PubMed

Related Articles Longan (Dimocarpus longan Lour.) Aril ameliorates cognitive impairment in AD mice induced by combination of D-gal/AlCl3 and an irregular diet via RAS/MEK/ERK signaling pathway. J Ethnopharmacol. 2020 Nov 26;:113612 Authors: Li H, Lei T, Zhang J, Yan Y, Wang N, Song C, Li C, Sun M, Li J, Guo Y, Yang J, Kang T Abstract ETHNOPHARMACOLOGICAL RELEVANCE: According to the theory of traditional Chinese medicine (TCM), Alzheimer's disease (AD) is identified as "forgetfulness" or "dementia", and it can be caused by spleen deficiency. Longan Aril (the aril of Dimocarpus longan Lour., LA) is a kind of Chinese medicine, and it can improve intelligence attributed to entering the spleen-meridian. This study aimed to explore the therapeutic effects of LA on AD mice with spleen deficiency, and to understand anti-AD mechanism of LA. MATERIAL AND METHODS: A mouse model of AD with spleen deficiency was established by D-gal (140 mg/kg, intraperitoneal injection) and AlCl3 (20 mg/kg, intragastrical administration) in combination with an irregular diet for 60 days, in which mice in LA group were daily given LA (0.5, 1.0 or 2.0 g/kg). The anti-AD effects of LA were evaluated by the Morris water maze, enzyme-linked immunosorbent assay (ELISA), hematoxylin and eosin (H&E), Nissl, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. The anti-AD mechanism of LA was studied by using metabolomics, and the expressions of RAS/MEK/extracellular signal-regulated kinase (ERK) signaling pathway-related proteins were detected by Western blotting. RESULTS: LA improved learning and memory abilities, superoxide dismutase (SOD) level, and form and number of Nissl bodies, while reduced the levels of Aβ42, phosphorylated-tau (p-tau), reactive oxygen species (ROS), malondialdehyde (MDA), monoamine oxidase-B (MAO-B), histological injury, and apoptosis rate in AD group (P < 0.05, P < 0.01 or P < 0.001). The anti-AD mechanism of LA may be related to RAS/MEK/ERK and other signaling pathways, in which the expressions of RAS/MEK/ERK signaling pathway-related proteins significantly reduced (P < 0.05 or P < 0.01). CONCLUSIONS: LA could improve the cognitive ability and reduce the pathologic impairment in AD mice, which might be partly mediated via inhibition of RAS/MEK/ERK singling pathway. PMID: 33249246 [PubMed - as supplied by publisher]

Related Articles Metabolomics in posttraumatic stress disorder: Untargeted metabolomic analysis of plasma samples from Croatian war veterans. Free Radic Biol Med. 2020 Nov 26;: Authors: Konjevod M, Erjavec GN, Perkovic MN, Sáiz J, Tudor L, Uzun S, Kozumplik O, Strac DS, Zarkovic N, Pivac N Abstract Posttraumatic stress disorder (PTSD) is a severe, multifactorial and debilitating neuropsychiatric disorder, which can develop in a subset of individuals as a result of the exposure to severe stress or trauma. Such traumatic experiences have a major impact on molecular, biochemical and cellular systems, causing psychological and somatic alterations that affect the whole organism. Although the etiology of PTSD is still unclear, it seems to involve complex interaction between various biological genetic and environmental factors. Metabolomics, as one of the rapidly developing "omics" techniques, might be a useful tool for determining altered metabolic pathways and stress-related metabolites as new potential biomarkers of PTSD. The aim of our study was to identify metabolites whose altered levels allow us to differentiate between patients with PTSD and healthy control individuals. The study included two cohorts. The first, exploratory, group included 50 Croatian veterans with PTSD and 50 healthy control subjects, whereas a validation group consisted of 52 veterans with PTSD and 52 control subjects. The metabolomic analysis of plasma samples was conducted using liquid chromatography coupled with mass spectrometry (LC-MS), as well as gas chromatography coupled with mass spectrometry (GC-MS). The LC-MS analysis determined significantly different levels of two glycerophospholipids, PE(18:1/0:0) and PC(18:1/0:0), between control subjects and PTSD patients in both cohorts. The altered metabolites might play a role in multiple cellular processes, including inflammation, mitochondrial dysfunction, membrane breakdown, oxidative stress and neurotoxicity, which could be associated with PTSD pathogenesis. PMID: 33249139 [PubMed - as supplied by publisher]

