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Modern lifestyle changes, especially the consumption of a diet high in salt, sugar, and fat, have contributed to the increasing incidence and prevalence of chronic metabolic diseases such as diabetes, obesity, and gout. Changing lifestyles continuously shape the gut microbiota which is closely related to the occurrence and development of metabolic diseases due to its specificity of composition and structural diversity. A large number of pathogenic bacteria such as Yersinia , Salmonella , Shigella , and pathogenic E. coli in the gut utilize the type III secretion system (T3SS) to help them resist host defenses and cause disease. Although the T3SS is critical for the virulence of many important human pathogens, its relationship with metabolic diseases remains unknown. This article reviews the structure and function of the T3SS, the disruption of intestinal barrier integrity by the T3SS, the changes in intestinal flora containing the T3SS in metabolic diseases, the possible mechanisms of the T3SS affecting metabolic diseases, and the application of the T3SS in the treatment of metabolic diseases. The aim is to provide insights into metabolic diseases targeting the T3SS, thereby serving as a valuable reference for future research on disease diagnosis, prevention, and treatment., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2024 Le Zhou et al.)

Background: Atherosclerosis (AS) is the most prevalent cardiovascular disease and remains the major contributor to death and mortality globally. Leonurine (LEO) is a unique alkaloid compound with protective effects on the cardiovascular system. However, the exact mechanisms underlying its cardiovascular-protecting action are still not fully elucidated. The methyltransferase 3 (METTL3), the catalytic core of the N6-methyladenosine modification (m 6 A) methyltransferase complex, has been shown to inhibit autophagy and exacerbate the process of AS via regulation of m 6 A modification of mRNA., Purpose: We aimed to determine whether the inhibited effect of LEO on AS is related to METTL3-mediated AKT1S1 stability., Methods: The apolipoprotein E (ApoE) knockout mice was subjected to a high-fat diet (HFD), and THP-1 derived macrophages was exposed to oxidized low-density lipoprotein (ox-LDL), to establish the animal and cellular models of AS, respectively., Results: We found that LEO effectively improved AS and reduced the plaque area and inflammation via diminishing macrophage lipid accumulation and remodeling the lipid metabolism profile. LEO activated ox-LDL-induced macrophage autophagy, enhancing lipid metabolism decrease, according to the lipidomic and molecular biology analyses. Additionally, LEO caused a marked increase in autophagy marker levels in mouse models with advanced AS. Furthermore, we found that LEO reactivated autophagy and reversed lipid accumulation by suppressing METTL3 expression. The m 6 A-seq from ox-LDL-induced macrophages showed that a total of five autophagy-related mRNA transcripts (AKT1S1, AKT1, RB1CC1, CFLAR, and MTMR4) were altered, and AKT1S1 was significantly upregulated by LEO. Mechanistically, LEO-mediated regulation of METTL3 decreased AKT1S1 expression by attenuating its mRNA stability. Silencing AKT1S1 inhibited LEO-METTL3 axis-mediated autophagy and enhanced lipid accumulation in ox-LDL-induced macrophages., Conclusion: The study first revealed that LEO exerts anti-atherosclerotic effect by activating METTL3-mediated macrophage autophagy in vivo and in vitro. The mechanism of LEO was further found to be the enhancement of METTL3-mediated AKT1S1 stability to activate autophagy thereby reducing lipid accumulation. This study provides a new perspective of natural medicines on the treatment of AS via an epigenetic manner., Competing Interests: Declaration of competing interest The authors declare that they have no conflict of interest., (Copyright © 2024 Elsevier GmbH. All rights reserved.)

Lower olefins are widely used in the chemical industry as basic carbon-based feedstocks. Here, we report the catalytic system featuring isolated single-atom sites of iridium (Ir 1 ) that can function within the entire temperature range of 300-600 °C and transform alkanes with conversions close to thermodynamics-dictated levels. The high turnover frequency values of the Ir 1 system are comparable to those of homogeneous catalytic reactions. Experimental data and theoretical calculations both indicate that Ir 1 is the primary catalytic site, while the coordinating C and N atoms help to enhance the activity and stability, respectively; all three kinds of elements cooperatively contribute to the high performance of this novel active site. We have further immobilized this catalyst on particulate Al 2 O 3 , and we found that the resulting composite system under mimicked industrial conditions could still give high catalytic performances; in addition, we have also developed and established a new scheme of periodical in situ regeneration specifically for this composite particulate catalyst.

Background: Diabetic nephropathy (DN) is a common microvascular complication of diabetes mellitus (DM). Ferroptosis is an atypical form of iron-dependent, modulated cell death that has been shown to occur in human umbilical vein endothelial cells (HUVECs). Leonurine (LEO) is a single active ingredient extracted from Leonurus japonicus Houtt . It has various biological activities, including anti-inflammatory and anti-cancer effects. However, whether LEO affects ferroptosis in DN has yet to be investigated., Methods: An animal model of DN was established by subjecting C57/BL6 mice to a high-fat diet (HFD) while being induced with Streptozotocin (STZ). A cellular model of DN was established by exposing HUVECs to a high glucose (HG) concentration of 30 mM., Results: LEO was found to improve DN and to attenuate the degree of glomerulosclerosis and tubular atrophy in the mouse model. Additionally, it markedly decreased the levels of ferroptosis markers. Molecular analyses revealed that LEO inhibited HG-induced oxidative stress in HUVECs, thereby decreasing endothelial cell (EC) dysfunction. Furthermore, LEO was found to reduce ferroptosis and reverse EC dysfunction by increasing the expression of glutathione peroxidase 4 (GPX4) and nuclear factor erythroid 2-related factor 2 (Nrf2). The suppression of Nrf2 in HG-induced HUVECs inhibited LEO-GPX4 axis-mediated ferroptosis and increased EC dysfunction., Conclusions: LEO exerts anti-DN effects both in vivo and in vitro by suppressing GPX4-mediated EC ferroptosis. Mechanistically, LEO appears to induce Nrf2-mediated GPX4 expression to inhibit ferroptosis, thereby reducing EC dysfunction. This study provides a new perspective on the treatment of diseases using natural medicines. It involves a novel form of cell death that could potentially lead to better treatment of DN., Competing Interests: The authors declare no conflict of interest., (© 2024 The Author(s). Published by IMR Press.)

The aromatization of light alkane is an important process for increasing the aromatic production and utilization efficiency of light alkane resources simultaneously. Herein, Ga-modified HZSM-5 catalysts were prepared and investigated by a series of characterization techniques such as X-ray diffraction, nuclear magnetic resonance spectroscopy, transmission electron microscopy, N 2 adsorption-desorption, and NH 3 temperature-programmed desorption to study their physicochemical properties. The catalytic performance in propane aromatization was also tested. Importantly, the structure-activity relationship, reaction pathway, and coke formation mechanism in propane aromatization were systematically explored. It was found that different Ga introduction methods would affect the amounts of Brønsted and Lewis acid sites, and Ga-HZSM-5 prepared by the hydrothermal method exhibited higher amounts of Brønsted and Lewis acid sites but a lower B/L ratio. As a result, Ga-HZSM-5 showed higher propane conversion and benzene, toluene, and xylene yield compared with that of Ga 2 O 3 /HZSM-5. The propane aromatization reaction pathway indicated that propane dehydrogenation to propene was a crucial step for aromatic formation. The increase of the Lewis acid density in Ga-HZSM-5 can effectively improve the dehydrogenation rate and promote the aromatization reaction. Furthermore, the formation of coke species was studied by thermogravimetry-mass spectrometry and Raman approaches, the results of which indicated that the graphitization degree of coke formed over spent Ga-HZSM-5 is lower, resulting in enhanced anticoking stability.

Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease with a clear genetic component. While most SLE patients carry rare gene variants in lupus risk genes, little is known about their contribution to disease pathogenesis. Amongst them, SH2B3-a negative regulator of cytokine and growth factor receptor signaling-harbors rare coding variants in over 5% of SLE patients. Here, we show that unlike the variant found exclusively in healthy controls, SH2B3 rare variants found in lupus patients are predominantly hypomorphic alleles, failing to suppress IFNGR signaling via JAK2-STAT1. The generation of two mouse lines carrying patients' variants revealed that SH2B3 is important in limiting the number of immature and transitional B cells. Furthermore, hypomorphic SH2B3 was shown to impair the negative selection of immature/transitional self-reactive B cells and accelerate autoimmunity in sensitized mice, at least in part due to increased IL-4R signaling and BAFF-R expression. This work identifies a previously unappreciated role for SH2B3 in human B cell tolerance and lupus risk., (© 2024 Zhang et al.)

The synthesis of laser coherence and the accuracy of beam scanning, which are based on an optical phased array (OPA), are severely constrained by phase noise. This limitation hampers their applications in various fields. Currently, the most widely utilized calibration method is adaptive optics, which can effectively mitigate phase noise and enhance the quality of the output beam. However, because of the multiple array elements of the OPA and the large optimization range for each element, the adaptive optimization method experiences slow convergence and a high risk of falling into local optima. We propose a narrowing search range algorithm that can quickly reduce phase noise by narrowing the search range of the optimal value. After initial optimization, the SPGD algorithm was used. This study was verified through simulations and experiments utilizing the OPA of various array elements. These findings indicate that the hybrid algorithm expedites the calibration process, requires simple experimental equipment, and can be broadly utilized.

Pulpitis is a common dental emergency that presents with intense pain; there is still no specific medicine to treat pulpitis-induced pain to date. Herein, differentially expressed genes in mouse anterior cingulate cortex (ACC) were investigated 7 days after pulp exposure via a combination of high-throughput transcriptomic and proteomic analyses. We screened 34 key genes associated with 8 critical pathways. Among these, genes (Elovl5, Ikbke, and Nbeal2) involved in immune or inflammatory responses exhibited exclusive regulation at the transcriptomic level, as confirmed by qRT-PCR. We also investigated the comprehensive expression profiles of genes (Erg1, Shank2, Bche, Serinf1, and Pax6) related to synaptic plasticity. Furthermore, the underlying mechanisms for pulpitis-induced pain through immune or inflammatory responses and synaptic plasticity were discussed. Taken together, our findings shed light on the mechanisms underlying pulpitis-induced pain, deepening our understanding of the molecular pathways and providing potential therapeutic and diagnostic targets., Competing Interests: The authors declare no competing financial interest., (© 2024 The Authors. Published by American Chemical Society.)

Background: Pain is a rapid response mechanism that compels organisms to retreat from the harmful stimuli and triggers a repair response. Nonetheless, when pain persists for extended periods, it can lead to adverse changes into in the individual's brain, negatively impacting their emotional state and overall quality of life. Microglia, the resident immune cells in the central nervous system (CNS), play a pivotal role in regulating a variety of pain-related disorders. Specifically, recent studies have shed light on the central role that microglial purinergic ligand-gated ion channel 7 receptor (P2X7R) plays in regulating pain. In this respect, the P2X7R on microglial membranes represents a potential therapeutic target., Aims: To expound on the intricate link between microglial P2X7R and pain, offering insights into potential avenues for future research., Methods: We reviewed 140 literature and summarized the important role of microglial P2X7R in regulating pain, including the structure and function of P2X7R, the relationship between P2X7R and microglial polarization, P2X7R-related signaling pathways, and the effects of P2X7R antagonists on pain regulation., Results: P2X7R activation is related to M1 polarization of microglia, while suppressing P2X7R can transfer microglia from M1 into M2 phenotype. And targeting the P2X7R-mediated signaling pathways helps to explore new therapy for pain alleviation. P2X7R antagonists also hold potential for translational and clinical applications in pain management., Conclusions: Microglial P2X7R holds promise as a potential novel pharmacological target for clinical treatments due to its distinctive structure, function, and the development of antagonists., (© 2023 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.)

Background: Studies have found that the plasma content of gut-derived 4-hydroxyphenylacetic acid (4-HPA) was significantly increased in septic patients. However, the mechanism of 4-HPA elevation during sepsis and its relationship with sepsis-induced acute kidney injury (SAKI) remain unclear., Methods: Cecal ligation and puncture (CLP) was performed in C57BL/6 mice to establish the SAKI animal model. Human renal tubular epithelial (HK-2) cells stimulated with lipopolysaccharide were used to establish the SAKI cell model. The widely targeted metabolomics was applied to analyze the renal metabolite changes after CLP. Proteomics was used to explore potential target proteins regulated by 4-HPA. The blood sample of clinical sepsis patients was collected to examine the 4-HPA content., Results: We found that renal gut-derived 4-HPA levels were significantly increased after CLP. The high permeability of intestinal barrier after sepsis contributed to the dramatic increase of renal 4-HPA. Intriguingly, we demonstrated that exogenous 4-HPA administration could further significantly reduce CLP-induced increases in serum creatinine, urea nitrogen, and cystatin C, inhibit renal pathological damage and apoptosis, and improve the survival of mice. Mechanistically, 4-HPA inhibited necroptosis in renal tubular epithelial cells by upregulating the protein expression of apoptosis repressor with caspase recruitment domain (ARC) and enhancing the interaction between ARC and receptor-interacting protein kinase 1 (RIPK1)., Conclusions: The increase of gut-derived 4-HPA in the kidney after sepsis could play a protective effect in SAKI by upregulating ARC to inhibit necroptosis., Competing Interests: Declaration of competing interest The authors declare no conflicts of interest., (Copyright © 2023. Published by Elsevier B.V.)

Abbreviations: AKI: acute kidney injury; ATP: adenosine triphosphate; BUN: blood urea nitrogen; CLP: cecal ligation and puncture; eGFR: estimated glomerular filtration rate; H&E: hematoxylin and eosin staining; LCN2/NGAL: lipocalin 2; LPS: lipopolysaccharide; LTL: lotus tetragonolobus lectin; mKeima: mitochondria-targeted Keima; mtDNA: mitochondrial DNA; PAS: periodic acid - Schiff staining; RTECs: renal tubular epithelial cells; SAKI: sepsis-induced acute kidney injury; Scr: serum creatinine; SIRT3: sirtuin 3; TFAM: transcription factor A, mitochondrial; TMRE: tetramethylrhodamine.

In recent years, the silicon-based optical phased array has been widely used in the field of light detection and ranging (LIDAR) due to its great solid-state steering ability. At the same time, the optical phased array transceiver integration scheme provides a feasible solution for low-cost information exchange of small devices in the future. Based on this, this paper designs a two-dimensional optical phased array transceiver with high efficiency and a large field of view, which can realize a dense array with antenna spacing of 5.5 μm × 5.5 μm by using low crosstalk waveguide wiring. Additionally, it can realize the conversion between the receiving mode and the transmitting mode by using the optical switch. The simulation results show that the scanning range of 16.3° × 16.3° can be achieved in the transmitting mode, and the overall loss is lower than 10dB. In the receiving mode, we can achieve a collection efficiency of more than 27%, and the antenna array receiving loss is lower than 12.1 dB.

Cell division cycle 42 (CDC42) regulates T helper (Th) cell differentiation and is related to psychological disorders. This study aimed to assess the correlation between blood CDC42 and Th cells, and their association with mental issues in stroke patients. Peripheral blood samples were obtained from 264 stroke patients and 50 controls. Then, serum CDC42 was measured by enzyme-linked immunosorbent assay, and Th1, Th2, and Th17 cells were detected by flow cytometry. Hospital Anxiety and Depression Scale (HADS) and Mini Mental State Examination (MMSE) were applied to patients. CDC42 was decreased (P<0.001), Th1 (P=0.013) and Th17 (P<0.001) cells were elevated, while Th2 cells (P=0.108) showed no difference in stroke patients compared to controls. In addition, CDC42 was negatively associated to Th1 (P=0.013) and Th17 (P<0.001) cells in stroke patients but were not associated with Th2 cells (P=0.223). Interestingly, CDC42 was negatively associated with HADS-anxiety (P<0.001) and HADS-depression scores (P=0.034) and positively associated with MMSE score (P<0.001) in stroke patients. Lower CDC42 was associated to lower occurrence of anxiety (P=0.002), depression (P=0.001), and cognitive impairment (P=0.036) in stroke patients. Furthermore, increased Th17 cells were positively correlated with HADS-anxiety and HADS-depression scores and inversely correlated with MMSE score, which were also associated with higher occurrence of anxiety, depression, and cognitive impairment in stroke patients (all P<0.05). Blood CDC42 and Th17 cells were correlated, and both of them were linked to the risk of anxiety, depression, and cognitive impairment. However, the findings need further large-scale validation, and the implicated mechanism needs more investigation.

