Relevant bibliographies by topics / Pathways metabolici

Academic literature on the topic 'Pathways metabolici'

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Published: 10 March 2023

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Journal articles on the topic "Pathways metabolici"

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Le Grazie, Giulia, Nicola Marrano, Annalisa Natalicchio, and Francesco Giorgino. "L’irisina: un ormone con benefici multiorgano." L'Endocrinologo 23, no. 2 (March 3, 2022): 189–92. http://dx.doi.org/10.1007/s40619-022-01046-z.

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SommarioL’irisina è una miochina secreta dal muscolo scheletrico in seguito ad attività fisica, in grado di regolare l’omeostasi glucidica ed energetica, agendo su numerosi tessuti e intervenendo su diversi pathways metabolici. Un’alterazione dei livelli sierici di irisina potrebbe promuovere l’insorgenza di patologie metaboliche, tra cui il diabete mellito di tipo 2. Numerosi studi su modelli animali di diabete e/o obesità hanno dimostrato che la somministrazione di irisina esogena è in grado di esercitare effetti antidiabetici e antiobesità.
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Šindelář, L., and M. Šindelářová. "Regulation of metabolic pathways PVY-RNA biosynthesis in tobacco: glycolytic pathway." Plant Protection Science 40, No. 3 (March 7, 2010): 101–6. http://dx.doi.org/10.17221/991-pps.

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Tobacco plants infected with potato virus <I>Y</I> were studied at the stage of acute infection. Key enzymes of the glycolytic pathway, their regulation and the content of involved intermediates were monitored. The activities of the key enzymes of the glycolytic pathway (6-phosphofructokinase, fructosebisphosphatase and pyruvate kinase), determined in both crude homogenates and after partial purification, did not differ from the activities found in healthy control tissues. In virus-infected tissues the content of ATP was higher than in the healthy control. The levels of ADP and AMP decreased soon after inoculation, but increased at the end of the experimental period. The content of inorganic phosphate was not influenced by infection. No difference in adenylate energy charge was observed between healthy and virus-infected tissues. This implies that the rates of the glycolytic pathway <I>in vivo </I>are not altered during the acute stage of infection.
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Giri, Shailendra, Poisson Laila, Hamid Suhail, Jaspreet Singh, Mandar Deshpande, Indrani Datta, Aleksandar Denic, Moses Rodriguez, Ramandeep Rattan, and Ashutosh Mangalam. "Nontargeted urinary metabolite profiling of a chronic mouse model of multiple sclerosis (THER3P.884)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 136.10. http://dx.doi.org/10.4049/jimmunol.192.supp.136.10.

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Abstract In search of metabolites signature as biomarkers during EAE disease, we profiled urine from B6 EAE using global untargeted metabolomics. Evaluation of metabolomic profiling of urine from EAE and healthy B6 group by using a combination of high-throughput liquid-and-gas chromatography with mass spectrometry, we found that 132 out of 322 (41%) metabolites were differentially altered (P&lt;0.05) indicating robust alteration in the urine metabolomics profile during disease. Among the perturbed metabolites, 11 were up regulated in EAE urine whereas 121 were down regulated. We conducted pathway analysis of the biochemical pathways of the KEGG and considered both concerted changes in metabolite intensity within the pathway (GlobalTest) and alterations of high impact, and found that a number of pathways were significantly altered including glyoxylate and dicarboxylate, phenylanine metabolism, porphyrin & chlorophyll metabolism, primary bile acid biosynthesis, cysteine & methione metabolism, taurine and hypotaurine metabolism, glycine, serine & threonine metabolism, and beta-alanine metabolism. Alteration in these pathways during EAE disease suggesting that perturbation of certain central metabolites could have impact on multiple metabolic pathways. While some of these metabolite changes could easily be developed as biomarkers, the key to translating metabolomics into therapeutics would require figuring out the central altered metabolic pathway(s), once studied in detail.
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Haj, Amelia K., Haytham Hasan, and Thomas J. Raife. "Heritability of Protein and Metabolite Biomarkers Associated with COVID-19 Severity: A Metabolomics and Proteomics Analysis." Biomolecules 13, no. 1 (December 27, 2022): 46. http://dx.doi.org/10.3390/biom13010046.

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Objectives: Prior studies have characterized protein and metabolite changes associated with SARS-CoV-2 infection; we hypothesized that these biomarkers may be part of heritable metabolic pathways in erythrocytes. Methods: Using a twin study of erythrocyte protein and metabolite levels, we describe the heritability of, and correlations among, previously identified biomarkers that correlate with COVID-19 severity. We used gene ontology and pathway enrichment analysis tools to identify pathways and biological processes enriched among these biomarkers. Results: Many COVID-19 biomarkers are highly heritable in erythrocytes. Among heritable metabolites downregulated in COVID-19, metabolites involved in amino acid metabolism and biosynthesis are enriched. Specific amino acid metabolism pathways (valine, leucine, and isoleucine biosynthesis; glycine, serine, and threonine metabolism; and arginine biosynthesis) are heritable in erythrocytes. Conclusions: Metabolic pathways downregulated in COVID-19, particularly amino acid biosynthesis and metabolism pathways, are heritable in erythrocytes. This finding suggests that a component of the variation in COVID-19 severity may be the result of phenotypic variation in heritable metabolic pathways; future studies will be necessary to determine whether individual variation in amino acid metabolism pathways correlates with heritable outcomes of COVID-19.
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Midford, Peter E., Mario Latendresse, Paul E. O’Maille, and Peter D. Karp. "Using Pathway Covering to Explore Connections among Metabolites." Metabolites 9, no. 5 (May 2, 2019): 88. http://dx.doi.org/10.3390/metabo9050088.

