% R

@Manual{r,
title = {R: A Language and Environment for Statistical Computing},
author = {{R Core Team}},
organization = {R Foundation for Statistical Computing},
address = {Vienna, Austria},
year = {2017},
url = {https://www.R-project.org/},
}

% camera

@article{camera,
  title={CAMERA: an integrated strategy for compound spectra extraction and annotation of liquid chromatography/mass spectrometry data sets},
  author={Kuhl, Carsten and Tautenhahn, Ralf and Bottcher, Christoph and Larson, Tony R and Neumann, Steffen},
  journal={Analytical chemistry},
  volume={84},
  number={1},
  pages={283--289},
  year={2011},
  publisher={ACS Publications}
}

@article{xcms,
  title={XCMS: processing mass spectrometry data for metabolite profiling using nonlinear peak alignment, matching, and identification},
  author={Smith, Colin A and Want, Elizabeth J and O'Maille, Grace and Abagyan, Ruben and Siuzdak, Gary},
  journal={Analytical chemistry},
  volume={78},
  number={3},
  pages={779--787},
  year={2006},
  publisher={ACS Publications}
}

% kegggraph

@article{kegggraph,
  title={KEGGgraph: a graph approach to KEGG PATHWAY in R and bioconductor},
  author={Zhang, Jitao David and Wiemann, Stefan},
  journal={Bioinformatics},
  volume={25},
  number={11},
  pages={1470--1471},
  year={2009},
  publisher={Oxford University Press}
}

% KEGGREST

@Manual{keggrest,
title = {KEGGREST: Client-side REST access to KEGG},
author = {Dan Tenenbaum},
year = {2017},
note = {R package version 1.16.1},
}

% igraph

@Article{igraph,
title = {The igraph software package for complex network research},
author = {Gabor Csardi and Tamas Nepusz},
journal = {InterJournal},
volume = {Complex Systems},
pages = {1695},
year = {2006}
}

% gene ontology

@article{geneontology,
  title={Gene ontology consortium: going forward},
  author={Gene Ontology Consortium and others},
  journal={Nucleic acids research},
  volume={43},
  number={D1},
  pages={D1049--D1056},
  year={2015},
  publisher={Oxford Univ Press}
}

% KEGG

@article{kegg,
title={KEGG for integration and interpretation of large-scale molecular data sets},
author={Kanehisa, Minoru and Goto, Susumu and Sato, Yoko and Furumichi, Miho and Tanabe, Mao},
journal={Nucleic acids research},
volume={40},
number={D1},
pages={D109--D114},
year={2011},
publisher={Oxford University Press}
}

% reactome

@article{reactome,
  title={The reactome pathway knowledgebase},
  author={Fabregat, Antonio and Sidiropoulos, Konstantinos and Garapati, Phani and Gillespie, Marc and Hausmann, Kerstin and Haw, Robin and Jassal, Bijay and Jupe, Steven and Korninger, Florian and McKay, Sheldon and others},
  journal={Nucleic acids research},
  volume={44},
  number={D1},
  pages={D481--D487},
  year={2015},
  publisher={Oxford University Press}
}

% ten years

@article{review10years,
author = {Purvesh Khatri and Marina Sirota and Atul J. Butte},
journal = {PLoS Computational Biology},
number = 2,
title = {{Ten Years of Pathway Analysis: Current Approaches and Outstanding Challenges}},
volume = 8,
year = 2012
}

% metaboanalyst

@article{metaboanalyst,
title={{MetaboAnalyst 3.0 -- making metabolomics more meaningful}},
author={Xia, Jianguo and Sinelnikov, Igor V and Han, Beomsoo and Wishart, David S},
journal={Nucleic Acids Research},
volume={43},
number={Web Server issue},
pages={W251--W257},
year={2015},
publisher={Oxford Univ Press}
}

% impala

@article{impala,
  title={Integrated pathway-level analysis of transcriptomics and metabolomics data with IMPaLA},
  author={Kamburov, Atanas and Cavill, Rachel and Ebbels, Timothy MD and Herwig, Ralf and Keun, Hector C},
  journal={Bioinformatics},
  volume={27},
  number={20},
  pages={2917--2918},
  year={2011},
  publisher={Oxford University Press}
}

% metabolomics article

@article{metabopicart,
author = {Picart-Armada, Sergio and Fern{\'a}ndez-Albert, Francesc and Vinaixa, Maria and Rodr{\'i}guez, Miguel Angel and Aivio, Suvi and Stracker, Travis H. and Yanes, Oscar and Perera-Lluna, Alexandre},
title = {{Null diffusion-based enrichment for metabolomics data}},
journal={PLOS ONE},
volume={12},
number={12},
pages={e0189012},
year={2017},
publisher={Public Library of Science}
}

% metabolomics review

@article{metaboreview,
  title={Chemometrics in metabolomics -- a review in human disease diagnosis},
  author={Madsen, Rasmus and Lundstedt, Torbj{\"o}rn and Trygg, Johan},
  journal={Analytica chimica acta},
  volume={659},
  number={1},
  pages={23--33},
  year={2010},
  publisher={Elsevier}
}

% MAIT

@article{mait,
  title={{An R package to analyse LC/MS metabolomic data: MAIT (Metabolite Automatic Identification Toolkit)}},
  author={Fern{\'a}ndez-Albert, Francesc and Llorach, Rafael and Andr{\'e}s-Lacueva, Cristina and Perera, Alexandre},
  journal={Bioinformatics},
  volume={30},
  number={13},
  pages={1937--1939},
  year={2014},
  publisher={Oxford Univ Press}
}

% meltdb

@article{meltdb,
  title={MeltDB 2.0--advances of the metabolomics software system},
  author={Kessler, Nikolas and Neuweger, Heiko and Bonte, Anja and Langenk{\"a}mper, Georg and Niehaus, Karsten and Nattkemper, Tim W and Goesmann, Alexander},
  journal={Bioinformatics},
  volume={29},
  number={19},
  pages={2452--2459},
  year={2013},
  publisher={Oxford Univ Press}
}

% gosemsim

@article{gosemsim,
  title={GOSemSim: an R package for measuring semantic similarity among GO terms and gene products},
  author={Yu, Guangchuang and Li, Fei and Qin, Yide and Bo, Xiaochen and Wu, Yibo and Wang, Shengqi},
  journal={Bioinformatics},
  volume={26},
  number={7},
  pages={976--978},
  year={2010},
  publisher={Oxford University Press}
}

% clusterprofiler

@article{clusterprofiler,
  title={clusterProfiler: an R package for comparing biological themes among gene clusters},
  author={Yu, Guangchuang and Wang, Li-Gen and Han, Yanyan and He, Qing-Yu},
  journal={Omics: a journal of integrative biology},
  volume={16},
  number={5},
  pages={284--287},
  year={2012},
  publisher={Mary Ann Liebert, Inc. 140 Huguenot Street, 3rd Floor New Rochelle, NY 10801 USA}
}

% msea

@article{msea,
  title={MSEA: a web-based tool to identify biologically meaningful patterns in quantitative metabolomic data},
  author={Xia, Jianguo and Wishart, David S},
  journal={Nucleic acids research},
  volume={38},
  number={suppl\_2},
  pages={W71--W77},
  year={2010},
  publisher={Oxford University Press}
}

% wikipathways

@article{wikipathways,
  title={WikiPathways: capturing the full diversity of pathway knowledge},
  author={Kutmon, Martina and Riutta, Anders and Nunes, Nuno and Hanspers, Kristina and Willighagen, Egon L and Bohler, Anwesha and M{\'e}lius, Jonathan and Waagmeester, Andra and Sinha, Sravanthi R and Miller, Ryan and others},
  journal={Nucleic acids research},
  volume={44},
  number={D1},
  pages={D488--D494},
  year={2015},
  publisher={Oxford University Press}
}

% hmdb

@article{hmdb,
  title={HMDB 3.0 -- the human metabolome database in 2013},
  author={Wishart, David S and Jewison, Timothy and Guo, An Chi and Wilson, Michael and Knox, Craig and Liu, Yifeng and Djoumbou, Yannick and Mandal, Rupasri and Aziat, Farid and Dong, Edison and others},
  journal={Nucleic acids research},
  volume={41},
  number={D1},
  pages={D801--D807},
  year={2012},
  publisher={Oxford University Press}
}

% egsea

@article{egsea,
  title={Combining multiple tools outperforms individual methods in gene set enrichment analyses},
  author={Alhamdoosh, Monther and Ng, Milica and Wilson, Nicholas J and Sheridan, Julie M and Huynh, Huy and Wilson, Michael J and Ritchie, Matthew E},
  journal={Bioinformatics},
  volume={33},
  number={3},
  pages={414--424},
  year={2017},
  publisher={Oxford University Press}
}

% papi

@article{papi,
  title={Pathway Activity Profiling (PAPi): from the metabolite profile to the metabolic pathway activity},
  author={Aggio, Raphael BM and Ruggiero, Katya and Villas-B{\^o}as, Silas Granato},
  journal={Bioinformatics},
  volume={26},
  number={23},
  pages={2969--2976},
  year={2010},
  publisher={Oxford University Press}
}

