Angular distributions of 16O + 16O elastic scattering at energies that range from 124 to 1120 MeV have been analyzed in the framework of the double folding (DF) optical model. Based upon the α-cluster structure of the 16O nucleus, two different versions of the real DF optical potential have been generated by using three effective α-α, α-nucleon (N) and nucleon-nucleon (NN) interactions. A microscopic optical potential built upon the M3Y effective NN interaction and the matter density distribution of the 16O nucleus has also been extracted. The obtained real potentials, in conjunction with phenomenological squaredWoods-Saxon imaginary parts, have successfully reproduced seven sets of elastic-scattering data. No renormalization of the real folded α-cluster potentials is required to fit the data. The energy dependence of the extracted real and imaginary volume integrals and total reaction cross section has also been investigated.

The elastic scattering of 6,7Li+28Si reactions has been analyzed in the framework of the double folding optical model. Semi-microscopic folded potentials are generated based on the alpha (α)-cluster structure of the colliding nuclei. Successful reproduction of the observed angular distributions of the elastic scattering differential cross section and reaction cross sections has been obtained at different energies using the derived potentials. A microscopic folding approach based on the effective DDM3Y nucleon–nucleon interaction and the nuclear matter densities of the interacting nuclei is also considered.

The elastic scattering of 6,7Li+28Si reactions has been analyzed in the framework of the double folding optical model. Semi-microscopic folded potentials are generated based on the alpha (α)-cluster structure of the colliding nuclei. Successful reproduction of the observed angular distributions of the elastic scattering differential cross section and reaction cross sections has been obtained at different energies using the derived potentials. A microscopic folding approach based on the effective DDM3Y nucleon–nucleon interaction and the nuclear matter densities of the interacting nuclei is also considered.

The vector analyzing power and differential cross-section for the elastic scattering of 8He nucleus from polarized protons at 71MeV/nucleon have been analyzed in the framework of the optical model potentials. Microscopic single folding (SF) optical potentials (OP) have been constructed based upon two different effective nucleon–nucleon (NN) interactions, namely Jeukenne–Lejeune–Mahaux (JLM) and BDM3Y1 effective interactions. The effect of 8He nuclear structure has been tested through two different choices of the nuclear density distribution. It is concluded that the nucleus 8He may be considered as a thick skin exotic nucleus. In order to investigate the vector analyzing power data, besides the Thomas phenomenological representation, three different forms of the spin–orbit (SO) part of the OP have been considered. These forms are based directly or indirectly upon the density distribution of 8He nucleus. It is found that SO potentials of larger root mean square radii are able to successfully describe the vector analyzing power data more than those of shorter radii.

The structureoftheas-preparedandthermalannealedAg10As30S60 chalcogenide glassischaracterized using theX-raydiffraction(XRD)andscanningelectronmicroscopy(SEM).Differentialscanning calorimetry (DSC)curvesrecordedatfourdifferentheatingratesareanalyzedtodeterminetheglass and crystallizationtransitiontemperatures,thermalstabilityandenthalpyrelease.Twoseparated crystallization peaksareobservedintheDSCcurves.XRDresultsindicatetheprecipitationofAgAsS4 crystal phaseisresponsibleforthe first peak.NumerousphaseswithS8 dominant phaseareaccountable for thesecondpeak.Thecrystallizationkineticssuchastheactivationenergyforthecrystallization(Ec), the frequencyfactor(Ko) andthecrystallizationrateconstant K are determinedforeachcrystallization stage. Theresultsshowthatthecrystallizationrateconstantforthe first crystallizationstageisaboutsix times largerthanthatofthesecondcrystallizationstep.

Coating nonmetallic-chalcogenide film material is developed to avoid oxidation and corrosion of the thin films. The chalcogenide part consists of a thin film of Se60Te30S10 prepared by the thermal evaporation technique. On the other hand, the nonmetallic carbon thin film is applied onto the as-plated chalcogenide surface by deposition from an electrically heated carbon rod (arc discharge). The products obtained are characterized with X-ray diffraction and Scanning Electron Microscopy. It is observed an enhancement in crystallinity upon annealing for the as prepared uncoated and coated carbon films is observed. Optical studies reveal that carbon coating influences the optical energy gap, absorption coefficient and refractive index of the Se60Te30S10 thin film.

Background: DJ 1 PARK7 was reported as an oncogene in a Ras-dependent manner. Recent studies have shown that DJ 1 stimulates cell proliferation, cell invasion, and cancer metastasis. However, the molecular mehchanism by which DJ 1 induces cancer cell invasion and metastasis remains unclear. Methods: Breast cancer cells were transfected with DJ 1 siRNA or DJ 1 overexpression to investigate the effect of DJ 1 on KLF17 expression. ID 1 luciferase promoter assay was performed to evaluate DJ-1-dependent KLF17 expression changes. In addition, Epistasis analysis of DJ 1 and KLF17 was performed to evaluate their regulatory interactions. Ras inhibitors were pretreated to determine whether DJ 1 regulates cell invasion in a Ras-dependent manner. Results: In the present study, we found increased DJ 1 expression in highly invasive breast cancer cells as compared with nonmetastatic cells. Furthermore, DJ 1 promoted breast cancer cell invasion by downregulating E cadherin and increasing Snail expression. Interestingly, exogenous DJ 1 overexpression markedly decreased mRNA and protein expression of KLF17, the EMT negative regulator. These data were confirmed by ID 1 promoter activity, which is directly regulated by DJ-1-dependent KLF17 transcription factor. Epistasis analysis showed that KLF17 overexpression overcomes increased cell invasion by DJ 1, suggesting that KLF17 might be one of the downstream signalling molecules of DJ 1. Acceleration of cell invasion by DJ 1 was alleviated by Ras inhibitors, suggesting that DJ 1 cooperates with Ras to increase cell invasion.

