Genetic KCa3.1-deficiency produces locomotor hyperactivity and alterations in cerebral monoamine levels.

PLoS One · 2012 · PMC3471871 · PMID 23077667

Europe PMC DOI

hedged sentences

0.0640

closest p · 1.3× alpha

0.0900

boldest claim

The sentences

a clear trendP = 0.064so close (0.05 < p ≤ 0.1)

Even though there was a clear trend, the ratio of center time/perimeter time for KCa3.2 T/T mice was not statistically different from that of KCa3.1 −/− /KCa2.3 T/T mice (P = 0.064; Figure 2G ).

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showed a trendP = 0.065so close (0.05 < p ≤ 0.1)

However, after exclusion of the KCa3.2 T/T mice with less than 20 entries, alteration rates appeared normal in the KCa3.2 T/T mice (P = 0.81) while DOX-treated KCa3.1 −/− /KCa3.2 T/T mice showed a trend towards decreased alteration rates compared to DOX-treated KCa3.2 T/T (P = 0.065; Figure 3E ).

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did not reach statistical significanceP = 0.09so close (0.05 < p ≤ 0.1)

However, there was a trend for DOX treatment to reduce the grip strength in KCa3.1 −/− /KCa2.3 T/T mice ( Figure 3C ), even though the difference did not reach statistical significance (P = 0.09).

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