ABSTRACT
AIM: To evaluate the therapeutic effect of amniotic membrane (AM) for covering high myopic macular hole associated with retinal detachment following failed primary surgery. METHODS: Seventeen eyes of 17 patients whose axial length was more than 29 mm suffered from macular hole (MH) or MH associated with retinal detachment (RD), and had previously surgery of pars plana vitrectomy (PPV) with internal limiting membrane (ILM) peeling and silicone oil (SO) tamponade. Half a year after the surgery, optical coherence tomography (OCT) showed that MH did not heal in all 17 eyes and RD was still maintained in 13 eyes of these 17 eyes. We performed SO removal combined with AM covering on macular area and C3F8 tamponade, and phacoemulsification combined with intraocular lens implantation simultaneously cataract eyes. We followed up these patients for one year. RESULTS: In all 17 eyes, SO was removed successfully, MHs were healed and RDs were reattached. One eye (5.89%, 1/17) had AM shifted half a month after surgery and underwent a second surgery to adjust the position of the AM and supplement C3F8. After surgery, the visual acuity (VA) improved in 15 eyes (88.24%, 15/17), no change in two eyes (11.76%, 2/17). No serious complications occurred in all eyes. CONCLUSION: AM covering is helpful to rescue the previous failure surgery of high myopic MH.
ABSTRACT
Background: As a rare disease in children, necrotizing enterocolitis (NEC) leads to high morbidity and mortality. However, its pathophysiology is largely unclear. Transient receptor potential melastatin 7 (TRPM7) is a membrane protein, which plays key roles in the inflammatory response. This study sought to examine the promoting effect of TRPM7 on NEC in children and explore the therapeutic effect of a TRPM7 inhibitor NS8593. Methods: First, we detected TRPM7 and NLR family pyrin domain containing 3 (NLRP3) expression and the state of inflammation in children with NEC through quantitative real-time polymerase chain reaction (RT-PCR), Western blot, and enzyme-linked immunosorbent assays. Next, Human intestinal epithelial cell lines were induced to NEC by lipopolysaccharides (LPSs). The level of cytokines and reactive oxygen species (ROS) were tested by RT-PCR and flow cytometry. The TRPM7 mediated calcium flux were determined by fluorescence. In addition, we used the TRPM7 inhibitor NS8593 to treat the in vivo rat model. The mRNA and protein expression were determined by real-time PCR and Elisa analysis, respectively. Results: TRPM7 and NLRP3 expression was more increased in the samples from children with NEC compared to the control samples. Additionally, the elevated secretion of interleukin-1ß, interleukin-6, and tumor necrosis factor alpha was also detected in the serum of children with NEC. These results showed that TRPM7 had a promoting effect on NEC development, possibly via the activation of NLRP3. To test our hypothesis, the TRPM7 inhibitor NS8593 was used to treat the LPS-stimulated IEC-6 cells. We found that the TRPM7 inhibitor NS8593 inhibited LPS-induced cytokine production and exhibited an anti-inflammatory effect by alleviating TRPM7-mediated NLRP3 inflammasome activation. Through in-vivo experiments, we found that TRPM7 was involved in the occurrence of NEC, and its inhibitor NS8593 played a certain therapeutic role in the rat model. Conclusions: Our study revealed TRPM7 inhibitors attenuated LPS-induced ROS and reduced the release of pro-inflammatory cytokines. It also exhibited protective effects on the NEC model.
