{"title":"Finite Universe of Discourse:The Systems Biology of Walter Elsasser (1904-1991)","authors":"D. Gatherer","doi":"10.2174/1874196700801010009","DOIUrl":"https://doi.org/10.2174/1874196700801010009","url":null,"abstract":"Walter Elsasser (1904-1991), an eminent quantum physicist and geophysicist, was also active in theoretical biology over a 35-year period from the early 1950s to the late 1980s. Although increasingly estranged from the biological establishment during the last fifteen years of his life, Elsasser’s central concern with complexity has resulted in a revival of interest in his theories over the last decade, particularly among those who see biology from a systems holist rather than a molecular reductionist viewpoint. This article reviews the development of Elsasser’s thought from his early opposition to genetic deter- minism, through the radical epistemology of his middle period, to his later more broadly philosophical ideas. After a summary of existing responses to Elsasser in the literature, a fresh critique and assessment of his work is presented, with particu- lar attention to the implications for systems biology. It is concluded that although Elsasser drew some conclusions from his epistemology that are not justifiable in the light of subsequent research, his insistence on the existence of biotonic phenomena in biology, irreducible (either at present, or in principle) to physics, is correct. Ironically, the most significant biotonic princi- ple is one which Elsasser largely ignored in his own work, that of Natural Selection.","PeriodicalId":22949,"journal":{"name":"The Open Biology Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72802834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
S. Nistri, T. Persichini, C. Sassoli, M. Colasanti, D. Bani
{"title":"Up-Regulation of Inducible Nitric Oxide Synthase by Relaxin in Rat Coronary Endothelial Cells is Not Mediated by Proinflammatory Cytokines","authors":"S. Nistri, T. Persichini, C. Sassoli, M. Colasanti, D. Bani","doi":"10.2174/1874196700801010001","DOIUrl":"https://doi.org/10.2174/1874196700801010001","url":null,"abstract":"Relaxin, best known for its reproductive effects can be also viewed as a cardiovascular hormone. Its action in- cludes a marked increase in coronary blood flow, exerted through the up-regulation of inducible nitric oxide (NO) syn- thase (NOS II) and NO production in vascular endothelial and smooth muscle cells. This effect seems to involve NF- B, a classical transcription factor controlling NOS II induction by proinflammatory cytokines. The present study was designed to clarify the mechanisms underlying the relaxin-induced up-regulation of NOS II gene in endothelial cells. Rat coronary endothelial (RCE) cells were grown for 30 min, 2, 6 and 12 h in the absence or presence of 60 ng/ml porcine relaxin. Time-course analysis of the expression of NOS II and the proinflammatory cytokines IL-1 and TNF was per- formed. Relaxin induced the expression of NOS II transcript and protein at all these time points. No correlation was ob- served with the expression profiles of the genes for the assayed cytokines: IL-1 expression showed a first peak at 30 min. followed by a decline and a second peak at 12 h, whereas faint TNF- expression was only detected at 2 h. Relaxin re- tained the ability to induce NOS II transcript and to generate NO even in the presence of neutralizing anti- IL1 and/or anti-TNF- antibodies. The current findings suggest that the induction of NOS II by relaxin in coronary endothelial cells is a direct effect of this hormone and does not depend on a primary cytokine-mediated pathway that eventually results in NF- B activation and NOS II induction.","PeriodicalId":22949,"journal":{"name":"The Open Biology Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86103014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Isabella B R Scheiber, Brigitte M Weiß, Katharina Hirschenhauser, Claudia A F Wascher, Iulia T Nedelcu, Kurt Kotrschal
{"title":"Does 'Relationship Intelligence' Make Big Brains in Birds?","authors":"Isabella B R Scheiber, Brigitte M Weiß, Katharina Hirschenhauser, Claudia A F Wascher, Iulia T Nedelcu, Kurt Kotrschal","doi":"10.2174/1874196700801010006","DOIUrl":"https://doi.org/10.2174/1874196700801010006","url":null,"abstract":"<p><p>Lately, Emery et al. developed a bird-specific modification of the \"social brain hypothesis\", termed \"relationship intelligence hypothesis\". Although the idea may be valuable, we doubt that it is supported by sufficient evidence and critically discuss some of the arguments raised by the authors in favour of their new idea.</p>","PeriodicalId":22949,"journal":{"name":"The Open Biology Journal","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2008-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3188405/pdf/ukmss-36469.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30197170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}