Since epithelial-mesenchymal transition (EMT) plays a critical role in cancer progression and in maintaining cancer stem cell properties, EMT is emerging as a therapeutic target for inhibiting the metastatic progression of cancer cells. 20-Hydroxycinnamaldehyde (HCA) and its derivative, 20-benzoyloxycinnamaldehyde, have recently been suggested as promising therapeutic candidates for cancer treatment. The purpose of this study is to investigate the anti-metastatic effect of HCA on breast cancer and the molecular mechanisms by which HCA regulates the transcriptional program during EMT. HCA induces epithelial reversion at nanomolar concentrations by suppressing Snail via the nuclear translocalization of GSK-3b, which results in the transcriptional upregulation of E-cadherin. HCA also activates the transcription factor KLF17, which suppresses Id-1, indicating that HCA inhibits EMT by multiple transcriptional programs. Further, HCA treatment significantly inhibits lung metastasis in a mouse orthotopic breast cancer model. This study demonstrates the anti-metastatic effect of the non-toxic natural compound HCA through attenuation of EMT in a breast cancer model.

Most anti-cancer agents induce apoptosis, however, a development of multidrug resistance in cancer cells and defects in apoptosis contribute often to treatment failure. Here, the mechanism of curcumin-induced apoptosis was investigated in human leukemia HL60 cells and their HL60/VCR multidrug-resistant counterparts. In both cell lines curcumin induced a bi-phasic ceramide generation with a slow phase until 6 h followed by a more rapid one. The level of the ceramide accumulation correlated inversely with the cell viability. We found that the ceramide elevation resulted from multifarious changes of the activity of sphingolipid-modifying enzymes. In both cell lines curcumin induced relatively fast activation of neutral sphingomyelinase (nSMase), which peaked at 3 h, and was followed by inhibition of sphingomyelin synthase activity. In addition, in HL60/VCR cells the glucosylceramide synthase activity was diminished by curcumin. This process was probably due to curcumin-induced down-regulation of P-gp drug transporter, since cyclosporine A, a P-gp blocker, also inhibited the glucosylceramide synthase activity. Inhibition of nSMase activity with GW4869 or silencing of SMPD3 gene encoding nSMase2 reversed the curcumin-induced inhibition of sphingomyelin synthase without affecting the glucosylceramide synthase activity. The early ceramide generation by nSMase was indispensable for the later lipid accumulation, modulation of Bax, Bcl-2 and caspase 3 levels, and for reduction of cell viability in curcumin-treated cells, as all these events were inhibited byGW4869 or nSMase2 depletion. These data indicate that the early ceramide generation by nSMase2 induced by curcumin intensifies the later ceramide accumulation via inhibition of sphingomyelin synthase, and controls pro-apoptotic signaling.

Most anti-cancer agents induce apoptosis, however, a development of multidrug resistance in cancer cells and defects in apoptosis contribute often to treatment failure. Here, the mechanism of curcumin-induced apoptosis was investigated in human leukemia HL60 cells and their HL60/VCR multidrug-resistant counterparts. In both cell lines curcumin induced a bi-phasic ceramide generation with a slow phase until 6 h followed by a more rapid one. The level of the ceramide accumulation correlated inversely with the cell viability. We found that the ceramide elevation resulted from multifarious changes of the activity of sphingolipid-modifying enzymes. In both cell lines curcumin induced relatively fast activation of neutral sphingomyelinase (nSMase), which peaked at 3 h, and was followed by inhibition of sphingomyelin synthase activity. In addition, in HL60/VCR cells the glucosylceramide synthase activity was diminished by curcumin. This process was probably due to curcumin-induced down-regulation of P-gp drug transporter, since cyclosporine A, a P-gp blocker, also inhibited the glucosylceramide synthase activity. Inhibition of nSMase activity with GW4869 or silencing of SMPD3 gene encoding nSMase2 reversed the curcumin-induced inhibition of sphingomyelin synthase without affecting the glucosylceramide synthase activity. The early ceramide generation by nSMase was indispensable for the later lipid accumulation, modulation of Bax, Bcl-2 and caspase 3 levels, and for reduction of cell viability in curcumin-treated cells, as all these events were inhibited byGW4869 or nSMase2 depletion. These data indicate that the early ceramide generation by nSMase2 induced by curcumin intensifies the later ceramide accumulation via inhibition of sphingomyelin synthase, and controls pro-apoptotic signaling.