-aqueous barrier. Most notably, this results in the development of GBS, a rare neurological complication in acute ZIKV infection. This can yield ocular symptoms and signs. Additionally, infants to whom ZIKV is transmitted congenitally develop congenital Zika syndrome (CZS). The ocular manifestations are widely variable, and include nonpurulent conjunctivitis, anterior uveitis, keratitis, trabeculitis, congenital glaucoma, microphthalmia, hypoplastic optic disc, and optic nerve pallor. There are currently no FDA approved therapeutic agents for treating ZIKV infections and, as such, a meticulous ocular examination is an important aspect of the diagnosis. This review utilized several published articles regarding the ocular findings of ZIKV, antiviral immune responses to ZIKV infection, and the pathogenesis of ocular manifestations in individuals with ZIKV infection. This review summarizes the current knowledge on the viral immunology of ZIKV, interactions between ZIKV and the host’s immune defense mechanism, pathological mechanisms, as well as anterior and posterior segment findings associated with ZIKV infection.

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17

Solomon, Abraham, Ilaria Puxeddu, and Francesca Levi-Schaffer. "Fibrosis in ocular allergic inflammation: recent concepts in the pathogenesis of ocular allergy." Current Opinion in Allergy and Clinical Immunology 3, no. 5 (October 2003): 389–93. http://dx.doi.org/10.1097/00130832-200310000-00012.

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18

Kalayoglu, M. "Ocular Chlamydial Infections: Pathogenesis and Emerging Treatment Strategies." Current Drug Target -Infectious Disorders 2, no. 1 (March 1, 2002): 85–91. http://dx.doi.org/10.2174/1568005024605918.

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19

Stone, Donald U., and James Chodosh. "Ocular rosacea: an update on pathogenesis and therapy." Current Opinion in Ophthalmology 15, no. 6 (December 2004): 499–502. http://dx.doi.org/10.1097/01.icu.0000143683.14738.76.

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20

Deshpande, Shilpa P., Mei Zheng, Sujin Lee, and Barry T. Rouse. "Mechanisms of pathogenesis in herpetic immunoinflammatory ocular lesions." Veterinary Microbiology 86, no. 1-2 (April 2002): 17–26. http://dx.doi.org/10.1016/s0378-1135(01)00487-4.

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21

LIESEGANG, THOMAS J. "Ocular Herpes Simplex Infection: Pathogenesis and Current Therapy." Mayo Clinic Proceedings 63, no. 11 (November 1988): 1092–105. http://dx.doi.org/10.1016/s0025-6196(12)65504-9.

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22

Agrawal, Rupesh, Ilaria Testi, Andres Rousselot, Elizabeth J. Chen, Rajamani Lakshminarayanan, Amit Singhal, Manish Bundele, et al. "Insights into the molecular pathogenesis of ocular tuberculosis." Tuberculosis 126 (January 2021): 102018. http://dx.doi.org/10.1016/j.tube.2020.102018.

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23

Stern, M. E., C. S. Schaumburg, R. Dana, M. Calonge, J. Y. Niederkorn, and S. C. Pflugfelder. "Autoimmunity at the ocular surface: pathogenesis and regulation." Mucosal Immunology 3, no. 5 (May 19, 2010): 425–42. http://dx.doi.org/10.1038/mi.2010.26.

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24

Capiz, Daniel, Hans E. Grossniklaus, and Steven Yeh. "Pathogenesis of Ocular Findings in Congenital Zika Syndrome." JAMA Ophthalmology 135, no. 10 (October 1, 2017): 1077. http://dx.doi.org/10.1001/jamaophthalmol.2017.3285.

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25

Hanbazazh, Mehenaz, and Kymberly A. Gyure. "Ocular Human Papillomavirus Infections." Archives of Pathology & Laboratory Medicine 142, no. 6 (June 1, 2018): 706–10. http://dx.doi.org/10.5858/arpa.2017-0571-ra.

