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Article ; Online: Integrate chaos theory with Epoker and leave God out of it!

Root-Bernstein, Robert

2024

Language	English
Publishing date	2024-02-07
Publishing country	England
Document type	Letter
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP286233
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Article ; Online: T-Cell Receptor Sequences Identify Combined Coxsackievirus-

Root-Bernstein, Robert

International journal of molecular sciences

2024 Volume 25, Issue 3

Abstract: Recent research suggests that T-cell receptor (TCR) sequences expanded during human immunodeficiency virus and SARS-CoV-2 infections unexpectedly mimic these viruses. The hypothesis tested here is that TCR sequences expanded in patients with type 1 ... ...

Abstract	Recent research suggests that T-cell receptor (TCR) sequences expanded during human immunodeficiency virus and SARS-CoV-2 infections unexpectedly mimic these viruses. The hypothesis tested here is that TCR sequences expanded in patients with type 1 diabetes mellitus (T1DM) and autoimmune myocarditis (AM) mimic the infectious triggers of these diseases. Indeed, TCR sequences mimicking coxsackieviruses, which are implicated as triggers of both diseases, are statistically significantly increased in both T1DM and AM patients. However, TCRs mimicking
MeSH term(s)	Animals ; Humans ; Diabetes Mellitus, Type 1 ; Myocarditis ; Autoimmune Diseases/complications ; Enterovirus ; Coxsackievirus Infections/complications ; Autoantigens ; Streptococcus ; Streptococcal Infections/complications ; Antigens, Bacterial ; Receptors, Antigen, T-Cell
Chemical Substances	Autoantigens ; Antigens, Bacterial ; Receptors, Antigen, T-Cell
Language	English
Publishing date	2024-02-01
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25031797
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Article ; Online: From Co-Infections to Autoimmune Disease via Hyperactivated Innate Immunity: COVID-19 Autoimmune Coagulopathies, Autoimmune Myocarditis and Multisystem Inflammatory Syndrome in Children.

Root-Bernstein, Robert

International journal of molecular sciences

2023 Volume 24, Issue 3

Abstract: Neutrophilia and the production of neutrophil extracellular traps (NETs) are two of many measures of increased inflammation in severe COVID-19 that also accompany its autoimmune complications, including coagulopathies, myocarditis and multisystem ... ...

Abstract	Neutrophilia and the production of neutrophil extracellular traps (NETs) are two of many measures of increased inflammation in severe COVID-19 that also accompany its autoimmune complications, including coagulopathies, myocarditis and multisystem inflammatory syndrome in children (MIS-C). This paper integrates currently disparate measures of innate hyperactivation in severe COVID-19 and its autoimmune complications, and relates these to SARS-CoV-2 activation of innate immunity. Aggregated data include activation of Toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD) receptors, NOD leucine-rich repeat and pyrin-domain-containing receptors (NLRPs), retinoic acid-inducible gene I (RIG-I) and melanoma-differentiation-associated gene 5 (MDA-5). SARS-CoV-2 mainly activates the virus-associated innate receptors TLR3, TLR7, TLR8, NLRP3, RIG-1 and MDA-5. Severe COVID-19, however, is characterized by additional activation of TLR1, TLR2, TLR4, TLR5, TLR6, NOD1 and NOD2, which are primarily responsive to bacterial antigens. The innate activation patterns in autoimmune coagulopathies, myocarditis and Kawasaki disease, or MIS-C, mimic those of severe COVID-19 rather than SARS-CoV-2 alone suggesting that autoimmunity follows combined SARS-CoV-2-bacterial infections. Viral and bacterial receptors are known to synergize to produce the increased inflammation required to support autoimmune disease pathology. Additional studies demonstrate that anti-bacterial antibodies are also required to account for known autoantigen targets in COVID-19 autoimmune complications.
MeSH term(s)	Child ; Humans ; COVID-19 ; Myocarditis ; Coinfection ; SARS-CoV-2 ; Immunity, Innate ; Systemic Inflammatory Response Syndrome ; Autoimmune Diseases/complications
Language	English
Publishing date	2023-02-03
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24033001
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Article: Biased, Bitopic, Opioid-Adrenergic Tethered Compounds May Improve Specificity, Lower Dosage and Enhance Agonist or Antagonist Function with Reduced Risk of Tolerance and Addiction.

