LuYuxing/MetaBench huggingface dataset:
Question: Write a study description for the study titled 'Effect of gut microbiota on depressive-like behaviors in mice is mediated by the endocannabinoid system'.
Answer: Depression is the leading cause of disability worldwide. Recent observations have revealed an association between mood disorders and alterations of the intestinal microbiota, but causality remains yet to be established. Here, using unpredictable chronic mild stress (UCMS) as a mouse model of depression, we show that UCMS mice display phenotypic alterations which could be transferred from UCMS donors to naïve recipient mice by fecal microbiota transplantation. The cellular and behavioral alterations observed in recipient mice were accompanied by a decrease in the endocannabinoid (eCB) signaling due to lower peripheral levels of fatty acid precursors of eCB ligands. The adverse effects of UCMS-transferred microbiota were alleviated by selectively enhancing the central eCB or by complementation with a strain of the Lactobacilli genus. Our findings provide a mechanistic scenario for how chronic stress, diet and gut microbiota generate a pathological feed-forward loop that contributes to despair behavior via the central eCB system.
Question: Write a study description for the study titled 'Melatonin enhances function of porcine immature Sertoli cells via modulating gene expression and metabolism'.
Answer: Melatonin (MT), a neurohormone synthesized and secreted primarily by the pineal gland, is of vital function to animal reproduction. However, the effect of MT treatment on porcine immature Sertoli cells (iSCs) remains unclear. Here, MT treatment (10 nM, 36 h) could elevate mitochondrial function and reduce oxidative stress, therefore inhibit apoptosis of porcine iSCs. Transcriptome profiling identified 39 differentially expressed genes (DEGs) (33 known and 6 novel) (MT vs Control), mainly involved in GO terms of steroid metabolic process, glutamine metabolic process, oxidoreductase activity and G protein coupled receptor binding, and KEGG pathways of steroid biogenesis, pyruvate metabolism, NF-kappa B and AMPK signal pathways. RT-qPCR validated 6 DEGs (Phgdh, Scd, Hmgcs1, Cytb, Pck2 and Sqle) induced by MT to be with the similar change trend to RNA-seq results. The protein level of HMGCS1 and the estradiol level were confirmed to be significantly decreased by MT (10 nM, 36 h) treatment of porcine iSCs. Inhibition of HMGCS1 in porcine iSCs could significantly reduce the level of estradiol. The levels of cholesterol content within cells and lactate in culture medium were unchanged by MT (10 nM, 36 h). 14 metabolites were significantly altered by MT (10 nM, 36 h) treatment of porcine iSCs. Which were involved in multiple vital metabolic pathways. Collectively, MT treatment of porcine iSCs could promote functions of porcine iSCs via modulating gene expression and metabolism.
Question: Write a study description for the study titled 'FDR-controlled metabolite annotation for high-resolution imaging mass spectrometry imaging MS (MALDI imaging assay)'.
Answer: High-mass-resolution imaging mass spectrometry promises to localize hundreds of metabolites directly from tissues, cell cultures, and agar plates with cellular resolution, but is hampered by the lack of bioinformatics for automated metabolite identification. We developed the first bioinformatics framework for False Discovery Rate (FDR)-controlled metabolite annotation for high-mass-resolution imaging mass spectrometry (https://github.com/alexandrovteam/pySM) introducing a Metabolite-Signal Match (MSM) score and a target-decoy FDR-estimate for spatial metabolomics. MALDI-FTICR datasets acquired from wild type adult mouse brain were used for the development of spatial metabolomics annotation bioinformatics. This study together with MTBLS317 and MTBLS378 provide the accompanying data for FDR-controlled metabolite annotation for high-resolution imaging mass spectrometry.
Question: Write a study description for the study titled 'Benthic exometabolites and their ecological significance on threatened Caribbean coral reefs (Metabolite uptake incubation assay)'.
