1. Bertalanffy, L, 1957, Quantitative laws in metabolism and growth: Quarterly Review of Biology, v. 32, p. 217-231.
BibTeX
@article{bertalanffy1957quantitative2,
author = "Bertalanffy, L",
title = "Quantitative laws in metabolism and growth",
year = "1957",
journal = "Quarterly Review of Biology, v. 32, p. 217-231",
note = "talkorigins\_source = {true}; raw\_reference = {Bertalanffy, L., 1957, Quantitative laws in metabolism and growth: Quarterly Review of Biology, v. 32, p. 217-231.}"
}
2. von Bertalanffy, Ludwig, 1957, Quantitative Laws in Metabolism and Growth: The Quarterly Review of Biology: v. 32, no. 3: p. 217-231.
BibTeX
@article{vonbertalanffy1957quantitative,
author = "von Bertalanffy, Ludwig",
title = "Quantitative Laws in Metabolism and Growth",
year = "1957",
journal = "The Quarterly Review of Biology",
url = "https://doi.org/10.1086/401873",
doi = "10.1086/401873",
number = "3",
openalex = "W2278685458",
pages = "217-231",
volume = "32",
references = "doi101002ar1091000306, doi101002jcp1030570302, doi101007bf00650112, doi101007bf01722007, doi101016s0021925818555757, doi101016s0021925818566928, doi101021j150446a008, doi101086physzool17130151829, doi101126science1092841579, doi101152physrev1956362255"
}
3. Bertalanffy, L., 1964, Basic concepts in quantitative biology of metabolism: Helgoländer wissenschaftliche Meeresuntersuchungen: v. 9, no. 1-4: p. 5-37.
DOI: 10.1007/BF01610024 Source
BibTeX
@article{doi101007bf01610024,
author = "Bertalanffy, L.",
title = "Basic concepts in quantitative biology of metabolism",
year = "1964",
journal = "Helgoländer wissenschaftliche Meeresuntersuchungen",
url = "https://link.springer.com/content/pdf/10.1007\%2FBF01610024.pdf",
doi = "10.1007/BF01610024",
is_oa = "true",
number = "1-4",
pages = "5-37",
semanticscholar_citation_count = "52",
semanticscholar_id = "0b47ec22e897e39541437b45049d5992201fa8a7",
volume = "9"
}
4. 1968, Quantitative Biology of Metabolism.
DOI: 10.1007/978-3-642-51065-6
BibTeX
@book{crossref1968quantitative,
title = "Quantitative Biology of Metabolism",
year = "1968",
url = "https://doi.org/10.1007/978-3-642-51065-6",
doi = "10.1007/978-3-642-51065-6",
openalex = "W562024091"
}
5. Bennett, A. F. and Dawson, W. R, 1976, Metabolism, in Gans, C., and Dawson, W. R., eds., Biology of the Reptilia: New York, Academic Press, p. 127-223.
BibTeX
@book{bennett1976metabolism1,
author = "Bennett, A. F. and Dawson, W. R",
title = "Metabolism, in Gans, C., and Dawson, W. R., eds., Biology of the Reptilia",
year = "1976",
publisher = "New York, Academic Press, p. 127-223",
note = "talkorigins\_source = {true}; raw\_reference = {Bennett, A. F., and Dawson, W. R., 1976, Metabolism, in Gans, C., and Dawson, W. R., eds., Biology of the Reptilia: New York, Academic Press, p. 127-223.}"
}
6. Ogilvie, D. M., 1982, Behavioral Response of Goldfish (Carassius auratus) to Deoxygenated Water: Copeia: v. 1982, no. 2: p. 434.
BibTeX
@article{doi1023071444625,
author = "Ogilvie, D. M.",
title = "Behavioral Response of Goldfish (Carassius auratus) to Deoxygenated Water",
year = "1982",
journal = "Copeia",
url = "https://www.semanticscholar.org/paper/52d4ce229829eae2ec33976b2d5c8afc14063c8a",
doi = "10.2307/1444625",
is_oa = "true",
number = "2",
pages = "434",
semanticscholar_citation_count = "19",
semanticscholar_id = "52d4ce229829eae2ec33976b2d5c8afc14063c8a",
volume = "1982"
}
7. Bernier, R�jane, 1983, Laws in biology: Acta Biotheoretica: v. 32, no. 4: p. 265-288.
BibTeX
@article{bernier1983laws,
author = "Bernier, R�jane",
title = "Laws in biology",
year = "1983",
journal = "Acta Biotheoretica",
url = "https://doi.org/10.1007/bf00048238",
doi = "10.1007/bf00048238",
number = "4",
openalex = "W2097522987",
pages = "265-288",
volume = "32",
references = "doi1010079789400764460, doi101126science1303374477, doi1023071907654, doi1023072023655, doi1023072090286, doi102307jctt5hjqm2, openalexw1562680794, openalexw1988585990, openalexw2065464699, openalexw3158856984"
}
8. Carpenter, Graham, 1985, Epidermal Growth Factor: Biology and Receptor Metabolism: Journal of Cell Science: v. 1985, no. Supplement_3: p. 1-9.
