In the casting process, alloying elements Mo and Cr are needed to improve the wear resistance of medium manganese steels for low impact energy. The element Ti is added to avoid the high cost of ...expenditure for using Mo. This paper studies the effect of Ti and Cr on microstructure and properties of medium manganese steel. It shows that a large number of polygon, column, and square (Ti, Cr) C particles (<13 μm) are formed in the casting samples using the present heat treatment process. A new type of Ti–Cr modified medium manganese steel (Ti content of 0.56%–1.48%) is produced by using (Ti, Cr) C reinforced phase particles. Compared with the traditional medium manganese steel (blank), the hardness increases twice with a slight decrease in impact toughness traditional and modified medium manganese steels (blank and steels A, B, and C) have values of 42.1 J/cm2, 47.5 J/cm2, 43.8 J/cm2, and 37.9 J/cm2, and the wear resistance also increased nearly two times.
Noble metal surfaces with intrinsic chirality serve as an ideal candidate for investigating enantioselective chemistry due to their superior chemical durability and high catalytic activity. Recently, ...significant advance has been made in synthesizing metal nanocrystals with intrinsic chirality. Nonetheless, the majority reports are limited to gold. Herein, through a heteroepitaxial growth strategy, the synthesis of metal nanocrystals with intrinsic chirality to palladium was extended for the first time and their application in enantioselective recognition was demonstrated. The heteroepitaxial growth strategy allows for transferring the chirality of homochiral Au nanocrystals to Au@Pd core–shell nanocrystals. By employing the chiral Au@Pd nanocrystals as enantiomeric recognizing elements, a series of electrochemical sensors for chiral discrimination were developed. Under optimal conditions, the peak potential between D-dihydroxyphenylalanine (D-DOPA) and L-dihydroxyphenylalanine (L-DOPA) is about 80 mV, and the peak current of D-DOPA is 2 times as much as that of L-DOPA, which enables the determination of the enantiomeric excess (EE, %) of L-DOPA. Overall, this report not only introduces a heteroepitaxial growth strategy to synthesize metal nanocrystals with intrinsic chirality, but also demonstrates the superior capability of integrating intrinsic chirality and catalytic properties into metal nanocrystals for chiral recognition.
Graphical abstract
A highly selective and sensitive bioluminescent sensor (DME) for human carboxylesterase 1 (hCE1) has been developed and well characterized. DME could be used for real-time monitoring of hCE1 ...activities in complex biological samples and for bio-imaging of endogenous hCE1 in living cells.
Trained immunity is driven by metabolism and epigenetics in innate immune cells in mammals. The phenomenon of trained immunity has been identified in invertebrates, including shrimp, but the ...underlying mechanisms remain unclear. To elucidate mechanisms of trained immunity in shrimp, the metabolomic changes in hemolymph of
trained by the UV-inactivated white spot syndrome virus (UV-WSSV) were analyzed using tandem gas chromatography-mass/mass spectrometry. The metabolomic profiles of shrimp trained with UV-WSSV followed WSSV infection showed significant differences comparison with the control groups, PBS injection followed WSSV infection. 16 differential metabolites in total of 154 metabolites were identified, including D-fructose-6-phosphate, D-glucose-6-phosphate, and D-fructose-6-phosphate, and metabolic pathways, glycolysis, pentose phosphate pathway, and AMPK signaling pathway were enriched in the UV-WSSV trained groups. Further study found that histone monomethylation and trimethylation at H3K4 (H3K4me1 and H3K4me3) were involved in the trained immunity. Our data suggest that the UV-WSSV induced trained immunity leads to metabolism reprogramming in the shrimp and provide insights for WSSV control in shrimp aquaculture.
A new ratiometric florescence probe derived from 3-hydroxyflavone (3-HF) has been developed for selective and sensitive detection of human carboxylesterase 2 (CE2). The probe is designed by ...modulating the excited state intramolecular proton transfer (ESIPT) emission of 3-HF via introducing of 4-ethylbenzoyloxy group. Under physiological conditions, probe 1 displays satisfying stability with very low background signal, but it can be selectively hydrolyzed by CE2 to release free 3-HF which brings remarkable changes in fluorescence spectrum. Both reaction phenotyping and chemical inhibition assays demonstrate that probe 1 is highly selective for CE2 over other human hydrolases including carboxylesterase 1, cholinesterases and paraoxonases. Probe 1 has been applied successfully to measure the real activities of CE2 in human biological samples, as well as to screen CE2 inhibitors by using tissue preparations as the enzymes sources. Additionally, probe 1 is cell membrane permeable and can be used for cellular imaging of endogenous CE2 in living cells. All of these features make it possible to serve as a promising tool for exploring the individual differences in biological function of CE2, as well as for rapid screening of selective and potent inhibitors of CE2 for further clinical use.
