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This study aims to determine the ultrastructural changes in collagen fibrils in rabbit conjunctiva after conjunctival crosslinking using riboflavin and ultraviolet A (UVA) light at an irradiation intensity of 45 mW/cm2. Conjunctival crosslinking may increase conjunctival stiffness. The supertemporal quadrants of the right eyes of 24 adult rabbits were treated with a topical riboflavin solution (0.25%) before irradiation with UVA light at 45 mW/cm2 for 4 min. After 3 weeks, the collagen fibrils in fibril bundles were examined by electron microscopy. Immunohistochemical staining was used to detect the expression levels of collagen I and collagen III in the rabbits’ conjunctiva. The diameter of the collagen fibrils in the fibril bundles varied slightly, ranging from 30 to 60 nm in the conjunctival stroma of the control group. In the treatment group, the diameter of collagen fibrils ranged from 60 to 90 nm. The thickest collagen fibrils were observed in the treatment group (up to 90 nm in diameter). In contrast, those in the conjunctival stroma of the control group were considerably smaller (up to 60 nm in diameter). However, thicknesses of collagen fibrils displayed a unimodal distribution. Both collagen I and collagen III increased after treatment with riboflavin and UVA light irradiation at 45 mW/cm2. The data indicate that in rabbits, conjunctival crosslinking with riboflavin and UVA light at 45 mW/cm2 for 4 min is safe and does not induce ultrastructural alterations of the conjunctival cells. The conjunctival crosslinking with riboflavin and UVA light at 45 mW/cm2 can increase the diameter of collagen fibrils, but the average densities of collagen I and collagen III have no statistical significance.

Although all kinds of complication have been reported after wasp stings, multiple organ failure following wasp attacks is very rare. In the past, the mortality of patients with multiple organ failure treated by conventional therapy after wasp stings was very high. Here, we report on a 65-year-old individual who developed multiple organ failure following wasp stings. When the patient was admitted at our hospital, 3 days after he had been stung by the wasps, he was unconscious. He was suffering from acute renal failure, hepatic, respiratory, and circulatory failures, and intravascular hemolysis. In addition to conventional therapy, plasma exchange was applied twice and followed by continuous venovenous hemofiltration. In the end, this elderly patient made a complete recovery, with his renal function returning to normal.

Aim: To investigate the expression of matrix metalloproteinases 1 and 3 (MMP-1 and MMP-3) and their tissue inhibitors of metalloproteinases 1 and 3 (TIMP-1 and TIMP-3) in the conjunctiva of eyes with conjunctivochalasis (CCh)., Methods: The conjunctival tissue was obtained from the CCh patients and controls, the MMPs/TIMPs expression concentration was determined by enzyme-linked immuno-sorbent assay (ELISA) and immunofluorescence staining. The expression levels of MMPs/TIMPs in the CCh fibro-blasts were determined by analyzing its concentration in the cellular supernatant that was abstracted from the in vitro cultured CCh fibroblasts., Results: MMP-1 and MMP-3 levels determined by ELISA were both significantly higher in the CCh group than that in the control group ( P =0.042, 0.022, respectively), so was the levels of TIMP-1 ( P =0.010). No significant difference in the expression of TIMP-3 in conjunctiva was found between the two groups ( P =0.298). The expression of MMP-1 and MMP-3 were both up-regulated significantly in the CCh group ( P =0.040, 0.001, respectively) on immuno-fluorescence staining. MMP-1 and MMP-3 expression in the fibroblasts were both significantly higher in the CCh group than that in the control group ( P =0.027, 0.001, respectively), while neither the TIMP-1 nor TIMP-3 expression was significantly different between the two groups ( P =0.421, 0.237, respectively)., Conclusion: The overexpression of MMP-1 and MMP-3 in conjunctival tissue and fibroblasts may play an important role in the pathogenesis and development of CCh.