TOWARDS AN UNDERSTANDING OF HOW TUBE INSERTS MITIGATE FOULING IN HEAT EXCHANGERS

A number of studies undertaken by Total have measured the improvement that can be expected when TurbotalTM inserts are installed in heat exchangers. These studies have fully established that TurbotalTM both improve heat transfer coefficient and mitigate fouling. It has been found that fouling levels vary with application. Consequently, economics of installing inserts are difficult to quantify. Gains must be estimated through specific tests. A model that predicts fouling development solves this problem. In this paper first steps towards the understanding of how TurbotalTM limits the fouling rate are described. Authors suggest that the calculation of both pressure drop and heat transfer coefficient in a tube equipped with insert can be used to extend the Ebert & Panchal fouling model to predict the fouling rate in tube equipped with TurbotalTM. This extension of the Ebert-Panchal Model requires adjustment of both the deposition term and the removal term. The deposition term can be adjusted by multiplying by the ratio of plain to enhanced heat transfer coefficients and the removal term can be based on the pressure drop imposed by the insert. This modified model is then compared with operating cases to verify its reliability. Further issues that require consideration are a mechanical effect that gives rise to limiting growth of the fouling deposit, and total suppression of fouling in parts of the exchanger into account

Toxoplasma seroprevalence in a rural population in France: detection of a household effect

<p>Abstract</p> <p>Background</p> <p><it>Toxoplasma gondii</it>, the agent of toxoplasmosis, has a complex life cycle. In humans, the parasite may be acquired either through ingestion of contaminated meat or through oocysts present in the environment. The importance of each source of contamination varies locally according to the environment characteristics and to differences concerning human eating habits and the presence of cats; thus, the risk factors may be determined through fine-scale studies. Here, we searched for factors associated with seropositivity in the population of two adjacent villages in Lorraine region, France.</p> <p>Methods</p> <p>All voluntary inhabitants filled out a questionnaire and gave a blood sample. The seroprevalence was estimated globally and according to the inhabitants' ages using a cubic spline regression. A mixed logistic regression model was used to quantify the effect of individual and household factors on the probability of seropositivity.</p> <p>Results</p> <p>Based on serological results from 273 persons, we estimated seroprevalence to be 47% (95% confidence interval: 41 to 53%). That seroprevalence increased with age: the slope was the steepest up to the age of 40 years (OR = 2.48 per 10-year increment, 95% credibility interval: [1.29 to 5.09]), but that increase was not significant afterwards. The probability of seropositivity tended to be higher in men than in women (OR = 2.01, 95% credibility interval: [0.92 to 4.72]) and in subjects eating raw vegetables at least once a week than in the others (OR = 8.4, 95% credibility interval: [0.93 to 72.1]). These effects were close to statistical significance. The multivariable analysis highlighted a significant seroprevalence heterogeneity among households. That seroprevalence varied between 6 and 91% (5^thand 95^thpercentile of the household seropositivity distribution).</p> <p>Conclusion</p> <p>The major finding is the household effect, with a strong heterogeneity of seroprevalence among households. This effect may be explained by common exposures of household members to local risk factors. Future work will quantify the link between the presence of oocysts in the soil and the seroprevalence of exposed households using a spatial analysis.</p

Chronic Toxoplasma Infection Modifies the Structure and the Risk of Host Behavior

The intracellular parasite Toxoplasma has an indirect life cycle, in which felids are the definitive host. It has been suggested that this parasite developed mechanisms for enhancing its transmission rate to felids by inducing behavioral modifications in the intermediate rodent host. For example, Toxoplasma-infected rodents display a reduction in the innate fear of predator odor. However, animals with Toxoplasma infection acquired in the wild are more often caught in traps, suggesting that there are manipulations of intermediate host behavior beyond those that increase predation by felids. We investigated the behavioral modifications of Toxoplasma-infected mice in environments with exposed versus non-exposed areas, and found that chronically infected mice with brain cysts display a plethora of behavioral alterations. Using principal component analysis, we discovered that most of the behavioral differences observed in cyst-containing animals reflected changes in the microstructure of exploratory behavior and risk/unconditioned fear. We next examined whether these behavioral changes were related to the presence and distribution of parasitic cysts in the brain of chronically infected mice. We found no strong cyst tropism for any particular brain area but found that the distribution of Toxoplasma cysts in the brain of infected animals was not random, and that particular combinations of cyst localizations changed risk/unconditioned fear in the host. These results suggest that brain cysts in animals chronically infected with Toxoplasma alter the fine structure of exploratory behavior and risk/unconditioned fear, which may result in greater capture probability of infected rodents. These data also raise the possibility that selective pressures acted on Toxoplasma to broaden its transmission between intermediate predator hosts, in addition to felid definitive hosts