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Tao Li

Publications and source records attributed to Tao Li.

At least 145 records · Page 8Linked to original sources

Linkage disequilibrium analysis of polymorphisms in the gene for myelin oligodendrocyte glycoprotein in Tourette's syndrome patients from a Chinese sample.

Gilles de la Tourette syndrome (GTS) is a neuropsychiatric disorder characterised by multiple motor and phonic tics, which wax and wane. Recently, evidence has accumulated supporting the role of autoimmune mechanisms in the aetiology of GTS, suggesting that it is within the paediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS) spectrum of childhood neurobehavioural disorders. An immunopathogenic role of antibodies against myelin oligodendrocyte glycoprotein (MOG) has been suggested in this syndrome. In this study, we investigate the association of three microsatellite polymorphisms (MOGa, MOGb, MOGc) in the gene for MOG with GTS in 197 family trios collected from southwest China. Linkage disequilibrium between these three markers was observed with the strongest between MOGa and MOGc (D' = 0.541, P = 0.000). We did not find overall significant evidence for distorted transmission of any of these three markers of MOG gene in GTS, although we observed a weak preferential transmission of the 148 bp allele of MOGc (chi(2) = 4.000, P = 0.046) which did not survive correction for multiple testing. Our results suggest that there is no association between the MOG gene polymorphisms we tested and GTS.

China↗

The 1239G/C polymorphism in exon 5 of BACE1 gene may be associated with sporadic Alzheimer's disease in Chinese Hans.

Beta-site amyloid-precursor protein cleaving enzyme (BACE1) is a candidate risk factor for Alzheimer's disease (AD) because of involving in generating beta-amyloid peptide, which is thought to play a central role in the pathogenesis of the disease. A single nucleotide polymorphism 1239G/C in exon 5 of BACE1 gene and a weak association between this polymorphism and AD in Caucasian APOEepsilon4 allele carriers has been reported. To examine possible association of the polymorphism with sporadic AD, two Chinese Han cohorts including 257 patients and 242 age-matched controls in Guangzhou and 112 patients and 113 controls in Chengdu were genotyped using PCR-RFLP techniques. The frequency of the C allele in controls of both cohorts was 0.65, which was higher than that in Caucasian populations [0.39 by Nowotny et al. 2001: Neuroport 12:1799-1802; 0.44 by Nicolaou et al. 2001: Neurogenetics 3:203-206]. There was a significant excess of C allele among the patients in both cohorts (Guangzhou, 0.71 vs. 0.65, chi(2) = 5.20, P = 0.02; Chengdu, 0.74 vs. 0.65, chi(2) = 4.36, P = 0.04). The CC genotype was found to be associated with AD (Guangzhou cohort, OR = 1.56, 95% CI = 1.09-2.23; Chengdu cohort, OR = 1.74, 95% CI = 1.03-2.95; combined sample: OR = 1.61, 95% CI = 1.20-2.17). The association remained in non-APOE epsilon4 allele carriers when all subjects were divided on the basis of the APOEepsilon4 status. Our findings suggest that the 1239G/C polymorphism in exon 5 of BACE1 gene may be associated with sporadic AD in Chinese Hans.

Age of Onset↗

Existence of heme oxygenase-carbon monoxide-cyclic guanosine monophosphate pathway in human trabecular meshwork cells in vitro.

To confirm the existence of heme oxygenase (HO)- carbon monoxide (CO)- cyclic guanosine monophosphate (cGMP) pathway in the cultured human trabecular meshwork cells (HT-MCs) in vitro, and to evaluate the inductive role of hemin on this pathway, HTMCs of the third to fourth generation were cultured in vitro. Reverse transcripase-polymerase chain reaction (RT-PCR) was employed for detection of HO-1 and HO-2 mRNA. Immunohistochemical staining was used to detect HO-1 and HO-2 proteins. Hemin was added into the culture solution. The HO-1 mRNA levels were quantified by RT-PCR. The relative amount of carbon monoxide released into the media was measured with the quantifying carbon monoxide hemoglobin (HbCO) by spectrophotometry. Radioimmunoassay was used to determine changes of cGMP in HTMCs. The results showed that cultured cells had the specific characteristics of HTMCs. Both HO-1 and HO-2 genes were expressed in HTMCs, as well as HO-1 and HO-2 proteins in HTMCs. Hemin induced HO-1 mRNA, HbCO and cGMP in a dose-dependent manner. In conclusion, HO-CO-cGMP pathway exists in the cultured HTMCs and can be induced by hemin. Pharmacological stimulation of HO-CO-cGMP pathway may constitute a novel therapeutic approach to rescuing glaucoma.