Key Message: Thirty-three stable QTL for 13 yield-related traits across ten environments were identified in the PD34/MY47 RIL population, and a candidate gene TaGS5-3D in Qmt.nwafu.3D was preliminarily identified to affect grain-related traits through accumulation of specific transcripts. Dissecting the genetic basis of yield-related traits is pivotal for improvement of wheat yield potential. In this study, a recombinant inbred line (RIL) population genotyped by SNP markers was used to detect quantitative trait loci (QTL) related to yield-related traits in ten environments. A total of 102 QTL were detected, including 33 environmentally stable QTL and 69 putative QTL. Among them, Qmt.nwafu.3D was identified as a pleiotropic QTL in the physical interval of 149.77-154.11 Mb containing a potential candidate gene TaGS5-3D. An SNP (T > C) was detected in its ninth intron, and TaGS5-3D-C was validated as a superior allele associated with larger grains using a CAPS marker. Interestingly, we found that TaGS5-3D-C was closely related to significantly up-regulated expression of intron-retained transcript (TaGS5-3D-PD34.1), while TaGS5-3D-T was related to dominant expression of normal splicing transcript (TaGS5-3D-MY47.1). Our results indicated that alternative splicing associated with the SNP T/C could be involved in the regulation of grain-related traits, laying a foundation for the functional analysis of TaGS5-3D and its greater potential application in high-yield wheat breeding., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Cardiac fibrosis plays a key role in the progression of diabetic cardiomyopathy (DCM). Previous studies demonstrated the cardioprotective effects of natriuretic peptides. However, the effects of natriuretic peptide receptor C (NPRC) on cardiac fibrosis in DCM remains unknown. Here, we observed that myocardial NPRC expression was increased in mice and patients with DCM. NPRC -/- diabetic mice showed alleviated cardiac fibrosis, as well as improved cardiac function and remodeling. NPRC knockdown in both cardiac fibroblasts and cardiomyocytes decreased collagen synthesis and proliferation of cardiac fibroblasts. RNA sequencing identified that NPRC deletion up-regulated the expression of TGF-β-induced factor homeobox 1 (TGIF1), which inhibited the phosphorylation of Smad2/3. Furthermore, TGIF1 up-regulation was mediated by the activation of cAMP/PKA and cGMP/PKG signaling induced by NPRC deletion. These findings suggest that NPRC deletion attenuated cardiac fibrosis and improved cardiac remodeling and function in diabetic mice, providing a promising approach to the treatment of diabetic cardiac fibrosis.

The increase of lactate is an independent risk factor for patients with sepsis-induced acute kidney injury (SAKI). However, whether elevated lactate directly promotes SAKI and its mechanism remain unclear. Here we revealed that downregulation of the deacetylase Sirtuin 3 (SIRT3) mediated the hyperacetylation and inactivation of pyruvate dehydrogenase E1 component subunit alpha (PDHA1), resulting in lactate overproduction in renal tubular epithelial cells. We then found that the incidence of SAKI and renal replacement therapy (RRT) in septic patients with blood lactate ≥ 4 mmol/L was increased significantly, compared with those in septic patients with blood lactate < 2 mmol/L. Further in vitro and in vivo experiments showed that additional lactate administration could directly promote SAKI. Mechanistically, lactate mediated the lactylation of mitochondrial fission 1 protein (Fis1) lysine 20 (Fis1 K20la). The increase in Fis1 K20la promoted excessive mitochondrial fission and subsequently induced ATP depletion, mitochondrial reactive oxygen species (mtROS) overproduction, and mitochondrial apoptosis. In contrast, PDHA1 activation with sodium dichloroacetate (DCA) or SIRT3 overexpression decreased lactate levels and Fis1 K20la, thereby alleviating SAKI. In conclusion, our results show that PDHA1 hyperacetylation and inactivation enhance lactate overproduction, which mediates Fis1 lactylation and exacerbates SAKI. Reducing lactate levels and Fis1 lactylation attenuate SAKI., (© 2023. The Author(s).)

Endemic fluorosis is a global public health problem. Cardiovascular diseases caused by fluoride are closely related to endothelial cell injury. Metabolism disorder of endothelial cells (ECs) are recognized as the key factor of endothelial dysfunction which has been a hot topic in recent years. However, the toxic effect of fluoride on vascular endothelium has not been elucidated. The aim of this study was to explore the alteration of endothelial cell metabolites in Human Umbilical Vein Endothelial Cells (HUVECs) exposed to NaF using LC-MS/MS technique. The screening conditions were Variable Importance for the Projection (VIP) > 1 and P < 0.05. It was found that the expression of the metabolites Lumichrome and S-Methyl-5'-thioadenosine was upregulated and of the other metabolites, such as Creatine, L-Glutamate, Stearic acid was downregulated. Differential metabolites were found to be primarily related to FoxO、PI3K/Akt and apoptosis signaling pathways by Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. From the perspective of metabolism, this study explored the possible mechanism of fluoride induced endothelial cell injury which providing theories and clues for subsequent studies., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier B.V. All rights reserved.)

Objective: Increased Toll-like receptor 7 (TLR-7) signaling leading to the production of type I interferon (IFN) is an important contributor to human systemic lupus erythematosus (SLE). Protein kinase C and casein kinase substrate in neurons 1 (PACSIN1), a molecule that regulates synaptic vesicle recycling, has been linked to TLR-7/TLR-9-mediated type I IFN production in humans and mice, but the underlying mechanism is unknown. We undertook this study to explore the pathogenicity and underlying mechanism of a de novo PACSIN1 missense variant identified in a child with SLE., Methods: PACSIN1 Q59K de novo and null variants were introduced into a human plasmacytoid dendritic cell line and into mice using CRISPR/Cas9 editing. The effects of the variants on TLR-7/TLR-9 signaling in human and mouse cells, as well as PACSIN1 messenger RNA and IFN signature in SLE patients, were assessed using real-time polymerase chain reaction and flow cytometry. Mechanisms were investigated using luciferase reporter assays, RNA interference, coimmunoprecipitation, and immunofluorescence., Results: We established that PACSIN1 forms a trimolecular complex with tumor necrosis factor receptor-associated factor 4 (TRAF4) and TRAF6 that is important for the regulation of type I IFN. The Q59K mutation in PACSIN1 augments binding to neural Wiskott-Aldrich syndrome protein while it decreases binding to TRAF4, leading to unrestrained TRAF6-mediated activation of type I IFN. Intriguingly, PACSIN1 Q59K increased TLR-7 but not TLR-9 signaling in human cells, leading to elevated expression of IFNβ and IFN-inducible genes. Untreated SLE patients had high PACSIN1 expression in peripheral blood cells that correlated positively with IFN-related genes. Introduction of the Pacsin1 Q59K mutation into mice caused increased surface TLR-7 and TRAIL expression in B cells., Conclusion: PACSIN1 Q59K increases IFNβ activity through the impairment of TRAF4-mediated inhibition of TLR-7 signaling, possibly contributing to SLE risk., (© 2023 American College of Rheumatology.)

