ObjectiveTo observe the inhibitory effect of endostatin (ES) on oxygen-induced retinal neovascularization.MethodsThirtyfour 7-day-old C57BL/6J mice were randomly divided into 3 groups: oxygen-exposed group (12 mice), ES group (12 mice) and the control group (8 mice). The mice in oxygen-exposed and ES group were exposed to (75±5)％ oxygen for 5 days and then back to the normal air. In ES group, 1 μg ES endostatin were injected into vitreous in one eye, while PBS was injected into the other eye as the control 12 and 36 hours after being exposed to oxygen. The mice in the control group were fed in normal circumstance. The changes of retinal neovascularization was examined by fluorescence angiography with fluorescein isothiocyanatedextran. The number of endothelial cells breaking through the internal limiting membrane (ILM) was counted and the inhibitory effects of ES on retinal neovascularization was observed.ResultsCompared with the oxygen-exposed group, the branches of retinal vessels went normal without any un-perfused area in ES group. The number of nuclei of endothelial cells breaking through ILM on each retinal crosssection decreased to (5.39±1.52), which differed much from that in the oxygen-exposed group (22.56±2.13) (plt;0.001).ConclusionES can effectively inhibit the formation of retinal neovascularization in rats and might be a new path of the treatment for proliferative retinopathy.(Chin J Ocul Fundus Dis, 2005,21:314-317)
Objective To explore the effects of overexpression of human tissue inhibitors of metalloproteinase-1 (hTIMP-1) on proliferation of human liver cancer cell line HepG2 in vitro. Methods A recombinant adenoviral vector containing full-length cDNA of hTIMP-1 was generated and transfected into HepG2. The viral titer was checked by measuring GFP, and the expression of hTIMP-1 in vitro was detected by the techniques of Western blot and semi-quantitative RT-PCR. The ultrastructure was observed by transmission electron microscope and the effects of overexpression of hTIMP-1 on proliferation of HepG2 in vitro was analyzed by MTT assay and growth curve. Results The resultant AdhTIMP-1 was successfully constructed and the expression of hTIMP-1 was detected by Western blot and RT-PCR. The growth and proliferation of HepG2, which had been transfected with AdhTIMP-1, was significantly inhibited. Conclusion The proliferation of HepG2 was markedly inhibited by recombinant adenovirus-mediated overexpression of hTIMP-1, which may pave the way for further application in liver gene therapy.
In the expert consensus published by the Pediatrics in 2013, it was first proposed that anti-VEGF drugs can be considered for retinopathy of prematurity (ROP) with stage 3, zone Ⅰ with plus disease. However, there are many problems worth the attention of ophthalmologists, including the advantages and disadvantages of anti-VEGF therapy compared with traditional laser therapy, systemic and ocular complications after anti-VEGF therapy, and what indicators are the end points of anti-VEGF therapy. Combined with this consensus and numerous research findings, we recommend that the first treatment for anti-VEGF or laser therapy should be considered from disease control effects. For the threshold and pre-threshold lesions, the effect of anti-VEGF therapy for zoneⅡ lesions is better than that for zone Ⅰ lesions and the single-time effective rate is high. So, it is suggested that anti-VEGF therapy should be preferred for the first treatment. The choice of repeat treatment should be considered from the final retinal structure and functional prognosis. Laser therapy is advisable for the abnormal vascular regression slower and abnormalities in the posterior pole. It can reduce the number of reexaminations and prolong the interval between re-examinations. However, the premature use of laser has an inevitable effect on peripheral vision field. Excluding the above problems, supplemental therapy can still choose anti-VEGF therapy again. Most of the children with twice anti-VEGF therapy are sufficient to control the disease. Anti-VEGF therapy should be terminated when there are signs such as plus regression, threshold or pre-threshold lesions controlled without recurrence, peripheral vascularization, etc.
Most immune-related adverse event (irAE) associated with immune checkpoint inhibitors (ICIs) resulted from excessive immune response against normal organs. The severity, timing, and organs affected by these events were often unpredictable. Adverse reactions could cause treatment delays or interruptions, in rare cases, pose a life-threatening risk. The mechanisms underlying irAE involved immune cell dysregulation, imbalances in inflammatory factor expression, alterations in autoantibodies and complement activation, even dysbiosis of intestinal microorganisms. However, the mechanisms of irAE occurrence might differ slightly among organs due to variations in their structures and the functions of resident immune cells. Future research should focus on the development of targeted drugs for the prevention or treatment of irAE based on the mechanisms by which irAE occurs in different organs. A deeper understanding of the mechanisms underlying irAE occurrence would aid clinicians in effectively utilizing ICIs and provide valuable guidance for their clinical application.
