325 resultados para IVA


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XVIII. Astronomical observations for latitude made during the period 1885 to 1895 and deduced values of the deflections of the plumb-line. Prepared under the directions of...S.G. Burrard. 1906.--XIX. Levelling of precision in India (1858-190) by S.G. Burrard..1910.--XIXA. Descriptions and heights of bench-marks on southern lines of levelling. Prepared under the directions of S.G. Burrard. 1910.--XIXB. Descriptions and heights of bench-marks on the northern lines of levelling. Prepared under the directions of S.G. Burrard. 1910.

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Bibliography: p. 38-41.

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The present study describes the isolation of the first neurotoxin (acantoxin IVa) from Acanthophis sp. Seram death adder venom and an examination of its activity at nicotinic acetylcholine receptor (naChR) subtypes. Acantoxin IVa (MW 6815; 0.1-1.0 muM) caused concentration-dependent inhibition of indirect twitches (0.1 Hz, 0.2 ms, supramaximal V) and inhibited contractile responses to exogenous nicotinic agonists in the chick biventer cervicis nerve-muscle, confirming that this toxin is a postsynaptic neurotoxin. Acantoxin IVa (1-10 nM) caused pseudo-irreversible antagonism at skeletal muscle nAChR with an estimated pA(2) Of 8.36 +/- 0.17. Acantoxin IVa was approximately two-fold less potent than the long-chain (Type 11) neurotoxin, alpha-bungarotoxin. With a pK(i) value of 4.48, acantoxin IVa was approximately 25,000 times less potent than a-bungarotoxin at alpha7-type neuronal nAChR. However, in contrast to alpha-bungarotoxin, acantoxin IVa completely inhibited specific [H-3]-methyllycaconitine (MLA) binding in rat hippocampus homogenate. Acantoxin IVa had no activity at ganglionic nAChR, alpha4beta2 subtype neuronal nAChR or cytisine-resistant [H-3]-epibatidine binding sites. While long-chain neurotoxin resistant [H-3]-MLA binding in hippocampus homogenate requires further investigation, we have shown that a short-chain (Type 1) neurotoxin is capable of fully inhibiting specific [H-3]-MLA binding. (C) 2004 Elsevier Inc. All rights reserved.

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Stable expression of human groups IIA and X secreted phospholipases A(2) (hGIIA and hGX) in CHO-K1 and HEK293 cells leads to serum- and interleukin-1beta-promoted arachidonate release. Using mutant CHO-K1 cell lines, it is shown that this arachidonate release does not require heparan sulfate proteoglycan- or glycosylphosphatidylinositol-anchored proteins. It is shown that the potent secreted phospholipase A(2) inhibitor Me-Indoxam is cell-impermeable. By use of Me-Indoxam and the cell-impermeable, secreted phospholipase A(2) trapping agent heparin, it is shown that hGIIA liberates free arachidonate prior to secretion from the cell. With hGX-transfected CHO-K1 cells, arachidonate release occurs before and after enzyme secretion, whereas all of the arachidonate release from HEK293 cells occurs prior to enzyme secretion. Immunocytochemical studies by confocal laser and electron microscopies show localization of hGIIA to the cell surface and Golgi compartment. Additional results show that the interleukin-1beta-dependent release of arachidonate is promoted by secreted phospholipase A(2) expression and is completely dependent on cytosolic (group IVA) phospholipase A(2). These results along with additional data resolve the paradox that efficient arachidonic acid release occurs with hGIIA-transfected cells, and yet exogenously added hGIIA is poorly able to liberate arachidonic acid from mammalian cells.

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Sequences of small-subunit rRNA genes were determined for Dermocystidium percae and a new Dermocystidium species established as D. fennicum sp. n. from perch in Finland. On the basis of alignment and phylogenetic analysis both species were placed in the Dermocystidium-Rhinosporidium clade within Ichthyosporea, D. fennicum as a specific sister taxon to D. salmonis, and D. percae in a clade different from D. fennicum. The ultrastructures of both species well agree with the characteristics approved within Ichthyosporea: walled spores produce uniflagellate zoospores lacking a collar or cortical alveoli. The two Dermocystidium species resemble Rhinosporidium seeberi (as described by light microscope), a member of the nearest relative genus, but differ in that in R. seeberi plasmodia have thousands of nuclei discernible, endospores are discharged through a pore in the wall of the sporangium, and zoospores have not been revealed. The plasmodial stages of both Dermocystidium species have a most unusual behaviour of nuclei, although we do not actually know how the nuclei transform during the development. Early stages have an ordinary nucleus with double, fenestrated envelope. In middle-aged plasmodia ordinary nuclei seem to be totally absent or are only seldom discernible until prior to sporogony, when rather numerous nuclei again reappear. Meanwhile single-membrane vacuoles with coarsely granular content, or complicated membranous systems were discernible. Ordinary nuclei may be re-formed within these vacuoles or systems. In D. percae small canaliculi and in D. fennicum minute vesicles may aid the nucleus-cytoplasm interchange of matter before formation of double-membrane-enveloped nuclei. Dermocystidium represents a unique case when a stage of the life cycle of an eukaryote lacks a typical nucleus.