Introduction: The energy imbalance when energy intake exceeds expenditure acts as an essential factor in the development of insulin resistance (IR). The activity of brown adipose tissue, which is involved in the dissipation of energy via heat expenditure decreases under type 2 diabetic mellitus (T2DM) state when the number of pathological aging adipocytes increases. Protein tyrosine phosphatase non-receptor type 2 (PTPN2) regulates several biological processes by dephosphorylating several cellular substrates; however, whether PTPN2 regulates cellular senescence in adipocytes and the underlying mechanism has not been reported. Methods: We constructed a model of type 2 diabetic mice with PTPN2 overexpression to explore the role of PTPN2 in T2DM. Results: We revealed that PTPN2 facilitated adipose tissue browning by alleviating pathological senescence, thus improving glucose tolerance and IR in T2DM. Mechanistically, we are the first to report that PTPN2 could bind with transforming growth factor-activated kinase 1 (TAK1) directly for dephosphorylation to inhibit the downstream MAPK/NF-κB pathway in adipocytes and regulate cellular senescence and the browning process subsequently. Discussion: Our study revealed a critical mechanism of adipocytes browning progression and provided a potential target for the treatment of related diseases., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Liu, Han, Zhu, Song, Zhang, Meng, Zhang, Zhang and Zhong.)

The integration of multiple sensors is a crucial and emerging trend in the development of autonomous driving technology. The depth image obtained by stereo matching of the binocular camera is easily influenced by environment and distance. The point cloud of LiDAR has strong penetrability. However, it is much sparser than binocular images. LiDAR-stereo fusion can neutralize the advantages of the two sensors and maximize the acquisition of reliable three-dimensional information to improve the safety of automatic driving. Cross-sensor fusion is a key issue in the development of autonomous driving technology. This study proposed a real-time LiDAR-stereo depth completion network without 3D convolution to fuse point clouds and binocular images using injection guidance. At the same time, a kernel-connected spatial propagation network was utilized to refine the depth. The output of dense 3D information is more accurate for autonomous driving. Experimental results on the KITTI dataset showed that our method used real-time techniques effectively. Further, we demonstrated our solution's ability to address sensor defects and challenging environmental conditions using the p-KITTI dataset., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Wei, Zhu, Zhang, Wang and Sun.)

Alkane catalytic cracking is regarded as one of the most significant processes for light olefin production; however, it suffers from serve catalyst deactivation due to coke formation. Herein, HZSM-5/MCM-41 composites with different Si/Al 2 ratios were first prepared by the hydrothermal method. The physicochemical properties of the prepared catalysts were analyzed by a series of bulk and surface characterization methods, and the catalytic performance was tested in n -decane catalytic cracking. It was found that HZSM-5/MCM-41 showed a higher selectivity to light olefins and a lower deactivation rate compared with the parent HZSM-5 due to an enhanced diffusion rate and decreased acid density. Moreover, the structure-reactivity relationship revealed that conversion, light olefin selectivity, and the deactivation rate strongly depended on the total acid density. Furthermore, HZSM-5/MCM-41 was further extruded with γ-Al 2 O 3 to obtain the catalyst pellet, which showed an even higher selectivity to light olefins (∼48%) resulting from the synergy effect of the fast diffusion rate and passivation of external acid density.

Physiologically, the intestinal barrier plays a crucial role in homeostasis and nutrient absorption and prevents pathogenic entry, harmful metabolites, and endotoxin absorption. Recent advances have highlighted the association between severely damaged intestinal barriers and diabetes, obesity, fatty liver, and cardiovascular diseases. Evidence indicates that an abated intestinal barrier leads to endotoxemia associated with systemic inflammation, insulin resistance, diabetes, and lipid accumulation, accelerating obesity and fatty liver diseases. Nonetheless, the specific mechanism of intestinal barrier damage and the effective improvement of the intestinal barrier remain to be explored. Here, we discuss the crosstalk between changes in the intestinal barrier and metabolic disease. This paper also highlights how to improve the gut barrier from the perspective of natural medicine, gut microbiota remodeling, lifestyle interventions, and bariatric surgery. Finally, potential challenges and prospects for the regulation of the gut barrier-metabolic disease axis are discussed, which may provide theoretical guidance for the treatment of metabolic diseases., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Zhang, Zhu, Yu, Novák, Gui and Yin.)

Background: Hepatocellular carcinoma (HCC), as an aggressive cancer with a high mortality rate, needs high-efficiency and low-toxicity drug therapy. Natural products have great potential as candidate lead compounds for the development of new HCC drugs. Crebanine is an isoquinoline alkaloid derived from Stephania with various potential pharmacological effects such as anti-cancer. However, the molecular mechanism underlying crebanine-induced liver cancer cells apoptosis has not been reported. Here, we investigated the effect of crebanine on HCC and identified a potential mechanism of action. Methods: In this paper, we intend to detect the toxic effects of crebanine on hepatocellular carcinoma HepG2 cells through a series of in vitro experiments, including detecting the effects of crebanine on the proliferation of HepG2 cells using the CCK8 method and plate cloning assay, observing the growth status and morphological changes of crebanine on HepG2 cells by inverted microscopy; and using the Transwell method to determine the the effect of crebanine on the migration and invasion ability of HepG2 cells; using Hoechst 33258 assay to stain cancer cells, thus observing the effect of crebanine on the morphology of HepG2 apoptotic cells, and detecting the apoptotic state and level of HepG2 cells by flow cytometry; using ROS kit and JC-1 assay kit to detect the changes of reactive oxygen species and mitochondrial membrane potential of HepG2 The immunofluorescence assay was taken to verify whether crebanine had an effect on the expression of p-FoxO3a in cancer cells; the Wetern blot assay was also used to examine the effect of crebanine on proteins related to the mitochondrial apoptotic pathway and its effect on the regulation of the relative protein expression of AKT/FoxO3a axis; after this, NAC and AKT inhibitor LY294002 were used to cells were pretreated with NAC and AKT inhibitor LY294002, respectively, in order to further validate the inhibitory effect of crebanine. Results: It was shown that crebanine effectively inhibited the growth and capacity of HepG2 cells migration and invasion in a dose-dependent manner. Furthermore, the effect of crebanine on the morphology of HepG2 cells was observed through microscopy. Meanwhile, crebanine induced apoptosis by causing reactive oxygen species (ROS) burst and mitochondrial membrane potential (MMP) disrupt. We found that crebanine could down-regulate Bcl-2 and up-regulate Bax, cleaved-PARP, cleaved-caspase-3 and cleaved-caspase-9, but these effects were overturned by ROS inhibitor N-acetylcysteine (NAC). Crebanine also down-regulated p-AKT and p-FoxO3a, and the PI3K inhibitor LY294002 significantly enhances this effect. We also found that the expression of AKT/FoxO3a signaling pathway was ROS-dependent. As shown by Western blots, NAC could partially attenuate the inhibitory effect of crebanine on AKT and FoxO3a phosphorylation. Conclusion: Based on our results, our results suggest that crebanine, as a compound with potential anticancer activity, has significant cytotoxic effects on hepatocellular carcinoma,and it likely induces apoptosis via ROS in the mitochondrial pathway and simultaneously affects the biological function of HCC via the ROS-AKT-FoxO3a signaling axis., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Tan, Xiang, Xiong, Zhang, Qiao and Zhang.)

Novel reusable acid-resistant magnetic polymer nanospheres-immobilized MIL-100 (CoFe 2 O 4 @Polymer@MIL-100) catalyst was prepared by a layer-by-layer method to achieve a controllable structure. The obtained core-shell catalyst consisted of modified magnetic nanoparticles as the core, a carboxylic-functionalized polymer as the protective layer, and an MIL-100 shell as the active catalytic layer by chemical bonds on the polymer. The catalysts showed good stability, good magnetic saturation, and acid corrosion resistance. The thickness of the MIL-100 shell could be adjusted by controlling the metal salt concentration and the number of layer-by-layer cycles. Nano-sized MIL-100 showed better mass transfer efficiency and catalytic activity. A conversion of 97.7% after 10 min was observed during acetalization when using CoFe 2 O 4 @Polymer@MIL-100 as the catalyst. CoFe 2 O 4 @Polymer@MIL-100 could be reused at least five times. The use of a polymer layer on CoFe 2 O 4 @Polymer@MIL-100 prevented acidic ligands from corroding the magnetic core. Chemical bonds between MIL-100 and functional magnetic polymer cores improved the catalyst's stability. CoFe 2 O 4 @Polymer@MIL-100 exhibited high activity, excellent stability, and easy magnetic separation., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022. Published by Elsevier Inc.)

