Magnus S. Magnusson

Biography

Magnus S. Magnusson, PhD, Emeritus Research Professor, founder and director of the Human Behavior Laboratory (hbl.hi.is), University of Iceland. Author of the T-pattern, T-string and T-system model and the corresponding detection algorithms and software THEMETM (PatternVision.com), initially focusing on real-time organization of behavior. Co-directed DNA analysis. Numerous papers, talks and keynotes in ethology, neuroscience, mathematics, religion, proteomics, mass spectrometry, A.I., robotics and nanoscience. Deputy Director 1983-1988 in Museum of Mankind, National Museum of Natural History, Paris. Repeatedly invited Professor at the University of Paris, V, VIII and XIII in psychology and the biology of behavior.  Now works in formal collaboration between 32 European and American universities initiated 1995 at the University Rene Descartes of Paris V, Sorbonne, based on “Magnusson’s analytical model

Abstract

Statement of the Problem: Attempts to understand human behavior continue in modern times of explosive growth in scientific knowledge, technology and population sizes in the biologically extremely recent human mass-societies of millions of highly specialized members only paralleled in insects using very different mechanisms. Can biological and possibly mathematical models be found to explain such a revolution occurring in a biological eye-blink?

Methodology & Theoretical Orientation: Ethology, the biology of behavior, received its first Nobel prize in 1973 (in Medicine or physiology) shared between N. Tinbergen, K. Lorenz and K. von Frisch and in 1975 E.O. Wilson’s Sociobiology pointed to social insect societies as biological models for human mass-societies. But none of the studied organisms were components of any others, so Lorenz’s Nobel lecture, “Analogy as a source of knowledge”, had no mention of self-similarity/analogy.

Diana Anderson

Biography

Diana Anderson (H index 64) holds the Established Chair in Biomedical Sciences at the University of Bradford. She obtained her first degree in the University of Wales and second degrees in the Faculty of Medicine, University of Manchester. She has 500+ peer-reviewed papers, 10 books, has successfully supervised 34 PhDs, is an Editorial Board Member of 10 international journals. She is Editor-in-Chief of a book series on Toxicology for the Royal Society of Chemistry. She gives plenary and key note addresses at various international meetings. She is a consultant for many international organizations, including WHO, EU, NATO, TWAS, UNIDO, OECD.

Abstract

Sertoli cells (SCs) are highly differentiated epithelial cells which play an essential role in the functional development of the testis and hence in the expression of the male phenotype. Sertoli cells form the blood-testis barrier making an extraordinary microenvironment where male germ cells develop and are under strict hormonal control. Sertoli cells express the cytokine glial cell line-derived neurotrophic factor (GDNF) under control of the follicle-stimulating hormone. GDNF is an essential regulator of SCs self-renewal and survival in vitro and is required for maintenance of the undifferentiated spermatogonial stem cells population in vivo. Various drugs, particularly alkylating agents, have been shown to be gonadotoxic. Methotrexate (MTX) is an anti-metabolite widely used in the treatment of neoplastic disorders, rheumatoid arthritis and psoriasis. The present study explored the mechanism of cytotoxic and genotoxic effects of MTX on a primary culture of Sertoli cells in vitro. DNA damage was evaluated using the Comet assay and the cell death was identified as apoptosis using terminal deoxynucleotidyl transferase- (TdT-) mediated dUTP nick end labeling (TUNEL) assay. mRNA expression and proteins levels of GDNF, P53 and ataxia telangiectasia mutated (ATM) were also investigated using quantitative polymerase chain reaction (qPCR) and Western blot methods. Results of the present study clearly showed that MTX -induced DNA damage as evident from the different Comet assay parameters. The GDNF disruption seen in our in vivo experiments correlates with the sudden increase of activation of p53 and ATM in Sertoli cells. These results imply that MTX affects the Sertoli cells, inducing GDNF proteins. This disruption signifies the loss of some support mechanism for spermatogenic cells and could be the cause of the increased apoptotic cells.

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