bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ordovician sea-level change and rapid change in crustal subsidence rates in East Siberia and Baltoscandia
Authors: Artyushkov E.V. , Tesakov Yu.I. , Chekhovich P.A. 
Published: August 2008

Abstract
Sea-level change has been commonly interpreted to be of eustatic origin, and many eustatic events were hypothesized for the Phanerozoic, including several 1–3 Myr long cycles in the Ordovician with magnitudes up to 100 or 200 m. However, sea-level change modeling using stratigraphic data from Northern Estonia, which was an area of slow shallow-marine (&lt;10 m) deposition through most of the Ordovician, indicates fluctuations of no more than 20 m. In the Late Ordovician the sea level fell only twice for ∼100 m within 1 Myr during the Gondwanian glaciation. Although the sea level remained relatively stable, there were frequent 100–200 m changes of sea depths we inferred with reference to the time spans of stratigraphic units and intervals between tectonic events estimated reliably against stable durations of East Siberian chronozones (biochrons) of the Ordovician. In the absence of eustatic events, the sea-depth changes most likely resulted from rapid crustal uplift and subsidence. According to correlated well-documented Ordovician sections from East Siberia, the rate of crustal subsidence changed rapidly in different periods and in different places of the area, thus being of a regional scale. The controversy between the sea-level stability and the regional-scale variations in sea depths controlled by rates of crustal uplift and subsidence can be resolved assuming a model of variable eclogitization rates in the lower crust caused by lithospheric stress change. Our inferences undermine the traditional petroleum prediction approach implying formation of depositional traps due to rapid eustatic sea-level change.
Hilbert-semblance method for acoustic logging data processing
Authors: Akhmetsafin R.D. , Dubinskii V. , Patterson D. 
Published: August 2008

Abstract
We suggest a method of multi-element low-frequency acoustic logging data processing which combines advantages of the semblance and phase velocity processing (PVP) techniques, namely, the interference resistance in the former and better accuracy in the latter. The new method is based on point (windowless) semblance by the Hilbert transformation. The introduced concept of phase semblance makes it possible to estimate the signal distribution semblance and the phase. Also suggested are an algorithm for preliminary estimation of formation S-wave slowness from signal group power variations and improved forms of processed data imaging.
Historical seismicity on the southern margin of the Siberian craton: new data
Authors: Radziminovich Ya.B. , Shchetnikov A.A. 
Published: August 2008

Abstract
We discuss historical evidence for seismicity on the southern margin of the Siberian craton collected from old local newspapers. The reported earthquakes vary in magnitude from M = 2.5 to 4.5, and their macroseismic locations agree well with the regional tectonic framework. The new data prove seismic activity in the area and can be used in seismic risk assessment.
Mesozoic-Cenozoic tectonics and geodynamics of Altai, Tien Shan, and Northern Kazakhstan, from apatite fission-track data
Authors: Buslov M.M. , Kokh D.A. , De Grave J. 
Published: August 2008

Abstract
Apatite fission-track (AFT) thermochronological modeling as a diagnostic tool for periods of stability (peneplanation) and tectonic activity (orogeny) has been broadly used in tectonic studies of Central Asia in recent years. We discuss more than 100 AFT ages of samples from the Kyrgyz Tien Shan and Altai and compare them with AFT data from northern Kazakhstan. Geological, geomorphological, and AFT data indicate intense activity in the Late Cenozoic Eurasian continental interior. The impact from the India-Eurasia collision on the northern Tien Shan, Altai, and northern Kazakhstan regions showed up at 11, 5, and 3 Ma, respectively, as a result of stress propagation into the continent, with the ensuing reactivation and mountain growth. We hypothesize that a distant effect of the Late Cenozoic India-Eurasia collision was to rejuvenate Paleozoic fault zones and to deform the Mesozoic sedimentary cover north of the collision front as far as the West Siberian Plate. The reactivation facilitated formation of tectonic oil and gas traps. The activity in northern Central Asia under the effect of the Indian indentation into Eurasia appears to continue and may evolve to include uplift of southern West Siberian plate with uplift.
Contact coal transformation under the influence of dolerite dike (Kaierkan deposit, Noril’sk district)
Authors: Melenevsky V.N. , Fomin A.N. , Konyshev A.S. , Talibova O.G. 
Published: August 2008