Invertase (INV) irreversibly catalyzes the conversion of sucrose into glucose and fructose, playing important role in plant development and stress tolerance. However, the functions of INV genes in wheat have been less studied. In this study, a total of 126 TaINV genes were identified using a genome-wide search method, which could be classified into five classes (TaCWI-α, TaCWI-β, TaCI-α, TaCI-β, and TaVI) based on phylogenetic relationship. A total of 101 TaINVs were collinear with their ancestors in the synteny analysis, and we speculated that polyploidy events were the main force in the expansion of the TaINV gene family. Compared with TaCI, TaCWI and TaVI are more similar in gene structure and protein properties. Transcriptome sequencing analysis showed that TaINVs expressed in multiple tissues with different expression levels. Among 19 tissue-specific expressed TaINVs , 12 TaINVs showed grain-specific expression pattern and might play an important role in wheat grain development. In addition, qRT-PCR results further confirmed that TaCWI50 and TaVI27 show different expression in grain weight NILs. Our results demonstrated that the high expression of TaCWI50 and TaVI27 may be associated with a larger TGW phenotype. This work provides the foundations for understanding the grain development mechanism.

Mitochondrial dysfunction has been regarded as a hallmark of diabetic cardiomyopathy. In addition to their canonical metabolic actions, mitochondria influence various other aspects of cardiomyocyte function, including oxidative stress, iron regulation, metabolic reprogramming, intracellular signaling transduction and cell death. These effects depend on the mitochondrial quality control (MQC) system, which includes mitochondrial dynamics, mitophagy and mitochondrial biogenesis. Mitochondria are not static entities, but dynamic units that undergo fission and fusion cycles to maintain their structural integrity. Increased mitochondrial fission elevates the number of mitochondria within cardiomyocytes, a necessary step for cardiomyocyte metabolism. Enhanced mitochondrial fusion promotes communication and cooperation between pairs of mitochondria, thus facilitating mitochondrial genomic repair and maintenance. On the contrary, erroneous fission or reduced fusion promotes the formation of mitochondrial fragments that contain damaged mitochondrial DNA and exhibit impaired oxidative phosphorylation. Under normal/physiological conditions, injured mitochondria can undergo mitophagy, a degradative process that delivers poorly structured mitochondria to lysosomes. However, defective mitophagy promotes the accumulation of nonfunctional mitochondria, which may induce cardiomyocyte death. A decline in the mitochondrial population due to mitophagy can stimulate mitochondrial biogenesis), which generates new mitochondrial offspring to maintain an adequate mitochondrial number. Energy crises or ATP deficiency also increase mitochondrial biogenesis, because mitochondrial DNA encodes 13 subunits of the electron transport chain (ETC) complexes. Disrupted mitochondrial biogenesis diminishes the mitochondrial mass, accelerates mitochondrial senescence and promotes mitochondrial dysfunction. In this review, we describe the involvement of MQC in the pathogenesis of diabetic cardiomyopathy. Besides, the potential targeted therapies that could be applied to improve MQC during diabetic cardiomyopathy are also discussed and accelerate the development of cardioprotective drugs for diabetic patients., Competing Interests: Declaration of competing interest The authors declared no conflict of interest in the study., (Copyright © 2022 Elsevier Inc. All rights reserved.)

The construction of yolk-shell composites with dielectric/magnetic multiple loss mechanisms has become a promising strategy to obtain high-efficiency microwave absorbing materials. An ideal microwave absorber should possess dielectric and magnetic loss abilities, thereby leading to the attenuation and absorption of incident electromagnetic radiation. Herein, the yolk-shell structured CoFe 2 O 4 @carbon (YS-CoFe 2 O 4 @C) and Co 3 Fe 7 /FeO@carbon (YS-Co 3 Fe 7 /FeO@C) composites were designed and synthesized through a series of processes, which include in-situ coating, heat-treating, etching and subsequent carbonization reduction reaction. The composite materials with specific structure, composition, and electromagnetic parameters could be effectively obtained by controlling the reaction conditions. The combination of alloy with high magnetic loss and carbon with advanced dielectric loss as well as the unique yolk-shell structure endow YS-Co 3 Fe 7 /FeO@C improved impendence matching and large attenuation constant. The YS-Co 3 Fe 7 /FeO@C composites show optimized microwave absorption behaviors, the minimum reflection loss is up to -57.6 dB at 12.30 GHz with the of 2.5 mm and the corresponding effective absorption bandwidth is 5.27 GHz (10.10-15.37 GHz). Moreover, the widest effective bandwidth could reach 7.0 GHz (11-18 GHz) with the thickness of 2.3 m. This design provides a novel concept for tuning microwave absorption efficiency of magnetic/dielectric composites to prepare high-performance microwave absorbers., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Improving yield potential is a major goal of wheat breeding that depends on identifying key genetic loci. In this study, two residual heterozygous line RHL351- and RHL78-derived populations were employed for genetic linkage map construction and QTL detection. Two genetic populations indicated a robust grain-size QTL between Marker6 and Marker10. It covered a 95.54-99.38 Mb physical interval and was named Qpleio.nwafu.3D, containing the candidate gene Tasg (TraesCS3D02G137200). Intriguingly, RNA-seq analysis and sequencing revealed two different allelic variants in Tasg, named Tasg-D1 (G>A) and Tasg-D2 (C>G), respectively. Although the relationship between Tasg-D1 and grain size had been demonstrated previously, here we provided the first genetic evidence that C/G allelic variation in Tasg-D2 was associated with grain shape and size through a newly developed dCAPS marker. In addition, transcriptome comparison indicated that Tasg-D1/2 might primarily contribute to significant expression differences in brassinolide (BR) metabolism-related genes rather than those related to BR responses in developing grains and spikes. Our study provided new evidence and a breeder-friendly dCAPS marker for improving grain size through the selection of Tasg, as well as a basis to understand Tasg function in the future., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: Many studies demonstrated no improved survival in patients with pulmonary artery catheter placement. However, no consistent conclusions have been drawn regarding the impact of pulmonary artery catheter in critically ill patients with heart disease. This study aimed to investigate the association of early pulmonary artery catheter use with 28-day mortality in that population., Methods: The Multiparameter Intelligent Monitoring in Intensive Care IV (MIMIC-IV) database, a single-center critical care database, was employed to investigate this issue. This study enrolled a total of 11,887 critically ill patients with cardiac disease with or without pulmonary artery catheter insertion. The primary outcome was 28-day mortality. The multivariate regression was modeled to examine the association between pulmonary artery catheter and outcomes. Additionally, we examined the effect modification by cardiac surgeries. Propensity score matching was conducted to validate our findings., Results: No improvement in 28-day mortality was observed among the pulmonary artery catheter group compared to the non-pulmonary artery catheter group (odds ratio 95% confidence interval: 1.18 [1.00-1.38], P = .049). When stratified by cardiac surgeries, the results were consistent. The patients in the pulmonary artery catheter group had fewer ventilation-free days and vasopressor-free days than those in the nonpulmonary artery catheter group after surgery stratification. In the surgical patients, pulmonary artery catheter insertion was not associated with the occurrence of acute kidney injury, and it was associated with a higher daily fluid input (mean difference 95% confidence interval: 0.13 [0.05-0.20], P = .001). In nonsurgical patients, the pulmonary artery catheter group had a higher risk of acute kidney injury occurrence (odds ratio 95% confidence interval: 1.94 [1.32-2.84], P = .001)., Conclusion: Early pulmonary artery catheter placement is not associated with survival benefits in critically ill patients with cardiac diseases, either in surgical or nonsurgical patients., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Side-chain type sulfonated poly(phenylquinoxaline) (SPPQ)-based proton exchange membranes (PEMs) with different ionic exchange capacity (IEC) were successfully synthesized by copolymerization from 4,4'-bis (2-diphenyletherethylenedione) diphenyl ether, 4,4'-bis (2-phenylethylenedione) diphenyl ether and 3,3',4,4'-tetraaminobiphenyl, and post-sulfonation process. The sulfonic acid groups were precisely grafted onto the p -position of phenoxy groups in the side chain of PPQ after the convenient condition of the post-sulfonation process, which was confirmed by 1 H NMR spectra and FTIR. The sulfonic acid groups of side-chain type SPPQ degraded at around 325 °C, and their maximum stress was higher than 47 MPa, indicating great thermal and mechanical stability. The water uptake increased with the increasing IEC and temperature. The size change in their plane direction was shown to be lower than 6%, indicating the stability of membrane electrode assembly. The SPPQ PEMs displayed higher proton conductivity than that of main chain. In the single cell test, the maximum power density of side-chain type SPPQ-5 was 63.8 mW cm -2 at 20 wt% methanol solution and O 2 at 60 °C, which is largely higher than 18.4 mW cm -2 of NR212 under the same conditions. The SPPQ PEMs showed high performance (62.8 mW cm -2 ) even when the methanol concentration was as high as 30 wt%.

