The pathogenesis of diabetic retinopathy is complicated. The vast network of multiple factors including unifying mechanism, inflammatory reaction, neuron degeneration and metabolic memory of glucose, and the four established pathogenic molecular pathways are hotspots of mechanism research for diabetic retinopathy. Nevertheless, these researches may be only one corner of the ldquo;icebergrdquo; of DR mechanism, and we still face enormous challenges in DR mechanism research. Collaboration with multiple disciplines to study the relationship between DR and diabetes and other systemic diseases, search novel therapy targets may increase the result in an unexpected windfall for DR basic research.
Objective To observe the relationship between retinal microglial activations and ganglion cell (RGC) damages in early-stage diabetic rats. Methods A total of 20 SpragueDawley（SD）rats were randomly divided into 4 groups (each with 5 rats): 1 month control group, 1 month diabetes group, 3 month control group, 3 month diabetes group. Diabetes was induced by intraperitoneal injection of streptozotocin (STZ). The RGCs of all rats were retrograde labeled by carbocyanine dye DiI injected at the superior colliculi.Microglial cells and RGCs in retinal flat-mounts and sections were stained immunohistochemically and recorded under confocal microscope.Results The diabetic microglial cells were amoeboid and ovoid with fewer processes on retinal flat mounts. The density of microglial cells which phagocytosed DiI particles in the RGC layer significantly increased in the 3month diabetes group（P＜0.01）. The density of microglial cells in the RGC layer significantly increased in the 1- and 3- month diabetes group（P＜0.05）. However there were more microglial cells in the RGC layer in the 3- month diabetes group than the 1-month diabetes group（P＜0.0001）. Significant correlation was found between the amount of microglial cells and that of RGCs in the early-stage of diabetes. Conclusions Microglial cell activation has close relationship with the RGC damages in early-stage diabetic rats.
ObjectiveTo investigate the relationship between retinal vessel diameters and cerebral infarction of carotid artery stenosis patients. MethodsEighty-seven patients (174 eyes) with carotid stenosis were included in this study. There were 49 males and 38 females, with an average age of (65.25±7.85) years. Thirty-four patients were suffered from cerebral infarction (cerebral infarction group), and the other 53 patients had no cerebral infarction (control group). There was no significant difference in age (t=1.916), male rate (χ2=0.142) and carotid stenosis extent (χ2=0.785) between the two groups (P=0.059, 0.706, 0.675). All patients underwent color fundus photography after mydriasis. Retinal vascular caliber measurements were performed using IVAN software. The main parameters were central retinal artery diameter (central retinal artery equivalent, CRAE), the diameter of the central retinal vein (central retinal vein equivalent, CRVE) and the retinal arteriole to venular ratio (AVR). The relationship between retinal vessel diameter and cerebral vascular disease were analyzed with logistic regression analysis. ResultsIn cerebral infarction group, CRVE, CRAE and AVR ratios were (132.90±20.67) μm, (243.47±43.92) μm and 0.56±0.10, while the control group was (145.26±21.59) μm, (224.99±32.35) μm and 0.68±0.13 respectively. There were significant differences between the two groups (t=-2.648, 2.257, -4.631; P < 0.05). After correction for risk factors, such as age, smoking history, CRAE reduction and CRVE increases were significantly correlated with cerebral infarction. ConclusionCRAE reduction and CRVE increases are risk factors of cerebral infarction in patients with carotid stenosis, and it is useful in the prediction.
Objective To investigate the relationship between dyslipidemia and diabetic retinopathy in non-insulin-dependent diabetes mellitus（NIDDM） patients． Methods In 55 health controls，60 NIDDM patients with DR and 75 NIDDM patients without DR，the plasma total cholesterol（TC），triglycerides（TG），high-density lipoprotein（HDL）and HDL subfractions，fasting plasma glucose（FPG），fasting plasma insulin（FINS）and glycosylated hemogolbin（HbA 1C）were measured，and the plasma lowdensity lipoprotein （LDL） and very lowdensity lipoprotein（VLDL）were caculated． Results In NIDDM patients with DR，the TC，LDL，FPG，HbA 1C and duration of NIDDM were higher or longer than those in NIDDM patients without DR．Moreover，the TC，LDL，FPG、FINS、HbA 1C and dutation of NIDDM were increased or lengthened in NIDDM patients with proliferative DR as compared with those with backgroud DR．The correlation analysis showed the severity of DR was positively correlated with TC，LDL，HbA 1C and duration of NIDDM． Conclusion Dyslipidemia may play some role in the onset and development of DR． (Chin J Ocul Fundus Dis,1998,14:21-23)