% subpathwayminer

@article{subpathwayminer,
  title={SubpathwayMiner: a software package for flexible identification of pathways},
  author={Li, Chunquan and Li, Xia and Miao, Yingbo and Wang, Qianghu and Jiang, Wei and Xu, Chun and Li, Jing and Han, Junwei and Zhang, Fan and Gong, Binsheng and others},
  journal={Nucleic acids research},
  volume={37},
  number={19},
  pages={e131--e131},
  year={2009},
  publisher={Oxford University Press}
}

% metscape

@article{metscape,
  title={Metscape 2 bioinformatics tool for the analysis and visualization of metabolomics and gene expression data},
  author={Karnovsky, Alla and Weymouth, Terry and Hull, Tim and Tarcea, V Glenn and Scardoni, Giovanni and Laudanna, Carlo and Sartor, Maureen A and Stringer, Kathleen A and Jagadish, HV and Burant, Charles and others},
  journal={Bioinformatics},
  volume={28},
  number={3},
  pages={373--380},
  year={2011},
  publisher={Oxford University Press}
}

% cytoscape

@article{cytoscape,
  title={Cytoscape 2.8: new features for data integration and network visualization},
  author={Smoot, Michael E and Ono, Keiichiro and Ruscheinski, Johannes and Wang, Peng-Liang and Ideker, Trey},
  journal={Bioinformatics},
  volume={27},
  number={3},
  pages={431--432},
  year={2010},
  publisher={Oxford University Press}
}

% mpinet

@article{mpinet,
  title={MPINet: Metabolite pathway identification via coupling of global metabolite network structure and metabolomic profile},
  author={Li, Feng and Xu, Yanjun and Shang, Desi and Yang, Haixiu and Liu, Wei and Han, Junwei and Sun, Zeguo and Yao, Qianlan and Zhang, Chunlong and Ma, Jiquan and others},
  journal={BioMed research international},
  volume={2014},
  year={2014},
  publisher={Hindawi Publishing Corporation}
}

% metamapr

@article{metamapr,
  title={MetaMapR: pathway independent metabolomic network analysis incorporating unknowns},
  author={Grapov, Dmitry and Wanichthanarak, Kwanjeera and Fiehn, Oliver},
  journal={Bioinformatics},
  volume={31},
  number={16},
  pages={2757--2760},
  year={2015},
  publisher={Oxford University Press}
}

% metabosignal

@article{metabosignal,
  title={MetaboSignal: a network-based approach for topological analysis of metabotype regulation via metabolic and signaling pathways},
  author={Rodriguez-Martinez, Andrea and Ayala, Rafael and Posma, Joram M and Neves, Ana L and Gauguier, Dominique and Nicholson, Jeremy K and Dumas, Marc-Emmanuel},
  journal={Bioinformatics},
  volume={33},
  number={5},
  pages={773--775},
  year={2017},
  publisher={Oxford University Press}
}

% review secondary analysis

@article{reviewsecondary,
  title={Tools for the functional interpretation of metabolomic experiments},
  author={Chagoyen, Monica and Pazos, Florencio},
  journal={Briefings in bioinformatics},
  volume={14},
  number={6},
  pages={737--744},
  year={2012},
  publisher={Oxford University Press}
}

% ovarian cancer cells 150

@article{ovarian,
  title={Distinct metabolic responses of an ovarian cancer stem cell line},
  author={Vermeersch, Kathleen A and Wang, Lijuan and McDonald, John F and Styczynski, Mark P},
  journal={BMC systems biology},
  volume={8},
  number={1},
  pages={134},
  year={2014},
  publisher={BioMed Central}
}

% epithelial cell data 214

@article{epithelial,
  title={{Global metabonomic and proteomic analysis of human conjunctival epithelial cells (IOBA-NHC) in response to hyperosmotic stress}},
  author={Chen, Liyan and Li, Jing and Guo, Tiannan and Ghosh, Sujoy and Koh, Siew Kwan and Tian, Dechao and Zhang, Liang and Jia, Deyong and Beuerman, Roger W and Aebersold, Ruedi and others},
  journal={Journal of proteome research},
  volume={14},
  number={9},
  pages={3982--3995},
  year={2015},
  publisher={ACS Publications}
}

% malaria 315

@article{malaria,
  title={Towards Improving Point-of-Care Diagnosis of Non-malaria Febrile Illness: A Metabolomics Approach},
  author={Decuypere, Saskia and Maltha, Jessica and Deborggraeve, Stijn and Rattray, Nicholas JW and Issa, Guiraud and B{\'e}renger, Kabor{\'e} and Lompo, Palpouguini and Tahita, Marc C and Ruspasinghe, Thusitha and McConville, Malcolm and others},
  journal={PLoS neglected tropical diseases},
  volume={10},
  number={3},
  pages={e0004480},
  year={2016},
  publisher={Public Library of Science}
}

% technologies

@article{metabolomicstechnologiescomplete,
  author = {Weckwerth, Wolfram},
  title = {{Annual Review of Plant Biology}},
  volume = {54},
  number = {1},
  pages = {669--689},
  year = {2003}
}

% shiny

@Manual{shiny,
title = {shiny: Web Application Framework for R},
author = {Winston Chang and Joe Cheng and JJ Allaire and Yihui Xie and Jonathan McPherson},
year = {2017},
note = {R package version 1.0.5},
url = {https://CRAN.R-project.org/package=shiny},
}

% metabolights

@article{metabolights,
  title={{MetaboLights -- an open-access general-purpose repository for metabolomics studies and associated meta-data}},
  author={Haug, Kenneth and Salek, Reza M and Conesa, Pablo and Hastings, Janna and de Matos, Paula and Rijnbeek, Mark and Mahendraker, Tejasvi and Williams, Mark and Neumann, Steffen and Rocca-Serra, Philippe and others},
  journal={Nucleic Acids Res.},
  volume={41},
  number={D1},
  pages={D781--D786},
  year={2012},
  publisher={Oxford University Press}
}

@article{hotnet,
  title={{Algorithms for detecting significantly mutated pathways in cancer}},
  author={Vandin, Fabio and Upfal, Eli and Raphael, Benjamin J},
  journal={J. Comput. Biol.},
  volume={18},
  number={3},
  pages={507--522},
  year={2011},
  publisher={Mary Ann Liebert, Inc. 140 Huguenot Street, 3rd Floor New Rochelle, NY 10801 USA}
}

@article{tiedie,
  title={{Discovering causal pathways linking genomic events to transcriptional states using Tied Diffusion Through Interacting Events (TieDIE)}},
  author={Paull, Evan O and Carlin, Daniel E and Niepel, Mario and Sorger, Peter K and Haussler, David and Stuart, Joshua M},
  journal={Bioinformatics},
  volume={29},
  number={21},
  pages={2757--2764},
  year={2013},
  publisher={Oxford Univ Press}
}

@article{gwadata,
  title={Prioritizing candidate disease genes by network-based boosting of genome-wide association data},
  author={Lee, Insuk and Blom, U Martin and Wang, Peggy I and Shim, Jung Eun and Marcotte, Edward M},
  journal={Genome research},
  volume={21},
  number={7},
  pages={1109--1121},
  year={2011},
  publisher={Cold Spring Harbor Lab}
}

% genemania

@article{genemania,
  title={GeneMANIA: a real-time multiple association network integration algorithm for predicting gene function},
  author={Mostafavi, Sara and Ray, Debajyoti and Warde-Farley, David and Grouios, Chris and Morris, Quaid},
  journal={Genome biology},
  volume={9},
  number={1},
  pages={S4},
  year={2008},
  publisher={BioMed Central}
}

@techreport{pagerank,
  title={The PageRank citation ranking: Bringing order to the web.},
  author={Page, Lawrence and Brin, Sergey and Motwani, Rajeev and Winograd, Terry},
  year={1999},
  institution={Stanford InfoLab}
}

