Tracer release experiments in the tropical North Atlantic

Lateral diffusivity is computed from a tracer release experiment in the northeastern tropical Atlantic thermocline. The uncertainties of the estimates are inferred from a synthetic particle release using a high-resolution ocean circulation model. The main method employed to compute zonal and meridional components of lateral diffusivity is the growth of the second moment of a cloud of tracer. The application of an areal comparison method for estimating tracer-based diffusivity in the field experiments is also discussed. The best estimate of meridional eddy diffusivity in the Guinea Upwelling region at about 300 m depth is estimated to be inline image m2 s-1. The zonal component of lateral diffusivity is estimated to be inline image m2 s-1, while areal comparison method yields areal equivalent zonal diffusivity component of inline image m2 s?1. In comparison to Ky, Kx is about twice larger, resulting from the tracer patch stretching by zonal jets. Employed conceptual jet model indicates that zonal jet velocities of about inline image m s?1 are required to explain the enhancement of the zonal eddy diffusivity component. Finally, different sampling strategies are tested on synthetic tracer release experiments. They indicate that the best sampling strategy is a sparse regular sampling grid covering most of the tracer patch.

Climatological observations from ship logbooks between 1750 and 1854 (release 2.1)

The Climatological Database for the World's Oceans: 1750-1854 (CLIWOC) project, which concluded in 2004, abstracted more than 280,000 daily weather observations from ships' logbooks from British, Dutch, French, and Spanish naval vessels engaged in imperial business in the eighteenth and nineteenth centuries. These data, now compiled into a database, provide valuable information for the reconstruction of oceanic wind field patterns for this key period that precedes the time in which anthropogenic influences on climate became evident. These reconstructions, in turn, provide evidence for such phenomena as the El Niño-Southern Oscillation and the North Atlantic Oscillation. Of equal importance is the finding that the CLIWOC database the first coordinated attempt to harness the scientific potential of this resource represents less than 10 percent of the volume of data currently known to reside in this important but hitherto neglected source.

Bond Modelling of prestressed concrete during the prestressing force release

This paper presents an analytical model for simulating the bond between steel and concrete, in precast prestressed concrete elements, during the prestressing force release. The model establishes a relationship between bond stress, steel and concrete stress and slip in such concrete structures. This relationship allows us to evaluate the bond stress in the transmission zone, where bond stress is not constant, along the whole prestressing force release process. The model is validated with the results of a series of tests and is extended to evaluate the transmission length. This capability has been checked by comparing the transmission length predicted by the model and one measured experimentally in a series of tests.

Bond modelling of prestressed concrete during the prestressing force release

This paper presents an analytical model for simulating the bond between steel and concrete, in precast prestressed concrete elements, during the prestressing force release. The model establishes a relationship between bond stress, steel and concrete stress and slip in such concrete structures. This relationship allows us to evaluate the bond stress in the transmission zone, where bond stress is not constant, along the whole prestressing force release process. The model is validated with the results of a series of tests, considering different steel indentation depths and concrete covers and is extended to evaluate the transmission length. This capability has been checked by comparing the transmission length predicted by the model and one measured experimentally in two series of tests.

An analytical model for simulating the bond of prestressed concrete during the prestressed force release

A bond analytical model is proposed in this paper. The model is capable of reproducing the bond stress developed between the steel and concrete, in precast prestressed elements, during the entire process of prestressing force release. The bond stress developed in the transmission zone, where the bond stress is not constant, is also obtained. The steel and concrete stresses as well as the slip between both materials can be also estimated by means of the relation established in the model between these parameters and the bond stress. The model is validated with the results of a series of tests, considering different steel indentation depths and concrete covers and it is extended to evaluate the transmission length. This has been checked by comparing the transmission length predicted by the model and one measured experimentally in two series of tests.

An analytical model for simulating the bond of prestressed concrete during the prestressed force release

A bond analytical model is proposed in this paper. The model is capable of reproducing the bond stress developed between the steel and concrete, in precast prestressed elements, during the entire process of prestressing force release. The bond stress developed in the transmission zone, where the bond stress is not constant, is also obtained. The steel and concrete stresses as well as the slip between both materials can be also estimated by means of the relation established in the model between these parameters and the bond stress. The model is validated with the results of a series of tests, considering different steel indentation depths and concrete covers and it is extended to evaluate the transmission length. This has been checked by comparing the transmission length predicted by the model and one measured experimentally in two series of tests.

