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Special Issue "Biosemiotic Entropy: Disorder, Disease, and Mortality"

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A special issue of Entropy (ISSN 1099-4300).

Deadline for manuscript submissions: closed (31 October 2012)

Special Issue Editor

Guest Editor
Prof. Dr. John W. Oller, Jr.

Department of Communicative Disorders, University of Louisiana at Lafayette, P. O. Box 43170, Lafayette, LA 70504-3170, USA
Website | E-Mail
Phone: 337 962-4649
Interests: biosemiotics; etiology of communication disorders; measurement of human abilities and severity of disabilities; intelligence theory; pragmatic information; pragmatic mapping theory; systems grammar

Special Issue Information

Dear Colleagues,

The simplest and most informative linguistic messages are the kind found in ordinary true narratives. Such valid messages ― laden with pragmatic information ― provide the limiting antithesis of biosemiotic entropy. Generalizing from linguistic to biological systems, and taking account of some of the countless ways any complex arrangement of symbols can be rendered senseless, the thesis to be explored in this special issue is that the corruption of biological messages from genetics upward to epigenetics, proteins, cells, tissues, and the organs of viable organisms ― which can be described as biosemiotic entropy ― is, unsurprisingly, the proximate cause of disorders, diseases, and mortality. We invite contributions ― pro, con, or offering any plausible alternative ― to the idea that corrupted biological messages account for (but, of course, are not limited to) anaphylaxis, preeclampsia, sudden death syndrome, immune disorders, autism, and so forth. Empirical and theoretical articles are invited exploring pathways by which toxins, disease agents, and their interactions, and/or injuries from microwave, electromagnetic, radiological, or other energy sources can be shown to increase biosemiotic entropy. Empirically grounded arguments showing how cascading series of effects lead to certain injuries, diseases, and/or known disorders are preferred.

Prof. Dr. John W. Oller, Jr.
Guest Editor

Keywords

  • abstraction theory
  • autism
  • biosemiotic entropy
  • immune disorders
  • mortality theory
  • pragmatic mapping
  • pragmatic information
  • preeclampsia
  • theoretical linguistics
  • theory of true narratives

Published Papers (12 papers)

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Editorial

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Open AccessEditorial Biosemiotic Entropy: Concluding the Series
Entropy 2014, 16(7), 4060-4087; doi:10.3390/e16074060
Received: 21 October 2013 / Revised: 9 June 2014 / Accepted: 1 July 2014 / Published: 18 July 2014
Cited by 1 | PDF Full-text (859 KB) | HTML Full-text | XML Full-text
Abstract
This article concludes the special issue on Biosemiotic Entropy looking toward the future on the basis of current and prior results. It highlights certain aspects of the series, concerning factors that damage and degenerate biosignaling systems. As in ordinary linguistic discourse, well-formedness (coherence)
[...] Read more.
This article concludes the special issue on Biosemiotic Entropy looking toward the future on the basis of current and prior results. It highlights certain aspects of the series, concerning factors that damage and degenerate biosignaling systems. As in ordinary linguistic discourse, well-formedness (coherence) in biological signaling systems depends on valid representations correctly construed: a series of proofs are presented and generalized to all meaningful sign systems. The proofs show why infants must (as empirical evidence shows they do) proceed through a strict sequence of formal steps in acquiring any language. Classical and contemporary conceptions of entropy and information are deployed showing why factors that interfere with coherence in biological signaling systems are necessary and sufficient causes of disorders, diseases, and mortality. Known sources of such formal degeneracy in living organisms (here termed, biosemiotic entropy) include: (a) toxicants, (b) pathogens; (c) excessive exposures to radiant energy and/or sufficiently powerful electromagnetic fields; (d) traumatic injuries; and (e) interactions between the foregoing factors. Just as Jaynes proved that irreversible changes invariably increase entropy, the theory of true narrative representations (TNR theory) demonstrates that factors disrupting the well-formedness (coherence) of valid representations, all else being held equal, must increase biosemiotic entropy—the kind impacting biosignaling systems. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)