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Context.— Human papillomavirus (HPV) has a well-known role in the pathogenesis of squamous cell carcinoma and precursor lesions of the cervix, anogenital region, and head and neck, but its role in the development of squamous neoplasms of the eye, particularly the conjunctiva, remains unclear. Objective.— To review recent evidence implicating HPV in the pathophysiology of ocular lesions. Data Sources.— Published articles obtained from a PubMed search of the English literature were the primary sources for this review. Conclusions.— The low-risk HPV types 6 and 11 appear to play a role in the development of at least a subset of conjunctival squamous papillomas. The role of HPV in the pathogenesis of pterygium and ocular surface squamous neoplasia is less well defined. There is evidence to suggest that HPV may be a cofactor in the development of these lesions, acting in concert with ultraviolet radiation and/or human immunodeficiency virus infection in a subgroup of cases.

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26

Park, Un Chul, Tae Wan Kim, and Hyeong Gon Yu. "Immunopathogenesis of Ocular Behçet’s Disease." Journal of Immunology Research 2014 (2014): 1–13. http://dx.doi.org/10.1155/2014/653539.

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Behçet’s disease (BD) is a chronic recurrent systemic inflammatory disorder of unknown etiology characterized by oral and genital ulcerations, skin lesions, and uveitis. The ocular involvement of BD, or Behçet’s uveitis (BU), is characterized by panuveitis or posterior uveitis with occlusive retinal vasculitis and tends to be more recurrent and sight threatening than other endogenous autoimmune uveitides, despite aggressive immunosuppression. Although pathogenesis of BD is unclear, researches have revealed that immunological aberrations may be the cornerstone of BD development. General hypothesis of BD pathogenesis is that inflammatory response is initiated by infectious agents or autoantigens in patients with predisposing genetic factors and perpetuated by both innate and acquired immunity. In addition, a network of immune mediators plays a substantial role in the inflammatory cascade. Recently, we found that the immunopathogenesis of BU is distinct from other autoimmune uveitides regarding intraocular effector cell profiles, maturation markers of dendritic cells, and the cytokine/chemokine environment. In addition, accumulating evidence indicates the involvement of Th17 cells in BD and BU. Recent studies on genetics and biologics therapies in refractory BU also support the immunological association with the pathogenesis of BU. In this review, we provide an overview of novel findings regarding the immunopathogenesis of BU.

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27

Hu, Mark S., Joseph D. Schwartzman, Grant R. Yeaman, Jane Collins, Rosanne Seguin, Imtiaz A. Khan, and Lloyd H. Kasper. "Fas-FasL Interaction Involved in Pathogenesis of Ocular Toxoplasmosis in Mice." Infection and Immunity 67, no. 2 (February 1, 1999): 928–35. http://dx.doi.org/10.1128/iai.67.2.928-935.1999.

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ABSTRACT Ocular toxoplasmosis is a potentially blinding intraocular inflammation. The intent of this study was to investigate the role of Fas-FasL interaction in a murine model of acquired ocular toxoplasmosis induced by intracameral inoculation of Toxoplasma gondii. Intraocular inflammation, Fas and FasL expression on lymphocytes and on ocular tissues, the occurrence of apoptosis, and the frequency of CD8+ and CD4+ T cells in the infected eyes were analyzed in C57BL/6 (B6) mice. Susceptibility to parasite-induced intraocular inflammation was observed in Fas-deficient (B6-lpr) and FasL-deficient (B6-gld) mice. Inoculation of 5,000 T. gondii tachyzoites induced significant intraocular inflammation associated with increase of Fas and FasL expression in the inoculated eyes of wild-type B6 mice. Flow cytometry demonstrated a significant increase of Fas and FasL expression on the splenocytes from naive mice incubated in vitro with the parasite and on the splenocytes harvested from the infected mice at day 8 after parasite inoculation. Apoptosis of inflammatory cells and cells in ocular tissues was seen, and a greater frequency of CD8+ than CD4+ T cells was observed in the infected eyes. The intensity of intraocular inflammation was greater in B6-lpr and B6-gldmice than in wild-type B6 mice (P < 0.05). The results suggest that Fas-FasL interaction associated with apoptosis is involved in the pathogenesis of acquired ocular toxoplasmosis in mice.

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28

Maurya, Rajendra Prakash, Vibha Singh, Kajal Pal, Shivangi Singh, Virendra P. Singh, and Kartika Anand. "Ocular surface squamous neoplasia: An overview." IP International Journal of Ocular Oncology and Oculoplasty 8, no. 1 (May 15, 2022): 1–11. http://dx.doi.org/10.18231/j.ijooo.2022.001.

