Condiciones bio-oceanográficas en San José, islas Lobos de Afuera, Perú. 2010

En este estudio se muestra la variabilidad oceanográfica que se presenta en Lambayeque. Se evidenció con la generación del evento frío La Niña, después que se registrara el arribo de ondas Kelvin hacia la costa desde fines del 2009, lo que se llegó a considerar como la ocurrencia de un evento El Niño de intensidad moderada. Esta situación propició que los recursos pesqueros se ausentaran de sus áreas habituales de pesca, sumado a la presencia de oleajes anómalos y fuertes vientos que dificultaron las faenas de pesca. Durante el 2010, la Extensión Sur de la Corriente de Cromwell (ESCC) se presentó moderadamente fortalecida en marzo, evidenciada por la relativa alta concentración de oxígeno disuelto en las áreas más profundas de San José, situación inusual para la época en la zona. La proyección de la ESCC se vio intensificada en abril, pero comenzó a debilitarse en junio hasta ausentarse en noviembre, como se puede deducir de los valores de oxígeno encontrados cerca del fondo durante las prospecciones realizadas.

Uppbåds(1904-Krets)nämnderna 1881-1905 : krigskommisarier och sekreterare

Åke Backström

Solos do topo da Serra São José (Minas Gerais) e suas relações com o paleoclima no Sudeste do Brasil

A diversidade de ecossistemas do sudeste do Brasil nem sempre pode ser relacionada com fatores edáficos, geomorfológicos ou hidrológicos. Topos de elevações, onde os solos são caracterizados pela unicidade de material de origem, podem constituir ambiente especial para estudos de gênese de solos e datações de eventos cíclicos relacionados com a dinâmica do clima regional. Depois de um levantamento detalhado de solos no topo da Serra São José (Prados - Minas Gerais), dois perfis de solo (P1 e P2), originados de metarenitos da Formação Tiradentes e caracterizados por deposições sucessivas de camadas arenosas alternadas com camadas arenosas enriquecidas com matéria orgânica, foram estudados, com intuito de encontrar testemunhos de paleoambientes. O pequeno platô localiza-se a 1.350 m acima do nível de mar e 350 m acima do nível topográfico regional dominante. No P1, foram identificadas trinta e três camadas enriquecidas com matéria orgânica, alternadas com camadas de areia. Três camadas no P1 (20-30, 70-80 e 100-110 cm), com conteúdo de C orgânico respectivamente de 0.5, 7 e 1 dag kg-1, apresentam idades radiocarbônicas < 40, 180 ± 60 e 350 ± 80 anos AP, respectivamente, e taxas de deposição de 0,177 cm ano-1 entre 110 e 70 cm e de 0,357 cm ano-1 entre 70 e 20 cm de profundidade. No P2, as camadas enriquecidas com matéria orgânica são mais espessas (entre 10 e 130 mm) e apresentam descontinuidades abruptas. Situam-se entre 20-30, 80-90, 110-120 e 170-180 cm de profundidade, têm um conteúdo de C orgânico de 3, 2.5, 21 e 1.5 dag kg-1 e idade radiocarbônica de 3580 ± 80, 3750 ± 80, 21210 ± 180 e 24060 ± 130 anos AP, respectivamente. Suas taxas de deposição são de 0,352 cm ano-1, entre 20 e 80 cm; de 0,002 cm ano-1, entre 80 e 110 cm, e de 0,021 cm ano-1, entre 110 e 170 cm de profundidade. Nos dois perfis, a relação C/N aumenta com a profundidade e com a idade das camadas. Os teores de Ti e Zr, elementos de baixa mobilidade, são mais elevados nas camadas mais antigas dos perfis, enquanto o Cu e o Pb concentram-se nas camadas mais ricas em matéria orgânica. Um fragmento de planta de 5 cm de diâmetro e 62 cm de comprimento, situado na base de P2, foi datado de 32220 ± 290 anos AP e relacionado com o início da gênese deste perfil. Os solos do topo da Serra São José são formados a partir de metarenitos da Formação Tiradentes, sem aporte de materiais de outra litologia. A água pluvial é o principal fator que adiciona energia a este ambiente, relacionando os atributos dos solos com o clima. P1 é um solo holocênico (Neossolo Flúvico Psamítico típico), formado a partir de deposições episódicas de areia, alternadas com material enriquecido com matéria orgânica. A formação de P2 (Paleossolo) iniciou-se no Pleistoceno, prolongou-se até o Holoceno e a morfologia de suas camadas enterradas de turfa relaciona-se com a oscilação do espelho d'água de uma lagoa, decorrente de fases mais secas e mais úmidas do clima. As idades radiocarbônicas encontradas estão relacionadas com alternâncias climáticas pleistocênicas e holocênicas em P2 e holocênicas em P1. O perfil P2 está situado em um local propício para realização de estudos palinológicos, com intuito de identificar ecótipos que ocuparam a área a partir do Pleistoceno tardio, relacionando-os com os paleoclimas.

