欧洲联盟步入新世纪时所面临的问题

欧洲一体化运动兴起以来，欧洲联盟面临一第列严重的问题，其中台刀约的修订，欧共体成员国扩大而引起的矛盾，与高生活水平同时存在的高失业率等。由此说明，欧盟的组织结构已不适应新形势的需要，需对其进行彻底“检修”。     

Organization of cell assemblies in the hippocampus

Neurons can produce action potentials with high temporal precision. A fundamental issue is whether, and how, this capability is used in information processing. According to the 'cell assembly' hypothesis, transient synchrony of anatomically distributed groups of neurons underlies processing of both external sensory input and internal cognitive mechanisms. Accordingly, neuron populations should be arranged into groups whose synchrony exceeds that predicted by common modulation by sensory input. Here we find that the spike times of hippocampal pyramidal cells can be predicted more accurately by using the spike times of simultaneously recorded neurons in addition to the animals location in space. This improvement remained when the spatial prediction was refined with a spatially dependent theta phase modulation. The time window in which spike times are best predicted from simultaneous peer activity is 10-30 ms, suggesting that cell assemblies are synchronized at this timescale. Because this temporal window matches the membrane time constant of pyramidal neurons, the period of the hippocampal gamma oscillation and the time window for synaptic plasticity, we propose that cooperative activity at this timescale is optimal for information transmission and storage in cortical circuits.     

Conformations of amino acids calculated from molecular orbital theory

Zusammenfassung Die Konformation einiger natürlicher Aminosäuren wird auf Grund einer erweiterten Hückel-Molekular-Orbital-Theorie berechnet.

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Recipient of a Public Health Service Research Career Development Award No. AM1159.     

Effects of long-term feeding of glibenclamide on normal rats

Summary Prolonged administration of glibenclamide decreased blood sugar, liver glycogen and protein and increased liver and serum lipids and organic phosphates of liver in normal rats. A significant weight increase observed in glibenclamide group of rats is attributed to lipid accumulation.     

The nature of DNA synthesis by isolated nuclei from cells of a rat tumour

Summary The DNA synthetic activity of nuclei isolated from a solid rat tumour was determined. The nuclei had DNA synthetic properties similar to nuclei from other sources but the time course of the reactions was different.     

Algebraic formulae for the Moon,Saturn and Jupiter in the Pancasiddhantika

Summary The daily motion of the Moon, and the synodic arcs and periods of Saturn and Jupiter are derived from the algebraic formulae given in the Pancasiddhantika.     

Mutations in UBQLN2 cause dominant X-linked juvenile and adult-onset ALS and ALS/dementia

Amyotrophic lateral sclerosis (ALS) is a paralytic and usually fatal disorder caused by motor-neuron degeneration in the brain and spinal cord. Most cases of ALS are sporadic but about 5-10% are familial. Mutations in superoxide dismutase 1 (SOD1), TAR DNA-binding protein (TARDBP, also known as TDP43) and fused in sarcoma (FUS, also known as translocated in liposarcoma (TLS)) account for approximately 30% of classic familial ALS. Mutations in several other genes have also been reported as rare causes of ALS or ALS-like syndromes. The causes of the remaining cases of familial ALS and of the vast majority of sporadic ALS are unknown. Despite extensive studies of previously identified ALS-causing genes, the pathogenic mechanism underlying motor-neuron degeneration in ALS remains largely obscure. Dementia, usually of the frontotemporal lobar type, may occur in some ALS cases. It is unclear whether ALS and dementia share common aetiology and pathogenesis in ALS/dementia. Here we show that mutations in UBQLN2, which encodes the ubiquitin-like protein ubiquilin?2, cause dominantly inherited, chromosome-X-linked ALS and ALS/dementia. We describe novel ubiquilin?2 pathology in the spinal cords of ALS cases and in the brains of ALS/dementia cases with or without UBQLN2 mutations. Ubiquilin?2 is a member of the ubiquilin family, which regulates the degradation of ubiquitinated proteins. Functional analysis showed that mutations in UBQLN2 lead to an impairment of protein degradation. Therefore, our findings link abnormalities in ubiquilin?2 to defects in the protein degradation pathway, abnormal protein aggregation and neurodegeneration, indicating a common pathogenic mechanism that can be exploited for therapeutic intervention.