As ROS have short diffusion lengths due to their high reactivity, one might hypothesize that ROS created by the construct react primarily within their local protein-bound environment, thereby causing less damage to the host cell at large.
Because of apparent overlap in cognitive processes required for relational thinking and mental computation, one might hypothesize that instruction that targets fluency in mental computation would enhance children's conceptions of the equal sign and their relational thinking more generally.
Consequently, one might hypothesize that altered levels or function of ARNTL may contribute to hypertension and type 2 diabetes via mechanisms related to disturbed sleep and mood.
With regard to the final item, we might hypothesize that first time transplant recipients may be more clinically urgent or more likely to have an undiagnosed immuno-incompatability than repeat transplant patients.
In this sense, we might hypothesize that mitochondrial genetic background could be one of these host genetic factors determining the response to Neisseria meningitides infection and the individual course of meningococcal disease.
Since NT2 cells are EC cells which are derived from a restricted embryonic/neonatal precursor cell developed in an adult niche one might hypothesize that expression of GFAP in theses adult-derived cancerous stem cells may occur.
One might hypothesize that LeX positive cells from the cortex and spinal cord would be essentially similar, while LeX negative cells would be fundamentally different, as indicated by their differential neurosphere-forming capacity.
The observed correlation between empathic concern and rightward attentional bias may be interpreted in this context; one might hypothesize that empathic concern is not possible when one is feeling threatened.
Altogether, we might hypothesize that hypoglycemia is of clinical relevance in more than one aspect.
Based on this result, we might hypothesize that apoptosis and organ damage were induced by these inflammatory mediators.
One might hypothesize that rather than shedding light on protein features, our results are caused by those prediction mistakes.
