"A L C L A D" A New Corrosion Resistant Aluminum Product

Described here is a new corrosion resistant aluminum product which is markedly superior to the present strong alloys. Its use should result in greatly increased life of a structural part. Alclad is a heat-treated aluminum, copper, manganese, magnesium alloy that has the corrosion resistance of pure metal at the surface and the strength of the strong alloy underneath. Of particular importance is the thorough character of the union between the alloy and the pure aluminum. Preliminary results of salt spray tests (24 weeks of exposure) show changes in tensile strength and elongation of Alclad 17ST, when any occurred, to be so small as to be well within the limits of experimental error. Some surface corrosion of the pure metal had taken place, but not enough to cause the specimens to break through those areas

The Politics of Income Distribution in Colombia

Paper by Robert H. Di

Polypus of the Iris

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Sperm competition in mated first generation hermaphrodite females of the HP 88 strain of Heterorhabditis (Nematoda : Heterorhabditidae) and progeny sex ratios in mated and unmated females

Nous avons utilisé un mutant "obèse" pour étudier le processus de la fécondation chez #Heterorhabditis. Nous avons observé que, chez les femelles hermaphrodites de première génération inséminées, les spermatozoïdes provenant du mâle possèdent un avantage dans leur compétition avec les spermatozoïdes provenant de la femelle hermaphrodite elle-même. Les observations en microscopie optique ont montré qu'il n'y a pas de spermathèque chez les femelles hermaphrodites de première génération et que les spermatozoïdes introduits sont stockés dans la partie proximale de l'ovotestis où ils se mélangent avec les spermatozoïdes d'origine hermaphrodite. Les spermatozoïdes introduits ont des pseudopodes bien développés et paraissent plus actifs que les spermatozoïdes d'origine hermaphrodite. Les femelles amphimictiques de deuxième génération possèdent une spermathèque où sont stockés les spermatozoïdes introduits, et non dans la partie proximale de l'ovaire ou de l'utérus. La proportion des sexes dans la descendance croisée de femelles tant hermaphrodites qu'amphimictiques varie de 2,2 à 6,6 mâles pour mille descendants, chiffres très différents du rapport 1/1 qui aurait pu être attendu dans la descendance croisée de mâles hétérogamiques. Des mâles, en proportion 20 à 30 fois supérieure, ont été observés dans la descendance d'hermaphrodites autofécondés. Ainsi, l'origine des spermatozoïdes, suivant qu'ils proviennent de mâles ou d'individus hermaphrodites, influencent nettement la proportion des sexes de la descendance chez la souche HP 88 d'#Heterorhabditis. (Résumé d'auteur

