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571. Attachment of Agrobacterium to plant surfaces

Title Tesim:
Attachment of Agrobacterium to plant surfaces
Creator:
Matthysse, Ann G.
Date of publication:
2014
Abstract Tesim:
Agrobacterium tumefaciens binds to the surfaces of inanimate objects, plants, and fungi. These bacteria are excellent colonizers of root surfaces. In addition, they also bind to soil particles and to the surface of artificial or man-made substances, such as polyesters and plastics. The mechanisms of attachment to these different surfaces have not been completely elucidated. At least two types of binding have been described unipolarpolysaccharide-dependent polar attachment and unipolar polysaccharide-independent attachment (both polar and lateral). The genes encoding the enzymes for the production of the former are located on the circular chromosome, while the genes involved in the latter have not been identified. The expression of both of these types of attachment is regulated in response to environmental signals. However, the signals to which they respond differ so that the two types of attachment are not necessarily expressed coordinately.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/4fhg-fj79
Identifier:
PMID: 24926300, PMCID: PMC4046570, Publisher DOI: https://doi.org/10.3389/fpls.2014.00252, and Onescience id: 6d7cf5a736466c920d80640f87fadca1001110ba
ISSN:
1664-462X
Journal Title:
Frontiers in Plant Science
Journal Volume:
5
Keyword:
attachment, adhesion, bacterial binding, Agrobacterium, and exopolysaccharides
Language Label:
English
Person:
Matthysse, Ann G.
Rights Statement Label:
In Copyright
Source:
n583z2196

572. How complex are intracellular immune receptor signaling complexes?

Title Tesim:
How complex are intracellular immune receptor signaling complexes?
Creator:
Bonardi, Vera and Dangl, Jeffery L.
Date of publication:
2012
Abstract Tesim:
Nucleotide binding leucine-rich repeat proteins (NLRs) are the major class of intracellular immune receptors in plants. NLRs typically function to specifically recognize pathogen effectors and to initiate and control defense responses that severely limit pathogen growth in plants (termed effector-triggered immunity, or ETI). Despite numerous reports supporting a central role in innate immunity, the molecular mechanisms driving NLR activation and downstream signaling remain largely elusive. Recent reports shed light on the pre- and post-activation dynamics of a few NLR-containing protein complexes. Recent technological advances in the use of proteomics may enable high-resolution definition of immune protein complexes and possible activation-relevant post-translational modifications of the components in these complexes. In this review, we focus on research aimed at characterizing pre- and post-activation NLR protein complexes and the molecular events that follow activation. We discuss the use of new or improved technologies as tools to unveil the molecular mechanisms that define NLR-mediated pathogen recognition.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/gm4w-wj47
Identifier:
Publisher DOI: https://doi.org/10.3389/fpls.2012.00237, PMCID: PMC3478704, PMID: 23109935, and Onescience id: c9d977e8628162db3a2feb62a28b6d41c54315a9
ISSN:
1664-462X
Journal Title:
Frontiers in Plant Science
Journal Volume:
3
Keyword:
immune system, effector, Review Article, plant, Plant Science, protein complex, Disease Resistance, disease resistance, NLR, Protein complex, and Immune System
Language Label:
English
Person:
Bonardi, Vera and Dangl, Jeffery L.
Rights Statement Label:
In Copyright
Source:
3b591g74d

