LuYuxing/MetaBench huggingface dataset:
Question: Write a study description for the study titled 'Metabolic profiling of ob/ob mouse fatty liver using HR-MAS 1H-NMR combined with gene expression analysis reveals alterations in betaine metabolism and the transsulfuration pathway'.
Answer: Metabolic perturbations resulting from excessive hepatic fat accumulation are poorly understood. Thus, in this study, leptin-deficient ob/ob mice, a mouse model of fatty liver disease, were used to investigate metabolic alterations in more detail. Metabolites were quantified in intact liver tissues of ob/ob (n=8) and control (n=8) mice using high-resolution magic angle spinning (HR-MAS) 1H-NMR. In addition, after demonstrating that HR-MAS 1H-NMR does not affect RNA integrity, transcriptional changes were measured by quantitative real-time PCR on RNA extracted from the same specimens after HR-MAS 1H-NMR measurements. Importantly, the gene expression changes obtained agreed with those observed by Affymetrix microarray analysis performed on RNA isolated directly from fresh-frozen tissue. In total, 40 metabolites could be assigned in the spectra and subsequently quantified. Quantification of lactate was also possible after applying a lactate-editing pulse sequence that suppresses the lipid signal, which superimposes the lactate methyl resonance at 1.3 ppm. Significant differences were detected for creatinine, glutamate, glycine, glycolate, trimethylamine-N-oxide, dimethylglycine, ADP, AMP, betaine, phenylalanine, and uridine. Furthermore, alterations in one-carbon metabolism, supported by both metabolic and transcriptional changes, were observed. These included reduced demethylation of betaine to dimethylglycine and the reduced expression of genes coding for transsulfuration pathway enzymes, which appears to preserve methionine levels, but may limit glutathione synthesis. Overall, the combined approach is advantageous as it identifies changes not only at the single gene or metabolite level but also deregulated pathways, thus providing critical insight into changes accompanying fatty liver disease. Graphical abstract A Evaluation of RNA integrity before and after HR-MAS 1H-NMR of intact mouse liver tissue. B Metabolite concentrations and gene expression levels assessed in ob/ob (steatotic) and ob/+ (control) mice using HR-MAS 1H-NMR and qRT-PCR, respectively.
Question: Write a study description for the study titled 'Community metabolomics provides insights into mechanisms of pollution-induced community tolerance of periphyton'.
Answer: Chemical pollution is a major concern for freshwater ecosystems, but the impact and mechanisms of chemical stressors on communities are barely understood. Pollution stress beyond natural homeostatic capacities can trigger succession of tolerant species within a community, enhancing the overall community tolerance. This process was operationalized in the Pollution-Induced Community Tolerance (PICT) concept and applied in many case studies, however, the molecular mechanisms of community tolerance and implications for ecological functions remain largely unexplored. Our study aimed to demonstrate that 1) community metabolomics can unravel potential mechanisms of PICT in periphyton and 2) induced tolerance helps to maintain primary production under re-occuring pollution. To this end, we grew periphyton for 5 weeks with and without the model herbicide diuron in microcosms, quantified PICT, and determined the related metabolic fingerprint of periphyton by GC–MS-based untargeted metabolomics. Further, we explored the autotrophic community based on pigment composition and functional parameters including photosynthesis and gross primary production. Chronic diuron exposure resulted in a shift in pigment composition, higher community tolerance and an individual metabolic fingerprint in the contaminated communities. Opposing responses of selected metabolites during a short-term exposure indicated differences in diuron pre-adaptation in the different communities. Metabolites (threonic acid and two sugar acid lactones) were found to be related to tolerance development, suggesting that ascorbate metabolism was induced in contaminated communities. Despite these compensating mechanism, contaminated communities were compromised in production-to-respiration ratio and biomass. A ranking of sensitivity thresholds of different biological endpoints revealed that metabolites were less sensitive than photosynthetic parameters, which reflects the mode-of-action of the herbicide. In conclusion, we could demonstrate that community metabolomics is able to unravel complex biochemical changes and allows mechanistic insights into community tolerance. Moreover, we were able to show that induced community tolerance was insufficient to safeguard functions like primary production.