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Interpreting changes in metabolite abundance in response to experimental treatments or disease states remains a major challenge in metabolomics. Pathway Covering is a new algorithm that takes a list of metabolites (compounds) and determines a minimum-cost set of metabolic pathways in an organism that includes (covers) all the metabolites in the list. We used five functions for assigning costs to pathways, including assigning a constant for all pathways, which yields a solution with the smallest pathway count; two methods that penalize large pathways; one that prefers pathways based on the pathway’s assigned function, and one that loosely corresponds to metabolic flux. The pathway covering set computed by the algorithm can be displayed as a multi-pathway diagram (“pathway collage”) that highlights the covered metabolites. We investigated the pathway covering algorithm by using several datasets from the Metabolomics Workbench. The algorithm is best applied to a list of metabolites with significant statistics and fold-changes with a specified direction of change for each metabolite. The pathway covering algorithm is now available within the Pathway Tools software and BioCyc website.
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Brister, Danielle, Brianna A. Werner, Geoffrey Gideon, Patrick J. McCarty, Alison Lane, Brian T. Burrows, Sallie McLees, et al. "Central Nervous System Metabolism in Autism, Epilepsy and Developmental Delays: A Cerebrospinal Fluid Analysis." Metabolites 12, no. 5 (April 20, 2022): 371. http://dx.doi.org/10.3390/metabo12050371.

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Neurodevelopmental disorders are associated with metabolic pathway imbalances; however, most metabolic measurements are made peripherally, leaving central metabolic disturbances under-investigated. Cerebrospinal fluid obtained intraoperatively from children with autism spectrum disorder (ASD, n = 34), developmental delays (DD, n = 20), and those without known DD/ASD (n = 34) was analyzed using large-scale targeted mass spectrometry. Eighteen also had epilepsy (EPI). Metabolites significantly related to ASD, DD and EPI were identified by linear models and entered into metabolite–metabolite network pathway analysis. Common disrupted pathways were analyzed for each group of interest. Central metabolites most involved in metabolic pathways were L-cysteine, adenine, and dodecanoic acid for ASD; nicotinamide adenine dinucleotide phosphate, L-aspartic acid, and glycine for EPI; and adenosine triphosphate, L-glutamine, ornithine, L-arginine, L-lysine, citrulline, and L-homoserine for DD. Amino acid and energy metabolism pathways were most disrupted in all disorders, but the source of the disruption was different for each disorder. Disruption in vitamin and one-carbon metabolism was associated with DD and EPI, lipid pathway disruption was associated with EPI and redox metabolism disruption was related to ASD. Two microbiome metabolites were also detected in the CSF: shikimic and cis-cis-muconic acid. Overall, this study provides increased insight into unique metabolic disruptions in distinct but overlapping neurodevelopmental disorders.
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Ahmed, Eman A., Marwa O. El-Derany, Ali Mostafa Anwar, Essa M. Saied, and Sameh Magdeldin. "Metabolomics and Lipidomics Screening Reveal Reprogrammed Signaling Pathways toward Cancer Development in Non-Alcoholic Steatohepatitis." International Journal of Molecular Sciences 24, no. 1 (December 22, 2022): 210. http://dx.doi.org/10.3390/ijms24010210.

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With the rising incidence of hepatocellular carcinoma (HCC) from non-alcoholic steatohepatitis (NASH), identifying new metabolic readouts that function in metabolic pathway perpetuation is still a demand. The study aimed to compare the metabolic signature between NASH and NASH-HCC patients to explore novel reprogrammed metabolic pathways that might modulate cancer progression in NASH patients. NASH and NASH-HCC patients were recruited and screened for metabolomics, and isotope-labeled lipidomics were targeted and profiled using the EXION-LCTM system equipped with a Triple-TOFTM 5600+ system. Results demonstrated significantly (p ≤ 0.05) higher levels of triacylglycerol, AFP, AST, and cancer antigen 19-9 in NASH-HCC than in NASH patients, while prothrombin time, platelet count, and total leukocyte count were decreased significantly (p ≤ 0.05). Serum metabolic profiling showed a panel of twenty metabolites with 10% FDR and p ≤ 0.05 in both targeted and non-targeted analysis that could segregate NASH-HCC from NASH patients. Pathway analysis revealed that the metabolites are implicated in the down-regulation of necroptosis, amino acid metabolism, and regulation of lipid metabolism by PPAR-α, biogenic amine synthesis, fatty acid metabolism, and the mTOR signaling pathway. Cholesterol metabolism, DNA repair, methylation pathway, bile acid, and salts metabolism were significantly upregulated in NASH-HCC compared to the NASH group. Metabolite–protein interactions network analysis clarified a set of well-known protein encoding genes that play crucial roles in cancer, including PEMT, IL4I1, BAAT, TAT, CDKAL1, NNMT, PNP, NOS1, and AHCYL. Taken together, reliable metabolite fingerprints are presented and illustrated in a detailed map for the most predominant reprogrammed metabolic pathways that target HCC development from NASH.
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Lin, Xiangping, Xinyu Liu, Mohamed N. Triba, Nadia Bouchemal, Zhicheng Liu, Douglas I. Walker, Tony Palama, et al. "Plasma Metabolomic and Lipidomic Profiling of Metabolic Dysfunction-Associated Fatty Liver Disease in Humans Using an Untargeted Multiplatform Approach." Metabolites 12, no. 11 (November 8, 2022): 1081. http://dx.doi.org/10.3390/metabo12111081.

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Metabolic dysfunction-associated fatty liver disease (MAFLD) is a complex disorder that is implicated in dysregulations in multiple biological pathways, orchestrated by interactions between genetic predisposition, metabolic syndromes and environmental factors. The limited knowledge of its pathogenesis is one of the bottlenecks in the development of prognostic and therapeutic options for MAFLD. Moreover, the extent to which metabolic pathways are altered due to ongoing hepatic steatosis, inflammation and fibrosis and subsequent liver damage remains unclear. To uncover potential MAFLD pathogenesis in humans, we employed an untargeted nuclear magnetic resonance (NMR) spectroscopy- and high-resolution mass spectrometry (HRMS)-based multiplatform approach combined with a computational multiblock omics framework to characterize the plasma metabolomes and lipidomes of obese patients without (n = 19) or with liver biopsy confirmed MAFLD (n = 63). Metabolite features associated with MAFLD were identified using a metabolome-wide association study pipeline that tested for the relationships between feature responses and MAFLD. A metabolic pathway enrichment analysis revealed 16 pathways associated with MAFLD and highlighted pathway changes, including amino acid metabolism, bile acid metabolism, carnitine shuttle, fatty acid metabolism, glycerophospholipid metabolism, arachidonic acid metabolism and steroid metabolism. These results suggested that there were alterations in energy metabolism, specifically amino acid and lipid metabolism, and pointed to the pathways being implicated in alerted liver function, mitochondrial dysfunctions and immune system disorders, which have previously been linked to MAFLD in human and animal studies. Together, this study revealed specific metabolic alterations associated with MAFLD and supported the idea that MAFLD is fundamentally a metabolism-related disorder, thereby providing new perspectives for diagnostic and therapeutic strategies.
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Thurley, Kevin, Christopher Herbst, Felix Wesener, Barbara Koller, Thomas Wallach, Bert Maier, Achim Kramer, and Pål O. Westermark. "Principles for circadian orchestration of metabolic pathways." Proceedings of the National Academy of Sciences 114, no. 7 (February 3, 2017): 1572–77. http://dx.doi.org/10.1073/pnas.1613103114.

