Acoustic records of the underwater soundscape at PALAOA with links to audio stream files, 2005-2011

Scientific background: Marine mammals use sound for communication, navigation and prey detection. Acoustic sensors therefore allow the detection of marine mammals, even during polar winter months, when restricted visibility prohibits visual sightings. The animals are surrounded by a permanent natural soundscape, which, in polar waters, is mainly dominated by the movement of ice. In addition to the detection of marine mammals, acoustic long-term recordings provide information on intensity and temporal variability of characteristic natural and anthropogenic background sounds, as well as their influence on the vocalization of marine mammals Scientific objectives: The PerenniAL Acoustic Observatory in the Antarctic Ocean (PALAOA, Hawaiian "whale") near Neumayer Station is intended to record the underwater soundscape in the vicinity of the shelf ice edge over the duration of several years. These long-term recordings will allow studying the acoustic repertoire of whales and seals continuously in an environment almost undisturbed by humans. The data will be analyzed to (1) register species specific vocalizations, (2) infer the approximate number of animals inside the measuring range, (3) calculate their movements relative to the observatory, and (4) examine possible effects of the sporadic shipping traffic on the acoustic and locomotive behaviour of marine mammals. The data, which are largely free of anthropogenic noise, provide also a base to set up passive acoustic mitigation systems used on research vessels. Noise-free bioacoustic data thereby represent the foundation for the development of automatic pattern recognition procedures in the presence of interfering sounds, e.g. propeller noise.

Holocene vegetation, fire and climate interactions in western Spain: El Maíllo mire

Interacciones entre la vegetación del Holoceno, el fuego y el clima en el oeste de España, ejemplo con datos de la turbera del Maíllo.

BALAÃO – O QUE OUVE AS PALAVRAS DE EL, TEM O CONHECIMENTO DE ELYON E VÊ A VISÃO DE SHADDAI: UM ESTUDO DE NÚMEROS 22-24

A presente pesquisa busca avaliar exegeticamente o texto que se encontra na Bíblia, especificamente no livro de Números capítulos 22-24 que relata sobre um personagem conhecido como Balaão. A pesquisa tem também como objeto o estudo sobre o panteão de divindades relatado no mesmo texto, assim como também o estudo dos textos descobertos em Deir Alla, na Jordânia, que apresentam um personagem designado como Balaão, possivelmente o mesmo personagem de Nm 22-24. A motivação que levou ao desenvolvimento dessa pesquisa foi o fato de se ter deparado com os conceitos dos diversos nomes divinos exibidos no texto, além da questão do profetismo fora de Israel, assim como as possibilidades hermenêuticas que se abrem para a leitura desse texto bíblico. O conceito geral sempre foi o de que Israel era a única nação onde existiam “verdadeiros” profetas e uma adoração a um único Deus, o “monoteísmo”. O que despertou interesse foi perceber, especialmente por meio da leitura dos livros bíblicos, que o profetismo não se restringiu somente a Israel. Ele antecede à formação do antigo Israel e já existia no âmbito das terras do antigo Oriente Médio, e que Israel ainda demorou muito tempo para ser monoteísta. Quem é esse Balaão, filho de Beor? Estudaremos sobre sua pessoa e sua missão. Examinaremos os textos de Deir Alla sobre Balaão e sua natureza de personagem mediador entre o divino e o humano. Esse personagem é apresentado como um grande profeta e que era famoso como intérprete de presságios divinos. Analisaremos a importante questão sobre o panteão de deuses que são apresentados na narrativa de Balaão nomeados como: El, Elyon Elohim e Shaddai, além de Yahweh. Entendemos, a princípio, que o texto possui uma conexão com a sociedade na qual foi criado e usando da metodologia exegética, faremos uma análise da narrativa em questão, buscando compreender o sentido do texto, dentro de seu cenário histórico e social. Cenário este, que nos apresentou esse profeta, não israelita, que profere bênçãos dos deuses sobre Israel e que, além disso, pronuncia maldições sobre os inimigos desse mesmo Israel. Percebemos que, parte do texto pesquisado é apresentado sob a ótica de Israel sobre as outras nações. A pesquisa defende, portanto, que o texto de Nm 22-24, além de nos apresentar um profeta fora de Israel igual aos profetas da Bíblia, defende que, o panteão de divindades também era adorado por Israel e que tais nomes são epítetos de uma mesma divindade, no caso YHWH. Defende, também, um delineamento de um projeto de domínio político e militar de Israel sobre as nações circunvizinhas.

