Mechanical Behavior of Two Ferrite–Martensite Dual-Phase Steels over a Broad Range of Strain Rates

The present study concerns the deformation and fracture behavior of two ferrite–martensite dual phase steels (FMDP660 and FMDP780) with different phase fractions subjected to different strain rate (0.001 s−1 to 1000 s−1) tensile testing. For both steels, the yield strength (YS) monotonically increased with strain rates, whereas the values of ultimate tensile strength (UTS), uniform elongation (UE) and post-uniform elongation (PUE) were maintained stable at the low strain rate range (0.001–0.1 s−1), followed by a significant increase with strain rate at high strain rate levels (0.1–1000 s−1). The FMDP780 steel with a higher fraction of martensite possessed a stronger strain rate sensitivity of tensile strength and elongation (UE and PUE) values at the high strain rate stage, compared with the FMDP660 sample. The change of UTS and UE with different strain rates and phase fractions was highly related to the strain hardening behavior, which was controlled by the dislocation multiplication in ferrite, as validated by transmission electron microscopy (TEM). The fracture surface of the two steels was characterized by dimpled-type fracture associated with microvoid formation at the ferrite–martensite interfaces, regardless of the strain rates. The change of the dimple size and PUE value of the two steels with strain rates was attributed to the effect of adiabatic heating during tensile testing

Comprehensive analysis of key genes, microRNAs and long non‐coding RNAs in hepatocellular carcinoma

Human hepatocellular carcinoma (HCC) is a common aggressive cancer whose molecular mechanism remains elusive. We aimed to identify the key genes, microRNAs (miRNAs) and long non‐coding RNAs (lncRNAs) involved with HCC. We obtained mRNA, miRNA and lncRNA profiles for HCC from The Cancer Genome Atlas and then identified differentially expressed mRNAs (DEmRNAs), miRNAs (DEmiRNAs) and lncRNAs (DElncRNAs). We performed functional annotation of DEmRNAs and then constructed HCC‐specific DEmiRNA–DEmRNA, DEmiRNA–DElncRNA and DElncRNA–DEmiRNA–DEmRNA interaction networks. We searched for nearby target cis‐DEmRNAs of DElncRNAs and performed receiver operating characteristic and survival analyses. A total of 1239 DEmRNAs, 33 DEmiRNAs and 167 DElncRNAs in HCC were obtained. Retinol metabolism [false discovery rate (FDR) = 7.02 × 10−14] and metabolism of xenobiotics by cytochrome P450 (FDR = 7.30 × 10−11) were two significantly enriched pathways in HCC. We obtained 545 DEmiRNA–DEmRNA pairs that consisted of 258 DEmRNAs and 28 DEmiRNAs in HCC. mir‐424, miR‐93 and miR‐3607 are three hub DEmiRNAs of the HCC‐specific DEmiRNA–DEmRNA interaction network. HAND2‐AS1/ENSG00000232855–miR‐93–LRAT/RND3, ENSG00000232855–miR‐877–RCAN1 and ENSG00000232855–miR‐224–RND3 interactions were found in the HCC‐specific DElncRNA–DEmiRNA–DEmRNA interaction network. A total of three DElncRNA–nearby target DEmRNA pairs (HCG25–KIFC1, LOC105378687–CDC20 and LOC101927043–EPCAM) in HCC were obtained. Diagnostic and prognostic values of several selected DElncRNAs, DEmRNAs and DEmiRNAs for HCC were assessed. Our study identified several DEmRNAs, DEmiRNAs and DElncRNAs with great diagnostic or prognostic value for HCC, which may facilitate studies into the molecular mechanisms, and development of potential biomarkers and therapeutic target sites for HCC

Detection of the Late Quaternary activity of the Liaocheng-Lankao Fault in the south-central part of the North China Plain: Discussion on the seismogenic mechanism of the 1937 Heze M 7.0 earthquake