DOI: 10.1242/jcs.1985.supplement_3.1
Abstract
Epidermal growth factor (EGF) is a small (Mr 6045) protein that stimulates cell proliferation in cell culture systems and in intact animals. This growth factor has been isolated from rodents and human material and probably exists in nearly all animal species. In humans EGF has been detected in many body fluids and receptors for the growth factor are also ubiquitous. While the mitogenic activity of EGF has been most frequently reported, it clearly has other functions, such as the inhibition of gastric acid secretion, that are unrelated to mitogenic responses. Correspondingly, receptors for EGF have been localized on cells that are rapidly proliferating and cells that are essentially non-proliferating. Nevertheless, it has not been possible to define experimentally the biological function(s) of the endogenous EGF present in the intact animal. Studies of the mechanism of action of EGF have concentrated, to date, on the plasma membrane receptor that specifically binds this ligand. The receptor is undoubtedly the first cellular component that mediates the-eventual biological response(s) of the cell to this extracellular signal. Studies of the EGF receptor have shown that this molecule, which has no subunit structure, functions not only in ligand recognition, but also may produce an intracellular ‘second message’. The receptor contains a protein kinase activity that is activated by the binding of EGF and it is this enzymic function that may yield the critical ‘second messenger’, by phosphorylation of an intracellular protein. Although intracellular targets of this EGF-sensitive protein kinase have been identified, it has not been possible to demonstrate their relevance as regulatory mediators of EGF activity.
BibTeX
@article{carpenter1985epidermal,
author = "Carpenter, Graham",
title = "Epidermal Growth Factor: Biology and Receptor Metabolism",
year = "1985",
journal = "Journal of Cell Science",
abstract = "Epidermal growth factor (EGF) is a small (Mr 6045) protein that stimulates cell proliferation in cell culture systems and in intact animals. This growth factor has been isolated from rodents and human material and probably exists in nearly all animal species. In humans EGF has been detected in many body fluids and receptors for the growth factor are also ubiquitous. While the mitogenic activity of EGF has been most frequently reported, it clearly has other functions, such as the inhibition of gastric acid secretion, that are unrelated to mitogenic responses. Correspondingly, receptors for EGF have been localized on cells that are rapidly proliferating and cells that are essentially non-proliferating. Nevertheless, it has not been possible to define experimentally the biological function(s) of the endogenous EGF present in the intact animal. Studies of the mechanism of action of EGF have concentrated, to date, on the plasma membrane receptor that specifically binds this ligand. The receptor is undoubtedly the first cellular component that mediates the-eventual biological response(s) of the cell to this extracellular signal. Studies of the EGF receptor have shown that this molecule, which has no subunit structure, functions not only in ligand recognition, but also may produce an intracellular ‘second message’. The receptor contains a protein kinase activity that is activated by the binding of EGF and it is this enzymic function that may yield the critical ‘second messenger’, by phosphorylation of an intracellular protein. Although intracellular targets of this EGF-sensitive protein kinase have been identified, it has not been possible to demonstrate their relevance as regulatory mediators of EGF activity.",
url = "https://doi.org/10.1242/jcs.1985.supplement\_3.1",
doi = "10.1242/jcs.1985.supplement\_3.1",
number = "Supplement\_3",
openalex = "W2314943989",
pages = "1-9",
volume = "1985",
references = "doi1010160092867484905506, doi101016s0021925819445699, doi101016s0021925819837390, doi101038257325a0, doi101038309418a0, doi101073pnas7241317, doi101083jcb711159, doi101083jcb812382, doi101126science1172293, doi101146annurevbi48070179001205"
}
9. West, Geoffrey B. and Brown, James H., 2005, The origin of allometric scaling laws in biology from genomes to ecosystems: towards a quantitative unifying theory of biological structure and organization: Journal of Experimental Biology.
Abstract
Life is the most complex physical phenomenon in the Universe, manifesting an extraordinary diversity of form and function over an enormous scale from the largest animals and plants to the smallest microbes and subcellular units. Despite this many of its most fundamental and complex phenomena scale with size in a surprisingly simple fashion. For example, metabolic rate scales as the 3/4-power of mass over 27 orders of magnitude, from molecular and intracellular levels up to the largest organisms. Similarly, time-scales (such as lifespans and growth rates) and sizes (such as bacterial genome lengths, tree heights and mitochondrial densities) scale with exponents that are typically simple powers of 1/4. The universality and simplicity of these relationships suggest that fundamental universal principles underly much of the coarse-grained generic structure and organisation of living systems. We have proposed a set of principles based on the observation that almost all life is sustained by hierarchical branching networks, which we assume have invariant terminal units, are space-filling and are optimised by the process of natural selection. We show how these general constraints explain quarter power scaling and lead to a quantitative, predictive theory that captures many of the essential features of diverse biological systems. Examples considered include animal circulatory systems, plant vascular systems, growth, mitochondrial densities, and the concept of a universal molecular clock. Temperature considerations, dimensionality and the role of invariants are discussed. Criticisms and controversies associated with this approach are also addressed.