Abstract
The influence of 6.75 m thick dolerite dike on the sheet coal of the Kaierkan deposit (northwestern Siberian Platform) was studied by organogeochemical methods. It is shown that initial bituminous coal was transformed into anthracite in the immediate vicinity of the dike. Chemical kinetic modeling of the dike-induced cracking of coal’s organic matter was performed, and the maximum paleotemperatures were estimated.
Differential enhancement of leukaemia cell differentiation without elevation of intracellular calcium by plant‐derived sesquiterpene lactone compounds
Authors: Kim S H , Danilenko M , Kim T S 
Published: August 2008

Background and purpose:All‐trans retinoic acid (ATRA) induces complete remission in a majority of acute promyelocytic leukaemia patients, but resistance of leukaemic cells to ATRA and its toxicity, such as hypercalcaemia, lead to a limitation of treatment. Therefore, combination therapies with differentiation‐enhancing agents at non‐toxic concentrations of ATRA may overcome its side effects. Here, we investigated the effect of plant‐derived sesquiterpene lactone compounds and their underlying mechanisms in ATRA‐induced differentiation of human leukaemia HL‐60 cells.Experimental approach:HL‐60 cells were treated with four sesquiterpene lactones (helenalin, costunolide, parthenolide and sclareolide) and cell differentiation was determined by NBT reduction, Giemsa and cytofluorometric analyses. Signalling pathways were assessed by western blotting, gel‐shift assay and kinase activity determinations and intracellular calcium levels were determined using a calcium‐specific fluorescent probe.Key results:Helenalin, costunolide and parthenolide, but not sclareolide, increased ATRA‐induced HL‐60 cell differentiation into a granulocytic lineage. Signalling kinases PKC and ERK were involved in the ATRA‐induced differentiation enhanced by all of the effective sesquiterpene lactones, but JNK and PI3‐K were involved in the ATRA‐induced differentiation enhanced by costunolide and parthenolide. Enhancement of cell differentiation closely correlated with inhibition of NF‐κB DNA‐binding activity by all three effective compounds. Importantly, enhancement of differentiation induced by 50 nM ATRA by the sesquiterpene lactones was not accompanied by elevation of basal intracellular calcium concentrations.Conclusions and implications:These results indicate that plant‐derived sesquiterpene lactones may enhance ATRA‐mediated cell differentiation through distinct pathways.British Journal of Pharmacology (2008) 155, 814–825; doi:10.1038/bjp.2008.319; published online 25 August 2008
H2S‐donating sildenafil (ACS6) inhibits superoxide formation and gp91phox expression in arterial endothelial cells: role of protein kinases A and G
Authors: Muzaffar S , Jeremy J Y , Sparatore A , Del Soldato P , Angelini G D , Shukla N 
Published: August 2008