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Ocular surface squamous neoplasia (OSSN) is a diverse range of neoplasm arising from squamous epithelium of conjunctiva, limbus and cornea. OSSN is considered as a low grade malignancy but may be locally invasive and require exenteration. It has relatively high recurrence rate. It has multifactorial etiology and specific pathogenesis of lesion has yet to be attributed. Histopathology with immunohistochemistry is a gold standard diagnostic tool.This mini review highlights the pathogenesis, risk factors, various clinical manifestations, latest diagnostic tools and recent development in treatment of OSSN.

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29

Xu, Shunbin, and Linda D. Hazlett. "MicroRNAs in Ocular Infection." Microorganisms 7, no. 9 (September 17, 2019): 359. http://dx.doi.org/10.3390/microorganisms7090359.

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MicroRNAs (miRNAs) are small, non-coding, regulatory RNA molecules and constitute a newly recognized, important layer of gene-expression regulation at post-transcriptional levels. miRNAs quantitatively fine tune the expression of their downstream genes in a cell type- and developmental stage-specific fashion. miRNAs have been proven to play important roles in the normal development and function as well as in the pathogenesis of diseases in all tissues and organ systems. miRNAs have emerged as new therapeutic targets and biomarkers for treatment and diagnosis of various diseases. Although miRNA research in ocular infection remains in its early stages, a handful of pioneering studies have provided insight into the roles of miRNAs in the pathogenesis of parasitic, fungal, bacterial, and viral ocular infections. Here, we review the current status of research in miRNAs in several major ocular infectious diseases. We predict that the field of miRNAs in ocular infection will greatly expand with the discovery of novel miRNA-involved molecular mechanisms that will inform development of new therapies and identify novel diagnostic biomarkers.

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30

Urban, Beata, Alina Bakunowicz-Łazarczyk, and Marta Michalczuk. "Immune Recovery Uveitis: Pathogenesis, Clinical Symptoms, and Treatment." Mediators of Inflammation 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/971417.

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IRU is the most common form of immune reconstitution inflammatory syndrome in HIV-infected patients with cytomegalovirus retinitis who are receiving highly active antiretroviral therapy (HAART). Among patients with CMV in the HAART era, immune recovery may be associated with a greater number of inflammatory complications, including macular edema and epiretinal membrane formation. Given the range of ocular manifestations of HIV, routine ocular examinations and screening for visual loss are recommended in patients with CD4 counts <50 cells/μL. With the increasing longevity of these patients due to the use of HAART, treatment of IRU may become an issue in the future. The aim of this paper is to review the current literature concerning immune recovery uveitis. The definition, epidemiology, pathophysiology, clinical findings, complications, diagnosis, and treatment are presented.

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31

Lacy, H. Marie, Anne K. Bowlin, Leah Hennings, Amy M. Scurlock, Uma M. Nagarajan, and Roger G. Rank. "Essential Role for Neutrophils in Pathogenesis and Adaptive Immunity in Chlamydia caviae Ocular Infections." Infection and Immunity 79, no. 5 (March 14, 2011): 1889–97. http://dx.doi.org/10.1128/iai.01257-10.

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ABSTRACTTrachoma, the world's leading cause of preventable blindness, is produced by chronic ocular infection withChlamydia trachomatis, an obligate intracellular bacterium. While many studies have focused on immune mechanisms for trachoma during chronic stages of infection, less research has targeted immune mechanisms in primary ocular infections, events that could impact chronic responses. The goal of this study was to investigate the function of neutrophils during primary chlamydial ocular infection by using the guinea pig model ofChlamydia caviaeinclusion conjunctivitis. We hypothesized that neutrophils help modulate the adaptive response and promote host tissue damage. To test these hypotheses, guinea pigs with primaryC. caviaeocular infections were depleted of neutrophils by using rabbit antineutrophil antiserum, and immune responses and immunopathology were evaluated during the first 7 days of infection. Results showed that neutrophil depletion dramatically decreased ocular pathology, both clinically and histologically. The adaptive response was also altered, with increasedC. caviae-specific IgA titers in tears and serum and decreased numbers of CD4+and CD8+T cells in infected conjunctivae. Additionally, there were changes in conjunctival chemokines and cytokines, such as increased expression of IgA-promoting interleukin-5 and anti-inflammatory transforming growth factor β, along with decreased expression of T cell-recruiting CCL5 (RANTES). This study, the first to investigate the role of neutrophils in primary chlamydial ocular infection, indicates a previously unappreciated role for neutrophils in modulating the adaptive response and suggests a prominent role for neutrophils in chlamydia-associated ocular pathology.

