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The persistent consumption of citrus fruit mainly depends on its sweet–sour taste as well as pulp texture. To date, the simple facility by covering plastic film just over trees is commonly used in different citrus species for harvest time extension and quality improvement. In this study, the effect of covering trees of Citrus reticulata cv. Kinokuni with plastic films was investigated. Results indicated that simply covering plastic film over trees significantly decreased the soil water content, the light intensity, and then the photosynthetic rate, however, moderately increased the internal average temperature of 0–3 °C. Moreover, it significantly facilitated soluble sugar accumulation, increased water soluble pectin content, and decreased protopectin content. Investigating transcript profile showed that only 351 gene transcripts were significantly influenced by covering plastic film. Interestingly, most differently expressed genes (DEGs) were involved in carbohydrate and cell wall metabolisms except some DEGs were related to signal transduction and environmental adaption. Taken together, covering plastic film over trees comprehensively modified the internal environmental condition and improved the fruit sweetness and mastication trait by promoting soluble sugar accumulation, increasing water soluble pectin content, and decreasing protopectin content through the alteration of transcript level.

‘Hong Anliu’ (HAL, Citrus sinensis cv. Hong Anliu) is a bud mutant of ‘Anliu’ (AL), characterized by a comprehensive metabolite alteration, such as lower accumulation of citrate, high accumulation of lycopene and soluble sugars in fruit juice sacs. Due to carboxylic acid metabolism connects other metabolite biosynthesis and/or catabolism networks, we therefore focused analyzing citrate accumulation-related gene expression profiles and/or enzyme activities, along with metabolic fingerprinting between ‘HAL’ and ‘AL’. Compared with ‘AL’, the transcript levels of citrate biosynthesis- and utilization-related genes and/or the activities of their respective enzymes such as citrate synthase, cytosol aconitase and ATP-citrate lyase were significantly higher in ‘HAL’. Nevertheless, the mitochondrial aconitase activity, the gene transcript levels of proton pumps, including vacuolar H + -ATPase, vacuolar H + -PPase, and the juice sac-predominant p-type proton pump gene ( CsPH8 ) were significantly lower in ‘HAL’. These results implied that ‘HAL’ has higher abilities for citrate biosynthesis and utilization, but lower ability for the citrate uptake into vacuole compared with ‘AL’. Combined with the metabolites-analyzing results, a model was then established and suggested that the reduction in proton pump activity is the key factor for the low citrate accumulation and the comprehensive metabolite alterations as well in ‘HAL’.

Aim： The phosphorylation of histone H2AX, a novel tumor suppressor protein, is involved in regulation of cancer cell apoptosis. The aim of this study was to examine whether H2AX phosphorylation was required for resveratrol-induced apoptosis of human chronic myelogenous leukemia （CML） cells in vitro. Methods： K562 cells were tested. Cell apoptosis was analyzed using flow cytometry, and the phosphorylation of H2AX and other signaling proteins was examined with Western blotting. To analyze the signaling pathways, the cells were transfected with lentiviral vectors encoding H2AX-wt or specific siRNAs. Results： Treatment of K562 cells with resveratrol （20-100 μmol/L） induced apoptosis and phosphorylation of H2AX at Ser139 in time- and dose-dependent manners, but reduced phosphorylation of histone H3 at SerlO. Resveratrol treatment activated two MAPK family members p38 and JNK, and blocked the activation of another MAPK family member ERK. Pretreatment with the p38 inhibitor SB202190 or the JNK inhibitor SP600125 dose-dependently reduced resveratrol-induced phosphorylation of H2AX, which were also observed when the cells were transfected with p38- or JNK-specific siRNAs. Overexpression of H2AX in K562 cells markedly increased resveratrol-induced apoptosis, whereas overexpression of H2AX-139m （Ser139 was mutated to block phosphorylation） inhibited resveratrol-induced apoptosis. K562 cells transfected with H2AX-speciflc siRNAs were resistant to resveratrol-induced apoptosis. Conclusion： H2AX phosphorylation at Ser139 in human CML cells, which is regulated by p38 and JNK, is essential for resveratrolinduced apoptosis.