BibTeX
@article{doi101242jeb01589,
author = "West, Geoffrey B. and Brown, James H.",
title = "The origin of allometric scaling laws in biology from genomes to ecosystems: towards a quantitative unifying theory of biological structure and organization",
year = "2005",
journal = "Journal of Experimental Biology",
abstract = "Life is the most complex physical phenomenon in the Universe, manifesting an extraordinary diversity of form and function over an enormous scale from the largest animals and plants to the smallest microbes and subcellular units. Despite this many of its most fundamental and complex phenomena scale with size in a surprisingly simple fashion. For example, metabolic rate scales as the 3/4-power of mass over 27 orders of magnitude, from molecular and intracellular levels up to the largest organisms. Similarly, time-scales (such as lifespans and growth rates) and sizes (such as bacterial genome lengths, tree heights and mitochondrial densities) scale with exponents that are typically simple powers of 1/4. The universality and simplicity of these relationships suggest that fundamental universal principles underly much of the coarse-grained generic structure and organisation of living systems. We have proposed a set of principles based on the observation that almost all life is sustained by hierarchical branching networks, which we assume have invariant terminal units, are space-filling and are optimised by the process of natural selection. We show how these general constraints explain quarter power scaling and lead to a quantitative, predictive theory that captures many of the essential features of diverse biological systems. Examples considered include animal circulatory systems, plant vascular systems, growth, mitochondrial densities, and the concept of a universal molecular clock. Temperature considerations, dimensionality and the role of invariants are discussed. Criticisms and controversies associated with this approach are also addressed.",
url = "https://doi.org/10.1242/jeb.01589",
doi = "10.1242/jeb.01589",
openalex = "W2117184765",
references = "doi101001jama196203050110085031, doi101016jresp200401006, doi101017cbo9780511608551, doi101021j150446a008, doi10103835098076, doi101113jphysiol1952sp004719, doi101119113295, doi101126science1061967, doi101126science2765309122, doi101126science28454201677, doi103733hilgv06n11p315, openalexw1558456135"
}
10. Cianfarani, Stefano and Le Bouc, Yves and Savage, Martin, 2007, The evolving biology of growth and metabolism: European Journal of Endocrinology: v. 157, no. suppl_1: p. S1.
BibTeX
@article{cianfarani2007the,
author = "Cianfarani, Stefano and Le Bouc, Yves and Savage, Martin",
title = "The evolving biology of growth and metabolism",
year = "2007",
journal = "European Journal of Endocrinology",
url = "https://doi.org/10.1530/eje-07-0370",
doi = "10.1530/eje-07-0370",
number = "suppl\_1",
openalex = "W2038161403",
pages = "S1",
volume = "157"
}
11. Enquist, B. and Stark, S., 2007, Follow Thompson's map to turn biology from a science into a Science: Nature: v. 446, no. 7136: p. 611-611.
BibTeX
@article{doi101038446611a,
author = "Enquist, B. and Stark, S.",
title = "Follow Thompson's map to turn biology from a science into a Science",
year = "2007",
journal = "Nature",
url = "https://www.nature.com/articles/446611a.pdf",
doi = "10.1038/446611A",
is_oa = "true",
number = "7136",
pages = "611-611",
semanticscholar_citation_count = "11",
semanticscholar_id = "c01113a14eb56230fd429feb721bea5443290a22",
volume = "446"
}
12. Sousa, Tânia and Domingos, Tiago and Kooijman, S.A.L.M., 2008, From empirical patterns to theory: a formal metabolic theory of life: Philosophical Transactions of the Royal Society B Biological Sciences.
Abstract
The diversity of life on Earth raises the question of whether it is possible to have a single theoretical description of the quantitative aspects of the organization of metabolism for all organisms. However, similarities between organisms, such as von Bertalanffy's growth curve and Kleiber's law on metabolic rate, suggest that mechanisms that control the uptake and use of metabolites are common to all organisms. These and other widespread empirical patterns in biology should be the ultimate test for any metabolic theory that hopes for generality. The present study (i) collects empirical evidence on growth, stoichiometry, feeding, respiration and energy dissipation and exhibits it as stylized biological facts; (ii) formalizes assumptions and propositions in a metabolic theory that is fully consistent with the Dynamic Energy Budget theory; and (iii) proves that these assumptions and propositions are consistent with the stylized facts.
