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Biological Heterogeneity (biological + heterogeneity)
Selected AbstractsHeterogeneity, speciation/extinction history and climate: explaining regional plant diversity patterns in the Cape Floristic RegionDIVERSITY AND DISTRIBUTIONS, Issue 3 2002R. M. Cowling Abstract. This paper investigates the role of heterogeneity and speciation/extinction history in explaining variation in regional scale (c. 0.1,3000 km2) plant diversity in the Cape Floristic Region of south-western Africa, a species- and endemic-rich biogeographical region. We used species-area analysis and analysis of covariance to investigate geographical (east vs. west) and topographic (lowland vs. montane) patterns of diversity. We used community diversity as a surrogate for biological heterogeneity, and the diversity of naturally rare species in quarter degree squares as an indicator of differences in speciation/extinction histories across the study region. We then used standard statistical methods to analyse geographical and topographic patterns of these two measures. There was a clear geographical diversity pattern (richer in the west), while a topographic pattern (richer in mountains) was evident only in the west. The geographical boundary coincided with a transition from the reliable winter-rainfall zone (west) to the less reliable non-seasonal rainfall zone (east). Community diversity, or biological heterogeneity, showed no significant variation in relation to geography and topography. Diversity patterns of rare species mirrored the diversity pattern for all species. We hypothesize that regional diversity patterns are the product of different speciation and extinction histories, leading to different steady-state diversities. Greater Pleistocene climatic stability in the west would have resulted in higher rates of speciation and lower rates of extinction than in the east, where for the most, Pleistocene climates would not have favoured Cape lineages. A more parsimonious hypothesis is that the more predictable seasonal rainfall of the west would have favoured non-sprouting plants and that this, in turn, resulted in higher speciation and lower extinction rates. Both hypotheses are consistent with the higher incidence of rare species in the west, and higher levels of beta and gamma diversity there, associated with the turnover of species along environmental and geographical gradients, respectively. These rare species do not contribute to community patterns; hence, biological heterogeneity is uniform across the region. The weak topography pattern of diversity in the west arises from higher speciation rates and lower extinction rates in the topographically complex mountains, rather than from the influence of environmental heterogeneity on diversity. [source] How would I manage a case of essential thrombocythaemia presenting with an ischaemic toeHEMATOLOGICAL ONCOLOGY, Issue 1 2008DP McLornan Abstract Essential thrombocythaemia (ET) is an acquired myeloproliferative disorder. The phenotypic and biological heterogeneity of ET can make management of individual cases problematic, especially in the era of changing ideas on the molecular pathogenesis of this disease process. This case discussion will explore the evidence base and rationale that guides treatment of a 46-year-old individual with ET presenting with an ischaemic episode. Copyright © 2007 John Wiley & Sons, Ltd. [source] Plasticity of death rates in stationary phase in Saccharomyces cerevisiaeAGING CELL, Issue 1 2009Nadège Minois Summary For the species that have been most carefully studied, mortality rises with age and then plateaus or declines at advanced ages, except for yeast. Remarkably, mortality for yeast can rise, fall and rise again. In the present study we investigated (i) if this complicated shape could be modulated by environmental conditions by measuring mortality with different food media and temperature; (ii) if it is triggered by biological heterogeneity by measuring mortality in stationary phase in populations fractionated into subpopulations of young, virgin cells, and replicatively older, non-virgin cells. We also discussed the results of a staining method to measure viability instead of measuring the number of cells able to exit stationary phase and form a colony. We showed that different shapes of age-specific death rates were observed and that their appearance depended on the environmental conditions. Furthermore, biological heterogeneity explained the shapes of mortality with homogeneous populations of young, virgin cells exhibiting a simple shape of mortality in conditions under which more heterogeneous populations of older cells or unfractionated populations displayed complicated death rates. Finally, the staining method suggested that cells lost the capacity to exit stationary phase and to divide long before they died in stationary phase. These results explain a phenomenon that was puzzling because it appeared to reflect a radical departure from mortality patterns observed for other species. [source] Molecular characterization of tumour heterogeneity and malignant mesothelioma cell differentiation by gene profilingTHE JOURNAL OF PATHOLOGY, Issue 1 2005Xiaojuan Sun Abstract Malignant mesothelioma is an aggressive tumour, characterized by a variable differentiation pattern and poor prognosis. At present, the clinical outcome in patients with malignant mesothelioma is mainly predicted by the morphological phenotype of the tumour. However, this conventional clinicopathological parameter is of limited value, partly because of the biological heterogeneity of this tumour and poor understanding of the regulatory mechanisms underlying the various patterns of growth. To elucidate the intrinsic molecular programmes that determine tumour differentiation, oligonucleotide arrays were used in an in vitro model of mesothelioma differentiation. The analysis of 2059 genes detected 102 genes that were significantly deregulated. Clustering of these genes into functional categories showed distinctive patterns for the two phenotypes, namely epithelioid and sarcomatoid. The molecular fingerprint of the sarcomatoid tumour component indicates overrepresentation of growth factor receptors and growth factor binding proteins, whereas epithelioid mesothelioma cells express other tumour-promoting factors involved in differentiation, metabolism, and regulation of apoptosis. These differences in the molecular phenotype may give a better basis for diagnosis and for designing novel therapies. Copyright © 2005 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] | |||||||||||||