Research

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Open AccessArticle Empirical Data Confirm Autism Symptoms Related to Aluminum and Acetaminophen Exposure
Entropy 2012, 14(11), 2227-2253; doi:10.3390/e14112227
Received: 24 September 2012 / Revised: 16 October 2012 / Accepted: 5 November 2012 / Published: 7 November 2012
Cited by 13 | PDF Full-text (441 KB) | HTML Full-text | XML Full-text
Abstract
Autism is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. This paper investigates word frequency patterns in the U.S. CDC
[...] Read more.
Autism is a condition characterized by impaired cognitive and social skills, associated with compromised immune function. The incidence is alarmingly on the rise, and environmental factors are increasingly suspected to play a role. This paper investigates word frequency patterns in the U.S. CDC Vaccine Adverse Events Reporting System (VAERS) database. Our results provide strong evidence supporting a link between autism and the aluminum in vaccines. A literature review showing toxicity of aluminum in human physiology offers further support. Mentions of autism in VAERS increased steadily at the end of the last century, during a period when mercury was being phased out, while aluminum adjuvant burden was being increased. Using standard log-likelihood ratio techniques, we identify several signs and symptoms that are significantly more prevalent in vaccine reports after 2000, including cellulitis, seizure, depression, fatigue, pain and death, which are also significantly associated with aluminum-containing vaccines. We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen administered to control fever. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)

