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Numerous Hypotheses (numerous + hypothesis)
Selected AbstractsTolerance to herbivory, and not resistance, may explain differential success of invasive, naturalized, and native North American temperate vinesDIVERSITY AND DISTRIBUTIONS, Issue 2 2008Isabel W. Ashton ABSTRACT Numerous hypotheses suggest that natural enemies can influence the dynamics of biological invasions. Here, we use a group of 12 related native, invasive, and naturalized vines to test the relative importance of resistance and tolerance to herbivory in promoting biological invasions. In a field experiment in Long Island, New York, we excluded mammal and insect herbivores and examined plant growth and foliar damage over two growing seasons. This novel approach allowed us to compare the relative damage from mammal and insect herbivores and whether damage rates were related to invasion. In a greenhouse experiment, we simulated herbivory through clipping and measured growth response. After two seasons of excluding herbivores, there was no difference in relative growth rates among invasive, naturalized, and native woody vines, and all vines were susceptible to damage from mammal and insect herbivores. Thus, differential attack by herbivores and plant resistance to herbivory did not explain invasion success of these species. In the field, where damage rates were high, none of the vines were able to fully compensate for damage from mammals. However, in the greenhouse, we found that invasive vines were more tolerant of simulated herbivory than native and naturalized relatives. Our results indicate that invasive vines are not escaping herbivory in the novel range, rather they are persisting despite high rates of herbivore damage in the field. While most studies of invasive plants and natural enemies have focused on resistance, this work suggests that tolerance may also play a large role in facilitating invasions. [source] Occupancy frequency distributions: patterns, artefacts and mechanismsBIOLOGICAL REVIEWS, Issue 3 2002MELODIE A. McGEOCH ABSTRACT Numerous hypotheses have been proposed to explain the shape of occupancy frequency distributions (distributions of the numbers of species occupying different numbers of areas). Artefactual effects include sampling characteristics, whereas biological mechanisms include organismal, niche-based and metapopulation models. To date, there has been little testing of these models. In addition, although empirically derived occupancy distributions encompass an array of taxa and spatial scales, comparisons between them are often not possible because of differences in sampling protocol and method of construction. In this paper, the effects of sampling protocol (grain, sample number, extent, sampling coverage and intensity) on the shape of occupancy distributions are examined, and approaches for minimising artefactual effects recommended. Evidence for proposed biological determinants of the shape of occupancy distributions is then examined. Good support exists for some mechanisms (habitat and environmental heterogeneity), little for others (dispersal ability), while some hypotheses remain untested (landscape productivity, position in geographic range, range size frequency distributions), or are unlikely to be useful explanations for the shape of occupancy distributions (species specificity and adaptation to habitat, extinction,colonization dynamics). The presence of a core (class containing species with the highest occupancy) mode in occupancy distributions is most likely to be associated with larger sample units, and small homogenous sampling areas positioned well within and towards the range centers of a sufficient proportion of the species in the assemblage. Satellite (class with species with the lowest occupancy) modes are associated with sampling large, heterogeneous areas that incorporate a large proportion of the assemblage range. However, satellite modes commonly also occur in the presence of a core mode, and rare species effects are likely to contribute to the presence of a satellite mode at most sampling scales. In most proposed hypotheses, spatial scale is an important determinant of the shape of the observed occupancy distribution. Because the attributes of the mechanisms associated with these hypotheses change with spatial scale, their predictions for the shape of occupancy distributions also change. To understand occupancy distributions and the mechanisms underlying them, a synthesis of pattern documentation and model testing across scales is thus needed. The development of null models, comparisons of