From 1986 to 1994, 82 patients with brachial plexus root avulsion were operated on using a contralateral C7 nerve-root transfer. Forty-four patients underwent a one-stage procedure in which the distal end of the ulnar nerve was anastomosed to the contralateral C7 root, and the other 38 underwent a two-stage procedure (first phase: C7 root --> ulnar nerve; second phase: ulnar nerve --> recipient nerve). Twenty postoperative cases were followed-up for 2 years. Of them, the ulnar nerve was transferred to the musculocutaneous nerve in six cases, with recovery of the biceps up to M3 in four and S3 in five cases; the ulnar nerve was transferred to the median nerve in eight cases, with recovery of the wrist and finger flexors up to M3 in five and S3 in six cases; the ulnar nerve was transferred to the radial nerve in four cases, with recovery of the triceps up to M4 in two and S3 in three cases; and the ulnar nerve was transferred to the thoracodorsal nerve in two cases, with recovery of the latissimus dorsi to M4 in one case. The total muscle recovery rate (up to M3) of the series was 60 percent, and the sensory recovery rate (S3) was 78 percent. Outcomes were related to patient age, operative delay, and whether or not the ulnar nerve was used as a bridge for transfer.

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This paper presents a novel fixed-time sliding mode control for the global fixed-time trajectory tracking of robot manipulators subject to uncertain dynamics and bounded external disturbances. A fixed-time sliding surface is proposed and a singularity-free fixed-time sliding mode control (SFSMC) is constructed. Lyapunov stability theory is employed to prove the global fixed-time stability ensuring that both the sliding variable and tracking errors converge globally to the origin within a fixed time. The appealing advantages of the proposed control are that it is easy to implement with the global fixed-time tracking control for uncertain robot manipulators featuring with faster transient, higher steady-state tracking precision, and the settling time is independent of the initial states of robotic system. Extensive simulations and experimental results are presented to demonstrate the effectiveness and improved performances of the proposed approach. INDEX TERMS Robot manipulators, sliding mode control, robust control, fixed-time stability, single inverted pendulum.

Aflatoxin B1 (AFB1), a food contaminant derived from Aspergillus fungi, has been reported to cause hepatic immunotoxicity via inflammatory infiltration and cytokines release. As a pro-inflammatory factor, cyclooxygenase-2 (COX-2) is widely involved in liver inflammation induced by xenobiotics. However, the mechanism by which AFB1-induced COX-2 regulates liver inflammatory injury via hepatocytes-Kupffer cells (KCs) crosstalk remains unclear and requires further elucidation. Here, we established a COX-2 upregulated model with AFB1 treatment in vivo (C57BL/6 mice, 1 mg/kg body weight, i.g, 4 weeks) and in vitro (human liver HepaRG cells, 1 μM for 24 h). In vivo, AFB1-treated mice exhibited NLRP3 inflammasome activation, inflammatory infiltration, and increased recruitment of KCs. In vitro, dephosphorylated COX-2 by protein phosphatase 2A (PP2A)-B55δ promoted NLRP3 inflammasome activation, including mitochondrial translocation of NLRP3, caspase 1 cleavage, and IL-1β release. Moreover, phosphorylated COX-2 at serine 601 (p-COX-2 Ser601 ) underwent endoplasmic reticulum (ER) retention for proteasome degradation. Furthermore, pyroptosis and inflammatory response induced by AFB1 were relieved with COX-2 genetic (siPTGS2) intervention or pharmaceutic (celecoxib, 30 mg/kg body weight, i.g, 4 weeks) inhibition of COX-2 via NLRP3 inflammasome suppression in vivo and in vitro. Ex vivo, in a co-culture system with murine primary hepatocytes and KCs, activated KCs induced by damaged signals from pyroptotic hepatocytes, formed a feedback loop to amplify NLRP3-dependent pyroptosis of hepatocytes via pro-inflammatory signaling, leading to liver inflammatory injury. Taken together, our data suggest a novel mechanism that protein quality control of COX-2 determines the intracellular distribution and activation of NLRP3 inflammasome, which promotes liver inflammatory injury via hepatocytes-KCs crosstalk.

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