Sentence examples for pathogenic thresholds from inspiring English sources

A bacteriological sample was considered positive if bacteria isolated after culture were above the pathogenic thresholds following Cagle's microbiological criteria.

Numerous pathogenic mutations responsible for various mitochondrial diseases have been identified in mtDNA-encoded tRNA genes [ 1], and in most cases, such disease-causative heteroplasmic mutations (i.e., wild-type mtDNA and mutant mtDNA co-exist within a cell) exhibit their intrinsic pathogenic thresholds.

Although we did not obtain these iPSCs in this experiment, this might be because the fibroblasts derived from the patient carried a ratio of m.3243A>G mtDNA mutation above the pathogenic threshold level, which limited the proliferative ability of the cells, resulting in the failure of segregation of the heteroplasmic mtDNA.

The observed fluctuations in heteroplasmy levels could be due to the different reprogramming states of the cell lines, i.e., highly pluripotent iPSCs predominantly produce energy by anaerobic glycolysis and carry a high proportion of mutations, even above the pathogenic threshold level.

At the same time, a pathogenic threshold of ∼40 glutamines was observed in a large number of polyQ diseases like Huntington's disease or spinocerebellar ataxias [45].

Microbiological resolution (ie, absence of bacteria or their reduction below the pathogenic threshold) was assessed on D7.

Of these patients, 203 (71.0%) with baseline bacterial cultures at/above the pathogenic threshold in at least one eye were included in the MFAS.

Disease-causing CAGpolyQ-containing genes tend to be considered a homogeneous group in terms of their repeats, with an often-cited pathogenic threshold of about 35 glutamines.

The end result is a toxic buildup of protein aggregates and dysfunctional organelles until a pathogenic threshold is reached, resulting in neuronal cell death (Enquist et al., 2007).

Heterogeneous distribution of mitochondria with and without COX activity in single cells would be important for elucidating the reason why the pathogenic threshold load of ∆mtDNA in embryonic blood and liver was lower than that in other tissues.

This may suggest that Mef2 is a unique modifier of either polyleucine or CUG repeat RNA pathogenesis (or both), or that a critical pathogenic threshold was not reached in the flies expressing expanded CAG repeats.