bluuebunny/crossref_metadata_2025_split huggingface dataset:
Extraction of Radio‐Labelled Xanthine Derivatives by Artificial Receptors: Deep Insight into the Association Behaviour
Authors: Bomkamp Martin , Siering Carsten , Landrock Karin , Stephan Holger , Fröhlich Roland , Waldvogel Siegfried R. 
Published: February 2007

AbstractAssociation constants for the interaction of almost insoluble substrates with triphenylene ketal‐based receptors in toluene have been determined by means of an extraction method employing the corresponding radio‐labelled substrates. Flexible and more polar receptors tend to aggregate and exhibit inferior extraction qualities. Binding constants in toluene were found to be in the range 105–107 m−1, which is significantly higher than in dichloromethane. X‐ray analyses indicate the direct participation of a water molecule in the binding process, which may account for the surprisingly small effect of moisture in the solvent on the stability of the complexes.
Description of the Ground‐State Covalencies of the Bis(dithiolato) Transition‐Metal Complexes from X‐ray Absorption Spectroscopy and Time‐Dependent Density‐Functional Calculations
Authors: Ray Kallol , DeBeer George Serena , Solomon Edward I. , Wieghardt Karl , Neese Frank 
Published: February 2007

AbstractThe electronic structures of [M(LBu)2]− (LBu=3,5‐di‐tert‐butyl‐1,2‐benzenedithiol; M=Ni, Pd, Pt, Cu, Co, Au) complexes and their electrochemically generated oxidized and reduced forms have been investigated by using sulfur K‐edge as well as metal K‐ and L‐edge X‐ray absorption spectroscopy. The electronic structure content of the sulfur K‐edge spectra was determined through detailed comparison of experimental and theoretically calculated spectra. The calculations were based on a new simplified scheme based on quasi‐relativistic time‐dependent density functional theory (TD‐DFT) and proved to be successful in the interpretation of the experimental data. It is shown that dithiolene ligands act as noninnocent ligands that are readily oxidized to the dithiosemiquinonate(−) forms. The extent of electron transfer strongly depends on the effective nuclear charge of the central metal, which in turn is influenced by its formal oxidation state, its position in the periodic table, and scalar relativistic effects for the heavier metals. Thus, the complexes [M(LBu)2]− (M=Ni, Pd, Pt) and [Au(LBu)2] are best described as delocalized class III mixed‐valence ligand radicals bound to low‐spin d8 central metal ions while [M(LBu)2]− (M=Cu, Au) and [M(LBu)2]2− (M=Ni, Pd, Pt) contain completely reduced dithiolato(2−) ligands. The case of [Co(LBu)2]− remains ambiguous. On the methodological side, the calculation led to the new result that the transition dipole moment integral is noticeably different for S1s→valence‐π versus S1s→valence‐σ transitions, which is explained on the basis of the differences in radial distortion that accompany chemical bond formation. This is of importance in determining experimental covalencies for complexes with highly covalent metal–sulfur bonds from ligand K‐edge absorption spectroscopy.
Further studies on the interaction of loperamide with capacitative calcium entry in Leukemic HL‐60 cells
Authors: Daly John W. , Camerini‐Otero Carol , Shapiro Craig A. , Ma Jingyuan , Ziffer Herman , Vélez Leykza , Harper Jacquie L. 
Published: February 2007

AbstractLoperamide at 3–10 µM has augmentative effects on calcium levels elevated by capacitative calcium entry (CCE) in leukemic HL‐60 cells after release of intracellular calcium by ATP or thapsigargin (Harper et al. [1997] Proc Natl Acad Sci USA 94:14912–14917). The effect of loperamide on calcium levels was absent at a pH value of 6.8, a pH at which CCE is not active in HL‐60 cells. Further investigations of HL‐60 cells in recent years revealed a great reduction in the magnitude of the loperamide response. However, when preceded by a CCE blocker, namely N‐methylnitrendipine (MRS 1844) or N‐propargylnitrendipine (MRS 1845), loperamide caused a significant reversal of the blockade. Six structural analogs of loperamide were synthesized, but only two showed loperamide‐like activity. Drug Dev. Res. 67:842–851, 2006. Published 2007 Wiley‐Liss, Inc.
K201 Improves norepinephrine‐induced diastolic dysfunction with preserved ejection fraction
Authors: Kaneko Noboru , Matsuda Ryuko , Ohtani Naoyuki , Nakajima Takahide , Arikawa Takuo , Suzuki Hidehiko , Toyoda Shigeru , Kikuchi Migaku , Hata Yoshihito , Abe Shichiro , Taguchi Isao , Shimamoto Ken 
Published: February 2007