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Circadian rhythms govern multiple aspects of animal metabolism. Transcriptome-, proteome- and metabolome-wide measurements have revealed widespread circadian rhythms in metabolism governed by a cellular genetic oscillator, the circadian core clock. However, it remains unclear if and under which conditions transcriptional rhythms cause rhythms in particular metabolites and metabolic fluxes. Here, we analyzed the circadian orchestration of metabolic pathways by direct measurement of enzyme activities, analysis of transcriptome data, and developing a theoretical method called circadian response analysis. Contrary to a common assumption, we found that pronounced rhythms in metabolic pathways are often favored by separation rather than alignment in the times of peak activity of key enzymes. This property holds true for a set of metabolic pathway motifs (e.g., linear chains and branching points) and also under the conditions of fast kinetics typical for metabolic reactions. By circadian response analysis of pathway motifs, we determined exact timing separation constraints on rhythmic enzyme activities that allow for substantial rhythms in pathway flux and metabolite concentrations. Direct measurements of circadian enzyme activities in mouse skeletal muscle confirmed that such timing separation occurs in vivo.
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VILLAS-BÔAS, Silas G., Joel F. MOXLEY, Mats ÅKESSON, Gregory STEPHANOPOULOS, and Jens NIELSEN. "High-throughput metabolic state analysis: the missing link in integrated functional genomics of yeasts." Biochemical Journal 388, no. 2 (May 24, 2005): 669–77. http://dx.doi.org/10.1042/bj20041162.

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The lack of comparable metabolic state assays severely limits understanding the metabolic changes caused by genetic or environmental perturbations. The present study reports the application of a novel derivatization method for metabolome analysis of yeast, coupled to data-mining software that achieve comparable throughput, effort and cost compared with DNA arrays. Our sample workup method enables simultaneous metabolite measurements throughout central carbon metabolism and amino acid biosynthesis, using a standard GC-MS platform that was optimized for this purpose. As an implementation proof-of-concept, we assayed metabolite levels in two yeast strains and two different environmental conditions in the context of metabolic pathway reconstruction. We demonstrate that these differential metabolite level data distinguish among sample types, such as typical metabolic fingerprinting or footprinting. More importantly, we demonstrate that this differential metabolite level data provides insight into specific metabolic pathways and lays the groundwork for integrated transcription–metabolism studies of yeasts.
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Dissertations / Theses on the topic "Pathways metabolici"

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De, Rosa Maria Caterina. "Studio dell’espressione di geni coinvolti in pathways metabolici regolati da nutrienti." Doctoral thesis, Universita degli studi di Salerno, 2015. http://hdl.handle.net/10556/1864.

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2014-2015
Il profilo sierico, con particolare riferimento ai livelli di biomarkers, rappresenta uno strumento efficace ed affidabile per la diagnosi di malattie metaboliche, come il diabete o le malattie cardiovascolari. La composizione del siero è influenzata sia dal metabolismo endogeno che dall’apporto nutrizionale. In effetti, lo stile alimentare, con particolare riferimento alla qualità e alla quantità dell’apporto nutrizionale, può fortemente influenzare il rischio e la progressione di malattia, poiché alcuni nutrienti agiscono come composti bioattivi. A questo proposito, la letteratura attuale indica un importante ruolo di specifiche molecole nutrizionali provenienti dalla dieta che interessano specifiche vie metaboliche. L'obiettivo del nostro progetto è quello di individuare pathways metabolici regolati da nutrienti, con lo scopo di identificare possibili taget terapeutici in stati patologici. [ a cura dell'autore]
XIII n.s.
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Gupta, Apoorv. "Dynamic regulation of bacterial metabolic pathways using autonomous, pathway-independent control strategies." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/112511.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 86-91).
Metabolic engineering efforts have so far focused on strain optimization through careful metabolic modeling and tinkering with host genomes, through gene knockouts or knockins, to direct flux in desired channels. These efforts have borne fruit with the development of large manufacturing processes for numerous chemicals. The next challenge for metabolic engineering, however, lies in tackling issues associated with construction of more complex pathways, such as those that directly interfere with host metabolism, have branchpoints with promiscuous enzymes, or synthesize toxic intermediates or products. Dynamic metabolic engineering has emerged as a new frontier for tool development to allow regulation and control of native and cellular pathways during the course of a production run. Advantages in dynamic strategies are especially apparent in the aforementioned examples where traditional static strategies of gene knockouts or knockins are not an option. Instead, it is necessary to be able to control when certain genes are expressed, such as to build biomass before switching on growth-limiting production pathways, or accumulating intermediates to drive the reaction of a promiscuous enzyme along a certain branch. In this thesis, we propose enzyme control strategies that are independent of any biosynthetic pathway of interest. Therefore, they can theoretically be applied to a wide variety of contexts in a "plug-and-play" fashion to control pathway enzyme expression. After initial work to understand the limitations of nutrient starvation strategies to induce genetic circuits, we decided to use quorum sensing circuitry to create circuits that can be autonomously induced. We used parts of the Esa QS system (derived from Pantoea stewartii) to create circuit variants in the Lscherichia cohi genome, which switch off expression of the targeted gene at various times and cell densities. Switching times were varied by modulating the expression of the AHL synthase, and therefore the production rate of AHL, the quorum sensing molecule. Switching dynamics were characterized and ranked for the entire library of circuit variants using fluorescent reporters. The characterized device was used to identify optimal switching times for redirection of glycolytic fluxes into heterologous pathways, resulting in a 5.5-fold boost in myo-inositol (MI) and increasing glucaric acid titers from unmeasurable quantities up to >0.8 g/L. With a focus on industrial application, consistency of device performance was verified in benchtop bioreactors, achieving nearly 10-fold and 5-fold boosts in specific titers of myoinositol and glucaric acid, respectively. To demonstrate broad utility and "off-the-shelf" applicability, the control module was applied to dynamic downregulation of flux into aromatic amino acid biosynthesis to accumulate the industrially-relevant intermediate, shikimate, resulting in an increase in titers from unmeasurable quantities to >100 mg/L. Finally, this QS device was coupled with a MI-biosensor circuit to institute two layers of dynamic regulation and further improve glucaric acid titers. Production trials in these composite strains resulted in the highest glucaric titers (-2 g/L) reported to date from E. coli K-strains. This work reports the first completely autonomous dynamic regulation module and its application in bioproduction of multiple products from different metabolic pathways. We envision that the strategy presented here may be adapted to any pathway context and gene of interest. With increased prevalence of dynamic regulation, the relevant strategies may become standardized for general use.
by Apoorv Gupta.
Ph. D.
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Lisowska, Beata. "Genomic analysis and metabolic modelling of Geobacillus thermoglucosidasius NCIMB 11955." Thesis, University of Bath, 2016. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.690738.

