High-resolution palynology reveals the land-use history of a Sami renvall in northern Sweden

Acknowledgements: This research was funded by the Leverhulme Trust through the Footprints on the Edge of Thule project, and was written under the auspices of the ERC-funded project Arctic Domus. Thanks are offered to Audrey Innes for laboratory assistance; Ian Foster for 210Pb dating; Gordon Cook for AMS radiocarbon analyses; and Martin Konert and the late Sjoerd Bohncke for assistance with LOI and related analyses. The comments of Tim Mighall, Jeff Blackford, Mari Kuoppamaa, two anonymous referees and the editor helped to improve the paper.Peer reviewedPublisher PD

Механізми вдосконалення управління інноваційною діяльністю в умовах економічної нестабільності

Розглядаються особливості глобально-постіндустріального розвитку. Досліджено методичні основи системи моніторингу, прогнозування, планування і забезпечення реалізації інноваційної діяльності та головні засади механізму її функціонування.Peculiarities of the global post-industrial development are reviewed. Methodical fundamentals of the system for monitoring, forecasting, planning and provision of innovation activity implementation and main principles of its functioning mechanisms are reviewed

Phenylbutazone in the horse: a review

Phenylbutazone is an acidic, lipophilic, nonsteroidal anti-inflammatory drug (NSAID). It is extensively metabolized in the horse. The metabolites so far identified, oxyphenbutazone, y-hydroxyphenylbutazone and y-hydroxyoxyphenbutazone. account for some 25-30% of administered dose over 24 h. The plasma half-life of phenylbutazone and termination of its pharmacological action are determined primarily by its rate of hepatic metabolism. Phenylbutazone acts by inhibiting the cyclooxygenase enzyme system, which is responsible for synthesis of prostanoids such as PGE?. It appears to act on prostaglalidin-H synthase and prostacyclin synthase, after conversion by prostaglandin-H synthase to reactive intermediates. It markedly reduces prostanoid-dependent swelling, edema, erythema, and hypersensitivity to pain in inflamed tissues. Its principal use in the horse is for treatment of soft tissue inflammation. Phenylbutazone is highly bound (\u3e 98%) to plasma protein. After i.v. injection, blood levels decline with an elimination half-life of 3-10 h. The plasma kinetics of phenylbutazone may be dose dependent, with the plasma half-life increasing as the drug dosage level increases. Plasma residues of the drug at 24 h after a single i.v. dose of 2 g/450 kg average about 0.9 pg/ml, but considerable variation occurs. If dosing is repeated, the plasma residue accumulates to give mean residual blood levels of approxiniately 4.5 pg/ml on Day 5 after 4 days of dosing. Approximately similar blood levels are found after a combination of oral and i.v. dosing. Experiments on large numbers of horses in training have been undertaken to ascertain the population distributions of residual blood levels after such dosing schedules. Absorption of phenylbutazone from the gastrointestinal tract is influenced by the dose administered and the relationship of dosing to feeding. Access to hay can delay the time of peak plasma concentration to 18 h or longer. Under optimal conditions, the bioavailability of oral phenylbutazone is probably in the region of 70%. Paste preparations may be more slowly absorbed than other preparations and yield higher residual plasma levels at 24 h after dosing, but further controlled studies are required. Phenylbutazone is easily detected in the plasma and urine of horses but concentrations in saliva are low. It is quantitated for forensic purposes by HPLC. The variability of this method between laboratories is about k 25%. Increasing urinary pH increases the urinary concentration of phenylbutazone and its metabolites up to 200-fold. However, urinary pH has little effect on the plasma half-life of phenylbutazone, which is determined mainly by hepatic metabolism and possibly by biliary secretion. Phenylbutazone has a narrow therapeutic index in the horse. If the administered dose is greater than recommended by the manufacturer, toxic effects may be produced, especially if high dose administration is maintained for more than a few days. Signs of toxicity include anorexia, depression, oral and GI ulcers, plasma protein losing enteropathy, and death from shock. Other side-effects include toxic neutropenia, hepatotoxicity and renal papillary necrosis; the latter may occur if access to water is restricted. If phenylbutazone is withdrawn in the early stages of toxicity, the prognosis is good. Late withdrawal is associated with delayed recovery. Death may occur up to 50 days after withdrawal of the drug. This toxicity can be antagonized by administration of prostaglandins

