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This anatomical progression supports the prion-like propagation hypothesis [ 3, 16, 26, 31] and the dual-hit hypothesis of alpha-synuclein [ 41, 42] where pathology starts in the olfactory bulb and spreads towards the basal forebrain region (Fig. 5).
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Experimental results show single image layout recovery performance and the improvement obtained with the propagation of the hypothesis through the image sequence.
Chosen wave functions are encoded into computer-mediated feedback essential to atomic clocks, including clocks that step computers through their phases of computation and clocks in space vehicles that supply evidence of signal propagation explained by hypotheses of spacetimes with metric tensor fields.
In a more general context, the present observation suggests heterozygote advantage in clonal propagation as an interesting hypothesis to test in future studies, when asexual reproduction is associated with unusually large degrees of haplotype diversity (see also [ 21]).
Therefore, interacting contiguous alpha-synuclein molecules, which we demonstrate are not only present in human brain tissues but strongly associated with disease, would be a necessary although by no means a sufficient step for disease propagation according to this hypothesis.
However, the fact that PrPres generated in vitro was associated with approximately 10 times less infectivity than an equivalent quantity of brain-derived PrPSc casts doubt on the "protein-only" hypothesis of prion propagation and backs theories that suggest there are additional molecular species of infectious PrP or other agent-associated factors.
In this paper, we assume that agents individually face abductive or inductive tasks in a globally coherent environment, and we show that general mechanisms can be designed that abstractly regard both cases as special instances of a problem of hypothesis refinement through propagation.
In addition to a hypothesis of indirect propagation of PrPSc into the CNS, various combinations of clinical manifestations and brain lesions may influence the symptoms of dCJD patients.
Under the hypothesis of two propagation fronts, as shown in Fig. 1, the outermost front would correspond the tumor cells, [ T] (GBM in our case of study).
Within the protein -only hypothesis of prion propagation prion strains are thought to be encoded by distinct pathogenic PrP conformations or assembly states.
Within the framework of the protein-only hypothesis of prion propagation, the distinct clinical and neuropathological phenotypes that distinguish prion strains are thought to be determined by the propagation of PrPSc isoforms with divergent physicochemical properties [ 1, 2, 7– 12].
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