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Geobacillus thermoglucosidasius is a Gram-positive thermophilic eubacterium (45-70‰) that has the ability to convert pre-treated lignocellulosic material LCM into ethanol. This organism has been genetically engineered such that its yield of ethanol production is in excess of 90% of the theoretical maximum [38]. There remains considerable scope to develop G.thermoglucosidasius to produce alternative fuels and chemicals of industrial importance. For such a useful bacterium the understanding of the global metabolism remains poorly characterised. To gain a better insight into the metabolic pathways and capabilities of G. thermoglucosidasius a bottom-up approach to construct a comprehensive metabolic model of the organism was applied. The model was build from manually annotated genome and incorporates data from wet lab experiments for accurate in silico analyses. The model simulations has highlighted a potential experimental design for the in silico production of succinate and butane-2,3-diol. PathwayBooster is also introduced in this study as a tool for curating metabolic pathways. The methodology is based on the assumption that the core metabolic capabilities are shared among evolutionarily closely related species [80]. This approach led to the further analysis of members of the genus Geobacillus with respect to their core metabolic capabilities, genome re-arrangements and shared unique features. Theoretical route for the biosynthesis of Vitamin B12 is presented here, which is novel to the canonical aerobic and anaerobic pathways known to date and ubiquitous amongst Geobacillus spp. The analysis of the gene assignment for this bacterium has highlighted the presence of NADP-dependent GAPDH. The theoretical function of this novel and previously uncategorised enzyme in the genus Geobacillus has been confirmed through enzymatic assays.
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Leung, Shuen-yi, and 梁舜頤. "Predicting metabolic pathways from metabolic networks." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B42664317.

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Leung, Shuen-yi. "Predicting metabolic pathways from metabolic networks." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B42664317.

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Edwards-Hicks, Joy. "Metabolic remodelling driven by MYC overexpression regulates the p53 tumour suppressor response." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31223.

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The MYC onocogene is frequently overexpressed in human cancer due to its capacity to promote cell growth and cell proliferation. MYC overexpression activates the p53 tumour suppressor pathway, which resists the pro-tumourigeneic program elicited by MYC. How MYC overexpression engages p53 is yet to be elucidated, and in this study I carried out a large metabolic siRNA screen to determine whether p53 responds to a specific MYC-driven metabolic pathway. Two clear lipid metabolic pathways emerged from the siRNA screen: PPARγ/arachidonate metabolism and de novo sphingolipid synthesis. Knockdown or inhibition of PPARγ increased p53 levels, and PPARγ ligands decreased following MYC overexpression. Knockdown of ceramide synthesis depleted p53 levels, and MYC overexpression increased de novo ceramide synthesis. This demonstrated that MYC-driven ceramide synthesis positively regulates p53, and highlights the role of cell metabolism in the tumour suppressor response to MYC deregulation.
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Zumbaugh, Morgan Daughtry. "Signaling pathways regulating skeletal muscle metabolism and growth." Diss., Virginia Tech, 2021. http://hdl.handle.net/10919/101750.

