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Digital technology and artificial intelligence technology have built an open sharing environment of intellectualization. For start‐ups, which are restricted by their own limited resources, it is wise to take inbound open innovation as a strategy to get external advanced technical information quickly. However, how to match technology resources obtained from outside with the organisation's demand is still a problem for entrepreneurial teams and entrepreneurial researchers. Based on the literature review of existing research and considering entrepreneurial teams' demand to deal with the challenges, this paper firstly analyses the relationship between entrepreneurial teams' inbound open innovation strategy and the innovative use of information technology by individuals in teams of start‐ups and based on the Identity Theory to explore the mechanism of IT identity on the relationship mentioned above. Lastly, the paper further analyses two types of team authorisation (structural empowerment and psychological empowerment) that play different moderating roles in the relationship of inbound open innovation, IT identity and the innovative use of information technology by individuals in teams. Using 238 survey data from entrepreneurial teams with linear regression analysis, we found that IT identity moderates the relationship between inbound open innovation and individual new IT technology exploration positively, and team psychological empowerment has further moderated the relationship between inbound open innovation and the innovative use of information technology by individuals in teams positively, while team structure empowerment plays an inverted U‐shaped moderation. This study has certain guiding significance for entrepreneurial teams to take advantage of digitalised opportunities, and it also has important value for innovation and digitalisation research. [ABSTRACT FROM AUTHOR]

This paper considers an energy‐constrained sensor power allocation problem for remote estimation under Denial‐of‐Service attack. Due to power constraints, the sensor needs to make a decision on how much power it should employ to optimise the state estimation performance under Denial‐of‐Servic attacks without using real‐time acknowledgment information. Different from the existing works concerning non‐zero power value with discrete values or one power value, the authors consider the multilevel continuous‐valued energy allocation policy containing zero power value in this work. By analysing the effects on performance index under different energy allocation policies, an optimal off‐line power scheduling policy with non‐decreasing structure is derived. To obtain the optimal power scheduling sequences, the authors formulate the problem as non‐linear programming after analysing the probability distribution of the estimation error covariance matrix. Moreover, the two power values energy allocation policy is investigated as a special case. At last, simulation examples are presented to verify the effectiveness of their theoretical results. [ABSTRACT FROM AUTHOR]

This paper focuses on the observer‐based resilient event‐triggered security control issue for networked T‐S fuzzy‐model‐based systems suffered from energy‐limited Denial‐of‐Service (DoS) attacks. Firstly, a novel resilient adaptive event‐triggered mechanism (AETM) is designed to deal with the packet losses problem induced by energy‐limited DoS attacks. Specifically, the resilient AETM threshold is adaptively updated based on the latest available packages. Secondly, according to Lyapunov theory, membership‐function‐dependent stabilisation criterions are obtained to ensure the control systems are stable with H∞ performance. Besides, the mismatched premise variables between model and controller are considered, and a slack matrix with the membership functions information is introduced to relax stability conditions. Then, the relationship between allowable duration of DoS attack and resilient AETM parameter is clarified. An algorithm is also presented to derive the resilient AETM parameter and observer‐based controller gains simultaneously. Finally, two examples are provided to demonstrate the effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

A microdeletion within human chromosome 5q14.3 has been associated with the occurrence of neurodevelopmental disorders, such as autism and intellectual disability, and MEF2C haploinsufficiency was identified as main cause. Here, we report that a brain‐enriched long non‐coding RNA, NDIME, is located near the MEF2C locus and is required for normal neural differentiation of mouse embryonic stem cells (mESCs). NDIME interacts with EZH2, the major component of polycomb repressive complex 2 (PRC2), and blocks EZH2‐mediated trimethylation of histone H3 lysine 27 (H3K27me3) at the Mef2c promoter, promoting MEF2C transcription. Moreover, the expression levels of both NDIME and MEF2C were strongly downregulated in the hippocampus of a mouse model of autism, and the adeno‐associated virus (AAV)‐mediated expression of NDIME in the hippocampus of these mice significantly increased MEF2C expression and ameliorated autism‐like behaviors. The results of this study reveal an epigenetic mechanism by which NDIME regulates MEF2C transcription and neural differentiation and suggest potential effects and therapeutic approaches of the NDIME/MEF2C axis in autism. Synopsis: The lncRNA NDIME is required for proper neural differentiation of mESCs. Viral‐mediated expression of NDIME in the hippocampus of a mouse model of autism ameliorates autism‐like behaviors. LncRNA NDIME is a critical regulator of proper neural differentiation and functions upstream of its neighbor gene Mef2c.NDIME physically interacts with EZH2 and SUZ12, components of PRC2.NDIME is associated with autism. [ABSTRACT FROM AUTHOR]