Carbon Monoxide↗

Epigenetic regulation of the taxol resistance-associated gene TRAG-3 in human tumors.

TRAG-3, originally identified as a taxol resistance-associated gene from an ovarian carcinoma cell line, is upregulated in many human tumors. Like many tumor antigens, TRAG-3 mRNA is not detectable or is expressed at very low levels in normal fetal and adult human tissues except for testis, where TRAG-3 mRNA transcripts are detected abundantly. TRAG-3 mRNA is frequently overexpressed in tumors but is rarely detected in adjacent normal tissues. To delineate the transcriptional regulation of this tumor antigen, we cloned and sequenced the TRAG-3 promoter. A 539-base pair fragment upstream of the initiation site, which contains two unusual CT repeat stretches, was sufficient to drive the maximum activity of a luciferase reporter gene. Sodium bisulfite sequencing of genomic DNA revealed that the amount of DNA methylation in exon 2 and in the promoter regions is inversely correlated with gene expression. In normal tissues, TRAG-3 is hypermethylated and is thus transcriptionally silenced. In those tumors where TRAG-3 is actively transcribed, the TRAG-3 promoter and exon 2 are hypomethylated. Treatment of a TRAG-3-silenced cell line H23 with the demethylating reagent 5-aza-cytosine reduced DNA methylation and induced TRAG-3 expression in a dose-dependent manner. These results indicate that DNA demethylation is an important epigenetic mechanism that regulates the TRAG-3 tumor antigen in human tumors.

Antineoplastic Agents, Phytogenic↗

Targeting specific PDZ domains of PSD-95; structural basis for enhanced affinity and enzymatic stability of a cyclic peptide.

A cyclic peptide, Tyr-Lys-c[-Lys-Thr-Glu(betaAla)-]-Val, incorporating a beta-Ala lactam side chain linker and designed to target the PDZ domains of the postsynaptic density protein 95 (PSD-95), has been synthesized and structurally characterized by NMR while free and bound to the PDZ1 domain of PSD-95. While bound, the lactam linker of the peptide makes a number of unique contacts outside the canonical PDZ binding motif, providing a novel target for PDZ-domain specificity as well as producing a 10-fold enhancement in binding affinity. Additionally, the cyclization greatly enhances the enzymatic stability, increasing the duration that the peptide inhibits the association between PSD-95 and glutamate receptors, effectively inhibiting the clustering of kainate receptors for over 14 hr after application. Highly specific regulation of kainate receptor action may provide a novel route for treatment of drug addiction and epilepsy.

Enzyme Stability↗

Characterization of Tollip protein upon Lipopolysaccharide challenge.

Tollip protein serves as a suppressor of innate immunity signaling with unknown mechanism. In this report, we observed that Tollip preferentially bound with phosphatidylinositol-3-phosphate (PtdIns(3)P) and phosphatidylinositol-3,4,5-phosphate (PtdIns(3,4,5)P) in vitro. Mutation of lysine 150 to glutamic acid (Tollip(KE)) within the C2 domain abolished such binding, indicating that C2 domain is critically involved. We demonstrated that overexpression of Tollip inhibited NFkB reporter gene transcription. On the contrary, overexpression of Tollip(KE) mutant has no inhibitory effect on LPS-induced NFkB reporter activity. Tollip binding with 3'-phosphorylated phosphatidylinositides implies that PI3 kinase may regulate its function. We observed that Tollip-mediated inhibition could be alleviated by wortmannin. We also showed that pretreatment with wortmannin augmented LPS-induced endogenous IL-1beta gene expression in monocytic THP-1 cells. THP-1 cells with prolonged LPS treatment develop a state of hyporesponsiveness and no longer respond to further LPS challenge in terms of IL-1beta gene expression. Here we demonstrated that Tollip protein levels were increased following LPS treatment in THP-1 cells as well as in human primary blood mononuclear cells. Increased protein stability upon LPS challenge was likely the cause for the Tollip protein increase. Upon over expression with an enhanced green fluorescent tag, Tollip localized to Golgi apparatus. Our study provides yet another mechanism for suppressing excessive TLR signaling activation mediated by Tollip.

Androstadienes↗

Fast multi-planar gradient echo MR imaging: impact of variation in pulse sequence parameters on image quality and artifacts.