573. The iPlant Collaborative: Cyberinfrastructure for Plant Biology

Title Tesim:
The iPlant Collaborative: Cyberinfrastructure for Plant Biology
Creator:
Hilgert, Uwe, Koesterke, Lars, Vaughn, Matthew, Dooley, Rion, Matasci, Naim, Stapleton, Ann E., Muir, Andy, Wang, Liya, Skidmore, Edwin, Gessler, Damian, Hanlon, Matthew, Merchant, Nirav, Kubach, Adam, Noutsos, Christos, Lu, Zhenyuan, Pasternak, Shiran, Micklos, David, Grene, Ruth, Lenards, Andrew, Lowry, Sonya, McKay, Sheldon, Jordan, Chris, Mock, Stephen, Narro, Martha, McLay, Robert, Piel, William H., Goff, Stephen A., Helmke, Matthew, Hopkins, Nicole, Gonzales, Michael, Cazes, John, and Lyons, Eric
Date of publication:
2011
Abstract Tesim:
The iPlant Collaborative (iPlant) is a United States National Science Foundation (NSF) funded project that aims to create an innovative, comprehensive, and foundational cyberinfrastructure in support of plant biology research (PSCIC, 2006). iPlant is developing cyberinfrastructure that uniquely enables scientists throughout the diverse fields that comprise plant biology to address Grand Challenges in new ways, to stimulate and facilitate cross-disciplinary research, to promote biology and computer science research interactions, and to train the next generation of scientists on the use of cyberinfrastructure in research and education. Meeting humanity's projected demands for agricultural and forest products and the expectation that natural ecosystems be managed sustainably will require synergies from the application of information technologies. The iPlant cyberinfrastructure design is based on an unprecedented period of research community input, and leverages developments in high-performance computing, data storage, and cyberinfrastructure for the physical sciences. iPlant is an open-source project with application programming interfaces that allow the community to extend the infrastructure to meet its needs. iPlant is sponsoring community-driven workshops addressing specific scientific questions via analysis tool integration and hypothesis testing. These workshops teach researchers how to add bioinformatics tools and/or datasets into the iPlant cyberinfrastructure enabling plant scientists to perform complex analyses on large datasets without the need to master the command-line or high-performance computational services.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/5qzg-xt08
Identifier:
Onescience id: fc21eac4d518af7eca30b871138849fc036bbffa, PMCID: PMC3355756, PMID: 22645531, and Publisher DOI: https://doi.org/10.3389/fpls.2011.00034
ISSN:
1664-462X
Journal Title:
Frontiers in Plant Science
Journal Volume:
2
Keyword:
cyberinfrastructure, bioinformatics, databases, cross-disciplinary collaborations, genomics and proteomics, plant, and high performance computing
Language Label:
English
Person:
Hilgert, Uwe, Koesterke, Lars, Vaughn, Matthew, Dooley, Rion, Matasci, Naim, Stapleton, Ann E., Muir, Andy, Wang, Liya, Skidmore, Edwin, Gessler, Damian, Hanlon, Matthew, Merchant, Nirav, Kubach, Adam, Noutsos, Christos, Lu, Zhenyuan, Pasternak, Shiran, Micklos, David, Grene, Ruth, Lenards, Andrew, Lowry, Sonya, McKay, Sheldon, Jordan, Chris, Mock, Stephen, Narro, Martha, McLay, Robert, Piel, William H., Goff, Stephen A., Helmke, Matthew, Hopkins, Nicole, Gonzales, Michael, Cazes, John, and Lyons, Eric
Rights Statement Label:
In Copyright
Source:
r494vs199

574. Identification and characterization of CHCHD1, AURKAIP1, and CRIF1 as new members of the mammalian mitochondrial ribosome

Title Tesim:
Identification and characterization of CHCHD1, AURKAIP1, and CRIF1 as new members of the mammalian mitochondrial ribosome
Creator:
Koc, Emine C., Cimen, Huseyin, Akpinar, Gurler, Kumcuoglu, Beril, Haque, Md. Emdadul, Spremulli, Linda L., Koc, Hasan, and Abu, Nadiah
Date of publication:
2013
Abstract Tesim:
Defects in mitochondrial ribosomal proteins (MRPs) cause various diseases in humans. Because of the essential role of MRPs in synthesizing the essential subunits of oxidative phosphorylation (OXPHOS) complexes, identifying all of the protein components involved in the mitochondrial translational machinery is critical. Initially, we identified 79 MRPs; however, identifying MRPs with no clear homologs in bacteria and yeast mitochondria was challenging, due to limited availability of expressed sequence tags (ESTs) in the databases available at that time. With the improvement in genome sequencing and increased sensitivity of mass spectrometry (MS)-based technologies, we have established four previously known proteins as MRPs and have confirmed the identification of ICT1 (MRP58) as a ribosomal protein. The newly identified MRPs are MRPS37 (Coiled-coil-helix-coiled-coil-helix domain containing protein 1-CHCHD1), MRPS38 (Aurora kinase A interacting protein1, AURKAIP1), MRPS39 (Pentatricopeptide repeat-containing protein 3, PTCD3), in the small subunit and MRPL59 (CR-6 interacting factor 1, CRIF1) in the large subunit. Furthermore, we have demonstrated the essential roles of CHCHD1, AURKAIP1, and CRIF1in mitochondrial protein synthesis by siRNA knock-down studies, which had significant effects on the expression of mitochondrially encoded proteins.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/dhkg-dp94
Identifier:
Publisher DOI: https://doi.org/10.3389/fphys.2013.00183, PMCID: PMC3726836, PMID: 23908630, and Onescience id: 57e5e97d965be77f256330452b26bcb8905fe2e9
ISSN:
1664-042X
Journal Title:
Frontiers in Physiology
Journal Volume:
4
Keyword:
AURKA, AURKAIP1, Sensitivity and Specificity, Mitochondria, MRPS38 (AURKAIP1), Ribosomes, Saccharomyces cerevisiae, GADD45GIP1, ANXA2, Mass Spectrometry, Genome, PTCD3, Homo sapiens, Ribosomal Proteins, Proteins, Aurora Kinase A, Mitochondrial translation, MRPS37 (CHCHD1), ICT1, IPL1, Mitochondrial Proteins, GADD45G, CHCHD1, Oxidative Phosphorylation, Protein Structure, Tertiary, and Expressed Sequence Tags
Language Label:
English
Person:
Koc, Emine C., Cimen, Huseyin, Akpinar, Gurler, Kumcuoglu, Beril, Haque, Md. Emdadul, Spremulli, Linda L., Koc, Hasan, and Abu, Nadiah
Rights Statement Label:
In Copyright
Source:
n583z218x

