|
| ||
|
|
||
Biological Complexity (biological + complexity)
Selected AbstractsThe Center for the Study of Biological Complexity , The First Five YearsCHEMISTRY & BIODIVERSITY, Issue 12 2007Gregory No abstract is available for this article. [source] Biodiverse Research at the Center for the Study of Biological ComplexityCHEMISTRY & BIODIVERSITY, Issue 11 2007Lemont B. Kier No abstract is available for this article. [source] The Center for the Study of Biological Complexity at Virginia Commonwealth UniversityCHEMISTRY & BIODIVERSITY, Issue 1 2004Gregory [source] Genetics of human iris colour and patternsPIGMENT CELL & MELANOMA RESEARCH, Issue 5 2009Richard A. Sturm Summary The presence of melanin pigment within the iris is responsible for the visual impression of human eye colouration with complex patterns also evident in this tissue, including Fuchs' crypts, nevi, Wolfflin nodules and contraction furrows. The genetic basis underlying the determination and inheritance of these traits has been the subject of debate and research from the very beginning of quantitative trait studies in humans. Although segregation of blue-brown eye colour has been described using a simple Mendelian dominant-recessive gene model this is too simplistic, and a new molecular genetic perspective is needed to fully understand the biological complexities of this process as a polygenic trait. Nevertheless, it has been estimated that 74% of the variance in human eye colour can be explained by one interval on chromosome 15 that contains the OCA2 gene. Fine mapping of this region has identified a single base change rs12913832 T/C within intron 86 of the upstream HERC2 locus that explains almost all of this association with blue-brown eye colour. A model is presented whereby this SNP, serving as a target site for the SWI/SNF family member HLTF, acts as part of a highly evolutionary conserved regulatory element required for OCA2 gene activation through chromatin remodelling. Major candidate genes possibly effecting iris patterns are also discussed, including MITF and PAX6. [source] Water uptake and nutrient concentrations under a floodplain oak savanna during a non-flood period, lower Cedar River, Iowa,HYDROLOGICAL PROCESSES, Issue 21 2009Keith E. Schilling Abstract Floodplains during non-flood periods are less well documented than when flooding occurs, but non-flood periods offer opportunities to investigate vegetation controls on water and nutrient cycling. In this study, we characterized water uptake and nutrient concentration patterns from 2005 to 2007 under an oak savanna located on the floodplain of the Cedar River in Muscatine County, Iowa. The water table ranged from 0·5 to 2·5 m below ground surface and fluctuated in response to stream stage, plant water demand and rainfall inputs. Applying the White method to diurnal water table fluctuations, daily ET from groundwater averaged more than 3·5 mm/day in June and July and approximately 2 mm/day in May and August. Total annual ET averaged 404 mm for a growing season from mid-May to mid-October. Savanna groundwater concentrations of nitrate-N, ammonium-N, and phosphate-P were very low (mean <0·18, <0·14, <0·08 mg/l, respectively), whereas DOC concentrations were high (7·1 mg/l). Low concentrations of N and P were in contrast to high nutrient concentrations in the nearby Cedar River, where N and P averaged 7·5 mg/l and 0·13, respectively. In regions dominated by intensive agriculture, study results document valuable ecosystem services for native floodplain ecosystems in reducing watershed-scale nutrient losses and providing an oasis for biological complexity. Improved understanding of the environmental conditions of regionally significant habitats, including major controls on water table elevations and water quality, offers promise for better management aimed at preserving the ecology of these important habitats. Copyright © 2009 John Wiley & Sons, Ltd. [source] Inflammatory bowel disease: Established and evolving considerations on its etiopathogenesis and therapyJOURNAL OF DIGESTIVE DISEASES, Issue 5 2010Anja SCHIRBEL Modern studies of inflammatory bowel disease (IBD) pathogenesis have been pursued for about four decades, a period of time where the pace of progress has been steadily increasing. This progress has occurred in parallel with and is largely due to developments in multiple basic scientific disciplines that range from population and social studies, genetics, microbiology, immunology, biochemistry, cellular and molecular biology, and DNA engineering. From this cumulative and constantly expanding knowledge base the fundamental pillars of IBD pathogenesis appear to have been identified and consolidated during the last couple of decades. Presently there is a general consensus among basic IBD investigators that both Crohn's disease (CD) and ulcerative colitis (UC) are the result of the combined effects of four basic components: global changes in the environment, the input of multiple genetic variations, alterations in the intestinal microbiota, and aberrations of innate and adaptive immune responses. There is also agreement on the conclusion that none of these four components can by itself trigger or maintain intestinal inflammation. A combination of various factors, and most likely of all four factors, is probably needed to bring about CD or UC in individual patients, but each patient or set of patients seems to have a different combination of alterations leading to the disease. This would imply that different causes and diverse mechanisms underlie IBD, and this could also explain why every patient displays his or her own clinical manifestations and a personalized response to therapy, and requires tailored approaches with different medications. While we are becoming increasingly aware of the importance of this individual variability, we have only a superficial notion of the reasons why this occurs, as hinted by the uniqueness of the genetic background and of the gut flora in each person. So, we are apparently facing the paradox of having to deal with the tremendous complexity of the mechanisms responsible for chronic intestinal inflammation in the setting of each patient's individuality in the response to this biological complexity. This obviously poses considerable challenges to reaching a full understanding of IBD pathogenesis, but being aware of the difficulties is the first step in finding answers to them. [source] The rational design of biological complexity: A deceptive metaphorPROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 