Objective To analyze the relationship of human leukocyte antigen alleles (HLA-A/B, HLA-DRB/DQB) polymorphism and Eales disease, tuberculosis infection in a Han population in Zunyi city of China. Methods The subjects were analyzed by case control study, which consisted of three groups including Eales disease group (47 patients), pulmonary tuberculosis group (36 patients) and normal control group (100 healthy people). Thirty-nine patients in Eales disease group who had complete history were divided into 4 subgroups according to the history and tuberculin PPD test. Twelve patients with past or present pulmonary tuberculosis were in group A, 27 patients without pulmonary tuberculosis were in group B, 27 patients with positive PPD test were in group C, and 12 patients with negative PPD test were in group D. Fifty-nine alleles of HLA-A/B and HLA-DRB/DQB were analyzed by polymerase chain reaction with sequencespecific primers (PCR-SSP) in all subjects. Odds ratios between each group (OR) and 95% confidence interval (CI) were calculated; Frequency distribution of HLA-A02 gene were analyzed for the group A and the TB group. Results The frequency distribution of HLA-A02 （OR=9.719, OR95% CI:4.377-21.580,P=0.000）and HLA-B07 （OR=11.605, OR95% CI:2.397-56.191,P=0.001）alleles in Eales disease group were obviously higher than that in normal control group, but frequency distribution of HLA-A11（OR=0.495, OR95% CI:0.245-1.000,P=0.048）in Eales disease group was obviously lower than that in normal control group. There was no significant difference in frequency distribution of HLA-A02, HLA-A11 and HLA-B07 alleles between groups A and B, and between groups C and D (P＞0.05). The distribution frequency of HLA-A02, HLA-A24, HLA-B07 and HLA-DRB16 alleles among Eales disease group, pulmonary tuberculosis group and control group was statistically different (P＜0.05). The frequency distribution of HLA-A24 alleles in pulmonary tuberculosis group was lower than that in Eales disease group （chi;2=7.289,P=0.007）, but the frequency distribution of HLA-A02 alleles had no significant difference (OR=0.515,P=0.202) between two groups. Conclusions The alleles of HLA-A02 and HLA-B07 may be genetic predisposing genes of Eales disease, but HLA-A11 alleles may be protective gene in population of Han nationality from Zunyi city. The alleles of HLA-DRB16 and HLA-A02 may be genetic predisposing genes of pulmonay tuberculosis. The alleles of HLA-A02 may be a common susceptible gene for Eales disease and pulmonary tuberculosis. HLA-A11 and HLA-A24 alleles were protective genes of Eales disease and pulmonary tuberculosis respectively.
Objective To observe the effect of blue light on apoptosis of cultured human retinal pigment epithelial (RPE) cells in vitro. Methods Human RPE cells were exposed to blue light, and the cells were divided into 3 groups: group A, with various intensity of illumination; group B: with same intensity but different time of illumination; group C: with same intensity and time of illumination but different finish time of the culture. The apoptosis of RPE cells was observed by TdT-dUTP terminal nick-end labeling (TUNEL) and annexin V-fluoresein isothiocyanate (FITC)/propidium iodide (PI) flow cytometry, and transmission electron microscopy. Results The positive cells stained by TUNEL shrinked and turned round, whose nuclei concentrated and congregated like the crescent or hat. Cracked nuclei and membrane bleb were found. Swollen mitochondrial, disappeared inner limiting membrane of mitochondria, and dilation of the rough endoplasmic reticulum with metabolite were observed by transmission electronmicroscopy. In group A, mild damage of RPE cells was found when the threshold value of the intensity of illumination was less than（500±100）lx, and the apoptosis and necrosis of RPE cells aggravated as the intensity of illumination increased; in group B, as the time of illumination extended, the number of apoptotic RPE cells didn′t increase while the necrosis increased; in group C, 6 and 12 hours after illumination, apoptosis of cells was the main injury, while apoptosis with necrosis was found and necrotic cells increased as the time of illumination was prolonged. Conclusions Illumination with blue light may cause damages of human RPE cells in vitro, with the modalities of apoptosis, apoptotic necrosis and necrosis. The extent of injury is dependent on intensity and duration of the illumination. (Chin J Ocul Fundus Dis, 2005, 21: 384-387)