Background and purpose:Superoxide (O2•−), derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, is associated with acute respiratory distress syndrome (ARDS). NADPH oxidase activity and expression are blocked by nitric oxide (NO) and sildenafil. As another gas, hydrogen sulphide (H2S) is formed by blood vessels, the effect of sodium hydrosulphide (NaHS) and the H2S‐donating derivative of sildenafil, ACS6, on O2•− formation and the expression of gp91phox (a catalytic subunit of NADPH oxidase) in porcine pulmonary arterial endothelial cells (PAECs) was investigated.Experimental approach:PAECs were incubated with 10 ng mL−1 tumour necrosis factor‐α (TNFα) (±NaHS or ACS6), both of which released H2S, for 2 h or 16 h. O2•− was measured. Expression of gp91phox was measured by western blotting and the role of cyclic AMP (cAMP) and/or cyclic GMP was assessed using protein kinase inhibitors.Key results:After either 2‐ or 16‐h incubations, O2•− formation by PAECs was inhibited by NaHS or ACS6, with IC50 values of about 10 nM and less than 1 nM, respectively. Both 100 nM NaHS and 1 nM ACS6 completely inhibited gp91phox expression induced by TNFα. The effects of NaHS were blocked by the inhibition of protein kinase A (PKA), but not PKG, and not by the inhibition of guanylyl cyclase. Effects of ACS6 were blocked by inhibition of both PKA and PKG. Both NaHS and ACS6 augmented cAMP formation.Conclusion and implications:H2S inhibited O2•− formation and upregulation of NADPH oxidase in PAECs through the adenylyl cyclase‐PKA pathway. ACS6 may be effective in treating ARDS through both elevation of cAMP and inhibition of phosphodiesterase type 5 activity.British Journal of Pharmacology (2008) 155, 984–994; doi:10.1038/bjp.2008.326; published online 1 September 2008
Effects of levo‐ and dextrosimendan on NF‐κB‐mediated transcription, iNOS expression and NO production in response to inflammatory stimuli
Authors: Sareila O , Korhonen R , Auvinen H , Hämäläinen M , Kankaanranta H , Nissinen E , Moilanen E 
Published: August 2008

Background and purpose:Levosimendan is used in the treatment of decompensated heart failure. It increases the contractility of the myocardium by sensitizing troponin C to calcium. In addition, levosimendan has been reported to have beneficial effects in experimental models of septic shock. Because heart failure and sepsis have been associated with excessive nitric oxide (NO) production through inducible NOS (iNOS), we investigated the effects of the simendans on NO production and iNOS expression and on generation of pro‐inflammatory cytokines.Experimental approach:Macrophages and fibroblasts were exposed to inflammatory stimuli to induce iNOS expression. Proteins were measured by western blot and mRNA expression was determined by quantitative RT‐PCR. Promoter activity and nuclear factor‐κB (NF‐κB) and the γ‐activated site (GAS; binding site for signal transducer and activator of transcription 1; STAT1)‐mediated transcription were investigated using luciferase reporter constructs. Cytokines tumour necrosis factor‐α (TNF‐α) and interleukin‐6 (IL‐6) were measured by ELISA.Key results:Levosimendan and dextrosimendan decreased NO production in a dose‐dependent manner in cells exposed to inflammatory stimuli. The simendans decreased iNOS protein and mRNA expression but did not affect iNOS mRNA decay. These compounds decreased iNOS promoter activity and inhibited NF‐κB‐mediated transcription but not that mediated by STAT1/GAS. The simendans reduced IL‐6 production slightly but they had no effect on TNF‐α synthesis.Conclusions and implications:The simendans downregulated NF‐κB‐dependent transcription and decreased iNOS promoter activity, iNOS expression and NO production. These mechanisms may contribute to their beneficial clinical effects.British Journal of Pharmacology(2008)155, 884–895; doi:10.1038/bjp.2008.328; published online 18 August 2008
Activation of peroxisome proliferator‐activated receptor‐α in mice induces expression of the hepatic low‐density lipoprotein receptor
Authors: Huang Z , Zhou X , Nicholson A C , Gotto A M , Hajjar D P , Han J 
Published: August 2008