Question: Write a study description for the study titled 'Transcriptomic and metabolomic analysis of liver cirrhosis'.
Answer: Liver cirrhosis is one of the leading causes of decreased life expectancy worldwide. However, the molecular mechanisms underlying the development of liver cirrhosis remain unclear. In this study, we performed a comprehensive analysis using transcriptome and metabolome sequencing to explore the genes, pathways, and interactions associated with liver cirrhosis. We performed transcriptome and metabolome sequencing of blood samples from patients with cirrhosis and healthy controls (1:1 matched for sex and age). For transcriptome analysis, we screened for differentially expressed miRNAs and mRNAs, analyzed mRNAs to identify possible core genes and pathways, and performed co-analysis of miRNA and mRNA sequencing results. And we validated differentially expressed microRNA (miRNA) and mRNAs using real-time quantitative polymerase chain reaction. In terms of the metabolome, we screened five pathways that were substantially enriched in the differential metabolites. Next, we identified the metabolites with the most pronounced differences among these five metabolic pathways. We performed receiver operating characteristic curve analysis of these five metabolites to determine their diagnostic efficacy for cirrhosis. Finally, we explored possible links between the transcriptome and metabolome. Using a systems biology framework, We identified miRNAs and mRNAs that were differentially expressed in the blood of cirrhotic patients and healthy controls. And explored associated pathways as well as disease-specific networks. Additionally, We identified possible common pathways in the transcriptome and metabolome that can reveal coherent changes in cirrhosis from the transcriptional level to the metabolic level, which can be further studied from multiple perspectives.
Question: Write a study description for the study titled 'An online atlas of human plasma metabolite signatures of gut microbiome composition'.
Answer: Human gut microbiota produce a variety of molecules, some of which enter the bloodstream and impact health. Conversely, dietary or pharmacological compounds may affect the microbiota before entering the circulation. Characterization of these interactions is an important step towards understanding the effects of the gut microbiota on health. In this cross-sectional study, we used deep metagenomic sequencing and ultra-high-performance liquid chromatography linked to mass spectrometry for a detailed characterization of the gut microbiota and plasma metabolome, respectively, of 8583 participants invited at age 50 to 64 from the population-based Swedish CArdioPulmonary bioImage Study. Here, we find that the gut microbiota explain up to 58% of the variance of individual plasma metabolites and we present 997 associations between alpha diversity and plasma metabolites and 546,819 associations between specific gut metagenomic species and plasma metabolites in an online atlas (https://gutsyatlas.serve.scilifelab.se/). We exemplify the potential of this resource by presenting novel associations between dietary factors and oral medication with the gut microbiome, and microbial species strongly associated with the uremic toxin p-cresol sulfate. This resource can be used as the basis for targeted studies of perturbation of specific metabolites and for identification of candidate plasma biomarkers of gut microbiota composition.
Question: Write a study description for the study titled 'Inorganic Carbon Limitation in Cells of the Wild Type and Photorespiratory Mutants of the Cyanobacterium Synechocystis sp. Strain PCC 6803'.
Answer: The amount of inorganic carbon represents one of the main environmental factors determining productivity of photoautotrophic organisms. Using the model cyanobacterium Synechocystis sp. PCC 6803, we performed a first metabolome study with cyanobacterial cells shifted from high CO2 (5% in air) into conditions of low CO2 (LC; ambient air with 0.035% CO2). Using gas chromatography-mass spectrometry, 74 metabolites were reproducibly identified under different growth conditions. Shifting wild-type cells into LC conditions resulted in a global metabolic reprogramming and involved increases of, for example, 2-oxoglutarate (2OG) and phosphoenolpyruvate, and reductions of, for example, sucrose and fructose-1,6-bisphosphate. A decrease in Calvin-Benson cycle activity and increased usage of associated carbon cycling routes, including photorespiratory metabolism, was indicated by synergistic accumulation of the fumarate, malate, and 2-phosphoglycolate pools and a transient increase of 3-phosphoglycerate. The unexpected accumulation of 2OG with a concomitant decrease of glutamine pointed toward reduced nitrogen availability when cells are confronted with LC. Despite the increase in 2OG and low amino acid pools, we found a complete dephosphorylation of the PII regulatory protein at LC characteristic for nitrogen-replete conditions. Moreover, mutants with defined blocks in the photorespiratory metabolism leading to the accumulation of glycolate and glycine, respectively, exhibited features of LC-treated wild-type cells such as the changed 2OG to glutamine ratio and PII phosphorylation state already under high CO2 conditions. Thus, metabolome profiling demonstrated that acclimation to LC involves coordinated changes of carbon and interacting nitrogen metabolism. We hypothesize that Synechocystis has a temporal lag of acclimating carbon versus nitrogen metabolism with carbon leading.