%%%%%%%%%%%%%%%%%%%%%%%%%% POSTER REFERENCES

@article{malaria_cortisol_bouyou,
abstract = {We measured cortisol and prolactin concentrations in the peripheral venous blood of 23 non-pregnant and 59 pregnant Gabonese women from the second trimester of pregnancy until delivery. Cortisol concentrations were significantly higher in primigravidae women than in multigravidae women between 20 and 25:weeks' gestational age (166 vs. 132:ng/ml, respectively), between 28 and 37:weeks (226 vs. 161:ng/ml) and at delivery (287 vs. 188:ng/ml). Conversely, plasma prolactin levels were highest in multigravidae women. Cortisol and prolactin concentrations both increased with the period of pregnancy (P = 0.01 and P {\textless} 0.01, respectively), suggesting that a sustained increase in cortisol level underlies the increased susceptibility of pregnant women, particularly primigravidae women, to malaria. In support of this hypothesis, we found a significant association between cortisol concentration and Plasmodium falciparum infection, on the one hand, and strong correlations with parasite load in P. falciparum-infected primigravidae women, on the other hand (rho between 0.35 and 0.45 with P {\textless} 0.01). {\textcopyright} 2005 Elsevier SAS. All rights reserved.},
author = {Bouyou-Akotet, Marielle K. and Adegnika, Ayola A. and Agnandji, Selidji T. and Ngou-Milama, Edouard and Kombila, Maryvonne and Kremsner, Peter G. and Mavoungou, Elie},
doi = {10.1016/j.micinf.2005.04.008},
file = {:home/sergi/all/devel/articles/mendeley/2005/Cortisol and susceptibility to malaria during pregnancy.pdf:pdf},
isbn = {1286-4579 (Print)$\backslash$r1286-4579 (Linking)},
issn = {12864579},
journal = {Microbes and Infection},
keywords = {Cortisol,MTBLS315,Malaria,Pregnancy,Prolactin,cortisol},
mendeley-tags = {MTBLS315,cortisol},
number = {11-12},
pages = {1217--1223},
pmid = {16002311},
title = {{Cortisol and susceptibility to malaria during pregnancy}},
volume = {7},
year = {2005}
}
@article{malaria_phenylalanine_campbell,
abstract = {Background. Multiple international treatment guidelines recommend amphotericin-based combination regimens for induction therapy of cryptococcal meningitis. Yet, only 1 trial has reported a mortality benefit for combination amphotericin-flucytosine, and none have reported a mortality benefit for combination amphotericin- fluconazole. Methods. We conducted a Bayesian network meta-analysis to estimate the comparative effectiveness of recommended induction therapies for HIV-associated cryptococcal meningitis. We searched PubMed and Cochrane CENTRAL for clinical reports of induction therapy for HIV-associated cryptococcal meningitis. We extracted or calculated early (two-week) and late (six to 12-week) mortality by treatment arm for the following induction regimens: amphotericin B alone, amphotericin B + flucytosine, amphotericin B + triazoles, amphotericin B + flucytosine + triazoles, triazoles alone, triazoles + flucytosine, liposomal amphotericin B, and amphotericin B + other medicines. Results. In the overall sample (35 studies, n = 2483), we found no evidence of decreased mortality from addition of flucytosine or triazoles to amphotericin B, compared with amphotericin B alone. Although we did find a nonsignificant benefit for addition of flucytosine to amphotericin B in studies including participants with altered levels of consciousness, we did not identify a benefit for combination therapy in restricted analyses in either resource- rich or resource-limited settings, studies conducted before or after 2004, and studies restricted to a high dose of amphotericin B and fluconazole. Conclusions. Given considerations of drug availability and toxicity, there is an important need for additional data to clarify which populations are most likely to benefit from combination therapies for human immunodeficiency virusassociated cryptococcal meningitis.},
author = {Campbell, Jeffrey I. and Kanters, Steve and Bennett, John E. and Thorlund, Kristian and Tsai, Alexander C. and Mills, Edward J. and Siedner, Mark J.},
doi = {10.1093/o},
file = {:home/sergi/all/devel/articles/mendeley/2015/Comparative Effectiveness of Induction Therapy for Human Immunodeficiency Virus-Associated Cryptococcal Meningitis A Network Meta-Analys.pdf:pdf},
isbn = {2328-8957},
issn = {2328-8957},
journal = {Ofid},
keywords = {MTBLS315,art-associated tb,genexpert mtb,hiv,phenylalanine,rif,screening,tuberculosis},
mendeley-tags = {MTBLS315,phenylalanine},
pages = {1--8},
pmid = {25884008},
title = {{Comparative Effectiveness of Induction Therapy for Human Immunodeficiency Virus-Associated Cryptococcal Meningitis: A Network Meta-Analysis}},
year = {2015}
}