Objective  The North China Plain (NCP) is one of the most populated and economically developed areas in China and is a region with a high level of seismic hazards. Studying the Quaternary activity of the faults and the seismogenic mechanism of the large earthquakes in NCP is conducive to exploring the seismogenic pattern of intraplate earthquakes and reducing the damage caused by seismic hazards. The Liaocheng-Lankao fault (LLF) is an important buried deep major fault in the south-central part of the NCP. The activity of the LLF and its relationship with the 1937 Heze M 7.0 earthquake is still highly controversial.  Methods  In this study, the activity of the Liaocheng-Liaokao fault is finely studied by combining shallow seismic exploration, drilling, and Quaternary dating methods.  Results  Shallow seismic reflection profile ZF-2 reveals that the strata below 145 m are obviously displaced, and the strata above 145 m are disturbed. The Bachengsi drilling profile reveals 16 sets of marker layers and three west-dipping normal faults Fa, Fb, and Fc; they form a "compound Y" structure in the profile, of which Fa displaces the bottom boundary of the Holocene (burial depth of approximately 38.9 m) and is an early Holocene active fault. It also reveals four paleoseismic events since the Late Pleistocene, with vertical displacement of 1.2±0.2 to 3.7±0.2 m for a single event. Based on the stratigraphic offsets in the boreholes, the average vertical slip rate of this fault is calculated to be about 0.1±0.05 mm/a for the early Late Pleistocene and 0.35±0.04 mm/a for the late Late Pleistocene-middle Holocene. The fitted age-depth curves by the test results of seven 14C samples and four OSL samples can be divided into two segments. Within the depth range of 0 to 86.0 m (approximately 21 to 0 ka), the age and depth of the strata conform to the formula y=(253.69±16.56)x+(924.72±681.36), from which the average deposition rate of this section is calculated to be 3.94±0.26 mm/a. Within the depth range of 102.9 to 145.4 m (approximately 128 to 59 ka), the age and depth of the strata conform to the formula y=(1470.67±259.91)x+(-95061.92±30190.73), from which the average deposition rate of this section is calculated to be 0.68±0.12 mm/a. The vertical slip rate of the LLF and the sedimentation rate of the Dongpu Sag have increased significantly since the late Late Pleistocene. The intensity lines of the Heze M 7.0 earthquake show an asymmetric butterfly shape.  Conclusion  The 1937 Heze M 7.0 and M 6\begin{document}{\raise0.7ex\hbox{3} \!\mathord{\left/{\vphantom {3 4}}\right.}\!\lower0.7ex\hbox{4}} \end{document} earthquakes formed "Z" -shaped ground fissure zones, which can be divided into three sections: the southeastern section (section A), the middle section (section B), and the northwestern section (section C). The long axis of the intensity lines and the distribution of the surface rupture of the 1937 Heze M 7.0 coincide with the NNE-striking Xiaoliu-Xieyuanjie and NWW-striking Dongming-Chengwu faults in location and striking. The analysis of the intensity lines, surface rupture distribution, focal mechanism solution of the 1937 Heze M 7.0 earthquake and M 6\begin{document}{\raise0.7ex\hbox{3} \!\mathord{\left/{\vphantom {3 4}}\right.}\!\lower0.7ex\hbox{4}} \end{document} earthquakes, and regional stress implies that the Xiaoliu-Xieyuanji fault and the Dongming-Chengwu fault are the seismogenic faults of the 1937 Heze M 7.0 earthquake. The LLF, as the deep major fault in the region, controlled the accumulation of stress, stimulated the earthquake with its deep movement, and reduced the effect of the seismic energy westward, acting as the regional seismic controlling fault of the 1937 Heze M 7.0 earthquake.  Significance  This article proposes a method for fine detection of the localization, structure, latest activity age, sliding rate, and paleoseismic sequences of the buried fault and also proposes a pattern of seismicity in which seismogenic faults do not coincide with the regional seismic controlling fault. It provides new insights into the characterization of seismicity within the NCP and can provide the geological basis for urban and rural planning, high-speed railway design, and earthquake prevention and disaster reduction project construction in this region

Revealing Key Genes and Pathways in Potato Scab Disease Resistance through Transcriptome Analysis

Potato scab, a global soil-borne disease caused by Streptomyces, is pivotal in developing resistant cultivars due to its complex resistance mechanisms. This study investigates the transcriptomic responses in potato to common scab using resistant variety CS10 and susceptible CS11 post S. scabie inoculation (0 d and 10 d, 12 cDNA libraries). Differential expression analysis identified 147 key DEGs (Differentially Expressed Genes) essential in disease recognition, signal transduction, and defense. GO (Gene Ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analyses revealed several significant metabolic pathways, such as ADP binding, heme binding, chloroplast thylakoid membrane, photosynthesis, glutathione metabolism, and homologous recombination, among others. Notably, the correlation between chloroplast pathways (GO:0019745) and photosynthesis (map00195) highlights photosynthesis’s role in potato scab response, while the oxygen transport (GO:0031408)-related glutathione metabolism pathway (map00480) emphasizes antioxidant defenses. Furthermore, three potential resistance genes were validated: Ethylene Response Factor ERF010 (LOC102589042), Disease Resistance Protein RPP13 (LOC102605863), and Cytochrome P450 83B1 (LOC102604056), demonstrating the linkage between metabolic pathways and pathogen response. These findings offer insights into potato’s molecular resistance mechanisms against potato scab, supporting the breeding of resistant varieties and comprehensive disease management, thus advancing sustainable agriculture

