1,616 research outputs found

    Meroplankton in Jørgen Brønlund Fjord, North Greenland

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    Meroplanktonic larvae of at least 42 species of bottom invertebrates in Jørgen Brønlund Fjord, North Greenland (82°10'N, 30°30'W) are described with respect to species identification, occurrence, reproduction, development, growth, settlement, and relations to depth, light, hydrography, and primary production. A few Holoplankters and some "pseudoplanktonic" nematodes are included. The occurrence of such a large number of species with pelagic larvae does not invalidate "Thorson's rule" of 1950, stating that the number of species having pelagic larval development decreases, as one moves from the equator to the pole, but it does lead to a less strict interpretation of it. Several species have lecithotrophic pelagic development. The short period of primary production, however meager, seems vital to many of the planktotrophic larvae, in promoting growth and settling, although the spawning of many species is not strictly linked to this period. Larvae of Hiatella striata (Fleuriau) seem able to live in the plankton for a year, even surviving the long, dark winter

    The annual cycle of phytoplankton primary production and hydrography in the Disko Bugt area, West Greenland

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    The distribution and size of phytoplankton production and biomass in relation to physical and chemical parameters in the upper 50 m at Godhavn and in Kangikerdlak in the inner part of Disko Fjord was investigated through 2½ years (1973-75). Some data from other parts of Disko Bugt are presented. In both locations the hydrography alternates between an unstable winter situation with isothermal (-1.75°C) and isohaline (33.5-34.0‰) conditions throughout, and a highly stable summer situation when dilution and heating, especially of the upper 20- 30 m, raise the temperature at the surface to 9.9°C and at 50 m to 3.8°C at Godhavn, and to 12°C and 3.5°C respectively in Kangikerdlak. Salinities drop correspondingly to 30.6‰ in Kangikerdlak. The 1% depth for green light is greatly reduced beneath ice and snow. During the ice free period at Godhavn it varies from 12 m during the spring phytoplankton bloom to more than 60 m from Oct. through the winter. In Kangikerdlak the 1% depth reaches only 40 m in winter, and outflowing turbid fresh water creates I% depths of as little as 4-5 m in June-Aug. At Godhavn NO3-N reaches highs of 10.05 μgat /liter and 10.15 μgat /liter at 0 and 50 m respectively in winter, whereas during the summer, depletion to less than 0.01 μgat /liter occurs in the upper 40 m and to 1.0 μgat / liter at 50 m. PO4-P is similarly reduced from 0.8 μgat/liter and 1.1 μgat/liter to less than 0.01 μgat / liter in the upper 20 m and to 0.21 μgat /liter at 50 m. The N:P ratio drops from 13 to less than 0.01 in the upper 30 m and to 1.0 at 50 m. In Kangikerdlak depletion of NO3-N is similar to conditions at Godhavn, whereas PO4-P reaches a low of 0.1 μgat/liter only, while in mid summer it reaches 1.88 μgat /liter at the surface, giving an N:P ratio which is below 0.1 in the upper 5 m only. At Godhavn primary production is about 90 gC • m-2 • yr-1  (75-104 g) with a maximum of about 5 .5 gC • m-3 • yr-1   at 5- 10 m, whereas in Kangikerdlak production was concentrated near the surface with about 6.0 gC • m-3 • yr-1and a total of 35 gC • m-2 • yr-1 at most. Production at Jacobshavn off the glacier fjord is probably greater than at Godhavn, whereas at Christianshilb and Egedesminde it is definitely lower. Phytoplankters larger than 56 μ contribute about 50% of annual and up to 90% of daily production. Due to the great stability, production usually extends no deeper than compensation depth, and most of the chlorophyll is usually in the nutrient rich water below this depth, where it sinks, is consumed, or degrades into phaeopigment. P/B is highest where there is least chlorophyll. Light reduces production in the upper 5-10 m, and inhibition may extend to 30 m. Correlations between production, P/B, or P/8 / light and nutrients reveal possible saturation values of 0.08-0. 78 μgal NO3-N /liter and 0.17-0.22 μgat PO4-P/liter. PO4-P seems to be the limiting nutrient in some cases, although NO3-N is most quickly and thoroughly depleted. Dark fixation at Godhavn is about 24 gC • m-2 • yr-1, and at Kangikerdlak about 15 gC • m-2 • yr-1. 55-60% of dark fixation is presumed to be biotic and 16-64% is associated with particulate matter larger than 56 μ. Although oxygen is never at a minimum in Disko Bugt, saturation as well as absolute 0 2 values and pH show profiles in the bay that clearly reflect the high degree of stratification compared to waters south of the bay

    The annual cycle of temperature, salinity, currents and water masses in Disko Bugt and adjacent waters, West Greenland