AbstractHeart failure with preserved ejection fraction differs from systolic heart failure in pathogenesis, underlying disease, and prognosis; however, the onset mechanism of this type of heart failure remains unknown and there is no proven therapy. Recently, we showed that norepinephrine (NE) under Ca2+ loading induces severe diastolic dysfunction without a significant change in the left ventricular ejection fraction (LVEF), that is, increased left ventricular end‐diastolic pressure (LVEDP), norepinephrine‐induced diastolic contracture (NEIDC), and diastolic opening of the aortic valve. In this study, the effects of two benzothiazepine derivatives, K201 (JTV519) and diltiazem, on diastolic dysfunction were examined using this model. K201 significantly suppressed the increase in LVEDP, reduced the incidence of NEIDC, and significantly improved the Ea wave and DCT in a dose‐dependent manner, as well as reducing pulmonary hemorrhage. In contrast, diltiazem did not improve diastolic dysfunction and the mortality in the diltiazem group was 57%, compared to 0% in the K201 group. These results suggest that reduction of intracellular Ca2+ alone does not inhibit diastolic heart failure; in contrast, blocking of α‐adrenoceptors and regulation of proteins such as troponin I via protein kinase C are required for treatment of diastolic heart failure. These results also suggest that K201 may be an agent for treatment of diastolic heart failure. Drug Dev. Res. 67:852–861, 2006. © 2007 Wiley‐Liss, Inc.
Endothelin receptors as drug targets in chronic cardiovascular diseases: the rationale for dual antagonism
Authors: Clozel Martine , Flores Susan 
Published: February 2007

AbstractEndothelin has been described as the most potent vasoconstrictor known. Recent research shows that it is also a growth factor, a promoter of fibrosis and inflammation, and a key initiator of endothelial dysfunction. Endothelin becomes, therefore, a candidate in the pathogenesis of many chronic cardiovascular and fibrotic diseases, and inhibition of endothelin function is a potential therapeutic approach for those diseases. Endothelin receptor antagonists are now established therapy in the treatment of pulmonary arterial hypertension, and present promising perspectives in diabetic nephropathy, peripheral arterial disease, hypertension, heart failure, and pulmonary diseases. Endothelin binds to two endothelin receptors, ETA and ETB, and their respective roles are actively debated. A major challenge lies in the understanding of what is the preferred profile for new drugs: selective ETA antagonism or dual ETA and ETB receptor antagonism. A number of cardiovascular diseases are characterized by an up‐regulation of smooth muscle cell ETB receptors mediating vasoconstriction and proliferation, and a down‐regulation of endothelial ETB receptors, as compared to the physiological state, creating a situation where both ETA and ETB receptors contribute to vasoconstriction and remodeling. When these two receptor subtypes co‐exist, a cross‐talk between them, probably a result of receptor heterodimerization, suggests that dual ETA/ETB receptor antagonism may be necessary to obtain maximal efficacy. Drug Dev. Res. 67:825–834, 2006. © 2007 Wiley‐Liss, Inc.
Sex differences in and hormonal regulation of Kv1 potassium channel gene expression in the electric organ: Molecular control of a social signal
Authors: Few W. Preston , Zakon Harold H. 
Published: February 2007

AbstractElectric fish communicate with electric organ (EO) discharges (EODs) that are sexually dimorphic, hormone‐sensitive, and often individually distinct. The cells of the EO (electrocytes) of the weakly electric fish Sternopygus possess delayed rectifying K+ currents that systematically vary in their activation and deactivation kinetics, and this precise variation in K+ current kinetics helps shape sex and individual differences in the EOD. Because members of the Kv1 subfamily produce delayed rectifier currents, we cloned a number of genes in the Kv1 subfamily from the EO of Sternopygus. Using our sequences and those from genome databases, we found that in teleost fish Kv1.1 and Kv1.2 exist as duplicate pairs (Kv1.1a&b, Kv1.2a&b) whereas Kv1.3 does not. Using real‐time quantitative RT‐PCR, we found that Kv1.1a and Kv1.2a, but not Kv1.2b, expression in the EO is higher in high EOD frequency females (which have fast EO K+ currents) than in low EOD frequency males (which have slow EO K+ currents). Systemic treatment with dihydrotestosterone decreased Kv1.1a and Kv1.2a, but not Kv1.2b, expression in the EO, whereas treatment with human chorionic gonadotropin (hCG) increased Kv1.2a but not Kv1.1a or Kv1.2b expression in the EO. Thus, systematic variation in the ratios of Kv1 channels expressed in the EO is correlated with individual differences in and sexual dimorphism of a communication signal. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007
Activity‐dependent formation and functions of chondroitin sulfate‐rich extracellular matrix of perineuronal nets
Authors: Dityatev Alexander , Brückner Gert , Dityateva Galina , Grosche Jens , Kleene Ralf , Schachner Melitta 
Published: February 2007