Distinguishing surface effects of calcium ion from pore-occupancy effects in Na+ channels

The effects of calcium ion on the Na+ activation gate were studied in squid giant axons. Saxitoxin (STX) was used to block ion entry into Na+ channels without hindering access to the membrane surface, making it possible to distinguish surface effects of calcium from pore-occupancy effects. In the presence of STX, gating kinetics were measured from gating current (Ig). The kinetic effects of external calcium concentration changes were small when STX was present. In the absence of STX, lowering the calcium concentration (from 100 to 10 mM) slowed the closing of Na+ channels (measured from INa tails) by more than a factor of 2. Surprisingly, the voltage sensitivity of closing kinetics changed with calcium concentration, and it was modified by STX. Voltage sensitivity apparently depends in part on the ability of calcium to enter and block the channels as voltage is driven negative. In external medium with no added calcium, INa tail current initially increases in amplitude severalfold with the relief of calcium block, then progressively slows and gets smaller, as calcium diffuses out of the layers investing the axon. INa tails seen just before the current disappears suggest that closing in the absence of channel block is very slow or does not occur. INa amplitude and kinetics are completely restored when calcium is returned. The results strongly suggest that calcium occupancy is a requirement for channel closing and that nonoccupied channels fold reversibly into a nonfunctional conformation.

Cell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: A quantitative approach

The epithelial amiloride-sensitive sodium channel (ENaC) controls transepithelial Na+ movement in Na+-transporting epithelia and is associated with Liddle syndrome, an autosomal dominant form of salt-sensitive hypertension. Detailed analysis of ENaC channel properties and the functional consequences of mutations causing Liddle syndrome has been, so far, limited by lack of a method allowing specific and quantitative detection of cell-surface-expressed ENaC. We have developed a quantitative assay based on the binding of 125I-labeled M2 anti-FLAG monoclonal antibody (M2Ab*) directed against a FLAG reporter epitope introduced in the extracellular loop of each of the α, β, and γ ENaC subunits. Insertion of the FLAG epitope into ENaC sequences did not change its functional and pharmacological properties. The binding specificity and affinity (Kd = 3 nM) allowed us to correlate in individual Xenopus oocytes the macroscopic amiloride-sensitive sodium current (INa) with the number of ENaC wild-type and mutant subunits expressed at the cell surface. These experiments demonstrate that: (i) only heteromultimeric channels made of α, β, and γ ENaC subunits are maximally and efficiently expressed at the cell surface; (ii) the overall ENaC open probability is one order of magnitude lower than previously observed in single-channel recordings; (iii) the mutation causing Liddle syndrome (β R564stop) enhances channel activity by two mechanisms, i.e., by increasing ENaC cell surface expression and by changing channel open probability. This quantitative approach provides new insights on the molecular mechanisms underlying one form of salt-sensitive hypertension.

Dopamine receptor subtypes modulate olfactory bulb γ-aminobutyric acid type A receptors

The γ-aminobutyric acid type A (GABAA) receptor is the predominant Cl− channel protein mediating inhibition in the olfactory bulb and elsewhere in the mammalian brain. The olfactory bulb is rich in neurons containing both GABA and dopamine. Dopamine D1 and D2 receptors are also highly expressed in this brain region with a distinct and complementary distribution pattern. This distribution suggests that dopamine may control the GABAergic inhibitory processing of odor signals, possibly via different signal-transduction mechanisms. We have observed that GABAA receptors in the rat olfactory bulb are differentially modulated by dopamine in a cell-specific manner. Dopamine reduced the currents through GABA-gated Cl- channels in the interneurons, presumably granule cells. This action was mediated via D1 receptors and involved phosphorylation of GABAA receptors by protein kinase A. Enhancement of GABA responses via activation of D2 dopamine receptors and phosphorylation of GABAA receptors by protein kinase C was observed in mitral/tufted cells. Decreasing or increasing the binding affinity for GABA appears to underlie the modulatory effects of dopamine via distinct receptor subtypes. This dual action of dopamine on inhibitory GABAA receptor function in the rat olfactory bulb could be instrumental in odor detection and discrimination, olfactory learning, and ultimately odotopic memory formation.

Bimodal regulation of Na+–Ca2+ exchanger by β-adrenergic signaling pathway in shark ventricular myocytes

In shark heart, the Na+–Ca2+ exchanger serves as a major pathway for both Ca2+ influx and efflux, as there is only rudimentary sarcoplasmic reticulum in these hearts. The modulation of the exchanger by a β-adrenergic agonist in whole-cell clamped ventricular myocytes was compared with that of the Na+–Ca2+ exchanger blocker KB-R7943. Application of 5 μM isoproterenol and 10 μM KB-R7943 suppressed both the inward and the outward Na+–Ca2+ exchanger current (INa−Ca). The isoproterenol effect was mimicked by 10 μM forskolin. Isoproterenol and forskolin shifted the reversal potential (Erev) of INa−Ca by approximately −23 mV and −30 mV, respectively. An equivalent suppression of outward INa−Ca by KB-R7943 to that by isoproterenol produced a significantly smaller shift in Erev of about −4 mV. The ratio of inward to outward exchanger currents was also significantly larger in isoproterenol- than in control- and KB-R7943-treated myocytes. Our data suggest that the larger ratio of inward to outward exchanger currents as well as the larger shift in Erev with isoproterenol results from the enhanced efficacy of Ca2+ efflux via the exchanger. The protein kinase A-mediated bimodal regulation of the exchanger in parallel with phosphorylation of the Ca2+ channel and enhancement of its current may have evolved to satisfy the evolutionary needs for accelerated contraction and relaxation in hearts of animals with vestigial sarcoplasmic Ca2+ release stores.