@article{epithelial_main,
abstract = {"Dry eye" is a multifactorial inflammatory disease affecting the ocular surface. Tear hyperosmolarity in dry eye contributes to inflammation and cell damage. Recent research efforts on dry eye have been directed toward biomarker discovery for diagnosis, response to treatment, and disease mechanisms. This study employed a spontaneously immortalized normal human conjunctival cell line, IOBA-NHC, as a model to investigate hyperosmotic stress-induced changes of metabolites and proteins. Global and targeted metabonomic analyses as well as proteomic analysis were performed on IOBA-NHC cells incubated in serum-free media at 280 (control), 380, and 480 mOsm for 24 h. Twenty-one metabolites and seventy-six iTRAQ-identified proteins showed significant changes under at least one hyperosmotic stress treatment as compared with controls. SWATH-based proteomic analysis further confirmed the involvement of inflammatory pathways such as prostaglandin 2 synthesis in IOBA-NHC cells under hyperosmotic stress. This study is the first to identify glycerophosphocholine synthesis and O-linked beta-N-acetylglucosamine glycosylation as key activated pathways in ocular surface cells under hyperosmotic stress. These findings extend the current knowledge in metabolite markers of dry eye and provide potential therapeutic targets for its treatment.},
author = {Chen, Liyan and Li, Jing and Guo, Tiannan and Ghosh, Sujoy and Koh, Siew Kwan and Tian, Dechao and Zhang, Liang and Jia, Deyong and Beuerman, Roger W. and Aebersold, Ruedi and Chan, Eric Chun Yong and Zhou, Lei},
doi = {10.1021/acs.jproteome.5b00443},
file = {:home/sergi/all/devel/articles/mendeley/2015/Global metabonomic and proteomic analysis of human conjunctival epithelial cells (IOBA-NHC) in response to hyperosmotic stress.pdf:pdf},
issn = {15353907},
journal = {Journal of Proteome Research},
keywords = {MTBLS214,SWATH,dry eye,hyperosmolarity,iTRAQ,main{\_}paper,metabolomics,metabonomics,osmoprotectants,osmostic stress,proteomics},
mendeley-tags = {MTBLS214,main{\_}paper},
number = {9},
pages = {3982--3995},
pmid = {26260330},
title = {{Global metabonomic and proteomic analysis of human conjunctival epithelial cells (IOBA-NHC) in response to hyperosmotic stress}},
volume = {14},
year = {2015}
}
@article{malaria_main,
abstract = {INTRODUCTION: Non-malaria febrile illnesses such as bacterial bloodstream infections (BSI) are a leading cause of disease and mortality in the tropics. However, there are no reliable, simple diagnostic tests for identifying BSI or other severe non-malaria febrile illnesses. We hypothesized that different infectious agents responsible for severe febrile illness would impact on the host metabololome in different ways, and investigated the potential of plasma metabolites for diagnosis of non-malaria febrile illness.$\backslash$n$\backslash$nMETHODOLOGY: We conducted a comprehensive mass-spectrometry based metabolomics analysis of the plasma of 61 children with severe febrile illness from a malaria-endemic rural African setting. Metabolite features characteristic for non-malaria febrile illness, BSI, severe anemia and poor clinical outcome were identified by receiver operating curve analysis.$\backslash$n$\backslash$nPRINCIPAL FINDINGS: The plasma metabolome profile of malaria and non-malaria patients revealed fundamental differences in host response, including a differential activation of the hypothalamic-pituitary-adrenal axis. A simple corticosteroid signature was a good classifier of severe malaria and non-malaria febrile patients (AUC 0.82, 95{\%} CI: 0.70-0.93). Patients with BSI were characterized by upregulated plasma bile metabolites; a signature of two bile metabolites was estimated to have a sensitivity of 98.1{\%} (95{\%} CI: 80.2-100) and a specificity of 82.9{\%} (95{\%} CI: 54.7-99.9) to detect BSI in children younger than 5 years. This BSI signature demonstrates that host metabolites can have a superior diagnostic sensitivity compared to pathogen-detecting tests to identify infections characterized by low pathogen load such as BSI.$\backslash$n$\backslash$nCONCLUSIONS: This study demonstrates the potential use of plasma metabolites to identify causality in children with severe febrile illness in malaria-endemic settings.},
author = {Decuypere, Saskia and Maltha, Jessica and Deborggraeve, Stijn and Rattray, Nicholas J W and Issa, Guiraud and B??renger, Kabor?? and Lompo, Palpouguini and Tahita, Marc C. and Ruspasinghe, Thusitha and McConville, Malcolm and Goodacre, Royston and Tinto, Halidou and Jacobs, Jan and Carapetis, Jonathan R.},
doi = {10.1371/journal.pntd.0004480},
file = {:home/sergi/all/devel/articles/mendeley/2016/Towards Improving Point-of-Care Diagnosis of Non-malaria Febrile Illness A Metabolomics Approach.pdf:pdf},
isbn = {1935-2735 (Electronic) 1935-2727 (Linking)},
issn = {19352735},
journal = {PLoS Neglected Tropical Diseases},
keywords = {MTBLS315,main{\_}paper},
mendeley-tags = {MTBLS315,main{\_}paper},
number = {3},
pmid = {26943791},
title = {{Towards Improving Point-of-Care Diagnosis of Non-malaria Febrile Illness: A Metabolomics Approach}},
volume = {10},
year = {2016}
}
@article{malaria_linoleate_fitch,
abstract = {Mice infected with the NYU-2 strain of Plasmodium berghei were used to study the effect of chloroquine on masking of a lipid that promotes ferriprotoporphyrin IX dimerization. More than 40{\%} of this lipid was masked and unable to promote dimerization in membrane ghosts from erythrocytes of untreated, infected mice. Thus, preparations of membrane ghosts dimerized 57 +/- 6 nmol of ferriprotoporphyrin IX during a 2-h incubation, whereas the lipids extracted from these preparations dimerized 101 +/- 11 nmol of ferriprotoporphyrin IX (means +/- S.D. for four experiments). Exposure of membrane ghosts to sonication or cold significantly increased the extent of masking. In addition, chloroquine treatment of infected mice increased the extent of masking to approximately 90{\%}. The lipid could be unmasked by extracting it into acetone or by aging erythrocyte membrane ghosts from untreated or chloroquine-treated, infected mice for 24 h at pH 7.4 and 25 degrees C. These findings indicate that masking and unmasking of a lipid is central to the regulation of ferriprotoporphyrin IX dimerization in malaria parasites. They also indicate that chloroquine impairs the function of this regulatory process.},
author = {Fitch, Coy D. and feng Chen, Yi and zuan Cai, Guang},
doi = {10.1074/jbc.M301407200},
file = {:home/sergi/all/devel/articles/mendeley/2003/Chloroquine-induced masking of a lipid that promotes ferriprotoporphyrin IX dimerization in malaria.pdf:pdf},
isbn = {0021-9258 (Print)$\backslash$r0021-9258 (Linking)},
issn = {00219258},
journal = {Journal of Biological Chemistry},
keywords = {MTBLS315,linoleate},
mendeley-tags = {MTBLS315,linoleate},
number = {25},
pages = {22596--22599},
pmid = {12697766},
title = {{Chloroquine-induced masking of a lipid that promotes ferriprotoporphyrin IX dimerization in malaria}},
volume = {278},
year = {2003}
}
@article{malaria_phenylalanine_fuchs,
abstract = {The blood meal of the female malaria mosquito is a pre-requisite to egg production and also represents the transmission route for the malaria parasite. The proper and rapid assimilation of proteins and nutrients in the blood meal creates a significant metabolic challenge for the mosquito. To better understand this process we generated a global profile of metabolite changes in response to blood meal of Anopheles gambiae, using Gas Chromatography-Mass Spectrometry (GC-MS). To disrupt a key pathway of amino acid metabolism we silenced the gene phenylalanine hydroxylase (PAH) involved in the conversion of the amino acid phenylalanine into tyrosine. We observed increased levels of phenylalanine and the potentially toxic metabolites phenylpyruvate and phenyllactate as well as a reduction in the amount of tyrosine available for melanin synthesis. This in turn resulted in a significant impairment of the melanotic encapsulation response against the rodent malaria parasite Plasmodium berghei. Furthermore silencing of PAH resulted in a significant impairment of mosquito fertility associated with reduction of laid eggs, retarded vitellogenesis and impaired melanisation of the chorion. Carbidopa, an inhibitor of the downstream enzyme DOPA decarboxylase that coverts DOPA into dopamine, produced similar effects on egg melanization and hatching rate suggesting that egg chorion maturation is mainly regulated via dopamine. This study sheds new light on the role of amino acid metabolism in regulating reproduction and immunity.},
author = {Fuchs, Silke and Behrends, Volker and Bundy, Jacob G. and Crisanti, Andrea and Nolan, Tony},
doi = {10.1371/journal.pone.0084865},
file = {:home/sergi/all/devel/articles/mendeley/2014/Phenylalanine metabolism regulates reproduction and parasite melanization in the malaria mosquito.pdf:pdf},
isbn = {1932-6203 (Electronic)$\backslash$r1932-6203 (Linking)},
issn = {19326203},
journal = {PLoS ONE},
keywords = {MTBLS315,phenylalanine},
mendeley-tags = {MTBLS315,phenylalanine},
number = {1},
pmid = {24409310},
title = {{Phenylalanine metabolism regulates reproduction and parasite melanization in the malaria mosquito}},
volume = {9},
year = {2014}
}
@article{ovarian_succinate_dehydrogenase_he,
abstract = {Compared to other familial pheochromocytoma/paragangliomas (PHEO/PGLs), the succinate dehydrogenase subunit B (SDHB)-related PHEO/PGLs often present with aggressive and rapidly growing metastatic lesions. Currently, there is no proven effective treatment for malignant PHEO/PGLs. Here, we present a 35-year-old white man with primary malignant abdominal extra-adrenal 11 cm paraganglioma underwent surgical successful resection. But 6 months later, he developed extensive bone, liver, and lymph nodes metastasis, which were demonstrated by computed tomography scan and the (18)F-fluorodeoxyglucose positron emission tomography. However, his (123)I-metaiodobenzylguanidine scintigraphy was negative; therefore, the cyclophosphamide, vincristine, and dacarbazine (CVD) combination chemotherapy was initiated. The combination chemotherapy was very effective showing 80{\%} overall reduction in the liver lesions and 75{\%} overall reduction in the retroperitoneal mass and adenopathy, and normalization of plasma catecholamine and metanephrine levels. However, plasma levels of dopamine (DA) and methoxytyramine (MTY) were only partially affected and remained consistently elevated throughout the remaining period of follow-up evaluation. Genetic testing revealed an SDHB gene mutation. Here, we present an SDHB-related PHEO/PGL patient with extensive tumor burden, numerous organ lesions, and rapidly growing tumors, which responded extremely well to CVD therapy. We conclude patients with SDHB-related PHEO/PGLs can be particularly sensitive to CVD chemotherapy and may have an excellent outcome if this therapy is used and continued on periodic basis. The data in this patient also illustrate the importance of measuring plasma levels of DA and MTY to provide a more complete and accurate assessment of the biochemical response to therapy than provided by measurements restricted to other catecholamines and O-methylated metabolites.},
author = {He, J. and Makey, D. and Fojo, T. and Adams, K. T. and Havekes, B. and Eisenhofer, G. and Sullivan, P. and Lai, E. W. and Pacak, K.},
doi = {10.1007/s12020-009-9219-6},
file = {:home/sergi/all/devel/articles/mendeley/2009/Successful chemotherapy of hepatic metastases in a case of succinate dehydrogenase subunit B-related paraganglioma.pdf:pdf},
issn = {1355008X},
journal = {Endocrine},
keywords = {1.3.5.1,Chemotherapy,MTBLS150,Paraganglioma,Succinate dehydrogenase,succinate{\_}dehydrogenase},
mendeley-tags = {1.3.5.1,MTBLS150,succinate{\_}dehydrogenase},
number = {2},
pages = {189--193},
pmid = {19618298},
title = {{Successful chemotherapy of hepatic metastases in a case of succinate dehydrogenase subunit B-related paraganglioma}},
volume = {36},
year = {2009}
}
@article{ovarian_succinate_dehydrogenase_huang,