Answer: Benthic organisms sustain coral reefs through their growth and metabolism, but less is known about how their released metabolites influence reef seawater microorganisms. To investigate metabolite composition of benthic exudates and their ecological significance for reef microbial communities, we harvested exudates from six species of Caribbean benthic organisms including stony corals, octocorals, and an invasive encrusting algae, and subjected these exudates to untargeted and targeted metabolomics approaches using liquid chromatography-mass spectrometry. Incubations with reef seawater microorganisms were conducted to monitor changes in microbial community composition using 16S rRNA gene sequencing and abundance in relation to exudate source and three specific metabolites. Exudates tended to be enriched in amino acids, nucleosides, and vitamins, indicating that benthic organisms contribute labile organic matter to reefs. The phytohormone indole-3-acetic acid was detected in octocoral exudates, suggesting that this metabolite facilitates microbial interactions within and outside of benthic organisms. Exudate compositions were species-specific and significantly enriched in the indole class of metabolites. Microbial abundances and specific microbial taxa responded differently in relation to exudates from stony corals and octocorals, demonstrating the link between benthic organismal composition, metabolite exudates, and microbial growth. Conversely, microbial communities did not respond to additions of the individual metabolites, suggesting that reef microorganisms likely provide diverse metabolite pools that support microbial growth. This work identifies, quantifies, and compares metabolites released from common Caribbean benthic organisms and indicates that recent shifts in benthic composition from stony to octocorals alter exudate composition and likely impact microbial community composition and function on coral reefs.UPLC-MS Metabolite uptake incubation assay is reported in the current study MTBLS3286UPLC-MS Metabolite collection incubation assays are reported in MTBLS2855
Question: Write a study description for the study titled 'Previous infestation by conspecifics leads to a transient increase of the performance of Sitobion avenae aphids on wheat leaves'.
Answer: 1. The ecological niche of aphids is largely defined by the phloem sap of plants, which they consume. Previous studies revealed that aphids may change the phloem sap metabolome and that a previous aphid infestation may benefit them. As aphids reproduce parthenogenetically, the performance and preference of aphids of the same monoclonal aphid lineage can be compared between previously uninfested and previously aphid-infested plants.2. Wheat (Triticum aestivum) leaves were infested by clonal lineages of Sitobion avenae aphids for 9–10 days. Leaf phloem exudates were analysed using amino acid profiling and metabolic fingerprinting, capturing mainly specialised metabolites. It was investigated whether aphid colony sizes differ between leaves that were previously uninfested or infested by aphids of a different clonal lineage or by aphids of the same clonal lineage and whether aphids show a preference for any of these leaves.3. The relative concentrations of metabolites in the phloem exudates were not affected by aphid infestation. Aphid colonies were partly larger on previously aphid-infested leaves than on control leaves. However, this effect was transient and finally colonies had similar sizes. Given a choice between previously aphid-infested and uninfested leaves, S. avenae nymphs showed no preferences.4. The findings that positive effects of previous aphid infestation on aphid performance are transient and that the performance but not the preference of the aphids was affected by previous aphid infestation highlight the temporal dynamics and complexity of aphid–plant interactions. Niche alteration processes may be partly involved in these interactions.
Question: Write a study description for the study titled 'Comparative Analyses of Metabolomic Fingerprints and Cytotoxic Activities of Soft Corals from the Colombian Caribbean'.
Answer: Soft corals (Cnidaria, Anthozoa, Octocorallia) are a diverse group of marine invertebrates that inhabit various marine environments in tropical and subtropical areas. Several species are recognized as prolific sources of compounds with a wide array of biological activities. Recent advances in analytical techniques, supported by robust statistical analyses, have allowed the analysis and characterization of the metabolome present in a single living organism. In this study, a liquid chromatography-high resolution mass spectrometry metabolomic approach was applied to analyze the metabolite composition of 28 soft corals present in the Caribbean coast of Colombia. Multivariate data analysis was used to correlate the chemical fingerprints of soft corals with their cytotoxic activity against tumor cell lines for anticancer purpose. Some diterpenoids were identified as specific markers to discriminate between cytotoxic and non-cytotoxic crude extracts of soft corals against tumor cell lines. In the models generated from the comparative analysis of PLS-DA for tumor lines, A549 and SiHa, the diterpene 13-keto-1,11-dolabell-3(E),7(E),12(18)-triene yielded a high score in the variable importance in projection. These results highlight the potential of metabolomic approaches towards the identification of cytotoxic agents against cancer of marine origin. This workflow can be useful in several studies, mainly those that are time consuming, such as traditional bioprospecting of marine natural products.
