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A new model of scattering kernel for gas-surface interaction was developed and its results were compared with the experimental data for the drag, lift and heat transfer coefficients in hypersonic free-molecular flow. Rarefied gas wind tunnel experiments at Gottingen were made to obtain these experimental data. It was found that the new model provides good results that are similar to the conditions of satellites orbiting the Earth at the upper atmosphere.

Fault diagnostic methods aim to recognize when faults exist on a system and to identify the failures that have caused the fault. The symptoms of the fault are obtained from readings from sensors located on the system. When the observed readings do not match those expected then a fault can exist. Using the detailed information provided by the sensors, a list of the failures (singly or in combinations) that could cause the symptoms can be deduced. In the last two decades, fault diagnosis has received growing attention due to the complexity of modern systems and the consequent need for more sophisticated techniques to identify the failures when they occur. Detecting the causes of a fault quickly and efficiently means reducing the costs associated with the system unavailability and, in certain cases, avoiding the risks of unsafe operating conditions. Bayesian belief networks (BBNs) are probabilistic models that were developed in artificial intelligence applications but are now applied in many fields. They are ideal for modelling the causal relations between faults and symptoms used in the detection process. The probabilities of events within the BBN can be updated following observations (evidence) about the system state. In this paper we investigate how BBNs can be applied to diagnose faults on a system. Initially Fault trees (FTs) are constructed to indicate how the component failures can combine to cause unexpected deviations in the variables monitored by the sensors. Converting FTs into BNs enables the creation of a model that represents the system with a single network, which is constituted by sub-networks. The posterior probabilities of the components' failures give a measure of those components that have caused the symptoms observed. The method gives a procedure that can be generalized for any system where the causality structure can be developed relating the system component states to the sensor readings. The technique is demonstrated with a simple example system. Copyright © 2008 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Depriving cells of nutrients triggers an energetic crisis, which is resolved by metabolic rewiring and organelle reorganization. Primary cilia are microtubule-based organelles at the cell surface, capable of integrating multiple metabolic and signalling cues, but their precise sensory function is not fully understood. Here we show that primary cilia respond to nutrient availability and adjust their length via glutamine-mediated anaplerosis facilitated by asparagine synthetase (ASNS). Nutrient deprivation causes cilia elongation, mediated by reduced mitochondrial function, ATP availability and AMPK activation independently of mTORC1. Of note, glutamine removal and replenishment is necessary and sufficient to induce ciliary elongation or retraction, respectively, under nutrient stress conditions both in vivo and in vitro by restoring mitochondrial anaplerosis via ASNS-dependent glutamate generation. Ift88-mutant cells lacking cilia show reduced glutamine-dependent mitochondrial anaplerosis during metabolic stress, due to reduced expression and activity of ASNS at the base of cilia. Our data indicate a role for cilia in responding to, and possibly sensing, cellular glutamine levels via ASNS during metabolic stress., (© 2023. The Author(s).)

Mutations in the NPHP1 gene, coding for human nephrocystin-1 (NPHP1), cause the autosomal recessive disease nephronophthisis, the most common cause of end-stage renal disease in children and adolescents. The function and structure of NPHP1 are still poorly characterized. NPHP1 presents a modular structure well in keeping with its role as an adaptor protein: it harbors an SH3 domain flanked by two glutamic acid-rich regions and a conserved C-terminal nephrocystin homology domain (NHD). Similar to other NPHP protein family members, its N-terminus contains a putative coiled-coil domain (NPHP1 CC ) that is supposed to play an important role in NPHP1 self-association and/or protein-protein interactions. Structural studies proving its structure and its oligomerization state are still lacking. Here we demonstrate that NPHP1 CC is monomeric in solution and unexpectedly folds into an autonomous domain forming a three-stranded antiparallel coiled coil suitable for protein-protein interactions. Notably, we found that the NPHP1 CC shares remarkable structural similarities with the three-stranded coiled coil of the BAG domain protein family, which is known to mediate the anti-apoptotic function of these proteins, suggesting a possible similar role for NPHP1 CC . In agreement with this hypothesis, we show that in the context of the full-length protein the NPHP1 CC is fundamental to regulate resistance to apoptotic stimuli.