111 research outputs found
Molecular, spectroscopic, and magnetic properties of cobalt(II) complexes with heteroaromatic N(O)-donor ligands
New [Co(SCN)2(L)4/2] complexes, where
L = b-pic (1), pyCH2OH (2), py(CH2)3OH (3), 1,2,4-
triazolo[1,5-a]pyrimidine (4), [CoCl2(urotrop)2] (5), and
[Co(DMIM)3]Cl2 H2O (6) where urotrop = hexamethylenetetramine
and DMIM = 2,20-bis(4,5-dimethylimidazolyl)
were synthesized in simple reactions of CoCl2 6H2O
with ammonia thiocyanate and pyridine type ligands or
urotropine and diimidazolyl ligands with cobalt(II) chloride
in methanol solutions. The orthorhombic crystallization
for (1), (2), and (4), the monoclinic one for (3) and (5)
as well as the hexagonal one for (6) were found. The plots
of the overlap population density-of-states indicated nonbonding
character of the interactions between pyridine
derivatives ligands and cobalt(II) ions in the complexes
(1)–(4). The electronic spectra showed almost perfect
octahedral complex in the case of (6). The magnetic susceptibility
measurements revealed paramagnetic behavior
with low values of the Curie–Weiss temperature, positive
for complex (5) and negative for the other ones, although
the transition to collective magnetic state at low temperatures
for (4) and (5) was evidenced by an observation of
antiferromagnetic coupling with Ne´el temperature of 4.5 K
and the ferromagnetic one with Curie temperature of 10 K,
respectively
Applicability of a Representation for the Martin's Real-Part Formula in Model-Independent Analyses
Using a novel representation for the Martin's real-part formula without the
full scaling property, an almost model-independent description of the
proton-proton differential cross section data at high energies (19.4 GeV - 62.5
GeV) is obtained. In the impact parameter and eikonal frameworks, the extracted
inelastic overlap function presents a peripheral effect (tail) above 2 fm and
the extracted opacity function is characterized by a zero (change of sign) in
the momentum transfer space, confirming results from previous model-independent
analyses. Analytical parametrization for these empirical results are introduced
and discussed. The importance of investigations on the inverse problems in
high-energy elastic hadron scattering is stressed and the relevance of the
proposed representation is commented. A short critical review on the use of
Martin's formula is also presented.Comment: Two comments and one reference added at the end of Subsec. 3.3; 23
pages, 9 figures; to be published in Int. J. Mod. Phys.
Computational aeroelastic analysis of a hovering W3 Sokol blade with gurney flap
This paper demonstrates the potential effect of a gurney flap on the performance of the W3-Sokol rotor blade in hover. A rigid blade was first considered and the calculations were conducted at several thrust settings. The gurney flap was extended from 46%R to 66%R and it was located at the trailing edge of the main rotor blade. Four different sizes of gurney flaps were studied, 2%, 1%, 0.5% and 0.3% of the chord. The biggest flap proved to be the most effective. A second study considered elastic blades with and without the gurney flap. The results were trimmed at the same thrust values as the rigid blade and indicate an increase of aerodynamic performance when the gurney flap is used, especially for high thrust cases
One-dimensional quasi-relativistic particle in the box
Two-term Weyl-type asymptotic law for the eigenvalues of one-dimensional
quasi-relativistic Hamiltonian (-h^2 c^2 d^2/dx^2 + m^2 c^4)^(1/2) + V_well(x)
(the Klein-Gordon square-root operator with electrostatic potential) with the
infinite square well potential V_well(x) is given: the n-th eigenvalue is equal
to (n pi/2 - pi/8) h c/a + O(1/n), where 2a is the width of the potential well.
