152 research outputs found
The Grizzly, September 26, 1980
Equipment Stolen From New Ritter Center β’ Conversion Eases Skyrocketing Utility Costs β’ Dean\u27s Office Discloses Frat GPAs β’ New Windows for NMD β’ New Spanish Lecturers Interviewed β’ IF, USGA to Sponsor Fall Picnic β’ Anderson Addresses College Crowd At Phila. Rally β’ College Invaded By World Of Technology β’ Draft Registration Closely Examined β’ Campus Grounds Receive Face Lift β’ Hamilton Presents Astronomy Discoveries β’ Try-outs for Trial by Jury β’ Weekends at Ursinus β’ Harriers Place 2nd At Lafayette Invitational β’ Grizzly Football Handled By W. Maryland β’ Sports Profile: Craig Walck β’ Field Hockey Finishes Week Undefeated β’ Strong Hitting By Bear V-Ball Outdoes Moravian β’ Offense Sputters As Bears Lose β’ Kreiger Powers Heathenshttps://digitalcommons.ursinus.edu/grizzlynews/1041/thumbnail.jp
The CLV3 Homolog in Setaria viridis Selectively Controls Inflorescence Meristem Size.
The CLAVATA pathway controls meristem size during inflorescence development in both eudicots and grasses, and is initiated by peptide ligands encoded by CLV3/ESR-related (CLE) genes. While CLV3 controls all shoot meristems in Arabidopsis, evidence from cereal grasses indicates that different meristem types are regulated by different CLE peptides. The rice peptide FON2 primarily controls the size of the floral meristem, whereas the orthologous peptides CLE7 and CLE14 in maize have their most dramatic effects on inflorescence and branch meristems, hinting at diversification among CLE responses in the grasses. Setaria viridis is more closely related to maize than to rice, so can be used to test whether the maize CLE network can be generalized to all members of subfamily Panicoideae. We used CRISPR-Cas9 in S. viridis to knock out the SvFON2 gene, the closest homolog to CLV3 and FON2. Svfon2 mutants developed larger inflorescence meristems, as in maize, but had normal floral meristems, unlike Osfon2, suggesting a panicoid-specific CLE network. Vegetative traits such as plant height, tiller number and leaf number were not significantly different between mutant and wild type plants, but time to heading was shorter in the mutants. In situ hybridization showed strong expression of Svfon2 in the inflorescence and branch meristems, consistent with the mutant phenotype. Using bioinformatic analysis, we predicted the co-expression network of SvFON2 and its signaling components, which included genes known to control inflorescence architecture in maize as well as genes of unknown function. The similarity between SvFON2 function in Setaria and maize suggests that its developmental specialization in inflorescence meristem control may be shared among panicoid grasses
Dual theory of the superfluid-Bose glass transition in disordered Bose-Hubbard model in one and two dimensions
I study the zero temperature phase transition between superfluid and
insulating ground states of the Bose-Hubbard model in a random chemical
potential and at large integer average number of particles per site. Duality
transformation maps the pure Bose-Hubbard model onto the sine-Gordon theory in
one dimension (1D), and onto the three dimensional Higgs electrodynamics in two
dimensions (2D). In 1D the random chemical potential in dual theory couples to
the space derivative of the dual field, and appears as a random magnetic field
along the imaginary time direction in 2D. I show that the transition from the
superfluid state in both 1D and 2D is always controlled by the random critical
point. This arises due to a coupling constant in the dual theory with replicas
which becomes generated at large distances by the random chemical potential,
and represents a relevant perturbation at the pure superfluid-Mott insulator
fixed point. At large distances the dual theory in 1D becomes equivalent to the
Haldane's macroscopic representation of disordered quantum fluid, where the
