We report an improved precision measurement of the Casimir force. The force is measured between a large Al coated sphere and flat plate using an Atomic Force Microscope. The primary experimental improvements include the use of smoother metal coatings, reduced noise, lower systematic errors and independent measurement of surface separations. Also the complete dielectric spectrum of the metal is used in the theory. The average statistical precision remains at the same 1% of the forces measured at the closest separation.PACS: 12.20.Fv

This study first investigates the anticancer effect of plumbagin (5-hydroxy-2-methyl-1,4-naphthoquinone) in human nonsmall cell lung cancer cells, A549. Plumbagin has exhibited effective cell growth inhibition by inducing cancer cells to undergo G 2 /M phase arrest and apoptosis. Blockade of cell cycle was associated with increased levels of p21 and reduced amounts of cyclinB1, Cdc2, and Cdc25C. Plumbagin treatment also enhanced the levels of inactivated phosphorylated Cdc2 and Cdc25C. Blockade of p53 activity by dominant-negative p53 transfection partially decreased plumbagin-induced apoptosis and G 2 /M arrest, suggesting it might be operated by p53-dependent and independent pathway. Plumbagin treatment triggered the mitochondrial apoptotic pathway indicated by a change in Bax/Bcl-2 ratios, resulting in mitochondrial membrane potential loss, cytochrome c release, and caspase-9 activation. We also found that c-Jun NH 2 -terminal kinase (JNK) is a critical mediator in plumbagin-induced cell growth inhibition. Activation of JNK by plumbagin phosphorylated p53 at serine 15, resulting in increased stability of p53 by decreasing p53 and MDM2 interaction. SP600125 (anthra [1,9-cd]pyrazol-6(2H)-one-1,9-pyrazoloanthrone), a specific inhibitor of JNK, significantly decreased apoptosis by inhibiting the phosphorylation of p53 (serine 15) and subsequently increased the interaction of p53 and MDM2. SP6000125 also inhibited the phosphorylation of Bcl-2 (Ser70) induced by plumbagin. Further investigation revealed that plumbagin's inhibition of cell growth effect was also evident in a nude mice model. Taken together, these results suggest a critical role for JNK and p53 in plumbagin-induced G 2 /M arrest and apoptosis of human nonsmall cell lung cancer cells.Lung cancer is one of the leading causes of death in the world, and nonsmall cell lung carcinoma accounts for approximately 75 to 85% of all lung cancers (Raez and Lilenbaum, 2004). Nonsmall cell lung cancers commonly develop resistance to radiation and chemotherapy and often present at stages too late for surgical intervention. Since current treatment modalities are inadequate, novel therapies are needed to reduce the effects of the increasing incidence in pulmonary neoplasm (Raez and Lilenbaum, 2004;Kelly, 2005).The tumor suppressor protein p53 is targeted by a wide variety of intracellular and extracellular stimuli, such as withdrawal of growth factors, hypoxia, irradiation, chemicals, and defects in nucleotide synthesis (Harris and Levine, 2005). The activation of p53 leads, primarily through its transcriptional function, to either apoptosis, eliminating those cells harboring severely damaged DNA, or growth arrest, allowing damaged DNA to be repaired and thereby suppressing tumor formation (Harris Robles et al., 2002;Levine, 2005). Stability and activity of p53 are believed to be regulated in part by posttranslational modifications, such as phosphorylation and acetylation.