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32

Savige, Judy, Shivanand Sheth, Anita Leys, Anjali Nicholson, Heather G. Mack, and Deb Colville. "Ocular Features in Alport Syndrome: Pathogenesis and Clinical Significance." Clinical Journal of the American Society of Nephrology 10, no. 4 (February 3, 2015): 703–9. http://dx.doi.org/10.2215/cjn.10581014.

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33

Hosogai, Mayumi. "Elucidation of the Pathogenesis of Cytomegalovirus-related Ocular Diseases." Kitakanto Medical Journal 69, no. 1 (February 1, 2019): 71–72. http://dx.doi.org/10.2974/kmj.69.71.

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34

Zhang, Zhihan, Xiaotian Liang, Jing Zhou, Meijun Meng, Ya Gao, Guoguo Yi, and Min Fu. "Exosomes in the pathogenesis and treatment of ocular diseases." Experimental Eye Research 209 (August 2021): 108626. http://dx.doi.org/10.1016/j.exer.2021.108626.

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35

Hayashi, K., Y. Suwa, Y. Shimomura, and Y. Ohashi. "Pathogenesis of ocular cytomegalovirus infection in the immunocompromised host." American Journal of Ophthalmology 121, no. 4 (April 1996): 464–65. http://dx.doi.org/10.1016/s0002-9394(14)70463-5.

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36

Foulks, Gary N. "Ocular Surface Morphogenesis and Pathogenesis in Health and Disease." Ocular Surface 6, no. 1 (January 2008): 1. http://dx.doi.org/10.1016/s1542-0124(12)70100-3.

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37

Fleiszig, Suzanne, Michael Gilmore, and Mark Willcox. "New Paradigms in the Pathogenesis of Ocular Surface Infections." Ocular Surface 3 (January 2005): S21—S22. http://dx.doi.org/10.1016/s1542-0124(12)70328-2.

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38

Basu, Soumyava, Paul Elkington, and Narsing A. Rao. "Pathogenesis of ocular tuberculosis: New observations and future directions." Tuberculosis 124 (September 2020): 101961. http://dx.doi.org/10.1016/j.tube.2020.101961.

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39

Hayashi, Kozaburo, Yuzo Suwa, Yoshikazu Shimomura, and Yuichi Ohashi. "Pathogenesis of ocular cytomegalovirus infection in the immunocompromised host." Journal of Medical Virology 47, no. 4 (December 1995): 364–69. http://dx.doi.org/10.1002/jmv.1890470412.

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40

He, Xuejun, Ningzhi Zhang, Wenye Cao, Yiqiao Xing, and Ning Yang. "Application Progress of High-Throughput Sequencing in Ocular Diseases." Journal of Clinical Medicine 11, no. 12 (June 17, 2022): 3485. http://dx.doi.org/10.3390/jcm11123485.

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Ocular diseases affect multiple eye parts and can be caused by pathogenic infections, complications of systemic diseases, genetics, environment, and old age. Understanding the etiology and pathogenesis of eye diseases and improving their diagnosis and treatment are critical for preventing any adverse consequences of these diseases. Recently, the advancement of high-throughput sequencing (HTS) technology has paved wide prospects for identifying the pathogenesis, signaling pathways, and biomarkers involved in eye diseases. Due to the advantages of HTS in nucleic acid sequence recognition, HTS has not only identified several normal ocular surface microorganisms but has also discovered many pathogenic bacteria, fungi, parasites, and viruses associated with eye diseases, including rare pathogens that were previously difficult to identify. At present, HTS can directly sequence RNA, which will promote research on the occurrence, development, and underlying mechanism of eye diseases. Although HTS has certain limitations, including low effectiveness, contamination, and high cost, it is still superior to traditional diagnostic methods for its efficient and comprehensive diagnosis of ocular diseases. This review summarizes the progress of the application of HTS in ocular diseases, intending to explore the pathogenesis of eye diseases and improve their diagnosis.