abstract = {Succinate dehydrogenase (SDH) and fumarate hydratase (FH) are tricarboxylic acid (TCA) cycle enzymes that are also known to act as tumour suppressor genes. Increased succinate or fumarate levels as a consequence of SDH and FH deficiency inhibit hypoxia inducible factor-1alpha (HIF-1alpha) prolyl hydroxylases leading to sustained HIF-1alpha expression in tumours. Since HIF-1alpha is frequently expressed in breast carcinomas, DNA methylation at the promoter regions of the SDHA, SDHB, SDHC and SDHD and FH genes was evaluated as a possible mechanism in silencing of SDH and FH expression in breast carcinomas.},
author = {Huang, Katie T and Dobrovic, Alexander and Fox, Stephen B},
doi = {10.1186/1756-0500-2-194},
file = {:home/sergi/all/devel/articles/mendeley/2009/No evidence for promoter region methylation of the succinate dehydrogenase and fumarate hydratase tumour suppressor genes in breast canc.pdf:pdf},
isbn = {2416830322416},
issn = {1756-0500},
journal = {BMC research notes},
keywords = {1.3.5.1,MTBLS150,succinate{\_}dehydrogenase},
mendeley-tags = {1.3.5.1,MTBLS150,succinate{\_}dehydrogenase},
pages = {194},
pmid = {19778456},
title = {{No evidence for promoter region methylation of the succinate dehydrogenase and fumarate hydratase tumour suppressor genes in breast cancer.}},
volume = {2},
year = {2009}
}
@article{ovarian_hexokinase_kaelin,
abstract = {Interest in the abnormal metabolism exhibited by cancer cells has been reawakened by the discovery of oncogenic mutations in metabolic enzymes, and by tools that monitor metabolism in living cells. Existing and emerging therapies aim to target this abnormal metabolism in various ways.},
author = {Kaelin, William G and Thompson, Craig B},
doi = {10.1038/465562a},
file = {:home/sergi/all/devel/articles/mendeley/2010/Q{\&}A Cancer clues from cell metabolism.pdf:pdf},
isbn = {1476-4687 (Electronic)$\backslash$n0028-0836 (Linking)},
issn = {0028-0836},
journal = {Nature},
keywords = {2.7.1.1,MTBLS150,hexokinase},
mendeley-tags = {2.7.1.1,MTBLS150,hexokinase},
number = {7298},
pages = {562--564},
pmid = {20520704},
title = {{Q{\&}A: Cancer: clues from cell metabolism.}},
volume = {465},
year = {2010}
}
@article{ovarian_3_5_1_26_kelo,
abstract = {{\&}{\#}10;Depletion of L-asparagine supply and apoptosis of leukemia cells induced by human glycosylasparaginase{\&}{\#}10;{\&}{\#}10;Leukemia advance online publication, January 22, 2009. doi:10.1038/leu.2008.387{\&}{\#}10;{\&}{\#}10;Authors: E Kelo, T Noronkoski{\&}{\#}10;{\&} I Mononen},
author = {Kelo, E and Noronkoski, T and Mononen, I},
doi = {10.1038/leu.2008.387},
file = {:home/sergi/all/devel/articles/mendeley/2009/Depletion of L-asparagine supply and apoptosis of leukemia cells induced by human glycosylasparaginase.pdf:pdf},
isbn = {0887-6924},
issn = {0887-6924},
journal = {Leukemia},
keywords = {3.5.1.26,MTBLS150},
mendeley-tags = {3.5.1.26,MTBLS150},
number = {6},
pages = {1167--1171},
pmid = {19158835},
title = {{Depletion of L-asparagine supply and apoptosis of leukemia cells induced by human glycosylasparaginase}},
volume = {23},
year = {2009}
}
@article{ovarian_lysosome_kirkegaard,
abstract = {Lysosomes, with their arsenal of degradative enzymes are increasingly becoming an area of interest in the field of oncology. The changes induced in this compartment upon transformation are numerous and whereas most are viewed as pro-oncogenic the same processes also render cancer cells susceptible to lysosomal death pathways. This review will provide an overview of the pro- and anti-oncogenic potential of this compartment and how these might be exploited for cancer therapy, with special focus on lysosomal death pathways. {\textcopyright} 2008 Elsevier B.V. All rights reserved.},
author = {Kirkegaard, Thomas and J{\"{a}}{\"{a}}ttel{\"{a}}, Marja},
doi = {10.1016/j.bbamcr.2008.09.008},
file = {:home/sergi/all/devel/articles/mendeley/2009/Lysosomal involvement in cell death and cancer.pdf:pdf},
isbn = {0006-3002 (Print)$\backslash$r0006-3002 (Linking)},
issn = {01674889},
journal = {Biochimica et Biophysica Acta - Molecular Cell Research},
keywords = {Apoptosis,Cancer,Cathepsins,Cell death,Lysosomes,MTBLS150,Transformation,lysosome},
mendeley-tags = {MTBLS150,lysosome},
number = {4},
pages = {746--754},
pmid = {18948147},
publisher = {Elsevier B.V.},
title = {{Lysosomal involvement in cell death and cancer}},
volume = {1793},
year = {2009}
}
@article{ovarian_4_2_1_2_lehtonen,
abstract = {Hereditary leiomyomatosis and renal cell cancer (HLRCC) is a tumor predisposition syndrome caused by mutations in the fumarate hydratase (FH) gene. HLRCC is characterized by uterine and cutaneous leiomyomas, renal cell cancer, and uterine leiomyosarcoma. Typically, renal cell cancers in HLRCC are unilateral and display a papillary type 2 or ductal histology. We describe here a 23-year-old patient carrying a novel FH mutation (N330S) with a bilateral renal cell center. Carcinoma of the right kidney showed papillary structure, but the left tumor was diagnosed as a conventional (clear cell) renal carcinoma, a type not previously described in HLRCC. The clear cell renal carcinoma also displayed loss of the normal FH allele and the FH immunostaining. Our finding extends the number of cases in which HLRCC can be suspected, and the FH immunohistochemistry may serve as a useful tool to screen for HLRCC in young individuals with clear cell renal carcinoma. ?? 2007 Elsevier Inc. All rights reserved.},
author = {Lehtonen, Heli J. and Blanco, Ignacio and Piulats, Jose M. and Herva, Riitta and Launonen, Virpi and Aaltonen, Lauri A.},
doi = {10.1016/j.humpath.2006.10.011},
file = {:home/sergi/all/devel/articles/mendeley/2007/Conventional renal cancer in a patient with fumarate hydratase mutation.pdf:pdf},
isbn = {0046-8177 (Print)$\backslash$r0046-8177 (Linking)},
issn = {00468177},
journal = {Human Pathology},
keywords = {4.2.1.2,Bilateral renal cell cancer,Clear cell,FH,HLRCC,MTBLS150,fumarate hydratase},
mendeley-tags = {4.2.1.2,MTBLS150},
number = {5},
pages = {793--796},
pmid = {17270241},
title = {{Conventional renal cancer in a patient with fumarate hydratase mutation}},
volume = {38},
year = {2007}
}
@article{malaria_phenylalanine_lopansri,
abstract = {Cerebral malaria is associated with decreased production of nitric oxide and decreased levels of its precursor, l-arginine. Abnormal amino acid metabolism may thus be an important factor in malaria pathogenesis. We sought to determine if other amino acid abnormalities are associated with disease severity in falciparum malaria. Subjects were enrolled in Dar es Salaam, Tanzania (children) (n = 126), and Papua, Indonesia (adults) (n = 156), in two separate studies. Plasma samples were collected from subjects with WHO-defined cerebral malaria (children), all forms of severe malaria (adults), and uncomplicated malaria (children and adults). Healthy children and adults without fever or illness served as controls. Plasma amino acids were measured using reverse-phase high-performance liquid chromatography with fluorescence detection. Several plasma amino acids were significantly lower in the clinical malaria groups than in healthy controls. Despite the differences, phenylalanine was the only amino acid with mean levels outside the normal range (40 to 84 microM) and was markedly elevated in children with cerebral malaria (median [95{\%} confidence interval], 163 [134 to 193] microM; P {\textless} 0.0001) and adults with all forms of severe malaria (median [95{\%} confidence interval], 129 [111 to 155] microM; P {\textless} 0.0001). In adults who survived severe malaria, phenylalanine levels returned to normal, with clinical improvement (P = 0.0002). Maintenance of plasma phenylalanine homeostasis is disrupted in severe malaria, leading to significant hyperphenylalaninemia. This is likely a result of an acquired abnormality in the function of the liver enzyme phenylalanine hydroxylase. Determination of the mechanism of this abnormality may contribute to the understanding of neurological complications in malaria.},
author = {Lopansri, Bert K. and Anstey, Nicholas M. and Stoddard, Gregory J. and Mwaikambo, Esther D. and Boutlis, Craig S. and Tjitra, Emiliana and Maniboey, Helena and Hobbs, Maurine R. and Levesque, Marc C. and Weinberg, J. Brice and Granger, Donald L.},
doi = {10.1128/IAI.02106-05},
file = {:home/sergi/all/devel/articles/mendeley/2006/Elevated plasma phenylalanine in severe malaria and implications for pathophysiology of neurological complications.pdf:pdf},
isbn = {0019-9567 (Print)$\backslash$r0019-9567 (Linking)},
issn = {00199567},
journal = {Infection and Immunity},
keywords = {MTBLS315,phenylalanine},
mendeley-tags = {MTBLS315,phenylalanine},
number = {6},
pages = {3355--3359},
pmid = {16714564},
title = {{Elevated plasma phenylalanine in severe malaria and implications for pathophysiology of neurological complications}},
volume = {74},
year = {2006}
}
@article{malaria_sphingolipid_meyer,
abstract = {Plasmodium-infected erythrocytes have been shown to employ sphingolipids from both endogenous metabolism as well as existing host pools. Therapeutic agents that limit these supplies have thus emerged as intriguing, mechanistically distinct putative targets for the treatment of malaria infections. In an initial screen of our library of sphingolipid pathway modulators for efficacy against two strains of the predominant human malaria species Plasmodium falciparum and Plasmodium knowlesi, a series of orally available, 1-deoxysphingoid bases were found to possess promising in vitro antimalarial activity. To better understand the structural requirements that are necessary for this observed activity, a second series of modified analogues were prepared and evaluated. Initial pharmacokinetic assessments of key analogues were investigated to evaluate plasma and red blood cell concentrations in vivo.},
author = {Meyer, Esmeralda V S and Holt, Jason J. and Girard, Kathryn R. and Ballie, Mark T. and Bushnev, Anatoliy S. and Lapp, Stacey and Menaldino, David S. and Arrendale, Richard F. and Reddy, G. Prabhakar and Evers, Taylor J. and Howard, Randy B. and Culver, Deborah G. and Liotta, Dennis C. and Galinski, Mary R. and Natchus, Michael G.},
doi = {10.1021/ml2002136},
file = {:home/sergi/all/devel/articles/mendeley/2012/Sphingolipid analogues inhibit development of malaria parasites.pdf:pdf},
isbn = {1948-5875},
issn = {19485875},
journal = {ACS Medicinal Chemistry Letters},
keywords = {Enigmols,MTBLS315,Plasmodium,antimalarials,drugs,malaria,sphingolipid,sphingolipids},
mendeley-tags = {MTBLS315,sphingolipid},
number = {1},
pages = {43--47},
pmid = {24900369},
title = {{Sphingolipid analogues inhibit development of malaria parasites}},
volume = {3},
year = {2012}
}
@article{ovarian_kinase_muzi,
abstract = {Quantitative imaging of glucose metabolism of human brain tumors with PET utilizes 2-[18F]-fluorodeoxy-D-glucose (FDG) and a conversion factor called the lumped constant (LC), which relates the metabolic rate of FDG to glucose. Since tumors have greater uptake of FDG than would be predicted by the metabolism of native glucose, the characteristic of tumors that governs the uptake of FDG must be part of the LC. The LC is chiefly determined by the phosphorylation ratio (PR), which is comprised of the kinetic parameters (Km and Vmax) of hexokinase (HK) for glucose as well as for FDG (LC ??? (Kmglc ?? VmaxFDG)/(KmFDG ?? Vmaxglc). The value of the LC has been estimated from imaging studies, but not validated in vitro from HK kinetic parameters. In this study we measured the kinetic constants of bovine and 36B-10 rat glioma HK I (predominant in normal brain) and 36B-10 glioma HK II (increased in brain tumors) for the hexose substrates glucose, 2-deoxy-D-glucose (2DG) and FDG. Our principal results show that the KmGlc {\textless} KmFDG ??? Km2DG and that PR2DG {\textless} PRFDG. The FDG LC calculated from our kinetic parameters for normal brain, possessing predominantly HK I, would be higher than the normal brain LC predicted from animal studies using 2DG or human PET studies using FDG or 2DG. These results also suggest that a shift from HK I to HK II, which has been observed to increase in brain tumors, would have little effect on the value of the tumor LC. ?? 2001 Elsevier Science Inc.},
author = {Muzi, M. and Freeman, S. D. and Burrows, R. C. and Wiseman, R. W. and Link, J. M. and Krohn, K. A. and Graham, M. M. and Spence, A. M.},
doi = {10.1016/S0969-8051(00)00201-8},
file = {:home/sergi/all/devel/articles/mendeley/2001/Kinetic characterization of hexokinase isoenzymes from glioma cells Implications for FDG imaging of human brain tumors.pdf:pdf},
isbn = {0969-8051},
issn = {09698051},
journal = {Nuclear Medicine and Biology},