Root-Bernstein, Robert

Pharmaceuticals (Basel, Switzerland)

2022 Volume 15, Issue 2

Abstract: This paper proposes the design of combination opioid-adrenergic tethered compounds to enhance efficacy and specificity, lower dosage, increase duration of activity, decrease side effects, and reduce risk of developing tolerance and/or addiction. ... ...

Abstract	This paper proposes the design of combination opioid-adrenergic tethered compounds to enhance efficacy and specificity, lower dosage, increase duration of activity, decrease side effects, and reduce risk of developing tolerance and/or addiction. Combinations of adrenergic and opioid drugs are sometimes used to improve analgesia, decrease opioid doses required to achieve analgesia, and to prolong the duration of analgesia. Recent mechanistic research suggests that these enhanced functions result from an allosteric adrenergic binding site on opioid receptors and, conversely, an allosteric opioid binding site on adrenergic receptors. Dual occupancy of the receptors maintains the receptors in their high affinity, most active states; drops the concentration of ligand required for full activity; and prevents downregulation and internalization of the receptors, thus inhibiting tolerance to the drugs. Activation of both opioid and adrenergic receptors also enhances heterodimerization of the receptors, additionally improving each drug's efficacy. Tethering adrenergic drugs to opioids could produce new drug candidates with highly desirable features. Constraints-such as the locations of the opioid binding sites on adrenergic receptors and adrenergic binding sites on opioid receptors, length of tethers that must govern the design of such novel compounds, and types of tethers-are described and examples of possible structures provided.
Language	English
Publishing date	2022-02-10
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2193542-7
ISSN	1424-8247
ISSN	1424-8247
DOI	10.3390/ph15020214
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Article ; Online: From Co-Infections to Autoimmune Disease via Hyperactivated Innate Immunity

Robert Root-Bernstein

International Journal of Molecular Sciences, Vol 24, Iss 3001, p

COVID-19 Autoimmune Coagulopathies, Autoimmune Myocarditis and Multisystem Inflammatory Syndrome in Children

2023 Volume 3001

Abstract	Neutrophilia and the production of neutrophil extracellular traps (NETs) are two of many measures of increased inflammation in severe COVID-19 that also accompany its autoimmune complications, including coagulopathies, myocarditis and multisystem inflammatory syndrome in children (MIS-C). This paper integrates currently disparate measures of innate hyperactivation in severe COVID-19 and its autoimmune complications, and relates these to SARS-CoV-2 activation of innate immunity. Aggregated data include activation of Toll-like receptors (TLRs), nucleotide-binding oligomerization domain (NOD) receptors, NOD leucine-rich repeat and pyrin-domain-containing receptors (NLRPs), retinoic acid-inducible gene I (RIG-I) and melanoma-differentiation-associated gene 5 (MDA-5). SARS-CoV-2 mainly activates the virus-associated innate receptors TLR3, TLR7, TLR8, NLRP3, RIG-1 and MDA-5. Severe COVID-19, however, is characterized by additional activation of TLR1, TLR2, TLR4, TLR5, TLR6, NOD1 and NOD2, which are primarily responsive to bacterial antigens. The innate activation patterns in autoimmune coagulopathies, myocarditis and Kawasaki disease, or MIS-C, mimic those of severe COVID-19 rather than SARS-CoV-2 alone suggesting that autoimmunity follows combined SARS-CoV-2-bacterial infections. Viral and bacterial receptors are known to synergize to produce the increased inflammation required to support autoimmune disease pathology. Additional studies demonstrate that anti-bacterial antibodies are also required to account for known autoantigen targets in COVID-19 autoimmune complications.
Keywords	neutrophils ; SARS-CoV-2 ; cytokine storm ; bacterial co-infection ; LPS ; Kawasaki disease ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	572
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article: Pneumococcal and Influenza Vaccination Rates and Pneumococcal Invasive Disease Rates Set Geographical and Ethnic Population Susceptibility to Serious COVID-19 Cases and Deaths.