Question: Write a study description for the study titled 'Bile acid is a significant host factor shaping the gut microbiome of diet induced obese mice (untargeted metabolome profile assay)'.
Answer: BACKGROUND: Intestinal bacteria are known to regulate the bile acid (BA) homeostasis via intestinal biotransformation of BAs and stimulating the expression of fibroblast growth factor 19 through intestinal nuclear farnesoid X receptor (FXR). On the other hand, BAs directly regulate the gut microbiota with their strong antimicrobial activities. It remains unclear, however, how mammalian BAs cross-talk with gut microbiome and shape microbial composition in a dynamic and interactive way.﻿RESULTS: We quantitatively profiled small molecule metabolites derived from host-microbial co-metabolism in mice, demonstrating that Bas were the most significant factor correlated with microbial alterations among all types of endogenous metabolites. HFD intervention resulted in a rapid and significant increase in intestinal BA pool within 12 hrs followed by alteration in microbial composition at 24 hrs, providing supporting evidence that BAs are major dietary factors regulating gut microbiota. Feeding mice with BAs along with normal diet induced obese phenotype and obesity-associated gut microbial composition, similar to HFD fed mice. Finally, inhibition of hepatic BA biosynthesis under HFD conditions attenuated the HFD-induced gut microbiome alterations. Inhibition of BAs and direct suppression of micriobiota improved obese phenotypes.CONCLUSIONS: Our study highlights a liver - BAs - gut microbiome metabolic axis that drives significant modifications of BA and microbiota compositions capable of triggering metabolic disorders, suggesting new therapeutic strategies targeting BA metabolism for metabolic diseases.﻿The targeted short chain fatty acid analysis assay for this study can be found in the MetaboLights study MTBLS546.The targeted bile acid analysis assay for this study can be found in the MetaboLights study MTBLS547.The targeted fatty acid analysis assay for this study can be found in the MetaboLights study MTBLS548.
Question: Write a study description for the study titled '1H NMR metabolite monitoring during the differentiation of human induced pluripotent stem cells provides new insights into the molecular events that regulate embryonic chondrogenesis'.
Answer: The integration of cell metabolism with signalling pathways, transcription factor networks and epigenetic mediators is critical in coordinating molecular and cellular events during embryogenesis. Induced pluripotent stem cells (IPSCs) are an established model for embryogenesis, germ layer specification and cell lineage differentiation, advancing the study of human embryonic development and the translation of innovations in drug discovery, disease modelling and cell-based therapies. The metabolic regulation of IPSC pluripotency is mediated by balancing glycolysis and oxidative phosphorylation, but there is a paucity of data regarding the influence of individual metabolite changes during cell lineage differentiation. We used 1H NMR metabolite fingerprinting and footprinting to monitor metabolite levels as IPSCs are directed in a three-stage protocol through primitive streak/mesendoderm, mesoderm and chondrogenic populations. Metabolite changes were associated with central metabolism, with aerobic glycolysis predominant in IPSC, elevated oxidative phosphorylation during differentiation and fatty acid oxidation and ketone body use in chondrogenic cells. Metabolites were also implicated in the epigenetic regulation of pluripotency, cell signalling and biosynthetic pathways. Our results show that 1H NMR metabolomics is an effective tool for monitoring metabolite changes during the differentiation of pluripotent cells with implications on optimising media and environmental parameters for the study of embryogenesis and translational applications.
Question: Write a study description for the study titled 'Untargeted gas chromatography–mass spectrometry-based metabolomics analysis of kidney and liver tissue from the Lewis Polycystic Kidney rat'.