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Skeletal muscle can perceive cellular energy status and substrate availability and demonstrates remarkable plasticity in response to environmental changes. Nonetheless, how skeletal muscle and its resident stem cells (satellite cells; SCs) sense and respond to nutrient flux remains largely undefined. The dynamic post-translational modification O-GlcNAcylation has been shown to serve as a cellular nutrient sensor in a wide range of cells and tissues, yet its role in skeletal muscle and SCs remains unexplored. Here, we ablated skeletal muscle O-GlcNAc transferase (OGT), and thus O-GlcNAcylation, and found the knockout mice exhibited enhanced glucose uptake, insulin sensitivity, and resistance to high-fat diet induced obesity. Additionally, mKO mice had a 3-fold increase in circulating levels of interleukin-15 (IL-15), a potent anti-obesity cytokine, potentially through epigenetic regulation of Il15 by OGT. To further investigate if there was a causal relationship between OGT ablation and the lean phenotype, we generated muscle specific OGT and interleukin-15 receptor alpha (IL-15ra) double knockout mice (mDKO). As a result, mDKO mice had blunted IL-15 secretion and minimal protection against HFD-induced obesity. Together, these data indicate the skeletal muscle OGT-IL15 axis plays an essential role in the maintenance of skeletal muscle and whole-body metabolic homeostasis. As satellite cells (SCs) play an indispensable role in postnatal muscle growth and adult regenerative myogenesis, we investigated the role of O-GlcNAcylation in SC function. To this end, we conditionally ablated OGT in SCs (cKO) and found cKO mice had impaired SC proliferation, in vivo cycling properties, population stability, metabolic regulation, and adult regenerative myogenesis. Together these findings show that SCs require O-GlcNAcylation, presumably to gauge nutritional signals, for proper function and metabolic homeostasis. Another critical yet often neglected player in myogenesis are mitochondria. Traditionally depicted as a power plant in cells, mitochondria are critical for numerous nonconventional, energy-independent cellular process. To investigate the role of both mitochondrial energy production and alternative mitochondrial functions in myogenic regulation, we ablated ATP synthase subunit beta (ATP5b) and ubiquinol-cytochrome c reductase (UQCRFS1) in C2C12 myoblasts to disrupt mitochondrial ATP production and mitochondrial membrane potential, respectively. Ablation of UQCRFS1, but not ATP5b, impaired myoblast proliferation, although lack of either gene compromised myoblast fusion. Interestingly, addition of the potent myogenic stimulator IGF-1 rescued ATP5b fusion but could not override UQCRFS1 knockout effects on proliferation or differentiation. These data demonstrate mitochondrial ATP production is not the "metabolic switch" that governs myogenic progression but rather an alternative mitochondrial function. In summary, skeletal muscle and their resident stem cell population (SCs) both use O-GlcNAcylation, feasibly to sense and respond to nutritional cues, for the maintenance of metabolic homeostasis and normal physiology. A deeper understand of both muscle and SC metabolic regulation may provide therapeutic targets to improve global metabolism and muscle growth.
Doctor of Philosophy
Skeletal muscle is responsible for approximately 20% of basal energy expenditure and 70-90% of insulin-mediated glucose disposal, and as such changes in skeletal muscle metabolism and insulin sensitivity have profound impacts on whole body metabolism. Skeletal muscle is a plastic tissue that can perceive nutrient availability, which permits metabolic adaptations to environmental changes. Deletion of the nutrient sensing pathway O-GlcNAcylation in skeletal muscle (mKO) protected mice from high-fat diet induced obesity and ameliorates whole-body insulin sensitivity. Skeletal muscle can secrete myokines to elicit endocrine effects on other tissues in the body, and as such, we proposed perturbation of this nutrient sensing pathway in skeletal muscle alters myokine secretion to elicit responses in other metabolically active tissues to support its energy requirements. Indeed, circulating levels of interleukin-15, a potent anti-obesity myokine, increased 3-fold in mKO mice. To determine the contribution of IL-15 to the mKO phenotype, we used a genetic approach to blunt IL-15 secretion from skeletal muscle (mDKO), which partially negated the lean mKO phenotype. Our findings show the ability of skeletal muscle to "sense" changes in nutrients through O-GlcNAcylation is necessary for proper muscle and whole-body metabolism. Moreover, this nutrient sensing mechanism is also important for proper muscle stem cell function, also known as satellite cells (SCs). Loss of O-GlcNAcylation in SCs impairs their ability to regenerate muscle after injury, which can be attributed to a reduced capacity to proliferate and an inability to maintain a healthy SC population. Interestingly, SCs lacking O-GlcNAcylation have a greater mitochondrial content. Using a myoblast cell line, we investigated the contribution of mitochondria to myogenesis, the formation of muscle, and found mitochondrial energy production is dispensable in the myogenic process. Our studies show skeletal muscle and SCs rely on highly integrated signaling cascades that sense and respond to intrinsic metabolic changes and extrinsic nutritional cues to function properly.
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McArthur, George Howard IV. "Orthogonal Expression of Metabolic Pathways." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/3087.

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Microbial metabolism can be tailored to meet human specifications, but the degree to which these living systems can be repurposed is still unknown. Artificial biological control strategies are being developed with the goal of enabling the predictable implementation of novel biological functions (e.g., engineered metabolism). This dissertation project contributes genetic tools useful for modulating gene expression levels (extending promoters with UP elements) and isolating transcription and translation of engineered DNA from the endogenous cellular network (expression by orthogonal cellular machinery), which have been demonstrated in Escherichia coli for the production of lycopene, a 40-carbon tetraterpene carotenoid with antioxidant activity and a number of other desirable properties.
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Bhargava, Prerna. "Immunomodulatory Pathways and Metabolism." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10696.

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Energy metabolism plays a vital role in normal physiology, adaptive responses and host defense mechanisms. Research throughout the last decade has shown evidence that immune pathways communicate with metabolic pathways to alter the metabolic status in response to physiological or pathological signals. In this thesis, I will explore how immunomodulatory molecules affect metabolic homeostasis and conversely, how metabolic sensing pathways modulate immune responses. The first part my work utilizes an immunomodulatory sugar motif to determine mechanisms by which immune cells influence metabolism. Specifically, I show in chapter 2 that lacto-N-fucopentaose III (LNFPIII), a motif used by pathogens to attenuate inflammation, is capable of improving systemic insulin sensitivity by increasing Il-10 production in macrophages and dendritic cells and subsequently improving white adipose tissue insulin sensitivity. Chapter 3 will address the observation that this same glycan is capable of directly activating Fxra in hepatocytes. This direct effect manifests as a reduction in high-fat-diet-induced hepatic triglyceride accumulation and improvement in liver function. Lastly, in chapter 4, I will discuss the role of metabolic regulators in the macrophage and how this affects the ability of the macrophage to kill bacteria. Specifically, I will show that lipid sensing nuclear receptors, such as Ppard and Pparg, are critical regulators of phagosomal function and bacterial killing. Macrophage-specific deletion of these receptors prevents efficient killing of Streptococcus pneumoniae, the causative bacterium in many cases of respiratory pneumonia. Ligand activation improves survival, suggesting a potential therapeutic role for Ppar activation during infection. Taken together, all the data suggest a critical role for the evolutionary interaction between metabolic and immune pathways. These interactions may be important when developing new therapeutics for complex metabolic and immunological dysfunctions.
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Johnston, Hannah. "The role of lipid metabolism in melanoma and identifying therapeutic targets in lipid metabolic pathways." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/the-role-of-lipid-metabolism-in-melanoma-and-identifying-therapeutic-targets-in-lipid-metabolic-pathways(44800322-0da3-4056-bc19-b947058ff203).html.