keywords = {2-Deoxyglucose,2.7.1.1,Glioma,Glucose,Hexokinase,Lumped Constant,MTBLS150,Positron emission tomography,[18F]Fluorodeoxyglucose,kinase},
mendeley-tags = {2.7.1.1,MTBLS150,kinase},
number = {2},
pages = {107--116},
pmid = {11295420},
title = {{Kinetic characterization of hexokinase isoenzymes from glioma cells: Implications for FDG imaging of human brain tumors}},
volume = {28},
year = {2001}
}
@article{ovarian_succinate_dehydrogenase_ni,
abstract = {Individuals with PTEN mutations have Cowden syndrome (CS), associated with breast, thyroid, and endometrial neoplasias. Many more patients with features of CS, not meeting diagnostic criteria (termed CS-like), are evaluated by clinicians for CS-related cancer risk. Germline mutations in succinate dehydrogenase subunits SDHB-D cause pheochromocytoma-paraganglioma syndrome. One to five percent of SDHB/SDHD mutation carriers have renal cell or papillary thyroid carcinomas, which are also CS-related features. SDHB-D may be candidate susceptibility genes for some PTEN mutation-negative individuals with CS-like cancers. To address this hypothesis, germline SDHB-D mutation analysis in 375 PTEN mutation-negative CS/CS-like individuals was performed, followed by functional analysis of identified SDH mutations/variants. Of 375 PTEN mutation-negative CS/CS-like individuals, 74 (20{\%}) had increased manganese superoxide dismutase (MnSOD) expression, a manifestation of mitochondrial dysfunction. Among these, 10 (13.5{\%}) had germline mutations/variants in SDHB (n = 3) or SDHD (7), not found in 700 controls (p {\textless} 0.001). Compared to PTEN mutation-positive CS/CS-like individuals, those with SDH mutations/variants were enriched for carcinomas of the female breast (6/9 SDH versus 30/107 PTEN, p {\textless} 0.001), thyroid (5/10 versus 15/106, p {\textless} 0.001), and kidney (2/10 versus 4/230, p = 0.026). In the absence of PTEN alteration, CS/CS-like-related SDH mutations/variants show increased phosphorylation of AKT and/or MAPK, downstream manifestations of PTEN dysfunction. Germline SDH mutations/variants occur in a subset of PTEN mutation-negative CS/CS-like individuals and are associated with increased frequencies of breast, thyroid, and renal cancers beyond those conferred by germline PTEN mutations. SDH testing should be considered for germline PTEN mutation-negative CS/CS-like individuals, especially in the setting of breast, thyroid, and/or renal cancers. ?? 2008 The American Society of Human Genetics.},
author = {Ni, Ying and Zbuk, Kevin M. and Sadler, Tammy and Patocs, Attila and Lobo, Glenn and Edelman, Emily and Platzer, Petra and Orloff, Mohammed S. and Waite, Kristin A. and Eng, Charis},
doi = {10.1016/j.ajhg.2008.07.011},
file = {:home/sergi/all/devel/articles/mendeley/2008/Germline Mutations and Variants in the Succinate Dehydrogenase Genes in Cowden and Cowden-like Syndromes.pdf:pdf},
isbn = {1537-6605},
issn = {00029297},
journal = {American Journal of Human Genetics},
keywords = {1.3.5.1,MTBLS150,succinate{\_}dehydrogenase},
mendeley-tags = {1.3.5.1,MTBLS150,succinate{\_}dehydrogenase},
number = {2},
pages = {261--268},
pmid = {18678321},
title = {{Germline Mutations and Variants in the Succinate Dehydrogenase Genes in Cowden and Cowden-like Syndromes}},
volume = {83},
year = {2008}
}
@article{malaria_steroids_pabon,
abstract = {Resistance to antimalarials has been widely reported and constitutes a major problem around the world. In Colombia, resistance of P. falciparum to chloroquine has been reported as 47{\%}-97{\%}, to amodiaquine 3{\%}-7{\%} and to sulfadoxine-pyrimethamine as 9{\%}-13{\%}. The search for new antimalarials is a priority and with this aim we studied the in vitro antimalarial activity of plants used by traditional healers. Incorporation of (3)H-hypoxanthine by the strain FCB-2 of P. falciparum was used to measure the degree of inhibition produced by the steroids SN-1 tumacone A (C(29)H(44)O(5)), SN-2 tumacone B (C(27)H(42)O(4)), SN-3 tumacoside A (C(35)H(54)O(10)), and SN-4 tumacoside B (C(33)H(52)O(9)). All compounds were obtained from the dried stems and leaves of Solanum nudum. The mean growth inhibition of P. falciparum was 71{\%}, 56{\%}, 21{\%} and 12{\%} with each of the compounds SN-1, SN-2, SN-3 and SN-4. These results constitute an important discovery since they may account for the antimalarial properties of extracts of Solanum nudum by a sensitive method. Future work should include study of the in vivo anti-malarial effect of these extracts.},
author = {Pab{\'{o}}n, Adriana and Carmona, Jaime and Maestre, Amanda and Camargo, Mauricio and Blair, Silvia},
doi = {10.1002/ptr.1035},
file = {:home/sergi/all/devel/articles/mendeley/2002/Inhibition of P. falciparum by steroids isolated from Solanum nudum.pdf:pdf},
isbn = {0951-418X (Print)$\backslash$r0951-418X (Linking)},
issn = {0951418X},
journal = {Phytotherapy Research},
keywords = {3H-hypoxanthine,FCB-2,MTBLS315,Plasmodium falciparum,Solanaceae,Steroids,steroids},
mendeley-tags = {MTBLS315,steroids},
number = {1},
pages = {59--62},
pmid = {11807967},
title = {{Inhibition of P. falciparum by steroids isolated from Solanum nudum}},
volume = {16},
year = {2002}
}
@article{ovarian_fumarate_pithukpakorn,
abstract = {BACKGROUND: Hereditary leiomyomatosis and renal cell cancer (HLRCC) is the autosomal dominant heritable syndrome with predisposition to development of renal cell carcinoma and smooth muscle tumours of the skin and uterus.$\backslash$n$\backslash$nOBJECTIVE: To measure the fumarate hydratase (FH) enzyme activity in lymphoblastoid cell lines and fibroblast cell lines of individuals with HLRCC and other familial renal cancer syndromes.$\backslash$n$\backslash$nMETHODS: FH enzyme activity was determined in the whole cell, cytosolic, and mitochondrial fractions in 50 lymphoblastoid and 16 fibroblast cell lines including cell lines from individuals with HLRCC with 16 different mutations.$\backslash$n$\backslash$nRESULTS: Lymphoblastoid cell lines (n = 20) and fibroblast cell lines (n = 11) from individuals with HLRCC had lower FH enzyme activity than cells from normal controls (p{\textless}0.05). The enzyme activity in lymphoblastoid cell lines from three individuals with mutations in R190 was not significantly different from individuals with other missense mutations. The cytosolic and mitochondrial FH activity of cell lines from individuals with HLRCC was reduced compared with those from control cell lines (p{\textless}0.05). There was no significant difference in enzyme activity between control cell lines (n = 4) and cell lines from affected individuals with other hereditary renal cancer syndromes (n = 22).$\backslash$n$\backslash$nCONCLUSIONS: FH enzyme activity testing provides a useful diagnostic method for confirmation of clinical diagnosis and screening of at-risk family members.},
author = {Pithukpakorn, M and Wei, M-H and Toure, O and Steinbach, P J and Glenn, G M and Zbar, B and Linehan, W M and Toro, J R},
doi = {10.1136/jmg.2006.041087},
file = {:home/sergi/all/devel/articles/mendeley/2006/Fumarate hydratase enzyme activity in lymphoblastoid cells and fibroblasts of individuals in families with hereditary leiomyomatosis and.pdf:pdf},
isbn = {1468-6244 (Electronic)$\backslash$r0022-2593 (Linking)},
issn = {1468-6244},
journal = {Journal of medical genetics},
keywords = {4.2.1.2,Amino Acid,Amino Acid Sequence,Carcinoma,Case-Control Studies,Cells,Cultured,Fibroblasts,Fibroblasts: enzymology,Fumarate Hydratase,Fumarate Hydratase: chemistry,Fumarate Hydratase: metabolism,Hereditary,Hereditary: enzymology,Humans,Leiomyomatosis,Leiomyomatosis: enzymology,Lymphocytes,Lymphocytes: enzymology,MTBLS150,Models,Molecular,Molecular Sequence Data,Mutation,Mutation: genetics,Neoplastic Syndromes,Pedigree,Phenotype,Renal Cell,Renal Cell: enzymology,Sequence Homology,fumarate},
mendeley-tags = {4.2.1.2,MTBLS150,fumarate},
number = {9},
pages = {755--62},
pmid = {16597677},
title = {{Fumarate hydratase enzyme activity in lymphoblastoid cells and fibroblasts of individuals in families with hereditary leiomyomatosis and renal cell cancer.}},
volume = {43},
year = {2006}
}
@article{ovarian_tca_fumarate_succinate,
abstract = {It is well documented that disturbances in mitochondrial function are associated with rare childhood disorders and possibly with many common diseases of ageing, such as Parkinson's disease and dementia. There has also been increasing evidence linking mitochondrial dysfunction with tumorigenesis. Recently, heterozygous germline mutations in two enzymes of the Krebs tricarboxylic acid cycle (TCA cycle) have been shown to predispose individuals to tumours. The two enzymes, fumarate hydratase (FH) and succinate dehydrogenase (SDH), are ubiquitously expressed, playing a vital role in adenosine triphosphate (ATP) production through the mitochondrial respiratory chain. Germline mutations in FHare associated with leiomyomatosis and renal cell carcinoma, whilst SDHmutations are associated with predisposition to paraganglioma (PGL) and phaeochromocytoma (PCC). At present, there are few data to explain the pathway(s) involved in this predisposition to neoplasia through TCA cycle defects. We shall review the mechanis...},
author = {Pollard, Patrick and Wortham, Noel and Tomlinson, Ian},
doi = {10.1080/07853890310018458},
file = {:home/sergi/all/devel/articles/mendeley/2003/The TCA cycle and tumorigenesis the examples of fumarate hydratase and succinate dehydrogenase.pdf:pdf},
isbn = {0785-3890 (Print)},
issn = {0785-3890},
journal = {Annals of Medicine},
keywords = {1.3.5.1,Krebs/TCA cycle,MTBLS150,TCA cycle,apoptosis,fibroid,fumarate,fumarate hydratase,hypoxia,leiomyoma,mitochondria,oxidative stress,paraganglioma,phaeochromocytoma,renal cell carcinoma,succinate dehydrogenase,succinate{\_}dehydrogenase,tumorigenesis,tumour suppressor},
mendeley-tags = {1.3.5.1,MTBLS150,TCA cycle,fumarate,succinate{\_}dehydrogenase},
number = {8},
pages = {634--639},
pmid = {14708972},
title = {{The TCA cycle and tumorigenesis: the examples of fumarate hydratase and succinate dehydrogenase}},
volume = {35},
year = {2003}
}
@article{malaria_phenylalanine_sengupta,
abstract = {BACKGROUND: Plasmodium vivax is responsible for the majority of malarial infection in the Indian subcontinent. This species of the parasite is generally believed to cause a relatively benign form of the disease. However, recent reports from different parts of the world indicate that vivax malaria can also have severe manifestation. Host response to the parasite invasion is thought to be an important factor in determining the severity of manifestation. In this paper, attempt was made to determine the host metabolic response associated with P. vivax infection by means of NMR spectroscopy-based metabonomic techniques in an attempt to better understand the disease pathology.$\backslash$n$\backslash$nMETHODS: NMR spectroscopy of urine samples from P. vivax-infected patients, healthy individuals and non-malarial fever patients were carried out followed by multivariate statistical analysis. Two data analysis techniques were employed, namely, Principal Component Analysis [PCA] and Orthogonal Projection to Latent Structure Discriminant Analysis [OPLS-DA]. Several NMR signals from the urinary metabolites were further selected for univariate comparison among the classes.$\backslash$n$\backslash$nRESULTS: The urine metabolic profiles of P. vivax-infected patients were distinct from those of healthy individuals as well as of non-malarial fever patients. A highly predictive model was constructed from urine profile of malarial and non-malarial fever patients. Several metabolites were found to be varying significantly across these cohorts. Urinary ornithine seems to have the potential to be used as biomarkers of vivax malaria. An increasing trend in pipecolic acid was also observed. The results suggest impairment in the functioning of liver as well as impairment in urea cycle.$\backslash$n$\backslash$nCONCLUSIONS: The results open up a possibility of non-invasive analysis and diagnosis of P. vivax using urine metabolic profile. Distinct variations in certain metabolites were recorded, and amongst these, ornithine may have the potential of being used as biomarker of malaria. Pipecolic acid also showed increasing trend in the malaria patient compared to the other groups.},
