Limited Knowledge and Use of HIV Post- and Pre-Exposure Prophylaxis Among Gay and Bisexual Men

Liu, Albert Y.; Kittredge, Pravina V; Vittinghoff, Eric; Raymond, H. Fisher; Ahrens, Katherine A.; Matheson, Tim; Hecht, Jennifer; Klausner, Jeffrey D.; Buchbinder, Susan

doi:10.1097/qai.0b013e31815e4041

Cited by 181 publications

(96 citation statements)

References 19 publications

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“…In accordance with these reports, an up-regulation of the expression of human ·-defensins and S100 A8 and A9 in tear fluids of pterygium patients provides additional indications for a connection between pterygium and chronic ocular surface inflammation (38). Another study has reported the up-regulation of phospholipase D (PLD) types 2, 3 and 4 in pterygium, compared with normal conjunctiva (39). PLD are involved in various processes, including inflammation, cell differentiation, apoptosis and wound healing and the detection of PLD alterations in pterygium supports their potential role in pterygium pathogenesis (39).…”

Section: Concepts Of Inheritancesupporting

confidence: 59%

“…Another study has reported the up-regulation of phospholipase D (PLD) types 2, 3 and 4 in pterygium, compared with normal conjunctiva (39). PLD are involved in various processes, including inflammation, cell differentiation, apoptosis and wound healing and the detection of PLD alterations in pterygium supports their potential role in pterygium pathogenesis (39).…”

Section: Concepts Of Inheritancementioning

confidence: 99%

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Pathogenetic mechanisms and treatment options for ophthalmic pterygium: Trends and perspectives (Review)

Detorakis

Spandidos²

2009

Int J Mol Med

150

103

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Abstract. Pterygium is a fibrovascular lesion of the ocular surface that can display an aggressive clinical behavior and, occasionally, threaten vision. Although there is no consensus on its pathogenesis, recent evidence suggests that it is a proliferative, rather than degenerative condition strongly correlated with exposure to ultraviolet radiation (UVR) of solar light. Molecular genetic alterations reported in association with pterygium include loss of heterozygosity (LOH), point mutations of proto-oncogenes, such as K-ras and alterations in the expression of tumor suppressor genes, such as p53 or p63. Other findings in pterygium include the frequent detection of HPV DNA, ocular surface changes such as the overexpression of various proteins, including defensins and phospolipases D, as well as the up-regulation of growth factors, such as bFGF or VEGF. Although pterygium management has traditionally involved surgery, often enhanced by the use of antimetabolites, recent advancements in the understanding of molecular and biochemical events underlying pterygium pathogenesis may enable the use of less invasive treatment methods.

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Section: Concepts Of Inheritancesupporting

confidence: 59%

Section: Concepts Of Inheritancementioning

confidence: 99%

Pathogenetic mechanisms and treatment options for ophthalmic pterygium: Trends and perspectives (Review)

Detorakis

Spandidos²

2009

Int J Mol Med

150

103

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“…Hyperosmotic stress has been reported to induce cultured HCE-T cell death through various signaling pathways, mediated in part by activation of c-jun N-terminal kinase (JNK), extracellular signal-regulated kinase (ERK), and mitogenactivated protein kinase (MAPK) signaling pathways (Piacentini et al, 2002;Luo et al, 2004;Tong et al, 2008). However, these studies did not look at the relevance of TGM-2 in the JNK, ERK, or MAPK signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

Hyperosmolarity‐mediated mitochondrial dysfunction requires Transglutaminase‐2 in human Corneal epithelial cells