•A ratiometric fluorescent ESIPT probe for selective detection of human CE2 was developed for the first time.•The probe can be selectively hydrolyzed by CE2 to release 3-hydroxylflavone which brings the remarkable changes in fluorescence spectrum.•The probe can be used to efficiently detect the real activity of CE2 in biological samples.•The probe also can monitor the real function of endogenous CE2 in living cells.
Sepsis is an acute inflammatory reaction and a cause of acute respiratory distress syndrome (ARDS). In the present study, we explored the roles and underlying mechanism of the lncRNA Nuclear enriched ...abundant transcript 1 (NEAT1) in ARDS. The expression levels of genes, proteins and pro-inflammatory cytokines in patients with ARDS, LPS-stimulated cells and septic mouse models were quantified using qPCR, western blotting and ELISA assays, respectively. The molecular targeting relationship was validated by conducting a dual-luciferase reporter assay. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8) assay. The cell cycle phase was determined by flow cytometry assay. The expression levels of NEAT1 and pro-inflammatory cytokines were higher in patients with ARDS and septic models than in controls. Knockdown of NEAT1 significantly increased cell proliferation and cycle progression and prolonged mouse survival in vitro and in vivo. Mechanistically, miR-27a was identified as a downstream target of NEAT1 and directly inhibited PTEN expression. Further rescue experiments revealed that inhibition of miR-27a impeded the promoting effects of NEAT1 silence on cell proliferation and cycle progression, whereas inhibition of PTEN markedly weakened the inhibitory effects of NEAT1 overexpression on cell proliferation and cycle progression. Altogether, our study revealed that NEAT1 plays a promoting role in the progression of ARDS via the NEAT1/miR-27a/PTEN regulatory network, providing new insight into the pathologic mechanism behind ARDS.
Sepsis-induced acute lung injury has been clinically defined as acute respiratory distress syndrome (ARDS). In the present study, the authors reveal that NEAT1 plays a role in the inflammation and cell cycle progression of ARDS via the NEAT1/miR-27a/PTEN regulatory network, providing new insight into the pathologic mechanism behind ARDS.
Aims
We aim to explore the role and mechanism of vagus nerve stimulation (VNS) in coronary endothelial cells and angiogenesis in infarcted hearts.
Methods and results
Seven days after rat myocardial ...infarction (MI) was prepared by ligation of the left anterior descending coronary artery, the left cervical vagus nerve was treated with electrical stimulation 1 h after intraperitoneal administration of the α7‐nicotinic acetylcholine inhibitor mecamylamine or the mAChR inhibitor atropine or 3 days after local injection of Ad‐shSDF‐1α into the infarcted heart. Cardiac tissue acetylcholine (ACh) and serum ACh, tumour necrosis factor α (TNF‐α), interleukin 1β (IL‐1β) and interleukin 6 (IL‐6) levels were detected by ELISA to determine whether VNS was successful. An inflammatory injury model in human coronary artery endothelial cells (HCAECs) was established by lipopolysaccharide and identified by evaluating TNF‐α, IL‐1β and IL‐6 levels and tube formation. Immunohistochemistry staining was performed to evaluate CD31‐positive vessel density and stromal cell‐derived factor‐l alpha (SDF‐1α) expression in the MI heart in vivo and the expression and distribution of SDF‐1α, C‐X‐C motif chemokine receptor 4 and CXCR7 in HCAECs in vitro. Western blotting was used to detect the levels of SDF‐1α, V‐akt murine thymoma viral oncogene homolog (AKT), phosphorylated AKT (pAKT), specificity protein 1 (Sp1) and phosphorylation of Sp1 in HCAECs. Left ventricular performance, including left ventricular systolic pressure, left ventricular end‐diastolic pressure and rate of the rise and fall of ventricular pressure, should be evaluated 28 days after VNS treatment. VNS was successfully established for MI therapy with decreases in serum TNF‐α, IL‐1β and IL‐6 levels and increases in cardiac tissue and serum ACh levels, leading to increased SDF‐1α expression in coronary endothelial cells of MI hearts, triggering angiogenesis of MI hearts with increased CD31‐positive vessel density, which was abolished by the m/nAChR inhibitors mecamylamine and atropine or knockdown of SDF‐1α by shRNA. ACh promoted SDF‐1α expression and its distribution along with the branch of the formed tube in HCAECs, resulting in an increase in the number of tubes formed in HCAECs. ACh increased the levels of pAKT and phosphorylation of Sp1 in HCAECs, resulting in inducing SDF‐1α expression, and the specific effects could be abolished by mecamylamine, atropine, the PI3K/AKT blocker wortmannin or the Sp1 blocker mithramycin. Functionally, VNS improved left ventricular performance, which could be abolished by Ad‐shSDF‐1α.
Conclusions
VNS promoted angiogenesis to repair the infarcted heart by inducing SDF‐1α expression and redistribution along new branches during angiogenesis, which was associated with the m/nAChR‐AKT‐Sp1 signalling pathway.