Background and purpose:Mutations in the low‐density lipoprotein receptor (LDLR) gene cause familial hypercholesterolaemia in humans and deletion of the LDLR induces lesion development in mice fed a high‐fat diet. LDLR expression is predominantly regulated by sterol regulatory element‐binding protein 2 (SREBP2). Fenofibrate, a peroxisome proliferator‐activated receptor α (PPARα) ligand, belongs to a drug class used to treat dyslipidaemic patients. We have investigated the effects of fenofibrate on hepatic LDLR expression.Experimental approach:The effects of fenofibrate on hepatic LDLR expression (mRNA and protein) and function were evaluated by both in vitro (with AML12 cells) and in vivo experiments in mice.Key results:Fenofibrate increased LDLR expression and LDL binding in a mouse hepatoma cell line, AML12 cells. Fenofibrate restored sterol‐inhibited hepatocyte LDLR expression. Mechanistic studies demonstrated that induction of LDLR expression by fenofibrate was dependent on PPARα and sterol regulatory elements (SRE). Specifically, fenofibrate induced LDLR expression by increasing maturation of SREBP2 and phosphorylation of protein kinase B (Akt) but had no effect on SREBP cleavage‐activating protein. In vivo, a high‐fat diet suppressed LDLR expression in mouse liver while elevating total and LDL cholesterol levels in plasma. However, fenofibrate restored LDLR expression inhibited by high‐fat diets in the liver and reduced LDL cholesterol levels in plasma.Conclusions and implications:Our data suggest that fenofibrate increased hepatic LDLR expression in mice by a mechanism involving Akt phosphorylation and LDLR gene transcription mediated by SREBP2.British Journal of Pharmacology (2008) 155, 596–605; doi:10.1038/bjp.2008.331; published online 18 August 2008
Human embryonic stem cells and lung regeneration
Authors: Varanou A , Page C P , Minger S L 
Published: August 2008

Human embryonic stem cells are pluripotent cells derived from the inner cell mass of preimplantation stage embryos. Their unique potential to give rise to all differentiated cell types has generated great interest in stem cell research and the potential that it may have in developmental biology, medicine and pharmacology. The main focus of stem cell research has been on cell therapy for pathological conditions with no current methods of treatment, such as neurodegenerative diseases, cardiac pathology, retinal dysfunction and lung and liver disease. The overall aim is to develop methods of application either of pure cell populations or of whole tissue parts to the diseased organ under investigation. In the field of pulmonary research, studies using human embryonic stem cells have succeeded in generating enriched cultures of type II pneumocytes in vitro. On account of their potential of indefinite proliferation in vitro, embryonic stem cells could be a source of an unlimited supply of cells available for transplantation and for use in gene therapy. Uncovering the ability to generate such cell types will expand our understanding of biological processes to such a degree that disease understanding and management could change dramatically.British Journal of Pharmacology (2008) 155, 316–325; doi:10.1038/bjp.2008.333; published online 25 August 2008
Inhibition of fatty acid amide hydrolase produces PPAR‐α‐mediated analgesia in a rat model of inflammatory pain
Authors: Sagar D R , Kendall D A , Chapman V 
Published: August 2008

