Delaunay Ends of Constant Mean Curvature Surfaces

The generalized Weierstrass representation is used to analyze the asymptotic behavior of a constant mean curvature surface that arises locally from an ordinary differential equation with a regular singularity. We prove that a holomorphic perturbation of an ODE that represents a Delaunay surface generates a constant mean curvature surface which has a properly immersed end that is asymptotically Delaunay. Furthermore, that end is embedded if the Delaunay surface is unduloidal

Unitarization of monodromy representations and constant mean curvature trinoids in 3-dimensional space forms

We present a theorem on the unitarizability of loop group valued monodromy representations and apply this to show the existence of new families of constant mean curvature surfaces homeomorphic to a thrice-punctured sphere in the simply-connected 3-dimensional space forms $\R^3$, \bbS^3 and \bbH^3. Additionally, we compute the extended frame for any associated family of Delaunay surfaces.Comment: 18 pages, revised versio

Constant mean curvature surfaces of any positive genus

We show the existence of several new families of non-compact constant mean curvature surfaces: (i) singly-punctured surfaces of arbitrary genus $g \geq 1$, (ii) doubly-punctured tori, and (iii) doubly periodic surfaces with Delaunay ends.Comment: 14 pages, 10 figure

The Effects of Additives on the Physical Properties of Electroformed Nickel and on the Stretch of Photoelectroformed Nickel Components

The process of nickel electroforming is becoming increasingly important in the manufacture of MST products, as it has the potential to replicate complex geometries with extremely high fidelity. Electroforming of nickel uses multi-component electrolyte formulations in order to maximise desirable product properties. In addition to nickel sulphamate (the major electrolyte component), formulation additives can also comprise nickel chloride (to increase nickel anode dissolution), sulphamic acid (to control pH), boric acid (to act as a pH buffer), hardening/levelling agents (to increase deposit hardness and lustre) and wetting agents (to aid surface wetting and thus prevent gas bubbles and void formation). This paper investigates the effects of some of these variables on internal stress and stretch as a function of applied current density.Comment: Submitted on behalf of TIMA Editions (http://irevues.inist.fr/tima-editions

Estrogen and Vitamin D Control of Transcription in MCF-7 Cells

Abstract The Extracellular Signal-Regulated Kinase (ERK) is part of a key, signaling pathway that regulates both transcription and translation in many cell types. Increases in intracellular calcium levels results in the CaM Kinase-dependent activation of ERK and cell growth in MCF-7 breast cancer cells. ERK has also been shown to play a role in the regulation of MCF-7 cell proliferation through control of downstream transcription factors including Elk-1. The hormone, Vitamin D has been suggested to play an inhibitory role on cancer cells by blocking ERK activation. Our goal was to evaluate the ability of E2 to activate Elk-1, through a CaM Kinase/ERK dependent pathway, in MCF-7 cells. We also examined Vitamin D’s inhibitory regulation of ERK and Elk-1 activation. Interestingly, E2 stimulation of MCF-7 cells triggered Elk-1 phosphorylation an effect that was blocked by inhibiting either CaM KK or ERK. Similarly, E2 treatment of MCF-7 cells also triggered a significant increase in Elk-1-dependent luciferase activity. siRNA inhibition of CaM KK or ERK blocked E2-stimulated Elk-1 luciferase activity. Additionally, E2 triggered a sustained increase in ERK and Elk-1 phosphorylation, both of which were blocked by Vitamin D treatment. Vitamin D treatment of cells also inhibited Elk-1 luciferase activity downstream of E2 stimulation. In summary, our data suggests that E2 utilizes both CaM KK and ERK to activate Elk-1 transcriptional activity an effect that is blocked by the hormone Vitamin D

TRP Channel Regulation of Estrogen Signaling

Abstract Calcium regulates numerous cell functions including growth and development. Calcium can enter cells through transient receptor potential channels (TRPCs). Previous studies in MCF-7 cells have suggested that the expression of one particular TRPC, TRPC6, correlates with cell transformation and disease progression. Calcium has several cellular targets including the Calcium/Calmodulin-dependent protein kinases (CaM Ks) and ERK. Previous work has shown that estrogen (E2) may utilize CaM Ks and ERK to promote breast cancer cell proliferation, however the possible involvement of TRPCs in this pathway is currently unknown. Our objective was to understand which E2 receptor is used in our system and if TRPCs participate in the control of CaM Kinase activation of ERK in MCF-7 cells. Specifically, we wanted to explore if E2 may utilize TRPCs particularly, TRPC6, upstream of the ERK pathway in MCF-7 cells. E2 stimulation of MCF-7 cells and the estrogen receptor alpha (α) inhibitor, MPP, completely blocked ERK activity. In contrast, MPP did not block EGF stimulation of ERK. MCF-7 cells express endogenous TRPC6 protein and TRPC inhibitors, APB and SK&F, both blocked ERK activation downstream of E2. In addition, neither APB or SK&F inhibited EGF activation of ERK. Results from these studies suggest that E2 is capable of activating ERK through the specifically through the alpha form of the estrogen receptor and TRPCs

