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Examining GHS-R1a constitutive activity, receptor desensitisation and resensitisation kinetics, and the pharmacological consequences of selective GHS-R1a activation in peripheral tissues including cardiac, hepatic, and immune cell models where distinguishing GHS-R1a-specific from prolactin and cortisol-mediated biology is critical for mechanistic interpretation

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Behavioural data were evaluated by two-way ANOVA with a Bonferroni post hoc test

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