Anelasticidad de la zona estable euroasiática y de la zona europea occidental

La teoria de inversión en su forma estocastica ha sido aplicada a dos conjuntos de coeficientes de atenuación de las ondas de Rayleigh correspondientes a la zona estable Euroasiatica y a la zona Europea Occidental. Los resultados obtenidos muestran que las propiedades anelásticas bajo dichas zonas son distintas. Europa Occidental se halla caracterizada por valores mas bajos de los factores especificos de calidad de las ondas de cizalla(Qbeta) que los correspondientes a la zona Estable Euroasiática. Las profundiades a las que los valores de Qbeta decrecen más rápidamente son alrededorde 60 km para Europa Occidental y de 40 km para la zona Estable Euroasiática. La comparación con un estudio de atenuación en el Océano Atlántico muestra que los coeficientes de atenuación correspondientes a la zona Europea Occidental pueden ser considerados representativos para dicha zona.

Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding

Cellular prion protein (PrPC) is a glycosyl-phosphatidylinositol¿anchored glycoprotein. When mutated or misfolded, the pathogenic form (PrPSC) induces transmissible spongiform encephalopathies. In contrast, PrPC has a number of physiological functions in several neural processes. Several lines of evidence implicate PrPC in synaptic transmission and neuroprotection since its absence results in an increase in neuronal excitability and enhanced excitotoxicity in vitro and in vivo. Furthermore, PrPC has been implicated in the inhibition of N-methyl-D-aspartic acid (NMDA)¿mediated neurotransmission, and prion protein gene (Prnp) knockout mice show enhanced neuronal death in response to NMDA and kainate (KA). In this study, we demonstrate that neurotoxicity induced by KA in Prnp knockout mice depends on the c-Jun N-terminal kinase 3 (JNK3) pathway since Prnpo/oJnk3o/o mice were not affected by KA. Pharmacological blockage of JNK3 activity impaired PrPC-dependent neurotoxicity. Furthermore, our results indicate that JNK3 activation depends on the interaction of PrPC with postsynaptic density 95 protein (PSD-95) and glutamate receptor 6/7 (GluR6/7). Indeed, GluR6¿PSD-95 interaction after KA injections was favored by the absence of PrPC. Finally, neurotoxicity in Prnp knockout mice was reversed by an AMPA/KA inhibitor (6,7-dinitroquinoxaline-2,3-dione) and the GluR6 antagonist NS-102. We conclude that the protection afforded by PrPC against KA is due to its ability to modulate GluR6/7-mediated neurotransmission and hence JNK3 activation.

Involvement of Dab1 in APP processing and [beta]-amyloid deposition in sporadic Creutzfeldt-Jakob patients.

Alzheimer"s disease and prion pathologies (e.g., Creutzfeldt-Jakob disease) display profound neural lesions associated with aberrant protein processing and extracellular amyloid deposits. For APP processing, emerging data suggest that the adaptor protein Dab1 plays a relevant role in regulating its intracellular trafficking and secretase-mediated proteolysis. Although some data have been presented, a putative relationship between human prion diseases and Dab1/APP interactions is lacking. Therefore, we have studied the putative relation between Dab1, APP processing and Aβ deposition, targets in sCJD cases. Our biochemical results categorized two groups of sCJD cases, which also correlated with PrPsc types 1 and 2 respectively. One group, with PrPsc type 1 showed increased Dab1 phosphorylation, and lower βCTF production with an absence of Aβ deposition. The second sCJD group, which carried PrPsc type 2, showed lower levels of Dab1 phosphorylation and βCTF production, similar to control cases. Relevant Aβ deposition in the second sCJD group was measured. Thus, a direct correlation between Dab1 phosphorylation, Aβ deposition and PrPsc type in human sCJD is presented for the first time.