Simplicity of eigenvalues is proved. Some L^2 and L^infinity properties of
eigenfunctions are also studied. Eigenvalues represent energies of a `massive
particle in the box' quasi-relativistic model.Comment: 40 pages, 4 figures; minor correction
Ruthenium(II) 8-quinolinolates: Synthesis, characterization, crystal structure and catalysis in the synthesis of 2-oxazolines
New octahedral ruthenium(II) complexes (1e4) have been synthesized from the reaction of ruthenium(II) precursors [RuHCl(CO)(EPh3)3] (E ¼ P or As) with the bidentate Schiff base ligands, 2-((2,6-dimethylphenylimino)methyl)quinolin-8-ol (L1) and 2-((2,6-diisopropylphenylimino)methyl)quinolin-8-ol (L2) in ethanol. These complexes have been characterized by elemental analyses, IR, UVeVis, 1H, 13C and 31P NMR and ESI-Mass spectroscopy. The molecular structure of the complex [RuCl(CO)(PPh3)2(L2)] (2) was determined by single-crystal X-ray diffraction, which reveals a distorted octahedral geometry around ruthenium(II) ion. The catalytic activity of the new complexes was evaluated for the condensation of nitriles with ethanolamine under solvent free conditions. The processes were operative with aromatic and heteroaromatic nitriles and tolerated several substitutional groups. The studies on the effect of substitution over ligands, coligands, reaction time, temperature and catalyst loading were carried out in order to find the best catalyst in this series of complexes and favorable reaction conditions. A probable mechanism for the catalytic condensation of nitrile has also been proposed. The catalyst was recovered and recycled up to five times without significant loss of its activity
Molecular, spectroscopic, and magnetic properties of cobalt(II) complexes with heteroaromatic N(O)-donor ligands
New [Co(SCN)2(L)4/2] complexes, where
L = b-pic (1), pyCH2OH (2), py(CH2)3OH (3), 1,2,4-
triazolo[1,5-a]pyrimidine (4), [CoCl2(urotrop)2] (5), and
[Co(DMIM)3]Cl2 H2O (6) where urotrop = hexamethylenetetramine
and DMIM = 2,20-bis(4,5-dimethylimidazolyl)
were synthesized in simple reactions of CoCl2 6H2O
with ammonia thiocyanate and pyridine type ligands or
urotropine and diimidazolyl ligands with cobalt(II) chloride
in methanol solutions. The orthorhombic crystallization
for (1), (2), and (4), the monoclinic one for (3) and (5)
as well as the hexagonal one for (6) were found. The plots
of the overlap population density-of-states indicated nonbonding
character of the interactions between pyridine
derivatives ligands and cobalt(II) ions in the complexes
(1)–(4). The electronic spectra showed almost perfect
octahedral complex in the case of (6). The magnetic susceptibility
measurements revealed paramagnetic behavior
with low values of the Curie–Weiss temperature, positive
for complex (5) and negative for the other ones, although
the transition to collective magnetic state at low temperatures
for (4) and (5) was evidenced by an observation of
antiferromagnetic coupling with Ne´el temperature of 4.5 K
and the ferromagnetic one with Curie temperature of 10 K,
respectively
Fibronectin rescues estrogen receptor α from lysosomal degradation in breast cancer cells
Estrogen receptor α (ERα) is expressed in tissues as diverse as brains and mammary glands. In breast cancer, ERα is a key regulator of tumor progression. Therefore, understanding what activates ERα is critical for cancer treatment in particular and cell biology in general. Using biochemical approaches and superresolution microscopy, we show that estrogen drives membrane ERα into endosomes in breast cancer cells and that its fate is determined by the presence of fibronectin (FN) in the extracellular matrix; it is trafficked to lysosomes in the absence of FN and avoids the lysosomal compartment in its presence. In this context, FN prolongs ERα half-life and strengthens its transcriptional activity. We show that ERα is associated with β1-integrin at the membrane, and this integrin follows the same endocytosis and subcellular trafficking pathway triggered by estrogen. Moreover, ERα+ vesicles are present within human breast tissues, and colocalization with β1-integrin is detected primarily in tumors. Our work unravels a key, clinically relevant mechanism of microenvironmental regulation of ERα signaling.Fil: Sampayo, Rocío Guadalupe. Universidad Nacional de San Martin. Instituto de Nanosistemas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Toscani, Andrés Martin. Universidad Nacional de Luján; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; ArgentinaFil: Rubashkin, Matthew G.. University of California; Estados UnidosFil: Thi, Kate. Lawrence Berkeley National Laboratory; Estados UnidosFil: Masullo, Luciano Andrés. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; ArgentinaFil: Violi, Ianina Lucila. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Parque Centenario. Centro de Investigaciones en Bionanociencias "Elizabeth Jares Erijman"; ArgentinaFil: Lakins, Jonathon N.. University of California; Estados UnidosFil: Caceres, Alfredo Oscar. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra. Universidad Nacional de Córdoba. Instituto de Investigación Médica Mercedes y Martín Ferreyra; ArgentinaFil: Hines, William C.. Lawrence Berkeley National Laboratory; Estados UnidosFil: Coluccio Leskow, Federico. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Química Biológica de la Facultad de Ciencias Exactas y Naturales; Argentina. Universidad Nacional de Luján; ArgentinaFil: Stefani, Fernando Daniel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Ciudad Universitaria. Instituto de Física de Buenos Aires. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales. Instituto de Física de Buenos Aires; ArgentinaFil: Chialvo, Dante Renato. Universidad de Buenos Aires; Argentina. Universidad Nacional de San Martín. Escuela de Ciencia y Tecnología. Centro Internacional de Estudios Avanzados; ArgentinaFil: Bissell, Mina J.. Lawrence Berkeley National Laboratory; Estados UnidosFil: Weaver, Valerie M.. University of California; Estados UnidosFil: Simian, Marina. Universidad Nacional de San Martin. Instituto de Nanosistemas; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Oncología "Ángel H. Roffo"; Argentin
Genetički polimorfizmi u dijabetesu: Utjecaj na terapiju oralnim antidijabeticima
Due to new genetic insights, etiologic classification of diabetes is under constant scrutiny. Hundreds, or even thousands, of genes are linked with type 2 diabetes. Three common variants (Lys23 of KCNJ11, Pro12 of PPARG, and the T allele at rs7903146 of TCF7L2) have been shown to be predisposed to type 2 diabetes mellitus across many large studies. Individually, each of these polymorphisms is only moderately predisposed to type 2 diabetes. On the other hand, monogenic forms of diabetes such as MODY and neonatal diabetes are characterized by unique clinical features and the possibility of applying a tailored treatment.
