ABSTRACT
@#AIM: To compare the clinical effects and safety of single subthreshold micropulse(STMP)yellow laser and combined ranibizumab intravitreal injection on the treatment of diabetic macular edema(DME).<p>METHODS: Totally 33 patients(58 eyes)with DME were divided into two groups. Group A(laser group)received STMP yellow laser, and group B(combined treatment group)received ranibizumab intravitreal injection combined with STMP yellow laser. The best corrected visual acuity(BCVA), intraocular pressure(IOP), central macular thickness(CMT), total macular volume(TMV), fluorescein fundus angiography(FFA), multifocal ERG(MERG), autofluorescence(AF)and macular pigment optical density(MPOD)were compared before and after the treatments. And treatment times were counted. <p>RESULTS:Compared with those before treatment, there were significant differences in BCVA and TMV 6, 9, 12mo after treatment in the laser group(<i>P</i><0.05). And there were significant differences in BCVA and TMV 3, 6, 9, 12mo after treatment in the combined treatment group(<i>P</i><0.05). For both groups, there were significant differences in CMT before and 3, 6, 9, 12mo after treatment(<i>P</i><0.01). Compared with the P1 amplitude of MEG, Max OD and Mean OD before treatment, there were significant differences for the two groups 12mo after treatment(<i>P</i><0.01). And the differences were significant in TMV and P1 amplitudes between the two groups after 12mo of treatment(<i>P</i><0.01). During the follow-up period, the laser times was 3.32±1.09 in the laser group and 3.30±1.18 in the combined treatment group(<i>P</i>=0.943).<p>CONCLUSION:Both single STMP laser and combined with intravitreal injection of ranibizumab can effectively reduce macular edema, improve vision and safety in DME patients. And the combined treatment group has faster and better effect.
ABSTRACT
PURPOSE: Cancer cells develop acquired resistance induced by chemotherapeutic drugs. In this study, we investigated the effects of brief treatment with cytotoxic drugs on the phenotype of breast cancer cells. METHODS: Breast cancer cells MCF7 and BT-474 were briefly treated with paclitaxel or doxorubicin. Clonogenic, migration, and invasion assays were performed on the treated cells. Western blot analysis and RhoA activity assay were also performed. RESULTS: Breast cancer cells when briefly treated with paclitaxel or doxorubicin showed reduced clonogenic ability. Doxorubicin, but not paclitaxel, augmented cell migration and invasion. The invasion-promoting effects of doxorubicin were lost when the two drugs were sequentially used in combination. Myosin light chain (MLC) 2 phosphorylation and RhoA activity were upregulated by doxorubicin and downregulated by paclitaxel. Pretreatment with RhoA inhibitors abolished the migration- and invasion-promoting effects of doxorubicin. CONCLUSION: Doxorubicin activates the RhoA/MLC pathway and enhances breast cancer cell migration and invasion. Therefore, this pathway might be explored as a therapeutic target to suppress anthracycline-enhanced tumor progression.