The clinical manifestations of infectious retinal diseases are complicated, especially these result from serious infectious diseases such as acquired immune deficiency syndrome (AIDS), tuberculosis and syphilis infections. It is an important issue to differentiate infectious retinal disease from noninfectious intraocular inflammation in the clinic. It is, therefore, highly desirable to follow a proper steps to reach the correct diagnosis. Complete history review and comprehensive ocular examination remains the first step in diagnosing infectious retinal diseases. Although an array of laboratory and serological tests are available to assist in the diagnosis, some situations may require a diagnostic therapy or a tissue biopsy. Identification of the pathogen and histopathologic examination of the ocular specimen remain to be the gold standard of diagnosis. Initiation a specific and appropriate antimicrobial therapy needs multidisciplinary collaborations including ophthalmologists and infectious specialists. Updated knowledge of general medicine and management of infectious diseases, interdisciplinary collaborations and optimization of treatment processes will improve the diagnosis and treatment of retinal infectious diseases in the future.
Objective To observe the expression of alpha;A-and alpha;B-in retina after blue-light exposure.Methods Forty female Wistar rats were divided randomly into 4 groups:control group,and blue-light exposure for 6,12,and 24 hours groups, with 10 rats in each group. The rats in the control group were not intervened.The other three groups of rats were exposed to blue fluorescent lights for 6,12,and 24 hours respcetively. Then the rats were kept in darkness for 12 hours. The globes were enucleated after anaesthesia.The immunohistochemistry and Western blot were performed to detect the expression of alpha;A and alpha;B-crystallin in retina.Results The absorbance value (A value) of retina alpha;A-crystallin was 1.40573plusmn;0.70748 in the control group, and were 4.317 51plusmn;0.412 97, 7.397 08plusmn;1.947 90, 9.634 32plusmn;2.377 61, respectively in the other 3 groups; the difference among the groups was significant (F=24.569,P<0.001). The A value of retina alpha;B-crystallin is 0.129 36plusmn;0.033 93 in the control group, and were 0.507 17plusmn;0.117 55, 7.345 43plusmn;2.292 97, 4.042 26plusmn;3.890 23, respectively in the other 3 groups; the difference among the groups was significant(F=40.102,P<0.001). The results of Western blot showed that the expression of alpha;A and alpha;B crystallin in groups with bluelight exposure was obviously higher than that in the control group.Conclusions Blue light may up-regulate the expression of alpha;A-and alpha;B-crystallin in ratsprime; retina.
Objective To investigate the relationship of clinical indexes between retinopathy in systemic-lupus-erythematosus (SLE)nephritis and SLE,and to discuss its clinical significance. Method The clinical data of 43 cases of SLE nephritis with ocular fundus diseases were retrospectively analyzed.The relationships between retinopathy and kidney defect,general lesions,SLEDAI grade,antinuclear antibody (ANA),anti-double stranded DNA,complement 3 and antiphospholipid antibodies were analyzed with Logistic regression respectively. Results In 86 eyes of the43paitents,there were retinal cotton wool spots in51eyes(59.3%),edema of optic disk in 43 eyes(50.5%),retinal haemorrhage in 12 eyes(14.0%),retinal artery occlusion in 5 eyes(5.8%),central retinal vein occlusion in 2 eyes(2.3%),retinal detachment in 3 eyes(3.5%),optic atrophy in 2 eyes(2.3%),and neovascularization in 2 eyes(2.3%).Logistic regression analysis revealed that SLEDAI grade had linear dependent relation with cotton wool spots and optic disk edema(chi;2=42.154,6.498;P<0.001),and didnrsquo;t have any correlation with proteinuria,hematuria and kidney function.Linear relation between retinal vascular occlusion and antiphospholipid antibodies was found(chi;2=24.475,P<0.001).Retinal haemorrhages,retinal detachment,optic atrophy and neovascularization did not correlate with clinical features. Conclusion SLEDAI grade had linear dependent relation with cotton wool spots and optic disk edema in patients with SLE nephritis,and Linear relation between retinal vascular occlusion and antiphospholipid antibodies is ascertained. Ocular fundus diseases are clinically important for evaluating the therapeutic responses and prognosis in lupus nephritis. (Chin J Ocul Fundus Dis, 2006, 22: 239-241)
