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AIM:To investigate the clinical efficacy of pars plana vitrectomy and Baerveldt glaucoma implant(PPV-BGI) in the treatment of refractory glaucoma.METHODS:One hundred twenty-nine refractory glaucoma patient's clinical data from March 2013 to December 2015 that underwent PPV-BGI were retrospectively reviewed.Among them,63 eyes were neovascular glaucoma (NVG) and 69 eyes were other types of glaucoma (non-NVG).The changes of intraocular pressure(lOP),surgical results,visual acuity (VA),the number of glaucoma medications,complications,and the success rate of surgery were analyzed.RESULTS:Cumulative success rates for the NVG group and non-NVG group were 46.0% and 81.2%,respectively,within 1a after surgeries,the difference was significantly (P< 0.05).Preoperative lOP was 30.4 ± 10.2mmHg in the non-NVG group and 40.1±10.4mmHg in the NVG group,and lOP was reduced to 14.9±4.1mmHg in the non-NVG group and 17.8±4.9mmHg in the NVG,and the difference was significantly (P<0.05).Number of glaucoma medications decreased from 2.7 ± 1.2 in the non-NVG group and 2.9 ± 1.4 in the NVG group preoperatively to 0.51 ±0.96 in the non-NVG group and 0.96±1.18 in the NVG group,and the difference was significantly (P<0.05).Improvement in VA of in the NVG group and non-NVG group were observed in 14 eyes of 13 patients and 38 eyes and 37 patients respectively,and the difference was significantly (P<0.05).The postoperative complications of 1d and 1a follow-up in NVG group was significantly higher than non-NVG group (P<0.05).CONCLUSION:PPV-BGI is a viable surgical option for eyes with refractory glaucoma,but visual outcomes are frequently poor because of ocular comorbidities,especially in eyes with NVG.
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ABSTRACT This study aimed to investigate the expression and mechanism of N- methyl -D- aspartate receptor 1 (NMDAR1) in the pathogenesis of Alzheimer disease (AD). Eighty adult Wistar rats were randomly divided into 4 groups (n=20 each) to receive an injection of 0, 5, 7 and 10 μl of 1 μg/μl amyloid-β 42 (Aβ1-42) in the hippocampus. Twenty rats in normal control group were injected with equal volume of saline. After 10 days, the hippocampus was isolated from 5 randomly selected rats in each group. The NMDAR1 protein and mRNA expression was determined by immunohistochemical staining and qRT-PCR. The aquaporin-1 (AQP-1) mRNA expression was also measured by qRT-PCR. We found that both NMDAR1 and AQP-1 expression in Aβ1-42 groups was increased in a dose-dependent manner. NMDAR1 and AQP-1 expression in 7 and 10 μl Aβ1-42 groups was significantly higher compared with 0 μl Aβ1-42 group (P <0.01). Further, the 10 μl Aβ1-42 group was randomly divided into 3 subgroups: AD-NMDA, AD-MK-801, and AD-Ctrl subgroup, which was given an intraperitoneal injection of NMDAR agonist NMDA, NMDAR antagonist MK-801 and saline, respectively. The relative APQ-1 expression in each subgroup was determined by qRT-PCR and Western blot analysis after 24 h. The AQP-1 expression was significantly decreased in AD-MK-801 group (P < 0.05), but was markedly increased in AD-NMDA group when compared with AD-Ctrl group (P <0.01). Our study suggested that expression abnormity of NMDAR1 is involved in the pathogenesis of AD. NMDAR1 might regulate the pathogenic process through stimulating the expression of AQP-1.