Use of the energy-release rate in a 2 scale damage analysis of a bonded joint

Stress singularities appear at the extremities of an adhesive bond. They can produce a damage mechanism that we assimilate in this Note to a crack. The energy release rate permits to characterize its evolution. But a very refined mesh would be necessary for a real structure. Using an asymptotic method based on the small thickness of the bond a limit model with a different local behaviour is suggested. It leads to an approximation of the energy release rate

Mining mobile apps reviews to support release planning

The mobile apps market is a tremendous success, with millions of apps downloaded and used every day by users spread all around the world. For apps’ developers, having their apps published on one of the major app stores (e.g. Google Play market) is just the beginning of the apps lifecycle. Indeed, in order to successfully compete with the other apps in the market, an app has to be updated frequently by adding new attractive features and by fixing existing bugs. Clearly, any developer interested in increasing the success of her app should try to implement features desired by the app’s users and to fix bugs affecting the user experience of many of them. A precious source of information to decide how to collect users’ opinions and wishes is represented by the reviews left by users on the store from which they downloaded the app. However, to exploit such information the app’s developer should manually read each user review and verify if it contains useful information (e.g. suggestions for new features). This is something not doable if the app receives hundreds of reviews per day, as happens for the very popular apps on the market. In this work, our aim is to provide support to mobile apps developers by proposing a novel approach exploiting data mining, natural language processing, machine learning, and clustering techniques in order to classify the user reviews on the basis of the information they contain (e.g. useless, suggestion for new features, bugs reporting). Such an approach has been empirically evaluated and made available in a web-­‐based tool publicly available to all apps’ developers. The achieved results showed that the developed tool: (i) is able to correctly categorise user reviews on the basis of their content (e.g. isolating those reporting bugs) with 78% of accuracy, (ii) produces clusters of reviews (e.g. groups together reviews indicating exactly the same bug to be fixed) that are meaningful from a developer’s point-­‐of-­‐view, and (iii) is considered useful by a software company working in the mobile apps’ development market.

A mutation in the transmembrane/luminal domain of the ryanodine receptor is associated with abnormal Ca2+ release channel function and severe central core disease

Central core disease is a rare, nonprogressive myopathy that is characterized by hypotonia and proximal muscle weakness. In a large Mexican kindred with an unusually severe and highly penetrant form of the disorder, DNA sequencing identified an I4898T mutation in the C-terminal transmembrane/luminal region of the RyR1 protein that constitutes the skeletal muscle ryanodine receptor. All previously reported RYR1 mutations are located either in the cytoplasmic N terminus or in a central cytoplasmic region of the 5,038-aa protein. The I4898T mutation was introduced into a rabbit RYR1 cDNA and expressed in HEK-293 cells. The response of the mutant RyR1 Ca2+ channel to the agonists halothane and caffeine in a Ca2+ photometry assay was completely abolished. Coexpression of normal and mutant RYR1 cDNAs in a 1:1 ratio, however, produced RyR1 channels with normal halothane and caffeine sensitivities, but maximal levels of Ca2+ release were reduced by 67%. [3H]Ryanodine binding indicated that the heterozygous channel is activated by Ca2+ concentrations 4-fold lower than normal. Single-cell analysis of cotransfected cells showed a significantly increased resting cytoplasmic Ca2+ level and a significantly reduced luminal Ca2+ level. These data are indicative of a leaky channel, possibly caused by a reduction in the Ca2+ concentration required for channel activation. Comparison with two other coexpressed mutant/normal channels suggests that the I4898T mutation produces one of the most abnormal RyR1 channels yet investigated, and this level of abnormality is reflected in the severe and penetrant phenotype of affected central core disease individuals.

