Given its non-spherical nature, we argue that the Galactic centre excess is not a dark-matter phenomenon but rather associated with the stellar population of the Galactic bulge and the nuclear bulge.
This study suggests that there is a decrease in the diversity of species over time, uncorrelated with changes in oceanographic patterns, but rather associated with the increasing number of seismic surveys.
This pattern or response in which subjects tend to reset after longer gaps was reported previously [5], [14] [17], [30], [36] and suggests that the run/stop/reset rules are not associated with the responses (i.e., pressing on the 3 levers), but rather associated with specific clocks.
In contrast, recent evidence suggests that AFAP1L1 does not bind strongly to Src, but rather associates with cortactin, and that AFAP1L1 and cortactin colocalize within the invadopodia 12.
Importantly, we show that H3.3 is not found in the core of H3K9me3-enriched chromatin domains, but rather associates with the periphery (Additional file 2).
In contradiction of this model, Campbell and Desai (2013) recently described a truncated form of budding yeast Sli15, which does not accumulate at centromeres but rather associates with microtubules and chromatin, yet is proficient for tension-sensing and chromosome biorientation.
These observations suggest that the Q 10 increase may not be associated with the voltage-sensor movement (as reflected by the Q-V curve) but rather associated with the activation gate opening (as reflected by the G-V curve), that is, instead of the C→C′ transition, it seemed to be the C′→O transition that yielded the Q 10 increase.
Our estimates based on the continuation of forest management practice documented during 2000 2009 (Fig. 2) suggest that most of these potential KP-CP2 forest credits do not reflect a genuine change in management, but are rather associated with the high projected harvest rates assumed at the time of setting the reference level (2011), and which have in fact not yet materialized.
Taken together, overexpression of CTGF in cardiomyocytes did not induce fibrosis neither in murine nor in rat hearts, but was rather associated with hypertrophic changes at the cellular level.
Utilizing various mutants that induce melanotic capsule formation and also a real immune challenge provided by parasitic wasps, we show that the acute expression of the ADGF-A protein is not driven by one specific signaling cascade but is rather associated with the behavior of immune cells during the general inflammatory response.