575. Computational Modeling of Interacting VEGF and Soluble VEGF Receptor Concentration Gradients

Title Tesim:
Computational Modeling of Interacting VEGF and Soluble VEGF Receptor Concentration Gradients
Creator:
Hashambhoy, Yasmin L., Peirce-Cottler, Shayn M., Mac Gabhann, Feilim, Chappell, John C., and Bautch, Victoria L.
Date of publication:
2011
Abstract Tesim:
Experimental data indicates that soluble vascular endothelial growth factor (VEGF) receptor 1 (sFlt-1) modulates the guidance cues provided to sprouting blood vessels by VEGF-A. To better delineate the role of sFlt-1 in VEGF signaling, we have developed an experimentally based computational model. This model describes dynamic spatial transport of VEGF, and its binding to receptors Flt-1 and Flk-1, in a mouse embryonic stem cell model of vessel morphogenesis. The model represents the local environment of a single blood vessel. Our simulations predict that blood vessel secretion of sFlt-1 and increased local sFlt-1 sequestration of VEGF results in decreased VEGF–Flk-1 levels on the sprout surface. In addition, the model predicts that sFlt-1 secretion increases the relative gradient of VEGF–Flk-1 along the sprout surface, which could alter endothelial cell perception of directionality cues. We also show that the proximity of neighboring sprouts may alter VEGF gradients, VEGF receptor binding, and the directionality of sprout growth. As sprout distances decrease, the probability that the sprouts will move in divergent directions increases. This model is a useful tool for determining how local sFlt-1 and VEGF gradients contribute to the spatial distribution of VEGF receptor binding, and can be used in conjunction with experimental data to explore how multi-cellular interactions and relationships between local growth factor gradients drive angiogenesis.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/g65v-4q88
Identifier:
PMID: 22007175, Onescience id: a92ed516d6c54c58dca2544ac3d172836916e42b, PMCID: PMC3185289, and Publisher DOI: https://doi.org/10.3389/fphys.2011.00062
ISSN:
1664-042X
Journal Title:
Frontiers in Physiology
Journal Volume:
2
Keyword:
computational model, Angiogenesis, sflt1, Vascular Development, Developmental Biology, mathematical model, capillary sprouting, and VEGF
Language Label:
English
Person:
Hashambhoy, Yasmin L., Peirce-Cottler, Shayn M., Mac Gabhann, Feilim, Chappell, John C., and Bautch, Victoria L.
Rights Statement Label:
In Copyright
Source:
td96k876b

