Ferrovalley and Quantum Anomalous Hall Effect in Janus TiTeCl Monolayer.

Ferrovalley materials are garnering significant interest for their potential roles in advancing information processing and enhancing data storage capabilities. This study utilizes first-principles calculations to determine that the Janus monolayer TiTeCl exhibits the properties of a ferrovalley semiconductor. This material demonstrates valley polarization with a notable valley splitting of 80 meV. Additionally, the Berry curvature has been computed across the first Brillouin zone of the monolayer TiTeCl. The research also highlights that topological phase transitions ranging from ferrovalley and half-valley metals to quantum anomalous Hall effect states can occur in monolayer TiTeCl under compressive strains ranging from -1% to 0%. Throughout these strain changes, monolayer TiTeCl maintains its ferromagnetic coupling. These characteristics make monolayer TiTeCl a promising candidate for the development of new valleytronic and topological devices.

Homeostasis of cytoplasmic crowding by cell wall fluidization and ribosomal counterions.

In bacteria, algae, fungi, and plant cells, the wall must expand in concert with cytoplasmic biomass production, otherwise cells would experience toxic molecular crowding1,2 or lyse. But how cells achieve expansion of this complex biomaterial in coordination with biosynthesis of macromolecules in the cytoplasm remains unexplained3, although recent works have revealed that these processes are indeed coupled4,5. Here, we report a striking increase of turgor pressure with growth rate in E. coli, suggesting that the speed of cell wall expansion is controlled via turgor. Remarkably, despite this increase in turgor pressure, cellular biomass density remains constant across a wide range of growth rates. By contrast, perturbations of turgor pressure that deviate from this scaling directly alter biomass density. A mathematical model based on cell wall fluidization by cell wall endopeptidases not only explains these apparently confounding observations but makes surprising quantitative predictions that we validated experimentally. The picture that emerges is that turgor pressure is directly controlled via counterions of ribosomal RNA. Elegantly, the coupling between rRNA and turgor pressure simultaneously coordinates cell wall expansion across a wide range of growth rates and exerts homeostatic feedback control on biomass density. This mechanism may regulate cell wall biosynthesis from microbes to plants and has important implications for the mechanism of action of antibiotics6.

A real-time energy management strategy for fuel cell vehicle based on Pontryagin's minimum principle.

This paper proposes a Pontryagin's minimum principle (PMP) energy management strategy (EMS) based on driving cycle recognition for fuel cell vehicle powertrains, aiming to minimize hydrogen consumption and fuel cell degradation. Firstly, the neural network-based driving cycle recognizer is optimized using the tuna swarm optimization (TSO) algorithm and trained under four typical driving cycles. Then, the optimal co-state variables for the four driving cycles are obtained by iteration. Finally, the co-state variables are dynamically updated based on real-time driving cycle recognition results. Comparative analysis demonstrates that the PMP-DCR effectively improves fuel cell lifetime and vehicle economy under short-distance driving cycles. Based on the combined driving cycle, the proposed PMP-DCR EMS exhibits similar economy performance to optimal dynamic programming (DP) EMS, reducing equivalent hydrogen consumption by 13.8% and 9.2%, and decreasing fuel cell degradation rates by 93% and 8.7% in comparison to the conventional power-following and PMP EMS, respectively.

Plasticity of growth laws tunes resource allocation strategies in bacteria.