The purpose of this investigation was to quantitatively evaluate the practical impact of alteration of key imaging parameters on image quality and artifacts in fast multi-planar gradient echo (GRE) pulse sequences. These include multi-planar GRASS (MPGR) and fast multi-planar spoiled GRASS (FMPSPGR). We developed a composite phantom with different T(1) and T(2) values comprising the range of common biological tissues, which was also subjected to periodic motion in order to evaluate motion effects. Magnetic resonance imaging was performed on a GE Signa 1.5-T system. Experimental variations in key parameters included excitation flip angle (FL), echo time (TE), repetition time (TR), and receive bandwidth (BW). Quantitative analysis consisted of signal-to-noise-ratio (SNR) and contrast (CN), image nonuniformity (NU), full-width-at-half-maximum (FWHM) (i.e., blurring or geometric distortion), and ghosting ratio (GR). We found that flip angle, TE, and TR play particularly critical roles in determining image signal, homogeneity, and ghosting artifact with these sequences. Optimum clinical application of these pulse sequences requires careful attention to these imaging parameters and to their complex interactions.

Artifacts↗

Dampable waves along nucleic acid sequences mediating nucleotides' interactions.

This work studied the relationship of any two nucleotides in genomic sequences, coding sequences and full-length cDNAs. We made a statistical hypothesis that there exist no interactions between any two nucleotides in sequences, therefore, a hypothetical combination distribution of two nucleotides is considered and the difference between the hypothetical combination distribution and the actual distribution is used to measure the average interaction between the two nucleotides. As a result, we found that the interactions between any two nucleotides are clearly and closely related with dampable wavelike patterns along the sequences. Based on the results we daringly make some hypotheses on several biological topics. Further, studies on the wave may provide new clues for gene prediction and genome structure study.

Algorithms↗

Association analysis of dopamine D2-like receptor genes and methamphetamine abuse.

OBJECTIVES: Substance use disorders are familial, and genetic factors explain a substantial degree of their familial aggregation. This study employs an association approach to examine the genetic underpinning of methamphetamine (MAMP) use and MAMP-induced psychosis. METHODS: A total of 416 MAMP abusers from a hospital and a detention center in Taipei were interviewed with the Diagnostic Interview for Genetic Study and the Family Interview for Genetic Study. Genetic polymorphisms of D2-like dopamine receptor genes, DRD2 TaqI A, DRD3 Ser-9-Gly, and DRD4 exon III variable number of tandem repeats, were compared between: (a) MAMP users as a whole and 435 normal controls, and (b) those 154 individuals with MAMP-induced psychosis and the 252 MAMP users with no psychosis. RESULTS: None of the three markers we studied were associated with predisposition to psychosis among the MAMP abusers. The MAMP abusers had a higher (P=0.011) prevalence of the seven-repeat allele of DRD4 than normal controls. CONCLUSIONS: Chance fluctuations in the frequency of rare alleles and ascertainment differences in the case and control samples cannot be ruled out. Therefore, further studies of the seven-repeat allele in MAMP abusers and controls should be performed before an association can be established.

Female↗

Analysis of gene expression profile in gastric cancer cells stimulated with Helicobacter pylori isogenic strains.

To understand the biological processes within host cells induced by VacA, isogenic strains of Helicobacter pylori (NCTC 11638 or 11638-DeltavacA) were used to stimulate gastric cancer cells SGC7901, and differentially expressed genes in host cells were identified using cDNA microarray technology. More than 300 genes were found to alter their mRNA expression at different time points, among which 68 were related to the cytoskeleton, 87 were associated with cell cycle, cell death and proliferation, IL8 expression was also found to be up-regulated. Cells co-cultured with broth-culture supernatant (BCS) of NCTC 11638 showed more alteration in microtubule cytoskeleton morphology, as observed by laser scanning confocal microscopy, and a lower apoptosis rate, detected by flow cytometry, compared with those co-cultured with BCS of 11638-DeltavacA. The supernatants of cells co-cultured with NCTC 11638 showed significantly higher IL8 expression than those co-cultured with 11638-DeltavacA. It is concluded that VacA disrupts cytoskeletal architecture by influencing the expression of cytoskeleton-associated genes. VacA breaks the balance between cell proliferation and cell death by inducing the maladjustment of genes related to cell cycle. VacA is also able to induce the inflammatory response.

Apoptosis↗

Nocardia sp. carboxylic acid reductase: cloning, expression, and characterization of a new aldehyde oxidoreductase family.

