Transmissible spongiform encephalopathies (TSEs) or prion diseases are unique disorders that are not caused by infectious micro-organisms (bacteria or fungi), viruses or parasites, but rather seem to be the result of an infectious protein. TSEs are comprised of fatal neurodegenerative disorders affecting both human and animals. Prion diseases cause sponge-like degeneration of neuronal tissue and include (among others) Creutzfeldt–Jacob disease in humans, bovine spongiform encephalopathy (BSE) in cattle and scrapie in sheep. TSEs are characterized by the formation and accumulation of transmissible (infectious) disease-associated protease-resistant prion protein (PrPSc), mainly in tissues of the central nervous system. The exact molecular processes behind the conversion of PrPC into PrPSc are not clearly understood. Correlations between prion protein polymorphisms and disease have been found, however in what way these polymorphisms influence the conversion processes remains an enigma; is stabilization or destabilization of the prion protein the basis for a higher conversion propensity? Apart from the disease-associated polymorphisms of the prion protein, the molecular processes underlying conversion are not understood. There are some notions as to which regions of the prion protein are involved in refolding of PrPC into PrPSc and where the most drastic structural changes take place. Direct interactions between PrPC molecules and/or PrPSc are likely at the basis of conversion, however which specific amino acid domains are involved and to what extent these domains contribute to conversion resistance/sensitivity of the prion protein or the species barrier is still unknown. 相似文献
The objective was to determine the critical N dilution curve of linseed, which is the minimal total N concentration in shoots necessary to produce the maximal shoot dry matter, and to explain possible differences with other C3 species. One main experiment was carried out in 1998/1999 on winter linseed with four levels of fertilizer N. Two plant densities were also studied, the recommended one (600 seeds m−2) and the minimum for canopy closure (150 seeds m−2), in order to investigate the stability with plant density of the critical N dilution curve. Shoot dry weights (WS) and shoot N contents expressed in percentage (NS) were measured for the determination of the critical dilution curve, along with organ N percentages and relative weights. The results of four other experiments were used to validate the critical N dilution curve. Three of these four trials were conducted on winter linseed (one in 1996/1997 and two in 1997/1998) with five levels of fertilizer N, and one on spring linseed in 1999 with six levels of fertilizer N.
The critical N dilution curve of linseed was different from those of other C3 species. The curve was steeper, indicating a greater decrease in the critical shoot N concentration (NSC) as the critical shoot dry weight (WSC) increased. This linseed curve determined with the data of the main experiment was relevant when compared to the data of the four other experiments. Organ weight ratios and N concentration of organs were investigated in a fertilizer N treatment resulting in NS close to the critical N values, NSC. In this treatment, the decrease in NS was the result of both a decrease in the N percentage of all organs and a decrease in the leaf weight ratio. The difference between linseed and other C3 species was mainly due to an acceleration of the dilution of N when leaf emission stopped and the flower bud emission began. At this stage of development, the leaf weight ratio of linseed was less than that of wheat, resulting in lower NS. For a given WS, no significant differences in NS, organ N percentages nor organ weight ratios were observed between the two plant densities. This indicates that the difference between linseed and other C3 species could not result from very high plant densities in linseed. Hence, it is concluded that the linseed N accumulation in shoot is different from other C3 species. 相似文献