Review

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Open AccessReview The New Genetics and Natural versus Artificial Genetic Modification
Entropy 2013, 15(11), 4748-4781; doi:10.3390/e15114748
Received: 2 August 2013 / Revised: 9 October 2013 / Accepted: 10 October 2013 / Published: 4 November 2013
Cited by 4 | PDF Full-text (442 KB) | HTML Full-text | XML Full-text
Abstract
The original rationale and impetus for artificial genetic modification was the “central dogma” of molecular biology that assumed DNA carries all the instructions for making an organism, which are transmitted via RNA to protein to biological function in linear causal chains. This is
[...] Read more.
The original rationale and impetus for artificial genetic modification was the “central dogma” of molecular biology that assumed DNA carries all the instructions for making an organism, which are transmitted via RNA to protein to biological function in linear causal chains. This is contrary to the reality of the “fluid genome” that has emerged since the mid-1970s. In order to survive, the organism needs to engage in natural genetic modification in real time, an exquisitely precise molecular dance of life with RNA and DNA responding to and participating in “downstream” biological functions. Artificial genetic modification, in contrast, is crude, imprecise, and interferes with the natural process. It drives natural systems towards maximum biosemiotic entropy as the perturbations are propagated and amplified through the complex cascades of interactions between subsystems that are essential for health and longevity. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview Deepening the Conception of Functional Information in the Description of Zoonotic Infectious Diseases
Entropy 2013, 15(5), 1929-1962; doi:10.3390/e15051929
Received: 22 February 2013 / Revised: 2 May 2013 / Accepted: 10 May 2013 / Published: 22 May 2013
Cited by 3 | PDF Full-text (255 KB) | HTML Full-text | XML Full-text
Abstract
Infectious agents, their hosts, and relevant abiotic components are directly involved in the complex dynamic process of maintaining infectious diseases in Nature. The current tendency to focus on host-pathogen interactions at the molecular and organismal levels does not advance our knowledge about infectious
[...] Read more.
Infectious agents, their hosts, and relevant abiotic components are directly involved in the complex dynamic process of maintaining infectious diseases in Nature. The current tendency to focus on host-pathogen interactions at the molecular and organismal levels does not advance our knowledge about infectious diseases, as much as it potentially could, by ignoring the ecological context pivotal for understanding the biology of the diseases. A new model of investigation requires a dynamic shift of perspectives in the “simplicity-complexity” dimension: from virulence factors to multi-sided descriptions of the pathogens; from particular microbes to wide microbial communities; from clinical manifestations to a variety of infectious patterns; from findings of infectious agents to defining a natural focus of the infection as a self-regulated system; from single factors affecting host-parasite relations to the complex ecological context. Various aspects of interactions between hosts, vectors, pathogens, and environmental niches should be integrated at multiple spatiotemporal scales and at different levels of biological organization (molecular, genomic, organismal, population, and ecosystem). Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview Glyphosate’s Suppression of Cytochrome P450 Enzymes and Amino Acid Biosynthesis by the Gut Microbiome: Pathways to Modern Diseases
Entropy 2013, 15(4), 1416-1463; doi:10.3390/e15041416
Received: 15 January 2013 / Revised: 10 April 2013 / Accepted: 10 April 2013 / Published: 18 April 2013
Cited by 35 | PDF Full-text (518 KB) | HTML Full-text | XML Full-text | Supplementary Files
Abstract
Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of
[...] Read more.
Glyphosate, the active ingredient in Roundup®, is the most popular herbicide used worldwide. The industry asserts it is minimally toxic to humans, but here we argue otherwise. Residues are found in the main foods of the Western diet, comprised primarily of sugar, corn, soy and wheat. Glyphosate's inhibition of cytochrome P450 (CYP) enzymes is an overlooked component of its toxicity to mammals. CYP enzymes play crucial roles in biology, one of which is to detoxify xenobiotics. Thus, glyphosate enhances the damaging effects of other food borne chemical residues and environmental toxins. Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body. Here, we show how interference with CYP enzymes acts synergistically with disruption of the biosynthesis of aromatic amino acids by gut bacteria, as well as impairment in serum sulfate transport. Consequences are most of the diseases and conditions associated with a Western diet, which include gastrointestinal disorders, obesity, diabetes, heart disease, depression, autism, infertility, cancer and Alzheimer’s disease. We explain the documented effects of glyphosate and its ability to induce disease, and we show that glyphosate is the “textbook example” of exogenous semiotic entropy: the disruption of homeostasis by environmental toxins. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview Is Encephalopathy a Mechanism to Renew Sulfate in Autism?
Entropy 2013, 15(1), 372-406; doi:10.3390/e15010372
Received: 8 October 2012 / Revised: 14 January 2013 / Accepted: 15 January 2013 / Published: 22 January 2013
Cited by 6 | PDF Full-text (777 KB) | HTML Full-text | XML Full-text
Abstract
This paper makes two claims: (1) autism can be characterized as a chronic low-grade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is
[...] Read more.
This paper makes two claims: (1) autism can be characterized as a chronic low-grade encephalopathy, associated with excess exposure to nitric oxide, ammonia and glutamate in the central nervous system, which leads to hippocampal pathologies and resulting cognitive impairment, and (2), encephalitis is provoked by a systemic deficiency in sulfate, but associated seizures and fever support sulfate restoration. We argue that impaired synthesis of cholesterol sulfate in the skin and red blood cells, catalyzed by sunlight and nitric oxide synthase enzymes, creates a state of colloidal instability in the blood manifested as a low zeta potential and increased interfacial stress. Encephalitis, while life-threatening, can result in partial renewal of sulfate supply, promoting neuronal survival. Research is cited showing how taurine may not only help protect neurons from hypochlorite exposure, but also provide a source for sulfate renewal. Several environmental factors can synergistically promote the encephalopathy of autism, including the herbicide, glyphosate, aluminum, mercury, lead, nutritional deficiencies in thiamine and zinc, and yeast overgrowth due to excess dietary sugar. Given these facts, dietary and lifestyle changes, including increased sulfur ingestion, organic whole foods, increased sun exposure, and avoidance of toxins such as aluminum, mercury, and lead, may help to alleviate symptoms or, in some instances, to prevent autism altogether. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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Open AccessReview Is Endothelial Nitric Oxide Synthase a Moonlighting Protein Whose Day Job is Cholesterol Sulfate Synthesis? Implications for Cholesterol Transport, Diabetes and Cardiovascular Disease
Entropy 2012, 14(12), 2492-2530; doi:10.3390/e14122492
Received: 8 October 2012 / Revised: 28 November 2012 / Accepted: 4 December 2012 / Published: 7 December 2012
Cited by 8 | PDF Full-text (618 KB) | HTML Full-text | XML Full-text
Abstract
Theoretical inferences, based on biophysical, biochemical, and biosemiotic considerations, are related here to the pathogenesis of cardiovascular disease, diabetes, and other degenerative conditions. We suggest that the “daytime” job of endothelial nitric oxide synthase (eNOS), when sunlight is available, is to catalyze sulfate
[...] Read more.