We have cloned, sequenced, and expressed the gene for a unique ATP- and NADPH-dependent carboxylic acid reductase (CAR) from a Nocardia species that reduces carboxylic acids to their corresponding aldehydes. Recombinant CAR containing an N-terminal histidine affinity tag had K(m) values for benzoate, ATP, and NADPH that were similar to those for natural CAR, and recombinant CAR reduced benzoic, vanillic, and ferulic acids to their corresponding aldehydes. car is the first example of a new gene family encoding oxidoreductases with remote acyl adenylation and reductase sites.

Amino Acid Sequence↗

Inhibitory effect of topiramate on Lewis lung carcinoma metastasis and its relation with AQP1 water channel.

AIM: To study the effect of topiramate on tumor metastasis and its relation with aquaporin 1 (AQP1) water channel. METHODS: Lewis lung carcinoma metastatic model was used to determine the effect of topiramate on tumor growth and metastasis. Colorimetric estimation was used to investigate the action of topiramate on carbonic anhydrase (CA) activity. Western blotting and immunohistochemical analysis were used to study the influence of topiramate on AQP1 water channel expression in lungs or tumor tissues of mice bearing Lewis lung carcinoma. RESULTS: Treatment with topiramate (120 mg/kg/d, ig for 20 d) reduced the growth of primary tumor significantly (P<0.05). Its inhibitory rate of metastasis was 81.25 %. Topiramate inhibited CA activity in lungs of mice in a dose-dependent manner. Topiramate apparently decreased AQP1 protein expression and immunostaining in lungs or in tumor microvessel endothelial cells of mice. CONCLUSION: Suppression of AQP1 water channel expression may be an important pathway for the inhibitory effect of topiramate on tumor metastasis.

Animals↗

Effects of acetazolamide and anordiol on osmotic water permeability in AQP1-cRNA injected Xenopus oocyte.

AIM: To study the effects of acetazolamide and anordiol on osmotic water permeability in aquaporin 1 (AQP1)-cRNA injected Xenopus oocyte and their mechanisms. METHODS: AQP1 gene constructed in pBluescript was transcripted into cRNA in vitro and then the cRNA was injected in Xenopus oocytes. The effects of acetazolamide and anordiol on the water transport function of AQP1 were observed by assaying the osmotic swelling of oocytes. In addition, their effects on protein expression of AQP1 were quantitatively investigated by Western blotting method. RESULTS: After incubation for 15 min or 72 h, acetazolamide, a carbonic anhydrase inhibitor, equally reduced the water permeability of AQP1-cRNA injected oocyte in a dose-dependent manner. After incubation for 72 h, anordiol, an antiestrogen with partial estrogenic activity, reduced the osmotic water permeability dose dependently as well; however, no discernable action was observed after incubation with anordiol for 15 min. The Western blotting analysis showed that acetazolamide did not influence the protein expression of AQP1. However, after incubation for 72 h with anordiol (10 micromol/L), the quantity of AQP1 in the oocyte membrane was decreased dramatically (P<0.05). CONCLUSION: Both acetazolamide and anordiol inhibited the osmotic water permeability of AQP1-cRNA injected oocyte, but their mechanisms were different. Acetazolamide functionally inhibited the osmotic water permeability of AQP1, whereas anordiol primarily decreased the amount of AQP1 protein in the oocyte membrane.

Acetazolamide↗

[Effects of estradiol on deltamethrin-induced neurotoxicity in rat cerebro-cortical synaptosomes].

OBJECTIVE: To investigate the neuroprotective effect of estradiol on the release of excitatory amino acid (EAAs) mediator, and the activity of ATPase in cerebro-cortical synaptosome membrane of rats exposed to deltamethrin. METHODS: Using HPLC to detect EAAs release, and colorimeter method to measure the activities of Na(+)-K(+)-ATPase, Mg(2+)-ATPase, Ca(2+)-ATPase, Ca(2+)-Mg(2+)-ATPase in the cerebro-cortical synaptosomes of ovariectomized rats exposed to deltamethrin (2 x 10(-5)mol/L), and treated with different doses of 17beta estradiol (10(-5), 10(-8), 10(-11) mol/L). Meanwhile, the estrogen receptor (ER) antagonist, tamoxifen, was used to investigate the effect on estradiol. RESULTS: The release of Asp and Glu from the cerebro-cortical synaptosomes was significantly increased by 2 x 10(-5)mol/L deltamethrin exposure at the depolarizing state evoked by 50 mmol/L KCl, while 10(-8), 10(-11) mol/L 17beta estradiol could partly inhibit the effect of deltamethrin on the release of Asp (28.42%, 24.36%, respectively), Glu (21.52%, 14.57%, respectively). The activities of 4 kinds of ATPase were inhibited by 2 x 10(-4) mol/L deltamethrin, and these effects could be blocked by 10(-5) mol/L estradiol, while the activity of Ca(2+)-ATPase was increased by 10(-8), 10(-11) mol/L of estradiol. However, no obvious antagonistic effect of tamoxifen on the function of estradial on EAAs release or the activities of ATPase was found. CONCLUSION: Estradiol showed certain neuroprotective effect on the release of EAAs and the inhibition on ATPase induced by deltamethrin. The effect of estradiol on synaptosomes may indicate the nongenetic mechanism of estradiol.