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Qin, Dan-Yi, and Ying-Ping Deng. "Transgenic dry eye mouse models: powerful tools to study dry eye disease." International Journal of Ophthalmology 15, no. 4 (April 18, 2022): 635–45. http://dx.doi.org/10.18240/ijo.2022.04.18.

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Dry eye disease (DED) is one of the most common chronic multifactorial ocular surface diseases with high prevalence and complex pathogenesis. DED results in several ocular discomforts, vision fluctuation, and even potential damage of the ocular surface, bringing heavy burdens both on individuals and the society. The pathology of DED consists of tear film hyperosmolarity and immune responses on the ocular surface. Mice are widely used for developing models that simulate human DED features for investigating its pathogenesis and treatment. DED can be classified into aqueous-deficiency dry eye (ADDE) and evaporative dry eye (EDE). ADDE can be further divided into Sjögren syndrome dry eye (SSDE) and non-Sjögren syndrome dry eye (NSSDE). SSDE mouse models include natural strains, typified by non-obese diabetic (NOD) mice, and genetically engineered ones, like Aire-/- and Id3 knockout mice. Intrinsic EDE mainly refers to meibomian gland dysfunction (MGD). Eda-/- Tabby, Sod1-/-, Elovl1-/- are the most common transgenic MGD mouse models. Transgenic mouse models provide useful tools for studying the pathogenesis of DED and evaluating its novel therapies. This review compares the major transgenic dry eye mouse models and discusses their applications in DED research.

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Primitasari, Yulia, and Evelyn Komaratih. "THE ROLE OF OCULAR BLOOD FLOW IN THE PATHOGENESIS OF GLAUCOMA." Jurnal Kedokteran Syiah Kuala 19, no. 1 (April 1, 2019): 51–54. http://dx.doi.org/10.24815/jks.v19i1.18052.

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Abstract. Glaucoma is currently the second leading cause of blindness worldwide and the prevalence is expected to increase. Despite lowering of IOP, vascular risk factors, genetics, and other systemic conditions could progress the glaucoma damage. Ocular blood flow has emerged as an increasingly prevalent glaucoma risk factor in large population-based trials. Abnormal perfusion and the subsequent ischemia of the ONH play a major role in the glaucomatous damage. Ocular Blood flow is unstable if IOP fluctuates on a high enough or blood pressure on a low enough level to exceed temporarily the autoregulation capacity. IOP fluctuation is also related to both an increase in scotomas and an increase in diffuse visual fields damage. OBF is unstable if autoregulation itself is disturbed. In glaucoma the response of retinal and optic nerve head blood flow to flicker stimulation is reduced. Primary vascular dysregulation appears to be associated with abnormal retinal neurovascular coupling, because vasospastic subjects show a reduced response to flicker stimulation.Keywords: ocular blood flow, glaucoma

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Zeng, Jia, Min Wu, Yamei Zhou, Manhui Zhu, and Xiaojuan Liu. "Neutrophil Extracellular Traps (NETs) in Ocular Diseases: An Update." Biomolecules 12, no. 10 (October 8, 2022): 1440. http://dx.doi.org/10.3390/biom12101440.

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Neutrophil extracellular traps (NETs) are net-like complexes expelled from neutrophils, composing cell-free deoxyribonucleic acid (DNA), histones, and neutrophil granule proteins. Besides capturing and eliminating pathogens, NETs also exacerbate the inflammatory response associated with various diseases, including systemic lupus erythematosus, rheumatoid arthritis, and psoriasis. Currently, there are growing reports about NETs involved in the pathogenesis of ocular diseases. This review primarily focuses on the pathogenesis of NETs in the ophthalmology field, highlighting their importance in serving as potential targets for the therapy of ocular diseases.

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Singh, Sneha, Dustin Farr, and Ashok Kumar. "Ocular Manifestations of Emerging Flaviviruses and the Blood-Retinal Barrier." Viruses 10, no. 10 (September 28, 2018): 530. http://dx.doi.org/10.3390/v10100530.