Root-Bernstein, Robert

Vaccines

2021 Volume 9, Issue 5

Abstract: This study examines the relationship of pneumococcal vaccination rates, influenza, measles-mumps-rubella (MMR) diphtheria-tetanus-pertussis vaccinations (DTP), polio, Haemophilus influenzae type B (Hib), and Bacillus Calmette-Guerin (tuberculosis) ... ...

Abstract	This study examines the relationship of pneumococcal vaccination rates, influenza, measles-mumps-rubella (MMR) diphtheria-tetanus-pertussis vaccinations (DTP), polio, Haemophilus influenzae type B (Hib), and Bacillus Calmette-Guerin (tuberculosis) vaccination rates to COVID-19 case and death rates for 51 nations that have high rates of COVID-19 testing and for which nearly complete childhood, at-risk adult and elderly pneumococcal vaccination data were available. The study is unique in a large number of nations examined, the range of vaccine controls, in testing effects of combinations of vaccinations, and in examining the relationship of COVID-19 and vaccination rates to invasive pneumococcal disease (IPD). Analysis of Italian regions and the states of the United States were also performed. Significant positive correlations were found between IPD (but not lower respiratory infections) and COVID-19 rates, while significant negative correlations were found between pneumococcal vaccination and COVID-19 rates. Influenza and MMR vaccination rates were negatively correlated with lower respiratory infection (LRI) rates and may synergize with pneumococcal vaccination rates to protect against COVID-19. Pneumococcal and influenza vaccination rates were independent of other vaccination rates. These results suggest that endemic rates of bacterial pneumonias, for which pneumococci are a sentinel, may set regional and national susceptibility to severe COVID-19 disease and death.
Language	English
Publishing date	2021-05-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2703319-3
ISSN	2076-393X
ISSN	2076-393X
DOI	10.3390/vaccines9050474
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Article ; Online: COVID-19 coagulopathies: Human blood proteins mimic SARS-CoV-2 virus, vaccine proteins and bacterial co-infections inducing autoimmunity: Combinations of bacteria and SARS-CoV-2 synergize to induce autoantibodies targeting cardiolipin, cardiolipin-binding proteins, platelet factor 4, prothrombin, and coagulation factors.

Root-Bernstein, Robert

BioEssays : news and reviews in molecular, cellular and developmental biology

2021 Volume 43, Issue 12, Page(s) e2100158

Abstract: Severe COVID-19 is often accompanied by coagulopathies such as thrombocytopenia and abnormal clotting. Rarely, such complications follow SARS-CoV-2 vaccination. The cause of these coagulopathies is unknown. It is hypothesized that coagulopathies ... ...