Background: Severe COVID‐19 patients typically test positive for SARS‐CoV‐2 RNA for extended periods of time, even after recovery from severe disease. Due to the timeframe involved, these patients may have developed humoral immunity to SARS‐CoV‐2 while still testing positive for viral RNA in swabs. Data are lacking on exposure risks in these situations. Here, we studied SARS‐CoV‐2 environmental contamination in an ICU and an isolation ward caring for such COVID‐19 patients. Methods: We collected air and surface samples in a hospital caring for critical and severe COVID‐19 cases from common areas and areas proximal to patients. Results: Of the 218 ICU samples, an air sample contained SARS‐CoV‐2 RNA. Of the 182 isolation ward samples, nine contained SARS‐CoV‐2 RNA. These were collected from a facemask, the floor, mobile phones, and the air in the patient room and bathroom. Serum antibodies against SARS‐CoV‐2 were detected in these patients at the beginning of the study. Conclusions: While there is a perception of increased risk in the ICU, our study demonstrates that isolation wards may pose greater risks to healthcare workers and exposure risks remain with clinically improved patients, weeks after their initial diagnoses. As these patients had serum antibodies, further studies may be warranted to study the utility of serum antibodies as a surrogate of viral clearance in allowing people to return to work. We recommend continued vigilance even with patients who appear to have recovered from COVID‐19. [ABSTRACT FROM AUTHOR]

The aberrant expression of Pknox1 is associated with hepatic glucose and lipid dysmetabolism status of type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD). However, the underlying mechanism causing Pknox1 overexpression in this pathological status remains unclear. By using miRNA target prediction programs, we found that the 3′‐UTR of the Pknox1 mRNA sequence contains highly conserved target sites of miR‐17 family. In a rat model of streptozotocin and high‐fat diet‐induced T2DM and NAFLD complication, the increased hepatic expression of Pknox1 was consistent with decreased expressions of miR‐17 family, especially miR‐17 and miR‐20a. Furthermore, an inverse correlation was observed between Pknox1 and miR‐17 and miR‐20a in free fatty acids‐induced hepatocyte steatosis. Dual‐luciferase reporter assay further showed that Pknox1 was a valid target gene of miR‐17 family. The ectopic expression of miR‐17 or miR‐20a could markedly suppress Pknox1 expression in hepatocytes. MiR‐17 or miR‐20a overexpression also resulted in significantly enhanced insulin sensitivity and reduced hepatocyte steatosis in HepG2 and L02 cells, which were determined by altered phosphorylation on insulin receptor signaling pathway proteins and decreased intracellular triglyceride and lipid accumulation, respectively. These data implicate the upregulated hepatic expression of Pknox1 in T2DM complicated with NAFLD may be caused by the reduced expression of miR‐17 family, indicating that developing miRNA‐mediated regulation strategies on Pknox1 may provide new therapeutic options for metabolic disease. [ABSTRACT FROM AUTHOR]

The problem of adaptive fuzzy output feedback tracking control for a class of switched stochastic non‐linear systems with time‐varying delay and unknown control directions is addressed in this study. During the adaptive controller design procedure, a state observer is introduced to estimate the unmeasurable system states, an appropriate stochastic Lyapunov–Krasovskii functional is utilised to compensate the time‐varying delay terms, and fuzzy logic systems are employed to approximate a suitable unknown function which is composed of all the unknown non‐linearities of the switched systems. In addition, the Nussbaum‐type function is used to detect the unknown control directions. With the help of the designed controller independent of switching signals, the semi‐globally uniformly ultimately boundedness of all the closed‐loop signals is guaranteed and the tracking error converges to a small neighbourhood of the origin. Finally, a simulation example is given to illustrate the effectiveness of the proposed approach. [ABSTRACT FROM AUTHOR]