Breeding for biofuel production

Tese de doutoramento em Ciências Farmacêuticas, na especialidade de Biologia Celular e Molecular, apresentada à Faculdade de Farmácia da Universidade de CoimbraAs sinapses excitatórias são estruturas dinâmicas e a forma como neurónios vizinhos comunicam entre si é ajustada consoante a actividade neuronal. A esta propriedade chama-se plasticidade sináptica e a nível molecular está correlacionada com a aprendizagem e a memória. A potenciação sináptica de longa duração (LTP) é a forma de plasticidade sináptica mais estudada sendo definida como um fortalecimento duradouro na comunicação entre neurónios vizinhos desencadeado pela actividade neuronal. Pelo contrário, a depressão sináptica de longa duração (LTD) é caracterizada por uma diminuição duradoura da potência sináptica. Alterações moleculares nos mecanismos de plasticidade sináptica estão na base de muitas doenças neurológicas e psiquiátricas. Algumas das modificações sinápticas ao nível estrutural, bioquímico e funcional associadas com a plasticidade sináptica requerem a traducão de mRNAs (RNA mensageiros) localizados nas dendrites, resultando em alterações no proteoma sináptico. Várias evidências mostram que a síntese proteica em dendrites desempenha um papel fundamental em várias formas de plasticidade sináptica, incluindo a LTP mediada pelo BDNF (factor neurotrófico derivado do cérebro). Contudo, pouco se sabe sobre a identidade dos mRNA que são traduzidos ao nível da sinapse em resposta ao BDNF e sobre os mecanismos de regulação envolvidos. Além disso, também está ainda por esclarecer de que modo muitas das alterações no proteoma sináptico contribuem para os fenómenos de plasticidade sináptica. Neste trabalho investigámos o papel da Pyk2 (cinase de resíduos de tirosina rica em prolina do tipo 2) na mediação dos efeitos do BDNF na sinapse. A Pyk2 é uma cinase de resíduos de tirosina pertencente à família das FAK (cinases de adesão focal), que desempenha uma grande variedade de funções no sistema nervoso central, incluindo o control da LTP e da LTD por mecanismos que envolvem a regulação dos receptores NMDA (N-metil-D-aspartato). Além disso, pensa-se que esta cinase desempenha um papel importante na remodelação da arquitectura das espículas sinápticas e da arborização dendritica, induzidas pela actividade neuronal. Observámos que a Pyk2 é traduzida ao nível da sinapse e acumulada nas densidades pós-sinápticas de neurónios do hipocampo após a estimulação com BDNF. A acumulação dendritica da Pyk2 em resposta à estimulação com BDNF requer a participação da RBP (proteína que liga RNA), hnRNPK (ribonucleoproteína nuclear heterogénea do tipo K). Estas observações estão de acordo com os resultados anteriores do nosso laboratório mostrando que: (i) a hnRNPK é acumulada nas dendrites dos neurónios do hipocampo após o estimulação com BDNF; (ii) a ligação do mRNA da Pyk2 à hnRNPK é regulada por BDNF. Usando um protocolo químico para aumentar a actividade neuronal e induzir LTP também observámos que a Pyk2 se acumula na sinapse por um mecanismo dependente de BDNF. A principal função da Pyk2 ao nível da densidade pós-sináptica tem sido associada à regulação das correntes mediadas pelos recetores NMDA através da interação direta com a Src, outra cinase de resíduos de tirosina. Neste estudo, observámos que o tratamento com BDNF aumenta a expressão superficial dos receptores NMDA que contêm a subunidade GluN2B, ao nível da sinapse, por um mecanismo dependente da síntese proteica. De acordo com estas observações, observou-se que a estimulação com BDNF aumenta os níveis de Pyk2 fosforilada/activada de forma específica ao nível da sinapse, o que sugere uma regulação diferencial da atividade da cinase. O aumento dos níveis sinápticos dos recetores NMDA induzido pelo BDNF também depende da Pyk2 e da sua actividade de cinase. Por outro lado, também se observou que em condições de repouso a manutenção na membrana celular dos recetores NMDA contendo subunidades GluN2B depende da atividade de cinase da Pyk2. Finalmente, a sobreexpressão da Pyk2 em neurónios do hipocampo foi suficente para mimetizar os efeitos do BDNF na expressão superficial dos receptores NMDA que contêm a subunidade GluN2B. No seu conjunto, os resultados mostram que o BDNF induz a activação/acumulação da Pyk2 por um mecanismo que envolve a hnRNPK e a síntese dendritica da Pyk2, resultando num aumento da expressão superfical dos receptores NMDA que contêm a subunidade GluN2B. Este mecanismo pode mediar os efeitos do BDNF nos défices cognitivos que são característicos de certas doenças do cérebro.Excitatory synapses are dynamic entities and adjust their strength depending on the activity. This property is named synaptic plasticity and is considered the cellular correlate of learning and memory. Long-term potentiation (LTP) is the best studied form of synaptic plasticity and by definition it is considered as an activity-induced sustained increase in synaptic strength. Long-term depression (LTD) is the opposite form of plasticity, and is characterized by an activity-induced sustained decrease in synaptic strength. Alterations in the molecular basis of synaptic plasticity events underlie several neurological and psychiatric disorders. Some of the structural, biochemical and functional modifications of the synapse associated with synaptic plasticity require translation of dendritic-localized mRNAs, with concomitant alterations in the synaptic proteome. Multiple lines of evidence show that dendritic protein synthesis plays a key role in several forms of synaptic plasticity, including in brain-derived neurotrophic factor (BDNF)-mediated LTP. However, the identity of the mRNAs that are synaptically translated in response to BDNF and the regulatory mechanisms involved are poorly understood. Furthermore, how these changes in the proteome contribute to the plastic alterations of the synapse also remains to be uncovered. In this work, we investigated a role for Pyk2 (proline-rich tyrosine kinase 2) as a mediator of the effects of BDNF at the synapse. Pyk2 is a non-receptor tyrosine kinase, belonging to the FAK (focal adhesion kinase) family of proteins, which plays a wide range of functions in the central nervous system (CNS), including the control of LTP and LTD by mechanisms involving the regulation of NMDA (N-methyl-D-aspartate) receptors. Furthermore, this kinase is thought to play an important role in the activity-induced remodeling of spine architecture and dendritic arborization. We found that the protein kinase Pyk2 is synaptically translated in hippocampal neurons and accumulates at post-synaptic density following BDNF treatment. The dendritic accumulation of Pyk2 upon stimulation with BDNF requires the participation of the RNA-binding protein hnRNPK (heterogeneous nuclear ribonucleoprotein K). This is in accordance with previous results from our laboratory showing that (i) hnRNPK is accumulated in dendrites of hippocampal neurons upon BDNF treatment and (ii) the binding of Pyk2 mRNA to hnRNPK is regulated by BDNF. Using a chemical protocol to increase neuronal activity and to induce LTP, we also observed that Pyk2 accumulates at the synapse by a mechanism requiring BDNF. The main function of Pyk2 at the post-synaptic compartment has been attributed to the regulation of NMDA receptor currents through a direct interaction with a different tyrosine kinase, Src. Herein we found that BDNF treatment increases the surface expression of GluN2B-containing NMDA receptors (NMDAR) at synapses, by a mechanism dependent on protein synthesis. In agreement with these observations, the levels of phosphorylated/activated Pyk2 were specifically enhanced at the synapse upon BDNF treatment, suggesting a compartment-specific regulation of Pyk2 activity by BDNF. The BDNF-induced increase on surface NMDARs also requires Pyk2 and its kinase activity. The maintenance of basal levels of GluN2B-containing NMDAR at the cell surface was also dependent on Pyk2 kinase activity. Finally, overexpression of Pyk2 in hippocampal neurons was sufficient, per se, to mimic the BDNF-induced increase in GluN2B-NMDAR surface expression. Taken together, the results show that BDNF induces synaptic activation/accumulation of Pyk2 by a mechanism involving hnRNPK and dendritic Pyk2 synthesis, resulting in an enhancement in the surface levels of GluN2B-containing NMDAR. This mechanism may mediate the effects of BDNF on synaptic plasticity and may constitute a novel therapeutic target to restore the cognitive deficits characteristic of some brain disorders.FCT - SFRH/BD/80332/201