Related Articles An integrated metagenomics and metabolomics approach implicates the microbiota-gut-brain axis in the pathogenesis of Huntington's disease. Neurobiol Dis. 2020 Nov 26;:105199 Authors: Kong G, Ellul S, Narayana VK, Kanojia K, Ha HTT, Li S, Renoir T, Cao KL, Hannan AJ Abstract BACKGROUND: Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder with onset and severity of symptoms influenced by various environmental factors. Recent discoveries have highlighted the importance of the gastrointestinal microbiome in mediating the gut-brain-axis bidirectional communication via circulating factors. Using shotgun sequencing, we investigated the gut microbiome composition in the R6/1 transgenic mouse model of HD from 4 to 12 weeks of age (early adolescent through to adult stages). Targeted metabolomics was also performed on the blood plasma of these mice (n = 9 per group) at 12 weeks of age to investigate potential effects of gut dysbiosis on the plasma metabolome profile. RESULTS: Modelled time profiles of each species, KEGG Orthologs and bacterial genes, revealed heightened volatility in the R6/1 mice, indicating potential early effects of HD mutation in the gut. In addition to gut dysbiosis in R6/1 mice at 12 weeks of age, gut microbiome function was perturbed. In particular, the butanoate metabolism pathway was elevated, suggesting increased production of the protective SCFA, butyrate, in the gut. No significant alterations were found in the plasma butyrate and propionate levels in the R6/1 mice at 12 weeks of age. The statistical integration of the metagenomics and metabolomics unraveled several Bacteroides species that were negatively correlated with ATP and pipecolic acid in the plasma. CONCLUSIONS: The present study revealed the instability of the HD gut microbiome during the pre-motor symptomatic stage of the disease which may have dire consequences on the host's health. Perturbation of the HD gut microbiome function prior to significant cognitive and motor dysfunction suggest the potential role of the gut in modulating the pathogenesis of HD, potentially via specific altered plasma metabolites which mediate gut-brain signaling. PMID: 33249136 [PubMed - as supplied by publisher]

Related Articles Effect of neonicotinoid dinotefuran on root exudates of Brassica rapa var. chinensis. Chemosphere. 2020 Nov 19;:129020 Authors: Li X, Zhang M, Li Y, Yu X, Nie J Abstract Root exudates are released by plant roots and are important carrier substances for material exchange and information transmission among plants and the rhizosphere. In the present study, the effect of dinotefuran on root exudates of Chinese cabbage (Brassica rapa var. chinensis) was investigated. The physiological activities revealed that dinotefuran uptake caused oxidative stress in vegetable tissues even at low dinotefuran exposure levels. The metabolic profile of plant root exudates acquired by LC-QTOF/MS was clearly changed by dinotefuran, where the numbers of both up- and down-regulated MS peaks increased with increasing dinotefuran concentration. Under dinotefuran stress, some osmotic adjustment substances (proline and betaine) and defence-related metabolites (spermidine, phenylalanine and some phenolic acids) were significantly upregulated, which may help plants adapt to adverse environmental conditions. Specifically, the contents of some phenylalanine-derived secondary metabolites increased with increasing dinotefuran concentration, which may increase the external detoxification ability of plants. Moreover, respiration metabolism was significantly affected, where some intermediates in the TCA cycle (succinic acid and malic acid) were upregulated with low-level dinotefuran exposure; however, anaerobic respiration products (lactic acid and 3-phenyllactic acid) were accumulated at high exposure levels. In addition, the release of glucosinolates was significantly inhibited in both dinotefuran treatment groups. PMID: 33248730 [PubMed - as supplied by publisher]

Related Articles Multi-omics integration in biomedical research - A metabolomics-centric review. Anal Chim Acta. 2021 Jan 02;1141:144-162 Authors: Wörheide MA, Krumsiek J, Kastenmüller G, Arnold M Abstract Recent advances in high-throughput technologies have enabled the profiling of multiple layers of a biological system, including DNA sequence data (genomics), RNA expression levels (transcriptomics), and metabolite levels (metabolomics). This has led to the generation of vast amounts of biological data that can be integrated in so-called multi-omics studies to examine the complex molecular underpinnings of health and disease. Integrative analysis of such datasets is not straightforward and is particularly complicated by the high dimensionality and heterogeneity of the data and by the lack of universal analysis protocols. Previous reviews have discussed various strategies to address the challenges of data integration, elaborating on specific aspects, such as network inference or feature selection techniques. Thereby, the main focus has been on the integration of two omics layers in their relation to a phenotype of interest. In this review we provide an overview over a typical multi-omics workflow, focusing on integration methods that have the potential to combine metabolomics data with two or more omics. We discuss multiple integration concepts including data-driven, knowledge-based, simultaneous and step-wise approaches. We highlight the application of these methods in recent multi-omics studies, including large-scale integration efforts aiming at a global depiction of the complex relationships within and between different biological layers without focusing on a particular phenotype. PMID: 33248648 [PubMed - as supplied by publisher]