Aim： To investigate the effect and underlying mechanisms of polygalasaponin F （PGSF）, a triterpenoid saponin isolated from Polygala japonica, on long-term potentiation （LTP） in hippocampus dentate gyrus （DG） of anesthetized rats. Methods： Population spike （PS） of hippocampal DG was recorded in anesthetized male Wistar rats. PGSF, the NMDAR inhibitor MK801 and the CaMKII inhibitor KN93 were intracerebroventricularly administered. Western blotting analysis was used to examine the phosphorylation expressions of NMDA receptor subunit 2B （NR2B）, Ca^2＋/calmodulin-dependent kinase II （CaMKII）, extraceilular signal- regulated kinase （ERK）, and cAMP response element-binding protein （CREB）. Results： Intracerebroventricular administration of PGSF （1 and 10 μmol/L） produced long-lasting increase of PS amplitude in hippocampal DG in a dose-dependent manner. Pre-injection of MKS01 （100 μmol/L） or KN93 （100 μmol/L） completely blocked PGSF- induced LTP. Furthermore, the phosphorylation of NR2B, CaMKII, ERK, and CREB in hippocampus was significantly increased 5-60 min after LTP induction. The up-regulation of p-CaMKII expression could be completely abolished by pre-injection of MK801. The upregulation of p-ERK and p-CREB expressions could be partially blocked by pre-injection of KN93. Conclusion： PGSF could induce LTP in hippocampal DG in anesthetized rats via NMDAR activation mediated by CaMKII, ERK and CREB signaling pathway.

The sigma-1 receptor (Sig-1R) is encoded by the SIGMAR1 gene and is a nonopioid transmembrane receptor located in the mitochondrial-associated endoplasmic reticulum membrane (MAM). It helps to locate endoplasmic reticulum calcium channels, regulates calcium homeostasis, and acts as a molecular chaperone to control cell fate and participate in signal transduction. It plays an important role in protecting neurons through a variety of signaling pathways and participates in the regulation of cognition and motor behavior closely related to neurodegenerative diseases. Based on its neuroprotective effects, Sig-1R has now become a breakthrough target for alleviating Alzheimer’s disease and other neurodegenerative diseases. This article reviews the most cutting-edge research on the function of Sig-1R under normal or pathologic conditions and target drugs of the sigma-1 receptor in neurodegenerative diseases.

Background Juvenile hormone (JH) is an insect-exclusive hormone involved in regulating diverse aspects of insect physiology, and the evolution of its diverse function is widely interesting. Studying embryogenesis in basal wingless insects is important to understand the functional evolution of JH; however, experimental studies in this regard are scarce. In this study, we conducted CRISPR/Cas9-mediated knockout (KO) of genes involved in JH biosynthesis and signaling cascades in the ametabolous firebrat, Thermobia domestica . Additionally, we investigated whether the primitive action of JH is conserved in the hemimetabolous cricket, Gryllus bimaculatus . Results We observed that KO of JHAMT , CYP15A1 , Met , and Kr-h1 resulted in embryonic lethality in T. domestica . Deprivation of JH or JH signaling arrested the progression of extraembryonic fluid resorption after dorsal closure and hatching, which is consistent with the gene expression pattern showing high Kr-h1 expression in the late embryos of T. domestica . The embryos deficient in JH signaling displayed wrinkled and weak legs. Comparative transcriptome analysis revealed that JH signaling promotes embryonic leg maturation through inducing energy supply and muscle activity, as validated by transmission electron microscopy (TEM). In addition, JH signaling exhibited similar embryonic effects in G. bimaculatus . Conclusions This study reveals the indispensable role of JH signaling in facilitating the maturation of terminal tissues during late embryogenesis, as demonstrated by the regulation of leg development, in ametabolous and hemimetabolous insects. These findings further indicate that the embryonic functions of JH evolved earlier than its anti-metamorphic functions during postembryonic development.