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Despite flaviviruses remaining the leading cause of systemic human infections worldwide, ocular manifestations of these mosquito-transmitted viruses are considered relatively uncommon in part due to under-reporting. However, recent outbreaks of Zika virus (ZIKV) implicated in causing multiple ocular abnormalities, such as conjunctivitis, retinal hemorrhages, chorioretinal atrophy, posterior uveitis, optic neuritis, and maculopathies, has rejuvenated a significant interest in understanding the pathogenesis of flaviviruses, including ZIKV, in the eye. In this review, first, we summarize the current knowledge of the major flaviviruses (Dengue, West Nile, Yellow Fever, and Japanese Encephalitis) reported to cause ocular manifestations in humans with emphasis on recent ZIKV outbreaks. Second, being an immune privilege organ, the eye is protected from systemic infections by the presence of blood-retinal barriers (BRB). Hence, we discuss how flaviviruses modulate retinal innate response and breach the protective BRB to cause ocular or retinal pathology. Finally, we describe recently identified infection signatures of ZIKV and discuss whether these system biology-predicted genes or signaling pathways (e.g., cellular metabolism) could contribute to the pathogenesis of ocular manifestations and assist in the development of ocular antiviral therapies against ZIKV and other flaviviruses.

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Balikov, Daniel A., Adam Jacobson, and Lev Prasov. "Glaucoma Syndromes: Insights into Glaucoma Genetics and Pathogenesis from Monogenic Syndromic Disorders." Genes 12, no. 9 (September 11, 2021): 1403. http://dx.doi.org/10.3390/genes12091403.

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Monogenic syndromic disorders frequently feature ocular manifestations, one of which is glaucoma. In many cases, glaucoma in children may go undetected, especially in those that have other severe systemic conditions that affect other parts of the eye and the body. Similarly, glaucoma may be the first presenting sign of a systemic syndrome. Awareness of syndromes associated with glaucoma is thus critical both for medical geneticists and ophthalmologists. In this review, we highlight six categories of disorders that feature glaucoma and other ocular or systemic manifestations: anterior segment dysgenesis syndromes, aniridia, metabolic disorders, collagen/vascular disorders, immunogenetic disorders, and nanophthalmos. The genetics, ocular and systemic features, and current and future treatment strategies are discussed. Findings from rare diseases also uncover important genes and pathways that may be involved in more common forms of glaucoma, and potential novel therapeutic strategies to target these pathways.

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Lee, Hyung-Keun, Sang-Mok Lee, and Dong-Ihll Lee. "Corneal Lymphangiogenesis: Current Pathophysiological Understandings and Its Functional Role in Ocular Surface Disease." International Journal of Molecular Sciences 22, no. 21 (October 27, 2021): 11628. http://dx.doi.org/10.3390/ijms222111628.

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The cornea is a transparent and avascular tissue that plays a central role in light refraction and provides a physical barrier to the external environment. Corneal avascularity is a unique histological feature that distinguishes it from the other parts of the body. Functionally, corneal immune privilege critically relies on corneal avascularity. Corneal lymphangiogenesis is now recognized as a general pathological feature in many pathologies, including dry eye disease (DED), corneal allograft rejection, ocular allergy, bacterial and viral keratitis, and transient corneal edema. Currently, sizable data from clinical and basic research have accumulated on the pathogenesis and functional role of ocular lymphangiogenesis. However, because of the invisibility of lymphatic vessels, ocular lymphangiogenesis has not been studied as much as hemangiogenesis. We reviewed the basic mechanisms of lymphangiogenesis and summarized recent advances in the pathogenesis of ocular lymphangiogenesis, focusing on corneal allograft rejection and DED. In addition, we discuss future directions for lymphangiogenesis research.

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Inoue, Takuro, Hisao Hirai, Toshiki Shimizu, Masayuki Tsuji, Ayako Shima, Fumio Suzuki, and Masayuki Matsuda. "Ocular neuromyotonia treated by microvascular decompression: usefulness of preoperative 3D imaging." Journal of Neurosurgery 117, no. 6 (December 2012): 1166–69. http://dx.doi.org/10.3171/2012.9.jns112361.