Gluco-oligomers initially formed by the reuteransucrase enzyme of Lactobacillus reuteri 121 incubated with sucrose and malto-oligosaccharides

<p>The probiotic bacterium Lactobacillus reuteri 121 produces a complex, branched (1 -> 4, 1 -> 6)-alpha-d-glucan as extracellular polysaccharide (reuteran) from sucrose (Suc), using a single glucansucrase/glucosyltransferase (GTFA) enzyme (reuteransucrase). To gain insight into the reaction/product specificity of the GTFA enzyme and the mechanism of reuteran formation, incubations with Suc and/or a series of malto-oligosaccharides (MOSs) (degree of polymerization (DP2-DP6)) were followed in time. The structures of the initially formed products, isolated via high-performance anion-exchange chromatography, were analyzed by matrix-assisted laser-desorption ionization time-of-flight mass spectrometry and 1D/2D H-1/C-13 NMR spectroscopy. Incubations with Suc only, acting as both donor and acceptor, resulted in elongation of Suc with glucose (Glc) units via alternating (alpha 1 -> 4) and (alpha 1 -> 6) linkages, yielding linear gluco-oligosaccharides up to at least DP similar to 12. Simultaneously with the ensemble of oligosaccharides, polymeric material was formed early on, suggesting that alternan fragments longer than DP similar to 12 have higher affinity with the GTFA enzyme and are quickly extended, yielding high-molecular-mass branched reuteran (4 x 10(7) Da). MOSs (DP2-DP6) in the absence of Suc turned out to be poor substrates. Incubations of GTFA with Suc plus MOSs as substrates resulted in preferential elongation of MOSs (acceptors) with Glc units from Suc (donor). This apparently reflects the higher affinity of GTFA for MOSs compared with Suc. In accordance with the GTFA specificity, most prominent products were oligosaccharides with an (alpha 1 -> 4)/(alpha 1 -> 6) alternating structure.</p>

Palynological evidence for pre-agricultural reindeer grazing and the later settlement history of the Lycksele region, northern Sweden.

Funder: Leverhulme Trust; doi: http://dx.doi.org/10.13039/501100000275Funder: European Research Council; doi: http://dx.doi.org/10.13039/501100000781Analyses of high-resolution pollen data, coprophilous fungal spores, microscopic charcoal and sedimentology, combined with radiocarbon dating, allow the assessment of the impact of Sami and Nordic land use in the region surrounding the winter market town of Lycksele in northern Sweden. Such winter markets were established by the Crown during the seventeenth century AD to control the semi-nomadic movements of the Sami who traded here with Finnish settlers and were also taxed and educated. Little is known about Sami and Nordic co-existence beyond these market places, mainly due to a lack of archaeological evidence relating to Sami activity. Vegetation and land-use changes in the region between ~ AD 250 and 1825 reveal no signal for pre-seventeenth century agricultural activity, but the coprophilous fungal spore records suggest the increased regional presence of grazing herbivores (possibly reindeer) between ~ AD 800 and 1100. Sami activity in the parish of Lycksele has been suggested by rich metal finds dated to ~ AD 1000-1350 and they may have been attracted by an abundance of reindeer

Pyrrolo[2,3D]Pyrimidine Compounds

Described herein is pyrrolo{2,3-d}pyrimidine compounds, their use as Janus Kinase (JAK) inhibitors, pharmaceutical compositions containing this compounds, and methods for the preparation of these compounds