Background and purpose:We have previously demonstrated antinociceptive effects of fatty acid amide hydrolase (FAAH) inhibition that were accompanied by increases in the levels of endocannabinoids (ECs) in the hind paw. Here, the effects of the FAAH inhibitor URB597 (3′‐carbamoyl‐biphenyl‐3‐yl‐cyclohexylcarbamate) on responses of spinal neurons were studied.Experimental approach:Extracellular single‐unit recordings of dorsal horn neurons were made in anaesthetized rats with hind paw inflammation induced by λ‐carrageenan. Effects of intraplantar pre‐administration of URB597, or vehicle, on carrageenan‐evoked expansion of peripheral receptive fields of spinal neurons and mechanically evoked responses of neurons were studied. The cannabinoid receptor type 1 (CB1) antagonist AM251 (N‐(piperidin‐1‐yl)‐5‐(4‐iodophenyl)‐1‐(2,4‐dichlorophenyl)‐4‐ methyl‐1H‐pyrazole‐3‐carboxamide) and the peroxisome proliferator‐ activated receptor (PPAR)‐α antagonist GW6471 ([(2S)‐2‐[[(1Z)‐1‐ methyl‐3‐oxo‐3‐[4‐(trifluoromethyl)phenyl]‐1‐propenyl]amino]‐3‐[4‐[2‐ (5‐methyl‐2‐phenyl‐4‐oxa zolyl)ethoxy]phenyl]propyl]‐carbamic acid ethyl ester) were used to investigate the roles of these receptors in mediating the effects of URB597.Key results:URB597 (25 μg in 50 μL) pretreatment significantly inhibited carrageenan‐evoked receptive field expansion and this was significantly reversed by co‐administration of the PPAR‐α antagonist but not the CB1 antagonist. Pretreatment with the PPAR‐α receptor agonist WY14643 ([[4‐chloro‐6‐[(2,3‐dimethylphenyl)amino]‐2‐pyrimidinyl]thio]acetic acid) also significantly inhibited receptive field expansion. URB597 (25 or 100 μg in 50 μL) had no significant effect on mechanically evoked responses of spinal neurons.Conclusions and implications:URB597 inhibited receptive field expansions but not mechanically evoked responses of spinal neurons in rats with hind paw inflammation. These effects were blocked by PPAR‐α receptor antagonism. These data support the contention that URB597 exerts its antinociceptive effects by indirect inhibition of sensitization of neuronal responses at least partly through PPAR‐α activation due to enhanced EC levels.British Journal of Pharmacology (2008) 155, 1297–1306; doi:10.1038/bjp.2008.335; published online 25 August 2008
Endogenous and synthetic agonists of GPR119 differ in signalling pathways and their effects on insulin secretion in MIN6c4 insulinoma cells
Authors: Ning Y , O'Neill K , Lan H , Pang L , Shan L X , Hawes B E , Hedrick J A 
Published: August 2008

Background and purpose:GPR119 is a G protein‐coupled receptor that is preferentially expressed in islet cells and mediates insulin secretion. Oleoyl‐lysophosphatidylcholine and oleoylethanolamide (OEA) act as endogenous ligands for this receptor, whereas PSN375963 and PSN632408 are two recently reported synthetic agonists. In this study, we explored mechanisms underlying GPR119‐induced insulin secretion. In addition, we assessed the potential utility of the synthetic agonists as tools for exploring GPR119 biology.Experimental approach:We examined natural and synthetic GPR119 agonist activity at GPR119 in MIN6c4 and RINm5f insulinoma cells. We evaluated insulin secretion, intracellular calcium [Ca2+]i, ion channel involvement and levels of cAMP.Key results:We report that increases in insulin secretion induced by OEA were associated with increased cAMP and a potentiation of glucose‐stimulated increases in [Ca2+]i. We also demonstrate that ATP‐sensitive K+ and voltage‐dependent calcium channels were required for GPR119‐mediated increases in glucose‐stimulated insulin secretion. In contrast to OEA, the synthetic GPR119 agonist PSN375963 and PSN632408 have divergent effects on insulin secretion, cAMP and intracellular calcium in MIN6c4 cells.Conclusions and implications:The endogenous ligand OEA signals through GPR119 in a manner similar to glucagon‐like peptide‐1 (GLP‐1) and its receptor with respect to insulin secretion, [Ca2+]i and cAMP. In addition, PSN375963 and PSN632408 substantially differ from OEA and from one another. These studies suggest that the commercially available synthetic agonists, although they do activate GPR119, may also activate GPR119‐independent pathways and are thus unsuitable as GPR119‐specific pharmacological tools.British Journal of Pharmacology (2008) 155, 1056–1065; doi:10.1038/bjp.2008.337; published online 25 August 2008
5‐HT4‐elicited positive inotropic response is mediated by cAMP and regulated by PDE3 in failing rat and human cardiac ventricles
Authors: Afzal F , Andressen K W , Mørk H K , Aronsen J M , Sjaastad I , Dahl C P , Skomedal T , Levy F O , Osnes J‐B , Qvigstad E 
Published: August 2008