author = {Sengupta, Arjun and Ghosh, Soumita and Basant, Angika and Malusare, Suhas and Johri, Parul and Pathak, Sulabha and Sharma, Shobhona and Sonawat, Haripalsingh M},
doi = {10.1186/1475-2875-10-384},
file = {:home/sergi/all/devel/articles/mendeley/2011/Global host metabolic response to Plasmodium vivax infection a 1H NMR based urinary metabonomic study.pdf:pdf},
isbn = {1475-2875 (Electronic)$\backslash$r1475-2875 (Linking)},
issn = {1475-2875},
journal = {Malaria journal},
keywords = {Adult,Biological Markers,Biological Markers: metabolism,Biological Markers: urine,Case-Control Studies,Humans,MTBLS315,Magnetic Resonance Spectroscopy,Malaria,Male,Metabolome,Metabolomics,Metabolomics: methods,Middle Aged,Multivariate Analysis,Ornithine,Ornithine: metabolism,Ornithine: urine,Pipecolic Acids,Pipecolic Acids: metabolism,Pipecolic Acids: urine,Plasmodium vivax,Plasmodium vivax: pathogenicity,Predictive Value of Tests,Specimen Handling,Specimen Handling: methods,Vivax,Vivax: metabolism,Vivax: parasitology,Vivax: urine,phenylalanine,phenylpyruvate},
mendeley-tags = {MTBLS315,phenylalanine,phenylpyruvate},
number = {1},
pages = {384},
pmid = {22196439},
title = {{Global host metabolic response to Plasmodium vivax infection: a 1H NMR based urinary metabonomic study.}},
volume = {10},
year = {2011}
}
@article{ovarian_4_2_1_3_singh,
abstract = {BACKGROUND: In prostate cancer, normal citrate-producing glandular secretory epithelial cells undergo a metabolic transformation to malignant citrate-oxidizing cells. m-Aconitase is the critical step involved in this altered citrate metabolism that is essential to prostate malignancy. The limiting m-aconitase activity in prostate epithelial cells could be the result of a decreased level of m-aconitase enzyme and/or the inhibition of existing m-aconitase. Earlier studies identified zinc as an inhibitor of m-aconitase activity in prostate cells; and that the depletion of zinc in malignant cells is an important factor in this metabolic transformation. However, a possibility remains that an altered expression and level of m-aconitase enzyme might also be involved in this metabolic transformation. To address this issue, the in situ level of m-aconitase enzyme was determined by immunohistochemical analysis of prostate cancer tissue sections and malignant prostate cell lines.$\backslash$n$\backslash$nRESULTS: The immunocytochemical procedure successfully identified the presence of m-aconitase localized in the mitochondrial compartment in PC-3, LNCaP, and DU-145 malignant prostate cell lines. The examination of prostate tissue sections from prostate cancer subjects demonstrated that m-aconitase enzyme is present in the glandular epithelium of normal glands, hyperplastic glands, adenocrcinomatous glands, and prostatic intraepithelial neoplastic foci. Quantitative analysis of the relative level of m-aconitase in the glandular epithelium of citrate-producing adenomatous glands versus the citrate-oxidizing adenocarcinomatous glands revealed no significant difference in m-aconitase enzyme levels. This is in contrast to the down-regulation of ZIP1 zinc transporter in the malignant glands versus hyperplastic glands that exists in the same tissue samples.$\backslash$n$\backslash$nCONCLUSION: The results demonstrate the existence of m-aconitase enzyme in the citrate-producing glandular epithelial cells; so that deficient m-aconitase enzyme is not associated with the limiting m-aconitase activity that prevents citrate oxidation in these cells. The level of m-aconitase is maintained in the malignant cells; so that an altered enzyme level is not associated with the increased m-aconitase activity. Consequently, the elevated zinc level that inhibits m-aconitase enzyme is responsible for the impaired citrate oxidation in normal and hyperplastic prostate glandular epithelial cells. Moreover, the down-regulation of ZIP1 zinc transporter and corresponding depletion of zinc results in the increase in the activity of the existing m-aconitase activity in the malignant prostate cells. The studies now define the mechanism for the metabolic transformation that characterizes the essential transition of normal citrate-producing epithelial cells to malignant citrate-oxidizing cells.},
author = {Singh, Keshav K and Desouki, Mohamed M and Franklin, Renty B and Costello, Leslie C},
doi = {10.1186/1476-4598-5-14},
file = {:home/sergi/all/devel/articles/mendeley/2006/Mitochondrial aconitase and citrate metabolism in malignant and nonmalignant human prostate tissues.pdf:pdf},
isbn = {1476459851},
issn = {1476-4598},
journal = {Molecular cancer},
keywords = {4.2.1.3,Aconitate Hydratase,Aconitate Hydratase: analysis,Aconitate Hydratase: metabolism,Cell Line,Citric Acid,Citric Acid: metabolism,Humans,MTBLS150,Male,Mitochondria,Mitochondria: enzymology,Prostate,Prostate: enzymology,Prostatic Neoplasms,Prostatic Neoplasms: enzymology,Tumor},
mendeley-tags = {4.2.1.3,MTBLS150},
pages = {14},
pmid = {16595004},
title = {{Mitochondrial aconitase and citrate metabolism in malignant and nonmalignant human prostate tissues.}},
volume = {5},
year = {2006}
}
@article{malaria_coa_spry,
abstract = {Pantothenate, a precursor of the fundamental enzyme cofactor coenzyme A (CoA), is essential for growth of the intraerythrocytic stage of human and avian malaria parasites. Avian malaria parasites have been reported to be incapable of de novo CoA synthesis and instead salvage CoA from the host erythrocyte; hence, pantothenate is required for CoA biosynthesis within the host cell and not the parasite itself. Whether the same is true of the intraerythrocytic stage of the human malaria parasite, Plasmodium falciparum, remained to be established. In this study we investigated the metabolic fate of [(14)C]pantothenate within uninfected and P. falciparum-infected human erythrocytes. We provide evidence consistent with normal human erythrocytes, unlike rat erythrocytes (which have been reported to possess an incomplete CoA biosynthesis pathway), being capable of CoA biosynthesis from pantothenate. We also show that CoA biosynthesis is substantially higher in P. falciparum-infected erythrocytes and that P. falciparum, unlike its avian counterpart, generates most of the CoA synthesized in the infected erythrocyte, presumably necessitated by insufficient CoA biosynthesis in the host erythrocyte. Our data raise the possibility that malaria parasites rationalize their biosynthetic activity depending on the capacity of their host cell to synthesize the metabolites they require.},
author = {Spry, Christina and Saliba, Kevin J.},
doi = {10.1074/jbc.M109.025312},
file = {:home/sergi/all/devel/articles/mendeley/2009/The human malaria parasite Plasmodium falciparum is not dependent on host coenzyme A biosynthesis.pdf:pdf},
isbn = {6126125754},
issn = {00219258},
journal = {Journal of Biological Chemistry},
keywords = {CoA,MTBLS315},
mendeley-tags = {CoA,MTBLS315},
number = {37},
pages = {24904--24913},
pmid = {19584050},
title = {{The human malaria parasite Plasmodium falciparum is not dependent on host coenzyme A biosynthesis}},
volume = {284},
year = {2009}
}
@article{ovarian_main,
abstract = {BackgroundCancer metabolism is emerging as an important focus area in cancer research. However, the in vitro cell culture conditions under which much cellular metabolism research is performed differ drastically from in vivo tumor conditions, which are characterized by variations in the levels of oxygen, nutrients like glucose, and other molecules like chemotherapeutics. Moreover, it is important to know how the diverse cell types in a tumor, including cancer stem cells that are believed to be a major cause of cancer recurrence, respond to these variations. Here, in vitro environmental perturbations designed to mimic different aspects of the in vivo environment were used to characterize how an ovarian cancer cell line and its derived, isogenic cancer stem cells metabolically respond to environmental cues.ResultsMass spectrometry was used to profile metabolite levels in response to in vitro environmental perturbations. Docetaxel, the chemotherapeutic used for this experiment, caused significant metabolic changes in amino acid and carbohydrate metabolism in ovarian cancer cells, but had virtually no metabolic effect on isogenic ovarian cancer stem cells. Glucose deprivation, hypoxia, and the combination thereof altered ovarian cancer cell and cancer stem cell metabolism to varying extents for the two cell types. Hypoxia had a much larger effect on ovarian cancer cell metabolism, while glucose deprivation had a greater effect on ovarian cancer stem cell metabolism. Core metabolites and pathways affected by these perturbations were identified, along with pathways that were unique to cell types or perturbations.ConclusionsThe metabolic responses of an ovarian cancer cell line and its derived isogneic cancer stem cells differ greatly under most conditions, suggesting that these two cell types may behave quite differently in an in vivo tumor microenvironment. While cancer metabolism and cancer stem cells are each promising potential therapeutic targets, such varied behaviors in vivo would need to be considered in the design and early testing of such treatments.},
author = {Vermeersch, Kathleen a and Wang, Lijuan and McDonald, John F and Styczynski, Mark P},
doi = {10.1186/s12918-014-0134-y},
file = {:home/sergi/all/devel/articles/mendeley/2014/Distinct metabolic responses of an ovarian cancer stem cell line.pdf:pdf},
issn = {1752-0509},
journal = {BMC Systems Biology},
keywords = {MTBLS150,Metabolomics,Cancer stem cells,Ovarian cancer,Canc,biologically-inspired metabolic,cancer metabolism,cancer stem cells,main{\_}paper,metabolomics,ovarian cancer},
mendeley-tags = {MTBLS150,main{\_}paper},
number = {1},
pages = {134},
pmid = {25518943},
title = {{Distinct metabolic responses of an ovarian cancer stem cell line}},
volume = {8},
year = {2014}
}
@article{epithelial_hyperosmotic_stress_wang,
abstract = {PURPOSE: Hyperosmotic stress causes cell shrinkage, perturbs cell function, and damages DNA, resulting in cell cycle arrest and apoptosis. In the present study, the authors explore the mechanism involving hyperosmotic stress-induced activation of c-Jun/AP-1 through a novel Plk3 pathway in human corneal epithelial cells.$\backslash$n$\backslash$nMETHODS: Human primary corneal epithelial cells and cell line were cultured in a serum-free keratinocyte medium and DMEM/F12 medium containing 10{\%} FBS in a 37°C incubator supplied with 5{\%} CO(2), respectively. Western blot analysis was used to determine protein expression and phosphorylation levels. Protein kinase activities were measured by immunocomplex kinase assay. Cell viability and apoptosis were determined by MTT assay and caspase-3 (DEVDase) activity.$\backslash$n$\backslash$nRESULTS: It was found that hyperosmotic stress-induced increases in the phosphorylation of c-Jun, resulting in apoptosis through the activation of Plk3 in human corneal epithelial cells. Plk3 was activated by extracellular hyperosmotic stress to directly phosphorylate c-Jun in the serine 63 and 73 residues. Hyperosmotic stress-induced c-Jun phosphorylation was enhanced by overexpression of constitutively positive Plk3 mutants and suppressed by the knockdown of Plk3 mRNA with Plk3-specific siRNA. Further studies indicated that the phosphorylation of c-Jun by Plk3 was responsible for hyperosmotic stress-induced apoptosis, which was independent from activation of the JNK signaling pathway in human corneal epithelial cells.$\backslash$n$\backslash$nCONCLUSIONS: These results, for the first time, provide a novel and alternative signaling mechanism that involves hyperosmotic stress-induced activation of the Plk3 pathway in addition to JNK/p38 MAPK pathways to regulate the c-Jun/AP-1 transcriptional complex and human corneal epithelial cell fate.},
author = {Wang, Ling and Dai, Wei and Lu, Luo},
doi = {10.1167/iovs.10-6485},
file = {:home/sergi/all/devel/articles/mendeley/2011/Hyperosmotic stress-induced corneal epithelial cell death through activation of Polo-like kinase 3 and c-Jun.pdf:pdf},
issn = {01460404},
journal = {Investigative Ophthalmology and Visual Science},
keywords = {MTBLS214,hyperosmotic{\_}stress},
mendeley-tags = {MTBLS214,hyperosmotic{\_}stress},
number = {6},
pages = {3200--3206},
pmid = {21296815},
title = {{Hyperosmotic stress-induced corneal epithelial cell death through activation of Polo-like kinase 3 and c-Jun}},
volume = {52},
year = {2011}
}