Bacteria like E. coli grow at vastly different rates on different substrates, however, the precise reason for this variability is poorly understood. Different growth rates have been attributed to 'nutrient quality', a key parameter in bacterial growth laws. However, it remains unclear to what extent nutrient quality is rooted in fundamental biochemical constraints like the energy content of nutrients, the protein cost required for their uptake and catabolism, or the capacity of the plasma membrane for nutrient transporters. Here, we show that while nutrient quality is indeed reflected in protein investment in substrate-specific transporters and enzymes, this is not a fundamental limitation on growth rate, at least for certain 'poor' substrates. We show that it is possible to turn mannose, one of the 'poorest' substrates of E. coli, into one of the 'best' substrates by reengineering chromosomal promoters of the mannose transporter and metabolic enzymes required for mannose degradation. This result falls in line with previous observations of more subtle growth rate improvement for many other carbon sources. However, we show that this faster growth rate comes at the cost of diverse cellular capabilities, reflected in longer lag phases, worse starvation survival and lower motility. We show that addition of cAMP to the medium can rescue these phenotypes but imposes a corresponding growth cost. Based on these data, we propose that nutrient quality is largely a self-determined, plastic property that can be modulated by the fraction of proteomic resources devoted to a specific substrate in the much larger proteome sector of catabolically activated genes. Rather than a fundamental biochemical limitation, nutrient quality reflects resource allocation decisions that are shaped by evolution in specific ecological niches and can be quickly adapted if necessary.

Focusing of surface plasmon polaritons propagating at the SiO2/Ag interface with 2-level and 4-level Fresnel phase zone pad structures.

We propose and demonstrate dielectric Fresnel phase zone pad (FPZP) structures for focusing surface plasmon polaritons (SPPs) propagating at the SiO2/Ag interfaces. We exploited up-conversion fluorescence microscopy to characterize the SPP focusing. We first report on the SPP focusing with 2-level FPZP structures that introduced a π-phase shift in the SPP wavefront between adjacent zones. We optimized the SPP focusing by fine-tuning the longitudinal width of the FPZP structure. This led to the enhancement of the peak intensity of the SPP focal spot and the reduction of the focal spot size in both the longitudinal and transverse directions. Such focusing was also demonstrated with different focal lengths. To further improve the SPP focusing, we developed a 4-level FPZP structure, which introduced a π/2-phase shift in the SPP wavefront between adjacent zones. With the optimized 4-level FPZP structure, the SPP focal spot peak intensity is further improved, and the spot size is reduced. To assist the design of the FPZP structures, we carried out theoretical analysis and numerical calculations to determine the SPP wavelengths at various oxide/Ag interfaces. We also carried out finite difference time domain (FDTD) calculations to simulate the SPP focusing with the FPZP structures. The results of the FDTD simulation agree with the experimental results qualitatively.

A universal mechanism of biomass density homeostasis via ribosomal counterions.

In all growing cells, the cell envelope must expand in concert with cytoplasmic biomass to prevent lysis or molecular crowding. The complex cell wall of microbes and plants makes this challenge especially daunting and it unclear how cells achieve this coordination. Here, we uncover a striking linear increase of cytoplasmic pressure with growth rate in E. coli. Remarkably, despite this increase in turgor pressure with growth rate, cellular biomass density was constant across a wide range of growth rates. In contrast, perturbing pressure away from this scaling directly affected biomass density. A mathematical model, in which endopeptidase-mediated cell wall fluidization enables turgor pressure to set the pace of cellular volume expansion, not only explains these confounding observations, but makes several surprising quantitative predictions that we validated experimentally. The picture that emerges is that changes in turgor pressure across growth rates are mediated by counterions of ribosomal RNA. Profoundly, the coupling between rRNA and cytoplasmic pressure simultaneously coordinates cell wall expansion across growth rates and exerts homeostatic feedback control on biomass density. Because ribosome content universally scales with growth rate in fast growing cells, this universal mechanism may control cell wall biosynthesis in microbes and plants and drive the expansion of ribosome-addicted tumors that can exert substantial mechanical forces on their environment.

Long-term history dependence of growth rates of E. coli after nutrient shifts.

According to a widely accepted paradigm of microbiology, steady-state growth rates are determined solely by current growth conditions1-3 and adaptations between growth states are rapid, as recently recapitulated by simple resource allocation models4. However, even in microbes overlapping regulatory networks can yield multi-stability or long-term cellular memory. Species like Listeria monocytogenes5 and Bacillus subtilis "distinguish" distinct histories for the commitment to sporulation6, but it is unclear if these states can persist over many generations. Remarkably, studying carbon co-utilization of Escherichia coli, we found that growth rates on combinations of carbon sources can depend critically on the previous growth condition. Growing in identical conditions, we observed differences in growth rates of up to 25% and we did not observe convergence of growth rates over 15 generations. We observed this phenomenon occurs across combinations of different phosphotransferase (PTS) substrates with various gluconeogenic carbon sources and found it to depend on the transcription factor Mlc.