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There have been dramatic advances in melanoma therapy in the last 10 years, yet there is still a demand for effective and affordable therapies. To identify novel therapeutic pathways a transcriptome analysis was performed on zebrafish melanoma models representing the different stages of melanoma progression. Transcriptomic differences between pre-malignant and malignant conditions highlighted lipid metabolism as a potential mediator of progression. A mass spectrometry analysis confirmed multiple changes in lipid composition between wild type fish, pre-malignant and advanced melanoma models. To better investigate metabolism a positron emission tomography (PET) technique was developed in zebrafish. Tumours in the zebrafish were successfully scanned with FDG used to detect human tumours. A novel tracer of unconjugated FA was then developed and, consistent with inferences from the transcriptome and mass spectrometry, was shown to be incorporated into tumours. Demonstrating the feasibility of PET in zebrafish now opens the way to systematic use of this organism in tracer development with potential time-saving and cost benefits. One of the most significantly up-regulated genes exclusive to the malignant state encodes lipoprotein lipase (LPL). LPL is involved in the release and uptake of FA from circulating triglyceride. LPL was found to increase the rate of tumour appearance and tumour growth in a zebrafish tumour assay. LPL was expressed in human tumours and expression correlated with progression. Melanoma cell lines expressed LPL and knocking-down LPL resulted in reduced cell numbers. The effect was most dramatic in WM852 cells. A novel role for LPL in autophagy was identified. WM852 cells treated with LPL siRNA showed a stabilisation of p62/SQSTM and induction of LC3B II. Electron microscopy revealed large autolysosomal vacuoles in the cytoplasm. Additionally many cells showed damaged mitochondria with absent cristae. The dependency of cells on LPL seemed to be modified by the co-expression of fatty acid synthase (FASN) required for de novo FA synthesis, as the magnitude of the effect of LPL-knockdown was dependent on the levels of FASN expressed in melanoma cell lines. Moreover, combining LPL and FASN inhibitors synergised to kill cells previously less sensitive to LPL inhibitor. FASN and LPL co-inhibition could provide a unique combinatorial therapeutic strategy.
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Books on the topic "Pathways metabolici"

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Jensen, Michael Krogh, and Jay D. Keasling, eds. Synthetic Metabolic Pathways. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7295-1.

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1943-, Roberts T. R., Hutson D. H. 1935-, and Royal Society of Chemistry (Great Britain). Information Services., eds. Metabolic pathways of agrochemicals. Cambridge: Royal Society of Chemistry, 1998.

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Roberts, Terry R., David H. Hutson, Philip W. Lee, Peter H. Nicholls, and Jack R. Plimmer, eds. Metabolic Pathways of Agrochemicals. Cambridge: Royal Society of Chemistry, 2007. http://dx.doi.org/10.1039/9781847551375.

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Roberts, Terry R., David H. Hutson, Philip W. Lee, Peter H. Nicholls, and Jack R. Plimmer, eds. Metabolic Pathways of Agrochemicals. Cambridge: Royal Society of Chemistry, 2007. http://dx.doi.org/10.1039/9781847551382.

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Wang, Xiaoyuan, Jian Chen, and Peter Quinn, eds. Reprogramming Microbial Metabolic Pathways. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5055-5.

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Himmel, Michael E., and Yannick J. Bomble, eds. Metabolic Pathway Engineering. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0195-2.

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Carbonell, Pablo. Metabolic Pathway Design. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-29865-4.

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Waring, Rosemary. Pathways in drug metabolism. Birmingham: University of Birmingham, 1992.

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Wolfinbarger, Lloyd. Enzyme Regulation in Metabolic Pathways. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2017. http://dx.doi.org/10.1002/9781119155423.

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Lee, Philip W. Handbook of metabolic pathways of xenobiotics. Chichester, West Sussex: John Wiley & Sons Inc., 2014.

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Book chapters on the topic "Pathways metabolici"

1

Slenter, Denise N., Martina Kutmon, and Egon L. Willighagen. "WikiPathways: Integrating Pathway Knowledge with Clinical Data." In Physician's Guide to the Diagnosis, Treatment, and Follow-Up of Inherited Metabolic Diseases, 1457–66. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-67727-5_73.

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SummaryThroughout the chapters in this book, pathways are used to visualize how genetically inheritable metabolic disorders are related. These pathways provide common conceptual models which explain groups of chemical reactions within their biological context. Visual representations of the reactions in biological pathway diagrams provide intuitive ways to study the complex metabolic processes. In order to link (clinical) data to these pathways, they have to be understood by computers. Understanding how to move from a regular pathway drawing to its machine-readable counterpart is pertinent for creating proper models. This chapter outlines the various aspects of the digital counterparts of the pathway diagrams in this book, connecting them to databases and using them in data integration and analysis. This is followed by three examples of bioinformatics applications including a pathway enrichment analysis, a biological network extension, and a final example that integrates pathways with clinical biomarker data.
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Li, Ting, Christopher Copeland, and Anne Le. "Glutamine Metabolism in Cancer." In The Heterogeneity of Cancer Metabolism, 17–38. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_2.

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AbstractMetabolism is a fundamental process for all cellular functions. For decades, there has been growing evidence of a relationship between metabolism and malignant cell proliferation. Unlike normal differentiated cells, cancer cells have reprogrammed metabolism in order to fulfill their energy requirements. These cells display crucial modifications in many metabolic pathways, such as glycolysis and glutaminolysis, which include the tricarboxylic acid (TCA) cycle, the electron transport chain (ETC), and the pentose phosphate pathway (PPP) [1]. Since the discovery of the Warburg effect, it has been shown that the metabolism of cancer cells plays a critical role in cancer survival and growth. More recent research suggests that the involvement of glutamine in cancer metabolism is more significant than previously thought. Glutamine, a nonessential amino acid with both amine and amide functional groups, is the most abundant amino acid circulating in the bloodstream [2]. This chapter discusses the characteristic features of glutamine metabolism in cancers and the therapeutic options to target glutamine metabolism for cancer treatment.
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Paro, Renato, Ueli Grossniklaus, Raffaella Santoro, and Anton Wutz. "Epigenetics and Metabolism." In Introduction to Epigenetics, 179–201. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-68670-3_9.

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AbstractMost chromatin-modifying enzymes use metabolites as cofactors. Consequently, the cellular metabolism can influence the capacity of the cell to write or erase chromatin marks. This points to an intimate relationship between metabolic and epigenetic regulation. In this chapter, we describe the biosynthetic pathways of cofactors that are implicated in epigenetic and chromatin regulation and provide examples of how metabolic pathways can influence chromatin and epigenetic processes as well as their interplay in developmental and cancer biology.
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Mal, Chittabrata, Ayushman Kumar Banerjee, and Joyabrata Mal. "Genome Scale Pathway-Pathway Co-functional Synergistic Network (PcFSN) in Oryza Sativa." In Proceedings of the Conference BioSangam 2022: Emerging Trends in Biotechnology (BIOSANGAM 2022), 47–57. Dordrecht: Atlantis Press International BV, 2022. http://dx.doi.org/10.2991/978-94-6463-020-6_6.