Theoretical inferences, based on biophysical, biochemical, and biosemiotic considerations, are related here to the pathogenesis of cardiovascular disease, diabetes, and other degenerative conditions. We suggest that the “daytime” job of endothelial nitric oxide synthase (eNOS), when sunlight is available, is to catalyze sulfate production. There is a striking alignment between cell types that produce either cholesterol sulfate or sulfated polysaccharides and those that contain eNOS. The signaling gas, nitric oxide, a well-known product of eNOS, produces pathological effects not shared by hydrogen sulfide, a sulfur-based signaling gas. We propose that sulfate plays an essential role in HDL-A1 cholesterol trafficking and in sulfation of heparan sulfate proteoglycans (HSPGs), both critical to lysosomal recycling (or disposal) of cellular debris. HSPGs are also crucial in glucose metabolism, protecting against diabetes, and in maintaining blood colloidal suspension and capillary flow, through systems dependent on water-structuring properties of sulfate, an anionic kosmotrope. When sunlight exposure is insufficient, lipids accumulate in the atheroma in order to supply cholesterol and sulfate to the heart, using a process that depends upon inflammation. The inevitable conclusion is that dietary sulfur and adequate sunlight can help prevent heart disease, diabetes, and other disease conditions. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview Is Cholesterol Sulfate Deficiency a Common Factor in Preeclampsia, Autism, and Pernicious Anemia?
Entropy 2012, 14(11), 2265-2290; doi:10.3390/e14112265
Received: 12 September 2012 / Revised: 21 October 2012 / Accepted: 6 November 2012 / Published: 8 November 2012
Cited by 4 | PDF Full-text (447 KB) | HTML Full-text | XML Full-text
Abstract
In a recent paper, we proposed that a contributing factor in autism is a deficiency in cholesterol sulfate supply. In this paper, we investigate a link between preeclampsia and subsequent autism in the child, and we hypothesize that both conditions can be attributed
[...] Read more.
In a recent paper, we proposed that a contributing factor in autism is a deficiency in cholesterol sulfate supply. In this paper, we investigate a link between preeclampsia and subsequent autism in the child, and we hypothesize that both conditions can be attributed to a severe depletion of cholesterol sulfate. Through studies on the Vaccine Adverse Event Reporting System (VAERS) database, we demonstrate a strong statistical relationship among the signs and symptoms associated with autism and those associated with preeclampsia, pernicious anemia, and serious adverse reactions to vaccines. We show that VAERS reports associated with symptoms typical of pernicious anemia produce both a set of symptoms that are highly correlated with preeclampsia and another set highly correlated with autism. We explain this observation via an argument that, in a severe reaction, the cascade of events subsequent to vaccination reflects a profuse production of nitric oxide (NO) and consequential destruction of both red blood cells (RBCs) and cobalamin. This may explain the diverse signs and symptoms associated with both preeclampsia and severe vaccine adverse reactions. We argue that excess NO synthesis, induced by the aluminum and antigen in vaccines, results in hemolysis of RBCs, which allows hemoglobin to scavenge the excess NO, converting it to nitrate. The NO is also scavenged by cobalamin, leading to its inactivation and contributing to subsequent pernicious anemia. Finally, we demonstrate that severe adverse reactions to vaccines can be associated with life-threatening conditions related to the heart and brain, as well as stillbirth, when the vaccine is administered to a woman in the third-trimester of pregnancy, as demonstrated by statistical analysis of the Gardasil records. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview The Completed Self: An Immunological View of the Human-Microbiome Superorganism and Risk of Chronic Diseases
Entropy 2012, 14(11), 2036-2065; doi:10.3390/e14112036
Received: 13 September 2012 / Revised: 18 October 2012 / Accepted: 19 October 2012 / Published: 25 October 2012
Cited by 9 | PDF Full-text (467 KB) | HTML Full-text | XML Full-text
Abstract
In this review, we discuss an immunological-driven sign termed the Completed Self, which is related to a holistic determination of health vs. disease. This sign (human plus commensal microbiota) forms the human superorganism. The worldwide emergence of an epidemic of chronic
[...] Read more.
In this review, we discuss an immunological-driven sign termed the Completed Self, which is related to a holistic determination of health vs. disease. This sign (human plus commensal microbiota) forms the human superorganism. The worldwide emergence of an epidemic of chronic diseases has caused increased healthcare costs, increased premature mortality and reduced quality of life for a majority of the world’s population. In addition, it has raised questions concerning the interactions between humans and their environment and potential imbalances. Misregulated inflammation, a host defense-homeostasis disorder, appears to be a key biomarker connecting a majority of chronic diseases. We consider the apparent contributors to this disorder that promote a web of interlinked comorbid conditions. Three key events are suggested to play a role: (1) altered epigenetic programming (AEP) that may span multiple generations, (2) developmental immunotoxicity (DIT), and (3) failure to adequately incorporate commensal microbes as a newborn (i.e., the incomplete self). We discuss how these three events can combine to determine whether the human superorganism is able to adequately and completely form during early childhood. We also discuss how corruption of this event can affect the risk of later-life diseases. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview Impaired Sulfate Metabolism and Epigenetics: Is There a Link in Autism?
Entropy 2012, 14(10), 1953-1977; doi:10.3390/e14101953
Received: 28 September 2012 / Revised: 16 October 2012 / Accepted: 16 October 2012 / Published: 18 October 2012
Cited by 7 | PDF Full-text (415 KB) | HTML Full-text | XML Full-text
Abstract
Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the
[...] Read more.
Autism is a brain disorder involving social, memory, and learning deficits, that normally develops prenatally or early in childhood. Frustratingly, many research dollars have as yet failed to identify the cause of autism. While twin concordance studies indicate a strong genetic component, the alarming rise in the incidence of autism in the last three decades suggests that environmental factors play a key role as well. This dichotomy can be easily explained if we invoke a heritable epigenetic effect as the primary factor. Researchers are just beginning to realize the huge significance of epigenetic effects taking place during gestation in influencing the phenotypical expression. Here, we propose the novel hypothesis that sulfates deficiency in both the mother and the child, brought on mainly by excess exposure to environmental toxins and inadequate sunlight exposure to the skin, leads to widespread hypomethylation in the fetal brain with devastating consequences. We show that many seemingly disparate observations regarding serum markers, neuronal pathologies, and nutritional deficiencies associated with autism can be integrated to support our hypothesis. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
Open AccessReview The Initial Common Pathway of Inflammation, Disease, and Sudden Death
Entropy 2012, 14(8), 1399-1442; doi:10.3390/e14081399
Received: 29 June 2012 / Revised: 19 July 2012 / Accepted: 20 July 2012 / Published: 2 August 2012
Cited by 11 | PDF Full-text (1223 KB) | HTML Full-text | XML Full-text
Abstract
In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as
[...] Read more.
In reviewing the literature pertaining to interfacial water, colloidal stability, and cell membrane function, we are led to propose that a cascade of events that begins with acute exogenous surfactant-induced interfacial water stress can explain the etiology of sudden death syndrome (SDS), as well as many other diseases associated with modern times. A systemic lowering of serum zeta potential mediated by exogenous cationic surfactant administration is the common underlying pathophysiology. The cascade leads to subsequent inflammation, serum sickness, thrombohemorrhagic phenomena, colloidal instability, and ultimately even death. We propose that a sufficient precondition for sudden death is lowered bioavailability of certain endogenous sterol sulfates, sulfated glycolipids, and sulfated glycosaminoglycans, which are essential in maintaining biological equipose, energy metabolism, membrane function, and thermodynamic stability in living organisms. Our literature review provides the basis for the presentation of a novel hypothesis as to the origin of endogenous bio-sulfates which involves energy transduction from sunlight. Our hypothesis is amply supported by a growing body of data showing that parenteral administration of substances that lower serum zeta potential results in kosmotropic cationic and/or chaotropic anionic interfacial water stress, and the resulting cascade. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)