Plasticity of growth laws tunes resource allocation strategies in bacteria.

Bacteria like E. coli grow at vastly different rates on different substrates, however, the precise reason for this variability is poorly understood. Different growth rates have been attributed to 'nutrient quality', a key parameter in bacterial growth laws. However, it remains unclear to what extent nutrient quality is rooted in fundamental biochemical constraints like the energy content of nutrients, the protein cost required for their uptake and catabolism, or the capacity of the plasma membrane for nutrient transporters. Here, we show that while nutrient quality is indeed reflected in protein investment in substrate-specific transporters and enzymes, this is not a fundamental limitation on growth rate. We show that it is possible to turn mannose, one of the 'poorest' substrates of E. coli, into one of the 'best' substrates by reengineering chromosomal promoters of the mannose transporter and metabolic enzymes required for mannose degradation. However, we show that this faster growth rate comes at the cost of diverse cellular capabilities, reflected in longer lag phases, worse starvation survival and lower motility. We show that addition of cAMP to the medium can rescue these phenotypes but imposes a corresponding growth cost. Based on these data, we propose that nutrient quality is largely a self-determined, plastic property that can be modulated by the fraction of proteomic resources devoted to a specific substrate in the much larger proteome sector of catabolically activated genes. Rather than a fundamental biochemical limitation, nutrient quality reflects resource allocation decisions that are shaped by evolution in specific ecological niches and can be quickly adapted if necessary.

Study of the Effect of Cell Prestress on the Cell Membrane Penetration Behavior by Atomic Force Microscopy.

In recent years, atomic force microscopes have been used for cell transfection because of their high-precision micro-indentation mode; however, the insertion efficiency of the tip of AFM into cells is extremely low. In this study, NIH3T3 mouse fibroblast cells cultured on a flexible dish with micro-groove patterns were subjected to various substrate strains at 5%, 10%, 15%, and 20%. It was found that the cell stiffness depends on the prestress of the cell membrane, and that the insertion rate of AFM tips into the cell membrane is proportional to the stiffness through the AFM indentation experiment. The finite element analysis proves that prestress increases the bending stiffness of the cytoskeleton, allowing it to better support the cell membrane, which realizes the stress concentration in the contact area between the AFM tip and the cell membrane. The results indicate that the prestress contributes to the mechanical properties of the cell and suggest that the insertion efficiency could be greatly improved with an increase of the prestress of the cell membrane.

Analysis of proteome adaptation reveals a key role of the bacterial envelope in starvation survival.

Bacteria reorganize their physiology upon entry to stationary phase. What part of this reorganization improves starvation survival is a difficult question because the change in physiology includes a global reorganization of the proteome, envelope, and metabolism of the cell. In this work, we used several trade-offs between fast growth and long survival to statistically score over 2,000 Escherichia coli proteins for their global correlation with death rate. The combined ranking allowed us to narrow down the set of proteins that positively correlate with survival and validate the causal role of a subset of proteins. Remarkably, we found that important survival genes are related to the cell envelope, i.e., periplasm and outer membrane, because the maintenance of envelope integrity of E. coli plays a crucial role during starvation. Our results uncover a new protective feature of the outer membrane that adds to the growing evidence that the outer membrane is not only a barrier that prevents abiotic substances from reaching the cytoplasm but also essential for bacterial proliferation and survival.

MetA is a "thermal fuse" that inhibits growth and protects Escherichia coli at elevated temperatures.

