Reliability of 3D Depth Motion Sensors for Capturing Upper Body Motions and Assessing the Quality of Wheelchair Transfers.

Wheelchair users must use proper technique when performing sitting-pivot-transfers (SPTs) to prevent upper extremity pain and discomfort. Current methods to analyze the quality of SPTs include the TransKinect, a combination of machine learning (ML) models, and the Transfer Assessment Instrument (TAI), to automatically score the quality of a transfer using Microsoft Kinect V2. With the discontinuation of the V2, there is a necessity to determine the compatibility of other commercial sensors. The Intel RealSense D435 and the Microsoft Kinect Azure were compared against the V2 for inter- and intra-sensor reliability. A secondary analysis with the Azure was also performed to analyze its performance with the existing ML models used to predict transfer quality. The intra- and inter-sensor reliability was higher for the Azure and V2 (n = 7; ICC = 0.63 to 0.92) than the RealSense and V2 (n = 30; ICC = 0.13 to 0.7) for four key features. Additionally, the V2 and the Azure both showed high agreement with each other on the ML outcomes but not against a ground truth. Therefore, the ML models may need to be retrained ideally with the Azure, as it was found to be a more reliable and robust sensor for tracking wheelchair transfers in comparison to the V2.

The primary antimitotic mechanism of action of the synthetic halichondrin E7389 is suppression of microtubule growth.

E7389, which is in phase I and II clinical trials, is a synthetic macrocyclic ketone analogue of the marine sponge natural product halichondrin B. Whereas its mechanism of action has not been fully elucidated, its main target seems to be tubulin and/or the microtubules responsible for the construction and proper function of the mitotic spindle. Like most microtubule-targeted antitumor drugs, it inhibits tumor cell proliferation in association with G(2)-M arrest. It binds to tubulin and inhibits microtubule polymerization. We examined the mechanism of action of E7389 with purified microtubules and in living cells and found that, unlike antimitotic drugs including vinblastine and paclitaxel that suppress both the shortening and growth phases of microtubule dynamic instability, E7389 seems to work by an end-poisoning mechanism that results predominantly in inhibition of microtubule growth, but not shortening, in association with sequestration of tubulin into aggregates. In living MCF7 cells at the concentration that half-maximally blocked cell proliferation and mitosis (1 nmol/L), E7389 did not affect the shortening events of microtubule dynamic instability nor the catastrophe or rescue frequencies, but it significantly suppressed the rate and extent of microtubule growth. Vinblastine, but not E7389, inhibited the dilution-induced microtubule disassembly rate. The results suggest that, at its lowest effective concentrations, E7389 may suppress mitosis by directly binding to microtubule ends as unliganded E7389 or by competition of E7389-induced tubulin aggregates with unliganded soluble tubulin for addition to growing microtubule ends. The result is formation of abnormal mitotic spindles that cannot pass the metaphase/anaphase checkpoint.