We report, in this paper, several findings about the swimming and attachment mechanisms of Giardia lamblia trophozoites. These data were collected using a combination of a high-contrast CytoViva imaging system and a particle image velocimetry camera, which can capture images at speeds greater than 800 frames/s. Using this system, we discovered that, during rapid swimming of Giardia trophozoites, undulations of the caudal region contributed to forward propulsion combined with the beating of the flagella pairs. It was also discovered, in contrast to previous studies with 10 times slower image sampling technique, that the anterior and posterolateral flagella beat with a clearly defined power stroke and not symmetrical undulations. During the transition from free swimming to attachment, trophozoites modified their swimming behavior from a rapid rotating motion to a more stable planar swimming. While using this planar swimming motion, the trophozoites used the flagella for propulsion and directional control. In addition to examination of the posterolateral and anterior flagella, a model to describe the motion of the ventral flagella was derived, indicating that the ventral flagella beat in an expanding sine wave. In addition, the structure of the ventrocaudal groove creates boundary conditions that determine the form of beating of the ventral flagella. The results from this study indicate that Giardia is able to simultaneously generate both ciliary beating and typical eukaryotic flagellar beating using different pairs of flagella.cell motility | cytoskeleton | swimming microorganism | ciliary and flagellar motion | bio-robotics

Therapeutic/care management study, level IV.

Mechanisms by which Pco2 controls cerebral vascular tone remain uncertain. We hypothesize that potassium channel activation contributes to the neonatal cerebrovascular dilation in response to increases in Paco2. To test this hypothesis, experiments were performed on newborn pigs with surgically implanted, closed cranial windows. Hypercapnia was induced by ventilation with elevated Pco2 gas in the absence and presence of the KATP channel inhibitor, glibenclamide and/or the KCa channel inhibitor, paxillin. Dilations to pinacidil, a selective KATP channel activator, without and with glibenclamide, were used to evaluate the efficacy of KATP channel inhibition. Dilations to NS1619, a selective KCa channel activator, without and with paxillin, were used to evaluate the efficacy of KCa channel inhibition. Cerebrovascular responses to the KATP and KCa channel activators, pinacidil and NS1619, respectively, cAMP‐dependent dilator, isoproterenol, and cGMP‐dependent dilator, sodium nitroprusside (SNP), were used to evaluate the selectivity of glibenclamide and paxillin. Glibenclamide blocked dilation to pinacidil, but did not inhibit dilations to NS1619, isoproterenol, or SNP. Glibenclamide prior to hypercapnia decreased mean pial arteriole dilation ~60%. Glibenclamide treatment during hypercapnia constricted arterioles ~35%. The level of hypercapnia, Paco2 between 50 and 75 mmHg, did not appear to be involved in efficacy of glibenclamide in blocking dilation to Paco2. Similarly to glibenclamide and KATP channel inhibition, paxillin blocked dilation to the KCa channel agonist, NS1619, and attenuated, but did not block, arteriolar dilation to hypercapnia. Treatment with both glibenclamide and paxillin abolished dilation to hypercapnia. Therefore, either glibenclamide or paxillin that block dilation to their channel agonists, pinacidil or NS1619, respectively, only partially inhibit dilation to hypercapnia. Block of both KATP and KCa channels completely prevent dilation hypercapnia. These data suggest hypercapnia activates both KATP and KCa channels leading to cerebral arteriolar dilation in newborn pigs.