Related Articles Effects of different stocking densities on tracheal barrier function and its metabolic changes in finishing broilers. Poult Sci. 2020 Dec;99(12):6307-6316 Authors: Wang Y, Wang D, Wang J, Li K, Heng C, Jiang L, Cai C, Zhan X Abstract In the present study, we evaluated the effects of various stocking densities on the tracheal barrier and plasma metabolic profiles of finishing broilers. We randomly assigned 1,440 Lingnan Yellow feathered broilers (age 22 d) to 5 different stocking density groups (8 m-2, 10 m-2, 12 m-2, 14 m-2, and 16 m-2). Each of these consisted of 3 replicates. The interleukin (IL)-1β and IL-10 concentrations were substantially higher in the 16 m-2 treatment group than they were in the 8 m-2 and 10 m-2 treatment groups (P < 0.05). Nevertheless, IL-4 did not significantly differ among the 5 treatments (P > 0.05). The tracheal mucosae of the birds in the 16 m-2 group (high stocking density, HSD) were considerably thicker than those for the birds in the 10 m-2 group (control, CSD). Relative to CSD, the claudin1 expression level was lower, and the muc2 and caspase3 expression levels were higher for HSD. Compared with CSD, 10 metabolites were significantly upregulated (P < 0.05), and 7 were significantly downregulated (P < 0.05) in HSD. Most of these putative diagnostic biomarkers were implicated in matter biosynthesis and energy metabolism. A metabolic pathway analysis revealed that the most relevant and critical biomarkers were pentose and glucuronate interconversions and the pentose phosphate pathway. Activation of the aforementioned pathways may partially counteract the adverse effects of the stress induced by high stocking density. This work helped improve our understanding of the harmful effects of high stocking density on the tracheal barrier and identified 2 metabolic pathways that might be associated with high stocking density-induced metabolic disorders in broilers. PMID: 33248546 [PubMed - as supplied by publisher]

Related Articles High-throughput metabolomics discovers metabolite biomarkers and insights the protective mechanism of schisandrin B on myocardial injury rats. J Sep Sci. 2020 Nov 28;: Authors: Zhao LK, Zhao YB, Zhang PX Abstract Schisandrin B has been proved to possess anti-inflammatory and anti-endoplasmic effects, could improve cardiac function, inhibit apoptosis, and reduce inflammation after ischemic injury. However, the detailed metabolic mechanism and potential pathways of Schisandrin B effects on myocardial injury are unclear. Metabolomics could yield in-depth mechanistic insights and explore the potential therapeutic effect of natural products. In this study, the preparation of doxorubicin-induced myocardial injury rat model for evaluation of Schisandrin B on viral myocarditis sequelae related pathological changes and its mechanism. The metabolite profiling of myocardial injury rats was performed through ultra-high performance liquid chromatography combined with mass spectrometry combined with pattern recognition approaches and pathway analysis. A total of 15 metabolites (9 in positive ion mode and 6 in negative ion mode) were considered as potential biomarkers of myocardial injury, and these metabolites may correlate with the regulation of Schisandrin B treatment. A total of 6 metabolic pathways are closely related to Schisandrin B treatment, including glycerophospholipid metabolism, sphingolipid metabolism, purine metabolism, etc. This study revealed the potential biomarkers and metabolic network pathways of myocardial injury, and illuminated the protective mechanism of Schisandrin B on myocardial injury. This article is protected by copyright. All rights reserved. PMID: 33247873 [PubMed - as supplied by publisher]

