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In this paper, based on the viscosity approximation method and the hybrid steepest-descent iterative method, a new implicit iterative algorithm is presented for finding the common fixed points set of a finite family of nonexpansive mappings in a reflexive Hilbert space, which is called a symmetric space. We prove that the sequence generated by this new implicit rule strongly converges to the unique solution of a class of variational inequalities under certain appropriate conditions of the parameters. Moreover, we also study the applications to a broader family of strictly pseudo-contractive mappings and generalized equilibrium problems that involve several variational inequality problems, optimization problems, and fixed-point problems. Finally, numerical results are provided to clarify the stability and effectiveness of the algorithm and to compare with some existing iterative algorithms. [ABSTRACT FROM AUTHOR]

The interval exponential state estimation and robust exponential stability for the switched interval neural networks with discrete and distributed time delays are considered. Firstly, by combining the theories of the switched systems and the interval neural networks, the mathematical model of the switched interval neural networks with discrete and distributed time delays and the interval estimation error system are established. Secondly, by applying the augmented Lyapunov- Krasovskii functional approach and available output measurements, the dynamics of estimation error system is proved to be globally exponentially stable for all admissible time delays. Both the existence conditions and the explicit characterization of desired estimator are derived in terms of linear matrix inequalities (LMIs). Moreover, a delay-dependent criterion is also developed, which guarantees the robust exponential stability of the switched interval neural networks with discrete and distributed time delays. Finally, two numerical examples are provided to illustrate the validity of the theoretical results. [ABSTRACT FROM AUTHOR]

Background: Distal arthrogryposis (DA) is a group of congenital autosomal‐dominant disorders secondary to defects in joint and muscle function, characterized by multiple joint contractures of the hands and feet. DA can be divided into 10 types according to clinical features. DA has been confirmed to be caused by mutations in genes encoding components of the contractile apparatus of skeletal muscle fibers, such as troponin I2 (TNNI2). Methods: In this study, we report a three‐generation DA family belonging to the DA2B type. The clinical characteristics of affected members are genetically stable and consistent, with severe deformities in hands and feet, and two affected adults had short stature. None exhibited facial abnormalities. Blood from three affected and three healthy members were collected for whole‐exome sequencing and Sanger sequencing. Results: A missense variant in TNNI2 (NM_003282.4: c.525G>T: p.K175N) was successfully identified, which resulted in the substitution of amino acid at position 175 of TNNI2 from lysine to asparagines. Conclusion: The variant c.525G>T in TNNI2 explains the cause of DA in the family. This variant was identified in Chinese people for the first time, and the same variant had been reported in another study but no description of clinical symptoms. Our study comprehensively characterized the c.525G>T variant in TNNI2. [ABSTRACT FROM AUTHOR]

[Display omitted] • PAW pre-exposure and subsequent US treatment has energy-efficient in MRSA inactivation. • The enhanced inactivation was partly due to the in-situ generation of RONS. • Elevated arginine levels induced the formation of VBNC bacteria. • Regrowth potential of MRSA cells was negligible. Methicillin-resistant Staphylococcus aureus (MRSA) and antibiotic resistance gene (mecA) are considered emerging contaminants that have been extensively identified in aqueous environments due to their high resistance to disinfectants. Herein, we report for the first time the inactivation of MRSA through a sequential application of plasma-activated water and ultrasound (PAW-SU). While the impact of PAW alone on bacterial culturability and mecA integrity was negligible, the combined PAW-SU treatment outperformed the inactivation method involving PAW with direct US (PAW-DU). It exhibited a shorter lag phase and a higher maximum inactivation rate constant. We numerically demonstrated that sonolysis processes induced by external ultrasound sources considerably improved the intracellular and extracellular reactive oxygen and nitrogen species (RONS) of MRSA in PAW system, thereby increasing the PAW reactivity and applicability. The highest inactivation efficiency of PAW-SU can be attributed to the synergistic effect of enhanced intracellular RONS (i.e., peroxynitrite and singlet oxygen) and membrane disruption induced by US, resulting in irreparable oxidative damage to the Save our Soul response and energy metabolic system. In particular, the elevated arginine metabolites in MRSA cells were primarily responsible for the formation of the viable but nonculturable state (VBNC) bacteria associated with high resistance to PAW system. Surprisingly, a decrease in arginine synthesis capacity was observed to expedite the flow of the tricarboxylic acid cycle, accelerating the detrimental effects of PAW-SU on intracellular components in VBNC bacteria. Finally, the limited regrowth potential of injured MRSA caused by cyclic inactivation of PAW-SU process was further confirmed in wastewater from meat and dairy models and therefore, advocates the possible real-world applications. [ABSTRACT FROM AUTHOR]

Neurofibromatosis type I (NF1) is an autosomal dominant genetic disease that is caused by mutations in the NF1 gene. Various studies have previously demonstrated that the mTOR complex 1 signaling pathway is essential for the NF1-modulated osteogenic differentiation of bone mesenchymal stem cells (BMSCs). Additionally, the mTOR signaling pathway plays a notable role in autophagy. The present study hypothesized that NF1 could modulate the osteogenic differentiation of BMSCs by regulating the autophagic activities of BMSCs. In the present study, human BMSCs were cultured in an osteogenic induction medium. The expression of the NF1 gene was either knocked down or overexpressed by transfection with a specific small interfering RNA (siRNA) targeting NF1 or the pcDNA3.0 NF1-overexpression plasmid, respectively. Autophagic activities of BMSCs (Beclin-1, P62, LC3B I, and LC3B II) were determined using western blotting, electron microscopy, acridine orange (AO) staining and autophagic flux/lysosomal detection by fluorescence microscopy. In addition, the autophagy activator rapamycin (RAPA) and inhibitor 3-methyladenine (3-MA) were used to investigate the effects of autophagy on NF1-modulated osteogenic differentiation in BMSCs. Inhibiting NF1 with siRNA significantly decreased the expression levels of autophagy markers Beclin-1 and LC3B-II, in addition to osteogenic differentiation markers osterix, runt-related transcription factor 2 and alkaline phosphatase. By contrast, overexpressing NF1 with pcDNA3.0 significantly increased their levels. Transmission electron microscopy, AO staining and autophagic flux/lysosomal detection assays revealed that the extent of autophagosome formation was significantly decreased in the NF1-siRNA group but significantly increased in the NF1-pcDNA3.0 group when compared with the NC-siRNA and pcDNA3.0 groups, respectively. In addition, the activity of the PI3K/AKT/mTOR pathway [phosphorylated (p)-PI3K, p-AKT, p-mTOR and p-p70S6 kinase] was significantly upregulated in the NF1-siRNA group compared with the NC-siRNA group, and significantly inhibited in the NF1-pcDNA3.0 group, compared with the pcDNA3.0 group. The knockdown effects of NF1-siRNA on the autophagy and osteogenic differentiation of BMSCs were reversed by the autophagy activator RAPA, while the overexpression effects of NF1-pcDNA3.0 on the autophagy and osteogenic differentiation of BMSCs were reversed by the autophagy inhibitor 3-MA. In conclusion, results from the present study suggest at the involvement of autophagy in the NF1-modulated osteogenic differentiation of BMSCs. Furthermore, NF1 may partially regulate the autophagic activity of BMSCs through the PI3K/AKT/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]