In diabetic cardiomyopathy (DCM), a major diabetic complication, the myocardium is structurally and functionally altered without evidence of coronary artery disease, hypertension or valvular disease. Although numerous anti-diabetic drugs have been applied clinically, specific medicines to prevent DCM progression are unavailable, so the prognosis of DCM remains poor. Mitochondrial ATP production maintains the energetic requirements of cardiomyocytes, whereas mitochondrial dysfunction can induce or aggravate DCM by promoting oxidative stress, dysregulated calcium homeostasis, metabolic reprogramming, abnormal intracellular signaling and mitochondrial apoptosis in cardiomyocytes. In response to mitochondrial dysfunction, the mitochondrial quality control (MQC) system (including mitochondrial fission, fusion, and mitophagy) is activated to repair damaged mitochondria. Physiological mitochondrial fission fragments the network to isolate damaged mitochondria. Mitophagy then allows dysfunctional mitochondria to be engulfed by autophagosomes and degraded in lysosomes. However, abnormal MQC results in excessive mitochondrial fission, impaired mitochondrial fusion and delayed mitophagy, causing fragmented mitochondria to accumulate in cardiomyocytes. In this review, we summarize the molecular mechanisms of MQC and discuss how pathological MQC contributes to DCM development. We then present promising therapeutic approaches to improve MQC and prevent DCM progression., Competing Interests: Competing Interests: The authors have declared that no competing interest exists., (© The author(s).)

As an efficient non-precious metal catalyst for the oxygen evolution reaction (OER), phosphides suffer from poor electrical conductivity, so it is still a challenge to reasonably design their structures to further improve their conductivity and OER performances. Here, we present a novel Ni 5 P 4 /N-doped carbon@CoFeP/N-doped carbon composite (Ni 5 P 4 /NC@CoFeP/NC) as electrocatalysts for OER. This elaborate structure consists of Ni 5 P 4 /NC derived from Ni-MOF and CoFeP/NC derived from CoFe-Prussian blue analog MOF (Co-Fe PBA). The cube-like CoFeP/NC are scattered and uniformly coated on the sheet of Ni 5 P 4 /NC flowers. Among them, NC can enhance the conductivity of phosphides, while CoFeP/NC can increase the electrochemical active area, which benefit the properties of Ni 5 P 4 /NC@CoFeP/NC. Notably, the Ni 5 P 4 /NC@CoFeP/NC catalyst possesses outstanding OER performances with a low overpotential of 260 and 303 mV at a current density of 10 and 100 mA·cm -2 , an ultra-low Tafel slope of 31.1 mV·dec -1 and excellent stability in 1 M KOH. XPS analysis shows that proper chemical composition promotes the oxidation of transition metal species and the chemisorption of OH - , thus accelerating the OER kinetics. Therefore, this work provides a hopeful method for designing and preparing transition metal phosphide/carbon composite as OER electrocatalysts., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Accumulation of immunoglobulin and complement components within the kidneys is a hallmark of glomerulonephritis. Staining and detection of IgG, IgA, IgM, and C3 deposits can assist in diagnosing the underlying causes of nephritis and has implications for the pathological processes underpinning glomerulonephritis. Here, we describe a protocol to detect immune deposits within biological specimens such as mouse kidneys. We detail tissue isolation and processing, immunostaining, and fluorescence microscopy to characterize and quantify the extent of immunological deposits contributing to kidney injury. For complete details on the use and execution of this protocol, please refer to Jiang et al. (2021)., Competing Interests: The authors declare no competing interests., (© 2022 The Author(s).)

Although circumstantial evidence supports enhanced Toll-like receptor 7 (TLR7) signalling as a mechanism of human systemic autoimmune disease 1-7 , evidence of lupus-causing TLR7 gene variants is lacking. Here we describe human systemic lupus erythematosus caused by a TLR7 gain-of-function variant. TLR7 is a sensor of viral RNA 8 , 9 and binds to guanosine 10 - 12 . We identified a de novo, previously undescribed missense TLR7 Y264H variant in a child with severe lupus and additional variants in other patients with lupus. The TLR7 Y264H variant selectively increased sensing of guanosine and 2',3'-cGMP 10-12 , and was sufficient to cause lupus when introduced into mice. We show that enhanced TLR7 signalling drives aberrant survival of B cell receptor (BCR)-activated B cells, and in a cell-intrinsic manner, accumulation of CD11c + age-associated B cells and germinal centre B cells. Follicular and extrafollicular helper T cells were also increased but these phenotypes were cell-extrinsic. Deficiency of MyD88 (an adaptor protein downstream of TLR7) rescued autoimmunity, aberrant B cell survival, and all cellular and serological phenotypes. Despite prominent spontaneous germinal-centre formation in Tlr7 Y264H mice, autoimmunity was not ameliorated by germinal-centre deficiency, suggesting an extrafollicular origin of pathogenic B cells. We establish the importance of TLR7 and guanosine-containing self-ligands for human lupus pathogenesis, which paves the way for therapeutic TLR7 or MyD88 inhibition., (© 2022. The Author(s).)

Acute kidney injury (AKI) induced by renal ischemia reperfusion (RIR) is typically observed in renal surgeries and is a leading cause of renal failure. However, there is still an unmet medical need currently in terms of clinical treatments. Herein, we report the effect of Urolithin A (UA) in a mouse RIR model, wherein we demonstrated its underlying mechanism both in vitro and in vivo. The expression levels of p62 and Keap1 significantly decreased, while that of nuclear Nrf2 increased in vitro in a hypoxia cell model after UA treatment. Furthermore, the apoptosis of tubular cells was attenuated and the reactive oxygen species (ROS) levels were reduced in the kidneys in a mouse RIR model after UA administration. In this study, we demonstrated that UA can alleviate oxidative stress and promote autophagy by activating the p62-Keap1-Nrf2 signaling pathway, which could protect the kidneys from ischemia reperfusion injury., (© 2022 John Wiley & Sons Ltd.)

The SH2B family of adaptor proteins, SH2-B, APS, and LNK are key modulators of cellular signalling pathways. Whilst SH2-B and APS have been partially structurally and biochemically characterised, to date there has been no such characterisation of LNK. Here we present two crystal structures of the LNK substrate recognition domain, the SH2 domain, bound to phosphorylated motifs from JAK2 and EPOR, and biochemically define the basis for target recognition. The LNK SH2 domain adopts a canonical SH2 domain fold with an additional N-terminal helix. Targeted analysis of binding to phosphosites in signalling pathways indicated that specificity is conferred by amino acids one- and three-residues downstream of the phosphotyrosine. Several mutations in LNK showed impaired target binding in vitro and a reduced ability to inhibit signalling, allowing an understanding of the molecular basis of LNK dysfunction in variants identified in patients with myeloproliferative disease., (© 2021. The Author(s).)

