CS16Counter-Strike 1.6 (game)
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In addition, five CS14 embryos, three CS16 embryos, two CS17 embryos, and two CS19 embryos were obtained.
Three-dimensional (3D) reconstructions of serial sections of three embryos from CS14 to CS16 were performed using AMIRA software version 5.2 (AMIRA International Limited, Australia) to display the morphological differences in the embryonic hearts.
At CS16, septation of the OFT was initiated [Figure 5]a, [Figure 5]b, [Figure 5]c, [Figure 5]d, [Figure 5]e.
At CS19, in the aorta and the pulmonary trunk wall, more a-SMA-positive cells were observed than at CS16 [Figure 5]b, [Figure 5]d and [Figure 6]a, [Figure 6]b, [Figure 6]c.
From CS16, the cushion is shortened as the distal margin of the OFT myocardium regresses compared to that at CS15.
At CS16, the OFT is shortened and is still composed of nonmyocardial and myocardial portions.
Anderson demonstrated that in human embryos, the protrusion forms in the dorsal wall of the aortic sac between aortic arch arteries 4 and 6 and partitions the distal portion of the OFT.[5] In this study, at CS16, the protrusion extended into the nonmyocardial portion of the OFT and septated it into the aorta and pulmonary trunk.
This means that the arterial wall consists of endothelium and mesenchyme at CS16. Waldo confirmed that the second heart field progenitor cells migrate and differentiate into the a-SMA-positive smooth muscle cells of the two arteries.[22] Our data indicate that after aortopulmonary septation, the number of a-SMA-positive cells surrounding the endothelium increases gradually in the arterial wall, thus supporting smooth muscle formation in the arterial tunica media.
Se destaca que el polimorfismo CS16 analizado en el presente estudio es el unico al que se le pudo demostrar un sustento biologico in silico que concuerda con un fenotipico previamente reportado.