576. Non-Invasive Methods for Estradiol Recovery from Infant Fecal Samples

Title Tesim:
Non-Invasive Methods for Estradiol Recovery from Infant Fecal Samples
Creator:
Whitten, Patricia L., Thompson, Amanda L., Lampl, Michelle, and Johnson, Michael L.
Date of publication:
2010
Abstract Tesim:
While the activation of the infant hypothalamic–pituitary–gonadal axis and the existence of a postnatal gonadotropin surge were first documented in the early 1970s, study of the longitudinal development of gonadal hormones in infancy, and the potential physiological and behavioral correlates of this development, have been hampered by reliance on infrequent serum sampling. The present study reports the validation of a non-invasive method for repeated assessment of steroid hormones in infant fecal samples. Fecal samples were collected in and excised from cotton diaper liners and extracted using methanol. Extracts were analyzed for estradiol using a diluted assay modification. Method validity was supported by a steroid recovery rate of at least 80%, a sensitivity of 0.35 pg/ml, and inter- and intra-assay coefficients of variations of less than 10 and 20%, respectively. Variation in estradiol concentration was assessed across (1) sample type (scraped vs. cut from diaper liner), (2) time of day (morning vs. afternoon/evening samples), (3) time interval between samples, and (4) time-to-assay (1 day vs. 489 days after collection). Of these characteristics, only the time interval between samples within an individual was significantly associated with estradiol concentration. This is the first report of human infant fecal estradiol levels. The results support fecal recovery as a novel and powerful non-invasive tool for longitudinal studies of human infants, expanding research opportunities for investigating development of sex-specific behaviors in infancy, and the potential effects of endocrine disruptors on development.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/5xga-pr61
Identifier:
PMCID: PMC3059931, Onescience id: ea969f196c628ece5605a80b63770834449e5995, PMID: 21423388, and Publisher DOI: https://doi.org/10.3389/fphys.2010.00148
ISSN:
1664-042X
Journal Title:
Frontiers in Physiology
Journal Volume:
1
Keyword:
Physiology, QP1-981, Infant, Science, developmental endocrinology, Estradiol, noninvasive methods, Q, fecal steroids, and development
Language Label:
English
Person:
Whitten, Patricia L., Thompson, Amanda L., Lampl, Michelle, and Johnson, Michael L.
Rights Statement Label:
In Copyright
Source:
ng451q962

577. Identifying genes that mediate anthracyline toxicity in immune cells

Title Tesim:
Identifying genes that mediate anthracyline toxicity in immune cells
Creator:
Richards, Kristy L., Frick, Amber, Benton, Cristina, Thomas, Russell S., Suzuki, Oscar T., Parks, Bethany, Wiltshire, Tim, and Fedoriw, Yuri
Date of publication:
2015
Abstract Tesim:
The role of the immune system in response to chemotherapeutic agents remains elusive. The interpatient variability observed in immune and chemotherapeutic cytotoxic responses is likely, at least in part, due to complex genetic differences. Through the use of a panel of genetically diverse mouse inbred strains, we developed a drug screening platform aimed at identifying genes underlying these chemotherapeutic cytotoxic effects on immune cells. Using genome-wide association studies (GWAS), we identified four genome-wide significant quantitative trait loci (QTL) that contributed to the sensitivity of doxorubicin and idarubicin in immune cells. Of particular interest, a locus on chromosome 16 was significantly associated with cell viability following idarubicin administration (p = 5.01 × 10−8). Within this QTL lies App, which encodes amyloid beta precursor protein. Comparison of dose-response curves verified that T-cells in App knockout mice were more sensitive to idarubicin than those of C57BL/6J control mice (p < 0.05). In conclusion, the cellular screening approach coupled with GWAS led to the identification and subsequent validation of a gene involved in T-cell viability after idarubicin treatment. Previous studies have suggested a role for App in in vitro and in vivo cytotoxicity to anticancer agents; the overexpression of App enhances resistance, while the knockdown of this gene is deleterious to cell viability. Further investigations should include performing mechanistic studies, validating additional genes from the GWAS, including Ppfia1 and Ppfibp1, and ultimately translating the findings to in vivo and human studies.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/3n2v-y546
Identifier:
Onescience id: 334c90e57a72e9267c9e85a4147cd5e6ff50084a, Publisher DOI: https://doi.org/10.3389/fphar.2015.00062, PMID: 25926793, and PMCID: PMC4398020
ISSN:
1663-9812
Journal Title:
Frontiers in Pharmacology
Journal Volume:
6
Keyword:
Idarubicin, Cells, Ppfibp1, Mus musculus, Genome-Wide Association Study, Homo sapiens, App, Genes, Antineoplastic Agents, Ppfia1, pharmacogenomics, Immune System, Genome, T-Lymphocytes, PPFIBP1, Therapeutics, Amyloid beta-Protein Precursor, In Vitro Techniques, Drug Evaluation, Preclinical, APP, Chromosomes, Doxorubicin, Quantitative Trait Loci, PPFIA1, Cell Survival, and Sensitivity and Specificity
Language Label:
English
Person:
Richards, Kristy L., Frick, Amber, Benton, Cristina, Thomas, Russell S., Suzuki, Oscar T., Parks, Bethany, Wiltshire, Tim, and Fedoriw, Yuri
Rights Statement Label:
In Copyright
Source:
6682xb78b