Question: Write a study description for the study titled 'Giardiavirus infection mediates Enolase to the upregulation of Glycolysis in Giardia'.
Answer: Giardia duodenalis is a prevalent intestinal parasite that cause giardiasis, a condition characterized by diarrhea and frequently linked to malnutrition and growth impairments in children. The presence of Giardiavirus (GLV) can lead to reduced pathological damage in mice infected with Giardia and different pro-inflammatory responses in host cells stimulated by Giardia. As is well known, viruses as “non-cellular organisms” that control host proteins, metabolic resources to complete replication and transmission. However, the understanding of the impact of the Giardiavirus on the G. duodenalis itself is currently limited. Here, we found that GLV infection can reduce the mRNA and expression levels of Giardia genes, but lead to upregulation of translation efficiency in Giardia genes. Additionally, GLV infection causes Giardia's energy metabolic reprogramming, 21 significantly different energy metabolites were identified, and the most significant pathway by KEGG enrichment was Glycolysis/ Gluconeogenesis. After the viral load of GLV stabilizes, glycolysis is significantly upregulated with increasing GLV infection generations. The glycolytic enzyme enolase in Giardia is closely associated with the viral load of GLV. and it was found that knocking down the expression level of enolase also led to a decrease in the viral load of GLV. Overall, these results highlight that GLV infection can regulate the protein and energy metabolism of G. duodenalis for its own survival, and discover the potential of GLV as a novel intervention strategy for the development of drugs and vaccines for the prevention and treatment of giardiasis.
Question: Write a study description for the study titled 'Multi-Omics Unveils Strain-Specific Neuroactive Metabolite Production Linked to Inflammation Modulation by Bacteroides and Their Vesicles'.
Answer: 18 Bacteroidetes isoaltes were analyzed for their neuroactive potentail using un-targeted and targeted metabolomics. The bacteria were grown to stationary phase, the supernatant was separated and purified using 0.22 um filter. The metabolome from the supernatant was extracted using standard Methanol extraction. The reconstituted supernatant samples were transferred into LC vials and loaded onto a sample tray in the nanoLC coupled to the Q-Exactive Plus mass spectrometer (Thermo Fisher Scientific). Chromatographic separation of metabolites was performed on a Proxeon EASY nLC II System (Thermo Fisher Scientific) equipped with a Thermo Scientific Acclaim PepMap RSLC C18 column (P/N ES800A). The Xbridge BEH Amide (2.5 μm, 2.1 x 150 mm, Waters, Milford, MA, USA) column was used for metabolite separation.
Question: Write a study description for the study titled 'Development and validation of a liquid chromatography-electrospray ionization-time-of-flight mass spectrometry method for induced changes in Nicotiana attenuata leaves during simulated herbivory'.
Answer: Metabolite profiling of herbivory-induced changes in Nicotiana attenuata was used to construct a correlation-weighted network to visualize intra- and inter-compound spectra relationships from individual mass features, and to annotate 12 major network hubs, including 4 O-acyl sugars and 6 17-hydroxygeranyllinalool diterpene glycosides, metabolites with recently uncovered anti-herbivore functions.
Question: Write a study description for the study titled 'MFSD7C protects hemolysis-induced lung impairments by inhibiting ferroptosis'.
