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According to Dubet (2010), two hypotheses can be formulated to explain this paradox: the institutional hypothesis assumes that schools and teachers are still stuck in a male-dominated model where the division of roles is gendered.
Two hypothesis can be formulated to explain the correlation between the weak growth of H1N1 virus and the few changes of host transcription.
Two different, but not necessarily alternative hypotheses can be formulated to explain the involvement of ctsk in adipogenesis and in situations requiring increased adipose tissue plasticity, such as the postnatal period or feeding with HFD.
Two hypotheses can be formulated to explain host specificity: either it can be explained by the phylogenetic position of the strains, or by the association of virulence genes enabling a pathological convergence of phylogenically distant strains.
Various hypotheses can be formulated to explain the massive presence of contaminating pathological microorganisms in the gut flora.
Different hypotheses can be formulated to explain the lack of activity of the AtMYB60 and VvMYB60 promoters in seeds.
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New hypotheses can thus be formulated to explain the positive and negative training effects on performance.
Therefore, two hypotheses might be formulated to explain how a treatment can improve endothelial function in RA.
Rules of inference would be formulated to explain what one takes to be valid scientific reasoning, much as one might formulate deductive inference rules to explain valid inferences of mathematicians.
Other hypotheses could be formulated to explain the decrease of PON1 activity in PWS and non-PWS obese subjects.
The Differential Adhesion Hypothesis (DAH) was formulated to explain how the cell rearrangement and reorganization observed during the process of tissue self-assembly can be driven by tissue mechanical properties, i.e. cohesion, adhesion and surface tension [33], [34].
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