6 2007Marc H. V. Van Regenmortel Dr. Abstract Biologists often claim that they follow a rational design strategy when their research is based on molecular knowledge of biological systems. This claim implies that their knowledge of the innumerable causal connections present in biological systems is sufficient to allow them to deduce and predict the outcome of their experimental interventions. The design metaphor is shown to originate in human intentionality and in the anthropomorphic fallacy of interpreting objects, events, and the behavior of all living organisms in terms of goals and purposes. Instead of presenting rational design as an effective research strategy, it would be preferable to acknowledge that advances in biomedicine are nearly always derived from empirical observations based on trial and error experimentation. The claim that rational design is an effective research strategy was tested in the case of current attempts to develop synthetic vaccines, in particular against human immunodeficiency virus. It was concluded that in this field of biomedicine, trial and error experimentation is more likely to succeed than a rational design approach. Current developments in systems biology may give us eventually a better understanding of the immune system and this may enable us in the future to develop improved vaccines. [source] Cybernetic Model Predictive Control of a Continuous Bioreactor with Cell RecycleBIOTECHNOLOGY PROGRESS, Issue 5 2003Kapil G. Gadkar The control of poly-,-hydroxybutyrate (PHB) productivity in a continuous bioreactor with cell recycle is studied by simulation. A cybernetic model of PHB synthesis in Alcaligenes eutrophus is developed. Model parameters are identified using experimental data, and simulation results are presented. The model is interfaced to a multirate model predictive control (MPC) algorithm. PHB productivity and concentration are controlled by manipulating dilution rate and recycle ratio. Unmeasured time varying disturbances are imposed to study regulatory control performance, including unreachable setpoints. With proper controller tuning, the nonlinear MPC algorithm can track productivity and concentration setpoints despite a change in the sign of PHB productivity gain with respect to dilution rate. It is shown that the nonlinear MPC algorithm is able to track the maximum achievable productivity for unreachable setpoints under significant process/model mismatch. The impact of model uncertainty upon controller performance is explored. The multirate MPC algorithm is tested using three controllers employing models that vary in complexity of regulation. It is shown that controller performance deteriorates as a function of decreasing biological complexity. [source] "Natural restoration" can generate biological complexityCOMPLEXITY, Issue 2 2005Emile ZuckerkandlArticle first published online: 16 DEC 200 Abstract Factor complexes engaged in transcriptional regulation of gene expression and their cognate DNA elements recurrently suffer mutational damage that can result in deadaptations in the mutual fit of interacting macromolecules. Such mutations can spread in populations by drift if their functional consequences are not severe. Mutational restorations of the damaged complexes may ensue and can take many forms. One of these forms would represent spontaneous increases in gene interaction complexity and correlated aspects of organismic complexity. In this particular mode of restoration, restabilization of a factor/factor/DNA complex occurs through the binding of an additional factor. Factors added under such circumstances to regulatory kits of individual genes are thought to be at the origin of a slow but persistent "complexity drive." This drive seems to be resisted in many forms whose developmental outcome has reached a finish line difficult to pass, but imposes itself along other lines of phylogenetic descent. In the process of restoration by an additional factor, the chances are significant that the original regulatory control of a target gene is not recovered exactly and that the restored gene expression has novel spatial, temporal, or quantitative characteristics. These new characteristics, which represent a functional transfer of the gene to a new domain of activity, may be selectable, even when the physicochemical properties of the gene product have remained largely unchanged. As a consequence of such activity transfers under quasi-constancy of the molecular properties of the protein encoded by the regulation's target gene, the activity domain originally covered by that target gene may be left at least in part functionally vacant. At that point, an unmodified duplicate of the target gene and of its original regulatory dependencies probably becomes in turn selectable. A causal link is therefore predicted between the regulatory specialization and selection of one of two duplicates and the regulatory maintenance and selection of the other. A conserved increase in gene number would result indirectly from the regulatory shift in paralogs, and the organism's complexity would be increased in this sense also, complexity as number of genes in addition to complexity as number of regulatory factors per gene. It is thus proposed that increased biological complexity, innovation in the gene regulatory network, and the development of a novel evolutionary potential can be the result, counterintuitively, of conservative forces that intervene when mutations play a survivable form of havoc with the system of gene regulation. Increasing complexity, then, could be seen as one of the side effects of "natural restoration." This phrase designates the mutational re-establishment in the gene whose regulation has been damaged of a functionally effective activity pattern, albeit, perhaps, with changes in its mode of expression in regard to location, time, and rate. The higher complexity, innovation in the gene regulatory network, of higher organisms,their very character of higher organisms,would to a significant extent be a side effect of episodes of natural selection aimed at functional restoration, not at complexity itself. Regulatory impairment, the point of departure of the process outlined, represents a controller gene disease. It thus may well be the case that molecular diseases, the effects on the individual of inheritable structural decay, are among the conditions of the evolution of higher organisms. © 2005 Wiley Periodicals, Inc. Complexity 11: 14,27, 2005 [source] | |||||||||||||