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Summary: Transcriptional regulation mechanisms underlying chilling injury (CI) development have been widely investigated in model plants and cold‐sensitive fruits, such as banana (Musa acuminata). However, unlike the well‐known NAC and WRKY transcription factors (TFs), the function and deciphering mechanism of heat shock factors (HSFs) involving in cold response are still fragmented. Here, we showed that hot water treatment (HWT) alleviated CI in harvested banana fruits accomplishing with reduced reactive oxygen species (ROS) accumulation and increased antioxidant enzyme activities. A cold‐inducible but HWT‐inhibited HSF, MaHsf24, was identified. Using DNA affinity purification sequencing (DAP‐seq) combined with RNA‐seq analyses, we found three heat shock protein (HSP) genes (MaHSP23.6, MaHSP70‐1.1 and MaHSP70‐1.2) and three antioxidant enzyme genes (MaAPX1, MaMDAR4 and MaGSTZ1) were the potential targets of MaHsf24. Subsequent electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation coupled with quantitative PCR (ChIP‐qPCR) and dual‐luciferase reporter (DLR) analyses demonstrated that MaHsf24 repressed the transcription of these six targets via directly binding to their promoters. Moreover, stably overexpressing MaHsf24 in tomatoes increased cold sensitivity by suppressing the expressions of HSPs and antioxidant enzyme genes, while HWT could recover cold tolerance, maintaining higher levels of HSPs and antioxidant enzyme genes, and activities of antioxidant enzymes. In contrast, transiently silencing MaHsf24 by virus‐induced gene silencing (VIGS) in banana peels conferred cold resistance with the upregulation of MaHSPs and antioxidant enzyme genes. Collectively, our findings support the negative role of MaHsf24 in cold tolerance, and unravel a novel regulatory network controlling bananas CI occurrence, concerning MaHsf24‐exerted inhibition of MaHSPs and antioxidant enzyme genes. [ABSTRACT FROM AUTHOR]

Precise regulation of gene expression is essential for proper development and the maintenance of homeostasis in organisms. Studies have shown that some transcriptional regulatory proteins influence gene expression through the formation of dynamic, locally concentrated assemblies known as condensates, while dysregulation of transcriptional condensates was associated with several cancers, such as Ewing sarcoma and AML [Wang Y et al. (2023) Nat Chem Biol 19, 1223–1234; Chandra B et al. (2022) Cancer Discov 12, 1152–1169]. Mutations in the histone acetylation “reader” eleven‐nineteen‐leukemia (ENL) have been shown to form discrete condensates at endogenous genomic targets, but it remains unclear how ENL mutations drive tumorigenesis and whether it is correlated with their condensate formation property. Liu et al. now show, using a conditional knock‐in mouse model, that ENL YEATS domain mutation is a bona fide oncogenic driver for AML. This mutant ENL forms condensates in hematopoietic stem/progenitor cells at the genomic loci of key leukemogenic genes, including Meis1 and Hoxa cluster genes, and disrupting condensate formation via mutagenesis impairs its chromatin and oncogenic function. Furthermore, they show that small‐molecule inhibition of the acetyl‐binding activity displaces ENL mutant condensates from oncogenic target loci, and this inhibitor significantly impairs the onset and progression of AML driven by mutant ENL in vivo. [ABSTRACT FROM AUTHOR]

Inverse optimal control is a widely used technique for solving various optimal problems arising in the controlled system. However, this method becomes inapplicable to optimal problems when the system has disturbances. In this article, we propose a novel anti‐disturbance inverse optimal controller design for a class of high‐dimensional chain structure systems with any disturbances, matched, or mismatched. First, a disturbance observer is employed to get the estimates of the disturbances in the system. Then using backstepping approach, the disturbance estimation is incorporated in the virtual control laws, and consequently a control Lyapunov function (CLF) is obtained. Finally, a composite controller is designed by developing an inverse optimal control method using the obtained CLF function. We show the stability analysis of the anti‐disturbance controller with rigorous proofs, which minimizes an optimal index while the output converges. Moreover, simulation study and analysis for real application to DC–DC buck converters reveal that the proposed composite controller achieves good performance and stabilizes the system with disturbances. [ABSTRACT FROM AUTHOR]