BibTeX
@article{doi101098rstb20072230,
author = "Sousa, Tânia and Domingos, Tiago and Kooijman, S.A.L.M.",
title = "From empirical patterns to theory: a formal metabolic theory of life",
year = "2008",
journal = "Philosophical Transactions of the Royal Society B Biological Sciences",
abstract = "The diversity of life on Earth raises the question of whether it is possible to have a single theoretical description of the quantitative aspects of the organization of metabolism for all organisms. However, similarities between organisms, such as von Bertalanffy's growth curve and Kleiber's law on metabolic rate, suggest that mechanisms that control the uptake and use of metabolites are common to all organisms. These and other widespread empirical patterns in biology should be the ultimate test for any metabolic theory that hopes for generality. The present study (i) collects empirical evidence on growth, stoichiometry, feeding, respiration and energy dissipation and exhibits it as stylized biological facts; (ii) formalizes assumptions and propositions in a metabolic theory that is fully consistent with the Dynamic Energy Budget theory; and (iii) proves that these assumptions and propositions are consistent with the stylized facts.",
url = "https://doi.org/10.1098/rstb.2007.2230",
doi = "10.1098/rstb.2007.2230",
openalex = "W2148759670",
references = "doi101007s0028500302560"
}
13. Fleming, R. and Thiele, I. and Provan, G. and Nasheuer, H., 2010, Integrated stoichiometric, thermodynamic and kinetic modelling of steady state metabolism.: Journal of theoretical biology: v. 264, no. 3: p. 683-692.
DOI: 10.1016/j.jtbi.2010.02.044 Source
BibTeX
@article{doi101016jjtbi201002044,
author = "Fleming, R. and Thiele, I. and Provan, G. and Nasheuer, H.",
title = "Integrated stoichiometric, thermodynamic and kinetic modelling of steady state metabolism.",
year = "2010",
journal = "Journal of theoretical biology",
url = "https://europepmc.org/articles/pmc2868105?pdf=render",
doi = "10.1016/j.jtbi.2010.02.044",
is_oa = "true",
number = "3",
pages = "683-692",
semanticscholar_citation_count = "61",
semanticscholar_id = "16469b755c64082f47d8b61133f85dc847fc0214",
volume = "264"
}
14. Kartal, Boran and van Niftrik, Laura and Keltjens, Jan T. and Op den Camp, Huub J.M. and Jetten, Mike S.M., 2012, Anammox—Growth Physiology, Cell Biology, and Metabolism: Advances in Microbial Physiology: p. 211-262.
DOI: 10.1016/b978-0-12-398264-3.00003-6
BibTeX
@incollection{kartal2012anammoxgrowth,
author = "Kartal, Boran and van Niftrik, Laura and Keltjens, Jan T. and Op den Camp, Huub J.M. and Jetten, Mike S.M.",
title = "Anammox—Growth Physiology, Cell Biology, and Metabolism",
year = "2012",
booktitle = "Advances in Microbial Physiology",
url = "https://doi.org/10.1016/b978-0-12-398264-3.00003-6",
doi = "10.1016/b978-0-12-398264-3.00003-6",
openalex = "W1542578191",
pages = "211-262",
references = "doi101007s002530051340, doi10103822749, doi10103835054051, doi101038nature04159, doi101038nature08465, doi101038nature08883, doi1010991350087214282187, doi101111j157469411995tb00281x, doi101126science1136674, doi101128aem657324832501999"
}
15. Rauch, C. and Cherkaoui, M. and Egan, S. and Leigh, J., 2017, The bio-physics of condensation of divalent cations into the bacterial wall has implications for growth of Gram-positive bacteria.: Biochimica et biophysica acta. Biomembranes: v. 1859, no. 2: p. 282-288.
DOI: 10.1016/j.bbamem.2016.12.002
BibTeX
@article{doi101016jbbamem201612002,
author = "Rauch, C. and Cherkaoui, M. and Egan, S. and Leigh, J.",
title = "The bio-physics of condensation of divalent cations into the bacterial wall has implications for growth of Gram-positive bacteria.",
year = "2017",
journal = "Biochimica et biophysica acta. Biomembranes",
url = "https://doi.org/10.1016/j.bbamem.2016.12.002",
doi = "10.1016/j.bbamem.2016.12.002",
is_oa = "true",
number = "2",
pages = "282-288",
semanticscholar_citation_count = "7",
semanticscholar_id = "a889535a1a2fc9e1c586fcb6097f121b2b3e1551",
volume = "1859"
}
16. Hatton, Ian and Dobson, Andrew P. and Štorch, David and Galbraith, Eric D. and Loreau, Michel, 2019, Linking scaling laws across eukaryotes: Proceedings of the National Academy of Sciences.
