Outbreak of Human Trichinellosis in Northern California Caused by Trichinella murrelli

Abstract. In October of 2008, an outbreak of trichinellosis occurred in northern California that sickened 30 of 38 attendees of an event at which meat from a black bear was served. Morphologic and molecular testing of muscle from the leftover portion of bear meat revealed that the bear was infected with Trichinella murrelli, a sylvatic species of Trichinella found in temperate North America. Clinical records revealed a high attack rate for this outbreak: 78% for persons consuming any bear meat and 100% for persons consuming raw or undercooked bear meat. To our knowledge, this report is the first published report of a human trichinellosis outbreak in the United States attributed to T. murrelli, and it is the second such outbreak reported worldwide.     

The Molecular Mechanisms of Offspring Effects from Obese Pregnancy

The incidence of obesity, increased weight gain and the popularity of high-fat / high-sugar diets are seriously impacting upon the global population. Billions of individuals are affected, and although diet and lifestyle are of paramount importance to the development of adult obesity, compelling evidence is emerging which suggests that maternal obesity and related disorders may be passed on to the next generation by non-genetic means. The processes acting within the uteri of obese mothers may permanently predispose offspring to a diverse plethora of diseases ranging from obesity and diabetes to psychiatric disorders. This review aims to summarise some of the molecular mechanisms and active processes currently known about maternal obesity and its effect on foetal and neonatal physiology and metabolism. Complex and multifactorial networks of molecules are intertwined and culminate in a pathologically synergistic manner to cause disruption and disorganisation of foetal physiology. This altered phenotype may potentiate the cycle of intergenerational transmission of obesity and related disorders.Key Words: Maternal obesity, Epigenetics, Reactive oxygen species     

Maternal Diet and Weight at 3 Months Postpartum Following a Pregnancy Intervention with a Low Glycaemic Index Diet: Results from the ROLO Randomised Control Trial

Pregnancy increases the risk of being overweight at a later time period, particularly when there is excessive gestational weight gain. There remains a paucity of data into the effect of low glycaemic index (GI) pregnancy interventions postpartum. Aim: To examine the impact of a low glycaemic index diet during pregnancy on maternal diet 3 months postpartum. Methodology: This analysis examined the diet, weight and lifestyle of 460 participants of the ROLO study 3 months postpartum. Questionnaires on weight, physical activity, breastfeeding, supplement use, food label reading and dietary habits were completed. Results: The intervention group had significantly greater weight loss from pre-pregnancy to 3 months postpartum than the control group (1.3 vs. 0.1 kg, p = 0.022). The intervention group reported greater numbers following a low glycaemic index diet (p < 0.001) and reading food labels (p = 0.032) and had a lower glycaemic load (GL) (128 vs. 145, p = 0.014) but not GI (55 vs. 55, p = 0.809) than controls. Conclusions: Low GI dietary interventions in pregnancy result in improved health-behaviours and continued reported compliance at 3 months postpartum possibly through lower dietary GL as a result of portion control. Greater levels of weight loss from pre-pregnancy to 3 months postpartum in the intervention group may have important positive implications for overweight and obesity.     

Hypoproteinemic alkalosis

Hypoproteinemia by itself causes a nonrespiratory ("metabolic") alkalosis. On the average, a decrease in plasma albumin concentration of 1 g/dl produces an increase in "standard" bicarbonate of 3.4 mM/liter, and an apparent base excess of +3.7 meq/liter; it also reduces the value of the normal anion gap by about 3 meq/liter. Concentration of plasma protein should be measured as part of the analysis of acid-base status. Interpretation of acid-base data requires special consideration in "primary hypoproteinemic alkalosis."     