The spotted leaf lesion mimic trait simulates cell death in a plant responding to pathogen infection. Some spotted leaf genes are recessive, while others are dominant. A small number of plants with a lesion mimic phenotype appeared in a segregating population obtained by crossing two normal green wheat strains, XN509 and N07216. Here, we clarified the genetic model and its breeding value. Phenotyping of the consecutive progeny populations over six cropping seasons showed that the spotted leaf lesion mimic phenotype was controlled by a dominant gene designated TaSpl1, which was inhibited by two other dominant genes, designated TaSpl1-I 1 and TaSpl1-I 2 . Using bulked segregant analysis RNA-seq (BSR-Seq) and newly developed KASP-PCR markers, the TaSpl1 and TaSpl1-I 1 loci in N07216 were mapped to the end of chromosomes 3DS and 3BS, respectively. Plants with the spotted phenotype showed lower levels of stripe rust and powdery mildew than those with the normal green phenotype. Compared with normal leaves, the differentially expressed genes in spotted leaves were significantly enriched in plant-pathogen interaction and endocytosis pathways. There were no differences in the yield parameters of the F 5 and F 6 sister lines, N13039S with TaSpl1 and N13039 N without TaSpl1. These results provide a greater understanding of spotted leaf phenotyping and the breeding value of the lesion mimic allele in developing disease-resistance varieties., (Copyright © 2021 Elsevier B.V. All rights reserved.)

A novel pomegranate-like Ni-NSs@MSNSs nanocatalyst was successfully synthesized via a modified Stöber method, and its application in the hydrogenation of dicyclopentadiene (DCPD) was firstly reported. The Ni-NSs@MSNSs possessed a high specific area (658 m 2 /g) and mesoporous structure (1.7-3.3 nm). The reaction of hydrogenation of DCPD to endo -tetrahydrodicyclopentadiene ( endo -THDCPD) was used to evaluate the catalytic performance of the prepared materials. The distinctive pomegranate-like Ni-NSs@MSNSs core-shell nanocomposite exhibited superior catalytic activity (TOF = 106.0 h -1 and STY = 112.7 g·L -1 ·h -1 ) and selectivity (98.9%) than conventional Ni-based catalysts (experimental conditions: Ni/DCPD/cyclohexane = 1/100/1000 (w/w), 150 °C, and 2.5 MPa). Moreover, the Ni-NSs@MSNSs nanocatalyst could be rapidly and conveniently recycled by magnetic separation without appreciable loss. The Ni-NSs@MSNSs also exhibited excellent thermal stability (≥750 °C) and good recycling performance (without an activity and selectivity decrease in four runs). The superior application performance of the Ni-NSs@MSNSs nanocatalyst was mainly owing to its unique pomegranate-like structure and core-shell synergistic confinement effect., Competing Interests: The authors declare no competing financial interest., (© 2021 American Chemical Society.)

Efficient conversion of light alkanes is of essential significance for enhancing the utilization efficiency of resources and exploring the activation and evolution regulation of C-C and C-H bonds in stable molecules. The processes are often executed with catalysts under harsh conditions. The olefin yield and metal stability have been the long-standing concerns. Herein, we report a facile strategy of constructing a bifunctional Pt/HZSM-5-based catalyst by two-step atomic layer deposition (ALD) to achieve a high light olefin formation rate of 0.48 mmol gcat-1·min-1 in the catalytic cracking of n-butane at 600 °C, which is ∼2.2 times higher than that of the conventional Pt/HZSM-5 catalyst (0.22 mmol gcat-1·min-1). Moreover, the bifunctional Pt/HZSM-5-based catalyst exhibited outstanding recyclability and excellent metal stability against sintering in comparison with conventional Pt/HZSM-5. Detailed microscopic and spectroscopic characterization studies demonstrate that the metal oxide (TiO2 or Al2O3) coating not only prevents the metal from high-temperature sintering, but also regulates the proportion of coordinately unsaturated platinum surface atoms. Theoretical calculations further confirm the preference of nucleation of TiO2 or Al2O3 on coordinately unsaturated platinum sites, which in turn modulates the bifunctional dehydrogenation-cracking pathway to improve the olefin formation rate.

Mitochondria maintain mitochondrial homeostasis through continuous fusion and fission, that is, mitochondrial dynamics, which is precisely mediated by mitochondrial fission and fusion proteins, including dynamin-related protein 1 (Drp1), mitofusin 1 and 2 (Mfn1/2), and optic atrophy 1 (OPA1). When the mitochondrial fission and fusion of cardiomyocytes are out of balance, they will cause their own morphology and function disorders, which damage the structure and function of the heart, are involved in the occurrence and progression of cardiovascular disease such as ischemia-reperfusion injury (IRI), septic cardiomyopathy, and diabetic cardiomyopathy. In this paper, we focus on the latest findings regarding the molecular features and regulatory mechanisms of mitochondrial dynamic disorder in cardiovascular pathologies. Finally, we will address how these findings can be applied to improve the treatment of cardiovascular disease., Competing Interests: The authors have declared that they have no conflicts of interest., (Copyright © 2021 Ying Tan et al.)

Objective: This study examined the relationships between skeletal deformities and the pharyngeal airway of patients with nonsyndromic unilateral cleft lip and palate (UCLP)., Design: Retrospective study., Setting: Orthodontics and Oral and Maxillofacial Surgery Departments in the Affiliated Hospital of Stomatology, Nanjing Medical University, China., Patients, Participants: The sample comprised 30 nonsyndromic UCLP patients and 30 healthy controls. Each group has 23 males and 7 females., Interventions: All cone-beam computed tomography images were obtained with the participant in the standard supine position and asked to bite with intercuspal position without swallowing or moving their heads and tongues during scanning., Main Outcome Measure(s): SNA, SNB, ANB, anterior cranial base, Wits appraisal, maxillary length (PTM-ANS || FH), maxillary position (S-PTM || FH), mandibular length (Go-Pog || MP), FMA, posterior face height, anterior face height, Posterior-Anterior face height, lower face height, pharyngeal airway volumes, and areas were evaluated by Dolphin imaging software., Results: The UCLP group showed significantly decreased SNA, SNB, ANB, PTM-ANS || FH, S-PTM || FH, P-A Face Height compared with the controls. However, the airway volumes and areas showed no significant difference between 2 groups. The total airway volume and minimum cross-sectional area in UCLP patients were related to the Go-Pog || MP and FMA., Conclusions: Patients with UCLP have both the maxillary and mandibular deficiencies in the sagittal dimension. Both the sagittal and vertical relationships of the jaw might affect the airway volume and area. However, no significant difference was detected in airway volume and area in UCLP patients when compared with the controls.

Aim: The contemporary article aims to review and compare various literatures concerning different conclusions regarding the correlation between tooth size discrepancy (TSD) and Angle's malocclusion groups., Background: Acquiring the ideal occlusion plays one of the major roles while designing the treatment plan for an orthodontic patient, any alterations in the individual tooth sizes are called TSD and will hinder this prime requirement. By determining the correct tooth size ratio, it further helps in acquiring the accurate interdigitation, balanced occlusion, and also predicting the orthodontic treatment results. Various investigations were carried out to know the correlation between tooth size discrepancies and different malocclusion groups, of which, a few reported a statistically significant difference whereas others reported no significant difference., Review Results: A computerized database quest was operated utilizing the Medline database (Pubmed/Medline) for original research and review articles. Publications between 1946 and 2018 were included. Four hundred twenty-one articles were recovered from database search and, among them, 66 articles were selected to review the full-article., Conclusion: Although a comparison was done between the tooth-size ratios and malocclusion groups (classes I, II, and III), many investigators noted no significant difference but there is an inadequacy in the data particularly related to subgroups of Angle's classification of malocclusion among these investigations; therefore, further studies are required to interpret this correlation., Clinical Significance: As there is high incidence of tooth size discrepancies noted in the previous literature orthodontist, Bolton's analysis regardless of malocclusion group, sex, and ethnicity is highly recommended.