Sensitive short-wavelength infrared photodetection with a quinoidal ultralow band-gap n-type organic semiconductor

It is fundamentally challenging to achieve high responsivity and detectivity for organic photodetectors (OPDs) in the short-wavelength infrared (SWIR) region due to the challenges in designing ultralow band-gap organic semiconductors with a low energetic disorder and trap density. Herein, we report a quinoidal, ultralow band-gap, n-type small molecule with an absorption onset of up to 1,243 nm. The quinoidal central core contributes to reduced thermally generated carriers via decreasing energetic disorder and trap density. As a result, the self-powered OPD exhibited a detectivity of over 1012 Jones in 400–1,200 nm. Particularly, at 1,100 nm, the detection limit of commercial silicon photodetectors, an external quantum efficiency of 18.9% and a detectivity of 3.81 × 1012 Jones are achieved under zero bias, which renders the device the best self-powered OPD in photovoltaic mode below the silicon band gap to date. This work opens an avenue to develop sensitive SWIR photodetection technology based on organic semiconductors.</p

Apolipoprotein A-1 mimetic peptide 4F promotes endothelial repairing and compromises reendothelialization impaired by oxidized HDL through SR-B1

Disruption of endothelial monolayer integrity is the primary instigating factor for many cardiovascular diseases. High density lipoprotein (HDL) oxidized by heme enzyme myeloperoxidase (MPO) is dysfunctional in promoting endothelial repair. Apolipoprotein A-1 mimetic 4F with its pleiotropic benefits has been proven effective in many in vivo models. In this study we investigated whether 4F promotes endothelial repair and restores the impaired function of oxidized HDL (Cl/NO2-HDL) in promoting re-endothelialization. We demonstrate that 4F and Cl/NO2-HDL act on scavenger receptor type I (SR-B1) using human aorta endothelial cells (HAEC) and SR-B1 (-/-) mouse aortic endothelial cells. Wound healing, transwell migration, lamellipodia formation and single cell migration assay experiments show that 4F treatment is associated with a recovery of endothelial cell migration and associated with significantly increased endothelial nitric oxide synthase (eNOS) activity, Akt phosphorylation and SR-B1 expression. 4F increases NO generation and diminishes oxidative stress. In vivo, 4F can stimulate cell proliferation and re-endothelialization in the carotid artery after treatment with Cl/NO2-HDL in a carotid artery electric injury model but fails to do so in SR-B1(-/-) mice. These findings demonstrate that 4F promotes endothelial cell migration and has a potential therapeutic benefit against early endothelial injury in cardiovascular diseases

Diabetic HDL Is Dysfunctional in Stimulating Endothelial Cell Migration and Proliferation Due to Down Regulation of SR-BI Expression

<div><h3>Background</h3><p>Diabetic HDL had diminished capacity to stimulate endothelial cell (EC) proliferation, migration, and adhesion to extracellular matrix. The mechanism of such dysfunction is poorly understood and we therefore sought to determine the mechanistic features of diabetic HDL dysfunction.</p> <h3>Methodology/Principal Findings</h3><p>We found that the dysfunction of diabetic HDL on human umbilical vein endothelial cells (HUVECs) was associated with the down regulation of the HDL receptor protein, SR-BI. Akt-phosphorylation in HUVECs was induced in a biphasic manner by normal HDL. While diabetic HDL induced Akt phosphorylation normally after 20 minutes, the phosphorylation observed 24 hours after diabetic HDL treatment was reduced. To determine the role of SR-BI down regulation on diminished EC responses of diabetic HDL, Mouse aortic endothelial cells (MAECs) were isolated from wild type and SR-BI (−/−) mice, and treated with normal and diabetic HDL. The proliferative and migratory effects of normal HDL on wild type MAECs were greatly diminished in SR-BI (−/−) cells. In contrast, response to diabetic HDL was impaired in both types suggesting diminished effectiveness of diabetic HDL on EC proliferation and migration might be due to the down regulation of SR-BI. Additionally, SR-BI down regulation diminishes diabetic HDL’s capacity to activate Akt chronically.</p> <h3>Conclusions/Significance</h3><p>Diabetic HDL was dysfunctional in promoting EC proliferation, migration, and adhesion to matrix which was associated with the down-regulation of SR-BI. Additionally, SR-BI down regulation diminishes diabetic HDL’s capacity to activate Akt chronically.</p> </div

Clinical and laboratory characteristics.

<p>Data are presented as mean±SEM as indicated.</p><p>TC = total cholesterol; HDLc = high density lipoprotein cholesterol; LDLc = low density lipoprotein cholesterol; TG = triglyceride.</p