Animals↗

[Genetic damage in peripheral blood lymphocyte of coke oven workers].

OBJECTIVE: To investigate DNA and chromosome damage in peripheral blood lymphocyte of coke oven workers exposed to polycyclic aromatic hydrocarbons (PAHs). METHODS: One hundred and thirty-seven coke oven workers and 50 controls without occupational PAHs exposure were investigated. Comet assay and cytokinesis-block micronucleus (CBMN) detection were used to evaluate DNA and chromosomal damage levels in peripheral blood lymphocyte. Urinary 1-hydroxypyrene level was used to assess the personal internal PAHs exposure dose. Personal information including occupational history, age, sex, smoking and drinking status was collected by questionnaire. RESULTS: Urinary 1-hydroxypyrene level in coke oven workers [(5.76 +/- 1.04) micro mol/mol Cr] was significantly higher than that in controls [(0.70 +/- 0.32) micro mol/mol Cr]. The rate of CBMN and comet tail moment of lymphocyte in coke oven workers [8.0 per thousand (0.0 per thousand - 30.0 per thousand ) and 2.09 (0.31 - 75.41), respectively] were higher than those in controls [3.5 per thousand (0.0 per thousand - 13.0 per thousand ) and 1.05 (0.11 - 6.63), P < 0.05]. In controls, the comet moment in smokers was significantly higher than that in non-smokers [1.44 (0.23 - 6.63) vs 0.81 (0.11 - 3.47), P < 0.05]. According to the length of work, 137 coke oven workers were classified into 3 groups i.e. 0.5 yrs , 16.0 yrs and 22.0 yrs group, and the comet moments were 1.34 (0.31 - 37.84), 2.32 (0.49 - 52.97) and 3.20 (0.45 - 75.41) respectively after adjusting the age, sex, smoking, drinking and level of urinary 1-hydroxy-pyrene. There was a rising tendency along with the increase in length of work. CONCLUSION: Under present PAHs exposure levels, both comet assay and Cytokinesis-block micronucleus test could detect PAHs-induced genotoxicity in coke oven workers, and comet assay is more suitable to assess the cumulative damage effect on DNA.

Adult↗

[Expression of MAGE-B genes in hepatocellular carcinoma].

OBJECTIVE: To investigate the expression of MAGE-B genes in hepatocellular carcinoma (HCC) in order to find new targets for immunotherapy. METHODS: The expression of MAGE-B1, B2, A1 and A3 mRNA was detected using RT-PCR in HCC tissues and the corresponding adjacent non-HCC tissues from 47 HCC patients, 30 samples of cirrhosis and normal liver tissues. Four samples selected randomly from MAGE-B1 or B2 with positive RT-PCR results were sequenced to confirm the results of RT-PCR. The relationship between the expression of MAGE-B and some clinicopathological parameters was analyzed. RESULTS: MAGE-B1 mRNA and MAGE-B2 mRNA were detected in 44.7% (21/47) and 61.7% (29/47) of HCC samples, respectively, while neither MAGE-B1 nor MAGE-B2 could be detected in the corresponding adjacent non-HCC liver tissues. In addition, none of 30 samples of cirrhosis and normal liver tissues was shown to express both MAGE-B genes. The DNA sequence confirmed that the RT-PCR products were truly target cDNA. The frequency of the expression of MAGE-A1 and A3 was 74.5% (35/47) and 44.7% (21/47), respectively. There was significant correlation between the expression of MAGE-B and MAGE-A (P < 0.05). However, the positive expression of MAGE-B was observed in 5 out of 12 HCC tissues without expression of MAGE-A1 and/or A3. When all four MAGE genes were examined, the positive rate of expression of one, two, three and four genes was 83.0% (39/47), 55.3% (26/47), 48.9% (23/47), and 38.3% (18/47) of 47 HCC tissues, respectively. No correlation was found between the expression of MAGE-B and clinical parameters such as age, sex, tumor size, degree of tumor differentiation, serum alpha-fetoprotein level and hepatitis B virus or hepatitis C virus infection (P > 0.05). CONCLUSION: MAGE-B genes are expressed with relatively high frequency and specificity in HCC. Most HCC patients with positive expression of at least one member of MAGE-B or MAGE-A gene family are adequate candidates to receive specific immunotherapy. Frequent co-expression of multiple members of MAGE-B and MAGE-A subfamilies provides the possibility of using polyvalent vaccines to achieve more effective immunotherapeutic results.