What is known and Objective: It is well known that high in‐stent thrombotic risk due to the superimposition of a platelet‐rich thrombus was considered as the main origin of major adverse cardiac events after stent implantation. The clinical management of antiplatelet therapy strategy after percutaneous coronary intervention (PCI) remains controversial. This study is sought to explore the efficacy and safety of a maintained P2Y12 inhibitor monotherapy after shorter‐duration of dual antiplatelet therapy (DAPT) in these patients. Methods: Medline, Google Scholar, Web of Science, and the Cochrane Controlled Trials Registry were searched online for retrieving eligible citations. A composite of all‐cause death, myocardial infarction (MI) and stroke was defined as major adverse cardio‐ and cerebro‐vascular events (MACCE), which is analysed as the primary efficacy endpoint. The risk of bleeding events was chosen as safety endpoint. Results: Five randomized clinical trials (RCT) with 32,143 patients were finally analysed. A maintained P2Y12 inhibitor monotherapy after shorter‐duration of DAPT cloud not only reduce the incidence of MACCE [odds ratios (OR): 0.89, 95% confidence intervals (CI): 0.79–0.99, p = 0.037], but also the bleeding risk (OR 0.61, 95% CI: 0.44–0.85, p = 0.003). No higher incidence of any ischaemic events, including MI, stroke or definite stent thrombosis (ST) was observed with respect to this new antiplatelet therapy option. Conclusions: A maintained P2Y12 inhibitor monotherapy after shorter‐duration of DAPT was suggested as a more preferable antiplatelet therapy option in patients undergoing coronary drug‐eluting stents (DES) placement. Larger and more powerful randomized trials with precise sub‐analyses are still necessary for further confirming these relevant benefits. [ABSTRACT FROM AUTHOR]

SUMMARY: Fruit ripening in tomato (Solanum lycopersicum) is the result of selective expression of ripening‐related genes, which are regulated by transcription factors (TFs). The NAC (NAM, ATAF1/2, and CUC2) TF family is one of the largest families of plant‐specific TFs and members are involved in a variety of plant physiological activities, including fruit ripening. Fruit ripening‐associated NAC TFs studied in tomato to date include NAC‐NOR (non‐ripening), SlNOR‐like1 (non‐ripening like1), SlNAC1, and SlNAC4. Considering the large number of NAC genes in the tomato genome, there is little information about the possible roles of other NAC members in fruit ripening, and research on their target genes is lacking. In this study, we characterize SlNAM1, a NAC TF, which positively regulates the initiation of tomato fruit ripening via its regulation of ethylene biosynthesis. The onset of fruit ripening in slnam1‐deficient mutants created by CRISPR/Cas9 (clustered regularly interspaced short palindromic repeats and CRISPR‐associated protein 9) technology was delayed, whereas fruit ripening in OE‐SlNAM1 lines was accelerated compared with the wild type. The results of RNA‐sequencing (RNA‐seq) and promoter analysis suggested that SlNAM1 directly binds to the promoters of two key ethylene biosynthesis genes (1‐aminocyclopropane‐1‐carboxylate synthase: SlACS2 and SlACS4) and activates their expression. This hypothesis was confirmed by electrophoretic mobility shift assays and dual‐luciferase reporter assay. Our findings provide insights into the mechanisms of ethylene production and enrich understanding of the tomato fruit ripening regulatory network. [ABSTRACT FROM AUTHOR]