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AbstractCohesive network modelling and systems biology have emerged as extremely potent tools which helps understanding the combinatorial effects of biomolecules. Synergistic modulation among biomolecules (e.g., enzymes, transcription factors, microRNAs, drugs, etc.) are significant in finding out complex regulatory mechanisms in biological networks and pathways. In some cases, although combinatorial interactions among some biomolecules in specific biological networks is available, our knowledge in that particular domain is very limited with context to a genomic scale. Here we explore the pathway-pathway network to identify and understand the network architecture of metabolic pathway mediated regulations at genomic and co-functional levels, in rice. Using network transformation methods, a genome scale pathway-pathway co-functional synergistic network (PcFSN) was constructed. Finally, the PcFSN modules are extracted. This in turn helps to identify the miRNAs and genes associated with the pathways, especially linked to the central metabolic network in rice.
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Speedie, Marilyn K., James J. Zulty, Bonnie M. Fox, and Kimberlee K. Wallace. "Methylation Pathways in Antibiotic Producing Streptomycetes." In Secondary-Metabolite Biosynthesis and Metabolism, 61–76. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3012-1_5.

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Wünschiers, Röbbe, Martina Jahn, Dieter Jahn, Ida Schomburg, Susanne Peifer, Elmar Heinzle, Helmut Burtscher, et al. "Metabolism." In Biochemical Pathways, 37–209. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2013. http://dx.doi.org/10.1002/9781118657072.ch3.

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Gooch, Jan W. "Metabolic Pathway." In Encyclopedic Dictionary of Polymers, 907. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_14204.

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Floss, H. G., H. Cho, R. Casati, K. A. Reynolds, E. Kennedy, B. S. Moore, J. M. Beale, U. M. Mocek, and K. Poralla. "Diversions of the Shikimate Pathway — The Biosynthesis of Cyclohexanecarboxylic Acid." In Secondary-Metabolite Biosynthesis and Metabolism, 77–88. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3012-1_6.

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Carbonell, Pablo. "Pathway Modeling." In Metabolic Pathway Design, 27–44. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-29865-4_3.

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Carbonell, Pablo. "Pathway Discovery." In Metabolic Pathway Design, 83–97. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-29865-4_6.

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Conference papers on the topic "Pathways metabolici"

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Inoue, Katsumi, Andrei Doncescu, Gabriel Synaeve, and Nabil Kabbak. "Main Pathway Discovery in Metabolic Pathways." In 2010 IEEE 24th International Conference on Advanced Information Networking and Applications Workshops. IEEE, 2010. http://dx.doi.org/10.1109/waina.2010.88.

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El-fadl, Rihab, Nasser Rizk, Amena Fadel, and Abdelrahman El Gamal. "The Profile of Hepatic Gene Expression of Glucose Metabolism in Mice on High Fat Diet." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0213.

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Obesity is a growing problem worldwide, and recent data indicated that 20% of the populations would be obese. Obesity arises as a multifactorial disease caused by inherited traits that interact with lifestyle factors such as diet and physical activity. The liver plays an essential role in the gluco-regulation via regulating glucose, lipid and protein metabolism. The process of glucose metabolism is controlled by a range of molecular mechanisms and genes which affect the metabolism of the liver during intake of high fat diet (HFD). The objective of this research is to investigate the profile of hepatic gene expression of glucose metabolism in mice on HFD treated with leptin (5 mg/kg BW Ip injection). Ten wild type CD1 mice fed on HFD is used for this study, where groups are control (vehicle - leptin) and test group (vehicle + leptin). Body weight (BW) was measured, and blood chemistry, insulin and leptin were measured at the end of the experiments. Total RNA was isolated from the liver tissue, and RTPCR profiler array technology was used to evaluate the mRNA expression of 84 essential genes of hepatic glucose metabolism. The data of the BW and blood chemistry are not significantly different between the two groups. Leptin treatment enhanced the metabolic pathways and the candidate genes of the different metabolic pathway; glycogen metabolism such as Gys1, Gys2 and Pygm, pentose phosphate shunt such as Rpia and suppressed the glycolysis such as Aldob, and TCA cycle such as Mdh1b. In conclusion, this study has shown that leptin could affect the profile of the hepatic mouse genes of glucose metabolism in the early stages of HFD to induce obesity
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Kamareddine, Layla, Hoda Najjar, Abeer Mohbeddin, Nawar Haj Ahmed, and Paula Watnick. "Between Immunity, Metabolism, and Development: A story of a Fly Gut!" In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0141.

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In addition to its role in initiating immune response in the body, the innate immune system seems to also play a critical role in maintaining homeostatic balance in the gut epithelium. Our recent studies in the Drosophila melanogaster fruit fly model suggest that different innate immune pathways contribute to this homeostatic balance through activating the transcription of genes encoding antimicrobial peptides. We provide evidence that several metabolic parameters are altered in immune deficient flies. We also highlight a role of the gut flora, particularly through its short chain fatty acid, in contributing to this metabolic balance. Interestingly, our data suggest that impaired immunity and metabolic alteration, in turn, exhibit an effect on host development. Collectively, these findings provide evidence that innate immune pathways not only provide the first line of defense against infection but also contribute to host metabolism and development.
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Yuan, Tai-Yi, Hanan N. Fernando, Jessica Czamanski, Chong Wang, Wei Yong Gu, and Chun-Yuh Huang. "Effects of Static Compression on Energy Metabolism of Porcine Intervertebral Disc." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19600.

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Degeneration of the intervertebral disc (IVD) has been associated with low back pain, which is one of the major socio-economic problems in the United States. Since IVD is the largest avascular cartilaginous structure in the human body, poor nutrient supply has been suggested as a potential mechanism for IVD degeneration. Biosynthesis of extracellular matrix is an energy demanding process which is required to maintain tissue integrity [1]. Cells consume glucose and oxygen to produce adenosine triphosphate (ATP), the main energy form in cells. Glycolysis, the primary metabolic pathway for production of ATP in IVD cells, is strongly regulated by local oxygen concentration and pH (which is governed by lactate concentration) [2]. Therefore, energy metabolism may play an important role in the malnutrition pathway leading to IVD degeneration. The objective of this study was to investigate the effect of mechanical loading on cellular energy metabolism in whole disc and in agarose gels.
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Pireddu, L., B. Poulin, D. Szafron, P. Lu, and D. S. Wishart. "Pathway Analyst Automated Metabolic Pathway Prediction." In 2005 IEEE Symposium on Computational Intelligence in Bioinformatics and Computational Biology. IEEE, 2005. http://dx.doi.org/10.1109/cibcb.2005.1594924.