Genetic polymorphisms in drug-metabolizing enzymes, transporters, receptors, and other drug targets have been linked to interindividual differences in the efficacy and toxicity of a number of medications. Mutations in genes important in drug absorption, distribution, metabolism and excretion (ADME) play a critical role in pharmacogenetics of diabetes.
There are currently five major classes of oral pharmacological agents available to treat type 2 diabetes: sulfonylureas, meglitinides, metformin (a biguanide), thiazolidinediones, and α-glucosidase inhibitors. Other classes are also mentioned in literature.
In this work, different types of genetic mutations (mutations of the gene for glucokinase, HNF 1, HNF1ß and Kir6.2 and SUR1 subunit of KATP channel, PPAR-γ, OCT1 and OCT2, cytochromes, direct drug-receptor (KCNJ11), as well as the factors that influence the development of the disease (TCF7L2) and variants of genes that lead to hepatosteatosis caused by thiazolidinediones) and their influence on the response to therapy with oral antidiabetics will be reviewed.Dijabetes tipa 2 dosegao je proporcije epidemije u SAD (> 18 milijuna) i cijelom svijetu (170 milijuna oboljelih osoba) te ima tendenciju daljnjeg dramatičnog rasta. Stoga se u posljednje vrijeme ulažu napori da se otkriju i razviju novi farmakološki agensi za liječenje ove bolesti. Klasifikacija šećerne bolesti proširena je uspjesima istraživača na području genetike. Da bismo razumjeli farmakogenetiku antidijabetika neophodno je razumjeti genetiku samog dijabetesa. Kao što će biti prikazano u ovom radu veliki broj gena koji su povezani s razvojem dijabetesa takođe utječu i na odgovor na terapiju antidijabeticima. S druge strane, mutacije gena koji utječu na ADME (apsorpcija, distribucija, metabolizam i ekskrecija) lijeka imaju značajan utjecaj na farmakogenetiku oralnih antidijabetika.
Utvrđeno je da je dijabetes genetički heterogena bolest. Uobičajeni oblici dijabetesa su gotovo uvijek poligenski i za razvoj same bolesti vrlo su značajne snažne interakcije među različitim genima kao i između gena i okoliša. Zbog toga mutacije ili polimorfizmi koji u manjoj mjeri utječu na funkciju gena mogu postati klinički značajni samo u slučaju kada se kombiniraju s drugim faktorima odnosno genima. Smatra se da u razvoju dijabetesa mogu sudjelovati stotine pa čak i tisuće gena. Do 2006. identificirano je nekoliko uobičajenih alela koji povećavaju rizik za razvoj dijabetesa, od kojih su najznačajniji PPARG (Pro12), KCNJ11 (Lys23) i TCF7L2 (T na rs7903146). Do danas je najveći uspjeh postignut u identifikaciji gena odgovornih za razmjerno rijetke oblike ove bolesti poput ”Maturity-onset diabetes of the young” (MODY) i neonatalnog dijabetesa. Monogenske oblike dijabetesa odlikuju jedinstvene kliničke karakteristike i mogućnost primjene individualnog tretmana. Genetički polimorfizmi enzima koji utječu na metabolizam lijekova, transportera, receptora i drugih ciljeva djelovanja lijekova povezani su s interindividualnim razlikama u efikasnosti i toksičnosti mnogih lijekova. Vrlo je važno da se na temelju farmakogenetičkih istraživanja mogu predvidjeti neki neželjeni efekti lijekova.
Trenutačno postoji pet glavnih klasa oralnih antidijabetika: sulfoniluree, meglitinidi, metformin (bigvanid), tiazolidindioni i inhibitori α-glukozidaze. U literaturi se također spominju inhibitori dipeptidil peptidaze IV (DPP-IV), selektivni antagonisti kanabinoidnog receptora 1 (CB-1), glukagonu slični peptid 1 mimetici i amilin mimetici.
Razumijevanje mehanizama koji rezultiraju disfunkcijom β stanica na fiziološkom i molekularnom nivou neophodno je za napredak u razumijevanju tretmana dijabetesa. U ovom radu dat je pregled različitih genetičkih mutacija (mutacije gena za glukokinazu, HNF 1, HNF1ß, Kir6.2 i SUR 1 podjedinicu KATP kanala ß stanica, PPAR-γ, OCT1 i OCT2, citohrome, KCNJ11, faktore koji utječu na razvoj bolesti (TCF7L2) i varijante gena koji dovode do hepatosteatoze uzrokovane tiazolidindionima) te njihov utjecaj na odgovor na terapiju oralnim antidijabeticima
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