ABSTRACT
·AIM: To analyze the clinical manifestation of Alport syndrome, especially the ocular features.·METHODS: The physical, ophthalmologic and audiologic examination results of thirty two patients with Alport syndrome were analyzed retrospectively.·RESULTS: Thirty (93.7%) patients had some family history. All patients had renal disease: eighteen(56.3%) patients with chronic renal failure, four(12.5%) patients with renal insufficiency, and the other ten(31.3%) patients with hematuria. Twenty (62.5%) patients had sensorineural deafness. Thirteen (40.6%) patients had ocular deformity, five(15.6%) patients had typical ocular changes: three patients with anterior lenticonus, and two patients with macular flecks.·CONCLUSION: Ocular anomalies are not requisite for the diagnosis of Alport syndrome. But its typical ocular features should be recognized by the ophthalmologists which supports the diagnosis.
ABSTRACT
· AIM: To examine the expression of MMP-9 and TIMP-3 mRNA during choroidal neovascularization (CNV) in a murine model and to investigate the role of them in the development of CNV. · METHODS: CNV was induced in C57BL/6J mice by intensive diode laser (810nm) photocoagulation (120mW, 75μm, 0. 1s) of the fundus whereafter eyes were enucleated at 1, 3days, 1, 2, and 4 weeks. The MMP-9 and TIMP-3 mRNA expression were analyzed using in situ hybridization and image analysis system. · RESULTS: Both expression of MMP-9 and TIMP-3 mRNA had dynamic changes. For MMP-9, the expression was 1, 2, 4 wk > 3d > 1d (P < 0.05), whereas TIMP-3 mRNA, 3d, 1, 2, 4 wk>1d (P<0.05). · CONCLUSION: The imbalance between the changes of MMP-9 and TIMP-3 may accelerate the degrading of extracelluar matrix, and then be involved in the pathogenesis of CNV.
ABSTRACT
Objective To evaluate the feasibility of inducing choroidal neovascularization(CNV) in Brown Norway(BN) rats by diode laser with wavelength of 810 nm. Methods Thirty-five BN rats were divided into(7 groups.)In each groups,one rat served as control,while the other four recieved retinal photocoagulation by diode(laser) in two eyes,at a spot size of 75 ?m with a duration of 100 ms and power of 140 mW.On 1,3,7,14,21,28 and 56 days after photocoagulation,the formation and nature process of CNV were observed by fundus fluorescein(angiography)(FFA),indocyaninegreen angiography(ICGA) and light microscopy(LM). Results FFA,ICGA and LM demonstrated that CNV began to form on the seventh day after photocoagulation,increased on the fourteenth day,reached the peak on the twenty-first day and kept stable until the fifty-sixth day. Conclusion Diode Laser can successfully induced CNV in BN rats,and it is an ideal animal model for further study.
ABSTRACT
<p><b>OBJECTIVES</b>To study the inhibitory mechanism of tamoxifen on benign prostatic hyperplasia.</p><p><b>METHODS</b>The Wistar male adult rats were injected into muscle with testosterone propionate 4-6 mg/kg, simultaneously were irrigated into stomach with tamoxifen citrate 0.21 mg/kg. The partly rats of each group were decapitated at 7, 15 and 30 days, then their index numbers of prostate were calculated, and the structural changes of the prostatic histocyte were observed in the light microscopy and scan electronic microscopy.</p><p><b>RESULTS</b>At the 7th, 15th, and 30th day, the index numbers of prostate of those rats which had been injected only with testosterone propionate were higher than that of the control group and the irrigating group(P < 0.05). The hyperplasia of the prostatic epithelial cells and the ground substance of those rats, which had been irrigated with tamoxifen citrate, had not happened in light microscopy and the scan electronic microscopy.</p><p><b>CONCLUSIONS</b>Tamoxifen could block the effect of the estrogen, which could suppress the prostatic hyperplasia. This study could provide the experimental evidences for using Tamoxifen to treat the human benign prostatic hyperplasia.</p>