Abstract	Severe COVID-19 is often accompanied by coagulopathies such as thrombocytopenia and abnormal clotting. Rarely, such complications follow SARS-CoV-2 vaccination. The cause of these coagulopathies is unknown. It is hypothesized that coagulopathies accompanying SARS-CoV-2 infections and vaccinations result from bacterial co-infections that synergize with virus-induced autoimmunity due to antigenic mimicry of blood proteins by both bacterial and viral antigens. Coagulopathies occur mainly in severe COVID-19 characterized by bacterial co-infections with Streptococci, Staphylococci, Klebsiella, Escherichia coli, and Acinetobacter baumannii. These bacteria express unusually large numbers of antigens mimicking human blood antigens, as do both SARS-CoV-2 and adenoviruses. Bacteria mimic cardiolipin, prothrombin, albumin, and platelet factor 4 (PF4). SARS-CoV-2 mimics complement factors, Rh antigens, platelet phosphodiesterases, Factors IX and X, von Willebrand Factor (VWF), and VWF protease ADAMTS13. Adenoviruses mimic prothrombin and platelet factor 4. Bacterial prophylaxis, avoidance of vaccinating bacterially infected individuals, and antigen deletion for vaccines may reduce coagulopathy risk. Also see the video abstract here: https://youtu.be/zWDOsghrPg8.
MeSH term(s)	Autoantibodies ; Autoimmunity ; Bacteria ; COVID-19 ; COVID-19 Vaccines ; Cardiolipins ; Carrier Proteins ; Coinfection ; Humans ; Platelet Factor 4 ; Prothrombin ; SARS-CoV-2
Chemical Substances	Autoantibodies ; COVID-19 Vaccines ; Cardiolipins ; Carrier Proteins ; Platelet Factor 4 (37270-94-3) ; Prothrombin (9001-26-7)
Language	English
Publishing date	2021-10-22
Publishing country	United States
Document type	Journal Article ; Video-Audio Media
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.202100158
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Article ; Online: Innate Receptor Activation Patterns Involving TLR and NLR Synergisms in COVID-19, ALI/ARDS and Sepsis Cytokine Storms: A Review and Model Making Novel Predictions and Therapeutic Suggestions.

Root-Bernstein, Robert

International journal of molecular sciences

2021 Volume 22, Issue 4

Abstract: Severe COVID-19 is characterized by a "cytokine storm", the mechanism of which is not yet understood. I propose that cytokine storms result from synergistic interactions among Toll-like receptors (TLR) and nucleotide-binding oligomerization domain-like ... ...

Abstract	Severe COVID-19 is characterized by a "cytokine storm", the mechanism of which is not yet understood. I propose that cytokine storms result from synergistic interactions among Toll-like receptors (TLR) and nucleotide-binding oligomerization domain-like receptors (NLR) due to combined infections of SARS-CoV-2 with other microbes, mainly bacterial and fungal. This proposition is based on eight linked types of evidence and their logical connections. (1) Severe cases of COVID-19 differ from healthy controls and mild COVID-19 patients in exhibiting increased TLR4, TLR7, TLR9 and NLRP3 activity. (2) SARS-CoV-2 and related coronaviruses activate TLR3, TLR7, RIG1 and NLRP3. (3) SARS-CoV-2 cannot, therefore, account for the innate receptor activation pattern (IRAP) found in severe COVID-19 patients. (4) Severe COVID-19 also differs from its mild form in being characterized by bacterial and fungal infections. (5) Respiratory bacterial and fungal infections activate TLR2, TLR4, TLR9 and NLRP3. (6) A combination of SARS-CoV-2 with bacterial/fungal coinfections accounts for the IRAP found in severe COVID-19 and why it differs from mild cases. (7) Notably, TLR7 (viral) and TLR4 (bacterial/fungal) synergize, TLR9 and TLR4 (both bacterial/fungal) synergize and TLR2 and TLR4 (both bacterial/fungal) synergize with NLRP3 (viral and bacterial). (8) Thus, a SARS-CoV-2-bacterium/fungus coinfection produces synergistic innate activation, resulting in the hyperinflammation characteristic of a cytokine storm. Unique clinical, experimental and therapeutic predictions (such as why melatonin is effective in treating COVID-19) are discussed, and broader implications are outlined for understanding why other syndromes such as acute lung injury, acute respiratory distress syndrome and sepsis display varied cytokine storm symptoms.
MeSH term(s)	Acute Lung Injury/drug therapy ; Acute Lung Injury/immunology ; Acute Lung Injury/metabolism ; Animals ; COVID-19/drug therapy ; COVID-19/immunology ; Cytokine Release Syndrome/drug therapy ; Cytokine Release Syndrome/immunology ; Cytokine Release Syndrome/metabolism ; Humans ; Inflammation/drug therapy ; Inflammation/immunology ; NLR Proteins/immunology ; Respiratory Distress Syndrome/drug therapy ; Respiratory Distress Syndrome/immunology ; Respiratory Distress Syndrome/metabolism ; SARS-CoV-2/immunology ; Sepsis/drug therapy ; Sepsis/immunology ; Sepsis/metabolism ; Toll-Like Receptors/immunology ; Toll-Like Receptors/metabolism
Chemical Substances	NLR Proteins ; Toll-Like Receptors
Language	English
Publishing date	2021-02-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22042108
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Article ; Online: 'Evolutionary poker': an agent-based model of interactome emergence and epistasis tested against Lenski's long-term E. coli experiments.

