Verordeningen voor het Nederlandsch-Israëlietisch Kerkgenootschap : Verzameling uitg. op last der Centrale Commissie ... . Met aanteekeningen en alphabetisch register

door D. M. Sluys

Die Centrale der "Societatii Sionistilor din Romînia", (S. Pineles, Galatz) gibt folgende Ortsgruppen ihres Verbandes bekannt

Societatii Sionistilor din Romînia / Zentrale

Die Centrale der "Societatii Sionistilor din Romînia", (S. Pineles, Galatz) gibt folgende Ortsgruppen ihres Verbandes bekannt : (Fortsetzung)

Societatii Sionistilor din Romînia / Zentrale

A travers l'Afrique centrale du Congo au Niger : 1892 - 1893

par C. Maistre

Società e paesaggi nelle campagne dell’Italia Centrale : un’evoluzione senza ritorno

En la segunda mitad del novecientos las zonas rurales de Italia Central Romagna, Marche, Umbria e Toscana) registraron transformaciones sociales, económicas y paisajísticas, profundas e irreversibles. En este período, a la crisis agrícola posbélica y al éxodo rural, se sumó la crisis de la aparcería, que desapareció oficialmente con posterioridad en los años sesenta. La consolidación de la conducción directa de las propiedades rurales con asalariados, la difusión de la mecanización sobre las tierras de colinas y la urbanización de las poblaciones rurales, hicieron mutar la sociedad; comenzando por la familia, que dejó de ser extensa y solamente agrícola. Nacieron formas productivas híbridas entre tradición e innovación; entre agricultura e industria (agricultores a tiempo parcial, trabajadores a domicilio, proveedores de servicios a las pequeñas fincas agrícolas) y entre agricultura y actividades terciarias (agroturismo). La casa rural, abandonada primero, fue después transformada en segunda vivienda por parte de los citadinos, también provenientes del norte de Europa. Nacieron nuevos paisajes extensivos (cerealeros) que confinaron a reducidas áreas el antiguo paisaje rural definido por la forma de aparcería.

Deficits in memory and hippocampal long-term potentiation in mice with reduced calbindin D28K expression.

The influx of calcium into the postsynaptic neuron is likely to be an important event in memory formation. Among the mechanisms that nerve cells may use to alter the time course or size of a spike of intracellular calcium are cytosolic calcium binding or "buffering" proteins. To consider the role in memory formation of one of these proteins, calbindin D28K, which is abundant in many neurons, including the CA1 pyramidal cells of the hippocampus, transgenic mice deficient in calbindin D28K have been created. These mice show selective impairments in spatial learning paradigms and fail to maintain long-term potentiation. These results suggest a role for calbindin D28K protein in temporally extending a neuronal calcium signal, allowing the activation of calcium-dependent intracellular signaling pathways underlying memory function.

Expression of calbindin-D28K in motoneuron hybrid cells after retroviral infection with calbindin-D28K cDNA prevents amyotrophic lateral sclerosis IgG-mediated cytotoxicity.

Calbindin-D28K and/or parvalbumin appear to influence the selective vulnerability of motoneurons in amyotrophic lateral sclerosis (ALS). Their immunoreactivity is undetectable in motoneurons readily damaged in human ALS, and in differentiated motoneuron hybrid cells [ventral spinal cord (VSC 4.1 cells)] that undergo calcium-dependent apoptotic cell death in the presence of ALS immunoglobulins. To provide additional evidence for the role of calcium-binding proteins in motoneuron vulnerability, VSC 4.1 cells were infected with a retrovirus carrying calbindin-D28K cDNA under the control of the promoter of the phosphoglycerate kinase gene. Differentiated calbindin-D28K cDNA-infected cells expressed high calbindin-D28K and demonstrated increased resistance to ALS IgG-mediated toxicity. Treatment with calbindin-D28K antisense oligodeoxynucleotides, which significantly decreased calbindin-D28K expression, rendered these cells vulnerable again to ALS IgG toxicity.

Regulation of excitatory transmission at hippocampal synapses by calbindin D28k.

Distinct subpopulations of neurons in the brain contain one or more of the Ca(2+)-binding proteins calbindin D28k, calretinin, and parvalbumin. Although it has been shown that these high-affinity Ca(2+)-binding proteins can increase neuronal Ca2+ buffering capacity, it is not clear which aspects of neuronal physiology they normally regulate. To investigate this problem, we used a recently developed method for expressing calbindin D28k in the somatic and synaptic regions of cultured hippocampal pyramidal neurons. Ninety-six hours after infection with a replication-defective adenovirus containing the calbindin D28k gene, essentially all cultured hippocampal pyramidal neurons robustly expressed calbindin D28k. Our results demonstrate that while calbindin D28k does not alter evoked neurotransmitter release at excitatory pyramidal cell synapses, this protein has a profound effect on synaptic plasticity. In particular, we show that calbindin D28k expression suppresses posttetanic potentiation.