Related Articles Changes of embryonic development, locomotor activity, and metabolomics in zebrafish co-exposed to chlorpyrifos and deltamethrin. J Appl Toxicol. 2020 Nov 28;: Authors: Hu Y, Hu J, Li W, Gao Y, Tian Y Abstract Organophosphates (OPs) and pyrethroids (PYRs) are extensively used pesticides and often occur in the form of mixture, whereas little was known about their joint toxicities. We aim to investigate the individual and joint effects of OPs and PYRs exposure on zebrafish embryo by employing chlorpyrifos (CPF) and deltamethrin (DM) as representatives. Zebrafish embryos at 2 hours post fertilization (hpf) were exposed to CPF (4.80, 39.06, and 78.13 μg/L), DM exposure (0.06, 1.60, and 3.19 μg/L), and CPF + DM (4.80 + 0.06, 39.06 + 1.60, and 78.13 + 3.19 μg/L) until 144 hpf. Embryonic development, locomotor activity, and metabolomic changes were recorded and examined. Results displayed that individual exposure to CPF and DM significantly increased the mortality and malformation rate of zebrafish embryos, but decreased hatching rate was only found in CPF + DM co-exposure groups (p < .05). Meanwhile, individual CPF exposure had no detrimental effect on locomotor activity, high dose of individual CPF exposure decreased the swimming speed but had adaptability to the conversion from dark to light, whereas high dose of CPF + DM co-exposure exhibited not only significant decline in swimming speed but also no adaptability to the repeated stimulations, suggesting deficit in learning and memory function. In metabolomic analysis, individual CPF exposure mainly influenced the metabolism of glycerophospholipids and amino acids, individual DM exposure mainly influenced glycerophospholipids, and CPF + DM co-exposure mainly influenced glycerophospholipids and amino acids. Taken together, our findings suggested the embryonic toxicities and neurobehavioral changes caused by CPF and/or DM exposure. The disorder metabolomics of glycerophospholipids and amino acids might be involved in the underlying mechanism of those toxicities. PMID: 33247449 [PubMed - as supplied by publisher]

Related Articles Ustilago maydis effector Jsi1 interacts with Topless corepressor, hijacking plant JA/ET signaling. New Phytol. 2020 Nov 28;: Authors: Darino M, Chia KS, Marques J, Aleksza D, Soto Jiménez LM, Saado I, Uhse S, Borg M, Betz R, Bindics J, Zienkiewicz K, Feussner I, Petit-Houdenot Y, Djamei A Abstract Ustilago maydis (U. maydis) is the causal agent of maize smut disease. During the colonization process, the fungus secretes effector proteins which suppress immune responses and redirect the host metabolism in favor of the pathogen. As effectors play a critical role during plant colonization, their identification and functional characterization is essential to understanding biotrophy and disease. Using biochemical, molecular, and transcriptomic techniques, we performed a functional characterization of the U. maydis effector Jasmonate/Ethylene signaling inducer 1 (Jsi1). Jsi1 interacts with several members of the plant co-repressor family Topless/Topless related (TPL/TPR). Jsi1 expression in Zea mays (Z. mays) and Arabidopsis thaliana (A. thaliana) leads to transcriptional induction of the ethylene response factor (ERF) branch of the jasmonate/ethylene (JA/ET) signaling pathway. In A. thaliana, activation of the ERF-branch leads to biotrophic susceptibility. Jsi1 likely activates the ERF-branch via an EAR motif, which resembles EAR motifs from plant ERF transcription factors, that interacts with TPL/TPR proteins. EAR motif-containing effector candidates were identified from different fungal species including Magnaporthe oryzae, Sporisorium scitamineum, and Sporisorium reilianum. Interaction between plant TPL proteins and these effector candidates from biotrophic and hemibiotrophic fungi indicates the convergent evolution of effectors modulating the TPL/TPR co-repressor hub. PMID: 33247447 [PubMed - as supplied by publisher]

Related Articles Hyphenated high-resolution mass spectrometry-the "all-in-one" device in analytical toxicology? Anal Bioanal Chem. 2020 Nov 28;: Authors: Maurer HH Abstract This trend article reviews papers with hyphenated high-resolution mass spectrometry (HRMS) approaches applied in analytical toxicology, particularly in clinical and forensic toxicology published since 2016 and referenced in PubMed. The article focuses on the question of whether HRMS has or will become the all-in-one device in these fields as supposed by the increasing number of HRMS presentations at scientific meetings, corresponding original papers, and review articles. Typical examples for the different application fields are discussed such as targeted or untargeted drug screening, quantification, drug metabolism studies, and metabolomics approaches. Considering the reviewed papers, HRMS is currently the only technique that fulfills the criteria of an all-in-one device for the various applications needed in analytical toxicology.Graphical abstract. PMID: 33247339 [PubMed - as supplied by publisher]

