ABSTRACT
Objective To investigate the protective role of light preconditioning in retinal photoreceptor cells and the underlying mechanisms after light damage.Methods Together 42 BALB/c mice were randomly divided into normal control group,light damage group,light preconditioning + light damage group and light preconditioning group.Mice in the light damage group were exposed to 4000 Lux intensity of cool white fluorescent light for 4 h continually;mice in the light reconditioning + light damage group were maintained in 600 Lux cyclic bright light for preconditioning (12 h ON and 12 h OFF) for 6 days,and then exposed to 4000 Lux bright-light for the induction of the damage;mice in the light reconditioning group were maintained in 600 Lux cyclic bright light for preconditioning (12 h ON and 12 h OFF) for 2 days,4 days,6 days.Then the function and morphology of retinal photoreceptor cells were detected by flash electroretinogram (FERG) and histopathological examination in the normal control group,light damage group and light preconditioning + light damage group,while real-time polymerase chain reaction (PCR) was used to detect the mRNA relative expression of leukemia inhibitory factor (LIF) and Western blot analysis was used to detect the phosphoprotein relative expression of signal transducer and activator of transcription 3(STAT3) in the light preconditioning group.Results FERG results showed the amplitudes of scotopic ERG a wave of the light damage group were decreased when compared with the normal control group,with significant difference (P =0.000).Compared with the light damage group,the amplitudes of scotopic ERG a wave of the light preconditioning + light damage group were increased significantly (P =0.000).Histopathological examination results showed that the number of photoreceptor nuclei in the light damage group was decreased compared with the normal control group,and the difference was statistically significant (P =0.000).Compared with light damage group,the number of photoreceptor nuclei in light preconditioning + light damage group was increased significantly (P =0.000).Real-time PCR results showed light preconditioning enhanced the LIF mRNA relative expression in a time-dependent manner (F=128.776,P =0.000).Western blot results showed light preconditioning up-regulated the phosphoprotein relative expression of STAT3 protein in a time-dependent manner (F =73.493,P =0.000).Conelusion Light preconditioning can protect retinal photoreceptor cells against light damage which may results from the activation of LIF/STAT3 signaling pathway.
ABSTRACT
Objective To observe the efficacy and safety of conbercept in the treatment of central serous chorioretinopathy (CSC) by EDI-OCT.Methods From July 2015 to July 2017,42 patients (44 eyes) of central serous choriodal retinopathy received intravitreal injection of conbercept (0.5 mg,0.05 mL).Then,the best corrected visual acuity was recorded before injection and 1 week,4 weeks and 12 weeks after treatment;meanwhile,EDI-OCT was used to measure subfoveal choroidal thickness at different time points.Results In CSC patients,the BCVA of 1 week,4 weeks and 12 weeks after treatment were 0.57 ±0.23,0.62 ±0.23 and 0.59 ±0.71,respectively,which were significantly higher than those before treatment [(0.43 ± 1.11)] (all P ＜ 0.05).The subfoveal choroidal thickness was (308.17 ± 16.52) μm,(286.54 ± 37.52) μm and (274.58±41.38)μm at 1 week,4 weeks and 12 weeks after treatment,respectively,which were significantly lower than those before treatment [(346.31 ± 59.43) μm] (all P ＜ 0.05).Conclusion It is safe and effective for conbercept injection in the treatment of CSC.
