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Nfe2 mutant pups showed significantly reduced (p = 0.0027, n = 4) Gli1-GFP positive cells (A′ ).

Post-mortem analysis of mutant pups showed no milk in the stomach, thus indicating that their death might be due to a neurological phenotype impairing suckling.

Typically, recovered wild-type pups had suckled (55/84), whereas only 4/46 (11.5%) Cdkn1c mutant pups showed evidence of milk in their stomach (Fig. 1B).

Kaplan-Meier survival curve of 20 mutant pups showed that 50% of mice died within 5 d after birth (Fig. 3 C) with no survivors after P11.

Since mutant pups showed important neurological abnormalities due to bilirubin neurotoxicity, we determined whether gene therapy was enough to prevent that damage.

Similar(55)

In addition, no difference was observed in synaptic function between the wild type and SMA neurons in culture, in spite of several studies with mutant pups showing reduced excitability in the axon terminals, impaired synaptic vesicle release and neurotransmission failures at neuromuscular synapses [16], [23], [24].

As a result, all the data loggers attached to pups showed negative attachment angles.

PND15 normal pups showed a biphasic pain response with a concentration of 2% formalin injection.

Weight gain (normalized to BW) from nursing was significantly higher in OdLp pups compared to LdLp pups, while LdOp pups showed decreased intake compared to OdOp pups (both F>5.03, p<0.05, Figure 5d).

Their pups showed much the same responses to PBBs as did the original group of pups.

The litter was normal size (14 pups; another litter had the same number of pups) and the pups showed no gross anatomical abnormalities.

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