Retinoblastoma is the most common intraoeular malignant tumor in children.In its treatment,drug therapy is one of the most effective and irreplaceable methods.To reduce the toxicity of drugs,enhance the therapeutic effect and lessen drug resistance, some new drug deliver systems and new medicines for retinoblastoma are coming into being.Ophthalmic arterial infusion,fibrin sealant and iontophoresis are newly-found drug deliver systems.And the latest drugs under research include nutlins,phenoxazine derivative Phx-1,combretastatin A4 phosphate,2-deoxy-d-glucose and histone deacetylase inhibitors,etc.The following text is focused on the two aspects of the drug therapy for retinoblastoma.

Nowadays,with the sharply increasing morbidity and stable high mortality,tumor has become the greatest threaten for human health and life.After taking a view of preservations,diagnoses and treatments on tumor, oncologists considered the cure rate had not improved evidently in patients with advanced tumor in the past several decades even though the total cure rate and survival rate had increased.Facing the puzzle,people should evaluate original tumorigenic theories again.A review about it was presented here.

Mitochondria play an important role in energy ( ATP ) production through oxidative phosphorylation pathway and the regulation of cell death by apoptosis. Mitochondrial dysfunction has been implicated in the pathophysiology of a number of neurodegenerative diseases. Glaucoma as a neurodegenerative disorder, mitochondrial oxidative stress in the pathogenesis of glaucoma and the damage of RGCs has received close attention in recent years. ln this article, we reviewed the current evidences and recent advances in the relationship between mitochondrial oxidative stress and the RGCs apoptosis.

Objective To investigate the effects of silymarin on expressions of nuclear factor kappa B(NF-?B) and intercellular adhesion molecule-1(ICAM-1) in the kidneys of rats with unilateral ureteral obstruction(UUO)-induced renal fibrosis.Methods Seventy-two male Sprague-Dawley rats were randomly divided into 3 groups: sham-operated group(n=24),operated group(n=24) and silymarin treated group(n=24).Renal tubulointerstitial fibrosis model was established via UUO.Silymarin was given by gavage with 30 mg/(kg?d) in silymarin treated group,and the same volume normal saline was given by gavage in operated group and sham-operated group.In each group,8 rats were killed at 7,14 and 21 d after operation.Histological changes were observed in tubulointerstitial injury under microscope.The expressions of NF-?B and ICAM-1 in renal tissue were determined with immunohistochemical method.Results Tubuloin-terstitial injury scores in operated group at 7,14 and 21 d were 1.168?0.108,1.776?0.064 and 2.301?0.157,respectively,and Tubulointerstitial injury scores in the treated group at 7,14 and 21 d were 1.043?0.114,1.677?0.083 and 2.084?0.201,respectively.Tubulointerstitial injury scores in silymarin treated group were significantly lower than those in operated group(Pa

Drug-Eluting Stents ; Humans ; Prosthesis Failure

Objective: To investigate the effect of tumor specific antigen of HCA520 on the proliferation of HEK293 cells and to obtain some functional implications for HCA520. Methods: MTT assay was performed with HEK293 stable cell lines transfected with pcDNA3-HCA520-flag construct. Cytokines probably involved in HCA520 enhanced proliferation were screened by RT-PCR, and effect of these cytokines on the HEK293 cell proliferation was further confirmed by MTT assay. Results: HCA520 significantly promoted the proliferation of HEK293 cells, which was at least partially attributed to the up-regulation of IL-6 in HEK293 cells by HCA520. Conclusion: HCA520 might accelerate tumorigenesis by promoting proliferation of cancerous cells.

Objective To investigate induction of the expression of human ?-defensin-2 (hBD-2) mRNA and the changes in activation of I-?B? and NF-?B by IL-1? in the human airway epithelium. Methods Primary human respiratory tract epithelium were stimulated with IL-1? and and/or PDTC. The expression of hBD-2 mRNA was detected by reverse transcription polymerase chain reaction (RT-PCR). The I-?B? protein level in the cytoplasm was determined by Western blot, and the nuclear factor-kappaB (NF-?B) binding activity was analyzed by electrophoretic mobility shift assays. Results The hBD-2 mRNA expression could be detected after 1.5 hours of IL-1? stimulation at concentration of 1?g/L, and the expression of HBD-2 was in a dose dependent manner. Stimulation with IL-1? resulted in a reduction of I-?B? protein levels. The supershifts assays indicated that the p65-p50 heterodimer complexes of NF-?B were involved in the activation of NF-?B. Conclusions I-?B? can induce the expression of HBD-2 mRNA in a dose dependent manner; the p65-p50 heterodimer complexes of NF-?B play an important role in the regulation of hBD-2 gene expression in response to IL-1?.

Objective To explore a simple and effective method of culturing primary human bronchial epithelial cells.Methods Bronchial epithelial cells were obtained from human bronchial tissues obtained from lobectomy or pneumectomy.Epithelial cells were isolated by three methods as fellows:1.proteinase XIV digestion with mechanical scraping,2.proteinase XIV digestion with mechanical stripping,and 3.trypsin digestion with mechanical scraping.Subsequently the cells were cultured in serum-free hormone-supplemented DMEM/F12.The quantity,purity and viability of cells isolated by three methods were compared.The cultured cells were identified with cytokeratins AE1/AE3 by immunohistochemistry.Results The quantity of cells [(9.37?1.62)?105] obtained from proteinase XIV digestion with mechanical scraping was significantly higher than that of proteinase XIV digestion with mechanical stripping [(5.20?0.75)?105](P

Aim To explore the mechanisms of lovastatin protecting EPCs.Methods EPCs were preincubated with lovastatin or LOX-1 mAb for 24 h and then exposed to oxLDL for 48 h.The abilities of migration,adhesion,and tube structure formation of EPCs were examined.To explore the mechanisms,the level of NO,the expression of eNOS and LOX-1 protein and mRNA were assayed.Results Incubation of EPCs with oxLDL resulted in the impairment of migration,adhesion and tube structure formation.Furthermore,oxLDL caused the decrease of NO generation,the down-regulation of eNOS mRNA and protein expression,the up-regulation of LOX-1 mRNA and protein expression.However,the detrimental effects of oxLDL on EPCs function were attenuated by lovastatin and LOX-1 mAb.Moreover,the effects of oxLDL on NO generation,eNOS and LOX-1 expression were reversed by lovastatin and LOX-1 mAb.Conclusion Lovastatin protects EPCs by the regulation of eNOS and LOX-1 expression.

Objective　To assess the value of real-time myocardial contrast enhancement imaging (real-time MCE) on acute myocardial infarction.Methods　Eight open-chest canine models of myocardial infarction were established by ligating left anterior descent branch of coronary artery (LAD) on level after first diagonal branch. The real-time MCE, using intravenous instillation of a new kind of Perfluorocarbon contrast agent， were performed before the occlusion, 1 hour and 3 hours after the occlusion. The myocardial contrast agents perfusion and wall motion was observed on the middle of papillary muscles scan plane.Results　The real-time MCE showed not only the black aridity of contrast agents but also the wall motion abnormality 1 hour and 3 hours after the occlusion. In comparison with pathology, the defects of contrast perfusion were larger than the stained infarction zones. In addition, the flash contrast imaging revealed the reperfusion defect of adjacent zones.Conclusions　With the ability of showing the myocardial microcirculation and wall motion function simultaneously, the real-time MCE makes MCE exam significantly easier to perform. Finally, flash contrast imaging will be the cornerstone upon which perfusion quantification will be built.