@article{mala_nonmala_aldosterone,
  title={Metabolic response to infection},
  author={Beisel, William R},
  journal={Annual review of medicine},
  volume={26},
  number={1},
  pages={9--20},
  year={1975},
  publisher={Annual Reviews 4139 El Camino Way, PO Box 10139, Palo Alto, CA 94303-0139, USA}
}

@article{mala_nonmala_linoleic,
  title={A role for linoleic acid in erythrocytes infected with Plasmodium berghei},
  author={Fitch, Coy D and Cai, Guang-zuan and Shoemaker, James D},
  journal={Biochimica et Biophysica Acta (BBA)-Molecular Basis of Disease},
  volume={1535},
  number={1},
  pages={45--49},
  year={2000},
  publisher={Elsevier}
}

@article{mala_nonmala_sphingo,
  title={Sphingolipid metabolites in inflammatory disease},
  author={Maceyka, Michael and Spiegel, Sarah},
  journal={Nature},
  volume={510},
  number={7503},
  pages={58},
  year={2014},
  publisher={NIH Public Access}
}

@article{mala_nonmala_sphingo2,
  title={Does cytokine signaling link sphingolipid metabolism to host defense and immunity against virus infections?},
  author={Seo, Young-Jin and Alexander, Stephen and Hahm, Bumsuk},
  journal={Cytokine \& growth factor reviews},
  volume={22},
  number={1},
  pages={55--61},
  year={2011},
  publisher={Elsevier}
}