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Coronary heart disease (CHD) is one of the leading causes of heart‐associated deaths worldwide. Conventional diagnostic techniques are ineffective and insufficient to diagnose CHD with higher accuracy. To use the circulating microRNAs (miRNAs) as non‐invasive, specific and sensitive biomarkers for diagnosing of CHD, 203 patients with CHD and 144 age‐matched controls (126 high‐risk controls and 18 healthy volunteers) were enrolled in this study. The direct S‐Poly(T)Plus method was used to identify novel miRNAs expression profile of CHD patients and to evaluate their clinical diagnostic value. This method is an RNA extraction‐free and robust quantification method, which simplifies procedures, reduces variations, in particular increases the accuracy. Twelve differentially expressed miRNAs between CHD patients and high‐risk controls were selected, and their performances were evaluated in validation set‐1 with 96 plasma samples. Finally, six (miR‐15b‐5p, miR‐29c‐3p, miR‐199a‐3p, miR‐320e, miR‐361‐5p and miR‐378b) of these 12 miRNAs were verified in validation set‐2 with a sensitivity of 92.8% and a specificity of 89.5%, and the AUC was 0.971 (95% confidence interval, 0.948‐0.993, P < .001) in a large cohort for CHD patients diagnosis. Plasma fractionation indicated that only a small amount of miRNAs were assembled into EVs. Direct S‐Poly(T)Plus method could be used for disease diagnosis and 12 unique miRNAs could be used for diagnosis of CHD.

This review briefly examines the recent progress in knowledge about the synthesis and degradation of highly unsaturated fatty acids (HUFA) and their functions. Following the cloning of mammalian Δ6‐desaturase (D6D), the D6D mRNA was found in many tissues, including adult brain, maternal organs, and fetal tissue, suggesting an active synthesis of HUFA in these tissues. The cloning also confirmed the long‐postulated hypothesis that the same pathway is followed in n−6 and n−3 HUFA synthesis. Dietary n−6 and n−3 HUFA both induce fatty acid oxidation enzymes in peroxisomes when compared to their respective precursor polyunsaturated fatty acids. This suggests that peroxisomes may be the primary site of HUFA degradation when HUFA are supplied in excess from the diet. Peroxisome proliferators strongly induce the enzymes for the HUFA synthesis. The mechanism of this induction is currently unknown. Recent studies revealed new HUFA functions that are not mediated by eicosanoids. These functions include endocytosis/exocytosis, ionchannel modulation, DNA polymerase inhibition, and regulation of gene expression. These new discoveries will enable us to reexamine the underlying mechanisms for the classical symptoms of essential fatty acid deficiency as well as vitamin E deficiency. Progress has also been made in understanding the mechanism by which dietary HUFA reduce body fat deposition. One mechanism is induction of genes for fatty acid oxidation, which is mediated by peroxisome proliferator‐activated receptor‐α. Another likely mechanism is that HUFA suppress genes for fatty acid synthesis by reducing both mRNA and protein maturation of sterol regulatory element binding protein‐1.

The Western flower thrips, Frankliniella occidentalis Pergande (Thysanoptera: Thripidae) is an invasive polyphagous pest with an expanding global range that damages a wide variety of crops. F. occidentalis was first reported in China from Yunnan province during 2000, and has rapidly expanded its range since then. It is currently distributed across at least 10 provinces in China and has become a particularly devastating pest, causing substantial damage and economic losses. At present, the still heavy reliance on frequent use of insecticides for control of F. occidentalis, has lead to a series of ecological problems stemming from insecticide resistance, interspecific displacement and non-target effects. Thus, integrated pest management (IPM) programmes, multiple complementary tactics, including preventive tactics, biological controls, and judicious use of insecticides will likely provide a viable IPM strategy for control of F. occidentalis in the near future. This review provides an overview for information gained during the 10+ years since the invasion of F. occidentalis into China, reviews lessons that have been learned enhancing our overall understanding of the biology and ecology of F. occidentalis and discusses IPM practices relative to this widespread invasive insect pest.

The post-translational modification and stability regulation of RIG-I play critical roles in promoting IFN-I production and maintaining immune homeostasis. In this study, we found that ubiquitin-specific peptidase 1 (USP1) promotes RIG-I protein stability through deubiquitination, which in turn enhances antiviral immunity through the production of inflammatory cytokines, and inhibits the replication of influenza virus in MDCK cells. In contrast, USP1 knockdown inhibited the deubiquitination of RIG-I, decreased the RIG-I protein level, and significantly increased the influenza virus titer. Meanwhile, inhibition of USP1 expression did not have a significant effect on the proliferation of MDCK cells, suggesting that USP1 could be used as a target gene to establish a vaccine-producing MDCK cell line. The above results provide a more comprehensive understanding of the function of USP1 and the antiviral response mechanism, and provide a theoretical and methodological basis for the screening of target genes for the artificial establishment of high-yield MDCK cell lines for vaccine production.

Background The Syrian hamster ( Mesocricetus auratus ) has shown promise as a human diseases model, recapitulating features of different human diseases including COVID-19. However, the landscape of its genome and transcriptome has not been systematically dissected, restricting its potential applications. Results Here we provide a complete analysis of the genome and transcriptome of the Syrian hamster and found that its lineage diverged from that of the Chinese hamster ( Cricetulus griseus ) around 29.4 million years ago. 21,387 protein-coding genes were identified, with 90.03% of the 2.56G base pair sequence being anchored to 22 chromosomes. Further comparison of the transcriptomes from 15 tissues of the Syrian hamster revealed that the Syrian hamster shares a pattern of alternative splicing modes more similar to humans, compared to rats and mice. An integrated genomic-transcriptomic analysis revealed that the Syrian hamster also has genetic and biological advantages as a superior animal model for cardiovascular diseases. Strikingly, several genes involved in SARS-COV-2 infection, including ACE2, present a higher homology with humans compared to other rodents and show the same function as their human counterparts. Conclusion The detailed molecular characterisation of the Syrian hamster in the present study opens a wealth of fundamental resources from this small rodent for future research into human disease pathology and treatment.