Objective. To investigate the effects of lycopene-loaded microemulsion (LME) on the cognitive function and neurogenesis in the dentate gyrus (DG) of the hippocampus and subventricular (SVZ) region of rats with amyloid β- (Aβ-) induced Alzheimer's disease (AD) and its mechanism based on the Wnt/β-catenin pathway. Methods. Healthy Wistar rats were divided into four groups: the blank control (CON), AD control, traditional lycopene (LOO), and LME groups. The CON and AD groups were fed with normal saline, while the LOO group was fed with traditional lycopene, and the LME group was fed with lycopene-loaded microemulsion. Behavioral tests were performed after three weeks of gastric administration. Immunofluorescence-labeled cells were used to observe the differentiation and maturation of new nerve cells in the DG of the hippocampus and SVZ region. qRT-PCR and Western blotting detected the expression of neurogenesis genes and Wnt/β-catenin pathway-related proteins, respectively. Results. On the Morris water maze test, LME rats had significantly shortened movement trajectory on the searching platform, reduced escape latency time, and increased residence time on the original platform quadrant. In addition, more LME rats crossed the platform when it was removed. Thus, LME can improve the spatial learning and memory of Aβ-induced AD rats. On qRT-PCR, LME significantly increased Reelin, Nestin, and Pax6 gene expressions, which regulate neurogenesis. Immunofluorescence showed that LME could significantly increase BrdU+, Dcx+, BrdU+/Neun+, BrdU+/Dcx+ cells in the DG and SVZ regions, thus promoting neurogenesis. LME also reduced the number of Iba1+ and Iba1+/BrdU+ cells, thus reducing the neuroinflammatory response. On Western blot, LME upregulated the Wnt/β-catenin pathway by upregulating Wnt3a, β-catenin, Disheveled (Dvl), and p-GSK3β and downregulating p-β-catenin and GSK3β. Conclusion. LME attenuates cognitive impairment in Aβ-induced AD rats by promoting neurogenesis in the hippocampus and SVZ region through upregulating the Wnt/β-catenin pathway. [ABSTRACT FROM AUTHOR]

LINKED CONTENT: This article is linked to Lui et al papers. To view these articles, visit https://doi.org/10.1111/apt.17654 and https://doi.org/10.1111/apt.17713 [ABSTRACT FROM AUTHOR]

Summary: Starch degradation is a necessary process determining banana fruit quality during ripening. Many starch degradation‐related genes are well studied. However, the transcriptional regulation of starch degradation during banana fruit ripening remains poorly understood. In this study, we identified a MYB transcription factor (TF) termed MaMYB3, as a putative protein binding the promoter of MaGWD1, a member of glucan water dikinase (GWD) family which has been demonstrated as an important enzyme of starch degradation. MaMYB3 was ripening‐ and ethylene‐repressible, and its expression was negatively correlated with starch degradation. Acting as a nucleus‐localized transcriptional repressor, MaMYB3 repressed the transcription of 10 starch degradation‐related genes, including MaGWD1, MaSEX4, MaBAM7‐MaBAM8, MaAMY2B, MaAMY3, MaAMY3A, MaAMY3C, MaMEX1, and MapGlcT2‐1, by directly binding to their promoters. Interestingly, a previously identified activator of starch degradation‐related genes, MabHLH6, was also suppressed by MaMYB3. The ectopic overexpression of MaMYB3 in tomato down‐regulated the expression of starch degradation‐related genes, inhibited starch degradation and delayed fruit ripening. Based on these findings, we conclude that MaMYB3 negatively impacts starch degradation by directly repressing starch degradation‐related genes and MabHLH6, and thereby delays banana fruit ripening. Collectively, our study expands our understanding of the complex transcriptional regulatory hierarchy modulating starch degradation during fruit ripening. Significance Statement: MaMYB3 negatively impacts starch degradation by the direct repression of MabHLH6 and starch degradation‐related genes, and thus delays banana fruit ripening. Our findings illustrate the complex transcriptional regulatory hierarchy modulating starch degradation during fruit ripening. [ABSTRACT FROM AUTHOR]

Abstract: The high‐sulfur gas sweetening process is energy consuming. To analyze its energy efficiency effectively, and look for ways to improve this process, a novel energy‐efficiency evaluation method based on the yield‐energy‐selectivity and efficiency coefficient methods was proposed. First, the yield, energy, and selectivity are selected as evaluation indicators to establish the yield‐energy‐selectivity evaluation model. Then, the coefficient and score of each indicator were determined by using the analytical hierarchy process and efficacy coefficient method, respectively. Finally, the proposed energy‐efficiency evaluation method was applied to the actual high‐sulfur gas sweetening process. The evaluation results were in good agreement with those obtained by actual experiences. [ABSTRACT FROM AUTHOR]

