The ground state of liquid $^{3}\mathrm{He}$-$^{4}\mathrm{He}$ solution was represented by a Jastrow wave function times Slater determinants for the $^{3}\mathrm{He}$ atoms, and a Monte Carlo calculation was performed for $^{3}\mathrm{He}$ concentrations of 6.5, 12, and 44 at.%. The average binding energy per atom, the radial distribution functions, the structure functions, the momentum distribution of the $^{4}\mathrm{He}$ atoms, and the $^{4}\mathrm{He}$ condensate fraction ${n}_{0}$ were calculated. In the above concentrations, the values of ${n}_{0}$ were found to be 13.1\ifmmode\pm\else\textpm\fi{}1%, 13.7\ifmmode\pm\else\textpm\fi{}1%, and 19.0\ifmmode\pm\else\textpm\fi{}1%, respectively, compared to 11% for bulk liquid $^{4}\mathrm{He}$. This enhancement of ${n}_{0}$ is due mainly to the decreasing density of the solution as the $^{3}\mathrm{He}$ concentration increases. Similar calculations were done for mass-3---mass-4 boson solutions. The radial distribution function of the $^{3}\mathrm{He}$-$^{4}\mathrm{He}$ solution are different from those of the mass-3---mass-4 boson solutions due to the difference in statistics.
Aberrative nonlinear transfer matrices are introduced to treat the propagation of laser beam in Kerr medium with thermal lensing. The dependence of mode-locking regions on cavity symmetry and the distance between the fold mirror and the crystal, and the optimal agreement for Kerr-lens mode- locking are discussed with ABCD matrix method.
The class 1 carcinogen cadmium (Cd2+) disrupts the E-cadherin/beta-catenin complex of epithelial adherens junctions (AJs) and causes renal cancer. Deregulation of E-cadherin adhesion and changes in Wnt/beta-catenin signaling are known to contribute to carcinogenesis.We investigated Wnt signaling after Cd2+-induced E-cadherin disruption in sub-confluent cultured kidney proximal tubule cells (PTC). Cd2+ (25 microM, 3-9 h) caused nuclear translocation of beta-catenin and triggered a Wnt response measured by TOPflash reporter assays. Cd2+ reduced the interaction of beta-catenin with AJ components (E-cadherin, alpha-catenin) and increased binding to the transcription factor TCF4 of the Wnt pathway, which was upregulated and translocated to the nucleus. While Wnt target genes (c-Myc, cyclin D1 and ABCB1) were up-regulated by Cd2+, electromobility shift assays showed increased TCF4 binding to cyclin D1 and ABCB1 promoter sequences with Cd2+. Overexpression of wild-type and mutant TCF4 confirmed Cd2+-induced Wnt signaling. Wnt signaling elicited by Cd2+ was not observed in confluent non-proliferating cells, which showed increased E-cadherin expression. Overexpression of E-cadherin reduced Wnt signaling, PTC proliferation and Cd2+ toxicity. Cd2+ also induced reactive oxygen species dependent expression of the pro-apoptotic ER stress marker and Wnt suppressor CHOP/GADD153 which, however, did not abolish Wnt response and cell viability.Cd2+ induces Wnt signaling in PTC. Hence, Cd2+ may facilitate carcinogenesis of PTC by promoting Wnt pathway-mediated proliferation and survival of pre-neoplastic cells.
Background Pituitary homeobox 2 (Pitx2) is a master regulator of organ asymmetry during development but is reactivated in neoplastic cells, contributing to cell proliferation, tumor cell invasion and cancer progression. Upregulation of the multidrug resistance P‐glycoprotein ABCB1 confers chemotherapeutic drug resistance to tumor cells, hampering effective treatment. We have previously shown that Pitx2 is upregulated in a multidrug resistant (MDR) kidney cancer cell line and serves as a positive transcriptional regulator of ABCB1 thereby increasing resistance to the anthracycline chemotherapeutic drug, doxorubicin (DOX) (Lee, W.‐K. et al. Int J Cancer 113 , 556–67, 2013). The objective of this study was to determine if ABCB1 regulation by Pitx2 is also in engaged by other cancer types that exhibit intrinsic MDR. Methods Expression of Pitx2 and ABCB1 was determined by immunofluorescence microscopy, immunoblotting and immunohistochemistry. Cell viability was assessed by MTT and clonogenic survival assays. Pitx2 transcriptional activity was measured by luciferase reporter gene assay. Isolation of nuclei was performed by Tenbroeck homogenization in hypoosmotic buffer and a discontinuous sucrose gradient. Results In human colorectal adenocarcinoma Colo320DM cells, which exhibit MDR and harbor augmented ABCB1 expression, nuclear Pitx2 expression and Pitx2 reporter gene activity were significantly increased compared to less drug resistant Colo205 cells. The ABCB1 inhibitor PSC833 (0.1 μM) reversed drug resistance to 1 μM DOX after 24 h in Colo320DM cells. Further, knockdown of Pitx2 by RNAi in Colo320DM cells resulted in decreased ABCB1 protein by almost 3‐fold and diminished resistance to DOX resulting in attenuated cell survival. Moreover, the Pitx2 isoforms that are involved in regulation of ABCB1 in colon and kidney cancer cells were investigated. Both Pitx2A and Pitx2B were found to be present in the nuclear fraction of Colo320DM and MDR A498 kidney carcinoma cells. Analysis of human kidney and colon cancer tissue arrays by co‐immunostaining suggests a causal relationship between nuclear Pitx2 and ABCB1 expression. Conclusion Pitx2 is a transcriptional regulator of ABCB1 in cancers of the colon and kidney suggesting a contributory role to the MDR phenotype. Support or Funding Information Funded by an Internal Research Grant (UW/H) and ZBAF
The lasing properties of an oval-shaped resonant cavity (ORC) with a continuously variable aspect ratio have been studied. The ORC was formed with a dye-doped pendant drop placed inside a variable static electric field. When the drop ORC was pumped by a nitrogen laser, lasing from the ORC was found to have strong directional emission characteristics and an intensity enhancement factor as great as 19.5. Calculated results of light rays escaping from ORC's by refraction are in good agreement with the experimental data.
Ferroportin 1 (FPN1) is an iron export protein expressed in liver and duodenum, as well as in reticuloendothelial macrophages. Previously, we have shown that divalent metal transporter 1 (DMT1) is expressed in late endosomes and lysosomes of the kidney proximal tubule (PT), the nephron segment responsible for the majority of solute reabsorption. We suggested that following receptor mediated endocytosis of transferrin filtered by the glomerulus, DMT1 exports iron liberated from transferrin into the cytosol. FPN1 is also expressed in the kidney yet its role remains obscure. As a first step towards determining the role of renal FPN1, we localized FPN1 in the PT. FPN1 was found to be located in association with the basolateral PT membrane and within the cytosolic compartment. FPN1 was not expressed on the apical brush-border membrane of PT cells. These data support a role for FPN1 in vectorial export of iron out of PT cells. Furthermore, under conditions of iron loading of cultured PT cells, FPN1 was trafficked to the plasma membrane suggesting a coordinated cellular response to export excess iron and limit cellular iron concentrations.
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