Adaptive stress resistance in microbes is mostly attributed to the expression of stress response genes, including heat-shock proteins. Here, we report a response of E. coli to heat stress caused by degradation of an enzyme in the methionine biosynthesis pathway (MetA). While MetA degradation can inhibit growth, which by itself is detrimental for fitness, we show that it directly benefits survival at temperatures exceeding 50°C, increasing survival chances by more than 1,000-fold. Using both experiments and mathematical modeling, we show quantitatively how protein expression, degradation rates, and environmental stressors cause long-term growth inhibition in otherwise habitable conditions. Because growth inhibition can be abolished with simple mutations, namely point mutations of MetA and protease knockouts, we interpret the breakdown of methionine synthesis as a system that has evolved to halt growth at high temperatures, analogous to "thermal fuses" in engineering that shut off electricity to prevent overheating.

Phosphatidic acid species 34:1 mediates expression of the myo-inositol 3-phosphate synthase gene INO1 for lipid synthesis in yeast.

Depletion of exogenous inositol in yeast results in rising levels of phosphatidic acid (PA) and is correlated with increased expression of genes containing the inositol-dependent upstream activating sequence promoter element (UASINO). INO1, encoding myo-inositol 3-phosphate synthase, is the most highly regulated of the inositol-dependent upstream activating sequence-containing genes, but its mechanism of regulation is not clear. In the current study, we determined the relative timing and kinetics of appearance of individual molecular species of PA following removal of exogenous inositol in actively growing wild type, pah1Δ, and ole1ts strains. We report that the pah1Δ strain, lacking the PA phosphatase, exhibits a delay of about 60 min in comparison to wildtype before initiating derepression of INO1 expression. The ole1ts mutant on the other hand, defective in fatty acid desaturation, when grown at a semirestrictive temperature, exhibited reduced synthesis of PA species 34:1 and elevated synthesis of PA species 32:1. Importantly, we found these changes in the fatty acid composition in the PA pool of the ole1ts strain were associated with reduced expression of INO1, indicating that synthesis of PA 34:1 is involved in optimal expression of INO1 in the absence of inositol. Using deuterium-labeled glycerol in short-duration labeling assays, we found that changes associated with PA species 34:1 were uniquely correlated with increased expression of INO1 in all three strains. These data indicate that the signal for activation of INO1 transcription is not necessarily the overall level of PA but rather levels of a specific species of newly synthesized PA 34:1.

Subwavelength-resolution imaging of surface plasmon polaritons with up-conversion fluorescence microscopy.

Imaging and characterization of surface plasmon polaritons (SPPs) are crucial for the research and development of the plasmonic devices and circuits. Here, we report on direct imaging of SPPs propagation on SiO2/metal interface with subwavelength spatial resolution using up-conversion fluorescence microscopy, that exploits rare-earth ions, such as Er3+, Yb3+, and Nd3+, doped nanoparticles as the fluorophores. We demonstrated that by further taking the intensity ratio of the image obtained with fluorescent emission at different wavelengths, we are able to substantially enhance the features associated to the SPP wavefronts in the image for quantitative analysis, such as the wavevector and propagation direction of the SPPs. Our results agree with the theoretic prediction of the SPP wavelengths quantitatively. We further demonstrate the evolution of the SPP wavefronts due to refraction SPPs, and reproduced the experiment with finite difference time domain (FDTD) method simulations. The relative refractive index of SPP estimated from the experiment also agrees quantitatively with those extracted from the theory and the simulation.

From DNA Damage to Cancer Progression: Potential Effects of Cytolethal Distending Toxin.

Cytolethal distending toxin (CDT), one of the most important genotoxins, is produced by several gram-negative bacteria and is involved in bacterial pathogenesis. Recent studies have shown that bacteria producing this peculiar genotoxin target host DNA, which potentially contributes to development of cancer. In this review, we highlighted the recent studies focusing on the idea that CDT leads to DNA damage, and the cells with inappropriately repaired DNA continue cycling, resulting in cancer development. Understanding the detailed mechanisms of genotoxins that cause DNA damage might be useful for targeting potential markers that drive cancer progression and help to discover new therapeutic strategies to prevent diseases caused by pathogens.

Bacterial Genotoxin-Coated Nanoparticles for Radiotherapy Sensitization in Prostate Cancer.