Other

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Open AccessConcept Paper Biosemiotic Entropy of the Genome: Mutations and Epigenetic Imbalances Resulting in Cancer
Entropy 2013, 15(1), 234-261; doi:10.3390/e15010234
Received: 1 November 2012 / Revised: 30 December 2012 / Accepted: 11 January 2013 / Published: 16 January 2013
Cited by 5 | PDF Full-text (6400 KB) | HTML Full-text | XML Full-text
Abstract
Biosemiotic entropy involves the deterioration of biological sign systems. The genome is a coded sign system that is connected to phenotypic outputs through the interpretive functions of the tRNA/ribosome machinery. This symbolic sign system (semiosis) at the core of all biology has been
[...] Read more.
Biosemiotic entropy involves the deterioration of biological sign systems. The genome is a coded sign system that is connected to phenotypic outputs through the interpretive functions of the tRNA/ribosome machinery. This symbolic sign system (semiosis) at the core of all biology has been termed “biosemiosis”. Layers of biosemiosis and cellular information management are analogous in varying degrees to the semiotics of computer programming, spoken, and written human languages. Biosemiotic entropy — an error or deviation from a healthy state — results from errors in copying functional information (mutations) and errors in the appropriate context or quantity of gene expression (epigenetic imbalance). The concept of biosemiotic entropy is a deeply imbedded assumption in the study of cancer biology. Cells have a homeostatic, preprogrammed, ideal or healthy state that is rooted in genomics, strictly orchestrated by epigenetic regulation, and maintained by DNA repair mechanisms. Cancer is an eminent illustration of biosemiotic entropy, in which the corrosion of genetic information via substitutions, deletions, insertions, fusions, and aberrant regulation results in malignant phenotypes. However, little attention has been given to explicitly outlining the paradigm of biosemiotic entropy in the context of cancer. Herein we distill semiotic theory (from the familiar and well understood spheres of human language and computer code) to draw analogies useful for understanding the operation of biological semiosis at the genetic level. We propose that the myriad checkpoints, error correcting mechanisms, and immunities are all systems whose primary role is to defend against the constant pressure of biosemiotic entropy, which malignancy must shut down in order to achieve advanced stages. In lieu of the narrower tumor suppressor/oncogene model, characterization of oncogenesis into the biosemiotic framework of sign, index, or object entropy may allow for more effective explanatory hypotheses for cancer diagnosis, with consequence in improving profiling and bettering therapeutic outcomes. Full article
(This article belongs to the Special Issue Biosemiotic Entropy: Disorder, Disease, and Mortality)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.


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