Antigens, Neoplasm↗

[A study on the inherited susceptibility of chromosomal damage in peripheral blood lymphocytes among coke oven workers].

OBJECTIVE: To investigate the association between polymorphisms of metabolic enzyme genes and chromosomal damage risk in peripheral blood lymphocytes among coke oven workers. METHODS: One hundred and fourty-nine coke oven workers and 24 referents without occupational polycyclic aromatic hydrocarbons (PAH) exposure were recruited in this study. Urinary 1-hydroxypyrene levels were measured as the internal dose of PAH exposure. The 6 per 1 000 of micronucleus value was used as the cut-off value to determine whether the individual's chromosomal damage was positive. The genotypes of CYP1A1, GSTM1, GSTT1, GSTP1, CYP2E1, NQO1, NAT2 and mEH genes were determined by PCR-based methods. Multiple logistic regression was used to calculate the adjusted ORs and the 95% CI for the risk of chromosomal damage and to analyze the gene-gene interaction. RESULTS: In 173 subjects, after adjusting the occupational exposure, age, sex, smoking and drinking status, the subjects with GSTM1 null genotype have significantly higher risk for chromosomal damage than subjects with GSTM1 positive genotype (adjusted OR = 2.01, 95% CI = 1.03 -3.91). Compared with the wild homozygotes at P187S site of NQO1 gene, the variant homozygotes have significantly higher risk for chromosomal damage (adjusted OR = 3.18, 95% CI = 1.18 - 8.62). The subjects with variant allele at H113Y site of mEH gene have significantly lower risk for chromosomal damage (adjusted OR = 0.40, 95% CI = 0.19 - 0.88). No significant associations were found for other gene polymorphisms and chromosomal damage risk. In addition, the gene-gene interactions were also found among GSTM1, NQO1 gene P187S and mEH gene H113Y polymorphisms for the risk of chromosomal damage risk. CONCLUSION: Significant associations between genetic polymorphisms in GSTM1, NQO1 and mEH gene and risk for chromosomal damage were found among occupational PAH-exposed workers, which related to the mechanism of PAH carcinogenesis.

Adult↗

[Flourescein angiography and ultrastructure studies on retina after laser photocoagulation].

OBJECTIVE: The fluorescein angiographs and ultrastructure changes as well as the repairable process of retina after photocoagulation were analyzed to provide scientific basis for the rationale of using laser in the treatment of retinal lesions. METHODS: Normal retinae were coagulated using I, II, III grade photic spots and were exposed to fluorescein angiography 1, 3, 7 days before the necessary exenteration in conformity with the informed consent given by 7 patients with malignant tumor of orbit. The retina from the removed globe was cut into thin sections and observed by use of electron microscope. RESULTS: Fluorescein angiography: Fluorescein leaked in photic spots 1 day after photocoagulation. Leakage relieved with central small fluorescein block 3 days after photocoagulation. Leakage disappeared with central fluorescein block 7 days after photocoagulation. Ultrastructure: 1 day after photocoagulation, I grade photic spot, some retinal pigment epithelium(RPE) cells were swellen and necrotic. Partial photoreceptors were lysed and disarranged. Cells of outer nuclear layer decreased in number. II grade photic spot, RPE and photoreceptors were destroyed. Some necrotic and apoptotic cells appeared in the outer nuclear layer. Structure of outer plexiform layer became disorganized. III grade photic spot, retina was destroyed severely. 3 days after photocoagulation, cell edema and debris decreased. Phagocytes appeared, RPE and Müller cells started proliferation. 7 days after photocoagulation, proliferative RPE and Müller cells replaced the damaged areas of the retina. Retinal structure disorganization increased gradually from I to III spot. CONCLUSION: Photocoagulation caused fluorescein leakage of retina, apoptosis of RPE and neuron, and damage to other structure. Subsequently, the proliferous RPE and Müller cells repaired the destroyed areas of retina.

Fluorescein Angiography↗