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    All available data on bathymetry, temperature, salinity and currents up until and including 1975 are used in describing the seasonal changes and dynamics of the hydrography of Disko Bugt, the Vaigat and adjacent glacier and non glacier fjords. From a winter situation with well mixed -1.75°C cold water in the upper c. 100 m steep halo-and thermoclines develop during the summer between freshened and heated surface water leaving Disko Bugt and deeper more saline water entering from the West Greenland Current. Huge ice bergs have a decisive cooling effect upon the upper 150-200 m affecting the outflowing current as well as the inflowing water which is responsible for the high bottom temperatures and salinities (up to 3.5°C and 34-34.5‰ at 300-500 m) found the year round, and which contributes to raising the temperature in the upper 200 m in the summer, especially in the southern and eastern part of the bay and even into the Vaigat. Surface temperatures reach 12°C in the offshore waters of the bay where salinities may drop to 30‰, and inshore in the more diluted waters of Disko Fjord temperatures may even reach 14°C, whereas in the glacier fjords, where surface salinities come close to zero, 4°C is the highest temperature recorded and subzero temperatures are found even in July. An extensive upwelling of W Greenland water occurs in the northern part of the bay during the summer and fall and similar phenomena occur in Disko Fjord, driven by winds and apparently linked to tidal rhythms. Although TS diagrams show that deep Disko Bugt water and Baffin Bay water is of common origin, no water seems to enter Disko Bugt from Baffin Bay or from the Baffin Current

    Extending invariant complex structures

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    We study the problem of extending a complex structure to a given Lie algebra g, which is firstly defined on an ideal h of g. We consider the next situations: h is either complex or it is totally real. The next question is to equip g with an additional structure, such as a (non)-definite metric or a symplectic structure and to ask either h is non-degenerate, isotropic, etc. with respect to this structure, by imposing a compatibility assumption. We show that this implies certain constraints on the algebraic structure of g. Constructive examples illustrating this situation are shown, in particular computations in dimension six are given.Comment: 22 pages, plus an Addendu

    Central activation of alpha7 nicotinic signaling attenuates lps-induced neuroinflammation and sickness behavior in adult but not in aged animals

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    We previously reported that lipopolysaccharide (LPS) challenge caused microglial-mediated neuroinflammation and sickness behavior that was amplified in aged mice. As α7 nAChRs are im-plicated in the “Cholinergic anti-inflammatory pathway”, we aimed to determine how α7 nAChR stimulation modulates microglial phenotype in an LPS-induced neuroinflammation model in adult and aged mice. For this, BALB/c mice were injected intraperitoneally with LPS (0.33 mg/kg) and treated with the α7 nAChR agonist PNU282987, using different administration protocols. LPS challenge reduced body weight and induced lethargy and social withdrawal in adult mice. Peripheral (intraperitoneal) co-administration of the α7 nAChR agonist PNU282987 with LPS, attenuated body weight loss and sickness behavior associated with LPS challenge in adult mice, and reduced microglial activation with suppression of IL-1β and TNFα mRNA levels. Furthermore, central (intracerebroven-tricular) administration of the α7 nAChR agonist, even 2 h after LPS injection, attenuated the decrease in social exploratory behavior and microglial activation induced by peripheral administration of LPS, although this recovery was not achieved if activation of α7 nAChRs was performed peripherally. Finally, we observed that the positive results of central activation of α7 nAChRs were lost in aged mice. In conclusion, we provide evidence that stimulation of α7 nAChR signaling reduces microglial activation in an in vivo LPS-based model, but this cholinergic-dependent regulation seems to be dysfunctional in microglia of aged mice.This work was supported by the Spanish Ministry of Science, innovation and Universities Ref. SAF2015-63935-R and Ref. RTI2018-095793-B-I00 and General Council for Research and Innovation of the Community of Madrid and European Structural Funds Ref. B2017/BMD–3827–NRF24ADCM to M.G.L. Aging studies were supported by an NIA grant (R01-AG-033028) to J.P.G

    A more Tubulocentric View of Diabetic Kidney Disease

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    Diabetic nephropathy (DN) is a common complication of Diabetes Mellitus (DM) Types 1 and 2, and prevention of end stage renal disease (ESRD) remains a major challenge. Despite its high prevalence, the pathogenesis of DN is still controversial. Initial glomerular disease manifested by hyperfiltration and loss of glomerular size and charge permselectivity may initiate a cascade of injuries, including tubulo-interstitial disease. Clinically, ‘microalbuminuria’ is still accepted as an early biomarker of glomerular damage, despite mounting evidence that its predictive value for DN is questionable, and findings that suggest the proximal tubule is an important link in the development of DN. The concept of ‘diabetic tubulopathy’ has emerged from recent studies, and its causative role in DN is supported by clinical and experimental evidence, as well as plausible pathogenetic mechanisms. This review explores the ‘tubulocentric’ view of DN. The recent finding that inhibition of proximal tubule (PT) glucose transport (via SGLT2) is nephro-protective in diabetic patients is discussed in relation to the tubule’s potential role in DN. Studies with a tubulocentric view of DN have stimulated alternative clinical approaches to the early detection of diabetic kidney disease. There are tubular biomarkers considered as direct indicators of injury of the proximal tubule (PT), such as N-acetyl-β-D-glucosaminidase, Neutrophil Gelatinase-Associated Lipocalin and Kidney Injury Molecule-1, and other functional PT biomarkers, such as Urine free Retinol-Binding Protein 4 and Cystatin C, which reflect impaired reabsorption of filtered proteins. The clinical application of these measurements to diabetic patients will be reviewed in the context of the need for better biomarkers for early DN