Changes in myofibrillar activation and troponin C Ca2+ binding associated with troponin T isoform switching in developing rabbit heart

Postnatal development of the mammalian heart is associated with changes in the population of isoforms of the thin filament proteins. We correlated the change in thin filament proteins, which occur in rabbit hearts between 5 days and 22 days of age, with changes in Ca2+ dependence of myofibrillar ATPase activity, force generation, and troponin C Ca2+ binding. The preparations derived from the 5-day-old animals exhibited a high molecular weight isoform of troponin T not found in the hearts of the 22-day-old animals. Other troponin T isoforms were also found to be present in different relative amounts. No other major differences in thin filament protein composition could be identified. Compared with the 5-day-old rabbit heart preparations, the ATPase activity of myofibrils from 22-day-old rabbit hearts exhibited a reduced Ca2+ sensitivity. The pCa50 (negative log of the half-maximal-activity free Ca2+) of the MgATPase activity was shifted by 0.15 pCa units with maturation. Maturation of the myofibrils was also associated with an increased effect of Mg2+ on pCa50. On increasing the Mg2+ from 2 to 10 mM at constant MgATP2-, the pCa50 of 5-day myofibrils was increased (shifted to the right) by 0.39 pCa units for 5-day-old rabbit hearts and 0.45 pCa units for 22-day-old rabbit hearts. Although similar changes in pCa50 of force developed by myofibrils were marginally significant, fibers from hearts of 5-day-old rabbits exhibited a greater Hill coefficient than hearts from 22-day-old rabbits (3.0 vs. 2.1). Despite the increased sensitivity of 5-day-old rabbit hearts to Ca2+, these hearts exhibited significantly less Ca2+ bound to myofibrillar troponin C than did the 22-day-old rabbit hearts. Moreover, the models that best described the Ca2+ binding data are different for the two age groups. Our data indicate that the Ca2+ activation and Ca2+ binding properties of myofibrillar troponin C are altered in developing cardiac myofibrils and that the changes in these properties may be influenced by changes in the troponin T isoforms present in the myofibril.     

Piecemeal degranulation of mast cells in the inflammatory eyelid lesions of interleukin-4 transgenic mice. Evidence of mast cell histamine release in vivo by diamine oxidase-gold enzyme-affinity ultrastructural cytochemistry

We used light and electron microscopy to analyze the eyelid inflammation that develops in transgenic mice that overexpress interleukin-4 (IL-4; Tepper et al, Cell 62:457, 1990). Analysis of alkaline Giemsa-stained plastic sections examined by light microscopy (Dvorak et al, J Exp Med 132:558, 1970), as well as by routine transmission electron microscopy, indicated that the mast cells in the inflammatory eyelid lesions were undergoing piecemeal degranulation, a form of secretion in which the cells' cytoplasmic granules exhibit characteristic morphologic changes that are thought to be associated with the prolonged, vesicle-mediated release of the granules' constituents. Moreover, by using a newly reported enzyme affinity-gold method, which stains histamine based on binding to diamine oxidase-gold (Dvorak et al, J Histochem Cytochem 41:787, 1993), we show that these activated mast cells had released much of their histamine content. The eyelid lesions also exhibited increased numbers of mast cells; interstitial fibrosis, particularly around cutaneous nerves and blood vessels; activated fibroblasts; focal axonal damage; venules with endothelial cells containing numerous vesiculo-vacuolar organelles; and infiltrates of neutrophils and eosinophils. Our findings illustrate that overexpression of the IL-4 gene in vivo can result in eyelid lesions associated with piecemeal degranulation of mast cells, as well as tissue fibrosis and a variety of other pathologic changes. These results also represent the first direct morphologic evidence for histamine secretion by mast cells in vivo.     

Sharing Heterogeneous Data: The National Database for Autism Research

The National Database for Autism Research (NDAR) is a secure research data repository designed to promote scientific data sharing and collaboration among autism spectrum disorder investigators. The goal of the project is to accelerate scientific discovery through data sharing, data harmonization, and the reporting of research results. Data from over 25,000 research participants are available to qualified investigators through the NDAR portal. Summary information about the available data is available to everyone through that portal.