Effect of variable surrounding on species creation

We constructed a model of speciation from evolution in an ecosystem consisting of a limited amount of energy recources. The species possesses genetic information, which is inherited according to the rules of the Penna model of genetic evolution. The increase in the number of the individuals of each species depends on the quality of their genotypes and the available energy resources. The decrease in number of the individuals results from genetic death or maximum-age reaching by the individual. The amount of energy resources is represented by a solution of the differential logistic equation, where the growth rate of the amount of the energy resources has been modified to include the number of individuals from all species in the ecosystem under consideration. The fluctuating surrounding is modelled with the help of the function V(x, t) = 1/4 x4 + 1/2 b(t)x2, where x represents phenotype and the coefficient b(t) shows the cos(omega t) time dependence. The closer the value x of an individual to the minimum of V(x, t), the better adapted its genotype to the surrounding. We observed that the life span of the organisms strongly depends on the value of the frequency omega. It becomes shorter the more frequent the changes of the surrounding. However, there is a tendency for the species that have a higher value of the reproduction age aR to win the competition with the other species. Another observation is that small evolutionary changes of the inherited genetic information lead to spontaneous bursts of the evolutionary activity when many new species may appear in a short period.     

A hierarchical matrix model to assess the impact of habitat fragmentation on population dynamics: an elasticity analysis

To better understand the role of habitat quality and boundaries on population dynamics at the landscape scale, we develop a model combining a spatially implicit approach, a spatial population Leslie-type model and an implicit model of habitat fragmentation. An original approach of elasticity permits to identify which types of element and boundary influence the most population viability according to the wood fragmentation degree. The studied species is a corridor forest insect sensitive to fragmentation (Abax parallelepipedus, Coleoptera, Carabidae). We show that a single large patch of wood is better than several small patches for the population viability.     

Statistical analysis of microarray data: a Bayesian approach

The potential of microarray data is enormous. It allows us to monitor the expression of thousands of genes simultaneously. A common task with microarray is to determine which genes are differentially expressed between two samples obtained under two different conditions. Recently, several statistical methods have been proposed to perform such a task when there are replicate samples under each condition. Two major problems arise with microarray data. The first one is that the number of replicates is very small (usually 2-10), leading to noisy point estimates. As a consequence, traditional statistics that are based on the means and standard deviations, e.g. t-statistic, are not suitable. The second problem is that the number of genes is usually very large (approximately 10,000), and one is faced with an extreme multiple testing problem. Most multiple testing adjustments are relatively conservative, especially when the number of replicates is small. In this paper we present an empirical Bayes analysis that handles both problems very well. Using different parametrizations, we develop four statistics that can be used to test hypotheses about the means and/or variances of the gene expression levels in both one- and two-sample problems. The methods are illustrated using experimental data with prior knowledge. In addition, we present the result of a simulation comparing our methods to well-known statistics and multiple testing adjustments.     

Prevalence and distribution of MEFV mutations among Arabs from the Maghreb patients suffering from familial Mediterranean fever

Familial Mediterranean fever (FMF) is an autosomal recessive inherited disease caused by mutations in MEFV. This disease is characterized by recurrent episodes of fever accompanied with topical signs of inflammation. Some patients can develop renal amyloidosis. We prospectively investigated MEFV mutations in a cohort of 209 unrelated Arab patients from Maghreb (85 Algerians, 87 Moroccans, and 37 Tunisians) with a clinical suspicion of FMF. FMF is the main cause of periodic fever syndrome in Maghreb. The most frequent MEFV mutations in this cohort were M694V and M694I. These mutations account for different proportions of the MEFV mutations in Algeria (5%, 80%), Morocco (49%, 37%), and Tunisia (50%, 25%) patients. M694I mutation is specific to the Arab population from Maghreb. Other rare mutations were observed: M680L, M680I, A744S, V726A, and E148Q. We estimated the frequency of MEFV mutation carriers among the Arab Maghrebian population at around 1%, which is significantly lower than in non-Ashkenazi Jews, Armenians or Turks.     

In vitro viability of lymphoid cells from lines of mice genetically selected for high or low responsiveness to phytohemagglutinin

The kinetics of viability of lymph node and spleen cells of mice genetically selected for "high" or "low" in vitro lymphocyte responsiveness to PHA were studied in PHA or PPD-stimulated short-term cultures. Lo/PHA cells were found to be less viable than Hi/PHA cells in unstimulated control cultures. PHA improved the viability of Lo/PHA cells while inducing proliferation of Hi/PHA cells with the appearance of more and larger lymphoblasts in the latter. PPD only improved the viability of spleen cell cultures, more so for the Hi/PHA line. The interline difference in thymidine uptake was smaller after PPD than after PHA stimulation. Modifications of culture conditions designed to decrease the interline difference in cell viability lessened but did not abolish the separation between the two lines for the PHA response as measured by thymidine uptake.     

Genetic regulation networks: circuits,regulons and attractors

We deal in this paper with the concept of genetic regulation network. The genes expression observed through the bio-array imaging allows the geneticist to obtain the intergenic interaction matrix W of the network. The interaction graph G associated to W presents in general interesting features like connected components, gardens of Eden, positive and negative circuits (or loops), and minimal components having 1 positive and 1 negative loop called regulons. Depending on parameters values like the connectivity coefficient K(W) and the mean inhibition weight I(W), the genetic regulation network can present several dynamical behaviours (fixed configuration, limit cycle of configurations) called attractors, when the observation time increases. We give some examples of such genetic regulation networks and analyse their dynamical properties and their biological consequences.     