Background and Aims. Hypoxia regulates the survival of mesenchymal stem cells (MSCs) but the mechanism is unclear. In hypoxia, the level of high mobility group box 1 (HMGB1) was increased in many cells which may be involved in the regulation of cell biology. The aim is to determine whether hypoxia affects the expression of HMGB1 in bone marrow MSCs (BM-MSCs) and to investigate the role of HMGB1 in the apoptosis and adhesion. Methods. BM-MSCs were exposed to hypoxia (1% O2) and normoxia (20% O2) and the expression of HMGB1 was measured by RT-PCR and western blotting. The apoptosis and adhesion of BM-MSCs were evaluated after interfered by different concentrations of HMGB1. Results. Expression of HMGB1 in BM-MSCs showed a significant upregulation in hypoxia when compared to those in normoxia. The adhesion of BM-MSCs was increased by HMGB1 in a concentration-dependent manner; the apoptosis effect of HMGB1 depended on its concentrations: HMGB1 at low concentration (50 ng/mL) promoted the apoptosis of BM-MSCs while HMGB1 at high concentration (≥100 ng/mL) reduced this apoptosis. Conclusions. Hypoxia enhanced the expression of HMGB1 in BM-MSCs with influences on apoptosis and adhesion and this could have a significant effect on the regenerative potential of MSC-based strategies. [ABSTRACT FROM AUTHOR]

As a central event in liver fibrogenesis, hepatic stellate cell (HSC) transdifferentiation involves loss of regulation by adipogenic transcription factors such as peroxisome proliferator-activated receptor γ; (PPARγ), which is epigenetically silenced during HSC activation. We hypothesized that JMJD1A, an H3K9 demethylase involved in adipogenic metabolism, could regulate PPARγ. In human HSC cell line, rat primary HSCs, and carbontetrachlorideinducedmouse liverfibrogenesis model,wedown-regulated the expression of JMJD1A using small interfering or short hairpin RNAs, and overexpressed its wild-type and mutant. We analyzed the effects of JMJD1A manipulation on the histone di-methyl-H3K9 (H3k9me2) status of PPARγ gene and the expression of PPARγ and fibrosis markers using chromatin immunoprecipitation, real-time quantitative RTPCR and Western blot, and also investigated the in vitro and in vivoconsequencesonliverfibrosis andnecrosisbyMasson or hematoxylin-eosin staining, respectively. JMJD1A knockdown in HSCs correlated with reinforced H3K9me2 in the PPARγ gene promoter, and its down-regulation in both mRNA and protein led to increased expression of fibrosis markers, which could be consistently rescued by JMJD1A overexpression. Jmjd1a knockdown in situ resulted in significantly increased expression of a-smooth muscle actin (P = 0.005) and Col1a (P = 0.036), strengthened production of collagens (P = 0.028), and remarkably enhanced necrosis (P = 0.007) 4 weeks after treatment. This study suggests JMJD1A as a novel epigenetic regulator that modulates HSC activation and liver fibrosis through targeting PPARγ gene expression. [ABSTRACT FROM AUTHOR]

The sequences of 16S rDNA, cytochrome oxidase subunit I ( COI) and cytochrome b ( Cyt b) genes from nine field collections (seven provinces in China: Guangxi, Hubei, Guangdong, Guizhou, Zhejiang, Hunan, Jiangxi, and also southern and northern part of Iran), plus the sequences of Africa, Europe, Americas and Japan obtained form GenBank were used to re-analyse the genetic variation in the southern green stink bug Nezara viridula (Linnaeus). The phylogeographic re-analysis by using four algorithms (NJ, MP, ML and Bayesian) showed three main lineages. The Iranian haplotypes fell into lineage II formed from Europe and America, rather than in lineage III from Asia; the Chinese haplotypes fell into the Asian clade. Our results suggested that African and non-African gene pools have been isolated since the Miocene era with the molecular clock calibrations for Heteroptera mtDNA, and not since the Pliocene as mentioned previously. The corresponding age of the separation of the eastern and western Asia clades is estimated to be 4.0-1.6 million years ago, coinciding with the Pliocene-Pleistocene epoch and with acute rising events in the Tibet Plateau locates in the western China, which may have formed the barriers observed today. [ABSTRACT FROM AUTHOR]

Abstract: To investigate whether stem cell transplantation affects ventricular electrophysiology in vivo, either autologous bone marrow mesenchymal stem cells or skeletal myoblast cells were transplanted via a catheter into a doxorubicin-treated failing heart. Four weeks after transplantation, electrophysiological investigation showed that transplantation of either cell type prolonged the local activation time and increased the activation time dispersion. In the stem cell transplantation groups, a positive correlation was demonstrated between activation time dispersion and the number of stem cell-derived cells in the pacing site. It is concluded that transplantation of either mesenchymal stem cells or skeletal myoblast cells might exacerbate abnormalities of local ventricular conduction in the doxorubicin-treated failing heart. [Copyright &y& Elsevier]

The article presents a structural analysis of the compound, [Cd(C8H18NO8P2)2]n that was conducted by researchers from the Jinggangshan University, China. The compound was formed through hydrothermal processes, and shows a layered structure that was made from coordinating six oxygen atoms from four phosphonate ligands. Researchers note that the study of metal phosphonates is essential to understanding applications in catalysis, ion exchange, and intercalation chemistry.

