Sentence examples for lifespan defects from inspiring English sources

Recent findings in yeast indicate that deletion of Cld1-mediated deacylation rescues growth and lifespan defects in tafazzin-deficient cells [ 53, 54].

No lifespan defects were observed upon hMGS-9A(D) expression in TH neurons (mean survival = 29.2, n = 60, p = 0.232, maximum survival = 41 days, Fig 3B).

The resulting phenotypes include lethality or reduced lifespan, defects in axogenesis and neurite branching, altered synaptic morphology, axon and neuron degeneration, astrogliosis, defective fat metabolism, impaired motor behavior and cognitive deficits (11, 14).

In contrast, pan-neuronal overexpression of Drosophila GS (dGS), which has low sequence similarity to hMGS, was not able to induce glycogen accumulation or cause lifespan defects (mean survival = 34.9, n = 62, p = 0.233, maximum survival = 50 days) when compared to control GFP-expressing flies (mean survival = 36.1, n = 75, maximum survival = 56 days, Supporting Information Fig 2).

On Lemmon's sprawling farm, Chinese visitors learn how to take meticulous records: of the size of a litter, pig weights over their lifespan, genetic defects, and types of feed eaten, with varying amounts of corn, soybean meal, and vitamins.

Drosophila parkin knockout mutants exhibited reduced lifespan, locomotor defects resulting from apoptotic muscle degeneration and male sterility.

Indeed, a focused screen of pharmacological compounds that ameliorated the dnj-14 lifespan and neuronal defects identified the polyphenolic molecule resveratrol, which has been shown to be neuroprotective in a range of animal neurodegeneration models [71].

"Escaper" adults display sterility, shortened lifespan, and locomotion defects [24].

In this study, we first presented not only the behavioral abnormalities but also the shortened lifespan and ultrastructural defects of muscles in flies with mutations in rt and/or tw, the Drosophila orthologs of human POMT1 and POMT2, respectively.

Developing erythroid cells thus became abnormal before the reduced lifespan or other defects of mutant RBCs became consequential, indicating that impaired erythroid cell maturation is a primary cause of anemia upon Sox6 inactivation.

Does ecdysone supplementation rescue the extended larval lifespan and NMJ defects?