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Neurons in pelvic ganglia receive nicotinic excitatory post-synaptic potentials (EPSPs) from sacral preganglionic neurons via the pelvic nerve, lumbar preganglionic neurons via the hypogastric nerve or both. We tested the effect of a range of calcium channel antagonists on EPSPs evoked in paracervical ganglia of female guinea-pigs after pelvic or hypogastric nerve stimulation. omega-Conotoxin GVIA (CTX GVIA, 100 nM) or the novel N-type calcium channel antagonist, CTX CVID (100 nM) reduced the amplitude of EPSPs evoked after pelvic nerve stimulation by 50-75% but had no effect on EPSPs evoked by hypogastric nerve stimulation. Combined addition of CTX GVIA and CTX CVID was no more effective than either antagonist alone. EPSPs evoked by stimulating either nerve trunk were not inhibited by the P/Q calcium channel antagonist, omega-agatoxin IVA (100 nM), nor the L-type calcium channel antagonist, nifedipine (30 muM). SNX 482 (300 nM), an antagonist at some R-type calcium channels, inhibited EPSPs after hypogastric nerve stimulation by 20% but had little effect on EPSPs after pelvic nerve stimulation. Amiloride (100 muM) inhibited EPSPs after stimulation of either trunk by 40%, while nickel (100 muM) was ineffective. CTX GVIA or CTX CVID (100 nM) also slowed the rate of action potential repolarization and reduced afterhyperpolarization amplitude in paracervical neurons. Thus, release of transmitter from the terminals of sacral preganglionic neurons is largely dependent on calcium influx through N-type calcium channels, although an unknown calcium channel which is resistant to selective antagonists also contributes to release. Release of transmitter from lumbar preganglionic neurons does not require calcium entry through either conventional N-type calcium channels or the variant CTX CVID-sensitive N-type calcium channel and seems to be mediated largely by a novel calcium channel. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved.

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1 The effects of calcium channel blockers on co-transmission from different populations of autonomic vasomotor neurons were studied on isolated segments of uterine artery and vena cava from guinea-pigs. 2 Sympathetic, noradrenergic contractions of the uterine artery (produced by 200 pulses at 1 or 10 Hz; 600 pulses at 20 Hz) were abolished by the N-type calcium channel blocker omega-conotoxin (CTX) GVIA at 1-10 nM. 3 Biphasic sympathetic contractions of the vena cava (600 pulses at 20 Hz) mediated by noradrenaline and neuropeptide Y were abolished by 10 nM CTX GVIA. 4 Neurogenic relaxations of the uterine artery (200 pulses at 10 Hz) mediated by neuronal nitric oxide and neuropeptides were reduced < 50% by CTX GVIA 10-100 nM. 5 Capsaicin (3 muM) did not affect the CTX GVIA-sensitive or CTX GVIA-resistant neurogenic relaxations of the uterine artery. 6 The novel N-type blocker CTX CVID (100-300 nM), P/Q-type blockers agatoxin IVA (10-100 nM) or CTX CVIB (100 nM), the L-type blocker nifedipine (10 muM) or the 'R-type' blocker SNX-482 (100 nM), all failed to reduce CTX GVIA-resistant relaxations. The T-type channel blocker NiCl2 (100-300 muM) reduced but did not abolish the remaining neurogenic dilations. 7 Release of different neurotransmitters from the same autonomic vasomotor axon depends on similar subtypes of calcium channels. N-type channels are responsible for transmitter release from vasoconstrictor neurons innervating a muscular artery and capacitance vein, but only partly mediate release of nitric oxide and neuropeptides from pelvic vasodilator neurons.