Guar gum is an important raw material in the food, textile and oil industries, but the biosynthesis of guar gum remains unclear. To illuminate the genes involved in guar gum biosynthesis, guar beans from 30 and 40 days after flowering (DAF) were used for RNA sequencing in this study. A total of 2,535 and 2,724 preferentially expressed genes were found in 30 and 40 DAF endosperm, and 3,720 and 2,530 preferentially expressed genes were found in 30 and 40 DAF embryos, respectively. Of these, mannan synthase genes, α-galactosyltransferase genes and cellulose synthase genes were preferentially expressed in the endosperm from 30 and 40 DAF. The high expression level of these glycometabolism genes in endosperm is consistent with the expectation that the main component of guar gum is galactomannan. We believe that genes related to guar gum biosynthesis found in this study will be useful for both new variety development via genetic engineering and synthetic biology research on guar gum biosynthesis in the future.

Non-oxidative propane dehydrogenation (PDH) is an attractive reaction from both an industrial and a scientific viewpoint because it allows direct large-scale production of propene and fundamental analysis of C-H activation respectively. The main challenges are related to achieving high activity, selectivity, and on-stream stability of environment-friendly and cost-efficient catalysts without non-noble metals. Here, we describe an approach for the preparation of supported ultrasmall ZnO nanoparticles (2-4 nm, ZnO NPs) for high-temperature applications. The approach consists of encapsulation of NPs into a nitrogen-doped carbon (NC) layer in situ grown from zeolitic imidazolate framework-8 on a Silicalite-1 support. The NC layer was established to control the size of ZnO NPs and to hinder their loss to a large extent at high temperatures. The designed catalysts exhibited high activity, selectivity, and on-stream stability in PDH. Propene selectivity of about 90% at 44.4% propane conversion was achieved at 600°C after nearly 6 h on stream., (Copyright © 2019 The Author(s). Published by Elsevier Inc. All rights reserved.)

As a nicotinamide adenine dinucleotide (NAD) + -dependent protein deacetylase, SIRT3 is highly expressed in tissues with high metabolic turnover and mitochondrial content. It has been demonstrated that SIRT3 plays a critical role in maintaining normal mitochondrial biological function through reversible protein lysine deacetylation. SIRT3 has a variety of substrates that are involved in mitochondrial biological processes such as energy metabolism, reactive oxygen species production and clearance, electron transport chain flux, mitochondrial membrane potential maintenance, and mitochondrial dynamics. In the suppression of SIRT3, functional deficiencies of mitochondria contribute to the development of various cardiovascular disorders. Activation of SIRT3 may represent a promising therapeutic strategy for the improvement of mitochondrial function and the treatment of relevant cardiovascular disorders. In the current review, we discuss the emerging roles of SIRT3 in mitochondrial derangements and subsequent cardiovascular malfunctions, including cardiac hypertrophy and heart failure, ischemia-reperfusion injury, and endothelial dysfunction in hypertension and atherosclerosis.

Due to the complexity of heterogeneous catalysts, identification of active sites and the ways for their experimental design are not inherently straightforward but important for tailored catalyst preparation. The present study reveals the active sites for efficient C-H bond activation in C 1 -C 4 alkanes over ZrO 2 free of any metals or metal oxides usually catalysing this reaction. Quantum chemical calculations suggest that two Zr cations located at an oxygen vacancy are responsible for the homolytic C-H bond dissociation. This pathway differs from that reported for other metal oxides used for alkane activation, where metal cation and neighbouring lattice oxygen form the active site. The concentration of anion vacancies in ZrO 2 can be controlled through adjusting the crystallite size. Accordingly designed ZrO 2 shows industrially relevant activity and durability in non-oxidative propane dehydrogenation and performs superior to state-of-the-art catalysts possessing Pt, CrO x , GaO x or VO x species.

A novel Siphoviridae family Phage BS5, which infects Pseudoalteromonas atlantica, was isolated from the surface waters of the Yellow Sea. Morphological study by transmission electron microscopy revealed that the novel phage belongs to Siphoviridae. The complete genome sequence of PBS5 contained a linear, double-strand 39949-bp DNA molecule with a G + C content of 40.6% and 65 putative open reading frames. Twelve conserved domains were detected by BLASTP in NCBI, and of these the functions of 5 were known. The genome was grouped into four modules as follows: phage structure, phage packaging, DNA replication and regulation, and some additional functions.16 S rDNA sequence analysis was also applied to identify the host bacteria. After initial characterization of bacteriophage PBS5, it was found that the optimal pH was 7.0, the optimal temperature was 30 °C, and the burst size was about 95 virions per cell. This information will provide an important benchmark for further research on the interaction between bacteriophages and their hosts.

The family Pseudoalteromonas is highly adaptable to dissimilar ecological habitats and plays an important ecological role in the marine environment. In this study, a new Pseudoalteromonas phage PH1 was isolated from the Yellow Sea. To better understand the bacteriophage, its biological properties, including morphology, host range, growth phenotype, thermal and pH stability, and nucleic acid composition, were investigated in detail. The result showed that the phage PH1 is a Podoviridae-phage with an icosahedral head (60 nm of diameter) and a short tail (26 nm in length). The phage PH1 genome consists of 42,685 bp length double-stranded DNA with a G+C content of 42.24% and is predicted to have 55 open reading frames (ORFs) with an average length of 740 bp nucleotides each. The phage PH1 genome adds a new Podoviridae-phage genome to marine bacteriophage dataset, which will provide useful basic information for further molecular research on interaction mechanisms between bacteriophages and their hosts.

Sepsis is a threatening health problem and characterized by microvascular dysfunction. In this study, we verified that LPS caused the downregulation of Sirt1 and the hyperpermeability of endothelial cells. Inhibition of Sirt1 with ex527 or Sirt1 siRNA displayed a higher permeability, while activation of Sirt1 with SRT1720 reversed the LPS-induced hyperpermeability, formation of fiber stress, and disruption of VE-cadherin distribution. In pulmonary microvascular vein endothelial cells isolated from wild-type mice, Sirt1 was attenuated upon LPS, while Sirt1 was preserved in a receptor of advanced glycation end product-knockout mice. The RAGE antibody could also diminish the downregulation and ubiquitination of Sirt1 in LPS-exposed human umbilical vein endothelial cells. An LPS-induced decrease in Sirt1 activity was attenuated by the RAGE antibody and TLR4 inhibitor. In vivo study also demonstrated the attenuating role of Sirt1 and RAGE knockout in LPS-induced increases in dextran leakage of mesenteric venules. Furthermore, activation of Sirt1 prevented LPS-induced decreases in the activity and expression of superoxide dismutase 2, as well as the increases in NADPH oxidase 4 and reactive oxygen species, while inhibition of Sirt1 aggravated the SOD2 decline. It also demonstrated that Sirt1-deacetylated p53 is required for p53 inactivation, which reversed the downregulation of β -catenin caused by LPS.

The vascular endothelium is a layer of cells lining the inner surface of vessels, serving as a barrier that mediates microenvironment homeostasis. Deterioration of either the structure or function of endothelial cells (ECs) results in a variety of cardiovascular diseases. Previous studies have shown that reactive oxygen species (ROS) is a key factor that contributes to the impairment of ECs and the subsequent endothelial dysfunction. The longevity regulator Sirt1 is a NAD + -dependent deacetylase that has a potential antioxidative stress activity in vascular ECs. The mechanisms underlying the protective effects involve Sirt1/FOXOs, Sirt1/NF- κ B, Sirt1/NOX, Sirt1/SOD, and Sirt1/eNOs pathways. In this review, we summarize the most recent reports in this field to recapitulate the potent mechanisms involving the protective role of Sirt1 in oxidative stress and to highlight the beneficial effects of Sirt1 on cardiovascular functions.