Contribution to the logistic theory of growth: temporal structure and growth potential

The analysis of a structured population according to three (juvenile, mature and senescent) cellular states is carried out within the framework of Delattre's transformation systems theory. Growth in number, with the dissymmetry of cell divisions, is determined by an autocatalysis process under the constraint of the availability of a source. Two models are presented: their dynamics results in a growth of the exponential type or of the sigmoidal type, respectively. In the sigmoidal case, the logistic equation (Richards-Nelder's function with adjunction of a lower asymptote Y not equal to 0) fits satisfactorily the simulated data of the total cell number Y. The growth potential is defined as the instantaneous capacity of autocatalysis, which is expressed in relation to the present 'mitotic resources' (source + non-senescing mature cells). The acceleration variations d2Y/dt2 are in close agreement with the growth potential gradient. The analysis is then generalized to other population structuring. As a result, the logistic equation can be interpreted in terms of a formal model of growth of a structured population submitted to autocatalysis and competition.     

Management of disease resistance diversity of cultivars of a species in single fields: controlling epidemics

The use of a diversity of resistance genes limits the development of polycyclic epidemics caused by airborne pathogens and reduces the risk that resistance be overcome by virulent races. Diversity can be easily achieved by growing mixtures of cultivars with different resistance genes and homogeneous agronomic traits. The mechanisms by which disease is reduced in cultivar mixtures include the loss of inoculum due to the presence of resistant plants between susceptible ones and resistance induced by avirulent pathogens. The complementary effects of individual mixture components reacting to disease pressure and to abiotic stresses result in greater yield stability compared with pure stands. The quality of products from mixtures is at least equal to that obtained with pure stands. This type of resistance management is applicable to both annual and perennial crops.     

Electron microprobe analysis into interactions of a resin-modified glass-ionomer cement and a modified composite with human dentin in vitro

When materials used in restorative dentistry, such as a glass-ionomer cement or a compomer, were applied to dentin, ion exchanges occur between the material and the dentin. This work is based on an assessment in vitro of the ion exchanges occurring over time between (i) a glass-ionomer cement and dentin and (ii) a compomer and dentin. An electron microprobe analysis, technique not previously used for such a study, permitted qualitative and quantitative analysis of the interface and of the peripheral dentin. Analysis of the distribution of the elements in the interface and nearby showed continuous, progressive exchanges between the glass-ionomer cement and the dentin and absence of diffusion between the compomer and the dentin.     

Genetics of human obesity

We present the knowledge acquired in the field of the genetics of human obesity. The molecular approach proved to be powerful to define new syndromes associated to obesity. The pivotal role of leptin and melanocortin pathways were recognized but in rare obesity cases. In the commoner form of obesities, a multitude of polymorphisms located in genes and candidate regions participate in an individual susceptibility to weight gain in a permissive environment. The effects are often uncertain and the results not always confirmed. It is now necessary to integrate data of various origins (environment, genotype, expression) to clarify the domain.     

The origins of the strategy of codon use

We analyzed the DNA sequences taking as an elementary pattern segments of increasing length from the codon to the gene. We have thus been able to identify part of the constraints from which originates the use of the code degeneracy in each gene. Our results show that the strategy of codon use is not solely related to the translation apparatus characteristics.     

Oxidative stress: a theoretical model or a biological reality?

Although oxidative stress has been extensively studied the last fifteen years, many physicians and biologists are still sceptical concerning its interest in biology and medicine. This is probably due, in part, to the fact that this subject is a matter of biophysics, and the first studies reported were written using a physical language that inspired these people used to a more concrete problematic very little. Another problem is the difficulty to detect the species mediating oxidative stress, and to determine their role in biological processes. This review is aimed at presenting oxidative stress, as well as reactive oxygen species and free radicals--the molecules that mediate it--in a clear form able to convince all researchers involved in life sciences that these short-lived intermediates are indissociable from any aerobic organism. Moreover, if reactive oxygen species and free radicals are undoubtedly involved in many pathologies, they have physiological functions too.     

Web-building management in an orb-weaving spider, Zygiella x-notata: influence of prey and conspecifics

According to optimal foraging theory, spiders should adapt their web building to environmental variations. Until now, there was no data on the influence of simultaneous information coming from different environmental factors on web building behaviour. Under laboratory conditions, we studied the behaviour of Zygiella x-notata in the presence of prey, conspecifics, or both simultaneously. There was a stimulating effect of prey, but web building was not affected by the presence of conspecifics. When spiders and prey were present simultaneously, the effect was similar to that of prey alone; it seemed that there was no interactive influence of both factors. We discussed about the use of environmental information by spiders in foraging behaviour.     

Molecular biology and genetics of Alzheimer's disease

Like several other adult onset neurodegenerative diseases, Alzheimer's disease is a multifactorial illness with both genetic and non-genetic causes. Recent genetic studies have identified four genes associated with inherited risk for AD (presenilin 1, presenilin 2, amyloid precursor protein, and apolipoprotein E). These genes account for about half of the total genetic risk for Alzheimer's disease. It is suspected that several other Alzheimer's disease-susceptibility genes exist, and their identification is the subject of ongoing research. Nevertheless, biological studies on the effects of mutations in the four known genes has led to the conclusion that all of these genes cause dysregulation of amyloid precursor protein processing and in particular dysregulation of the handling of a proteolytic derivative termed Abeta. The accumulation of Abeta appears to be an early and initiating event that triggers a series of downstream processes including misprocessing of the tau protein. This cascade ultimately causes neuronal dysfunction and death, and leads to the clinical and pathological features of Alzheimer's disease. Knowledge of this biochemical cascade now provides several potential targets for the development of diagnostics and therapeutics.