A 10-Year Retrospective Case Series on Wound Dehiscence Following Corneal Transplant.

Background and objective Corneal transplants are associated with multiple well-known complications, one of them being wound dehiscence. It results in unfavorable outcomes, such as ocular structure damage, graft failure, repeated surgeries, and possibly a poor prognosis in terms of vision quality. Although the wound site may appear well-healed clinically, as the strength at the graft-host junction is weak, the site is susceptible to dehiscence. Wound dehiscence can be secondary to suture removal and/or trauma. In this study, we assessed the incidence of wound dehiscence secondary to trauma following corneal transplant and evaluated its occurrence in terms of patient age, type of corneal transplant performed, duration between corneal transplantation and wound dehiscence, mechanism of injury, and final outcome. Methods This was a case series that included all patients who suffered from wound dehiscence secondary to trauma post-corneal transplant between January 1, 2009, and December 31, 2019, at Hospital Kuala Lumpur. Results A total of 492 patients underwent corneal transplant surgery during the 10-year study period. Based on specified inclusion and exclusion criteria, only 13 patients were eligible for inclusion in this study. The incidence of wound dehiscence secondary to trauma post-penetrating keratoplasty (PK) was low (2.64%). Twelve patients had undergone PK, while one patient had undergone deep anterior lamellar keratoplasty (DALK). Blunt ocular trauma post-transplant can cause wound dehiscence regardless of patient age and duration post-corneal transplantation. Males are at a higher risk as their active lifestyle contributes to higher exposure to ocular injury. Conclusion As corneal transplant patients are at life-long risk of wound dehiscence post-transplant, they must be counseled about this possible risk and the need to take adequate precautions in their daily lives. Based on our findings, the use of newer technologies and partial- rather than full-thickness corneal transplants should be explored further.

Anticancer activity of a monobenzyltin complex C1 against MDA-MB-231 cells through induction of Apoptosis and inhibition of breast cancer stem cells.

In the present study, we examined the cytotoxic effects of Schiff base complex, [N-(3,5-dichloro-2-oxidobenzylidene)-4-chlorobenzyhydrazidato](o-methylbenzyl)aquatin(IV) chloride, and C1 on MDA-MB-231 cells and derived breast cancer stem cells from MDA-MB-231 cells. The acute toxicity experiment with compound C1 revealed no cytotoxic effects on rats. Fluorescent microscopic studies using Acridine Orange/Propidium Iodide (AO/PI) staining and flow cytometric analysis using an Annexin V probe confirmed the occurrence of apoptosis in C1-treated MDA-MB-231 cells. Compound C1 triggered intracellular reactive oxygen species (ROS) production and lactate dehydrogenase (LDH) releases in treated MDA-MB-231 cells. The Cellomics High Content Screening (HCS) analysis showed the induction of intrinsic pathways in treated MDA-MB-231 cells, and a luminescence assay revealed significant increases in caspase 9 and 3/7 activity. Furthermore, flow cytometric analysis showed that compound C1 induced G0/G1 arrest in treated MDA-MB-231 cells. Real time PCR and western blot analysis revealed the upregulation of the Bax protein and the downregulation of the Bcl-2 and HSP70 proteins. Additionally, this study revealed the suppressive effect of compound C1 against breast CSCs and its ability to inhibit the Wnt/ß-catenin signaling pathways. Our results demonstrate the chemotherapeutic properties of compound C1 against breast cancer cells and derived breast cancer stem cells, suggesting that the anticancer capabilities of this compound should be clinically assessed.

Synthesis, structural characterization, and anticancer activity of a monobenzyltin compound against MCF-7 breast cancer cells.

A new monoorganotin Schiff base compound, [N-(3,5-dichloro-2-oxidobenzylidene)-4-chlorobenzyhydrazidato](o-methylbenzyl)aquatin(IV) chloride, (compound C1), was synthesized, and its structural features were investigated by spectroscopic techniques and single-crystal X-ray diffractometry. Compound C1 was exposed to several human cancer cell lines, including breast adenocarcinoma cell lines MCF-7 and MDA-MB-231, ovarian adenocarcinoma cell lines Skov3 and Caov3, and prostate cancer cell line PC3, in order to examine its cytotoxic effect for different forms of cancer. Human hepatic cell line WRL-68 was used as a normal cell line. We concentrated on the MCF-7 cell line to detect possible underlying mechanism involvement of compound C1. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay revealed the strongest cytotoxicity of compound C1 against MCF-7 cells, with a half maximal inhibitory concentration (IC50) value of 2.5±0.50 µg/mL after 48 hours treatment. The IC50 value was >30 µg/mL in WRL-68 cells. Induced antiproliferative activity of compound C1 for MCF-7 cells was further confirmed by lactate dehydrogenase, reactive oxygen species, acridine orange/propidium iodide staining, and DNA fragmentation assays. A significant increase of lactate dehydrogenase release in treated cells was observed via fluorescence analysis. Luminescent analysis showed significant growth in intracellular reactive oxygen species production after treatment. Morphological changes of necrosis and early and late apoptosis stages were observed in treated cells after staining with acridine orange/propidium iodide. DNA fragmentation was observed as a characteristic of apoptosis in treated cells. Results of the present study obviously reveal potential cytotoxic effects of compound C1 against human breast cancer MCF-7 cells.