Retracted: Inhibition of Corneal Neovascularization by Hydrazinocurcumin

This article previously published in Volume 15 Issue 2 of this journal in February 2016 has been retracted in line with the guidelines from the Committee on Publication Ethics (COPE, http://publicationethics.org/resources/guidelines)Retracted: Zhan W, Zhu J, Zhang Y. Inhibition of corneal neovascularization by hydrazinecurcumin. Trop J Pharm Res 2016; 15(2):349-354 doi: http://dx.doi.org/10.4314/tjpr.v15i2.18

Inhibition of Corneal Neovascularization by Hydrazinocurcumin

Purpose: To investigate the effect of hydrazinocurcumin on a human vascular endothelial growth factor (VEGF)-induced corneal neovascularization in rabbit model.Methods: Murine corneal neovascularization (CorNV) was induced via two intrastromal implantations of VEGF polymer 2 mm from the limbus. Hydrazinocurcumin was administered topically on the cornea 4 times daily for 7 days. The therapeutic effects of hydrazinocurcumin were evaluated daily using slitlamp. At the end of the treatment, the corneas were harvested for H&E staining, masson trichrome staining, immuno-histochemical study, and semi quantification reverse transcription polymerase chain reaction (RT-PCR) was utilized for measurement of inflammation-related molecules.Results: Topical application of hydrazinocurcumin had significant therapeutic effects on CorNV Hydrazinocurcumin extract treatment was more effective in suppressing CorNV in terms of vessel length and levels of cluster of differentiation 31 (CD31) proteins or angiogenesis-related genes such as VEGF, matrix metalloproteinase-2 (MMP2) and matrix metalloproteinase-9 (MMP9). The average length of vessels in hydrazinocurcumin-treated group was only 17 % of that in the control group. Hydrazinocurcumin also inhibited inflammation more markedly by more effectively inhibiting mononuclear and polymorphonuclear cell infiltration into the corneal stroma and reducing levels of stromal cell-derived factor-1 (SDF1), tumor necrosis factor-alpha (TNFα) and macrophage inflammatory protein-3 (MIP3a). In addition, the corneas of hydrazinocurcumin group had a more regular and compact architecture of collagen with thinner corneal thickness than those of the untreated group.Conclusion: Hydrazinocurcumin inhibited human vascular endothelial growth factor (VEGF)-induced rabbit corneal neovascularization and thus can potentially be used for its treatment.Keywords: Hydrazinocurcumin, Corneal neovascularization, Inflammation, Vascular endothelial growth factor, Corneal thicknes

Inhibitory effect of puerarin on proliferation of retinoblastoma cells: An in-vitro study

Purpose: To investigate the anti-proliferative effect of puerarin on retinoblastoma cells.Methods: The effect of puerarin was examined on human retinoblastoma Y79 cells using cell proliferation assays and reverse transcription-polymerase chain reaction (RT-PCR). The effect of puerarin on the cell cycle was also investigated. Western blot and RT-PCR analyses were also performed to identify the putative mechanism of action.Results: The results showed that cell viability was suppressed by puerarin in a concentrationdependent manner with a half-maximal inhibitory concentration (IC50) of 0.184 ± 0.034 μmol/L. Moreover, puerarin increased the proportion of cells in G1 phase from 42.6 ± 3.1 to 62.83 ± 4.1, 75.76 ± 3.4 and 91.33 ± 5.1 % in a concentration-dependent manner at concentrations of 0.1, 0.2, and 0.4 μmol/L, respectively. The results also indicate that Bmi-1 mRNA and protein levels decreased after puerarin treatment. Additionally, flow cytometry data showed that Bmi-1 knock-down through siRNA resulted in G1-cell cycle arrest. The proportion of cells in G1 were 51.2 ± 2.5 and 71.4 ± 4.5 % for control and Bmi-1 siRNA-treated groups, respectively.Conclusions: The results show that puerarin exert suppressive effects on human retinoblastoma Y79 cells and therefore may find application in the treatment of intraocular tumor.Keywords: Cancer, Puerarin, Retinoblastoma Y79 cells, mTOR inhibition, Intraocular tumo

Low-energy Scattering of (D∗Dˉ∗)±(D^{*}\bar{D}^{*})^\pm System and the Resonance-like Structure Zc(4025)Z_c(4025)

