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The problem of finite-time attitude-tracking control (ATC) for a rigid spacecraft subject to inertial uncertainties, external disturbances, actuator saturations and faults is addressed. First, a fast nonsingular terminal sliding mode (FNTSM) manifold is constructed to improve robustness. Second, the fuzzy logic system (FLS) is integrated into the manifold derivative to deal with the lumped unknown function. The specific assumptions about uncertainties in most of the existing achievements are no longer needed. Combining the FNTSM and fuzzy approximation techniques, an enhanced fault-tolerant control scheme is developed. Compared to almost all finite-time ATC results based on FLS or neural network, a new Proof line is proposed to prove that the approximation errors are finite-time stable instead of asymptotically stable. Therefore, the attitude controller presented herein guarantees the real finite-time stability in a complete sense. Finally, numerical experiments are conducted to verify the effectiveness of the solution, and comparisons with related works are displayed. • Assumptions on uncertainties in the existing achievements are abolished. • Finite-time stability of fuzzy approximation errors is proved via a new Proof line. • Norm approximation is exploited to reduce the parameters to be estimated online. • The attitude controller guarantees the finite-time stability in a complete sense. [ABSTRACT FROM AUTHOR]

Lysosomes transcend the role of degradation stations, acting as key nodes for interorganelle crosstalk and signal transduction. Lysosomes communicate with the nucleus through physical proximity and functional interaction. In response to external and internal stimuli, lysosomes actively adjust their distribution between peripheral and perinuclear regions and modulate lysosome–nucleus signaling pathways; in turn, the nucleus fine-tunes lysosomal biogenesis and functions through transcriptional controls. Changes in coordination between these two essential organelles are associated with metabolic disorders, neurodegenerative diseases, and aging. In this review, we address recent advances in lysosome–nucleus communication by multi-tiered regulatory mechanisms and discuss how these regulations couple metabolic inputs with organellar motility, cellular signaling, and transcriptional network. Lysosomal–nuclear communication coordinates lysosomal positioning, metabolism, and signaling with nuclear transcription to support fundamental cellular activities. Lysosomal positioning between peripheral and perinuclear regions is subject to cooperative regulation in response to metabolic stimuli and contributes to lysosomal functions and signaling. Retrograde transport of chaperone proteins and transcription factors from the lysosome to the nucleus is actively regulated by metabolic signaling. Nuclear transcriptional networks comprise a variety of different transcription factors that act independently or coordinately to fine tune lysosomal-autophagic gene expression. [ABSTRACT FROM AUTHOR]

In this paper, to improve the dynamic performance of DFIG-based WT, a NADRC technology is proposed. The proposed NADRC can actively estimate and compensate the plant internal dynamics and external disturbances in real time. Therefore, it improves the tracking performance of the rotor current without any overshoot and steady-state error, and enhances the fault ride-through capability of DFIG-based wind turbine. Compared with the proportional PI control, the proposed NADRC during grid fault can significantly suppress the peak values of stator and rotor currents and DC-link voltage, and decrease the oscillation time of electromagnetic torque. Moreover, the proposed NADRC has a characteristic of one-parameter tuning by using the parameterization technique of controller, and parameter tuning of NADRC is only determined by the rise time of the system step response. A series of simulations for various cases on a 1.5-MW DFIG-based wind turbine are implemented, and the results validate the stability of the proposed NADRC and the strong robustness against the plant internal dynamics and external disturbances. [ABSTRACT FROM AUTHOR]

This paper studies the issue of finite-time prescribed performance control for spacecraft attitude tracking with inertia perturbations, external disturbances, actuator saturations and faults. To the best of the authors' knowledge, limited results have been reported in the relevant literature, and how to achieve the prescribed performance attitude tracking within a preset time interval is still an open problem. A novel finite-time prescribed performance function (FTPPF) whose settling time can be arbitrarily preset is first proposed. With the FTPPF predefining the envelope of tracking-error trajectories, the original spacecraft model is transformed into a new error system. Based on the barrier Lyapunov function of converted errors, the attitude controller is derived via backstepping design. During the process, the fuzzy approximation is used to handle inertia perturbations and external disturbances, while the Nussbaum gain technique is adopted to compensate for the efficiency loss caused by actuator saturations and faults. Finally, a finite-time fault-tolerant control scheme that guarantees both transient and steady-state performances (e.g., the maximum overshoot, steady-state error, and settling time) is developed. To verify the effectiveness of the solution, numerical experiments involving comparisons with related achievements are performed. [ABSTRACT FROM AUTHOR]

Healthy mitochondria are critical for reproduction. During aging, both reproductive fitness and mitochondrial homeostasis decline. Mitochondrial metabolism and dynamics are key factors in supporting mitochondrial homeostasis. However, how they are coupled to control reproductive health remains unclear. We report that mitochondrial GTP (mtGTP) metabolism acts through mitochondrial dynamics factors to regulate reproductive aging. We discovered that germline-only inactivation of GTP- but not ATP-specific succinyl-CoA synthetase (SCS) promotes reproductive longevity in Caenorhabditis elegans. We further identified an age-associated increase in mitochondrial clustering surrounding oocyte nuclei, which is attenuated by GTP-specific SCS inactivation. Germline-only induction of mitochondrial fission factors sufficiently promotes mitochondrial dispersion and reproductive longevity. Moreover, we discovered that bacterial inputs affect mtGTP levels and dynamics factors to modulate reproductive aging. These results demonstrate the significance of mtGTP metabolism in regulating oocyte mitochondrial homeostasis and reproductive longevity and identify mitochondrial fission induction as an effective strategy to improve reproductive health. [Display omitted] • Mitochondrial GTP-specific succinyl-CoA synthetase regulates reproductive longevity • Oocyte mitochondrial positioning influences reproductive health during aging • Mitochondrial fission in the oocyte promotes reproductive longevity • Bacterial vitamin B12 modulates reproductive aging via GTP succinyl-CoA synthetase Lee et al. identify a signaling nexus between mitochondrial GTP metabolism and mitochondrial dynamics in regulating C. elegans reproductive aging. They further demonstrate that bacterial metabolites act through this signaling mechanism to modulate the host's reproductive health during aging. [ABSTRACT FROM AUTHOR]

Summary Asymmetric stem cell division establishes an initial difference between a stem cell and its differentiating sibling, critical for maintaining homeostasis and preventing carcinogenesis. Yet the mechanisms that consolidate and lock in such initial fate bias remain obscure. Here, we use Drosophila neuroblasts to demonstrate that the super elongation complex (SEC) acts as an intrinsic amplifier to drive cell fate commitment. SEC is highly expressed in neuroblasts, where it promotes self-renewal by physically associating with Notch transcription activation complex and enhancing HES (hairy and E(spl)) transcription. HES in turn upregulates SEC activity, forming an unexpected self-reinforcing feedback loop with SEC. SEC inactivation leads to neuroblast loss, whereas its forced activation results in neural progenitor dedifferentiation and tumorigenesis. Our studies unveil an SEC-mediated intracellular amplifier mechanism in ensuring robustness and precision in stem cell fate commitment and provide mechanistic explanation for the highly frequent association of SEC overactivation with human cancers. [ABSTRACT FROM AUTHOR]