Answer: Hemolysis drives susceptibility to lung injury and predicts poor outcomes in diseases, such as malaria and sickle cell disease (SCD). However, the underlying pathological mechanism remains unknown. Here, we report that major facilitator superfamily domain containing 7C (MFSD7C) protects the lung from hemolytic-induced damage by preventing ferroptosis. Mechanistically, MFSD7C deficiency leads to mitochondrial dysfunction and lipid remodeling caused by increased fatty acid uptake and decreased consumption, the excess accumulation of lipids sensitizes cells to peroxidation and ferroptosis. Moreover, systematic delivery of MFSD7C mRNA-loaded nanoparticles to the lungs effectively prevented lung injury in mice with hemolysis. These findings present the detailed link between hemolytic complications and ferroptosis, providing potential therapeutic targets for patients with hemolytic disorders.
Question: Write a study description for the study titled 'Serine and 1-carbon metabolism are required for HIF-mediated protection against retinopathy of prematurity'.
Answer: We determined which metabolic pathways are activated by hypoxia-inducible factor 1-mediated (HIF-1-mediated) protection against oxygen-induced retinopathy (OIR) in newborn mice, the experimental correlate to retinopathy of prematurity, a leading cause of infant blindness. HIF-1 coordinates the change from oxidative to glycolytic metabolism and mediates flux through serine and 1-carbon metabolism (1CM) in hypoxic and cancer cells. We used untargeted metabolite profiling in vivo to demonstrate that hypoxia mimesis activates serine/1CM. Both [13C6] glucose labeling of metabolites in ex vivo retinal explants as well as in vivo [13C3] serine labeling of metabolites followed in liver lysates strongly suggest that retinal serine is primarily derived from hepatic glycolytic carbon and not from retinal glycolytic carbon in newborn pups. In HIF-1α2lox/2lox albumin-Cre-knockout mice, reduced or near-0 levels of serine/glycine further demonstrate the hepatic origin of retinal serine. Furthermore, inhibition of 1CM by methotrexate blocked HIF-mediated protection against OIR. This demonstrated that 1CM participates in protection induced by HIF-1 stabilization. The urea cycle also dominated pathway enrichment analyses of plasma samples. The dependence of retinal serine on hepatic HIF-1 and the upregulation of the urea cycle emphasize the importance of the liver to remote protection of the retina.
Question: Write a study description for the study titled 'Discovery and validation of metabolite markers in bloodstains for bloodstain age estimation'.
Answer: The age estimation of bloodstains measures the time-dependent changes in the levels of bloodstain biomolecules. Although several studies have identified bloodstain metabolites as markers for estimating bloodstain age, none has consider gender and age-related metabolomic differences or long-time bloodstain age. Therefore, we aimed to identify metabolite markers for estimating the age of bloodstains at weekly intervals within 28 d and validate them through the MRM technique. Interestingly, adenosine 5′-monophosphate (5′-AMP), choline and pyroglutamic acid were selected as markers. We validated a total of 7 metabolites, including 5 previously reported metabolites, ergothioneine, hypoxanthine, L-isoleucine, L-tryptophan and pyroglutamic acid. Choline and hypoxanthine might be used to differentiate between day 0 and day 14 at weekly intervals, while L-isoleucine and L-tryptophan might help distinguish between 7 d before and 14 d after. Evaluation of the changes in the levels of metabolites according to gender and age, revealed that the average level of all 7 metabolites was higher in women on day 0. Moreover, the level of ergothioneine was significantly higher in the elderly than the youth under all time conditions. In this study, we confirmed the potential effectiveness of metabolites in bloodstains as forensic markers, and provided a new perspective on metabolomic approaches linked to forensic science.
Question: Write a study description for the study titled 'LC−MS Based Serum Metabolomics for Identification of Hepatocellular Carcinoma Biomarkers in Egyptian Cohort'.
