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.

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.