Transcription Factor Regulation of ERK and Estrogen in MCF-7 Cells

Abstract ERK is activated by increased intracellular calcium downstream of the hormone estrogen (E2). E2 activates ERK via the CaM Kinases, specifically CaM KK and CaM KI in MCF-7 cells. ERK may control cell growth and proliferation through Elk-1, Rsk, SRF, CREB, and numerous other molecules and nuclear targets. Vitamin D, a hormone, has proven to be an effective antagonist of ERK and MCF-7 breast cancer cell growth. Our goal was to evaluate if the E2 pathway working through CaM KK and ERK regulated the transcription factors Elk-1, CREB, and SRF. We also examined the ability of vitamin D to antagonize ERK activation of its downstream targets. Interestingly, E2 stimulation of MCF-7 cells activated both ERK and Elk-1 an effect that was blocked by inhibiting both CaM KK and ERK. E2 treatment of MCF-7 cells also triggered a significant increase in SRF and CREB phosphorlation in a CaM KK- and ERK-dependent manner. Dimerization of transcription factors may enhance DNA binding and gene expression. E2 stimulation of MCF-7 cells promoted the formation of a molecular complex between endogenous Elk-1 and SRF. Finally, E2 triggered a prolonged increased in ERK and Elk-1 phosphorylation, both of which were blocked by vitamin D treatment. Taken together our data demonstrates several transcriptional targets for E2 working through CaM KK and their inhibition by vitamin D signaling

The Ca II infrared triplet's performance as an activity indicator compared to Ca II H and K

Aims. A large number of Calcium Infrared Triplet (IRT) spectra are expected from the GAIA- and CARMENES missions. Conversion of these spectra into known activity indicators will allow analysis of their temporal evolution to a better degree. We set out to find such a conversion formula and to determine its robustness. Methods. We have compared 2274 Ca II IRT spectra of active main-sequence F to K stars taken by the TIGRE telescope with those of inactive stars of the same spectral type. After normalizing and applying rotational broadening, we subtracted the comparison spectra to find the chromospheric excess flux caused by activity. We obtained the total excess flux, and compared it to established activity indices derived from the Ca II H & K lines, the spectra of which were obtained simultaneously to the infrared spectra. Results. The excess flux in the Ca II IRT is found to correlate well with $R_\mathrm{HK}'$ and $R_\mathrm{HK}^{+}$, as well as $S_\mathrm{MWO}$, if the $B-V$-dependency is taken into account. We find an empirical conversion formula to calculate the corresponding value of one activity indicator from the measurement of another, by comparing groups of datapoints of stars with similar B-V.Comment: 16 pages, 15 figures. Accepted for publication in Astronomy & Astrophysic

Non-Fermi liquid signatures in the Hubbard Model due to van Hove singularities

When a van-Hove singularity is located in the vicinity of the Fermi level, the electronic scattering rate acquires a non-analytic contribution. This invalidates basic assumptions of Fermi liquid theory and within perturbative treatments leads to a non-Fermi liquid self-energy and transport properties.Such anomalies are shown to also occur in the strongly correlated metallic state. We consider the Hubbard model on a two-dimensional square lattice with nearest and next-nearest neighbor hopping within the single-site dynamical mean-field theory. At temperatures on the order of the low-energy scale $T_0$ an unusual maximum emerges in the imaginary part of the self-energy which is renormalized towards the Fermi level for finite doping. At zero temperature this double-well structure is suppressed, but an anomalous energy dependence of the self-energy remains. For the frustrated Hubbard model on the square lattice with next-nearest neighbor hopping, the presence of the van Hove singularity changes the asymptotic low temperature behavior of the resistivity from a Fermi liquid to non-Fermi liquid dependency as function of doping. The results of this work are discussed regarding their relevance for high-temperature cuprate superconductors.Comment: revised version, accepted in Phys.Rev.