578. Influence of host iron status on Plasmodium falciparum infection

Title Tesim:
Influence of host iron status on Plasmodium falciparum infection
Creator:
Clark, Martha A., Cerami, Carla, and Goheen, Morgan M.
Date of publication:
2014
Abstract Tesim:
Iron deficiency affects one quarter of the world's population and causes significant morbidity, including detrimental effects on immune function and cognitive development. Accordingly, the World Health Organization (WHO) recommends routine iron supplementation in children and adults in areas with a high prevalence of iron deficiency. However, a large body of clinical and epidemiological evidence has accumulated which clearly demonstrates that host iron deficiency is protective against falciparum malaria and that host iron supplementation may increase the risk of malaria. Although many effective antimalarial treatments and preventive measures are available, malaria remains a significant public health problem, in part because the mechanisms of malaria pathogenesis remain obscured by the complexity of the relationships that exist between parasite virulence factors, host susceptibility traits, and the immune responses that modulate disease. Here we review (i) the clinical and epidemiological data that describes the relationship between host iron status and malaria infection and (ii) the current understanding of the biological basis for these clinical and epidemiological observations.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/qg1y-9t20
Identifier:
PMID: 24834053, PMCID: PMC4018558, Onescience id: 6ec21acdefbc2979a3006d6e4e25645beac7614c, and Publisher DOI: https://doi.org/10.3389/fphar.2014.00084
ISSN:
1663-9812
Journal Title:
Frontiers in Pharmacology
Journal Volume:
5
Keyword:
iron supplementation, Iron, plasmodium falciparu, iron deficiency anemia, and Malaria
Language Label:
English
Person:
Clark, Martha A., Cerami, Carla, and Goheen, Morgan M.
Rights Statement Label:
In Copyright
Source:
4t64gv56d

579. Exploring BSEP inhibition-mediated toxicity with a mechanistic model of drug-induced liver injury

Title Tesim:
Exploring BSEP inhibition-mediated toxicity with a mechanistic model of drug-induced liver injury
Creator:
Siler, Scott Q., Barton, Hugh A., Watkins, Paul B., Yang, Kyunghee, Brouwer, Kim L. R., Woodhead, Jeffrey L., and Howell, Brett A.
Date of publication:
2014
Abstract Tesim:
Inhibition of the bile salt export pump (BSEP) has been linked to incidence of drug-induced liver injury (DILI), presumably by the accumulation of toxic bile acids in the liver. We have previously constructed and validated a model of bile acid disposition within DILIsym®, a mechanistic model of DILI. In this paper, we use DILIsym® to simulate the DILI response of the hepatotoxic BSEP inhibitors bosentan and CP-724,714 and the non-hepatotoxic BSEP inhibitor telmisartan in humans in order to explore whether we can predict that hepatotoxic BSEP inhibitors can cause bile acid accumulation to reach toxic levels. We also simulate bosentan in rats in order to illuminate potential reasons behind the lack of toxicity in rats compared to the toxicity observed in humans. DILIsym® predicts that bosentan, but not telmisartan, will cause mild hepatocellular ATP decline and serum ALT elevation in a simulated population of humans. The difference in hepatotoxic potential between bosentan and telmisartan is consistent with clinical observations. However, DILIsym® underpredicts the incidence of bosentan toxicity. DILIsym® also predicts that bosentan will not cause toxicity in a simulated population of rats, and that the difference between the response to bosentan in rats and in humans is primarily due to the less toxic bile acid pool in rats. Our simulations also suggest a potential synergistic role for bile acid accumulation and mitochondrial electron transport chain (ETC) inhibition in producing the observed toxicity in CP-724,714, and suggest that CP-724,714 metabolites may also play a role in the observed toxicity. Our work also compares the impact of competitive and noncompetitive BSEP inhibition for CP-724,714 and demonstrates that noncompetitive inhibition leads to much greater bile acid accumulation and potential toxicity. Our research demonstrates the potential for mechanistic modeling to contribute to the understanding of how bile acid transport inhibitors cause DILI.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/919x-mc77
Identifier:
PMID: 25426072, PMCID: PMC4224072, Publisher DOI: https://doi.org/10.3389/fphar.2014.00240, and Onescience id: 22985988118a977f7f6fa6d6af3c43f9ed5db0b9
ISSN:
1663-9812
Journal Title:
Frontiers in Pharmacology
Journal Volume:
5
Keyword:
BSEP inhibition, CP-724, bosentan, population variability, mechanistic modeling, bile acids and salts, drug-induced liver injury, and 714
Language Label:
English
Person:
Siler, Scott Q., Barton, Hugh A., Watkins, Paul B., Yang, Kyunghee, Brouwer, Kim L. R., Woodhead, Jeffrey L., and Howell, Brett A.
Rights Statement Label:
In Copyright
Source:
xw42ng03d

