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Prion diseases are a family of progressive fatal neurodegenerative diseases of infectious, sporadic or inherited origin, which affect humans and other animals.
For ACC1-II-1 and DS1-II-2 whose parents' blood samples were available, pyrosequencing confirmed the absence of the alternative alleles in their parents, which suggested postzygotic but not inherited origin of the mutant pSNM alleles.
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Our study also clarifies that fascin protein is upregulated in precancerous lesions, of both inherited and sporadic origin.
This loosely refers to paternal and maternal strands but note that the assignment is entirely arbitrary and P/M are simply used to distinguish between the two paternal strands; i.e. the strands of grand-parental origin inherited from the sire.
This division of prokaryotes and eukaryotes in Figure 5, rather than the separation of the two groups, suggests that all eukaryote SiRs are either of prokaryotic origin, inherited from the progenitors of the mitochondrion and/or plastid, or that lateral gene transfers have occurred.
TSEs are characterized by abnormal deposits of a protease-resistant isoform of the host genome encoded prion protein (PrP) and are unique in that they can manifest through acquired, inherited, or sporadic origins [5].
TSEs are characterized by abnormal deposits of a protease-resistant isoform of the host genome encoded prion protein and are unique in that they can manifest through acquired, inherited, or sporadic origins [3].
Naturally occurring prion diseases may have acquired, inherited, or sporadic origins (i.e., no known environmental or genetic cause).
Many of the interactions between the sub-regions are inhibitory, which might be of V2 intra-cortical origin or inherited from V1 [17].
In 261 DMSs between MRC- and AM-iPS cells (MA-DMSs), 203 sites in AM-iPS cells and 165 in MRC-iPS cells showed no difference from their parental cells, suggesting that these sites in iPS cells are inherited from their tissue origin (Fig. 1E).
Two extreme possibilities implicate either a clonal origin with inherited molecular and phenotypic differences of oligo-or polymetastases, or sequential development of the metastatic process with oligometastases as an early but transient phase of polymetastatic disease (Fig. 1).
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