Purpose To investigate the expression of intercellular adhesion molecules ICAM-1 and Mac-1,in epiretinal membanes (ERM) of eyes wi th proliferative vitreoretinopathy (PVR). Methods Twenty epiretinal membranes were obtained from eyes undergone vitrectomy for retinal detachment complicated with PVR and observed by immunohistochemical examination. Results Expressions of ICMA-1 and Mac-1 were observed in 18 and 15 membranes respectively.Expression of both adhesion molecules in 12 membranes. Conclusion The findings indicate that adhesion molecules might be involved in the development of PVR. (Chin J Ocul Fundus Dis,2000,16:71-138)
Purpose To investigate the expression of the interleukin-6(IL-6)and tumor necrosis factor alpha(TNF-alpha;) in epiretinal membranes(ERM) of eyes with proliferative vitreoretinopathy(PVR). Methods Nineteen epiretinal membranes were obtained form eyes undergoing vitrectomy for retinal detachment complicated with PVR and observed by immunohistochemical methods. Results Expression of IL-6 and TNF-alpha; were observed in 12 and 15 membranes respectively with positive staining mostly in extracellular matrix of epiretinal membranes.Only one membrane showed positive to IL-6 intracellularly,and expression for IL-6 and TNF-alpha; simultaneously in membranes. Conclusion The findings indicate that IL-6、and TNF-alpha;might be involved in the development of PVR. (Chin J Ocul Fundus Dis,1998,14:219-221)
ObjectiveTo study morphological characteristics and microRNA (miR) expression profiling in a mouse model of oxygen-induced retinopathy (OIR). MethodsHealthy C57BL/6J female mice and pups were randomly divided into normal and OIR group at postnatal day 7 (P7). The normal group was raised in a conventional cage and exposed to room air for 10 days. The OIR group was raised in a sealed chamber and exposed to (75±2)% oxygen. The moms were alternated between the two groups every day to promote their survival under hyperoxia. The OIR group was returned to the room air at P12. At P17, mice from either group were retro-orbitally injected with high molecular weight fluorescein isothiocyanate-dextran (FITC-dextran), the eye balls were fixed in 4% paraformaldehyde, and the retinal whole mounts were prepared. The retinal vessels labeled with FITC-dextran were observed under a fluorescence microscope; the eye balls were also processed for paraffin sections and Hematoxylin and Eosin (H&E) staining. The cell nucleus in the newly-formed vessels beyond the inner limiting membrane was quantified. The miR was extracted from the eyes, reverse transcribed, and subjected to a customized miR array analysis. The real-time PCR was preformed to verify the results of the miR array. ResultsRetinal whole mounts labeled with FITC-dextran showed that the peripheral retinal microvessels in the OIR group were tortuous, disorganized with neovascular buds, and the avascular area was prominent in central retina. In contrast, the vessels were smooth, organized, and evenly distributed in the retinas of normal group. The percentage of avascular area in total retina area in OIR group (25.81±2.12)% was 4-fold that in normal group (6.57±3.6)% (P < 0.01, normal group vs OIR group). H & E staining showed that the number of the cell nuclei beyond inner limiting membrane was (28.41±4.01) in OIR retina, which was substantially higher than that (0.16±0.31) in normal retina (P < 0.01, normal group vs OIR group). More interestingly, the results of miR array showed that 21 out of the 80 miRs examined exhibited more than 1.5-fold changes at expression level. Among these 21 miRs, 9 were up-regulated, 12 were down-regulated; 4 miRs showed more than 3-fold expression changes, 3 were down-regulated and 1 was up-regulated. The expression of the 4 miRs was verified by real-time PCR. The expression trends of miR-3078, miR-140, miR-29b and miR-29c were consistent with those revealed by the miR array. MiR-3078 was significantly up-regulated (t=-2.380, P < 0.05. normal group vs OIR group), and the other 3 miRs were significantly down-regulated (t=2.638, 2.323, 2.415, P < 0.05. normal group vs OIR group). ConclusionsThe OIR mouse model has been established in our study. Differential expression of the microRNAs, including miR-3078, 140, 29b and 29c, was detected in normal and OIR mouse retinas. These miR expression changes may be associated with retinal neovascularization. These results would provide the new leads for further studying pathogenic mechanisms and therapeutic targets for neovascular retinopathy.