Background and purpose:The left ventricle in failing hearts becomes sensitive to 5‐HT parallelled by appearance of functional Gs‐coupled 5‐HT4receptors. Here, we have explored the regulatory functions of phosphodiesterases in the 5‐HT4receptor‐mediated functional effects in ventricular muscle from failing rat and human heart.Experimental approach:Extensive myocardial infarctions were induced by coronary artery ligation in Wistar rats. Contractility was measured in left ventricular papillary muscles of rat, 6 weeks after surgery and in left ventricular trabeculae from explanted human hearts. cAMP was quantified by RIA.Key results:In papillary muscles from postinfarction rat hearts, 5‐HT4stimulation exerted positive inotropic and lusitropic effects and increased cAMP. The inotropic effect was increased by non‐selective PDE inhibition (IBMX, 10 μM) and selective inhibition of PDE3 (cilostamide, 1 μM), but not of PDE2 (EHNA, 10 μM) or PDE4 (rolipram, 10 μM). Combined PDE3 and PDE4 inhibition enhanced inotropic responses beyond the effect of PDE3 inhibition alone, increased the sensitivity to 5‐HT, and also revealed an inotropic response in control (sham‐operated) rat ventricle. Lusitropic effects were increased only during combined PDE inhibition. In failing human ventricle, the 5‐HT4receptor‐mediated positive inotropic response was regulated by PDEs in a manner similar to that in postinfarction rat hearts.Conclusions and implications:5‐HT4receptor‐mediated positive inotropic responses in failing rat ventricle were cAMP‐dependent. PDE3 was the main PDE regulating this response and involvement of PDE4 was disclosed by concomitant inhibition of PDE3 in both postinfarction rat and failing human hearts. 5‐HT, PDE3 and PDE4 may have pathophysiological functions in heart failure.British Journal of Pharmacology(2008)155, 1005–1014; doi:10.1038/bjp.2008.339; published online 1 September 2008
Dexmedetomidine and ST‐91 analgesia in the formalin model is mediated by α2A‐adrenoceptors: a mechanism of action distinct from morphine
Authors: Nazarian A , Christianson C A , Hua X‐Y , Yaksh T L 
Published: August 2008

Background and purpose:Intrathecal administration of α2‐adrenoceptor agonists produces potent analgesia. This study addressed the subtype of spinal α2‐adrenoceptor responsible for the analgesic effects of i.t. dexmedetomidine and ST‐91 in the formalin behavioural model and their effects on primary afferent substance P (SP) release and spinal Fos activation.Experimental approach:The analgesic effects of i.t. dexmedetomidine and ST‐91 (α2agonists) were tested on the formalin behavioural model. To determine the subtype of α2‐adrenoceptor involved in the analgesia, i.t. BRL44408 (α2Aantagonist) or ARC239 (α2B/Cantagonist) were given before dexmedetomidine or ST‐91. Moreover, the ability of dexmedetomidine and ST‐91 to inhibit formalin‐induced release of SP from primary afferent terminals was measured by the internalization of neurokinin1(NK1) receptors. Finally, the effects of dexmedetomidine on formalin‐induced Fos expression were assessed in the dorsal horn.Key results:Intrathecal administration of dexmedetomidine or ST‐91 dose‐dependently reduced the formalin‐induced paw‐flinching behaviour in rats. BRL44408 dose‐dependently blocked, whereas ARC239 had no effect on the analgesic actions of dexmedetomidine and ST‐91. Dexmedetomidine and ST‐91 had no effect on the formalin‐induced NK1receptor internalization, while morphine significantly reduced the NK1receptor internalization. On the other hand, both dexmedetomidine and morphine diminished the formalin‐induced Fos activation. The effect of dexmedetomidine on formalin‐induced Fos activation was reversed by BRL44408, but not ARC239.Conclusion and implications:These findings suggest that α2A‐adrenoceptors mediate dexmedetomidine and ST‐91 analgesia. This effect could be through a mechanism postsynaptic to primary afferent terminals, distinct from that of morphine.British Journal of Pharmacology(2008)155, 1117–1126; doi:10.1038/bjp.2008.341; published online 1 September 2008