Abstract
Scaling laws relating body mass to species characteristics are among the most universal quantitative patterns in biology. Within major taxonomic groups, the 4 key ecological variables of metabolism, abundance, growth, and mortality are often well described by power laws with exponents near 3/4 or related to that value, a commonality often attributed to biophysical constraints on metabolism. However, metabolic scaling theories remain widely debated, and the links among the 4 variables have never been formally tested across the full domain of eukaryote life, to which prevailing theory applies. Here we present datasets of unprecedented scope to examine these 4 scaling laws across all eukaryotes and link them to test whether their combinations support theoretical expectations. We find that metabolism and abundance scale with body size in a remarkably reciprocal fashion, with exponents near ±3/4 within groups, as expected from metabolic theory, but with exponents near ±1 across all groups. This reciprocal scaling supports "energetic equivalence" across eukaryotes, which hypothesizes that the partitioning of energy in space across species does not vary significantly with body size. In contrast, growth and mortality rates scale similarly both within and across groups, with exponents of ±1/4. These findings are inconsistent with a metabolic basis for growth and mortality scaling across eukaryotes. We propose that rather than limiting growth, metabolism adjusts to the needs of growth within major groups, and that growth dynamics may offer a viable theoretical basis to biological scaling.
BibTeX
@article{doi101073pnas1900492116,
author = "Hatton, Ian and Dobson, Andrew P. and Štorch, David and Galbraith, Eric D. and Loreau, Michel",
title = "Linking scaling laws across eukaryotes",
year = "2019",
journal = "Proceedings of the National Academy of Sciences",
abstract = {Scaling laws relating body mass to species characteristics are among the most universal quantitative patterns in biology. Within major taxonomic groups, the 4 key ecological variables of metabolism, abundance, growth, and mortality are often well described by power laws with exponents near 3/4 or related to that value, a commonality often attributed to biophysical constraints on metabolism. However, metabolic scaling theories remain widely debated, and the links among the 4 variables have never been formally tested across the full domain of eukaryote life, to which prevailing theory applies. Here we present datasets of unprecedented scope to examine these 4 scaling laws across all eukaryotes and link them to test whether their combinations support theoretical expectations. We find that metabolism and abundance scale with body size in a remarkably reciprocal fashion, with exponents near ±3/4 within groups, as expected from metabolic theory, but with exponents near ±1 across all groups. This reciprocal scaling supports "energetic equivalence" across eukaryotes, which hypothesizes that the partitioning of energy in space across species does not vary significantly with body size. In contrast, growth and mortality rates scale similarly both within and across groups, with exponents of ±1/4. These findings are inconsistent with a metabolic basis for growth and mortality scaling across eukaryotes. We propose that rather than limiting growth, metabolism adjusts to the needs of growth within major groups, and that growth dynamics may offer a viable theoretical basis to biological scaling.},
url = "https://doi.org/10.1073/pnas.1900492116",
doi = "10.1073/pnas.1900492116",
openalex = "W2979688413",
references = "doi101126scienceaac6284"
}
17. Adler, Stephan O. and Klipp, E., 2019, Entropic regulation of dynamical metabolic processes: bioRxiv.
Abstract
Life depends on the input of energy, either directly provided by sunlight or in form of high-energy matter. The rules and conditions for the conversion of chemical or electromagnetic energy into living structure and all the processes related with life are governed by the laws of thermodynamics. Hence, to understand the potential and the limitations of cell growth and metabolism, it is unavoidable to take these laws into account. During the last years, systems biology has developed many mathematical models aiming to describe steady states and dynamic behavior of cellular processes in qualitative and quantitative terms. The validity of the model predictions depends strongly on whether the model formulation is in agreement with the laws of physics, chemistry, and, specifically, thermodynamics. Here, we review basic principles of thermodynamics for equilibrium and non-equilibrium processes as well as for closed and open systems as far as they concern metabolic processes, especially in their dynamics. We illustrate the application of thermodynamic laws for some practical cases that are currently intensively studied in systems and computational biology. Specifically, we will discuss the concept of entropy production and energy dissipation for isolated and open systems and its interpretation for the feasibility of biological processes, especially metabolism. We demonstrate that steady states of metabolic systems cannot show energy dissipation, while in dynamical modes entropy of the system can be both increased or decreased, depending on the type of perturbation and the kinetics of the reaction system. These findings are very important for biotechnological processes where energy dissipation should be limited, but also for analysis of healthy and diseased cellular metabolism.