occupancy distributions across spatial scales and taxa, documentation of the movement of individual species between occupancy classes with changes in spatial scale, as well as further testing of biological mechanisms are all necessary for an improved understanding of the distribution of species and assemblages within their geographic ranges. [source] Molecular mechanisms of calorie restriction's protection against age-related sclerosisIUBMB LIFE, Issue 12 2006Elena Chiarpotto Abstract The current knowledge on the molecular mechanisms of the protective effect of calorie restriction (CR) against age-related fibrosclerosis is tentatively reviewed with specific reference to the role of oxidative stress in aging. The effects of oxidative stress are often mediated by its own final products. Of these, 4-hydroxy-2,3-nonenal (HNE) induces the expression and synthesis of transforming growth factor ,1 (TGF,1) and activates nuclear binding of transcription factor activator protein 1 (AP-1) thus stimulating fibrogenesis. Several studies have shown that, as well as extending mean and maximum life span in a variety of species, CR delays the onset and slows the progression of a variety of age-associated diseases, including diabetes, cardiovascular diseases and neoplasia. However, the anti-aging mechanisms of CR are still not clearly understood. Of the numerous hypotheses put forward, one that still remains popular is protection against the age-associated increase of oxidative stress and consequent cell damage. CR protects the rat aorta from the age-related increase of both oxidative damage and fibrosis; as regards the possible mechanism/s of CR's protection against fibrosclerosis, it is conceivable that, by decreasing oxidative stress, CR reduces HNE levels and consequently TGF,1 expression and collagen deposition, likely by down-regulating the activation of Jun-N terminal kinase and of AP-1. Through the modulation of reactive oxygen species and oxidative stress CR may also attenuate the age-associated increase in the inflammatory milieu, thus preserving vascular functional integrity by suppressing the age-associated increase in inflammatory enzyme activities and prostanoids. iubmb Life, 58: 695-702, 2006 [source] Subcutaneous pseudomembranous fat necrosis: new observations,/linkr>JOURNAL OF CUTANEOUS PATHOLOGY, Issue 1 2002Carlos Diaz-Cascajo Background: Pseudomembranous fat necrosis is a peculiar manifestation of necrosis of adipose tissue characterized by formation of pseudocystic cavities lined by crenulated membranes. The underlying mechanism for the formation of pseudomembranes is unknown and numerous hypotheses have been proposed. Despite divergent interpretations, most authors consider necrotic fat cells to be the anatomic substrate for the formation of pseudomembranes. Methods: A total of 341 panniculitides were reviewed for the presence of pseudomembranous fat necrosis. The specific diagnoses were established after correlation of all available clinical and laboratory data with the histopathology. Special attention was given to the time in the evolution of the disease when the biopsy was taken. Additional immunohistochemical studies were performed in 12 cases. Results: Thirty of 341 cases of different types of panniculitides were found to show pseudomembranous fat necrosis, namely: 10 of 15 cases of sclerosing panniculitis (lipodermatosclerosis), 6 of 95 cases of erythema nodosum, 7 of 34 cases of traumatic panniculitis, 1 of 7 cases of lupus panniculitis, 1 of 20 cases of erythema induratum Bazin (nodular vasculitis), 1 of 9 cases of necrobiosis lipoidica, 1 of 4 cases of sclerotic lipogranuloma, 1 of 9 cases of infectious panniculitis (erysipelas), 1 of 2 cases of pancreatic panniculitis, and 1 of 4 cases of subcutaneous sarcoidosis. Pseudomembranous fat necrosis labelled strongly for the histiocytic markers CD68 and lysozyme. Conclusions: Our series provides data suggesting that pseudomembranous fat necrosis represents a dynamic process that varies according to the evolution of the lesion at the time of the biopsy. In biopsies taken from early foci of panniculitides pseudomembranes show vescicular or picnotic nuclei. Later, pseudomembranes retain their crenulated appearance but lack nuclear elements. Furthermore, we present histopathologic, histochemical, and immunohistochemical evidence that pseudomembranous fat necrosis results from the interaction of residual products of disintegrated fat cells and macrophages. Histiocytic markers such as CD68 and lysozyme may be used as reliable tools in order to detect pseudomembranes in panniculitides. [source] | ||||||||||