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These mechanisms could explain why application of increasing mechanical treatment intensity for longer physical stability against coalescence is accompanied by hindered shelf-life of resulting low size vitamin-loaded particles formed in protein-stabilised nanoemulsions.
According to Elder and Lubotsky (2009), two potential mechanisms could explain why later entrants outperform their peers.
However, none of these three mechanisms could explain the abnormal activation behavior observed at electrodes prepared at 600 °C in CH3OH solution.
At least two possible mechanisms could explain this result.
Several mechanisms could explain this transition in WUE.
Two major mechanisms could explain the TrkB-dependent Ret activation.
Several conjugative-dependent mechanisms could explain the formation of tandem SGI1 arrays.
One or both of these mechanisms could explain the autoinhibition observed in intersectin-1L.
Different mechanisms could explain the existence of a sub-populations susceptible to carcinoma.
However, neither of these two mechanisms could explain the behaviour of both U1A and U1C Arabidopsis proteins.
Several possible mechanisms could explain how post-translational modification of Adr1 may regulate promoter binding and transcription activation.
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