generated term is identified with random backscattering. In 2D the generated
coupling corresponds to the random mass of the complex field which represents
vortex loops. I calculate the critical exponents at the superfluid-Bose glass
fixed point in 2D to be \nu=1.38 and z=1.93, and the universal conductivity at
the transition \sigma_c = 0.26 e_{*}^2 /h, using the one-loop field-theoretic
renormalization group in fixed dimension.Comment: 25 pages, 6 Postscript figures, LaTex, references updated, typos
corrected, final version to appear in Phys. Rev. B, June 1, 199
Scaling critical behavior of superconductors at zero magnetic field
We consider the scaling behavior in the critical domain of superconductors at
zero external magnetic field. The first part of the paper is concerned with the
Ginzburg-Landau model in the zero magnetic field Meissner phase. We discuss the
scaling behavior of the superfluid density and we give an alternative proof of
Josephson's relation for a charged superfluid. This proof is obtained as a
consequence of an exact renormalization group equation for the photon mass. We
obtain Josephson's relation directly in the form , that
is, we do not need to assume that the hyperscaling relation holds. Next, we
give an interpretation of a recent experiment performed in thin films of
. We argue that the measured mean field like
behavior of the penetration depth exponent is possibly associated with a
non-trivial critical behavior and we predict the exponents and
for the correlation lenght and specific heat, respectively. In the
second part of the paper we discuss the scaling behavior in the continuum dual
Ginzburg-Landau model. After reviewing lattice duality in the Ginzburg-Landau
model, we discuss the continuum dual version by considering a family of
scalings characterized by a parameter introduced such that
, where is the bare mass of the magnetic
induction field. We discuss the difficulties in identifying the renormalized
magnetic induction mass with the photon mass. We show that the only way to have
a critical regime with is having , that
is, with having the scaling behavior of the renormalized photon mass.Comment: RevTex, 15 pages, no figures; the subsection III-C has been removed
due to a mistak
Volume 02
Introduction from Dean Dr. Charles Ross
Mike\u27s Nite: New Jazz for an Old Instrument by Joseph A. Mann
Investigation of the use of Cucumis Sativus for Remediation Of Chromium from Contaminated Environmental Matrices: An Interdisciplinary Instrumental Analysis Project by Kathryn J. Greenly, Scott E. Jenkins, and Andrew E. Puckette
Development of GC-MS and Chemometric Methods for the Analysis of Accelerants in Arson Cases by Scott Jenkins
Building and Measuring Scalable Computing Systems by Daniel M. Honey and Jeffery P. Ravenhorst
Nomini Hall: A Case Study in the Use of Archival Resources as Guides for Excavation at An Archaeological Site by Jamie Elizabeth Mesrobian
Two Stories: In Ohio and How to Stay Out of the Brazilian Army by Thomas Scott
Forgerson des Hommes/Stealing the Steel in Zola\u27s Men by Jay Crowell
Paul Gauguin\u27s Escape into Primitivism by Sarah Spangenberg
Lee Krasner, Abstract Expressionist by Amy S. Eason
Artist Book βParisβ by Kenny Wolfe
Artist Book βSequence of Every Dayβ by Liz Hale
Artist Book βApple Treeβ by Rachel Bouchard
Artist Book βNot so Pretty in Pinkβ by Will Semonco
Artist Book βLook into the Moonβ by Carley York
Artist Books βExtraβ and βGreenβ by Ryan Higgenbothom
Artist Book βRe-growing Appalachiaβ by Adrienne Heinbaugh
Artist Books βCheeziestβ, βUh-ohβ and βThe Girl with the Glassesβ by Melissa Dorton
βSelf-Reflectionβ by Madeline Hunter
Artist Book βThe Princess and the Frogβ by June Ashmore
βHunterβs Nicheβ and βThe Wildβ by Clark Barkley
βTo Thine Own Self be Trueβ by Jay Haley
βNot Funnyβ Ten-Minute Play Festiva
Lovastatin Inhibits VEGFR and AKT Activation: Synergistic Cytotoxicity in Combination with VEGFR Inhibitors