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Ocular neuromyotonia is a rare ocular motility disorder characterized by involuntary contraction of extraocular muscles resulting in paroxysmal diplopia. Although ocular neuromyotonia is reported as a rare complication after radiation therapy, there are a few cases of ocular neuromyotonia in the absence of irradiation. In the reported cases the possibility of vascular compression has been suggested on radiological imaging. The authors report a case of ocular neuromyotonia treated by microvascular decompression of the third cranial nerve, supporting the hypothesis that neurovascular compression may play a role in its pathogenesis. The usefulness of preoperative 3D imaging for microvascular decompression is also discussed.

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Ekici, Feyzahan, Şafak Korkmaz, Emine Esra Karaca, Sabahattin Sül, Hasan Ali Tufan, Bahri Aydın, and Ergin Dileköz. "The Role of Magnesium in the Pathogenesis and Treatment of Glaucoma." International Scholarly Research Notices 2014 (October 13, 2014): 1–7. http://dx.doi.org/10.1155/2014/745439.

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Glaucoma is characterized by chronic optic neuropathy resulting in progressive vision loss. Not only is glaucoma considered as a condition of elevated intraocular pressure (IOP), but also other risk factors may play a role in the pathogenesis of glaucomatous optic nerve damage. Vascular dysregulation in ocular blood flow and oxidative stress are currently suggested as important risk factors for glaucomatous retinal ganglion cell loss. New treatment modalities that improve ocular blood flow and reduce oxidative stress have been investigated in many studies. Magnesium (Mg) is thought to be one of the molecules that has a treatment potential in glaucoma. Mg has been shown to improve blood flow by modifying endothelial function via endothelin-1 (ET-1) and endothelial nitric oxide (NO) pathways. Mg also exhibits neuroprotective role by blocking N-methyl-D-aspartate (NMDA) receptor-related calcium influx and by inhibiting the release of glutamate, and hence protects the cell against oxidative stress and apoptosis. Both improvement in ocular blood flow and prevention of ganglion cell loss would make magnesium a good candidate for glaucoma management. Further studies on the effect of Mg may open a new therapeutic era in glaucoma.

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Stefanovic, Alexandra, and Izidore S. Lossos. "Extranodal marginal zone lymphoma of the ocular adnexa." Blood 114, no. 3 (July 16, 2009): 501–10. http://dx.doi.org/10.1182/blood-2008-12-195453.

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Abstract Lymphomas of the ocular adnexa are a heterogeneous group of malignancies, composing approximately 1% to 2% of non-Hodgkin lymphomas (NHLs) and 8% of extranodal lymphomas. The most common subtype, accounting for up to 80% of cases of primary ocular adnexal lymphoma, is marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT) type. In the recent past, there have been significant advances in our understanding of the clinical characteristics, morphology and phenotype, etiology, pathogenesis, diagnosis, natural history, treatment approaches, outcome, and prognostic factors of this disease entity. Novel immunologic and molecular techniques have aided in the distinction between MALT lymphoma and other lymphoproliferative disorders and led to the identification of tissue markers of prognostic significance. Modern imaging modalities provide invaluable tools for accurate staging and treatment planning. Besides radiotherapy and chemotherapy, a variety of new treatment options have emerged in the management of patients with ocular adnexal MALT lymphoma, especially monoclonal antibody therapy and antibiotic therapy against Chlamydia psittaci, which has been associated with the pathogenesis of ocular adnexal lymphomas in some parts of the world. In this review, we present a state-of-the-art summary of ocular adnexal MALT lymphomas.

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Andrew, SE. "Ocular Manifestations of Feline Herpesvirus." Journal of Feline Medicine and Surgery 3, no. 1 (March 2001): 9–16. http://dx.doi.org/10.1053/jfms.2001.0110.

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Feline herpesvirus-1 (FHV-1) infection is ubiquitous in the domestic cat population worldwide. The most common clinical ocular manifestations of infection with FHV-1 are conjunctivitis and keratitis. This paper reviews the pathogenesis of feline herpesvirus-1 and discusses the various clinical ocular manifestations, diagnostic techniques and treatment of FHV-1-induced diseases. Ocular manifestations include: conjunctivitis, keratitis, stromal keratitis, keratoconjunctivitis sicca, ophthalmia neonatorium, symblepharon, corneal sequestrum, eosinophilic keratitis and anterior uveitis. Diagnostic techniques discussed include: virus isolation, fluorescent antibody testing, serum neutralising titers, ELISA and polymerase chain reaction. Various therapies are also discussed.

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