Objective To review the treatment methods and techniques of ischemia-reperfusion injury of flap. Methods Recent basic research l iterature concerning ischemia-reperfusion injury of flap was reviewed and analyzed in terms of treatment techniques. Results Ischemia-reperfusion injury is one of the leading causes of flap necrosis postoperatively. Interventions against any l ink of the ischemia-reperfusion injury progress could effectively reduce the damageand improve the survival rate of flaps. Conclusion Including production of reactive oxygen species, neutrophil infiltrationetc are thought to be the main mechanisms of ischemia-reperfusion injury. Treatment including medicine administration and physical intervention against any specific l ink of ischemia-reperfusion injury can interfere or block the whole progress, which reduce the damage of ischemia-reperfusion injury and improve the survival rate of animal flap models eventually.
Objective To study and compare the clinical efficacy between intravitreal conbercept injection and (or) macular grid pattern photocoagulation in treating macular edema secondary to non-ischemic branch retinal vein occlusion (BRVO). Methods Ninety eyes of 90 patients diagnosed as macular edema secondary to non-ischemic BRVO were enrolled in this study. Forty-eight patients (48 eyes) were male and 42 patients (42 eyes) were female. The average age was (51.25±12.24) years and the course was 5–17 days. All patients were given best corrected visual acuity (BCVA), intraocular pressure, slit lamp with preset lens, fluorescence fundus angiography (FFA) and optic coherent tomography (OCT) examination. The patients were divided into conbercept and laser group (group Ⅰ), laser group (group Ⅱ) and conbercept group (group Ⅲ), with 30 eyes in each group. The BCVA and central macular thickness (CMT) in the three groups at baseline were statistically no difference (F=0.072, 0.286;P=0.930, 0.752). Patients in group Ⅰ received intravitreal injection of 0.05 ml of 10.00 mg/ml conbercept solution (conbercept 0.5 mg), and macular grid pattern photocoagulation 3 days later. Group Ⅱ patients were given macular grid pattern photocoagulation. Times of injection between group Ⅰ and Ⅲ, laser energy between group Ⅰ and Ⅱ, changes of BCVA and CMT among 3 groups at 1 week, 1 month, 3 months and 6 months after treatment were compared. Results Patients in group Ⅰ and Ⅲ had received conbercept injections (1.20±0.41) and (2.23±1.04) times respectively, and 6 eyes (group Ⅰ) and 22 eyes (group Ⅲ) received 2-4 times re-injections. The difference of injection times between two groups was significant (P＜0.001). Patients in group Ⅱ had received photocoagulation (1.43±0.63) times, 9 eyes had received twice photocoagulation and 2 eyes had received 3 times of photocoagulation. The average laser energy was (96.05±2.34) μV in group Ⅰ and (117.41±6.85) μV in group Ⅱ, the difference was statistical significant (P=0.003). BCVA improved in all three groups at last follow-up. However, the final visual acuity in group Ⅰ and group Ⅲ were better than in group Ⅱ (t=4.607, –4.603;P＜0.001) and there is no statistical significant difference between group Ⅲ and group Ⅰ (t=–0.802,P=0.429). The mean CMT reduced in all three groups after treating for 1 week and 1 month, comparing that before treatment (t=–11.855, –10.620, –10.254;P＜0.001). There was no statistical difference of CMT between group Ⅰand Ⅲ at each follow up (t=0.404, 1.723, –1.819, –1.755;P=0.689, 0.096, 0.079, 0.900). CMT reduction in group Ⅰ was more than that in group Ⅱ at 1 week and 1 month after treatments (t=–4.621, –3.230;P＜0.001, 0.003). The CMT in group Ⅲ at 3 month after treatment had increased slightly comparing that at 1 month, but the difference was not statistically significant (t=1.995,P=0.056). All patients had no treatment-related complications, such as endophthalmitis, rubeosis iridis and retinal detachment. Conclusions Intravitreal conbercept injection combined with macular grid pattern photocoagulation is better than macular grid pattern photocoagulation alone in treating macular edema secondary to non-ischemic BRVO. Combined therapy also reduced injection times comparing to treatment using conbercept injection without laser photocoagulation.