Adeno-associated viral vector-mediated gene transfer results in long-term enzymatic and functional correction in multiple organs of Fabry mice

Fabry disease is a lysosomal storage disorder caused by a deficiency of the lysosomal enzyme α-galactosidase A (α-gal A). This enzyme deficiency leads to impaired catabolism of α-galactosyl-terminal lipids such as globotriaosylceramide (Gb3). Patients develop painful neuropathy and vascular occlusions that progressively lead to cardiovascular, cerebrovascular, and renal dysfunction and early death. Although enzyme replacement therapy and bone marrow transplantation have shown promise in the murine analog of Fabry disease, gene therapy holds a strong potential for treating this disease in humans. Delivery of the normal α-gal A gene (cDNA) into a depot organ such as liver may be sufficient to elicit corrective circulating levels of the deficient enzyme. To investigate this possibility, a recombinant adeno-associated viral vector encoding human α-gal A (rAAV-AGA) was constructed and injected into the hepatic portal vein of Fabry mice. Two weeks postinjection, α-gal A activity in the livers of rAAV-AGA-injected Fabry mice was 20–35% of that of the normal mice. The transduced animals continued to show higher α-gal A levels in liver and other tissues compared with the untouched Fabry controls as long as 6 months after treatment. In parallel to the elevated enzyme levels, we see significant reductions in Gb3 levels to near normal at 2 and 5 weeks posttreatment. The lower Gb3 levels continued in liver, spleen, and heart, up to 25 weeks with no significant immune response to the virus or α-gal A. Also, no signs of liver toxicity occurred after the rAAV-AGA administration. These findings suggest that an AAV-mediated gene transfer may be useful for the treatment of Fabry disease and possibly other metabolic disorders.

Single point mutations affect fatty acid block of human myocardial sodium channel α subunit Na+ channels

Suppression of cardiac voltage-gated Na+ currents is probably one of the important factors for the cardioprotective effects of the n-3 polyunsaturated fatty acids (PUFAs) against lethal arrhythmias. The α subunit of the human cardiac Na+ channel (hH1α) and its mutants were expressed in human embryonic kidney (HEK293t) cells. The effects of single amino acid point mutations on fatty acid-induced inhibition of the hH1α Na+ current (INa) were assessed. Eicosapentaenoic acid (EPA, C20:5n-3) significantly reduced INa in HEK293t cells expressing the wild type, Y1767K, and F1760K of hH1α Na+ channels. The inhibition was voltage and concentration-dependent with a significant hyperpolarizing shift of the steady state of INa. In contrast, the mutant N406K was significantly less sensitive to the inhibitory effect of EPA. The values of the shift at 1, 5, and 10 μM EPA were significantly smaller for N406K than for the wild type. Coexpression of the β1 subunit and N406K further decreased the inhibitory effects of EPA on INa in HEK293t cells. In addition, EPA produced a smaller hyperpolarizing shift of the V1/2 of the steady-state inactivation in HEK293t cells coexpressing the β1 subunit and N406K. These results demonstrate that substitution of asparagine with lysine at the site of 406 in the domain-1-segment-6 region (D1-S6) significantly decreased the inhibitory effect of PUFAs on INa, and coexpression with β1 decreased this effect even more. Therefore, asparagine at the 406 site in hH1α may be important for the inhibition by the PUFAs of cardiac voltage-gated Na+ currents, which play a significant role in the antiarrhythmic actions of PUFAs.

Climate forcings in the Industrial era

The forcings that drive long-term climate change are not known with an accuracy sufficient to define future climate change. Anthropogenic greenhouse gases (GHGs), which are well measured, cause a strong positive (warming) forcing. But other, poorly measured, anthropogenic forcings, especially changes of atmospheric aerosols, clouds, and land-use patterns, cause a negative forcing that tends to offset greenhouse warming. One consequence of this partial balance is that the natural forcing due to solar irradiance changes may play a larger role in long-term climate change than inferred from comparison with GHGs alone. Current trends in GHG climate forcings are smaller than in popular “business as usual” or 1% per year CO2 growth scenarios. The summary implication is a paradigm change for long-term climate projections: uncertainties in climate forcings have supplanted global climate sensitivity as the predominant issue.