The problem of fault detection for switched systems with quantisation effects and packet dropout is presented in this study. A dynamic quantiser is introduced, which is composed of a dynamic scaling and a static quantiser. Since a novel switched system is modelled according to packet dropout, a switching strategy which combines average dwell time switching with event‐driven switching is proposed. The systems performance and the relationship between the switching signal and the packet dropout rate are simultaneously developed. Furthermore, sufficient conditions for the existence of fault detection filters are given in the framework of linear matrix inequality, and the filter gains and the quantiser range are derived by a convex optimised method. Finally, two illustrative examples demonstrate the effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

Excess in mitochondrial reactive oxygen species ( ROS) is considered as a major cause of cellular oxidative stress. NADPH, the main intracellular reductant, has a key role in keeping glutathione in its reduced form GSH, which scavenges ROS and thus protects the cell from oxidative damage. Here, we report that SIRT5 desuccinylates and deglutarylates isocitrate dehydrogenase 2 ( IDH2) and glucose-6-phosphate dehydrogenase (G6 PD), respectively, and thus activates both NADPH-producing enzymes. Moreover, we show that knockdown or knockout of SIRT5 leads to high levels of cellular ROS. SIRT5 inactivation leads to the inhibition of IDH2 and G6 PD, thereby decreasing NADPH production, lowering GSH, impairing the ability to scavenge ROS, and increasing cellular susceptibility to oxidative stress. Our study uncovers a SIRT5-dependent mechanism that regulates cellular NADPH homeostasis and redox potential by promoting IDH2 desuccinylation and G6 PD deglutarylation. [ABSTRACT FROM AUTHOR]

This study considers the distributed fault‐tolerant consensus problem for uncertain multi‐agent systems using adaptive protocol. A more general time‐varying actuator fault model is given, which includes loss of effectiveness, stuck, bias and outage fault. A new distributed adaptive control scheme is developed to compensate the effect of fault, multiple delayed state perturbations, mismatched parameter uncertainties and external disturbances on leader–follower multi‐agent systems. Based on the local state information of neighbouring agents, the adaptive updating protocol gains are adjusted online, which remove the assumption that the upper bounds of unknown uncertainty, delayed state perturbation and external disturbances should be known. Moreover, the consensus errors of leader–follower systems can asymptotically converge to zero. Finally, a simulation example is given to show the effectiveness of the theoretical analysis. [ABSTRACT FROM AUTHOR]

This study proposes an integral sliding mode control (ISMC) scheme for a class of uncertain non‐linear systems subject to actuator faults including outage. It is noted that traditional ISMC method cannot handle actuator outage. To tackle the problem, matrix full‐rank factorisation technique and adaptive mechanism are incorporated. Based on the above technique, two novel integral sliding surfaces using construction methods I and II are then introduced and existence conditions of sliding modes are given in terms of linear matrix inequalities, in which less conservativeness and better robustness against actuator faults are obtained using construction method II than I. The fuzzy logic systems are applied to approximate the bounds of unknown non‐linear functions. Furthermore, an integral sliding mode controller, without an fault detection and isolation mechanism, is synthesised to guarantee the asymptotic stability and the robustness of the closed‐loop system against actuator faults and non‐linearities from the every beginning. Finally, simulation results for a model of B747‐100/200 aircraft confirm the effectiveness of the proposed control method. [ABSTRACT FROM AUTHOR]

In this study, we examined the relationships among proactive vitality management (PVM), work engagement, and mental health. A total of 392 call center employees completed the survey. The results of structural equation modeling analyses supported that work engagement meditated the positive relationship between PVM and mental health. [ABSTRACT FROM AUTHOR]