Root-Bernstein, Robert S / Bernstein, Morton I

The Journal of physiology

2023

Abstract: A simple agent-based model is presented that produces results matching the experimental data found by Lenski's group for ≤50,000 generations of Escherichia coli bacteria under continuous selective pressure. Although various mathematical models have been ... ...

Abstract	A simple agent-based model is presented that produces results matching the experimental data found by Lenski's group for ≤50,000 generations of Escherichia coli bacteria under continuous selective pressure. Although various mathematical models have been devised previously to model the Lenski data, the present model has advantages in terms of overall simplicity and conceptual accessibility. The model also clearly illustrates a number of features of the evolutionary process that are otherwise not obvious, such as the roles of epistasis and historical contingency in adaptation and why evolution is time irreversible ('Dollo's law'). The reason for this irreversibility is that genomes become increasingly integrated or organized, and this organization becomes a novel selective factor itself, against which future generations must compete. Selection for integrated or synergistic networks, systems or sets of mutations or traits, not for individual mutations, confers the main adaptive advantage. The result is a punctuated form of evolution that follows a logarithmic occurrence probability, in which evolution proceeds very quickly when interactomes begin to form but which slows as interactomes become more robust and the difficulty of integrating new mutations increases. Sufficient parameters exist in the game to suggest not only how equilibrium or stasis is reached but also the conditions in which it will be punctuated, the factors governing the rate at which genomic organization occurs and novel traits appear, and how population size, genome size and gene variability affect these.
Language	English
Publishing date	2023-09-14
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	3115-x
ISSN	1469-7793 ; 0022-3751
ISSN (online)	1469-7793
ISSN	0022-3751
DOI	10.1113/JP284421
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Article ; Online: T Cell Receptor Sequences Amplified during Severe COVID-19 and Multisystem Inflammatory Syndrome in Children Mimic SARS-CoV-2, Its Bacterial Co-Infections and Host Autoantigens.

Root-Bernstein, Robert / Churchill, Elizabeth / Oliverio, Shelby

International journal of molecular sciences

2023 Volume 24, Issue 2

Abstract: Published hypervariable region V-beta T cell receptor (TCR) sequences were collected from people with severe COVID-19 characterized by having various autoimmune complications, including blood coagulopathies and cardiac autoimmunity, as well as from ... ...

Abstract	Published hypervariable region V-beta T cell receptor (TCR) sequences were collected from people with severe COVID-19 characterized by having various autoimmune complications, including blood coagulopathies and cardiac autoimmunity, as well as from patients diagnosed with the Kawasaki disease (KD)-like multisystem inflammatory syndrome in children (MIS-C). These were compared with comparable published v-beta TCR sequences from people diagnosed with KD and from healthy individuals. Since TCR V-beta sequences are supposed to be
MeSH term(s)	Child ; Humans ; COVID-19 ; SARS-CoV-2 ; Autoantigens ; Coinfection ; Receptors, Antigen, T-Cell/genetics ; Autoimmune Diseases ; Receptors, Antigen, T-Cell, alpha-beta ; Connective Tissue Diseases ; Bacteria ; Bacterial Infections ; Mucocutaneous Lymph Node Syndrome
Chemical Substances	Autoantigens ; Receptors, Antigen, T-Cell ; Receptors, Antigen, T-Cell, alpha-beta
Language	English
Publishing date	2023-01-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24021335
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