Objective To determine the effects of lensspecific overexpression of OSM on the eye development. Methods A truncated mouse OSM c DNA (661 bp) was linked to the αA-crystallin promoter. Transgenic mice were characterized by routine histological and immunohistochemical techiniques. TUNEL assays were used to de tect cell death. The mRNA expression of caspase-3 was detected by in situhybridization, Rabbit anti-cleavage caspase-3 antibody was used to detectactive capase-3. Results At embryonic day (E) 14.5 and 17.5, expression of the OSM transgenic protein was detected specifically in lens fiber cells. The onset of retinal degeneration in the mid portion of the transgenic retinae was observed started from E17.5. By the time of birth 50% or more of the retinal cells were missing. The OSM transgenic retinal cells underwent apoptosis indicated by TUNEL assays. Most strikingly, activation of caspase-3 protein were observed throughout the transgenic retinas. Conclusions Lens-specific overexpression of OSM activate caspase-3, leading to abnormal eye development,apoptosis and widespread retinal degeneration. (Chin J Ocul Fundus Dis，2003，19：201-268)
Diabetic macular ischemia (DMI) is one of the manifestation of diabetic retinopathy (DR). It could be associated with diabetic macular edema (DME), which may affect the vision of DR patients. FFA is the gold standard for the diagnosis of DMI, but with the advent of OCT angiography, a more convenient and diversified method for the evaluation of DMI has been developed, which makes more and more researchers start to study DMI. Intravitreal injection of anti-VEGF has become the preferred treatment for DME. When treating with DME patients, ophthalmologists usually avoid DMI patients. But if intravitreal anti-VEGF should be the contradiction of DME is still unclear. To provide references to the research, this article summarized the risk factors, assessment methods and influence of DMI. This article also analyzed the existing studies, aiming to offer evidences to a more reasonable and effective treatment decision for DME individual.
Objective Non-small cell lung cancer ( NSCLC) cells are relatively resistant to chemotherapy, and the outcomes are not always satisfactory. This study was designed to explore the relationship between the content of Ku80 protein of human lung cancer cells and their sensitivity to cisplatin.Methods The lung cancer cells isolated frommalignant pleural effusion samples frompatients with primary lung cancer were cultured in vitro. The sensitivity to cisplatin was tested with the method of CCK-8 expressed as half maximal inhibitory concentration ( IC50 ) . The relative content of Ku80 protein was determined by Western blot. The correlation between sensitivity to cisplatin of lung cancer cells and the relative content of Ku80 protein was analyzed. Results The IC50 of NSCLC group was significantly higher than that of SCLCgroup [ ( 4. 40 ±3. 39) mg/L vs. ( 1. 02 ±0. 54) mg/L, P lt; 0. 001] . The relative content of Ku80 protein of NSCLC group was statistically higher than that of SCLC group [ ( 0. 80 ±0. 45) vs. ( 0. 48 ±0. 25) , P lt;0. 05] . The correlation coefficient between content of Ku80 protein and IC50 was 0. 618 ( P lt; 0. 001) .Conclusions The content of Ku80 protein of NSCLC patients is higher than that of SCLC patients. Itmay be one of the mechanisms contributing to chemotherapeutic resistance of NSCLC. There is a negative relationship between Ku80 protein content of cancer cells and their sensitivity to cisplatin suggesting that the content of Ku80 protein may be served as a candidate index for predicting sensitivity of lung cancer cells to cisplatin.
PURPOSE:To investigale the influence of orally administered aldose reduetace inhibitor(ARI) and myo-inositol (MI)for contents of gluecose,sorbitol and myo-inositol in experimental diabetic retinal tissue in rat. METHODS :The STZ-induced diabetic rats were administered ARI or MI by oral. The glucose sorbitol and myo-inositol in retinal tissues were analysed by high performance liquid chromatography after experimental period of 6 montbs. RESULTS:It was found that the contents of glucose and sorhitol were increased and myo inosltol was decreased in diabetic group. In diabetes with ARI group.the content of sorbitol was increased although the glucose was in high level. In diabetes wilb MI group,the sorbitol accumulaled and coment of myo-inositol was close to the normal control group. CONCLUSIONS:The ARI can effectively obstruct sorbitol accumulation in retina. MI increase myo-inositol level but fail to reduce sorbitol contenl of retina. （Chin J Ocul Fundus Dis,1997,13: 75-77 ）