The malate-aspartate shuttle is indispensable for the net transfer of cytosolic NADH into mitochondria to maintain a high rate of glycolysis and to support rapid tumor cell growth. The malate-aspartate shuttle is operated by two pairs of enzymes that localize to the mitochondria and cytoplasm, glutamate oxaloacetate transaminases ( GOT), and malate dehydrogenases ( MDH). Here, we show that mitochondrial GOT2 is acetylated and that deacetylation depends on mitochondrial SIRT3. We have identified that acetylation occurs at three lysine residues, K159, K185, and K404 (3K), and enhances the association between GOT2 and MDH2. The GOT2 acetylation at these three residues promotes the net transfer of cytosolic NADH into mitochondria and changes the mitochondrial NADH/ NAD+ redox state to support ATP production. Additionally, GOT2 3K acetylation stimulates NADPH production to suppress ROS and to protect cells from oxidative damage. Moreover, GOT2 3K acetylation promotes pancreatic cell proliferation and tumor growth in vivo. Finally, we show that GOT2 K159 acetylation is increased in human pancreatic tumors, which correlates with reduced SIRT3 expression. Our study uncovers a previously unknown mechanism by which GOT2 acetylation stimulates the malate-aspartate NADH shuttle activity and oxidative protection. [ABSTRACT FROM AUTHOR]

This study is concerned with the robust H∞ static output feedback control of discrete Markov jumps systems with norm bounded uncertainties on system input and output matrices. With resorting to a new separating technique, the coupling relationship among Lyapunov variables, controller gains, input and output matrices is eliminated. Based on this new technique, sufficient conditions are developed to guarantee that the closed loop system is robust stochastically stable with the prescribed H∞ performance level. Moreover, these conditions are expressed in terms of linear matrix inequalities. A numerical example is further given to demonstrate the effectiveness of the proposed method. [ABSTRACT FROM AUTHOR]

Glucose-6-phosphate dehydrogenase (G6 PD) is a key enzyme in the pentose phosphate pathway ( PPP) and plays an essential role in the oxidative stress response by producing NADPH, the main intracellular reductant. G6 PD deficiency is the most common human enzyme defect, affecting more than 400 million people worldwide. Here, we show that G6 PD is negatively regulated by acetylation on lysine 403 ( K403), an evolutionarily conserved residue. The K403 acetylated G6 PD is incapable of forming active dimers and displays a complete loss of activity. Knockdown of G6 PD sensitizes cells to oxidative stress, and re-expression of wild-type G6 PD, but not the K403 acetylation mimetic mutant, rescues cells from oxidative injury. Moreover, we show that cells sense extracellular oxidative stimuli to decrease G6 PD acetylation in a SIRT2-dependent manner. The SIRT2-mediated deacetylation and activation of G6 PD stimulates PPP to supply cytosolic NADPH to counteract oxidative damage and protect mouse erythrocytes. We also identified KAT9/ ELP3 as a potential acetyltransferase of G6 PD. Our study uncovers a previously unknown mechanism by which acetylation negatively regulates G6 PD activity to maintain cellular NADPH homeostasis during oxidative stress. [ABSTRACT FROM AUTHOR]

In this study, a direct adaptive control scheme is developed to solve the robust fault‐tolerant control problem for linear systems with mismatched parameter uncertainties, disturbances and actuator faults including loss of effectiveness, outage and stuck. Although the unparameterisable time‐varying stuck faults and the upper bounds of disturbances are unknown, the adaptive laws are proposed to estimate the unknown controller parameters online. Then, by using the information from the adaptive mechanism, a class of robust adaptive state feedback controllers are constructed for automatically compensating the actuator faults, external disturbances and mismatched parameter uncertainties. Moreover, on the basis of Lyapunov stability theory, it is proved that the resulting adaptive closed‐loop system can be guaranteed to be asymptotically stable in the presence of actuator faults, disturbances and mismatched parameter uncertainties. Finally, simulation results are presented to illustrate the efficiency of the proposed fault‐tolerant design approach. [ABSTRACT FROM AUTHOR]

Abstract: Foam cell formation due to excessive accumulation of cholesterol by macrophages is a pathological hallmark of atherosclerosis. Macrophages cannot limit the uptake of cholesterol and therefore depend on cholesterol efflux pathways for preventing their transformation into foam cells. Several ABC-transporters, including ABCA1 and ABCG1, facilitate the efflux of cholesterol from macrophages. These transporters, however, also affect membrane lipid asymmetry which may have important implications for cellular endocytotic pathways. We propose that in addition to the generally accepted role of these ABC-transporters in the prevention of foam cell formation by induction of cholesterol efflux from macrophages, they also influence the macrophage endocytotic uptake. [Copyright &y& Elsevier]