We demonstrate the charge state of C 60 on a Cu(111) surface can be made optimal, i.e., forming C 60 3À as required for superconductivity in bulk alkali-doped C 60 , purely through interface reconstruction rather than with foreign dopants. We link the origin of the C 60 3À charge state to a reconstructed interface with ordered (4 Â 4) 7-atom vacancy holes in the surface. In contrast, C 60 adsorbed on unreconstructed Cu(111) receives a much smaller amount of electrons. Our results illustrate a definitive interface effect that affects the electronic properties of molecule-electrode contact. DOI: 10.1103/PhysRevLett.104.036103 PACS numbers: 68.43.Àh, 61.05.jh, 68.35.Ct, 73.20.Àr In bulk fulleride A n C 60 (A ¼ Na, K, etc.) [1], an ''optimal doping'' state favoring superconductivity is known to occur for n ¼ 3, with 3 electrons on each C 60 (C 60 3À ). Since C 60 films on metallic surfaces typically involve substrate-to-C 60 electron transfer that partially populates the C 60 lowest unoccupied molecular orbital (LUMO), it has been of great interest to pursue optimally doped C 60 films. Earlier studies show that the electron transfer amount does not simply depend on the substrate work function [2]. This raises the question of the role of the C 60 =metal interface structure. Although strong C 60 -metal interactions are not expected for, e.g., C 60 on noble metal surfaces, there is increasing evidence of C 60 -induced interface reconstruction for C 60 =Auð110Þ [3], C 60 =Ptð111Þ [4], C 60 =Alð111Þ [5], C 60 =Agð100Þ [6], and even for C 60 =Agð111Þ [7] and C 60 =Cuð111Þ [8], etc. The typical scenario is that C 60 tends to dig a ''vacancy'' in the surface. Calculations, including our own, show this geometry increases the adsorption strength that compensates the energy cost of vacancy creation. No studies, however, have discussed how the electronic structure and hence the charge state of a C 60 film are affected by its interface structure. Here, we discovered that a C 60 monolayer on Cu(111) is optimally electron doped purely by interface reconstruction and without intercalating alkali atoms. We convincingly establish the C 60 3À charge state and trace its origin to a reconstructed interface with ordered (4 Â 4) large 7-atom vacancy holes in the surface. The key link between molecular doping and a reconstructed interface indicates the practical needs of tackling the often neglected difficult interface structure problems which could prove essential in understanding the physics and chemistry of thin film materials.Many inconsistencies between experiment and theory in heteroepitaxial systems, such as the charge state of a C 60 film on a surface, are likely rooted in the application of an incorrect interface model. For C 60 =Cuð111Þ, it has been measured to range from 1-3 electrons per C 60 by photoemission spectroscopy (PES) [9]. Calculations predict a much smaller amount, <0:8e À , for an unreconstructed interface [10]. The electronic band structure measured by a recent PES study is also at odds with theoretical analysi...

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1. The present study was conducted to evaluate the cytotoxic effects of Coptis chinensis and Epimedium sagittatum extracts and their major constituents on hepatoma and leukaemia cells in vitro. 2. Four human liver cancer cell lines, namely HepG2, Hep3B, SK-Hep1 and PLC/PRF/5, and four leukaemia cell lines, namely K562, U937, P3H1 and Raji, were used in the present study. 3. Of the two crude drugs, C. chinensis exhibited the strongest activity against SK-Hep1 (IC50 = 7 microg/mL) and Raji (IC50 = 4 microg/mL) cell lines. The IC50 values for C. chinensis on HepG2, Hep3B and PLC/PRF/5 cell lines were 20, 55 and 35 microg/mL, respectively. The IC50 values for C. chinensis on K562, U937 and P3H1 cell lines were 29, 29 and 31 microg/mL, respectively. 4. With the exception of HepG2 and Hep3B, the E. sagittatum extract inhibited the proliferation of all cell lines (SK-Hep1, PLC/PRF/5, K562, U937, P3H1 and Raji), with IC50 values of 15, 57, 74, 221, 40 and 80 microg/mL, respectively. 5. Interestingly, the two major compounds of C. chinensis, berberine and coptisine, showed a strong inhibition on the proliferation of both hepatoma and leukaemia cell lines, with IC50 values varying from 1.4 to 15.2 microg/mL and from 0.6 to 14.1 microg/mL, respectively. However, icariin (the major compound of E. sagittatum) showed no inhibition of either the hepatoma or leukaemia cell lines. 6. The results of the present study suggest that the C. chinensis extract and its major constituents berberine and coptisine possess active antihepatoma and antileukaemia activities.