Objective:The aim of this study was to compare the efficacy of augmenting trabeculectomy with subconjunctival mitomycin C (TMMC) versus 5-fluorouracil (T5-FU) in lowering intraocular pressure (IOP).Methods:Forty eyes from 40 patients referred to the Nikoukari Ophthalmology University Hospital, Tabriz University of Medical Sciences, Tabriz, Iran, were enrolled in a randomized clinical trial. Patients with high-risk open angle glaucoma were allocated to receive either subconjunctival TMMC or T5-FU.Results:Mean overall preoperative IOP was 30.8 mmHg. Mean preoperative IOPs in the TMMC and T5-FU groups were 31.2 ± 9.8 and 30.6 ± 9.9 mmHg, respectively. Postoperatively, mean IOPs were 11.4.3 ± 4.9 and 13.6 ± 3.9 mmHg, respectively for TMMC and T5-FU groups after 6 months. In spite of some existing descriptive differences in IOP between the groups, statistical tests showed no difference in mean and median IOP. Three cases of hypotonia (IOP < 6 mmHg) and 1 case of epithelial keratitis were detected.Conclusion:TMMC and T5-FU appeared to have similar efficacy in lowering IOP.

Cell proliferation, migration, and capillary network formation of endothelial cells are the fundamental steps for angiogenesis, which involves the formation of new blood vessels. The purpose of this study is to investigate the effect of a novel aminothiazole SNS-032 on these critical steps for in vitro angiogenesis using a coculture system consisting of human umbilical vein endothelial cells (HUVECs) and human glioblastoma cells (U87MG). SNS-032 is a potent selective inhibitor of cyclin-dependent kinases 2, 7, and 9, and inhibits both transcription and cell cycle. In this study, we examined the proliferation and viability of HUVECs and U87MG cells in the presence of SNS-032 and observed a dose-dependent inhibition of cellular proliferation in both cell lines. SNS-032 inhibited threedimensional capillary network formations of endothelial cells. In a coculture study, SNS-032 completely prevented U87MG cell-mediated capillary formation of HUVECs. This inhibitor also prevented the migration of HUVECs when cultured alone or cocultured with U87MG cells. In addition, SNS-032 significantly prevented the production of vascular endothelial growth factor (VEGF) in both cell lines, whereas SNS-032 was less effective in preventing capillary network formation and migration of endothelial cells when an active recombinant VEGF was added to the medium. In conclusion, SNS-032 prevents in vitro angiogenesis, and this action is attributable to blocking of VEGF.

growth rate and twinning rate are economic traits that can be used in goat breeding objectives. the aim of this study was to investigate polymorphisms in the insulin-like growth factor 1(IGF-I) and insulin-like growth factor binding protein (IGFBP-3) genes and their relationship with growth traits and twinning in Markhoz goats. Two sets of specific primers were used to amplify a 249bp fragment of IGF-I gene and a 316bp fragment of IGFBP-3 gene. pCr-ssCp analysis revealed three banding patterns for each gene that confirmed presence of a mutation in position 1617 of the IGF-I gene and a mutation in position 58 of IGFBP-3 gene. the genotype frequencies of IGF-I gene were 0.81 (gg), 0.16 (ga) and 0.03 (aa). also, the genotype frequencies of IGFBP-3 gene were 0.79 (TT), 0.17 (TC) and 0.04 (CC). The Odds Ratio estimated for twinning rate was 1.11 for second on first parity, 0.19 for third on first parity and 5.71 for second on third parity. The chi-square statistics were 6.46 for IGF-I gene and 3.32 for IGFBP-3 gene. the results also indicated that different genotypes of these genes had no significant effect on birth weight, weight at 6 months, at 9 months and at 12 months but the interactions between different genotypes of IGF-I and IGFBP-3 genes were significant for weaning weight and average daily gain from birth to weaning. These results suggest that twinning rate in markhoz breed is statistically affected by these genes and can be considered in breeding programs.

No abstract

Overexpression of cyclooxygenase-2 (COX-2) is frequently observed in several human cancers, including lung, colon, and head and neck. Malignancies are also associated with the dysregulation of cell cycle events and concomitant elevated activity of cyclin-dependent kinases (CDK). CDK2 is a key cell cycle regulatory protein that controls the transition of cells from G 1 to S phase. In this study, we furnish several lines of evidence that show a functional role for the CDK2 in interleukin-1B (IL-1B)-induced COX-2 expression in H358 human non-small cell lung carcinoma cell line by blocking CDK2 activity. First, we show that BMS-387032, a potent CDK2 inhibitor, blocks IL-1B-induced expression as well as steadystate mRNA levels of COX-2. Second, we show that small interfering RNA that abrogates CDK2 expression also blocks IL-1B-induced COX-2 expression. Third, results from in vitro kinase assays clearly show that IL-1B induces CDK2 activity in H358 cells and this activity is significantly inhibited by BMS-387032. Moreover, CDK2 inhibition blocks IL-1B-induced binding to the NF-IL6 element of the COX-2 promoter and inhibits transcription of the COX-2 gene. We also observed that BMS-387032 does not inhibit endogenous expression of COX-2 or prostaglandin synthesis in lung carcinoma cells. Finally, we provide evidence showing that IL-1B-induced signaling events, such as p38 mitogen-activated protein kinase, phosphorylated stress-activated protein kinase/c-Jun NH 2 -terminal kinase, phosphorylated AKT, and phosphorylated extracellular signal-regulated kinase 1/2, are not inhibited by CDK2 inhibitor. Taken together, the data suggest that CDK2 activity may play an important event in the IL-1B-induced COX-2 expression and prostaglandin E 2 synthesis and might represent a novel target for BMS-387032. (Cancer Res 2006; 66(3): 1758-66)