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)
Objective To investigate the relationship between keloid proliferation and destruction of skin appendages(SAs). Methods Pathological biopsies of keloids were derived from 17 patients whounderwent scar resection. All samples were divided into 4 groups: infiltrating growth locus of keloids（K-I,n=9），proliferative keloids (K-P,n=17), atrophic keloids (K-A,n=10), and edging normal skin (K-N,n=6). Normal skin derived from thorax of patients was used as control (NS, n=6). The density of SAs and the expressive characteristics of pan-cytokeratin (CKp), cytokeratin19 (CK19), secretory component of glandular epithelium(SC), proliferating cell nuclear antigen(PCNA), and apoptosis related proteins (Bcl-2 and Bax) were observed with immunohistochemical method. Results Compared with K-N and NS, the density of SAs expressing CKP and SC in keloids was apparently decreased, and remnant of CKp protein was observed after the disappearance of SAs structures. Protein expression of Bax was increased in epithelial cellsof most SAs. SAs containing postive immunostaining signals of Bcl-2, PCNA and CK19 exhibited squamous epithelization and abnormal structure. The structure of SAs underwent 3 morphological stages: infiltrating, proliferating, and maturing.In correspondence to each stage, SAs underwent proliferation, structural destruction, and fibrosis which were caused by cellular migration, nflammatory reaction, and vascular occlusion respectively. Conclusion Abnormal proliferation of epithelial cells and their structural destruction of SAs may beassociated with tissue fibrosis in keloid lesion.
OBJECTIVE: To explore the expression of alpha-smooth muscle actin (alpha-SMA) induced by transforming growth factor beta 1 (TGF-beta 1). METHODS: Five samples of hypertrophic scars and three samples of normal mature scars were collected as the experimental and control groups respectively. The fibroblasts were isolated from scars, and cultured in 2-dimension or 3-dimension culture system. The immunohistochemical staining method of LSAB were used to investigate the expression of alpha-SMA in fibroblasts in the different concentration of TGF-beta 1. RESULTS: The expression of alpha-SMA in 3-dimension culture system were markedly lower than those in 2-dimension culture system with respect to the fibroblasts in the experimental group. The expression of alpha-SMA in fibroblasts were different in response to various TGF-beta 1 concentration, it was more effective at the concentration of 5 ng/ml. The expression of alpha-SMA in the fibroblasts from hypertrophic scars seemed to be more sensitive to TGF-beta 1 compared to that of the normal mature scars. CONCLUSION: There are concentration-dependent in the expression of alpha-SMA induced by TGF-beta 1 in scar fibroblasts in vitro. The biological characteristics of the fibroblasts from hypertrophic scars and normal mature scars and their sensitivity to the inducement of TGF-beta 1 were different. The inducement of TGF-beta 1 may be depressed by extracellular matrix components and that may decrease the expression of alpha-SMA.
ObjectiveTo evaluate the diagnostic value of 99Tcm-methoxy isobutyl isonitrile (MIBI) dual-time imaging for parathyroid adenoma (PA) and parathyroid hyperplasia (PH).MethodsClinical data of 187 patients with pathologically confirmed hyperparathyroidism (HPT) who admitted to the First Affiliated Hospital of Xi’an Jiaotong University School of Medicine from July 2011 to December 2018 were retrospectively collected. Taking postoperative pathology as the standard, the diagnostic value of preoperative 99Tcm-MIBI dual-time imaging was analyzed.ResultsThe serum PTH level of PH patients was higher than that of PA patients (Z=–3.23, P<0.01). Te/N (T: focal area radioactive count, N: the normal tissue radioactivity count of the corresponding thyroid gland on the opposite side of the lesion) in PA and PH patients were lower than Td/N (Z=–3.61, P<0.01; Z=–3.47, P<0.01). The positive rates of 99Tcm-MIBI dual-time imaging in the diagnosis of PA and PH lesions were 67.9% (36/53) and 20.6% (86/418), respectively, and the positive rate of PA were higher (χ2=52.51, P<0.01). The positive rate of 99Tcm-MIBI dual-time imaging in the diagnosis of PA and PH single lesions was higher than that of multiple lesions (χ2=15.79, P<0.01; χ2=64.73, P<0.01). Conclusions99Tcm-MIBI dual-time imaging shows a higher positive rate for PA and a lower positive rate for PH. When HPT is clinically suspected, but 99Tcm-MIBI dual-time imaging is negative and serum PTH is positive, PH should be considered, and B ultrasound and other examinations should be performed to determine the lesion site.
ObjectiveTo observe the longterm effect of suramin on the inhibition of proliferation of human retinal pigment epithelial (RPE) cells in vitro.
MethodsRPE cells grown in 9 pieces of 96well plate (12 wells each plate) were divided into experimental and control group, with 6 wells in each group. The concentration of 0.1 ml RPE cells in each well is 5×104 cells/ml. After the change of the medium, RPE cells were treated with suramin (250 μg/ml) in experimental group while treated with nothing in the control group. The medium of the 2 groups were changed to the normal medium after 4 days. At the 1st, 2nd, and 4thday after the addition of suramin and at the 1st, 2nd, 3rd, 5th, 6th, 7th, 9th , 11th and 13th day after removing suramin, 1 plate was randomly selected to stop culturing, and the proliferation of RPE cells were detected by methyl thiazolyl tetrazolium (MTT) assay. ResultsUnder reversed microscope, RPE cells in control group were fused completely at the 7th day after inoculation. The extracellular space of RPE cells in experimental groups was larger than that in the control group, and remained unfused at the 13th day after inoculation. The inhibitory rate of proliferation of RPE cells at the first day after treated with suramin was 14.85% and increased to the highest 25.79% at the 4th day. The first day after the suramincontaining media was removed, the inhibitory rate decreased to 12.35%, and then raised gradually to over 20% at the 3rd to 5th day. Finally, the rate drop to 14.71%.
ConclusionSuramin has the long-term effect on the inhibition of RPE cells induced by serum, especially the inhibitive effect after the remove of suramin, which indicates the specific double-peak inhibition during the whole process.(Chin J Ocul Fundus Dis, 2005,21:25-27)
Objective To investigate the effects of asiaticoside onthe proliferation and the Smad signal pathway of the hypertrophic scar fibroblasts.Methods The hypertrophic scar fibroblasts were cultured with tissue culture method. The expressions of Smad2 and Smad7 mRNA after asiaticoside treatment were determined by reverse transcriptionpolymerase chain reaction 48 hours later. Thecell cycle, the cell proliferation, the cell apoptosis and the expression of phosphorylated Smad2 and Smad7 with(experimental group) or without(control group) asiaticoside were detected with flow cytometry, immunocytochemistry and Western blot. Results Asiaticoside inhibited the hypertrophic scar fibroblasts from phase S to phase M. The Smad7 content and the expression of Smad7 mRNA were (1.33±1.26)% and (50.80±22.40)% in experimental group, and (9.15±3.36)% and (32.18±17.84)% in control group; there were significant differences between two groups (P＜0.05). While the content and the mRNA expression of Smad2 had no significant difference between two groups. Conclusion Asiaticoside inhibits the scar formation through Smad signal pathway.