Regulation of GABA(A) and glutamate receptor expression, synaptic facilitation and long-term potentiation in the hippocampus of prion mutant mice

Background: Prionopathies are characterized by spongiform brain degeneration, myoclonia, dementia, and periodic electroencephalographic (EEG) disturbances. The hallmark of prioniopathies is the presence of an abnormal conformational isoform (PrP(sc)) of the natural cellular prion protein (PrP(c)) encoded by the Prnp gene. Although several roles have been attributed to PrP(c), its putative functions in neuronal excitability are unknown. Although early studies of the behavior of Prnp knockout mice described minor changes, later studies report altered behavior. To date, most functional PrP(c) studies on synaptic plasticity have been performed in vitro. To our knowledge, only one electrophysiological study has been performed in vivo in anesthetized mice, by Curtis and coworkers. They reported no significant differences in paired-pulse facilitation or LTP in the CA1 region after Schaffer collateral/commissural pathway stimulation. Principal Findings: Here we explore the role of PrP(c) expression in neurotransmission and neural excitability using wild-type, Prnp -/- and PrP(c)-overexpressing mice (Tg20 strain). By correlating histopathology with electrophysiology in living behaving mice, we demonstrate that both Prnp -/- mice but, more relevantly Tg20 mice show increased susceptibility to KA, leading to significant cell death in the hippocampus. This finding correlates with enhanced synaptic facilitation in paired-pulse experiments and hippocampal LTP in living behaving mutant mice. Gene expression profiling using Illumina microarrays and Ingenuity pathways analysis showed that 129 genes involved in canonical pathways such as Ubiquitination or Neurotransmission were co-regulated in Prnp -/- and Tg20 mice. Lastly, RT-qPCR of neurotransmission-related genes indicated that subunits of GABA(A) and AMPA-kainate receptors are co-regulated in both Prnp -/- and Tg20 mice. Conclusions/Significance: Present results demonstrate that PrP(c) is necessary for the proper homeostatic functioning of hippocampal circuits, because of its relationships with GABA(A) and AMPA-Kainate neurotransmission. New PrP(c) functions have recently been described, which point to PrP(c) as a target for putative therapies in Alzheimer's disease. However, our results indicate that a "gain of function" strategy in Alzheimer's disease, or a "loss of function" in prionopathies, may impair PrP(c) function, with devastating effects. In conclusion, we believe that present data should be taken into account in the development of future therapies.

State of Iowa : Something of its History, its Institutions, its Resources and Natural Advantages, Published by Iowa Commissioners to the Louisiana Purchase Exposition, 1904.

The Commissioners for the State of Iowa to the Louisisana Purchase Exposition believed it wise to place the facts contained in this booklet in the hands of Commissioners from other States and other Nations to be preserved as souvenirs of the year and the occasion which brought together at St. Louis the marvelous exhibition of the world's wealth. This booklet contains facts of Iowa and its citizens and history.

Neuroprotective role of PrPC against kainate-induced epileptic seizures and cell death depends on the modulation of JNK3 activation by GluR6/7-PSD-95 binding

Cellular prion protein (PrPC) is a glycosyl-phosphatidylinositol¿anchored glycoprotein. When mutated or misfolded, the pathogenic form (PrPSC) induces transmissible spongiform encephalopathies. In contrast, PrPC has a number of physiological functions in several neural processes. Several lines of evidence implicate PrPC in synaptic transmission and neuroprotection since its absence results in an increase in neuronal excitability and enhanced excitotoxicity in vitro and in vivo. Furthermore, PrPC has been implicated in the inhibition of N-methyl-D-aspartic acid (NMDA)¿mediated neurotransmission, and prion protein gene (Prnp) knockout mice show enhanced neuronal death in response to NMDA and kainate (KA). In this study, we demonstrate that neurotoxicity induced by KA in Prnp knockout mice depends on the c-Jun N-terminal kinase 3 (JNK3) pathway since Prnpo/oJnk3o/o mice were not affected by KA. Pharmacological blockage of JNK3 activity impaired PrPC-dependent neurotoxicity. Furthermore, our results indicate that JNK3 activation depends on the interaction of PrPC with postsynaptic density 95 protein (PSD-95) and glutamate receptor 6/7 (GluR6/7). Indeed, GluR6¿PSD-95 interaction after KA injections was favored by the absence of PrPC. Finally, neurotoxicity in Prnp knockout mice was reversed by an AMPA/KA inhibitor (6,7-dinitroquinoxaline-2,3-dione) and the GluR6 antagonist NS-102. We conclude that the protection afforded by PrPC against KA is due to its ability to modulate GluR6/7-mediated neurotransmission and hence JNK3 activation.