BACKGROUND: In a recent study, we demonstrated the ability of lovastatin, a potent inhibitor of mevalonate synthesis, to inhibit the function of the epidermal growth factor receptor (EGFR). Lovastatin attenuated ligand-induced receptor activation and downstream signaling through the PI3K/AKT pathway. Combining lovastatin with gefitinib, a potent EGFR inhibitor, induced synergistic cytotoxicity in a variety of tumor derived cell lines. The vascular endothelial growth factor receptor (VEGFR) and EGFR share similar activation, internalization and downstream signaling characteristics. METHODOLOGY/PRINCIPAL FINDINGS: The VEGFRs, particularly VEGFR-2 (KDR, Flt-1), play important roles in regulating tumor angiogenesis by promoting endothelial cell proliferation, survival and migration. Certain tumors, such as malignant mesothelioma (MM), also express both the VEGF ligand and VEGFRs that act in an autocrine loop to directly stimulate tumor cell growth and survival. In this study, we have shown that lovastatin inhibits ligand-induced VEGFR-2 activation through inhibition of receptor internalization and also inhibits VEGF activation of AKT in human umbilical vein endothelial cells (HUVEC) and H28 MM cells employing immunofluorescence and Western blotting. Combinations of lovastatin and a VEGFR-2 inhibitor showed more robust AKT inhibition than either agent alone in the H28 MM cell line. Furthermore, combining 5 Β΅M lovastatin treatment, a therapeutically relevant dose, with two different VEGFR-2 inhibitors in HUVEC and the H28 and H2052 mesothelioma derived cell lines demonstrated synergistic cytotoxicity as demonstrated by MTT cell viability and flow cytometric analyses. CONCLUSIONS/SIGNIFICANCE: These results highlight a novel mechanism by which lovastatin can regulate VEGFR-2 function and a potential therapeutic approach for MM through combining statins with VEGFR-2 inhibitors
A novel inhibitor of the PI3K/Akt pathway based on the structure of inositol 1,3,4,5,6-pentakisphosphate
Background: Owing to its role in cancer, the phosphoinositide 3-kinase (PI3K)/Akt pathway is an attractive target for therapeutic intervention. We previously reported that the inhibition of Akt by inositol 1,3,4,5,6- pentakisphosphate (InsP5) results in anti-tumour properties. To further develop this compound we modified its structure to obtain more potent inhibitors of the PI3K/Akt pathway.Methods: Cell proliferation/survival was determined by cell counting, sulphorhodamine or acridine orange/ethidium bromide assay; Akt activation was determined by western blot analysis. In vivo effect of compounds was tested on PC3 xenografts, whereas in vitro activity on kinases was determined by SelectScreen Kinase Profiling Service.Results: The derivative 2-O-benzyl-myo-inositol 1,3,4,5,6-pentakisphosphate (2-O-Bn-InsP5) is active towards cancer types resistant to InsP5 in vitro and in vivo. 2-O-Bn-InsP5 possesses higher pro-apoptotic activity than InsP 5 in sensitive cells and enhances the effect of anti-cancer compounds. 2-O-Bn-InsP5 specifically inhibits 3-phosphoinositide- dependent protein kinase 1 (PDK1) in vitro (IC 50 in the low nanomolar range) and the PDK1-dependent phosphorylation of Akt in cell lines and excised tumours. It is interesting to note that 2-O-Bn-InsP5 also inhibits the mammalian target of rapamycin (mTOR) in vitro.Conclusions: InsP5 and 2-O-Bn-InsP5 may represent lead compounds to develop novel inhibitors of the PI3K/Akt pathway (including potential dual PDK1/mTOR inhibitors) and novel potential anti-cancer drugs
Potential of Resveratrol Analogues as Antagonists of Osteoclasts and Promoters of Osteoblasts
