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A strategy combining an improved rapidly-exploring random tree (RRT) method with the artificial potential field (APF) method is proposed for the path planning of flexible tensegrity manipulators considering typical complex constraints, such as structural stability, obstacle avoidance, and cable no-slackening. The relationship between the node displacements and the elongations of active members is established for the kinematic analysis of tensegrity manipulators. The rest lengths of active members are taken as the design variables for the generation of random tree. The guide node is utilized for goal-biased samplings to expedite the exploration toward the final configuration, while the APF method is introduced to ensure that the obtained elongations of active members can satisfy the constraint of obstacle avoidance. The proportion of random and goal-biased samplings is adaptively adjusted based on the sampling success rate. Futile random samplings can be significantly reduced by dynamically modifying the random sampling range according to the obtained configuration nearest to the final configuration. The computational procedure of the proposed method is presented. An illustrative flexible tensegrity manipulator is employed to demonstrate the adaptability of the proposed path planning method to complex constraints, especially structural stability.

Colorectal cancer (CRC) ranks third in incidence and second in mortality worldwide. Metabolic disorders are known to be closely associated with CRC. Functional metabolomics aims to translate metabolomics-derived biomarkers to disease mechanisms. Previous work based on untargeted liquid chromatography identified 30 differential metabolites of CRC. Among them, only β-hydroxybutyrate (BHB) was elevated in CRC. Here, we first confirm the increased level of β-hydroxybutyrate by targeted metabolomic analysis using an independent cohort of 400 serum samples by UPLC-QQQ-MS/MS analysis. Using appropriate cell and animal models, we find that treatment with pathological levels of β-hydroxybutyrate expedites CRC proliferation and metastasis. Out of four major rate-limiting enzymes of ketolysis, only acetyl-coenzyme A acetyltransferase1 (ACAT1) expression is increased in paired human CRC tissues. These findings suggest probable clinical relevance for the functional implications of β-hydroxybutyrate in CRC. We demonstrate that β-hydroxybutyrate may exert its tumorigenic effects via regulation of ACAT1, due to induction of downstream isocitrate dehydrogenase1 (IDH1) acetylation. Genetic silencing of ACAT1 significantly suppresses the progression of CRC and abrogates the effects of β-hydroxybutyrate both in vitro and in vivo. Overall, this study suggests that targeting β-hydroxybutyrate and its major rate-limiting enzyme ACAT1 may provide a new avenue for therapeutic intervention in CRC.