Purpose: To compare the incidence, risk factors, treatment, and outcomes associated with intravitreal triamcinolone-acetonide (TA) and dexamethasone-implant (Dex) induced ocular hypertension (OHT). Methods: This retrospective study reviewed 1549 TA and Dex administrations in 1075 eyes of 897 patients. Intraocular pressure (IOP) values were monitored for a period of 6-months following intravitreal injection(s) and patients were categorized as steroid-responders (SR): IOP ≥ 21mmHg, and non-responders (NR): IOP ≤ 20mmHg. Glaucoma patients, glaucoma suspects, uveitis, trauma, and less than one month IOP follow-up cases were excluded from the study. Incidence of IOP rise, time and magnitude of IOP rise, and its management procedures were studied. Ocular and systemic association with OHT incidence was investigated. Statistical analysis was performed using SPSS.23 and p < 0.05 was considered significant. Result: 28% of TA and 17% of Dex administered eyes developed OHT. Male subjects and elderly people (greater than 40 years) are at higher risk for OHT following steroid treatment. A high percentage of IOP rise was observed at day-1 (41%) for TA-SR, and after 1-month (50%) among Dex-SR. IOP rise was found to be more severe (>30mmHg) for TA-SR compared to Dex-SR (p=0.006). 6% TA-SR required trabeculectomy with medically uncontrollable IOP. Myopia is a risk factor for secondary OHT, whereas diabetes mellitus and hypercholesterolemia were protective of it. Conclusion: 28% of TA and 17% of Dex administrations developed OHT. Early and severe IOP rise was more common in TA than among Dex administrations. Myopia is a risk for Dex-OHT.
In the era of personalized medicine as well as precision medicine, targeted therapy has become an integral part of cancer treatment in conjunction with conventional chemo-and radiotherapy. We designed aptamer-siRNA chimeras that can specifically target cancers expressing EpCAM, a stem cell marker and deliver the specific siRNA required for therapy response. The siRNAs were chosen against PLK1, BCL2 and STAT3 as these oncogenes play prominent role in tumour progression of several cancers. Targeted delivery of EpCAM-siRNA chimeras resulted in cell death in several cancer cell lines such as cancers of the breast, lung, head and neck, liver and retinoblastoma. In vivo analysis of EpCAM-siRNA chimera mediated silencing on RB xenografts tumour model showed increased tumor reduction in all the three EpCAM-siRNA treated conditions. However, regulation of PLK1 exhibited higher efficacy in tumour reduction. Therefore. We studied signaling mechanism using global phosphoproteomics analysis. An increased P53 mediated downstream signalling pathway might have enabled increased apoptosis in the cancer cells. In conclusion, this study demonstrated the efficacy of EpCAM aptamer chimeras coupled to siRNA gene silencing for targeted anti-cancer therapy.
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