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Little is known about the nature of the calcium channels controlling neurotransmitter release from preganglionic parasympathetic nerve fibres. In the present study, the effects of selective calcium channel antagonists and amiloride were investigated on ganglionic neurotransmission. Conventional intracellular recording and focal extracellular recording techniques were used in rat submandibular and pelvic ganglia, respectively. Excitatory postsynaptic potentials and excitatory postsynaptic currents preceded by nerve terminal impulses were recorded as a measure of acetylcholine release from parasympathetic and sympathetic preganglionic fibres following nerve stimulation. The calcium channel antagonists omega-conotoxin GVIA (N type), nifedipine and nimodipine (L type), omega-conotoxin MVIIC and omega-agatoxin IVA (P/Q type), and Ni2+ (R type) had no functional inhibitory effects on synaptic transmission in both submandibular and pelvic ganglia. The potassium-sparing diuretic, amiloride, and its analogue, dimethyl amiloride, produced a reversible and concentration-dependent inhibition of excitatory postsynaptic potential amplitude in the rat submandibular ganglion. The amplitude and frequency of spontaneous excitatory postsynaptic potentials and the sensitivity of the postsynaptic membrane to acetylcholine were unaffected by amiloride. In the rat pelvic ganglion, amiloride produced a concentration-dependent inhibition of excitatory postsynaptic currents without causing any detectable effects on the amplitude or configuration of the nerve terminal impulse. These results indicate that neurotransmitter release from preganglionic parasympathetic and sympathetic nerve terminals is resistant to inhibition by specific calcium channel antagonists of N-, L-, P/Q- and R-type calcium channels. Amiloride acts presynaptically to inhibit evoked transmitter release, but does not prevent action potential propagation in the nerve terminals, suggesting that amiloride may block the pharmacologically distinct calcium channel type(s) on rat preganglionic nerve terminals. (C) 1999 IBRO. Published by Elsevier Science Ltd.

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We consider a 3-dimensional Riemannian manifold V with a metric g and an a±nor structure q. The local coordinates of these tensors are circulant matrices. In V we define an almost conformal transformation. Using that definition we construct an infinite series of circulant metrics which are successively almost conformaly related. In this case we get some properties.

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Ива Р. Докузова, Димитър Р. Разпопов - В настоящата статия е разгледан клас V оттримерни риманови многообразия M с метрика g и два афинорни тензора q и S. Дефинирана е и друга метрика ¯g в M. Локалните координати на всички тези тензори са циркулантни матрици. Намерени са: 1) зависимост между тензора на кривина R породен от g и тензора на кривина ¯R породен от ¯g; 2) тъждество за тензора на кривина R в случая, когато тензорът на кривина ¯R се анулира; 3) зависимост между секционната кривина на прозволна двумерна q-площадка {x, qx} и скаларната кривина на M.

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Fish stomach content records extracted from the DAPSTOM 4.5 database (held at the UK Centre for Environment, Fisheries and Aquaculture Science - CEFAS). Data collated as part of the EU Euro-Basin project and specifically concerning herring (Clupea harengus), mackerel (Scomber scombrus), blue whiting (Micromesistius poutassou), albacore (Thunnus alalunga) and bluefin tuna (Thunnus thynnus). The data set consist of 20720 records - collected throughout the northeast Atlantic, between 1906 and 2011 - mostly during routine fisheries monitoring research cruises.

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La messa a punto di processi in grado di utilizzare le biomasse lignocellulosiche per la produzione di molecole piattaforma, utilizzabili per la sintesi di intermedi per la chimica fine, l’industria polimerica ed i combustibili, è attualmente un argomento di ricerca di grande interesse. Tra le molecole più studiate vi è la furfurale (FU), che si può ottenere mediante disidratazione dei monosaccaridi pentosi contenuti nei materiali lignocellulosici. Il prodotto di riduzione della furfurale, l’alcol furfurilico (FAL), è commercialmente interessante perché trova applicazione nell’industria polimerica e viene utilizzato come intermedio nella produzione di lisina, vitamina C, lubrificanti e agenti dispersanti. In letteratura sono riportati numerosi processi che permettono di ottenere questo prodotto, utilizzando la riduzione catalitica con H2 in pressione, che però presentano problemi di selettività, costo, sostenibilità e tossicità del catalizzatore utilizzato. La possibilità di effettuare la riduzione selettiva della furfurale senza fare ricorso all’idrogeno molecolare, utilizzando un processo di H-transfer e catalizzatori eterogenei a base di ossidi misti, risulta quindi di estremo interesse perché permette di eliminare i suddetti problemi. Lo scopo di questa tesi è stato quello di ottimizzare il processo, confrontando catalizzatori basici, quali MgO, CaO e SrO ottenuti tramite calcinazione a diverse temperature dei rispettivi precursori. In particolare, è stata valutata l’influenza che la temperatura di calcinazione, il tempo e la temperatura di reazione hanno sulla reattività e la stabilità dei sistemi catalitici sintetizzati. La caratterizzazione dei catalizzatori tramite diffrazione ai raggi X (XRD), analisi termiche (TGA, DTA) e misure di area superficiale con tecnica BET ha permesso di correlare le proprietà chimico-fisiche dei materiali con la loro attività catalitica.