Prostate cancer (PCa) is one of the most commonly diagnosed cancers in men and usually becomes refractory because of recurrence and metastasis. CD44, a transmembrane glycoprotein, serves as a receptor for hyaluronic acid (HA). It has been found to be abundantly expressed in cancer stem cells (CSCs) that often exhibit a radioresistant phenotype. Cytolethal distending toxin (CDT), produced by Campylobacter jejuni, is a tripartite genotoxin composed of CdtA, CdtB, and CdtC subunits. Among the three, CdtB acts as a type I deoxyribonuclease (DNase I), which creates DNA double-strand breaks (DSBs). Nanoparticles loaded with antitumor drugs and specific ligands that recognize cancerous cell receptors are promising methods to overcome the therapeutic challenges. In this study, HA-decorated nanoparticle-encapsulated CdtB (HA-CdtB-NPs) were prepared and their targeted therapeutic activity in radioresistant PCa cells was evaluated. Our results showed that HA-CdtB-NPs sensitized radioresistant PCa cells by enhancing DSB and causing G2/M cell-cycle arrest, without affecting the normal prostate epithelial cells. HA-CdtB-NPs possess maximum target specificity and delivery efficiency of CdtB into the nucleus and enhance the effect of radiation in radioresistant PCa cells. These findings demonstrate that HA-CdtB-NPs exert target specificity accompanied with radiomimetic activity and can be developed as an effective strategy against radioresistant PCa.

A universal trade-off between growth and lag in fluctuating environments.

The rate of cell growth is crucial for bacterial fitness and drives the allocation of bacterial resources, affecting, for example, the expression levels of proteins dedicated to metabolism and biosynthesis1,2. It is unclear, however, what ultimately determines growth rates in different environmental conditions. Moreover, increasing evidence suggests that other objectives are also important3-7, such as the rate of physiological adaptation to changing environments8,9. A common challenge for cells is that these objectives cannot be independently optimized, and maximizing one often reduces another. Many such trade-offs have indeed been hypothesized on the basis of qualitative correlative studies8-11. Here we report a trade-off between steady-state growth rate and physiological adaptability in Escherichia coli, observed when a growing culture is abruptly shifted from a preferred carbon source such as glucose to fermentation products such as acetate. These metabolic transitions, common for enteric bacteria, are often accompanied by multi-hour lags before growth resumes. Metabolomic analysis reveals that long lags result from the depletion of key metabolites that follows the sudden reversal in the central carbon flux owing to the imposed nutrient shifts. A model of sequential flux limitation not only explains the observed trade-off between growth and adaptability, but also allows quantitative predictions regarding the universal occurrence of such tradeoffs, based on the opposing enzyme requirements of glycolysis versus gluconeogenesis. We validate these predictions experimentally for many different nutrient shifts in E. coli, as well as for other respiro-fermentative microorganisms, including Bacillus subtilis and Saccharomyces cerevisiae.

Fault diagnosis in a current sensor and its application to fault-tolerant control for an air supply subsystem of a 50 kW-Grade fuel cell engine.

The safety, reliability and stability of air supply subsystems are still problems for the commercial applications of fuel cells; therefore, engine fault diagnosis and fault-tolerant control are essential to protect the fuel cell stack. In this study, a fault diagnosis and fault-tolerant control method based on artificial neural networks (ANNs) has been proposed. The offline ANN modification model was trained with a Levenberg-Marquardt (LM) algorithm based on other sensors' signals relevant to the current sensor of a 50 kW-grade fuel cell engine test bench. The output current was predicted via the ANN identification model according to other relevant sensors and compared with the sampled current sensor signal. The faults in the current sensor were detected immediately once the difference exceeded the given threshold value, and the invalid signals of the current sensor were substituted with the predictive output value of the ANN identification model. Finally, the reconstructed current sensor signals were sent back to a fuel cell controller unit (FCU) to adjust the air flow and rotate speeds of the air compressor. Experimental results show that the typical faults in the current sensor can be diagnosed and distinguished within 0.5 s when the threshold value is 15 A. The invalid signal of current sensor can be reconstructed within 0.1 s. Which ensures that the air compressor operate normally and avoids oxygen starvation. The proposed method can protect the fuel cell stack and enhance the fault-tolerant performance of air supply subsystem used in the fuel cell engine, and it is promising to be utilized in the fault diagnosis and fault-tolerant control of various fuel cell engines and multiple sensor systems.