Patients with gastric and esophageal (GE) adenocarcinoma tumors in which the oncogene ERBB2 has been amplified are routinely treated with a combination of cytotoxic chemotherapy and the ERBB2-directed antibody trastuzumab; however, the addition of trastuzumab, even when tested in a selected biomarker-positive patient population, provides only modest survival gains. To investigate the potential reasons for the modest impact of ERBB2-directed therapies, we explored the hypothesis that secondary molecular features of ERBB2-amplified GE adenocarcinomas attenuate the impact of ERBB2 blockade. We analyzed genomic profiles of ERBB2-amplified GE adenocarcinomas and determined that the majority of ERBB2-amplified tumors harbor secondary oncogenic alterations that have the potential to be therapeutically targeted. These secondary events spanned genes involved in cell-cycle regulation as well as phosphatidylinositol-3 kinase and receptor tyrosine kinase signaling. Using ERBB2-amplified cell lines, we demonstrated that secondary oncogenic events could confer resistance to ERBB2-directed therapies. Moreover, this resistance could be overcome by targeting the secondary oncogene in conjunction with ERBB2-directed therapy. EGFR is commonly coamplified with ERBB2, and in the setting of ERBB2 amplification, higher EGFR expression appears to mark tumors with greater sensitivity to dual EGFR/ERBB2 kinase inhibitors. These data suggest that combination inhibitor strategies, guided by secondary events in ERBB2-amplified GE adenocarcinomas, should be evaluated in clinical trials.

Aiming at the problems of poor welding quality and low degree of automatic welding on the engineering site, a welding process parameter control method based on machine vision and nonlinear regression technology is proposed. Firstly, a vision unit and a peripheral sensor unit are designed to obtain the information of each influencing factor of the welding process parameters. Secondly, a clustering algorithm is used to improve the extraction accuracy of feature point coordinates of weld images. Thirdly, a nonlinear regression fitting method is proposed to determine the mathematical relationship between welding quality at different welding positions and corresponding process parameters. Experimental results show that the control system is easy to operate, and the flexible control of welding process parameters in the whole process is realized. The weld cumulative height and width deviations are less than 0.5 and 0.3 mm, respectively. The welding surface is stable and meets welding requirements. Therefore, this method is of great practical significance in engineering field welding.

In the complex interactions between plants and pathogens, the regulation of nutrient allocation plays a critical role in determining plant health and susceptibility to diseases. Root‐knot nematodes (RKNs, Meloidogyne incognita) extract sugar from plants during their interactions with the hosts. SWEET (Sugars Will Eventually be Exported Transporters) proteins are a class of non‐energy‐consuming sugar uniporters that regulate the allocation of sugars in plant. Here, it is find that SlSWEET17 (Solanum lycopersicum SWEET17), a member of the SWEET family in tomato, is localized to the plasma membrane, Golgi body and small vacuoles, and is highly expressed in galls. Further studies show that SlSWEET17 negatively regulates the sugar transport capacity of other SlSWEETs via protein interactions. Overexpression of SlSWEET17 significantly decreases the soluble sugar content in galls and susceptibility to RKNs, while SlSWEET17 knockout‐mutation (ko‐mutation) has the opposite effect. It is also identified SlDOF9 (Solanum lycopersicum DNA binding with one finger 9), an upstream negative regulator of SlSWEET17, using ChIP (chromatin immunoprecipitation) analysis, electrophoretic mobility shift assays and dual‐Luciferase assays. SlDOF9‐overexpressing plants show increased sugar content in galls and susceptibility to RKNs, and sldof9cr ko‐mutants have the opposite phenotype. This results show how SlDOF9‐SlSWEET17 affects RKN infection through sugar partitioning from roots to galls. Root‐knot nematode (RKN) disease seriously affects the yield and quality of vegetable crops. SlDOF9‐SlSWEET17 model helps plants resist RKN infection during early stage by switching off the sugar transport capacity of other SlSWEET proteins that are hijacked by RKNs. This study provides new insights into the molecular mechanisms of sugar distribution and crop susceptibility to pathogen mediated by SWEETs.

Background: The Madin–Darby canine kidney (MDCK) cell line constitutes a key component of influenza vaccine production, but its dependence on adherent growth limits cell culture density and hinders vaccine yield. There is evidence that the use of gene editing techniques to inhibit cell adhesion and establish an easily suspended cell line can improve vaccine yield; however, the mechanisms underlying MDCK cell adhesion are unclear. Methods: In this study, we used transcriptomics to analyse differentially expressed mRNAs and miRNAs in adherent and suspension cultures of MDCK cells. Results: We found that claudin-1 (CLDN1) expression was downregulated in the suspension MDCK cells and that CLDN1 promotes MDCK cell–extracellular matrix adhesion. Additionally, microRNA (miR)-175 expression was upregulated in the suspension MDCK cells. Importantly, we demonstrated that miR-175 inhibits MDCK cell adhesion by targeting the CLDN1 3′-untranslated region (UTR). These findings contribute to a more comprehensive understanding of the regulatory mechanisms modulating cell adhesion and provide a basis for establishing suspension-adapted, genetically engineered cell lines. Our work could also facilitate the identification of targets for tumour therapy.