Stable Characteristics Optimization of Anti-Symmetric Cylindrical Shell with Laminated Carbon Fiber Composite.

This paper proposes a multi-objective optimization model for anti-symmetric cylindrical shell in the bionic gripper structure. Here, the response surface method is used to establish multiple surrogate models of the anti-symmetric cylindrical shell, and the non-dominated sorting genetic algorithm-II (NSGA-II) is used to optimize the design space of the anti-symmetric cylindrical shell; the design points of the anti-symmetric cylindrical shell are verified by experimental methods. The optimization goals are that the first steady state transition load (the transition process of the bionic gripper structure from the open state to the closed state) of the anti-symmetric cylindrical shell is minimized, and the second steady state transition load (the transition process of the bionic gripper structure from the closed state to the open state) is the largest. At the same time, in order to prevent stable instability caused by stress concentration in the second steady state of the anti-symmetric cylindrical shell, the maximum principal plane stress is given as the constraint condition. The validity of the optimization results is verified by finite element and experimental methods. Due to the stable transition load of the anti-symmetric cylindrical shell being significantly larger than that of the orthogonal laminated plate, therefore, the anti-symmetric cylindrical shell has potential application prospects in the application of deformable structures and bionic structures that require composite functions such as having light weight, high strength, and large clamping force. The novelty of this paper lies in the multi-objective optimization of the application of the antisymmetric bistable cylindrical shell in the bionic gripper structure.

Delayed stress-induced colonic hypersensitivity in male Wistar rats: role of neurokinin-1 and corticotropin-releasing factor-1 receptors.

The mechanism(s) underlying stress-induced colonic hypersensitivity (SICH) are incompletely understood. Our aims were to assess the acute and delayed (24 h) effect of water avoidance (WA) stress on visceral nociception in awake male Wistar rats and to evaluate the role of two stress-related modulation systems: the substance P/neurokinin-1 receptor (SP/NK(1)R) and the corticotropin-releasing factor (CRF)/CRF(1) receptor (CRF/CRF(1)R) systems, as well as the possible involvement of the sympathetic nervous system. Visceral pain responses were measured as the visceromotor response to colorectal distension (CRD) at baseline, immediately after WA and again 24 h later. The NK(1)R antagonists RP-67580 and SR-140333 and the CRF(1)R antagonist CP-154526 were injected 15 min before WA or 1 h before the CRD on day 2. Chemical sympathectomy was performed by repeated injection of 6-hydroxydopamine. WA stress resulted in a significant increase in the visceromotor response on day 2, but no change immediately after WA. Injection of CP-154526 abolished delayed SICH when applied either before WA stress or before the CRD on day 2. Both NK(1)R antagonists only decreased SICH when injected before the CRD on day 2. Chemical sympathectomy did not affect delayed SICH. Our results indicate that in male Wistar rats, both NK(1)R and CRF(1)R activation, but not sympathetic nervous system activation, play a role in the development of SICH.

A novel water-soluble selective CRF1 receptor antagonist, NBI 35965, blunts stress-induced visceral hyperalgesia and colonic motor function in rats.

The stress response involves the activation of two corticotropin-releasing factor (CRF) receptor subtypes. We investigated the role of CRF1 in stress-related visceral responses. A novel water-soluble tricyclic CRF1 antagonist, NBI 35965 was developed that displayed a high affinity for CRF1 (Ki approximately 4 nM) while having no binding affinity to CRF2. This antagonist also inhibited the stimulation of cAMP induced by sauvagine in CRF1 transfected cells. NBI 35965 administered per orally (p.o.) in rats (1, 3, 10 or 30 mg/kg) inhibited dose-dependently [125I]sauvagine binding selectively at brain sites of CRF1 distribution as shown by ex vivo receptor autoradiography. At the highest doses, NBI 35965 completely prevented [125I]sauvagine labeling in the cortex. NBI 35965 (10 mg/kg) administered p.o. or subcutaneously (s.c.) 1 h before intravenous CRF completely blocked the 81% shortening of distal colonic transit time induced by CRF. NBI 35965 (20 mg/kg s.c.) significantly reduced the defecation in response to water avoidance stress but not that induced by s.c. carbachol. In adult male Long-Evans rats that had undergone maternal separation, acute water avoidance stress significantly increased the visceromotor response to colorectal distention (20-80 mmHg) by 42+/-19% compared with the response before stress. Stress-induced visceral hyperalgesia was abolished by NBI 35965 (20 mg/kg, s.c.). The data show that NBI 35965 is a novel water-soluble selective CRF1 antagonist with bioavailability to the brain upon peripheral administration and that CRF1 receptor signaling pathways are involved in water avoidance stress-induced hyperalgesia to colorectal distention and stimulation of colonic transit.