On the relationship between niche and distribution

Applications of Hutchinson's n -dimensional niche concept are often focused on the role of interspecific competition in shaping species distribution patterns. In this paper, I discuss a variety of factors, in addition to competition, that influence the observed relationship between species distribution and the availability of suitable habitat. In particular, I show that Hutchinson's niche concept can be modified to incorporate the influences of niche width, habitat availability and dispersal, as well as interspecific competition per se . I introduce a simulation model called NICHE that embodies many of Hutchinson's original niche concepts and use this model to predict patterns of species distribution. The model may help to clarify how dispersal, niche size and competition interact, and under what conditions species might be common in unsuitable habitat or absent from suitable habitat. A brief review of the pertinent literature suggests that species are often absent from suitable habitat and present in unsuitable habitat, in ways predicted by theory. However, most tests of niche theory are hampered by inadequate consideration of what does and does not constitute suitable habitat. More conclusive evidence for these predictions will require rigorous determination of habitat suitability under field conditions. I suggest that to do this, ecologists must measure habitat specific demography and quantify how demographic parameters vary in response to temporal and spatial variation in measurable niche dimensions.     

Comparative studies of oxidative stress and mitochondrial function in aging

The oxidative stress theory and its correlate the mitochondrial theory of aging are among the most studied and widely accepted of all hypotheses of the mechanism of aging. To date, most of the supporting evidence for these theories has come from investigations using common model organisms such as Caenorhabditis elegans, Drosophila melanogaster, and laboratory rodents. However, comparative data from a wide range of endotherms provide equivocal support as to whether oxidative stress is merely a correlate, rather than a determinant, of species' maximum lifespan. The great majority of studies in this area have been devoted to the relationship between reactive oxygen species and maximal longevity in young adult organisms, with little emphasis on mitochondrial respiratory efficiency, age-related alterations in mitochondrial physiology or oxidative damage. The advantage of studying a broader spectrum of species is the broad range of virtually every biological phenotype/trait, such as lifespan, body weight and metabolic rate. Here we summarize the results from a number of comparative studies in an effort to correlate oxidant production and oxidative damage among many species with their maximal lifespan and briefly discuss the pitfalls and limitations. Based on current information, it is not possible to accept or dispute the oxidative stress theory of aging, nor can we exclude the possibility that private mechanisms might offer an explanation for the longevity of exceptionally long-lived animal models. Thus, there is need for more thorough and controlled investigations with more unconventional animal models for a deeper understanding of the role of oxidative stress in longevity.     

Contributions of the hippocampus and medial prefrontal cortex to energy and body weight regulation

The effects of selective ibotenate lesions of the complete hippocampus (CHip), the hippocampal ventral pole (VP), or the medial prefrontal cortex (mPFC) in male rats were assessed on several measures related to energy regulation (i.e., body weight gain, food intake, body adiposity, metabolic activity, general behavioral activity, conditioned appetitive responding). The testing conditions were designed to minimize the nonspecific debilitating effects of these surgeries on intake and body weight. Rats with CHip and VP lesions exhibited significantly greater weight gain and food intake compared with controls. Furthermore, CHip-lesioned rats, but not rats with VP lesions, showed elevated metabolic activity, general activity in the dark phase of the light-dark cycle, and greater conditioned appetitive behavior, compared with control rats without these brain lesions. In contrast, rats with mPFC lesions were not different from controls on any of these measures. These results indicate that hippocampal damage interferes with energy and body weight regulation, perhaps by disrupting higher-order learning and memory processes that contribute to the control of appetitive and consummatory behavior.     

The COP9 signalosome controls jasmonic acid synthesis and plant responses to herbivory and pathogens

The COP9 signalosome (CSN) is a multi‐protein complex that regulates the activities of cullin‐RING E3 ubiquitin ligases (CRLs). CRLs ubiquitinate proteins in order to target them for proteasomal degradation. The CSN is required for proper plant development. Here we show that the CSN also has a profound effect on plant defense responses. Silencing of genes for CSN subunits in tomato plants resulted in a mild morphological phenotype and reduced expression of wound‐responsive genes in response to mechanical wounding, attack by Manduca sexta larvae, and Prosystemin over‐expression. In contrast, expression of pathogenesis‐related genes was increased in a stimulus‐independent manner in these plants. The reduced wound response in CSN‐silenced plants corresponded with reduced synthesis of jasmonic acid (JA), but levels of salicylic acid (SA) were unaltered. As a consequence, these plants exhibited reduced resistance against herbivorous M. sexta larvae and the necrotrophic fungal pathogen Botrytis cinerea. In contrast, susceptibility to tobacco mosaic virus (TMV) was not altered in CSN‐silenced plants. These data demonstrate that the CSN orchestrates not only plant development but also JA‐dependent plant defense responses.     

Effect of leukocytic endogenous mediator on C-reactive protein in rabbits.

Elevation in the plasma levels of the acute phase proteins--C-reactive protein (C-RP) and fibrinogen--were found after injection of leukocytic endogenous mediator (LEM) into rabbits. C-RP in the plasma was elevated 8 hr after injection of LEM, and maximum elevation occurred 24 hr after injection. Injection of LEM into rabbits also produced alterations in body temperature, in levels of plasma iron and zinc, and in the number of neutrophils in the peripheral blood.     

Evidence from bioinformatics, expression and inhibition studies of phosphoinositide-3 kinase signalling in Giardia intestinalis

Background  

Giardia intestinalis is a parasitic protozoan and major cause of diarrhoeal disease. Disease transmission is dependent on the ability of the parasite to differentiate back and forth between an intestine-colonising trophozoite and an environmentally-resistant infective cyst. Our current understanding of the intracellular signalling mechanisms that regulate parasite replication and differentiation is limited, yet such information could suggest new methods of disease control. Phosphoinositide-3 kinase (PI3K) signalling pathways have a central involvement in many vital eukaryotic processes, such as regulation of cell growth, intracellular membrane trafficking and cell motility. Here we present evidence for the existence of functional PI3K intracellular signalling pathways in G. intestinalis.