Answer: Polycystic kidney disease (PKD) encompasses a spectrum of inherited disorders that lead to end-stage renal disease (ESRD). There is no cure for PKD and current treatment options are limited to renal replacement therapy and transplantation. A better understanding of the pathobiology of PKD is needed for the development of new, less invasive treatments. The Lewis Polycystic Kidney (LPK) rat phenotype has been characterized and classified as a model of nephronophthisis (NPHP9, caused by mutation of the Nek8 gene) for which polycystic kidneys are one of the main pathologic features. The aim of this study was to use a GC-MS-based untargeted metabolomics approach to determine key biochemical changes in kidney and liver tissue of the LPK rat. Tissues from 16-week old LPK (n = 10) and Lewis age- and sex-matched control animals (n = 11) were used. Principal component analysis (PCA) distinguished signal corrected metabolite profiles from Lewis and LPK rats for kidney (PC-1 77%) and liver (PC-1 46%) tissue. There were marked differences in the metabolite profiles of the kidney tissues with 122 deconvoluted features significantly different between the LPK and Lewis strains. The metabolite profiles were less marked between strains for liver samples with 30 features significantly different. Five biochemical pathways showed three or more significantly altered metabolites: transcription/translation, arginine and proline metabolism, alpha-linolenic and linoleic acid metabolism, the citric acid cycle, and the urea cycle. The results of this study validate and complement the current literature and are consistent with the understood pathobiology of PKD.
Question: Write a study description for the study titled 'Sensing Ceramides by CYSLTR2 and P2RY6 to Aggravate Atherosclerosis'.
Answer: Recent evidence shows elevated circulating long-chain ceramide levels predicts atherosclerotic cardiovascular disease (ASCVD) independently of cholesterol. Although targeting ceramides signaling may provide therapeutic benefits beyond the treatment of hypercholesterolemia, the underlying mechanism by which circulating ceramides aggravate ASCVD remains elusive. We examined whether circulating long-chain ceramides activate membrane G protein-coupled receptors (GPCRs) to exacerbate atherosclerosis. We performed a systematic screen combining G protein signaling quantification, bioinformatic analysis of GPCRs expression, and functional examination of NLRP3 inflammasome activation, and the results suggested CYSLTR2 and P2RY6 as potential endogenous receptors of C16:0 ceramide-evoked inflammasome activation in both endothelial cells and macrophages. We found that inhibiting CYSLTR2/P2RY6 genetically or pharmacologically alleviated ceramide-evoked atherosclerosis aggravation. Additionally, increased ceramide levels correlated with the severity of coronary artery disease in patients with varying degrees of renal impairment. Notably, CYSLTR2/P2RY6 deficiency mitigated chronic kidney disease (CKD)-aggravated atherosclerosis in mice without affecting cholesterol or ceramide levels. Structural analysis of the ceramide-CYSLTR2-Gq complexes revealed that both C16:0 and C20:0 ceramides bind within an inclined channel-like ligand binding pocket on CYSLTR2. We further revealed an unconventional mechanism underlying ceramides-induced CYSLTR2 activation and CYSLTR2-Gq interface. Overall, our study provided structural and molecular mechanisms that long-chain ceramides initiated transmembrane Gq and inflammasome signaling through directly binding to CYSLTR2 and P2RY6 receptors, and blocking these signaling may provide new therapeutic potential to treat atherosclerosis-related diseases.
Question: Write a study description for the study titled 'Macrophage ATP citrate lyase deficiency stabilizes atherosclerotic plaques'.
Answer: Macrophages represent a major immune cell population in atherosclerotic plaques and play central role in the progression of this lipid-driven chronic inflammatory disease. Targeting immunometabolism is proposed as a strategy to revert aberrant macrophage activation to improve disease outcome. Here, we show ATP citrate lyase (Acly) to be activated in inflammatory macrophages and human atherosclerotic plaques. We demonstrate that myeloid Acly deficiency induces a stable plaque phenotype characterized by increased collagen deposition and fibrous cap thickness, along with a smaller necrotic core. In-depth functional, lipidomic, and transcriptional characterization indicate deregulated fatty acid and cholesterol biosynthesis and reduced liver X receptor activation within the macrophages in vitro. This results in macrophages that are more prone to undergo apoptosis, whilst maintaining their capacity to phagocytose apoptotic cells. Together, our results indicate that targeting macrophage metabolism improves atherosclerosis outcome and we reveal Acly as a promising therapeutic target to stabilize atherosclerotic plaques.