Summary: With five sub towers and a maximum height of 246.8 m, the Beijing Olympic Tower (BOT) is a landmark of Beijing. The complex structural properties and slenderness of the BOT render it prone to wind loading. As far as the wind‐induced performance of this structure is concerned, this paper thus aims at a tuned mass damper‐based mitigation system for controlling the wind‐induced acceleration response of the BOT. To this end, the three‐dimensional wind loading of various wind directions are simulated based on the fluctuating wind force obtained by the wind tunnel test, by which the wind‐induced vibration is evaluated in the time domain by using the finite element model. A double‐stage pendulum tuned mass damper (DPTMD), which is capable of controlling the long period dynamic response and requires only a limited space of installation, is optimally designed at the upper part of the tower. Finally, the wind‐induced response of the structure with and without DPTMD is compared with respect to various wind directions and in both the time and frequency domains. The comparative results show that the wind‐induced accelerations atop the tower with the wind directions of 45, 135, 225, and 315° are larger than those with the other directions. The DPTMD significantly reduces the wind‐induced response by the maximum acceleration reduction ratio of 30.05%. Moreover, it is revealed that the control effect varies noticeably for the five sub towers, depending on the connection rigidity between Tower1 and each sub tower. [ABSTRACT FROM AUTHOR]

The title triazole compound, C15H8Cl4N4S·C3H7NO, has been obtained as an unexpected product when attempting to prepare Schiff bases of thio­carbohydrazide (TCH). The triazole ring is planar within 0.004 (8) Å because of conjugation. The dihedral angles between the 1,2,4-triazole ring and the two benzene rings are 24.9 (2) and 70.0 (2)°. The interplanar angle between the two benzene rings is 83.4 (2)°. The packing of the mol­ecules is stabilized both by van der Waals interactions and by N—H·O intermolecular hydrogen bonds between the triazole N atom and the carbonyl O atom of the di­methyl­form­amide solvent mol­ecule. [ABSTRACT FROM AUTHOR]

Melatonin and abscisic acid (ABA) play contrasting roles in regulating leaf senescence in plants. The molecular mechanism underlying the interaction between melatonin and ABA involved in leaf senescence, however, remains poorly defined. Herein, we found that exogenous application of melatonin delayed the senescence of Chinese flowering cabbage, accompanied by reduced expression of chlorophyll catabolic and ABA biosynthetic genes, and a lower endogenous ABA level. Significantly, three nucleus‐localized transcriptional activators BrABF1, BrABF4, and BrABI5 were identified, and their expressions were repressed by melatonin. In vitro and in vivo binding experiments revealed that BrABF1, BrABF4, and BrABI5 activated the transcription of a series of ABA biosynthetic and chlorophyll catabolic genes by physically binding to their promoters. Moreover, transient over‐expression of BrABF1, BrABF4, and BrABI5 in tobacco leaves induced ABA accumulation and promoted chlorophyll degradation by upregulating tobacco ABA biosynthetic and chlorophyll catabolic genes, resulting in the accelerated leaf senescence. These effects were significantly attenuated by melatonin treatment. Our findings suggest that melatonin‐mediated inhibition of leaf senescence involves suppression of ABFs‐mediated ABA biosynthesis and chlorophyll degradation. Unraveling of the molecular regulatory mechanism of leaf senescence controlled by ABA and melatonin expands our understanding of the regulation of this phenomenon and offers potentially more effective molecular breeding strategies for extending the shelf‐life of Chinese flowering cabbage. [ABSTRACT FROM AUTHOR]

In the title complex, [Ni(C7H3N2O6)(C10H8N2)(H2O)]ClO4, the NiII ion adopts a distorted square-pyramidal coordination geometry, with the coordinated water molecule occupying the apical position. The NiII complex cation is linked to the ClO4− anion by O—H...O hydrogen bonding. [ABSTRACT FROM AUTHOR]