Modern pollution signals in sediments from Windermere, NW England, determined by micro-XRF and lead isotope analysis

High resolution geochemical (Itrax micro-XRF and wavelength dispersive XRF) data, radiochronology (210Pb and 137Cs analyses) and ultra-high precision double-spike lead isotope measurements from lacustrine sediment cores are used in combination with historical research of former mining landscapes to investigate modern pollution signals in sediments from Windermere, the largest lake in the English Lake District. The sediment record suggests that while most element concentrations have been stable, there has been a significant increase since the 1930s in lead, zinc and copper concentrations. Double-spike lead isotope measurements reveal a mixture of natural lead, and three major contributory sources of anthropogenic (industrial) lead, comprising gasoline lead, coal combustion lead (from coal-fired steam ships) and lead derived from Carboniferous Pb–Zn mineralisation (mining activities). A number of up-system sediment traps have limited the amount of mining related heavy metals entering Windermere, and as a result, periods of metal workings do not correlate with peaks in heavy metals. Increases could also be due to flood-induced metal inwash or weathering of bedrock in the catchment. Application of these non-destructive and high precision analytical techniques provides new insights into the pollutant depositional history of Windermere

A 500 year sediment lake record of anthropogenic and natural inputs to Windermere (English Lake District) using double-spike lead isotopes, radiochronology, and sediment microanalysis

A high-resolution record of pollution is preserved in recent sediments from Windermere, the largest lake in the English Lake District. Data derived from X-ray core scanning (validated against wavelength dispersive X-ray fluorescence), radiochronological techniques (210Pb and 137Cs) and ultrahigh precision, double-spike mass spectrometry for lead isotopes are combined to decipher the anthropogenic inputs to the lake. The sediment record suggests that while most element concentrations have been stable, there has been a significant increase in lead, zinc, and copper concentrations since the 1930s. Lead isotope down-core variations identify three major contributory sources of anthropogenic (industrial) lead, comprising gasoline lead, coal combustion lead (most likely source is coal-fired steam ships), and lead derived from Carboniferous Pb–Zn mineralization (mining activities). Periods of metal workings do not correlate with peaks in heavy metals due to the trapping efficiency of up-system lakes in the catchment. Heavy metal increases could be due to flood-induced metal inwash after the cessation of mining and the weathering of bedrock in the catchment. The combination of sediment analysis techniques used provides new insights into the pollutant depositional history of Windermere and could be similarly applied to other lake systems to determine the timing and scale of anthropogenic inputs