AbstractExtracellular matrix molecules—including chondroitin sulfate proteoglycans, hyaluronan, and tenascin‐R—are enriched in perineuronal nets (PNs) associated with subsets of neurons in the brain and spinal cord. In the present study, we show that similar cell type‐dependent extracellular matrix aggregates are formed in dissociated cell cultures prepared from early postnatal mouse hippocampus. Starting from the 5th day in culture, accumulations of lattice‐like extracellular structures labeled with Wisteria floribunda agglutinin were detected at the cell surface of parvalbumin‐expressing interneurons, which developed after 2–3 weeks into conspicuous PNs localized around synaptic contacts at somata and proximal dendrites, as well as around axon initial segments. Physiological recording and intracellular labeling of PN‐expressing neurons revealed that these are large fast‐spiking interneurons with morphological characteristics of basket cells. To study mechanisms of activity‐dependent formation of PNs, we performed pharmacological analysis and found that blockade of action potentials, transmitter release, Ca2+ permeable AMPA subtype of glutamate receptors or L‐type Ca2+ voltage‐gated channels strongly decreased the extracellular accumulation of PN components in cultured neurons. Thus, we suggest that Ca2+ influx via AMPA receptors and L‐type channels is necessary for activity‐dependent formation of PNs. To study functions of chondroitin sulfate‐rich PNs, we treated cultures with chondroitinase ABC that resulted in a prominent reduction of several major PN components. Removal of PNs did not affect the number and distribution of perisomatic GABAergic contacts but increased the excitability of interneurons in cultures, implicating the extracellular matrix of PNs in regulation of interneuronal activity. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007
Differential contribution of extracellular and intracellular calcium sources to basal transmission and long‐term potentiation in the sympathetic ganglion of the rat
Authors: Vargas R. , Cifuentes F. , Morales M.A. 
Published: February 2007

AbstractCalcium involved in basal ganglionic transmission and long‐term potentiation (LTP) can arise either by influx from the extracellular medium or release from intracellular stores. No attempts have yet been made to concurrently explore the contributions of extracellular and intracellular Ca2+ to basal ganglionic transmission or LTP. Here, we investigate this subject using the superior cervical ganglion of the rat. To explore the extracellular Ca2+ contribution, we evaluated basal transmission and LTP at different extracellular Ca2+ concentrations. To assess intracellular Ca2+ release, we explored the contribution of the calcium‐induced calcium release process by overactivation or blockade of ryanodine‐sensitive Ca2+ receptor channel with caffeine, and also by blocking either IP3R with Xestospongin C or the sarco(endo)plasmic reticulum Ca2+‐ATPase pump with thapsigargin. Extracellular Ca2+ affected ganglionic basal transmission and LTP to different extents. While 25% of the physiological Ca2+ concentration supported 80% of basal transmission, 50% of normal Ca2+ was required to achieve 80% of LTP. Notably, disruption of intracellular Ca2+ release by all the drugs tested apparently did not affect basal ganglionic transmission but impaired LTP. We conclude that basal transmission requires only a small level of Ca2+ entry, while LTP expression not only requires more Ca2+ entry but is also dependent on Ca2+ release from intracellular stores. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007
Exposure to neonatal separation stress alters exploratory behavior and corticotropin releasing factor expression in neurons in the amygdala and hippocampus
Authors: Becker Katja , Abraham Andreas , Kindler Jennifer , Helmeke Carina , Braun Katharina 
Published: February 2007