ABSTRACT
<p><b>BACKGROUND</b>Neovascular glaucoma (NVG) is a refractory glaucoma. The management of NVG is very difficult, and it is more difficult when combined with vitreous hemorrhage. The aim of this study was to investigate the effects of ranibizumab plus combined surgery for NVG with vitreous hemorrhage.</p><p><b>METHODS</b>A total of 26 eyes of 26 NVG patients with vitreous hemorrhage were recruited in this study. The patients aged from 36 to 63 years with a mean age of 51.97 ± 7.60 years. The mean intraocular pressure (IOP) was 46.38 ± 5.75 mmHg (1 mmHg = 0.133 kPa) while being treated with the maximum medical therapy. The mean best-corrected visual acuities converted to logarithm of the minimum angle of resolution (logMAR BCVA) was 2.62 ± 0.43. All the patients underwent intravitreal injection of 0.5 mg (0.05 ml) ranibizumab combined with pars plana vitrectomy (PPV), pars plana lensectomy (PPL) with a preserved anterior capsule, panretinal photocoagulation (PRP), and trabeculectomy (intravitreal ranibizumab [IVR] + PPV + PPL + PRP + trabeculectomy). The IOP and logMAR BCVA were the main outcome measures in this study.</p><p><b>RESULTS</b>The follow-up period was 12 months. The mean postoperative IOPs were 26.38 ± 3.75 mmHg, 21.36 ± 3.32 mmHg, 18.57 ± 3.21 mmHg, and 16.68 ± 2.96 mmHg, respectively at 7 days, 1 month, 3 months, and 12 months after PPV + PPL + PRP + trabeculectomy. At the last follow-up, the mean IOP was significantly lower than the preoperative one (t = 6.612, P = 0.001). At 7 days, 1 month, 3 months, and 12 months after PPV + PPL + PRP + trabeculectomy, the mean logMAR BCVA were 1.30 ± 0.36, 1.29 ± 0.37, 1.29 ± 0.39, and 1.26 ± 0.29, respectively. At the last follow-up, the mean logMAR BCVA was significantly improved, and the difference was statistically significant compared with preoperative one (t = 6.133, P = 0.002). The logMAR BCVA improved in 22 eyes (84.62%), and remained stable in 4 eyes (15.38%). The neovascularization in the iris and the angle regressed significantly in all patients 7 days after ranibizumab injection. No serious complications occurred during 12 months of the study.</p><p><b>CONCLUSIONS</b>IVR + PPV + PPL + PRP + trabeculectomy can control IOP well and improve BCVA without severe complication for NVG patients with vitreous hemorrhage.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Glaucoma, Neovascular , Drug Therapy , General Surgery , Intraocular Pressure , Postoperative Complications , Ranibizumab , Therapeutic Uses , Trabeculectomy , Vitrectomy , Vitreous Hemorrhage , Drug Therapy , General SurgeryABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of 4OH-Tamoxifen (OHT) on proliferation and apoptosis of primary cultured prostate stromal cells.</p><p><b>METHODS</b>Primarily cultured prostate stromal cells in vitro were treated with various concentrations (10(-8) mol/L - 10(-5) mol/L) of estradiol (E2), diethylstilbestrol (DES), OHT and the mixture of E2 (10(-8) mol/L - 10(-6) mol/L) with OHT (10(-7) mol/L) and then MTT and TUNEL were used to detect their proliferation and apoptosis respectively.</p><p><b>RESULTS</b>There was a significant difference (P < 0.05) between OHT and estrogens in the effects on the apoptosis and proliferation of the primarily cultured prostate stromal cells. OHT suppressed proliferation of the prostate stromal cells at the concentrations from 10(-7) mol/L to 10(-5) mol/L (P < 0.05), and this effect was concentration related (r = -0.383, P = 0.005); OHT (10(-7) mol/L) suppressed the proliferation stimulation effect of E2 at the concentrations from 10(-8) mol/L to 10(-6) mol/L (P < 0.05). OHT induced apoptosis at the concentrations from 10(-8) mol/L to 10(-5) mol/L (P < 0.05), and this effect was concentration related (r = 0.349, P = 0.012). The apoptosis induced by OHT could not be reversed by E2 at the concentrations from 10(-8) mol/L to 10(-5) mol/L (P > 0.05).</p><p><b>CONCLUSION</b>OHT can obviously suppressed the proliferation and promote the apoptosis of primarily cultured prostate stromal cells, which might not be totally attributed to the competitive inhibition of the estrogen receptor.</p>