BibTeX
@article{doi101101643601,
author = "Adler, Stephan O. and Klipp, E.",
title = "Entropic regulation of dynamical metabolic processes",
year = "2019",
journal = "bioRxiv",
abstract = "Life depends on the input of energy, either directly provided by sunlight or in form of high-energy matter. The rules and conditions for the conversion of chemical or electromagnetic energy into living structure and all the processes related with life are governed by the laws of thermodynamics. Hence, to understand the potential and the limitations of cell growth and metabolism, it is unavoidable to take these laws into account. During the last years, systems biology has developed many mathematical models aiming to describe steady states and dynamic behavior of cellular processes in qualitative and quantitative terms. The validity of the model predictions depends strongly on whether the model formulation is in agreement with the laws of physics, chemistry, and, specifically, thermodynamics. Here, we review basic principles of thermodynamics for equilibrium and non-equilibrium processes as well as for closed and open systems as far as they concern metabolic processes, especially in their dynamics. We illustrate the application of thermodynamic laws for some practical cases that are currently intensively studied in systems and computational biology. Specifically, we will discuss the concept of entropy production and energy dissipation for isolated and open systems and its interpretation for the feasibility of biological processes, especially metabolism. We demonstrate that steady states of metabolic systems cannot show energy dissipation, while in dynamical modes entropy of the system can be both increased or decreased, depending on the type of perturbation and the kinetics of the reaction system. These findings are very important for biotechnological processes where energy dissipation should be limited, but also for analysis of healthy and diseased cellular metabolism.",
url = "https://doi.org/10.1101/643601",
doi = "10.1101/643601",
is_oa = "true",
semanticscholar_citation_count = "1",
semanticscholar_id = "2512cf870e73d1a2d4f66ced29c483240e082769"
}
18. Huang, Shu and Jiang, Yizhao and Yang, Lin-Jie and Yang, Jie and Liang, Meiyan and Zhou, Hua-Fu and Luo, Jiao and Yang, Da-Ping and Mo, Wei-jia and Chen, Gang and Shi, Lin and Gan, T., 2020, Downregulation of miR-125b-5p and Its Prospective Molecular Mechanism in Lung Squamous Cell Carcinoma: Cancer Biotherapy & Radiopharmaceuticals: v. 37, no. 2: p. 125-140.
DOI: 10.1089/cbr.2020.3657 Source
Abstract
Background: To explore the clinical significance of miR-125b-5p and its potential mechanisms in lung squamous cell carcinoma (LUSC). Materials and Methods: An integrated analysis of data from in-house quantitative real-time polymerase chain reaction (qRT-PCR), microRNA-sequencing, and microarray assays to appraise the expression level of miR-125b-5p in LUSC tissues compared to adjacent noncancerous controls. The authors identified the candidate targets of miR-125b-5p and conducted functional analysis using computational biology strategies from gene ontology, the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, disease ontology (DO), and protein–protein interaction (PPI) network analyses to investigate the prospective mechanisms. Results: According to qRT-PCR results, the expression level of miR-125b-5p was markedly decreased in LUSC tissues compared to noncancerous control tissues. Receiver operating characteristic and summary receiver operating characteristic analyses showed that miR-125b-5p had good specificity and sensitivity for distinguishing LUSC tissue from noncancerous lung tissue. The standard mean difference revealed that men and women with lower expression levels of miR-125b-5p may have a higher risk for LUSC. KEGG analysis and DO analysis intimated that target genes were evidently enriched in pyrimidine metabolism and pancreatic carcinoma. The PPI network of the top assembled KEGG pathway indicated that RRM2, UMPS, UCK2, and CTPS1 were regarded as crucial target genes for miR-125b-5p, and RRM2 was eventually deemed a key target. Conclusions: The authors' findings implicate a low expression level of miR-125b-5p in LUSC. A tumor-suppressive role of miR-125b-5p is proposed, based on its effects on LUSC tumor growth, clinical stage progression, and lymph node metastasis.
BibTeX
@article{doi101089cbr20203657,
author = "Huang, Shu and Jiang, Yizhao and Yang, Lin-Jie and Yang, Jie and Liang, Meiyan and Zhou, Hua-Fu and Luo, Jiao and Yang, Da-Ping and Mo, Wei-jia and Chen, Gang and Shi, Lin and Gan, T.",
title = "Downregulation of miR-125b-5p and Its Prospective Molecular Mechanism in Lung Squamous Cell Carcinoma",
year = "2020",
journal = "Cancer Biotherapy \& Radiopharmaceuticals",
abstract = "Background: To explore the clinical significance of miR-125b-5p and its potential mechanisms in lung squamous cell carcinoma (LUSC). Materials and Methods: An integrated analysis of data from in-house quantitative real-time polymerase chain reaction (qRT-PCR), microRNA-sequencing, and microarray assays to appraise the expression level of miR-125b-5p in LUSC tissues compared to adjacent noncancerous controls. The authors identified the candidate targets of miR-125b-5p and conducted functional analysis using computational biology strategies from gene ontology, the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, disease ontology (DO), and protein–protein interaction (PPI) network analyses to investigate the prospective mechanisms. Results: According to qRT-PCR results, the expression level of miR-125b-5p was markedly decreased in LUSC tissues compared to noncancerous control tissues. Receiver operating characteristic and summary receiver operating characteristic analyses showed that miR-125b-5p had good specificity and sensitivity for distinguishing LUSC tissue from noncancerous lung tissue. The standard mean difference revealed that men and women with lower expression levels of miR-125b-5p may have a higher risk for LUSC. KEGG analysis and DO analysis intimated that target genes were evidently enriched in pyrimidine metabolism and pancreatic carcinoma. The PPI network of the top assembled KEGG pathway indicated that RRM2, UMPS, UCK2, and CTPS1 were regarded as crucial target genes for miR-125b-5p, and RRM2 was eventually deemed a key target. Conclusions: The authors' findings implicate a low expression level of miR-125b-5p in LUSC. A tumor-suppressive role of miR-125b-5p is proposed, based on its effects on LUSC tumor growth, clinical stage progression, and lymph node metastasis.",
url = "https://www.semanticscholar.org/paper/3738913b253d45733ec2b3a934c33de38b427241",
doi = "10.1089/cbr.2020.3657",
is_oa = "true",
number = "2",
pages = "125-140",
semanticscholar_citation_count = "9",
semanticscholar_id = "3738913b253d45733ec2b3a934c33de38b427241",
volume = "37"
}
19. Bibeau, Jeffrey P. and Galotto, Giulia and Wu, Min and Tüzel, Erkan and Vidali, Luis, 2021, Quantitative cell biology of tip growth in moss: Plant Molecular Biology: v. 107, no. 4-5: p. 227-244.
