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Archive | 1996

The Sciences and Arts Share a Common Creative Aesthetic

Robert Root-Bernstein

The sciences and arts were once, not so very long ago, considered to be very similar, certainly complementary, and sometimes even overlapping ways of understanding the world. No longer. Today we accept such generalizations as that the sciences are objective, analytical, and rational whereas the arts are subjective, emotional, and based on intuition. But I am a controversialist. The fact that arts and sciences are not widely perceived to be similar does not mean that they are not. Fashions often dictate perceptions of beauty and knowledge alike, and fashions are notoriously changeable. Thus, I am willing — indeed eager — to challenge the new fashion of separating sciences and arts into two, uncommunicating and even antagonistic camps. I believe that such a challenge is not only necessary if we are to develop a viable theory of thinking, but also healthy, for it should create controversy. Unlike some people, who believe that knowledge is best advanced by the slow accumulation of validated and undoubtable bits of information, I believe that we learn most by challenging conventional wisdom with the biggest and best arguments we can muster. This is my style. Sometimes it fails; sometimes it succeeds. But in either case, the process of trying to undermine dogma often reveals new aspects of knowledge, or forces it to be utilized in new and innovative ways that justify the rethinkings.


Journal of Theoretical Biology | 2015

The ribosome as a missing link in the evolution of life

Meredith Root-Bernstein; Robert Root-Bernstein

Many steps in the evolution of cellular life are still mysterious. We suggest that the ribosome may represent one important missing link between compositional (or metabolism-first), RNA-world (or genes-first) and cellular (last universal common ancestor) approaches to the evolution of cells. We present evidence that the entire set of transfer RNAs for all twenty amino acids are encoded in both the 16S and 23S rRNAs of Escherichia coli K12; that nucleotide sequences that could encode key fragments of ribosomal proteins, polymerases, ligases, synthetases, and phosphatases are to be found in each of the six possible reading frames of the 16S and 23S rRNAs; and that every sequence of bases in rRNA has information encoding more than one of these functions in addition to acting as a structural component of the ribosome. Ribosomal RNA, in short, is not just a structural scaffold for proteins, but the vestigial remnant of a primordial genome that may have encoded a self-organizing, self-replicating, auto-catalytic intermediary between macromolecules and cellular life.


Creativity Research Journal | 1993

Identification of scientists making long‐term, high‐impact contributions, with notes on their methods of working

Robert Root-Bernstein; Maurine Bernstein; Helen Gamier

Abstract A two decade (1958–1978) study was made of 40 male scientists, including four Nobel Prize winners. Multiple psychological tests were administered, along with interviews and analysis of publication rates and citations. The data yielded two factors that had very high predictive ability for identifying long‐term, high‐impact investigators: a series of five or more high‐impact papers published by the age of 45 accompanied by simultaneous involvement in research in several areas. Scientists meeting these criteria all went on to produce high‐impact papers into their late‐50s and 60s, whereas the other scientists in the study did not. Other factors, such as number of publications, membership in the National Academy of Sciences, and the award of a Nobel Prize were not significantly predictive of continued impact. Thus, previous impact should not be used as a basis for further funding independent of other measures. Methods of working peculiar to long‐term, high‐impact individuals, such as frequent changes...


Brain Research Bulletin | 1990

Serotonin binding sites. II. Muramyl dipeptide binds to serotonin binding sites on myelin basic protein, LHRH, and MSH-ACTH 4-10

Robert Root-Bernstein; Fred Westall

Previously, we reported the existence of structurally similar serotonin binding sites on myelin basic protein, LHRH, and MSH-ACTH 4-10. We now report that the adjuvant peptide, muramyl dipeptide (N-acetyl-muramyl-L-Ala-D-isoGln) also binds to these sites. This observation may help to explain previous observations of serotonin-like activity by muramyl peptides, including the promotion of slow-wave sleep and fever induction. The observation may also provide an important link between the immune system and the nervous system that may explain the role of muramyl dipeptide adjuvants in causing autoimmune diseases to serotonin-regulated proteins and their receptors, as well as the alterations in serotonin levels that are often observed in autoimmune diseases. The observation provides concrete evidence for a dual-antigen hypothesis for the induction of autoimmune diseases by an adjuvant-peptide complex. Application of such a mechanism for induction of autoimmunity may be of importance in understanding a number of postinfectious and postvaccinal neuropathies, and suggests a possible etiology for autism, in which many patients have high blood serotonin levels, autoimmune reactions to myelin basic protein, and antibodies to serotonin binding sites. Finally, the observation suggests that glycopeptides may act as neurotransmitters.


Leonardo | 2001

Music, Creativity and Scientific Thinking

Robert Root-Bernstein

Are music and sci-ence different types of intel-ligence (as posited in the context of Howard Gardners multiple intelligences), or are they two manifestations of common ways of think-ing? By focusing on scien-tists who have been musi-cians and on the ways they have used their musical knowledge to inform their scientific work, the author argues in this article that music and science are two ways of using a common set of tools for thinking that unify all disciplines. He explores the notion that cre-ative individuals are usually polymaths who think in trans-disciplinary ways.


Autoimmunity | 2009

Antigenic complementarity between coxsackie virus and streptococcus in the induction of rheumatic heart disease and autoimmune myocarditis.