Effect of Ruellia tuberosa L. on aorta endothelial damage-associated factors in high-fat diet and streptozotocin-induced type 2 diabetic rats.

Hyperglycemia plays crucial roles in vascular disease development, including macrovascular and microvascular diseases from diabetes mellitus (DM). Our previous study demonstrated that Ruellia tuberosa L. (RTL) aqueous and ethanol extracts alleviate hyperglycemia and inhibit insulin resistance in diabetic rats. This study investigated the protective effect of RTL ethanol extract against aorta dysfunction in high-fat diet (HFD) and streptozotocin (STZ)-induced type 2 DM (T2DM) rats. Results showed that RTL ethanol extract (100 and 400 mg/kg BW/day) ameliorated serum lipid profiles, including triglyceride, free fatty acid, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol levels. It also significantly reduced the level of serum cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 in T2DM rats. Additionally, RTL extract decreased endothelin-1 and endothelial nitric oxide contents, reduced the level of cell adhesion factors, including monocyte chemoattractant protein-1 and cell adhesion factor vascular cell adhesion molecule-1, while decreasing content of damage factors, namely tissue factor and von Willebrand factor in aortic tissues of diabetic rats. Equally noteworthy is that RTL extract enhanced the activity of aorta antioxidative enzymes, including superoxidase dismutase and catalase in diabetic rats, suggesting that RTL ethanol extract may ameliorate aorta dysfunction via enhancing aortic antioxidative enzyme activity, which subsequently suppresses aorta endothelial damage-associated factors in HFD with STZ-induced T2DM rats.

Ameliorative effect of Ruellia tuberosa L. on hyperglycemia in type 2 diabetes mellitus and glucose uptake in mouse C2C12 myoblasts.

Ruellia tuberosa L. (RTL) exhibits a wide range of phytochemical activities, for example, on treatment of diabetes mellitus (DM), in Orient. There is, however, few study regarding the effect of RTL on glycemic-related homeostasis in type 2 DM (T2DM). We investigated the effect of RTL aqueous and ethanolic extracts on hypoglycemia in high-fat diet (HFD)-fed plus streptozotocin (STZ)-induced T2DM rats, and examined the effect of RTL on glucose uptake in tumor necrosis factor-α-induced insulin-resistant mouse C2C12 myoblasts, a mouse skeletal muscle cell line. The administration of 100 or 400 mg kg BW-1 day-1 of RTL aqueous or ethanolic extracts once a day for 4 weeks significantly ameliorated hyperglycemia, hyperinsulinemia, and the insulin resistance (IR) index in diabetic rats. RTL either aqueous or ethanolic extract at a concentration of 25-800 µg/ml significantly improved glucose uptake in insulin-resistant mouse C2C12 myoblasts, indicating inhibiting the IR in skeletal muscles. These evidences suggest that RTL ameliorates hyperglycemia in HFD/STZ-induced T2DM rats may be attributed to the alleviation of IR in skeletal muscles.

Magnetoresistance Effect and the Applications for Organic Spin Valves Using Molecular Spacers.

Organic spin devices utilizing the properties of both spin and charge inherent in electrons have attracted extensive research interest in the field of future electronic device development. In the last decade, magnetoresistance effects, including giant magetoresistance and tunneling magnetoresistance, have been observed in organic spintronics. Significant progress has been made in understanding spin-dependent transport phenomena, such as spin injection or tunneling, manipulation, and detection in organic spintronics. However, to date, materials that are effective for preparing organic spin devices for commercial applications are still lacking. In this report, we introduce basic knowledge of the fabrication and evaluation of organic spin devices, and review some remarkable applications for organic spin valves using molecular spacers. The current bottlenecks that hinder further enhancement for the performance of organic spin devices is also discussed. This report presents some research ideas for designing organic spin devices operated at room temperature.