DOI: 10.1007/s11103-021-01147-7
BibTeX
@article{bibeau2021quantitative,
author = "Bibeau, Jeffrey P. and Galotto, Giulia and Wu, Min and Tüzel, Erkan and Vidali, Luis",
title = "Quantitative cell biology of tip growth in moss",
year = "2021",
journal = "Plant Molecular Biology",
url = "https://doi.org/10.1007/s11103-021-01147-7",
doi = "10.1007/s11103-021-01147-7",
number = "4-5",
openalex = "W3147449270",
pages = "227-244",
volume = "107",
references = "doi1010079780387877105, doi101038349117a0, doi101038nature01485, doi101038nmeth1220, doi101046j1365313x199711061195x, doi101046j1365313x199800304x, doi101083jcb1452317, doi101105tpc11122283, doi101146annurevcellbio171159, doi101146annurevcellbio20082503103053"
}
20. Kumar, Manish and Zuniga, Cristal and Tibocha-Bonilla, Juan D. and Smith, Sarah R. and Coker, Joanna and Allen, Andrew E. and Zengler, Karsten, 2022, Constraint-Based Modeling of Diatoms Metabolism and Quantitative Biology Approaches: The Molecular Life of Diatoms: p. 775-808.
DOI: 10.1007/978-3-030-92499-7_26
BibTeX
@incollection{kumar2022constraintbased,
author = "Kumar, Manish and Zuniga, Cristal and Tibocha-Bonilla, Juan D. and Smith, Sarah R. and Coker, Joanna and Allen, Andrew E. and Zengler, Karsten",
title = "Constraint-Based Modeling of Diatoms Metabolism and Quantitative Biology Approaches",
year = "2022",
booktitle = "The Molecular Life of Diatoms",
url = "https://doi.org/10.1007/978-3-030-92499-7\_26",
doi = "10.1007/978-3-030-92499-7\_26",
openalex = "W4285211075",
pages = "775-808",
references = "doi101006jmbi20004315, doi101038nbt1614, doi101038nprot2007131, doi101038s415870190036z, doi101038srep08365, doi101093bioinformaticsbtu153, doi101093nargkm259, doi101093nargkv1164, doi101093nargkw1092, doi1011861471210512491"
}
21. Yeung, A. and Ksepka, Natalia and Matin, Maima and Wang, Dongdong and Souto, E. and Stoyanov, Jivko and Echeverría, Javier and Tewari, Devesh and Horbańczuk, J. and Lucarini, M. and Durazzo, A. and Marchewka, J. and Pirgozliev, V. and Gan, Ren-You and Tzvetkov, N. and Wysocki, Kamil and Matin, Farhan Bin and Litvinova, O. and Bishayee, A. and Devkota, H. and El‐Demerdash, A. and Brnčić, M. and Santini, A. and Horbańczuk, Olaf K. and Mickael, Michel-Edwar and Ławiński, Michał and Das, Niranjan and Siddiquea, B. and Hrg, Dalibor and Atanasov, Atanas G., 2023, Dietary factors in nonalcoholic fatty liver disease: impacts on human and animal health - a review: Animal Science Papers and Reports: v. 41, no. 3: p. 179-194.