Robert Root-Bernstein; Jessica Vonck; Abigail Podufaly

A variety of clinical, epidemiological, and experimental data suggest that rheumatic heart disease and autoimmune myocarditis are not only similar in their pathogenesis, but may often be due to combined infections with coxsackie virus (CX) and streptococcus A bacteria (SA). This paper reviews the evidence for this hypothesis, provides some new experimental data supporting the hypothesis, and suggests specific experiments for testing it. While, it is well-established that the M protein of SA mimics myosin, we demonstrate using homology search tools that various CX proteins mimic actin. We further demonstrate that antibody against CX recognizes actin as an antigen, and that anti-actin antibodies recognize CX antigen. Thus, anti-CX antibodies may also target muscle. Moreover, since myosin and actin are molecularly complementary, it follows that some SA and CX proteins may be molecularly complementary. Some antibodies against these complementary proteins in SA and CX should therefore act like idiotype-antiidiotype antibodies. We show that, indeed, CX and SA antibodies precipitate each other. Thus, it is possible that combined CX–SA infections produce more severe disease by producing pairs of idiotypic antibodies that act like antiidiotypic antibodies as well, thereby, disregulating immune control and triggering an autoimmune reaction against both myosin and actin simultaneously. We predict that combinations of the appropriate actin- and myosin-like antigens from CX and SA will, therefore, be much more autoimmunogenic than antigens from CX or SA alone, and that the combination will not require use of adjuvants or self-proteins that many current protocols require. It is possible that co-infections involving CX or SA with other infectious agents may produce similarly enhanced disease.


Creativity Research Journal | 2006

Imaginary worldplay in childhood and maturity and its impact on adult creativity

Michele Root-Bernstein; Robert Root-Bernstein

ABSTRACT: The childhood invention of imaginary worlds or paracosms may prepare for creative endeavor in adulthood. To test hypotheses concerning the incidence of childhood worldplay and its connection to mature work, this study queried MacArthur Fellows, selected for their creativity, and compared them to Michigan State University (MSU) students. Whereas previous research declared paracosm play to be uncommon and associated with the arts, this study found it reasonably common among MSU students (3%–12%), about twice as frequent among MacArthur Fellows (5%–26%), and prevalent in the backgrounds of scientists and social scientists as well as artists. A majority of Fellows with assessed worldplay in childhood reported connections between early paracosm play and mature endeavor. Childhood worldplay deserves further study as early apprenticeship in creative imagination.


Autoimmunity | 2001

Insulin binds to glucagon forming a complex that is hyper-antigenic and inducing complementary antibodies having an idiotype-antiidiotype relationship

Robert Root-Bernstein; Christopher Dobbelstein

We demonstrate using physico-chemical techniques that insulin binds to glucagon with a Kd of 0.89 micromolar. While such binding is of little significance physiologically, it has important immunological consequences. Hormone binding is mirrored by specific binding between insulin antibody and glucagon antibody to form idiotype-antiidiotype complexes observable by Ouchterlony immunodiffusion and ELISA. These complexes may provide new insights into the formation of circulating immune complexes in diabetes. The insulin-glucagon complex is hyper-antigenic, inducing antibody production at concentrations that do not elicit immune responses from the individual hormones. The resulting immune response is not primarily against the individual hormones, but against the complex. In fact, all so-called insulin antibodies tested (rabbit, guinea pig, mouse and human) show substantially higher affinity for insulin-glucagon complex than for insulin alone, suggesting that this complex is the primary antigen in most, if not all, cases. These results lead to several testable predictions, including the possibility that glucagon antibody will bind to insulin receptors to cause type 2 (antibody mediated) insulin resistance.


The International Handbook on Innovation | 2003

Problem Generation and Innovation

Robert Root-Bernstein

Abstract: Most of the literature on innovation concerns fostering better solutions to existing problems. Many innovators in the sciences and engineering argue, however, that problem generation is far more critical to innovation than problem solution, involving not just a thorough grasp of what is known (epistemology), but of what is not known (nepistemology). The proper definition of a problem gets an innovator more than half way to its solution; poorly posed questions divert energy, resources, and ideas. This chapter explores how problem definition and evaluation act as catalysts for insight and examines strategies used by successful innovators to generate productive problems.


Clinical & Developmental Immunology | 2006

Antigenic Complementarity in the Origins of Autoimmunity: A General Theory Illustrated With a Case Study of Idiopathic Thrombocytopenia Purpura

Robert Root-Bernstein; Jacob P. Couturier

We describe a novel, testable theory of autoimmunity, outline novel predictions made by the theory, and illustrate its application to unravelling the possible causes of idiopathic thrombocytopenia purpura (ITP). Pairs of stereochemically complementary antigens induce complementary immune responses (antibody or T-cell) that create loss of regulation and civil war within the immune system itself. Antibodies attack antibodies creating circulating immune complexes; T-cells attack T-cells creating perivascular cuffing. This immunological civil war abrogates the self-nonself distinction. If at least one of the complementary antigens mimics a self antigen, then this unregulated immune response will target host tissues as well. Data demonstrating that complementary antigens are found in some animal models of autoimmunity and may be present in various human diseases, especially ITP, are reviewed. Specific mechanisms for preventing autoimmunity or suppressing existing autoimmunity are derived from the theory, and critical tests proposed. Finally, we argue that Kochs postulates are inadequate for establishing disease causation for multiple-antigen diseases and discuss the possibility that current research has failed to elucidate the causes of human autoimmune diseases because we are using the wrong criteria.

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Ania Pathak

Michigan State University

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Jessica Vonck

Michigan State University

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Plamen L. Simeonov

Humboldt University of Berlin

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