R-type Ca2+ currents evoke transmitter release at a rat central synapse

Voltage-dependent Ca2+ currents evoke synaptic transmitter release. Of six types of Ca2+ channels, L-, N-, P-, Q-, R-, and T-type, only N- and P/Q-type channels have been pharmacologically identified to mediate action-potential-evoked transmitter release in the mammalian central nervous system. We tested whether Ca2+ channels other than N- and P/Q-type control transmitter release in a calyx-type synapse of the rat medial nucleus of the trapezoid body. Simultaneous recordings of presynaptic Ca2+ influx and the excitatory postsynaptic current evoked by a single action potential were made at single synapses. The R-type channel, a high-voltage-activated Ca2+ channel resistant to L-, N-, and P/Q-type channel blockers, contributed 26% of the total Ca2+ influx during a presynaptic action potential. This Ca2+ current evoked transmitter release sufficiently large to initiate an action potential in the postsynaptic neuron. The R-type current controlled release with a lower efficacy than other types of Ca2+ currents. Activation of metabotropic glutamate receptors and γ-aminobutyric acid type B receptors inhibited the R-type current. Because a significant fraction of presynaptic Ca2+ channels remains unidentified in many other central synapses, the R-type current also could contribute to evoked transmitter release in these synapses.

Adenosine acts by A1 receptors to stimulate release of prolactin from anterior-pituitaries in vitro

Adenosine has been identified in the anterior pituitary gland and is secreted from cultured folliculostellate (FS) cells. To determine whether adenosine controls the secretion of anterior pituitary hormones in vitro, adenosine was incubated with anterior pituitaries. It stimulated prolactin (PRL) release at the lowest concentration used (10−10 M); the stimulation peaked at 10−8 M with a threefold increase in release and declined to minimal stimulation at 10−4 and 10−3 M. Follicle-stimulating hormone release was maximally inhibited at 10−8 M, whereas luteinizing hormone release was not significantly inhibited. Two selective A1 adenosine receptor antagonists (10−7 or 10−5 M) had no effect on basal PRL release, but either antagonist completely blocked the response to the most effective concentration of adenosine (10−8 M). In contrast, a highly specific A2 receptor antagonist (10−7 or 10−5 M) had no effect on basal PRL release or the stimulation of PRL release induced by adenosine (10−8 M). We conclude that adenosine acts to stimulate PRL release in vitro by activating A1 receptors. Since the A1 receptors decrease intracellular-free calcium, this would decrease the activation of nitric oxide synthase in the FS cells, resulting in decreased release of nitric oxide (NO). NO inhibits PRL release by activating guanylate cyclase that synthesizes cGMP from GTP; cGMP concentrations increase in the lactotrophs leading to inhibition of PRL release. In the case of adenosine, NO release from the FS cells decreases, resulting in decreased concentrations of NO in the lactotrophs, consequent decreased cGMP formation, and resultant increased PRL release.

Bradykinin inhibits M current via phospholipase C and Ca2+ release from IP3-sensitive Ca2+ stores in rat sympathetic neurons

A variety of intracellular signaling pathways can modulate the properties of voltage-gated ion channels. Some of them are well characterized. However, the diffusible second messenger mediating suppression of M current via G protein-coupled receptors has not been identified. In superior cervical ganglion neurons, we find that the signaling pathways underlying M current inhibition by B2 bradykinin and M1 muscarinic receptors respond very differently to inhibitors. The bradykinin pathway was suppressed by the phospholipase C inhibitor U-73122, by blocking the IP3 receptor with pentosan polysulfate or heparin, and by buffering intracellular calcium, and it was occluded by allowing IP3 to diffuse into the cytoplasm via a patch pipette. By contrast, the muscarinic pathway was not disrupted by any of these treatments. The addition of bradykinin was accompanied by a [Ca2+]i rise with a similar onset and time to peak as the inhibition of M current. The M current inhibition and the rise of [Ca2+]i were blocked by depletion of Ca2+ internal stores by thapsigargin. We conclude that bradykinin receptors inhibit M current of sympathetic neurons by activating phospholipase C and releasing Ca2+ from IP3-sensitive Ca2+ stores, whereas muscarinic receptors do not use the phospholipase C pathway to inhibit M current channels.