Png

Samivelu

Yeo

et al. 2010

Journal Cellular Physiology

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Hyperosmolar-induced ocular surface cell death is a key mitochondria-mediated event in inflammatory eye diseases. Transglutaminase (TGM)-2, a cross-linking enzyme, is purported to mediate cell death, but its link to mitochondria is unclear. In the cornea, the integrity of the epithelial cells is important for maintaining transparency of the cornea and therefore functional vision. We evaluated the role of TGM-2 and its involvement in hyperosmolarity-stimulated mitochondrial cell death in human corneal epithelial (HCE-T) cells. HCE-T cell lines stably expressing either shRNA targeting TGM-2 (shTG) or scrambled shRNA (shRNA) were constructed. Hyperosmolar conditions reduced viability and increased mitochondrial depolarization in shRNA cells. However, hyperosmolarity failed to induce mitochondrial depolarization to the same extent in shTG cells. Transient overexpression of TGM-2 resulted in very high levels of TGM-2 expression in shTG and shRNA cells. In the case of shTG cells after overexpression of TGM-2, hyperosmolarity induced the same extent of mitochondrial depolarization as similarly treated shRNA cells. Overexpression of TGM-2 also elevated transamidase activity and reduced viability. It also induced mitochondrial depolarization, increased caspase-3/7 and -9 activity, and these increases were partially suppressed by pan-caspase inhibitor Z-VAD-FMK. Corneal epithelial apoptosis via mitochondrial dysfunction after hyperosmolar stimulation is partially dependent on TGM-2. This TGM-2-dependent mechanism occurs in part via caspase-3/7 and -9. Protection against mitochondrial stress in the ocular surface targeting TGM-2 may have important implications in the survival of cells in hyperosmolar stress.

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“…Further inflammatory cascades 31 Phospholipase D Further inflammation and cellular differentiation 121 Cystatin C Regulation of extracellular matrix modulators 122 increase in the expression levels of stem cell factor, 131 platelet-derived growth factor (PDGF), 120 connective tissue growth factor (CTGF), 132 and transforming growth factor-beta (TGF-b) 120 have been documented in pterygium. Inflammatory processes of pterygium can trigger reactive wound formation, which may induce dysregulated and inappropriate tissue remodeling, fibroproliferation, enhanced vascularization, and deposition of the extracellular matrix, leading to the formation of hypertrophic scarring.…”

Section: Cox2mentioning

confidence: 99%

“…31 An increase in phospholipase D, an enzyme involved in inflammation and cellular differentiation, was also found in pterygium. 121 Cystatin C, an inhibitor of cysteine proteinases, is overexpressed in pterygium and is more abundant in tears from patients with the disease. This protein could serve as a natural mechanism of protection against inflammation.…”

Section: Inflammatory Mediators and Growth Factorsmentioning

confidence: 99%

Molecular Basis of Pterygium Development

Cárdenas-Cantú

Zavala

Valenzuela

et al. 2014

Seminars in Ophthalmology

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Pterygium pathogenesis is mainly related to UV light exposure. However, the exact mechanisms by which it is formed have not been elucidated. Clinical advances in surgical treatment use conjunctival autografts and amniotic membranes in combination with adjuvant therapies, including mitomycin C, β-radiation, and 5-fluoroacil, to reduce recurrence. Several studies aim to unveil the molecular mechanisms underlying pterygium growth and proliferation. They demonstrate the role of different factors, such as viruses, oxidative stress, DNA methylation, apoptotic and oncogenic proteins, loss of heterozygosity, microsatellite instability, inflammatory mediators, extracellular matrix modulators, lymphangiogenesis, cell epithelial-mesenchymal transition, and alterations in cholesterol metabolism in pterygium development. Understanding the molecular basis of pterygium provides new potential therapeutic targets for its prevention and elimination. This review focuses on providing a broad overview of what is currently known regarding molecular mechanisms of pterygium pathogenesis.

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Limited Knowledge and Use of HIV Post- and Pre-Exposure Prophylaxis Among Gay and Bisexual Men

Abstract: PEP awareness and use were modest and PrEP use was rare among gay/bisexual men in California. Although PrEP is not currently recommended, community education on the availability of PEP is suggested.

Cited by 181 publications

References 19 publications

Pathogenetic mechanisms and treatment options for ophthalmic pterygium: Trends and perspectives (Review)

Pathogenetic mechanisms and treatment options for ophthalmic pterygium: Trends and perspectives (Review)

Hyperosmolarity‐mediated mitochondrial dysfunction requires Transglutaminase‐2 in human Corneal epithelial cells

Molecular Basis of Pterygium Development

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