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R S Root-Bernstein

Publications and source records attributed to R S Root-Bernstein.

48 records · Page 3Linked to original sources
PubMed1983

An explanation of prevention and suppression of experimental allergic encephalomyelitis.

An explanation of experimental allergic encephalomyelitis prevention and suppression is presented based upon evidence that the active unit in disease induction is an encephalitogen-adjuvant complex. The stereochemical complementarity in structure of the encephalitogen and adjuvant is mirrored in complementarity in the recognition sites of lymphocyte populations activated against encephalitogen and adjuvant. Since two complementary lymphocyte populations are necessary for disease induction, any procedure that prevents the development of one of these populations will prevent disease induction. Any procedure that eliminates one population after induction has occurred will suppress the disease. We argue that all extant data support the hypothesis. Several new experiments are proposed to further test it.

Adjuvants, Immunologic↗
PubMedDate not supplied

Toward a philosophy of cancer research.

Every theory and all research assumes, either explicitly or implicitly, a scientific philosophy. Making the philosophy of cancer research explicit is likely to improve our understanding both of what we know and what we still need to discover. The implications for cancer research of three different philosophies of science are therefore outlined here: 1) reduction-mechanism; 2) holism; and 3) complementarity. We show that each of these philosophies leads to a different notion of causation, a different expectation of what represents a valid explanation of cancer, and thus to different problems that are addressed by different types of experiments. We conclude that the development of an appropriate philosophy of science is not only a relevant but necessary element in research on carcinogenesis.

Humans↗
PubMedDate not supplied

A simple stochastic model of development and carcinogenesis.

Game theory can be a powerful tool for generating testable hypotheses concerning biological systems. We present a simple game that has many features analogous to a developing cellular system. The game mimics random turning on of genes in cells. Despite the randomness explicit in the mechanism, the game nonetheless results in deterministic outcomes that are extremely resistant to perturbation. Analysis of the types of mistakes or rule changes that are necessary in order to alter the outcome of the game suggests that there are a very limited number of mechanisms by which the differentiation process can result in tumor formation or carcinogenesis. The most significant causes of altered outcomes are alterations in gene order or number, and alteration of the rule by which the gene sequences are traversed. These alterations correspond to chromosomal defects or rearrangements, changes in chromosomal number, and changes in the "orders" delivered by regulatory genes. Notably, most common mistakes, which correspond to simple forms of mutations, have no effect on the outcome of the game, suggesting that mutation is relevant to tumorigenesis and carcinogenesis only to the extent that it results in altered "rules" for reading other gene sequences.

Cell Transformation, Neoplastic↗
PubMedDate not supplied

Complementarity and contradiction in cancer research: the role of hierarchies in carcinogenesis.

The essays on carcinogenesis in this volume tend to fall into groups according to the level of complexity at which the theories focus. Many investigators focus on events and processes involving genetic mutations. Others, however, identify events or processes at the chromosomal, cellular, tissue, or organsimal level as being of primary importance. While such different approaches to carcinogenesis may, at first, seem to be contradictory, they may be seen to be complementary in light of the general theory of hierarchical organization. Hierarchy theory, which is a development of general systems theory, describes the manner in which organized processes are formed by subunits that have unique properties of their own but which can acquire new properties through their interactions. Hierarchy theory suggests that carcinogenesis can only be understood as a set of interactions between organizational processes at every level from genetic to organismal.

Cell Transformation, Neoplastic↗
PubMedDate not supplied

Antisense-designed peptides: a comparative study focusing on possible complements to angiotensin II.

A comprehensive study of antisense peptides possibly complementary to angiotensin II (AII) is described. Antisense peptides of AII were designed using two different procedures outlined by Blalock and Root-Bernstein. Also, peptide complements designed to interact as homologs of AII were investigated. Three methods were used to detect binding between these peptides and AII. Several antisense-designed peptides were studied with unprotected termini to compare the effects of protected vs. unprotected termini. It was determined that the protected antisense-designed peptides derived from Root-Bernstein's methods interacted (high micro-molar range) directly with AII, while those protected antisense peptides derived from Blalock's method interacted only with the AII receptor. Two novel AII antagonists were discovered using this technology, a Root-Bernstein derived unprotected complementary peptide (H2N-K-G-V-Y-M-H-A-L-CO2H) and a Blalock derived unprotected antisense peptide (H2N-E-G-V-Y-V-H-P-V-CO2H), which exhibited 5 microM and 70 nM affinity toward the AII receptor, respectively.

Adrenal Glands↗