Related Articles Potential impact of tissue molecular heterogeneity on ambient mass spectrometry profiles: a note of caution in choosing the right disease model. Anal Bioanal Chem. 2020 Nov 27;: Authors: Katz L, Woolman M, Tata A, Zarrine-Afsar A Abstract This review provides a summary of known molecular alterations in commonly used cancer models and strives to stipulate how they may affect ambient mass spectrometry profiles. Immortalized cell lines are known to accumulate mutations, and xenografts derived from cell lines are known to contain tumour microenvironment elements from the host animal. While the use of human specimens for mass spectrometry profiling studies is highly encouraged, patient-derived xenografts with low passage numbers could provide an alternative means of amplifying material for ambient MS research when needed. Similarly, genetic preservation of patient tissue seen in some organoid models, further verified by qualitative proteomic and transcriptomic analyses, may argue in favor of organoid suitability for certain ambient profiling studies. However, to choose the appropriate model, pre-evaluation of the model's molecular characteristics in the context of the research question(s) being asked will likely provide the most appropriate strategy to move research forward. This can be achieved by performing comparative ambient MS analysis of the disease model of choice against a small amount of patient tissue to verify concordance. Disease models, however, will continue to be useful tools to orthogonally validate metabolic states of patient tissues through controlled genetic alterations that are not possible with patient specimens. PMID: 33247337 [PubMed - as supplied by publisher]

Related Articles Benford's law and metabolomics: A tale of numbers and blood. Transfus Apher Sci. 2020 Nov 21;:103019 Authors: D'Alessandro A Abstract The Newcomb-Benford law - also known as the "law of anomalous numbers" or, more commonly, Benford's law - predicts that the distribution of the first significant digit of random numbers obtained from mixed probability distributions follows a predictable pattern and reveals some universal behavior. Specifically, given a dataset of empirical measures, the likelihood of the first digit of any number being 1 is ∼30 %, ∼18 % for 2, 12.5 % for 3 and so on, with a decreasing probability all the way to number 9. If the digits were distributed uniformly, all the numbers 1 through 9 would have the same probability to appear as the first digit in any given empirical random measurement. However, this is not the case, as this law defies common sense and seems to apply seamlessly to large data. The use of omics technologies and, in particular, metabolomics has generated a wealth of big data in the field of transfusion medicine. In the present meta-analysis, we focused on previous big data from metabolomics studies of relevance to transfusion medicine: one on the quality of stored red blood cells, one on the phenotypes of transfusion recipients, i.e. trauma patients suffering from trauma and hemorrhage, and one of relevance to the 2020 SARS-COV-2 global pandemic. We show that metabolomics data follow a Benford's law distribution, an observation that could be relevant for future application of the "law of anomalous numbers" in the field of quality control processes in transfusion medicine. PMID: 33246837 [PubMed - as supplied by publisher]

Related Articles Morinda officinalis polysaccharides improve meat quality by reducing oxidative damage in chickens suffering from tibial dyschondroplasia. Food Chem. 2020 Nov 20;:128688 Authors: Huang SC, Cao QQ, Cao YB, Yang YR, Xu TT, Yue K, Liu F, Tong ZX, Wang XB Abstract Tibial dyschondroplasia (TD) is the common leg disease in commercial broilers. However, the effects of TD on meat quality and the protective of Morinda officinalis polysaccharide (MOP) are largely unknown. Three hundred broiler chicks (one-day-old) were equally allocated into control (CON), TD and MOP-treated groups for 15 days. The results indicated that TD influenced morphology and meat quality-related parameters of the breast muscle, and changed the activity and mRNA expression of antioxidant enzymes in plasma and breast muscles. Moreover, metabolomics profiling of breast muscle revealed that the main altered metabolites 4-guanidinobutyric acid and chenodeoxycholic acid, which are related to meat quality and oxidative stress. Additionally, 500 mg/L MOP effectively restored the content of meat metabolites and oxidative damage. These findings suggest that oxidative damage caused by TD may affect meat quality in broilers by changing the content of breast muscle metabolites and that MOP supplementation has a restorative effect. PMID: 33246686 [PubMed - as supplied by publisher]

20 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2020/11/28PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

18 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2020/11/27PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

42 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2020/11/26PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

23 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2020/11/25PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

23 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2020/11/25PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

26 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2020/11/24PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

26 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: metabolomics These pubmed results were generated on 2020/11/24PubMed comprises more than millions of citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.