DOI: 10.2478/aspr-2023-0007 Source
Abstract
Abstract Non-alcoholic fatty liver disease (NAFLD) is defined as a clinical syndrome characterized by excessive fat accumulation in liver, predominantly influenced by dietary choices. This study provides an extensive quantitative literature analysis on dietary influences on NAFLD. Bibliometric data were collected through the search string TOPIC = (“NAFLD*” OR “nonalcoholic fatty liver*” OR “non-alcoholic fatty liver*”) AND TOPIC = (“diet*” OR “nutrition*” OR “food*” OR “feed*”), which yielded 12,445 publications indexed within the Web of Science Core Collection. Utilizing VOSviewer software, term maps were generated to visually illustrate recurring phrases alongside citation data. The literature, which has seen exponential growth since the 2010s, predominantly consists of original articles, with a ratio of 4.7:1 compared to reviews. Notably, the significant contributors to this field were China and the United States. The majority of publications were found journals specialized in Gastroenterology & Hepatology, Nutrition & Dietetics, Biochemistry & Molecular Biology, Endocrinology & Metabolism, and Pharmacology & Pharmacy. Key dietary compounds/compounds classes such as resveratrol, polyphenols, curcumin, berberine, quercetin, flavonoids, omega-3 fatty acids, docosahexaenoic acid (DHA), genistein, and palmitic acid were frequently mentioned and cited. Many of them were demonstrated to have some potential benefits on NAFLD, both in human and animal studies.
BibTeX
@article{doi102478aspr20230007,
author = "Yeung, A. and Ksepka, Natalia and Matin, Maima and Wang, Dongdong and Souto, E. and Stoyanov, Jivko and Echeverría, Javier and Tewari, Devesh and Horbańczuk, J. and Lucarini, M. and Durazzo, A. and Marchewka, J. and Pirgozliev, V. and Gan, Ren-You and Tzvetkov, N. and Wysocki, Kamil and Matin, Farhan Bin and Litvinova, O. and Bishayee, A. and Devkota, H. and El‐Demerdash, A. and Brnčić, M. and Santini, A. and Horbańczuk, Olaf K. and Mickael, Michel-Edwar and Ławiński, Michał and Das, Niranjan and Siddiquea, B. and Hrg, Dalibor and Atanasov, Atanas G.",
title = "Dietary factors in nonalcoholic fatty liver disease: impacts on human and animal health - a review",
year = "2023",
journal = "Animal Science Papers and Reports",
abstract = "Abstract Non-alcoholic fatty liver disease (NAFLD) is defined as a clinical syndrome characterized by excessive fat accumulation in liver, predominantly influenced by dietary choices. This study provides an extensive quantitative literature analysis on dietary influences on NAFLD. Bibliometric data were collected through the search string TOPIC = (“NAFLD*” OR “nonalcoholic fatty liver*” OR “non-alcoholic fatty liver*”) AND TOPIC = (“diet*” OR “nutrition*” OR “food*” OR “feed*”), which yielded 12,445 publications indexed within the Web of Science Core Collection. Utilizing VOSviewer software, term maps were generated to visually illustrate recurring phrases alongside citation data. The literature, which has seen exponential growth since the 2010s, predominantly consists of original articles, with a ratio of 4.7:1 compared to reviews. Notably, the significant contributors to this field were China and the United States. The majority of publications were found journals specialized in Gastroenterology \& Hepatology, Nutrition \& Dietetics, Biochemistry \& Molecular Biology, Endocrinology \& Metabolism, and Pharmacology \& Pharmacy. Key dietary compounds/compounds classes such as resveratrol, polyphenols, curcumin, berberine, quercetin, flavonoids, omega-3 fatty acids, docosahexaenoic acid (DHA), genistein, and palmitic acid were frequently mentioned and cited. Many of them were demonstrated to have some potential benefits on NAFLD, both in human and animal studies.",
url = "https://sciendo.com/pdf/10.2478/aspr-2023-0007",
doi = "10.2478/aspr-2023-0007",
is_oa = "true",
number = "3",
pages = "179-194",
semanticscholar_citation_count = "8",
semanticscholar_id = "e86fdd388c6c11888061406abe79aba2a534d58f",
volume = "41"
}
22. Sethi, Sonia, 2023, Anammox Cell Biology, Metabolism, Growth, and Genetics: Anammox Technology in Industrial Wastewater Treatment: p. 51-71.
DOI: 10.1007/978-981-99-3459-1_4
BibTeX
@incollection{sethi2023anammox,
author = "Sethi, Sonia",
title = "Anammox Cell Biology, Metabolism, Growth, and Genetics",
year = "2023",
booktitle = "Anammox Technology in Industrial Wastewater Treatment",
url = "https://doi.org/10.1007/978-981-99-3459-1\_4",
doi = "10.1007/978-981-99-3459-1\_4",
openalex = "W4381051649",
pages = "51-71",
references = "doi10103822749, doi101038461472a, doi101038nature03911, doi101038nature04396, doi101038nature04647, doi101038nature10453, doi101093nargkt1178, doi101126science1170261, doi101126science1185941, doi101126science1186120"
}