In this paper, low-energy scattering of the $(D^{*}\bar{D}^{*})^\pm$ meson system is studied within L\"uscher's finite-size formalism using $N_{f}=2$ twisted mass gauge field configurations. With three different pion mass values, the $s$-wave threshold scattering parameters, namely the scattering length $a_0$ and the effective range $r_0$, are extracted in $J^P=1^+$ channel. Our results indicate that, in this particular channel, the interaction between the two vector charmed mesons is weakly repulsive in nature hence do not support the possibility of a shallow bound state for the two mesons, at least for the pion mass values being studied. This study provides some useful information on the nature of the newly discovered resonance-like structure $Z_c(4025)$ observed in various experiments.Comment: 11 pages, 6 figures. arXiv admin note: substantial text overlap with arXiv:1403.131

A Lattice Study of (Dˉ1D∗)±(\bar{D}_1 D^{*})^\pm Near-threshold Scattering

In this exploratory lattice study, low-energy near threshold scattering of the $(\bar{D}_1 D^{*})^\pm$ meson system is analyzed using lattice QCD with $N_f=2$ twisted mass fermion configurations. Both s-wave ($J^P=0^-$) and p-wave ($J^P=1^+$) channels are investigated. It is found that the interaction between the two charmed mesons is attractive near the threshold in both channels. This calculation provides some hints in the searching of resonances or bound states around the threshold of $(\bar{D}_1 D^{*})^\pm$ system.Comment: 20 pages, 15 figures, matches the version on PR

Two Photon Decays of ηc\eta_c from Lattice QCD

We present an exploratory lattice study for the two-photon decay of $\eta_c$ using $N_f=2$ twisted mass lattice QCD gauge configurations generated by the European Twisted Mass Collaboration. Two different lattice spacings of $a=0.067$fm and $a=0.085$fm are used in the study, both of which are of physical size of 2$fm$. The decay widths are found to be $1.025(5)$KeV for the coarser lattice and $1.062(5)$KeV for the finer lattice respectively where the errors are purely statistical. A naive extrapolation towards the continuum limit yields $\Gamma\simeq 1.122(14)$KeV which is smaller than the previous quenched result and most of the current experimental results. Possible reasons are discussed.Comment: 13 pages, 7 figures; matches the published versio

Extracellular Matrix Protein Tenascin C Increases Phagocytosis Mediated by CD47 Loss of Function in Glioblastoma.

Glioblastomas (GBM) are highly infiltrated by myeloid-derived innate immune cells that contribute to the immunosuppressive nature of the brain tumor microenvironment (TME). CD47 has been shown to mediate immune evasion, as the CD47-SIRPα axis prevents phagocytosis of tumor cells by macrophages and other myeloid cells. In this study, we established CD47 homozygous deletion (CD47-/-) in human and mouse GBM cells and investigated the impact of eliminating the "don't eat me" signal on tumor growth and tumor-TME interactions. CD47 knockout (KO) did not significantly alter tumor cell proliferation in vitro but significantly increased phagocytosis of tumor cells by macrophages in cocultures. Compared with CD47 wild-type xenografts, orthotopic xenografts derived from CD47-/- tumor cells grew significantly slower with enhanced tumor cell phagocytosis and increased recruitment of M2-like tumor-associated microglia/macrophages (TAM). CD47 KO increased tumor-associated extracellular matrix protein tenascin C (TNC) in xenografts, which was further examined in vitro. CD47 loss of function upregulated TNC expression in tumor cells via a Notch pathway-mediated mechanism. Depletion of TNC in tumor cells enhanced the growth of CD47-/- xenografts in vivo and decreased the number of TAM. TNC knockdown also inhibited phagocytosis of CD47-/- tumor cells in cocultures. Furthermore, TNC stimulated release of proinflammatory factors including TNFα via a Toll-like receptor 4 and STAT3-dependent mechanism in human macrophage cells. These results reveal a vital role for TNC in immunomodulation in brain tumor biology and demonstrate the prominence of the TME extracellular matrix in affecting the antitumor function of brain innate immune cells. SIGNIFICANCE: These findings link TNC to CD47-driven phagocytosis and demonstrate that TNC affects the antitumor function of brain TAM, facilitating the development of novel innate immune system-based therapies for brain tumors

3,5-Bis(4-methoxy­phen­yl)-1H-1,2,4-triazole monohydrate

In the title compound, C16H15N3O2·H2O, the two benzene rings and the triazole ring lie almost in the same plane, the triazole ring forming dihedral angles of 5.07 (9) and 5.80 (8)° with the benzene rings. In the crystal, there are three relatively strong inter­molecular O—H⋯N and N—H⋯O hydrogen bonds, which lead to the formation of a one-dimensional double chain running parallel to the a axis. Weak π—π inter­actions between the benzene rings of neighboring chains with a centroid–centroid distance of 3.893 (4) Å result in the formation of layers parallel to the ac plane