Conventional I/O Buffer Information Specification (IBIS) models often suffer from reduced fidelity in high-speed signaling because their static table-lookup mechanism cannot accurately reproduce complex transient I/O-buffer dynamics. To address this limitation, this study proposes a Verilog-AMS-based dynamic parameter compensation method. First, the conventional IBIS model is reformulated into a three-layer architecture comprising a data interface layer, an intermediate variable computation layer, and a port response synthesis layer. Then, based on Kirchhoff’s current law (KCL), the monotonic dependence of the output voltage on the pull-up and pull-down driving factors, kpu and kpd, is analytically derived to provide a directional criterion for parameter correction. Building on this criterion, a pulse-width-driven compensation algorithm is developed by constructing a pulse-width-indexed dual-factor empirical adjustment matrix and detecting the pulse width of the input bitstream in real time during transient simulation. The detected pulse width is then used to dynamically update kpu and kpd, enabling the IBIS response to converge toward the transistor-level SPICE reference waveform. Three representative device models were evaluated at 666 Mbps and 1.302 Gbps using pseudo-random binary sequence excitation, and the model fidelity was quantified using the normalized mean square error (NMSE). The proposed method reduced the NMSE from −6.73 to −1.03 dB before compensation to −54.79 to −44.19 dB after compensation, demonstrating a substantial improvement in high-frequency IBIS modeling fidelity and confirming the robustness and adaptability of the pulse-width-aware dynamic compensation strategy under random high-speed excitation.

In order to remove phosphorus element from steelmaking slag and decrease iron loss, malic acid was selected as the leaching agent to dissolve steelmaking slag. Firstly, the influences of different factors, such as malic acid concentration, slag particle size, temperature, liquid/solid ratio and stirring speed, on the leaching ratios of phosphorus and iron were studied. Then, the kinetics for the leaching process of phosphorus was analyzed. The results showed that the leaching ratios of phosphorus and iron increase significantly with increasing the malic acid solution concentration and liquid/solid ratio. When the concentration of malic acid solution increases up to 0.01492 mol/L, about 80% phosphorus can be dissolved, and iron leaching ratio is less than 17%. In addition, decreasing slag particle size can obviously increase the leaching ratio of phosphorus. However, temperature and stirring speed have no significant effect on the dissolution of phosphorus and iron. The leaching kinetics of phosphorus follows the unreacted shrinking core model. Diffusion through product layer is the rate-limiting step of the leaching process, and the corresponding apparent activation energy is determined to be 3.32 kJ/mol. Finally, a semi-empirical kinetic equation was established.

AlCrCuFeMn x ( x =0, 0.5, 1, 1.5, and 2) high-entropy alloys were prepared using the vacuum arc melting technology. The microstructure and mechanical properties of AlCrCuFeMn x were analyzed and tested by XRD, SEM, TEM, nanoindentation, and electronic universal testing. The results indicate that the AlCrCuFeMn x high-entropy alloy exhibits a dendritic structure, consisting of dendrites with a BCC structure, interdendrite regions with an FCC structure, and precipitates with an ordered BCC structure that form within the dendrite. Manganese (Mn) has a strong affinity for dendritic, interdendritic, and precipitate structures, allowing it to easily enter these areas. With an increase in Mn content, the size of the precipitated nanoparticles in the dendritic region initially increases and then decreases. Similarly, the area fraction initially decreases and then increases. Additionally, the alloy’s strength and wear resistance decrease, while its plasticity increases. The AlCrCuFeMn 1.5 alloy boasts excellent mechanical properties, including a hardness of 360 HV and a wear rate of 2.4×10 −5 mm 3 ·N −1 ·mm −1 . It also exhibits impressive yield strength, compressive strength, and deformation rates of 960 MPa, 1,700 MPa, and 27.5%, respectively.

The praseodymium-doped indium zinc oxide (PrIZO) thin-film transistor (TFT) is promising for applications in flat-panel displays, due to its high carrier mobility and stability. Nevertheless, there are few studies on the mechanism of annealing on PrIZO films and the fabrication of flexible devices. In this work, we first optimized the annealing-process parameters on the glass substrate. As the annealing temperature rises, the film tends to be denser and obtains a lower surface roughness, a narrower optical-band gap and less oxygen-vacancy content. However, the μ-PCD test shows the 250 °C-annealed film obtains the least defects. And the PrIZO TFT annealed at 250 °C exhibited a desired performance with a saturation mobility (μsat) of 14.26 cm2·V−1·s−1, a subthreshold swing (SS) of 0.14 V·dec−1, an interface trap density (Dit) of 3.17 × 1011, an Ion/Ioff ratio of 1.83 × 108 and a threshold voltage (Vth) of −1.15 V. The flexible devices were prepared using the optimized parameters on the Polyimide (PI) substrate and subjected to static bending tests. After bending at a radius of 5 mm, the mobility of devices decreases slightly from 12.48 to 10.87 cm2·V−1·s−1, demonstrating the great potential of PrIZO for flexible displays.