Objective To investigate the clinical features of polypoidal choroidal vasculopathy (PCV) in Chinese patients.Methods The clinical data of 71 continuous patients (142 eyes) who were diagnosed with PCV by fundus photography, fundus fluorescein angiography (FFA), indocyanine green angiography (ICGA) and optical coherence tomography (OCT) were analyzed retrospectively.Results Eleven patients (11 eyes) of 71 patients (142 eyes) were diagnosed with PCV to make up 15.49% and 7.75% of the numbers of patients and affected eyes respectivery. The patients included 7 males (63.6%)and 4 females (36.4%). The predominant location for these lesions was the macular region in 10 eyes (90.9%). Fundus examination demonstrated the reddish-orange nodular elevations in 6 eyes. ICGA revealed umbrellalike or twiglike branching vascular networks and polypoidal dilations at the vascular terminals of the branches in all patients, and feeder vassels within choroidal vascular networks were found in 8 eyes. OCT images of retinochoroidal structures showed prominent anterior protrusion of the orange subretinal mass corresponding to the polypoidal structure in the indocyanine green angiogram. An apparent discontinuity was observed in the highly reflective layer which delineates the polypoidal structure.Conclusions PCV mainly affects the male over 50 years and the eyes involved were mostly unilateral. Most of polypoidal vascular lesions are present in the macul ar area. (Chin J Ocul Fundus Dis，2003，19：269-332)
The occurrence and development of myopia is closely related to scleral remodeling. Therefore, in order to effectively prevent and cure myopia, it is very important to clarify the mechanism of scleral remodeling. In recent years, Chinese scholars have found that endoplasmic reticulum stress can regulate the expression of apoptotic proteins through the inositol demand protein-1/X box binding protein-1 pathway in the unfolded protein response, thus it is involved in regulating the state of scleral fibroblasts under hypoxia and regulating the occurrence and development of scleral remodeling. At the same time, some studies have found that inhibiting and knocking out protein kinase RNA-like endoplasmic reticulum kinase and activated transcription factor 6 in endoplasmic reticulum stress can effectively inhibit the growth of ocular axis. This proves that endoplasmic reticulum stress plays an important role in the occurrence and development of scleral remodeling. However, the comprehensive analysis of endoplasmic reticulum stress and scleral remodeling has not been reported at home and abroad. In-depth analysis of the relationship between endoplasmic reticulum and scleral remodeling is of great significance for the follow-up analysis and study of the mechanism of scleral remodeling.
Objective Mendelian randomization (MR) was used to analyze the potential relationship between blood pressure and proliferative diabetic retinopathy (PDR). MethodsTwo-sample MR analysis was performed using summary statistics from genome-wide association studies. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were selected as the exposure, PDR as the outcome. The instrumental variable of SBP and DBP came from the publicly available data of the the UK Medical Research Council Comprehensive Epidemiology Unit and Neale Laboratory; the outcome data (8 681 cases in the case group, 204 208 cases in the control group, European population) are from the FinnGen database. Inverse variance weighting (IVW) and weighted median (WM) were used to analyze the potential relationships between SBP, DBP and PDR. ResultsMR analysis showed that IVW [SBP: odds ratio (OR)=1.36, 95% confidence interval (CI) 1.17-1.57, P=4.22E-05; DBP: OR=1.29, 95%CI 1.11-1.51, P=8.6E-04], WM (SBP: OR=1.33, 95%CI 1.07-1.66, P=0.009; DBP: OR=1.28, 95%CI=1.03-1.59, P=0.002). The results showed that elevated SBP and DBP increased the risk of PDR. ConclusionBlood pressure (SBP, DBP) change is positively correlated with the risk of PDR.