青光眼引流器植入联合小梁切除术治疗难治性青光眼的临床观察

目的：观察青光眼引流器植入联合小梁切除术治疗难治性青光眼的疗效。方法对34例（46只眼）难治性青光眼行青光眼引流器植入联合小梁切除术治疗,观察术后视力、眼压、滤过泡及并发症等情况。结果34例难治性青光眼中,新生血管性青光眼12例（17只眼）,无晶状体眼4例（4只眼）,人工晶状体眼1例（1只眼）,外伤性青光眼2例（2只眼）,发育性青光眼9例（12只眼）,色素播散性青光眼2例（2只眼）。术前平均眼压（42．15±2．32）mmHg,术后眼压控制30只眼,眼压部分控制7只眼,眼压失控9只眼,术后平均眼压（18．34±3.55）mmHg,眼压有效控制率为80．43％。功能性滤过泡形成率67．39％,手术并发症较少。结论新型国产青光眼引流器植入联合小梁切除术治疗难治性青光眼疗效好,安全性高,术后并发症少,可以推广使用。     

Heat shock proteins in the retina: Focus on HSP70 and alpha crystallins in ganglion cell survival

Heat shock proteins (HSPs) belong to a superfamily of stress proteins that are critical constituents of a complex defense mechanism that enhances cell survival under adverse environmental conditions. Cell protective roles of HSPs are related to their chaperone functions, antiapoptotic and antinecrotic effects. HSPs' anti-apoptotic and cytoprotective characteristics, their ability to protect cells from a variety of stressful stimuli, and the possibility of their pharmacological induction in cells under pathological stress make these proteins an attractive therapeutic target for various neurodegenerative diseases; these include Alzheimer's, Parkinson's, Huntington's, prion disease, and others. This review discusses the possible roles of HSPs, particularly HSP70 and small HSPs (alpha A and alpha B crystallins) in enhancing the survival of retinal ganglion cells (RGCs) in optic neuropathies such as glaucoma, which is characterized by progressive loss of vision caused by degeneration of RGCs and their axons in the optic nerve. Studies in animal models of RGC degeneration induced by ocular hypertension, optic nerve crush and axotomy show that upregulation of HSP70 expression by hyperthermia, zinc, geranyl–geranyl acetone, 17-AAG (a HSP90 inhibitor), or through transfection of retinal cells with AAV2-HSP70 effectively supports the survival of injured RGCs. RGCs survival was also stimulated by overexpression of alpha A and alpha B crystallins. These findings provide support for translating the HSP70- and alpha crystallin-based cell survival strategy into therapy to protect and rescue injured RGCs from degeneration associated with glaucomatous and other optic neuropathies.