A new ratiometric fluorescent probe derived from 2-(2-hydroxy-3-methoxyphenyl) benzothiazole (HMBT) has been developed for selective monitoring of human carboxylesterase 1 (hCE1). The probe is ...designed by introducing benzoyl moiety to HMBT. The prepared latent spectroscopic probe 1 displays satisfying stability under physiological pH conditions with very low background signal. Both the reaction phynotyping and chemical inhibition assays demonstrated that hCE1 mediated the specific cleavage of the carboxylic ester bond of probe 1 in human biological samples. The release of HMBT leads to a remarkable red-shifted emission in fluorescence spectrum (120nm large emission shift). Furthermore, human cell-based assays show that probe 1 is cell membrane permeable, and it can be used for bioassay and cellular imaging of hCE1 activity in HepG2 cells. These findings lead to the development of a simple and sensitive fluorescent method for measurement of hCE1 activity in vitro or in living cells, in the presence of additional enzymes or endogenous compounds.
•A highly selective ratiometric fluorescent probe of hCE1 was synthesized and well-characterized for the first time.•Isoform specific hydrolysis mediated by hCE1 leads to a large emission shift with a desirable red-shifted.•The fluorescence intensity ratio (488nm/368nm) exhibited a good linearity increasing with both protein concentration and time.•The probe was successfully applied in measuring hCE1 activity and screening the inhibitors of hCE1 in a heterogeneous mixture containing multi-enzymes.•The probe was cell membrane permeable and can be used to image the hCE1 activity in living cells.
Background/Aims: Vagus nerve stimulation (VNS) suppresses arrhythmic activity and minimizes cardiomyocyte injury. However, how VNS affects angiogenesis/arteriogenesis in infarcted hearts, is poorly ...understood. Methods: Myocardial infarction (MI) was achieved by ligation of the left anterior descending coronary artery (LAD) in rats. 7 days after LAD, stainless-steel wires were looped around the left and right vagal nerve in the neck for vagus nerve stimulation (VNS). The vagal nerve was stimulated with regular pulses of 0.2ms duration at 20 Hz for 10 seconds every minute for 4 hours, and then ACh levels by ELISA in cardiac tissue and serum were evaluated for its release after VNS. Three and 14 days after VNS, Real-time PCR, immunostaining and western blot were respectively used to determine VEGF-A/B expressions and α-SMA- and CD31-postive vessels in VNS-hearts with pretreatment of α7-nAChR blocker mecamylamine (10 mg/kg, ip) or mACh-R blocker atropine (10 mg/kg, ip) for 1 hour. The coronary function and left ventricular performance were analyzed by Langendorff system and hemodynamic parameters in VNS-hearts with pretreatment of VEGF-A/B-knockdown or VEGFR blocker AMG706. Coronary arterial endothelial cells proliferation, migration and tube formation were evaluated for angiogenesis following the stimulation of VNS in coronary arterial smooth muscle cells (VSMCs). Results: VNS has been shown to stimulate VEGF-A and VEGF-B expressions in coronary arterial smooth muscle cells (VSMCs) and endothelial cells (ECs) with an increase of α-SMA- and CD31-postive vessel number in infarcted hearts. The VNS-induced VEGF-A/B expressions and angiogenesis were abolished by m-AChR inhibitor atropine and α7-nAChR blocker mecamylamine in vivo. Interestingly, knockdown of VEGF-A by shRNA mainly reduced VNS-mediated formation of CD31+ microvessels. In contrast, knockdown of VEGF-B powerfully abrogated VNS-induced formation of α-SMA+ vessels. Consistently, VNS-induced VEGF-A showed a greater effect on EC tube formation as compared to VNS-induced VEGF-B. Moreover, VEGF-A promoted EC proliferation and VSMC migration while VEGF-B induced VSMC proliferation and EC migration in vitro. Mechanistically, vagal neurotransmitter acetylcholine stimulated VEGF-A/B expressions through m/nACh-R/PI3K/Akt/Sp1 pathway in EC. Functionally, VNS improved the coronary function and left ventricular performance. However, blockade of VEGF receptor by antagonist AMG706 or knockdown of VEGF-A or VEGF-B by shRNA significantly diminished the beneficial effects of VNS on ventricular performance. Conclusion: VNS promoted angiogenesis/arteriogenesis to repair the infracted heart through the synergistic effects of VEGF-A and VEGF-B.
In this work, jute fiber and aluminum (Al) powder were used synergistically to improve the mechanical properties and color of polypropylene (PP) composites, which can be used as spray‐free materials. ...The effect of jute fiber and Al powder on the mechanical properties of PP composites was systematically investigated. The results show that jute fiber and Al powder can significantly improve the tensile strength and impact strength of PP. Compared with pure PP, the tensile strength, impact strength, and elastic modulus of jute/Al/PP composites were increased by 55.1%, 78.9%, and 263%, respectively. Compared with Al/PP spray‐free materials, they were increased by 11.2%, 9.07%, and 103%, respectively. Statistical analysis by one‐way analysis of variance confirmed that Al powder and jute fiber have significant improvement on the mechanical properties of PP composites.
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