During a train of work-loop contractions, the downstream hook and glass connecting rod are required to move upstream, repeatedly, to allow the muscle to shorten.
Phosphorylated STAT3 was evident in SCs 4 h after lengthening contraction, and the downstream genes, cyclin D1 and SOCS3 were significantly elevated 24 hours after the intervention.
Then, we defined two possible scenarios: gene 2 contracted or elongated, depending on whether the next in-frame start codon occurred downstream (gene contraction) or upstream (gene elongation) of the original (and disrupted) start codon, respectively.
In addition, the passage of a packet of ICG-laden lymph through ROI 66 to the ALN is represented by intensity peaks as shown in Fig. 2C, reflecting the contractile assembly upstream emptying (contraction) and the subsequent downstream filling (relaxation).
As shown in Fig. 6D, if we define Δt1 and Δt2 as the time delays between the fluorescence maxima or the onset of contraction of upstream and downstream regions of interest (i.e. Δt1 = tpeak ROI 30) - tpeak ROI 1) and Δt2 = tpeak ROI 91) - tpeak ROI 40)), we find negative values of Δt1 over the entire period of imaging, indicating that the contractions in ROI 30 preceded those in upstream ROI 1.
A possible limitation of our approach was that contraction-induced phosphorylation of downstream targets of CaMKII, was not assessed.
The elevated calcium initiates sarcomere shortening, that is, excitation-contraction coupling, and produces downstream effects on gene regulation, that is, excitation-transcription coupling [ 2– 5].
Furthermore, details of the droplet dynamics along downstream of the contraction have been explored as well to depict deformation, retraction and/or breakup of the droplet.
At the site of the atheroma rupture, platelet-released T×A2 leads to downstream micro-vessel contraction and thrombus propagation (7).