580. Flavonol-rich dark cocoa significantly decreases plasma endothelin-1 and improves cognition in urban children

Title Tesim:
Flavonol-rich dark cocoa significantly decreases plasma endothelin-1 and improves cognition in urban children
Creator:
Zhu, Hongtu, Solorio, Edelmira, Medina-Cortina, Humberto, Chao, Chih-kai, Mora-Tiscareño, Antonieta, Cross, Janet V., D'Angiulli, Amedeo, Engle, Randall, Gómez-Garza, Gilberto, Mukherjee, Partha S., Torres-Jardón, Ricardo, Ferreira-Azevedo, Lara, Jewells, Valerie, Franco-Lira, Maricela, Calderón-Garcidueñas, Lilian, and Aragón-Flores, Mariana
Date of publication:
2013
Abstract Tesim:
Air pollution exposures are linked to systemic inflammation, cardiovascular and respiratory morbidity and mortality, neuroinflammation and neuropathology in young urbanites. In particular, most Mexico City Metropolitan Area (MCMA) children exhibit subtle cognitive deficits, and neuropathology studies show 40% of them exhibiting frontal tau hyperphosphorylation and 51% amyloid-β diffuse plaques (compared to 0% in low pollution control children). We assessed whether a short cocoa intervention can be effective in decreasing plasma endothelin 1 (ET-1) and/or inflammatory mediators in MCMA children. Thirty gram of dark cocoa with 680 mg of total flavonols were given daily for 10.11 ± 3.4 days (range 9–24 days) to 18 children (10.55 years, SD = 1.45; 11F/7M). Key metabolite ratios in frontal white matter and in hippocampus pre and during cocoa intervention were quantified by magnetic resonance spectroscopy. ET-1 significantly decreased after cocoa treatment (p = 0.0002). Fifteen children (83%) showed a marginally significant individual improvement in one or both of the applied simple short memory tasks. Endothelial dysfunction is a key feature of exposure to particulate matter (PM) and decreased endothelin-1 bioavailability is likely useful for brain function in the context of air pollution. Our findings suggest that cocoa interventions may be critical for early implementation of neuroprotection of highly exposed urban children. Multi-domain nutraceutical interventions could limit the risk for endothelial dysfunction, cerebral hypoperfusion, neuroinflammation, cognitive deficits, structural volumetric detrimental brain effects, and the early development of the neuropathological hallmarks of Alzheimer's and Parkinson's diseases.
Resource type:
Article
Deposit Record:
http://windsor.libint.unc.edu:8181/fcrepo/rest/prod/f8/ca/d5/63/f8cad563-9b67-4053-a6f6-f544764d92b7
Type:
http://purl.org/dc/dcmitype/Text
DOI:
https://doi.org/10.17615/hz8k-zf86
Identifier:
PMID: 23986703, PMCID: PMC3749371, Publisher DOI: https://doi.org/10.3389/fphar.2013.00104, and Onescience id: d96ee0a3c153c92823dba208e3d52afe7e3d54b0
ISSN:
1663-9812
Journal Title:
Frontiers in Pharmacology
Journal Volume:
4
Keyword:
Amyloid, Cities, Air, Morbidity, Alzheimer’s and Parkinson’s disease risk, Endothelin-1, Brain, Cognition, Risk, Theobroma cacao, Fine Particulate Matter, Air Pollution, Children, Parkinson Disease, Inflammation, Biological Availability, Particulate Matter, Magnetic Resonance Spectroscopy, Therapeutics, Cocoa, Hippocampus, Flavonols, Plasma, Mortality, White Matter, and Homo sapiens
Language Label:
English
Person:
Zhu, Hongtu, Solorio, Edelmira, Medina-Cortina, Humberto, Chao, Chih-kai, Mora-Tiscareño, Antonieta, Cross, Janet V., D'Angiulli, Amedeo, Engle, Randall, Gómez-Garza, Gilberto, Mukherjee, Partha S., Torres-Jardón, Ricardo, Ferreira-Azevedo, Lara, Jewells, Valerie, Franco-Lira, Maricela, Calderón-Garcidueñas, Lilian, and Aragón-Flores, Mariana
Rights Statement Label:
In Copyright
Source:
3t945z13z