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Akella, Sridevi, and Chanchal K. Mitra. "Metabolic pathways as electronic circuits." In 2011 6th International Symposium on Health Informatics and Bioinformatics (HIBIT). IEEE, 2011. http://dx.doi.org/10.1109/hibit.2011.6450815.

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Umeton, Renato, Giovanni Stracquadanio, Anilkumar Sorathiya, Pietro Liò, Alessio Papini, and Giuseppe Nicosia. "Design of robust metabolic pathways." In the 48th Design Automation Conference. New York, New York, USA: ACM Press, 2011. http://dx.doi.org/10.1145/2024724.2024892.

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"METABOLIC MODELING OF CONVERGING METABOLIC PATHWAYS - Analysis of Non-steady State Stable Isotope-resolve Metabolism of UDP-GlcNAc and UDP-GalNAc." In International Conference on Bioinformatics Models, Methods and Algorithms. SciTePress - Science and and Technology Publications, 2011. http://dx.doi.org/10.5220/0003129401080115.

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Fardilha, Margarida, and Magda Carvalho Henriques. "How to motivate students to learn Metabolic Biochemistry in a Biomedical Sciences curricula." In Fifth International Conference on Higher Education Advances. Valencia: Universitat Politècnica València, 2019. http://dx.doi.org/10.4995/head19.2019.9315.

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Teaching methodologies used in biochemistry classes at the University level are traditionally dependent on theorical classes. The assessment is usually based on written tests performed at the end of the semester. However, most students who learn metabolism by this traditional method consider the study of metabolic biochemistry a terrifying and unforgettable experience. Understanding biochemical metabolic pathways was the proposed goal of the Medical Biochemistry curricular unit. To this end, the multi-method active learning approach was used in order to increase students’ motivation towards the learning process and to allow the development of skills associated with group conflict resolution, critical thinking and communication skills. Overall, students and learning facilitators were highly motivated by the diversity of learning activities, particularly due to the emphasis on correlating theoretical knowledge with human health and disease. As a quality control exercise, the students were asked to answer a questionnaire on their evaluation of the teaching/learning experience. Thus, the initial analysis of the student’s perception questionnaires permits to conclude that the approach undertaken yields results that surpass the traditional teaching methods. Investing in preparing attractive and motivating classes increases students and teacher’s general satisfaction and the learning/teaching process becomes more efficient.
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Makrydaki, Foteini, Kyongbum Lee, and Christos Georgakis. "Tendency Stoichiometric Modeling of Metabolic Pathways." In 2007 American Control Conference. IEEE, 2007. http://dx.doi.org/10.1109/acc.2007.4282891.

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Reports on the topic "Pathways metabolici"

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Knaff, David, and Hirasawa Mussakaz. Ferredoxin Dependent Plant Metabolic Pathways. Office of Scientific and Technical Information (OSTI), September 2007. http://dx.doi.org/10.2172/1417307.

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Schaffer, Arthur A., D. Mason Pharr, Joseph Burger, James D. Burton, and Eliezer Zamski. Aspects of Sugar Metabolism in Melon Fruit as Determinants of Fruit Quality. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7568770.bard.

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The cucurbit family, including melon, translocates the galactosyl-sucrose oligosaccharides, raffinose and stachyose, in addition to sucrose, from the source leaves to the fruit sink. The metabolism of these photoassimilates in the fruit sink controls fruit growth and development, including the horticulturally important phenomenon of sucrose accumulation, which determines melon fruit sweetness. During this research project we have characterized the complete pathway of galactosyl sucrose metabolism in developing fruit, from before anthesis until maturity. We have also compared the metabolic pathway in scurose accumulating genotypes, as compared to non-accumulating genotypes. Furthermore, we studied the pathway in different fruit tissues, in response to pollination, and also analyzed the response of the individual steps of the pathway to perturbations such as low temperature and leaf removal. The results of our studies have led to the conclusion that generally galactosyl-sucrose metabolism functions as a coordinately controlled pathway. In one case, as an immediate response to the absence of pollination, the activity of a single enzyme, UDPglu pyrophosphorylase, was drastically reduced. However, during young fruit development, sucrose accumulation, and in response to perturbations of the system, groups of enzymes, rather than single enzymes, respond in a concerted manner. Our research has characterized in detail the initial enzymes of galactosyl-sucrose metabolism, including the galactosidases, galactokinase and the UDPgal- and UDPglu pyrophosphorylases. We have discovered a novel alkaline a-galactoside which hydrolyzes both stachyose and reaffinose and thereby may have solved the dilemma of cytosolic-sucrose metabolism, since prior to this research there was no known alkaline a-galactosidase capable of hydrolyzing raffinose.
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Lee, L. Parallel Extreme Pathway Computation for Metabolic Networks. Office of Scientific and Technical Information (OSTI), June 2004. http://dx.doi.org/10.2172/827001.

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Jiao, Y., and A. Navid. Metabolic Engineering and Modeling of Metabolic Pathways to Improve Hydrogen Production by Photosynthetic Bacteria. Office of Scientific and Technical Information (OSTI), December 2014. http://dx.doi.org/10.2172/1179401.

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Karp, Peter D. Curation and Computational Design of Bioenergy-Related Metabolic Pathways. Office of Scientific and Technical Information (OSTI), September 2014. http://dx.doi.org/10.2172/1171111.

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Metallo, Christian. Targeting Metabolic Survival Pathways in Lung Cancer via Combination Therapy. Fort Belvoir, VA: Defense Technical Information Center, June 2014. http://dx.doi.org/10.21236/ada611017.

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Cheng, Yan. Targeting Energy Metabolic Pathways as Therapeutic Intervention for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada573205.

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Cheng, Yan. Targeting Energy Metabolic Pathways as Therapeutic Intervention for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada592686.

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Luthey-Schulten, Zaida. Computational Modeling of Fluctuations in Energy and Metabolic Pathways of Methanogenic Archaea. Office of Scientific and Technical Information (OSTI), January 2017. http://dx.doi.org/10.2172/1337955.

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Gregory Stephanopoulos. Development of DNA Microarrays for Metabolic Pathway and Bioprocess Monitoring. Office of Scientific and Technical Information (OSTI), July 2004. http://dx.doi.org/10.2172/837870.

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