AbstractEvidence is accumulating that early emotional experience interferes with the development of the limbic system, which is involved in perception and regulation of emotional behaviors as well as in learning and memory formation. Limbic brain regions, as well as hypothalamic regions and other, nonlimbic areas contain specific neuron subpopulations, which express and release corticotropin releasing factor (CRF). Since these neurons serve to connect limbic function to endocrine, stress‐related responses, we proposed that stressful experience during early postnatal brain development should interfere with the development of CRF‐containing neurons, particularly in brain regions essential for emotional regulation. Applying neonatal separation stress (daily 1 h separation from the parents and litter mates) as stressor, the number of immunocytochemically identified CRF‐expressing neurons/fibers was quantified in the amygdala, hippocampus, paraventricular nucleus of the hypothalamus, piriform cortex, and the somatosensory cortex of 3‐week‐old stressed and nonstressed Octodon degus, a semi‐precocial rodent. Compared to controls neonatally stressed animals showed significantly lower levels of CRF‐positive fibers (−60%) in the central amygdala, significantly less CRF‐positive neurons in the dentate gyrus (−28%) and the CA1 region (−29%) and significantly lower CRF cell densities in the somatosensory cortex (−26%). On the other hand, we found significantly higher numbers of CRF‐immunoreactive neurons in the basolateral amygdaloid complex (+192%) of stressed animals compared to nonstressed controls. No differences in CRF‐immunoreactive cell densities were detected in the other regions. Additional behavioral analysis revealed significantly elevated exploratory behavior (+34%) in stressed animals compared to controls, which might indicate reduced anxiety in the stressed animals. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007
Regulatory T cells inhibit Fas ligand‐induced innate and adaptive tumour immunity
Authors: Simon Anna Katharina , Jones Emma , Richards Hannah , Wright Kate , Betts Gareth , Godkin Andrew , Screaton Gavin , Gallimore Awen 
Published: February 2007

AbstractCD4+CD25+ regulatory T cells (Treg) are known to influence T cell responses to tumours. Here we have explored the role of Treg in inhibiting not only adaptive, but also innate immune responses to tumours. To this end we used a Fas ligand (FasL)‐expressing melanoma cell line in a mouse model. In this system, innate immunity is sufficient to reject the tumour. All mice depleted of Treg and challenged with FasL‐expressing melanoma remained tumour‐free. Investigation of the underlying cellular effector mechanisms revealed that depletion of Treg enhanced an NK cell response capable of tumour lysis. Furthermore, this initial innate immune response primed mice to make an effective adaptive immune response leading to complete rejection of challenge with the parental melanoma. Both antigen‐specific antibody and CD4+ T cells were implicated in protection via adaptive immunity. We conclude that removal of Treg and vaccination with whole tumour cells expressing FasL activates multiple arms of the immune system, leading to efficient tumour rejection. These findings highlight a novel role for FasL in inducing innate immune responses that are normally inhibited by Treg and uncover an adjuvant effect of FasL that can be used to stimulate tumour immunity after depletion of Treg.
Essential roles of IL‐12 and dendritic cells but not IL‐23 and macrophages in lupus‐like diseases initiated by cell surface HSP gp96
Authors: Dai Jie , Liu Bei , Cua Daniel J. , Li Zihai 
Published: February 2007

AbstractProinflammatory cytokine IL‐23 but not IL‐12 is critical for the pathogenesis of organ‐specific autoimmune diseases including experimental autoimmune encephalitis and collagen‐induced arthritis. The contribution by IL‐23 in systemic autoimmune diseases such as lupus is undefined. We addressed this question in a murine lupus‐like disease model, initiated by enforced cell‐surface expression of an ER HSP gp96 in C57BL/6 background. We found a significant increase of p40 in the sera in these mice that preceded the onset of diseases. However, autoimmunity was abrogated in transgenic mice expressing membrane‐bound gp96 reconstituted with p35–/– BM, but not with p19–/– BM. Moreover, we found that dendritic cells (DC) but not macrophages were the main producers of p40. To dissect the roles of DC further, we depleted DC using a diphtheria toxin‐based inducible DC depletion system. We demonstrated that the integrity of DC was essential for autoimmunity. Our results thus revealed that IL‐12 and DC are critical for the pathogenesis of lupus‐like disease precipitated by cell surface gp96. This study further highlighted the significant biological differences between IL‐12 and IL‐23.
Dinuclear and Polynuclear Bridged Azido–Nickel(II) Complexes: Synthesis, Structure Determination, and Magnetic Properties
Authors: Massoud Salah S. , Mautner Franz A. , Vicente Ramon , Gallo August A. , Ducasse Elodie 
Published: February 2007