Answer: Although hepatocellular carcinoma (HCC) has been subjected to continuous investigation and its symptoms are well-known, early stage diagnosis of this disease remains difficult and the survival rate after diagnosis is typically very low (3−5%). Early and accurate detection of metabolic changes in the sera of patients with liver cirrhosis can help improve the prognosis of HCC and lead to a better understanding of its mechanism at the molecular level, thus providing patients with in-time treatment of the disease. In this study, we compared metabolite levels in sera of 40 HCC patients and 49 cirrhosis patients from Egypt by using ultraperformance liquid chromatography coupled with quadrupole time-of-flight mass spectrometer (UPLC-QTOF MS). Following data preprocessing, the most relevant ions in distinguishing HCC cases from cirrhotic controls are selected by statistical methods. Putative metabolite identifications for these ions are obtained through mass-based database search. The identities of some of the putative identifications are verified by comparing their MS/MS fragmentation patterns and retention times with those from authentic compounds. Finally, the serum samples are reanalyzed for quantitation of selected metabolites as candidate biomarkers of HCC. This quantitation was performed using isotope dilution by selected reaction monitoring (SRM) on a triple quadrupole linear ion trap (QqQLIT) coupled to UPLC. Statistical analysis of the UPLC-QTOF data identified 274 monoisotopic ion masses with statistically significant differences in ion intensities between HCC cases and cirrhotic controls. Putative identifications were obtained for 158 ions by mass based search against databases. We verified the identities of selected putative identifications including glycholic acid (GCA), glycodeoxycholic acid (GDCA), 3β, 6β-dihydroxy-5β-cholan-24-oic acid, oleoyl carnitine, and Phe-Phe. SRM-based quantitation confirmed significant differences between HCC and cirrhotic controls in metabolite levels of bile acid metabolites, long chain carnitines and small peptide. Our study provides useful insight into appropriate experimental design and computational methods for serum biomarker discovery using LC−MS/MS based metabolomics. This study has led to the identification of candidate biomarkers with significant changes in metabolite levels between HCC cases and cirrhotic controls. This is the first MS-based metabolic biomarker discovery study on Egyptian subjects that led to the identification of candidate metabolites that discriminate early stage HCC from patients with liver cirrhosis.
Question: Write a study description for the study titled 'Integrated transcriptome and metabolome dynamics with phenotypic traits reveal regulatory basis of male morphotype differentiation in giant freshwater prawn Macrobrachium rosenbergii'.
Answer: This integrated multi-omics resource delineates the molecular and phenotypic trajectories underlying male morphotype differentiation (Blue Claw [BC], Orange Claw [OC], Small Male [SM]) in macrobrachium rosenbergii during determinative developmental stages (100, 110, and 120 days post-stocking). The dataset comprises paired testicular transcriptomic profiles, hemolymph serum metabolomes, and quantitative morphological trait data (15 key metrics), thereby establishing a holistic framework capturing concurrent gene expression dynamics, metabolic flux alterations, and phenotypic manifestations throughout morphotype specification. The synergistic integration of these multidimensional layers enables mechanistic dissection of regulatory networks governing crustacean growth polymorphism, facilitates identification of heritable biomarkers associated with commercially advantageous morphotypes, and provides foundational insights into arthropod phenotypic plasticity.
Question: Write a study description for the study titled 'Neuroactive metabolites and bile acids are altered in extremely premature infants with brain injury'.
Answer: The gut microbiome has been associated with pathological neurophysiological evolvement in extremely premature infants suffering from brain injury. The exact underlying mechanism and its associated metabolic signatures in infants are not fully understood. To decipher metabolite profiles linked to neonatal brain injury, we investigated the longitudinal fecal and plasma metabolome of 51 extremely premature infants using LC-HRMS-based untargeted metabolomics. This was expanded by an investigation of bile acids and amidated bile acid conjugates in feces and plasma by LC-MS/MS-based targeted metabolomics. The resulting data was integrated with 16S rRNA gene amplicon gut microbiome profiles as well as patient cytokine, growth factor and T-cell profiles. We identified an early onset of differentiation in neuroactive metabolites and bile acids between infants with and without brain injury. We detected several bacterially-derived bile acid amino acid conjugates and secondary bile acids in the plasma already 3 days after delivery, indicating the early establishment of a metabolically active gut microbiome. These results give new insights into the early life metabolome of extremely premature infants.