Calorific Ash Carbon And Nitrogen-Content In Relation To Length And Dry-Weight Of Parathemisto-Gaudichaudi (Amphipoda Hyperiidea) In The North-East Atlantic Ocean

The calorific, ash, carbon and nitrogen content, length and dry weight were determined for the hyperiid Parathemisto gaudichaudi (Guerin). Regression equations for all these variables were determined so that they can be estimated by calculation from measurements of length of the hyperiid. Mean values for total nitrogen and carbon were 7.79±0.85% and 36.80±4.18% of the dry weight, respectively. The carbon to calorific equivalent for P. gaudichaudi was 10.37 kcal g-1 carbon (9.13 kcal g-1 when corrected for nitrogen). The calorific value for ash-free adult P. gaudichaudi was 5.138 kcal g-1±1.309 (4.510 kcal g-1 when corrected for nitrogen). This large variation in the calorific content (coefficient of variation of 25.84%) can be accounted for largely by variation in the ash content (coefficient of variation of 21.84%). The calorific value determined for P. gaudichaudi is similar to that measured for other carnivorous crustaceans and adds support to the hypothesis that animals with high calorific content have a low fecundity and an energy-rich store which can be used as a buffer during unfavourable periods in their life.

Low molecular weight halocarbons in the Humber and Rhine estuaries determined using a new purge-and-trap gas chromatographic method

A number of chlorinated and brominated low molecular weight hydrocarbons (halocarbons) have been measured in and adjacent to the North Sea estuaries of the Humber and the Rhine. The measurements have been carried out using a newly constructed purge-and-trap sample work-up system coupled to megabore gas chromatography with electron capture detection. The results show that whereas the Humber is a pronounced source of the anthropogenic halocarbons carbon tetrachloride and perchloroethylene, the input from the Rhine into the North Sea of these compounds is more modest. Some halocarbons normally considered as mainly or even exclusively of natural origin are released from the two investigated estuaries into the North Sea. A distinct patch of high concentrations of the naturally produced compound bromoform was observed in the southwestern North Sea. The results have also been used to examine some of the halocarbons for common sources.

Effect of supplementation silage ("Festuca dolichophylla, Avena sativa and Vicia sativa") on weight gain and mortality in adult alpacas ("Vicugna pacos")

This study was conducted in order to evaluate the effect of supplementation with silage (Festuca dolichophylla, Avena sativa and Vicia sativa) on weight gain and mortality in adult alpacas, during the months of dry season (June to August) in Huancavelica region. 300 female alpacas 3 and 4 years of age (physiological state: pregnant) were used, which were assigned to the following treatments: SP, grazing only PSE15, grazing plus supplementation of 1.5 kg of silage. Alpacas were supplemented once daily. In each alpaca they were recorded live weight at the beginning and end of the experiment. The weight gain was -0.02 y 2.05 kg for SP and PSE15 respectively (p <0.001) treatments. Mortality was 5.3% and 2.7% for SP and PSE15 respectively (p=0.073) treatments. It can be concluded under the conditions of this trial silage supplementation has effect on weight gain and maybe also on mortality in alpacas.

TRANSIENT LIPOPOLYSACCHARIDE-INDUCED CYTOKINE RESPONSES IN THE MATERNAL AND FETAL GUINEA PIG

The aim of this study was to further investigate the role of pro-inflammatory cytokines in the pathogenesis of fetal cererbral white matter injury associated with chorioamnionitis by charaterizing the time course of the cytokine response in the pregnant guinea pig following a maternal inflammatory insult. Chorioamnionitis increases the risk for fetal brain injury. In the guinea pig, a threshold maternal inflammatory response must be reached for significant fetal brain injury to occur. However, a previous study demonstrated that, by seven days after an acute maternal inflammatory insult, cytokine levels in both maternal and fetal compartments are not different from controls. The purpose of this study, therefore, was to test the hypothesis that a significant cytokine response occurs within the first seven days following an acute maternal inflammatory response. Pregnant guinea pigs (n=34) were injected intraperitoneally with 100µg/kg lipopolysaccharide (LPS) at 70% gestation and euthanized at 24 hours, 48 hours or 5 days following endotoxin exposure. Control animals were euthanized at 70% gestation without exposure. Concentrations of interleukin-6, interleukin 1-β and tumour necrosis factor-α (IL-6, IL-1β, TNF-α) were quantified in the maternal serum and amniotic fluid by enzyme-linked immunosorbent assay. IL-6 and IL-1β concentrations were elevated in the maternal serum at 24 hours and returned to control levels by five days. In the amniotic fluid, IL-6 peaked at 48 hours and IL-1β at 24 hours. TNF-α levels were not significantly increased. A single maternal LPS injection produces transient increases in cytokine concentrations in the maternal serum and amniotic fluid. This further implicates the cytokines as potential mediators of fetal white matter damage. Although this response might not be sufficient to produce the brain injury itself, it may initiate harmful pro-inflammatory cytokine cascades, which could even continue to harm the fetus following delivery. A human diagnostic protocol was developed to assess the use of serial serum biomarkers, including IL-6 and TNF-α, in the prediction of histological chorioamnionitis. Preliminary analysis of the pilot study suggests that certain biomarkers might be worthy of further investigation in a larger-scale study.

Investigation of the effect of intrauterine inflammation and infection on fetal brain injury using human and animal models

In recent years, increased focus has been placed on the role of intrauterine infection and inflammation in the pathogenesis of fetal brain injury leading to neurodevelopmental disorders such as cerebral palsy. At present, the mechanisms by which inflammatory processes during pregnancy cause this effect on the fetus are poorly understood. Our previous work has indicated an association between experimentally-induced intrauterine infection, increased proinflammatory cytokines, and increased white matter injury in the guinea pig fetus. In order to further elucidate the pathways by which inflammation in the maternal system or the fetal membranes leads to fetal impairment, a number of studies investigating aspects of the disease process have been performed. These studies represent a body of work encompassing novel research and results in a number of human and animal studies. Using a guinea pig model of inflammation, increased amniotic fluid proinflammatory cytokines and fetal brain injury were found after a maternal inflammatory response was initiated using endotoxin. In order to more closely monitor the fetal response to chorioamnionitis, a model using the chronically catheterized fetal ovine was carried out. This study demonstrated the adverse effects on fetal white matter after intrauterine exposure to bacterial inoculation, though the physiological parameters of the fetus were relatively stable throughout the experimental protocol, even when challenged with intermittent hypoxic episodes. The placenta is an important mediator between mother and fetus during gestation, though its role in the inflammatory process is largely undefined. Studies on the placental role in the inflammatory process were undertaken, and the limited ability of proinflammatory cytokines and endotoxin to cross the placenta are detailed herein. Neurodevelopmental disorders can be monitored in animal models in order to determine effective disease models for characterization of injury and use in therapeutic strategies. Our characterizations of postnatal behaviour in the guinea pig model using motility monitoring and spatial memory testing have shown small but significant differences in pups exposed to inflammatory processes in utero. The data presented herein contributes a breadth of knowledge to the ongoing elucidation of the pathways by which fetal brain injury occurs. Determining the pathway of damage will lead to discovery of diagnostic criteria, while determining the vulnerabilities of the developing fetus is essential in formulating therapeutic options.