AbstractAzido–NiII complexes of dinuclear, [Ni2(trpn)2(μ1,3‐N3)2](ClO4)2 (1), and monodimensional structures cis‐[Ni(abap)(μ1,3‐N3)]n(ClO4)n (2) and cis‐[Ni(Me6trien)(μ1,3‐N3)]n(ClO4)n·nH2O (3a) as well as the monomer [Ni(Me6trien)(N3)]ClO4 (3b) {trpn = tris(3‐aminopropyl)amine; abap = N‐(2‐aminoethyl)‐N,N‐bis(3‐aminopropyl)amine; Me6trien = 1,1,4,7,10,10‐hexamethyltriethylene tetramine} were synthesized and structurally characterized by spectroscopic techniques, X‐ray crystallography, and variable‐temperature magnetic measurements. In the complexes 1–3a, the ClO4– groups are counterions and the Ni2+ centers are bridged by the azido ligands in an end‐to‐end bonding fashion. The coordination geometry around the NiII ions is six‐coordinate with a distorted octahedral environment achieved by the four N atoms of the tetradentate amines and two terminal N atoms of the azide groups. Complex 1 consists of dinuclear units with doubly bridged azido groups whereas in 2 and 3a, a polymeric 1D chain is formed in which the adjacent azido groups link the NiII centers in a cis arrangement. In complex 2, the structural parameters of the two adjacent azido bridging ligands are different and an alternating 1D system with two different end‐to‐end azido bridges is produced. Complex 3a is a uniform 1D system where the strong steric hindrance imposed by the methyl groups of the Me6trien ligand [diagonal N(azide)–Ni–N(amine) bond angles] causes pronounced deviation from the ideal octahedral geometry. Complex 3b exhibits a distorted square pyramidal geometry. The complexes 1–3a show antiferromagnetic coupling. In complex 1, the exchange coupling constant was J = –64(1) cm–1, whereas in the polynuclear species 2 and 3a, the calculated values were J1 = –63.7(2) (α = 0.52) and J = –26.8(1) cm–1, respectively. The magnetic parameters have been correlated to the structural data.(© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
(Pentabenzylcyclopentadienyl)molybdenum Complexes: Synthesis, Structures and Redox Properties
Authors: Namorado Sónia , Cui Jinlan , de Azevedo Cristina G. , Lemos M. Amélia , Duarte M. Teresa , Ascenso José R. , Dias Alberto R. , Martins Ana M. 
Published: February 2007

Abstract[MCpBz(CO)3]2 (M = Mo 3, W 4; CpBz = pentabenzylcyclopentadienyl) complexes were prepared by reaction of Li[MCpBz(CO)3] [M = Mo (1), W (2)] with FeIII. [MoCpBz(CO)2]2 (5) can be prepared by thermal elimination of CO from 3 and also by reaction of 1 with C3H5Br. The steric bulk of the CpBz ligands causes all the dimers to exist either in the solid state or in solution as the trans isomers. The hydrido complexes [MH(CpBz)(CO)3] [M = Mo (6), W (7)] were prepared by reactions of 1 and 2 with H+. Cyclic voltammetry and controlled potential coulometry of 5 in CH2Cl2, thf and CH3CN were performed and mechanisms for the redox behaviour are proposed. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)
Control of Intramolecular Ether‐Oxygen Coordination in the Crystal Structure of Copper(II) Complexes With Dipicolylamine‐Based Ligands
Authors: Mikata Yuji , Fujimoto Tomomi , Sugai Yuko , Yano Shigenobu 
Published: February 2007

AbstractThirteen crystal structures of copper(II) complexes with a series of dipicolylamine (DPA)‐derived ligands, N‐(2‐methoxyethyl)‐N,N‐bis(2‐pyridylmethyl)amine (L1), N‐[2‐(2‐hydroxyethyloxy)ethyl]‐N,N‐bis(2‐pyridylmethyl)amine (L2) and N‐(3‐methoxypropyl)‐N,N‐bis(2‐pyridylmethyl)amine (L3), have been determined and the factors that control the coordination of the ether‐oxygen atom of these ligands to the copper centre are discussed. Complexes that have +1 or +2 charges exhibit coordination of the ether‐oxygen atom, whereas neutral complexes in which two anions are bound to the copper(II) centre tend to lose the oxygen coordination. Upon chelation of the oxygen atom, L3 forms a six‐membered chelate ring with respect to the 3‐aminopropyl ether moiety whereas L1 and L2 form a five‐membered chelate. This difference, especially in the nitrate and bromide complexes, determines whether the ether‐oxygen atom chelates to the metal centre to give a monocationic complex, or the second anion coordinates to the metal centre to form the ether‐free, neutral complex. The terminal anchor hydroxy group of L2 facilitates the ether‐oxygen coordination via a hydrogen bond interaction to the donor atom located trans to the aliphatic nitrogen atom in the basal plane. (© Wiley‐VCH Verlag GmbH & Co. KGaA, 69451 Weinheim, Germany, 2007)