Sara P. Modjtahedi's research while affiliated with Jules Stein Eye Institute and other places

... RPE has vital physiological functions, including the formation of the outer blood retinal barrier (oBRB), transportation of nutrients to photoreceptors (PRs), absorption of scattered light, recycling of retinoid and phagocytosis of shed PR outer segment membrane [5]. Therefore, depicting the gene profile of RPE and studying their function could help en-rich the understanding of early DR and further develop novel diagnosis and treatment strategies [6,7]. ...

... For instance, dexamethasone and triamcinolone are commonly used in clinical practice to treat a wide range of retinal pathologies and both can induce glaucoma [26]. In mice, OPN1SW, GRIN2B, HTR1A, and HTR7 were found downregulated after retina postintravitreal injections of triamcinolone [27]. CNGB1, HTR1A, HTR7, OPN1SW, and CRX were downregulated by dexamethasone in the retinal pigment epithelium of mouse [28]. ...

... DEXA has long been used for treating several pathologies such as cancer, leukemia, rheumatoid arthritis, cerebral edema, asthma, edema, multiple sclerosis, gastrointestinal disorders, ulcerative colitis, psoriasis, and retinal diseases, among others [1,[11][12][13][14][15]. ...

... Relative to TA, dexamethasone displayed lower toxicity towards lens epithelial cells [23], trabecular meshwork cells [22,24] and retinal neurosensory and RPE cells [25,26] in vitro. However, dexamethasone (392.5 Da) suffers from a relatively short half-life within the eye (3.5 h), whereas TA (18 days) has been shown to persist for 3 months [27][28][29]. Therefore, releasing dexamethasone from a slow-releasing pNNAD scaffold (similar to Osurdex [30]) should help create persistent levels of the potent corticosteroid within the eye, extending its duration of action, minimizing the number of repeat injections required to maintain therapeutic concentrations and lower the incidence of steroid-related complications. ...

... An inflammatory reaction in the skin due to a single exposure to an offending chemical is termed acute irritant dermatitis [33]. Cumulative contact irritation, which is more common, is the result of ongoing contact with lowlevel irritants. ...

... However, it is important to note that, in some cases, persistent edema can occur, resulting in a decline in visual acuity and permanent vision loss, even after the resolution of the edema. Hunter et al. [31] reported that 26.8% of patients with PCME did not return to 20/20 visual acuity following the resolution of macular edema. However, there is still no consensus on the most appropriate treatment for patients with PCME who present preoperative pre-existing risk factors, such as ERM. ...

... Moreover, OTC products containing menthol, eucalyptus have been used for relieving insect bite reactions. [34][35][36][37] It was postulated that the Trikatu product exerting anti-inflammatory effects may have efficacy for controlling symptoms of mosquito bites. This study was conducted to determine the efficacy and safety of this product on mosquito bite reactions. ...

... DMSO, dimethyl sulfoxide; DEX, dexamethasone; Le135, specific inhibitor of RARβ; GR, glucocorticoid receptor; CRABPI, cellular retinoic acid binding protein I; CRABPII, cellular retinoic acid binding protein II; CYP26, cytochrome P450 26 because Serpina3n also acts as a reactive astroglial marker. It has been reported that DEX can remarkably enhance both the gene and protein levels of Serpina3n and that Serpina3n may act as a circulating biomarker for muscle atrophy induced by glucocorticoids [37,53]. In our study, DEX potentiated the expression of Serpi-na3n in a concentration-dependent manner (Fig. 6a, b), which is consistent with our RNA-seq results and previous reports involving different cell lines. ...

... Molecular mechanisms involved in AMD etiopathogenesis can be broadly categorized into abnormal (excessive) level of reactive oxygen species (ROS) and oxidative stress (OS), generated mainly in the RPE cells [1,10,11], dysregulated internal antioxidant mechanisms such as heterophagy and autophagy pathways [14,15], oxidative mitochondrial dysfunction and sluggish mitophagy pathway [10,16], dysregulated metabolism of lipoproteins [17,18], degeneration of photoreceptors/RPE cells complex and influence of regulated genetically programmed cells' death (PCD) mechanism leading to massive cells' death (apoptosis; classical and non-inflammatory PCD pathway, pyroptosis; pro-inflammatory PCD activated by inflammasomes, necroptosis; regulated and caspase-independent necrosis, as well as ferroptosis; novel PCD, all contribute to genetically programmed RPE cell death in AMD) [11,19], chronic inflammation; pathological parainflammation connected with macrophages and microglia recruitment [20,21], complement complex activation [22,23], inflammasomes activation [20,24,25], and dysregulation of angiogenesis [5]. ...

... Previously, Trikha et al. [24] reported the cell viability and diagnostic yield when applying 20-gauge and 25-gauge vitrectomy to cultured human Burkitt lymphoma cells (Raji B-cell lymphoma line). When comparing simple aspiration 20-gauge and 25-gauge vitrectomy based on flow cytometry, there was no difference in cell viability or diagnostic yield of the three cell surface markers CD19, CD45, and kappa light chain. ...