ObjectiveTo investigate the clinical characteristics of 40 patients with ocular toxocariasis (OT) on the first attendance. MethodsA total of 40 consecutive patients who were clinically and serologically diagnosed with OT were retrospectively reviewed. ResultsThe mean age of patients was (12.12±10.42) years. There were 29 males and 11 females. 29 cases presented with decreased vision, 4 children with leukocoria, 2 cases with strabismus and 5 cases was found abnormal during regular eye examination. Initially 8 eyes (20%) were misdiagnosed as retinoblastoma (1 eye), Coat's disease(1 eye), cataract (2 eyes), iridocyclitis (2 eyes) and retinal detachment (2 eyes). 23 eyes had retinal detachment, 19 eyes had cataract. OT was the initial diagnosis for 15 patients (37.5%). The best corrected visual acuity (BCVA) were NLP to 0.7. Ultrasound biomicroscopy (UBM) were performed in 29 eyes, and identified peripheral granulomas in 23 eyes and adjacent tractional retinal detachment in 12 eyes. We also identified 17 cases (68.0%) with elevated IgE level among 25 patients with positive serological antibody test. ConclusionsTractional retinal detachment, vitreous opacities and cataract are the common clinical findings at the first attendance of OT patients. The adjunctive test of serum total IgE level may be helpful for the diagnosis. The application of UBM and specific IgG detection in serum and intraocular fluid, can also improve the diagnosis.
Hypertensive retinopathy (HR) often coexist with carotid lesions in hypertensive patients. Carotid lesions are closely associated with cardiovascular and cerebrovascular diseases, as well as end events, offering early important evidence to screening high risk patients. HR has significant value to predict target organ damage (TOD) of hypertension including carotid lesion. In addition, hypertensive retinopathy and carotid lesions-related ischemic ocular diseases will cause serious vision function damage. This article is going to summarize the value and correlation between hypertensive retinopathy and carotid lesions in terms of clinical manifestations, pathological physiological mechanism and target organ damage.
ObjectiveTo reveal the pathogenic mutation in a three-generation Chinese family with autosomal dominant familial exudative vitreoretinopathy (FEVR). MethodsThree patients and a healthy spouse from the index family with FEVR were recruited. The proband was a 5 years old boy. His mother and grandpa were presented with typical FEVR presentations, while his father with normal ocular fundus. DNA was extracted from peripheral blood samples taken from all four participants. All coding and exon-intron boundary regions of five targeted genes, including NDP, FZD4, LRP5, TSPAN12 and ZNF408 were amplified with polymerase chain reaction and sequenced using direct sequencing. In silico analyses were applied to determine the conservation of the mutation site, pathogenic effect and the potential protein crystal structural changes caused by the mutation. ResultsFZD4 c.478G > A, a susceptible mutation was found after four high frequency mutation sites which MAF values were higher than 0.001 was filtered among 5 single nucleotide variations detected in four participants, leading to the residue 160 changing from glutamate to lysine (p.E160K). Co-segregation analysis between genotypes and phenotypes revealed FZD4 p.E160K as the disease-causing mutation for this family. Conservational analysis suggested that this mutation site was highly conserved among all tested species. Functional analysis predicated that this mutation may be a damaging mutation. Crystal structural analysis also indicated that this mutation could lead to the elimination of the hydrogen bond between residue 160 and asparagine at residue 152, thus altering the tertiary structure of the protein and further impairing the protein function. ConclusionOur study demonstrates FZD4 p.E160K as a novel pathogenic mutation for FEVR.
Retinal macrophages and (or) microglial cells play important roles in regulating inflammation, angiogenesis and tissue repairing, thus affect the development and prognosis of ischemic retinal disease, ocular immune diseases and ocular tumors. Reversing the polarization imbalance of these cells may provide new therapeutic strategies for ischemic retinal disease and ocular immune diseases. The duality of the polarization direction of these cells is still controversial in the inflammatory reaction and pathological angiogenesis of ischemic retinal disease. Meanwhile, the plasticity and diversity of the function need to be further studied and discussed.