The plant phytoalexin resveratrol was previously demonstrated to inhibit the differentiation and bone resorbing activity of osteoclasts, to promote the formation of osteoblasts from mesenchymal precursors in cultures, and inhibit myeloma cell proliferation, when used at high concentrations. In the current study, we screened five structurally modified resveratrol analogues for their ability to modify the differentiation of osteoclasts and osteoblasts and proliferation of myeloma cells. Compared to resveratrol, analogues showed an up to 5,000-fold increased potency to inhibit osteoclast differentiation. To a lesser extent, resveratrol analogues also promoted osteoblast maturation. However, they did not antagonize the proliferation of myeloma cells. The potency of the best-performing candidate in vitro was tested in vivo in an ovariectomy-induced model of osteoporosis, but an effect on bone loss could not be detected. Based on their powerful antiresorptive activity in vitro, resveratrol analogues might be attractive modulators of bone remodeling. However, further studies are required to establish their efficacy in vivo
What Is New for an Old Molecule? Systematic Review and Recommendations on the Use of Resveratrol
Stilbenes are naturally occurring phytoalexins that generally exist as their more stable E isomers. The most well known natural stilbene is resveratrol (Res), firstly isolated in 1939 from roots of Veratrum grandiflorum (white hellebore) (1) and since then found in various edible plants, notably in Vitis vinifera L. (Vitaceae) (2). The therapeutic potential of Res covers a wide range of diseases, and multiple beneficial effects on human health such as antioxidant, anti-inflammatory and anti-cancer activities have been suggested based on several in vitro and animal studies (3). In particular, Res has been reported to be an inhibitor of carcinogenesis at multiple stages via its ability to inhibit cyclooxygenase, and is an anticancer agent with a role in antiangiogenesis (4). Moreover, both in vitro and in vivo studies showed that Res induces cell cycle arrest and apoptosis in tumor cells (4). However, clinical studies in humans evidenced that Res is rapidly absorbed after oral intake, and that the low level observed in the blood stream is caused by a fast conversion into metabolites that are readily excreted from the body (5). Thus, considerable efforts have gone in the design and synthesis of Res analogues with enhanced metabolic stability. Considering that reduced Res (dihydro- resveratrol, D-Res) conjugates may account for as much as 50% of an oral Res dose (5), and that D-Res has a strong proliferative effect on hormone-sensitive cancer cell lines such as breast cancer cell line MCF7 (6), we recently devoted our synthetic efforts to the preparation of trans-restricted analogues of Res in which the E carbon-carbon double bond is embedded into an imidazole nucleus. To keep the trans geometry, the two aryl rings were linked to the heteroaromatic core in a 1,3 fashion. Based on this design, we successfully prepared a variety of 1,4-, 2,4- and 2,5-diaryl substituted imidazoles including Res analogues 1, 2 and 3, respectively, by procedures that involve transition metal-catalyzed Suzuki-Miyaura cross-coupling reactions and highly selective N-H or C-H direct arylation reactions as key synthetic steps.
The anticancer activity of compounds 1β3 was evaluated against the 60 human cancer cell lines panel of the National Cancer Institute (NCI, USA). The obtained results, that will be showed and discussed along with the protocols developed for the preparation of imidazoles 1β3, confirmed that a structural optimization of Res may provide analogues with improved potency in inhibiting the growth of human cancer cell lines in vitro when compared to their natural lead.
(1) Takaoka,M.J.Chem.Soc.Jpn.1939,60,1090-1100.
(2) Langcake, P.; Pryce, R. J. Physiological. Plant Patology 1976, 9, 77-86.
(3) Vang, O.; et al. PLoS ONE 2011, 6, e19881. doi:10.1371/journal.pone.0019881
(4) Kraft, T. E.; et al. Critical Reviews in Food Science and Nutrition 2009, 49, 782-799.
(5) Walle, T. Ann. N.Y. Acad. Sci. 2011, 1215, 9-15. doi: 10.1111/j.1749-6632.2010.05842.x
(6) Gakh,A.A.;etal.Bioorg.Med.Chem.Lett.2010,20,6149-6151
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