    A new bond fluctuation method for a polymer undergoing gel electrophoresis

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    We present a new computational methodology for the investigation of gel electrophoresis of polyelectrolytes. We have developed the method initially to incorporate sliding motion of tight parts of a polymer pulled by an electric field into the bond fluctuation method (BFM). Such motion due to tensile force over distances much larger than the persistent length is realized by non-local movement of a slack monomer at an either end of the tight part. The latter movement is introduced stochastically. This new BFM overcomes the well-known difficulty in the conventional BFM that polymers are trapped by gel fibers in relatively large fields. At the same time it also reproduces properly equilibrium properties of a polymer in a vanishing filed limit. The new BFM thus turns out an efficient computational method to study gel electrophoresis in a wide range of the electric field strength.Comment: 15 pages, 11 figure

    Dent disease: A window into calcium and phosphate transport

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    This review examines calcium and phosphate transport in the kidney through the lens of the rare X-linked genetic disorder Dent disease. Dent disease type 1 (DD1) is caused by mutations in the CLCN5 gene encoding ClC-5, a Cl- /H+ antiporter localized to early endosomes of the proximal tubule (PT). Phenotypic features commonly include low molecular weight proteinuria (LMWP), hypercalciuria, focal global sclerosis and chronic kidney disease; calcium nephrolithiasis, nephrocalcinosis and hypophosphatemic rickets are less commonly observed. Although it is not surprising that abnormal endosomal function and recycling in the PT could result in LMWP, it is less clear how ClC-5 dysfunction disturbs calcium and phosphate metabolism. It is known that the majority of calcium and phosphate transport occurs in PT cells, and PT endocytosis is essential for calcium and phosphorus reabsorption in this nephron segment. Evidence from ClC-5 KO models suggests that ClC-5 mediates parathormone endocytosis from tubular fluid. In addition, ClC-5 dysfunction alters expression of the sodium/proton exchanger NHE3 on the PT apical surface thus altering transcellular sodium movement and hence paracellular calcium reabsorption. A potential role for NHE3 dysfunction in the DD1 phenotype has never been investigated, either in DD models or in patients with DD1, even though patients with DD1 exhibit renal sodium and potassium wasting, especially when exposed to even a low dose of thiazide diuretic. Thus, insights from the rare disease DD1 may inform possible underlying mechanisms for the phenotype of hypercalciuria and idiopathic calcium stones

    Kinesins relocalize the chromosomal passenger complex to the midzone for spindle disassembly.

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    Mitotic spindle disassembly after chromosome separation is as important as spindle assembly, yet the molecular mechanisms for spindle disassembly are unclear. In this study, we investigated how the chromosomal passenger complex (CPC), which contains the Aurora B kinase Ipl1, swiftly concentrates at the spindle midzone in late anaphase, and we researched the role of this dramatic relocalization during spindle disassembly. We showed that the kinesins Kip1 and Kip3 are essential for CPC relocalization. In cells lacking Kip1 and Kip3, spindle disassembly is severely delayed until after contraction of the cytokinetic ring. Purified Kip1 and Kip3 interact directly with the CPC and recruit it to microtubules in vitro, and single-molecule experiments showed that the CPC diffuses dynamically on microtubules but that diffusion stops when the CPC encounters a Kip1 molecule. We propose that Kip1 and Kip3 trap the CPC at the spindle midzone in late anaphase to ensure timely spindle disassembly

    Extinction times in the subcritical stochastic SIS logistic epidemic

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    Many real epidemics of an infectious disease are not straightforwardly super- or sub-critical, and the understanding of epidemic models that exhibit such complexity has been identified as a priority for theoretical work. We provide insights into the near-critical regime by considering the stochastic SIS logistic epidemic, a well-known birth-and-death chain used to model the spread of an epidemic within a population of a given size NN. We study the behaviour of the process as the population size NN tends to infinity. Our results cover the entire subcritical regime, including the "barely subcritical" regime, where the recovery rate exceeds the infection rate by an amount that tends to 0 as NN \to \infty but more slowly than N1/2N^{-1/2}. We derive precise asymptotics for the distribution of the extinction time and the total number of cases throughout the subcritical regime, give a detailed description of the course of the epidemic, and compare to numerical results for a range of parameter values. We hypothesise that features of the course of the epidemic will be seen in a wide class of other epidemic models, and we use real data to provide some tentative and preliminary support for this theory.Comment: Revised; 34 pages; 6 figure
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