Purpose: To compare the long-term follow-up results of the bare sclera technique (BST), limbal-conjunctival autograft technique (LCAT) and amniotic membrane graft technique (AMGT) in primary pterygium excisions. Materials and Methods: In this study, 48 eyes of 48 patients who underwent pterygium surgery using BST (group 1), 63 eyes of 63 patients who underwent pterygium surgery using LCAT (group 2) and 52 eyes of 52 patients who underwent pterygium surgery using AMGT (group 3) were compared with respect to corneal epithelialization, recurrence and complication of the procedures. The mean ages of the groups were 47.88 ± 14.21 years in group 1, 49.63 ± 14.42 years in group 2 and 47.92 ± 15.52 years in group 3. Patients were followed up to 72.39 ± 11.03 months in group 1, 69.91 ± 12.41 months in group 2 and 61.43 ± 9.83 months in group 3. Results: Postoperative corneal epithelialization was completed in 5.62 ± 1.74 days in group 1, 4.33 ± 0.91 days in group 2 and 4.79 ± 1.39 days in group 3. Corneal epithelialization time was earlier in group 2 than in groups 1 (p < 0.01) and 3 (p < 0.05). Recurrences were detected in 19 eyes (39.58%) in group 1, 11 eyes (14.29%) in group 2 and 12 eyes (23.08%) in group 3. The recurrence rate was significantly lower in group 2 than in groups 1 and 3 (p < 0.001). Postoperative complications were not seen in any of the groups. Graft retraction and necrosis were not detected in the LCAT and AMGT groups during the follow-up period. Conclusions: LCAT was found to be a more effective procedure than BST and AMGT, with decreased recurrence rates after pterygium excision. Limbal-conjunctival autograft seems to be a useful treatment in pterygium surgery due to higher success rates and lower recurrence rates. Amniotic membrane grafts may be an alternative surgical technique for pterygium treatment for patients with or without glaucoma who might need glaucoma surgery in the future.

There was no significant difference in the success rate between the DCPC and AGV implantation in neovascular glaucoma treatment. However, DCPC is less time consuming and easier method for lowering IOP in patients with neovascular glaucoma.

We previously reported that mice with experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), develop profound urinary bladder dysfunction. Because neurogenic bladder in MS patients causes marked bladder remodeling, we next examined morphometric and molecular alterations of the bladder in EAE mice. EAE was created in female SJL/J mice by immunization with the p139-151 encephalitogenic peptide of myelin proteolipid protein in complete Freund's adjuvant, along with intraperitoneal injections of Bordetella pertussis toxin. Seventy days after immunization, mice were scored for the level of neurological impairment and then killed. Spinal cord sections were assessed for demyelination, inflammation, and T cell infiltration; the composition of the bladder tissue was measured quantitatively; and gene expression of markers of tissue remodeling and fibrosis was assessed. A significant increase in the bladder weight-to-body weight ratio was observed with increasing neurological impairment, and morphometric analysis showed marked bladder remodeling with increased luminal area and tissue hypertrophy. Despite increased amounts of all tissue components (urothelium, smooth muscle, and connective tissue), the ratio of connective tissue to muscle increased significantly in EAE mice compared with control mice. Marked increases in mRNA expression of collagen type I α(2), tropoelastin, transforming growth factor-β3, and connective tissue growth factor (CTGF) were observed in EAE mice, as were decreased levels of mRNAs for smooth muscle myosin heavy chain, nerve growth factors, and muscarinic and purinergic receptors. Our results suggest that bladder remodeling corresponding to EAE severity may be due to enhanced expression of CTGF and increased growth of connective tissue.

The cause of chronic pelvic pain in interstitial cystitis/painful bladder syndrome (IC/PBS) remains unclear; autoimmunity is a possible etiology. We have recently shown that injection of a single immunogenic peptide of uroplakin 3A (UPK3A 65-84) induces experimental autoimmune cystitis (EAC) in female BALB/cJ mice that is unique among experimental models in accurately reflecting both the urinary symptoms and pelvic pain of IC/PBS. The aim of this project was to identify the roles of mast cells and mast cell chemoattractant/activator monocyte chemoattractant protein-1 [chemokine (C-C motif) ligand 2 (CCL2)] in the allodynia in this model. We immunized 6- to 8-wk-old female BALB/cJ mice with UPK3A 65-84 peptide and, 5–40 days later, observed increased responses to stimulation of the suprapubic abdominal and hindpaw surfaces with von Frey monofilaments compared with mice injected with adjuvant alone. Suprapubic and hindpaw tactile allodynia responses by EAC mice were blocked by instillation of lidocaine into the bladder but not by lidocaine in the uterus, confirming the bladder as the source of the hypersensitivity. Markedly increased numbers of activated mast cells and expression of CCL2 were found in the bladder after immunization with UPK3A 65-84. Hypersensitive responses were inhibited by mast cell stabilizer cromolyn sodium and antagonists of histamine receptors 1 and 2. Furthermore, BALB/cJ mice with deletion of the Ccl2 or chemokine (C-C motif) receptor 2 gene exhibited markedly reduced allodynia and accumulation of mast cells after UPK3A 65-84 immunization. These results show that UPK3A 65-84 immunization causes chronic visceral allodynia and suggest that it is mediated by CCL2-driven mast cell accumulation in the bladder.