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Pollen analysis of Wisconsinan sediments from eleven localities in northern and central Illinois, combined with the results of older studies, allows a first general survey of the vegetational changes in Illinois during the last glaciation. In the late Altonian (after 40,000 B.P.), pine was already the most prevalent tree type in northern Illinois. Probably because of the influence of the last Altonian ice advance to northern Illinois, pine migrated to the south and reached south-central Illinois, which was at that time a region of prairie, with oak and hickory trees in favorable sites. Likewise in the late Altonian, spruce appeared in northern Illinois. Spruce also expanded its area to the south during the Wisconsinan, reaching south-central Illinois only after 21,000 B.P., in the early Woodfordian. Deciduous trees (predominantly oak) were present in south-central Illinois throughout the Wisconsinan. Their prevalence decreased to the north. The vegetation during the different subdivisions of the last glacial period in Illinois was approximately as follows: Late Altonian: Pine/spruce forest with some deciduous trees in northern and central Illinois; prairie and oak/hickory stands in south-central Illinois; immigration of pine. Farmdalian: Pine/spruce forest in central Illinois; deciduous trees and pine in south-central Illinois, with areas of open vegetation, perhaps similar to the present-day transition of prairie to forest in the northern Great Plains. Woodfordian: Northern and central Illinois ice covered; in south central Illinois, spruce and oak as dominant tree types, but also pine and grassland. During the Woodfordian, pine and spruce disappeared again from south-central Illinois, and oak/hickory forest and prairie again prevailed. The ice-free areas of northern Illinois become populated temporarily with spruce, but later there is proof of deciduous forest in this region. Pollen investigations in south-central Illinois have shown convincingly that deciduous trees could survive relatively close (less than 60 km) to the ice margin. Therefore the frequently presented view that arctic climatic conditions prevailed in North America during the last glaciation far south of the ice margin can be refuted for the Illinois area, confirming the opinion of other authors resulting from investigations of fossil mollusks and frost-soil features. The small number of localities investigated still permits no complete reconstruction of the vegetation zones and their possible movements in Illinois. During the Altonian and Farmdalian in Illinois, a vegetational zonation probably existed similar to that of today in North America. As the ice pushed southward as far as 39° 20' N. lat in the early Woodfordian, this zonation was apparently broken up under the influence of a relatively moderate climate. In any case, the Vandalia area, which was only about 60 km south of the ice, was at that time neither in a tundra zone nor in a zone of boreal coniferous forest.

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Background Lumacaftor/ivacaftor combination therapy demonstrated clinical benefits inpatients with cystic fibrosis homozygous for the Phe508del CFTR mutation.Pretreatment lung function is a confounding factor that potentially impacts the efficacyand safety of lumacaftor/ivacaftor therapy. Methods Two multinational, randomised, double-blind, placebo-controlled, parallelgroupPhase 3 studies randomised patients to receive placebo or lumacaftor (600 mgonce daily [qd] or 400 mg every 12 hours [q12h]) in combination with ivacaftor (250 mgq12h) for 24 weeks. Prespecified analyses of pooled efficacy and safety data by lungfunction, as measured by percent predicted forced expiratory volume in 1 second(ppFEV1), were performed for patients with baseline ppFEV1 <40 (n=81) and ≥40(n=1016) and screening ppFEV1 <70 (n=730) and ≥70 (n=342). These studies wereregistered with ClinicalTrials.gov (NCT01807923 and NCT01807949). Findings The studies were conducted from April 2013 through April 2014.Improvements in the primary endpoint, absolute change from baseline at week 24 inppFEV1, were observed with both lumacaftor/ivacaftor doses in the subgroup withbaseline ppFEV1 <40 (least-squares mean difference versus placebo was 3∙7 and 3.3percentage points for lumacaftor 600 mg qd/ivacaftor 250 mg q12h and lumacaftor 400mg q12h/ivacaftor 250 mg q12h, respectively [p<0∙05] and in the subgroup with baselineppFEV1 ≥40 (3∙3 and 2∙8 percentage points, respectively [p<0∙001]). Similar absoluteimprovements versus placebo in ppFEV1 were observed in subgroups with screening 4ppFEV1 <70 (3∙3 and 3∙3 percentage points for lumacaftor 600 mg qd/ivacaftor 250 mgq12h and lumacaftor 400 mg q12h/ivacaftor 250 mg q12h, respectively [p<0∙001]) and≥70 (3∙3 and 1∙9 percentage points, respectively [p=0.002] and [p=0∙079]). Increases inBMI and reduction in number of pulmonary exacerbation events were observed in bothLUM/IVA dose groups vs placebo across all lung function subgroups. Treatment wasgenerally well tolerated, although the incidence of some respiratory adverse events washigher with active treatment than with placebo. Interpretation Lumacaftor/ivacaftor combination therapy benefits patients homozygousfor Phe508del CFTR who have varying degrees of lung function impairment. Funding Vertex Pharmaceuticals Incorporated.