We have reported that epoxyeicosatrienoic acids (EETs), the cytochrome P450 (CYP) epoxygenase metabolites of arachidonic acid (AA), are potent sarcolemmal ATP-sensitive K+ (KATP) channel activators. However, activation of cardiac and vascular KATP channels by endogenously produced EETs under physiological intracellular conditions has not been demonstrated and direct comparison of the mechanisms whereby EETs activate the KATP channels in cardiac myocytes versus vascular smooth muscle cells has not been made. In this study, we examined the effects of AA on KATP channels in freshly isolated cardiac myocytes from rats, wild-type (WT) and transgenic mice overexpressing CYP2J2 cDNA, and mesenteric arterial smooth muscle cells from rats. We also compared the activation of cardiac and vascular KATP channels by extracellularly and intracellularly applied 11,12-EET. We found that 1 μm AA enhanced KATP channel activities in both cardiac and vascular smooth muscle cells, and the AA effects were inhibited by preincubation with CYP epoxygenase inhibitors. Baseline cardiac KATP current densities in CYP2J2 transgenic mice were 190% higher than those of WT mice, and both were reduced to similar levels by CYP epoxygenase inhibition. Western blot analysis showed that expression of Kir6.2 and SUR2A was similar between WT and CYP2J2 transgenic hearts. 11,12-EET (5 μm) applied intracellularly enhanced the KATP currents by 850% in cardiac myocytes, but had no effect in vascular smooth muscle cells. In contrast, 11,12-EET (5 μm) applied extracellularly increased KATP currents by 520% in mesenteric arterial smooth muscle cells, but by only 209% in cardiac myocytes. Preincubation with 100 μm m-iodobenzylguanidine or 5 μm myristoylated PKI amide did not alter the activation of cardiac KATP channels by 5 μm 11,12-EET, but significantly inhibited activation of vascular KATP channels. Moreover, EET only enhanced the inward component of cardiac KATP currents, but activated both the inward and outward components of vascular KATP currents. Our results indicate that endogenously derived CYP metabolites of AA potently activate cardiac and vascular KATP channels. EETs regulate cardiac electrophysiology and vascular tone by KATP channel activation, albeit through different mechanisms: the cardiac KATP channels are directly activated by EETs, whereas activation of the vascular KATP channels by EETs is protein kinase A dependent. [ABSTRACT FROM AUTHOR]

Summary The Helicobacter pylori vacuolating cytotoxin (VacA) induces degenerative vacuolation of sensitive mammalian cell lines. Although evidence is accumulating that VacA enters cells and functions from an intracellular site of action, the biochemical mechanism by which VacA mediates cellular vacuolation has not been established. In this study, we used functional complementation and biochemical approaches to probe the structure of VacA. VacA consists of two discrete fragments, p37 and p58, that are both required for vacuolating activity. Using a transient transfection system, we expressed genetically modified forms of VacA and identified mutations in either p37 or p58 that inactivated the toxin. VacA with an inactivating single-residue substitution in the p37 domain [VacA (P9A)] functionally complemented a second mutant form of VacA with an inactivating two-residue deletion in the p58 domain [VacA Δ(346–347)]. VacA (P9A) and VacA Δ(346–347) also co-immunoprecipitated from vacuolated monolayers, supporting the hypothesis that these two inactive mutants associate directly to function in trans . p37 and p58 interact directly when expressed as separate fragments within HeLa cells, suggesting that p37–p58 inter-actions facilitate VacA monomer associations. Collectively, these results support a model in which the active form of VacA requires assembly into a complex of two or more monomers to elaborate toxin function. [ABSTRACT FROM AUTHOR]

In the title compound, C(46)H(80)O(3), a natural ursane-type triperpenoid, four of the five six-membered rings adopt chair conformations; the fifth, which has a C=C double bond, adopts an approximate half-boat conformation. In the crystal, mol-ecules are linked by O-H⋯O hydrogen bonds, forming chains along [010].