Childhood solid tumours in relation to infections in the community in Cumbria during pregnancy and around thetime of birth

In a retrospective cohort study of all 99 976 live births in Cumbria, 1975–1992, we investigated whether higher levels of community infections during the mother's pregnancy and in early life were risk factors for solid tumours (brain/spinal and other tumours), diagnosed 1975–1993 under age 15 years. Logistic regression was used to relate risk to incidence of community infections in three prenatal and two postnatal quarters. There was an increased risk of brain/spinal tumours among children exposed around or soon after birth to higher levels of community infections, in particular measles (OR for trend=2.1, 95%CI : 1.3–3.6, P=0.008) and influenza (OR for exposure=3.3, 95%CI : 1.5–7.4, P=0.005). There was some evidence of an association between exposure to infections around and soon after birth and risk of other tumours, but this may have been a chance finding. The findings are consistent with other recent epidemiological studies suggesting brain tumours may be associated with perinatal exposure to infections

Does Reviewing Lead to Better Learning and Decision Making? Answers from a Randomized Stock Market Experiment

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Paracoccidioides brasilinsis-Induced Migration of Dendritic Cells and Subsequent T-Cell Activation in the Lung-Draining Lymph Nodes

Paracoccidioidomycosis is a mycotic disease caused by a dimorphic fungus, Paracoccidioides brasiliensis (Pb), that starts with inhalation of the fungus; thus, lung cells such as DC are part of the first line of defense against this microorganism. Migration of DC to the lymph nodes is the first step in initiating T cell responses. The mechanisms involved in resistance to Pb infection are poorly understood, but it is likely that DC play a pivotal role in the induction of effector T cells that control Pb infection. In this study, we showed that after Pb Infection, an important modification of lung DC receptor expression occurred. We observed an increased expression of CCR7 and CD103 on lung DC after infection, as well as MHC-II. After Pb infection, bone marrow-derived DC as well lung DC, migrate to lymph nodes. Migration of lung DC could represent an important mechanism of pathogenesis during PCM infection. In resume our data showed that Pb induced DC migration. Furthermore, we demonstrated that bone marrow-derived DC stimulated by Pb migrate to the lymph nodes and activate a T helper (Th) response. To the best of our knowledge, this is the first reported data showing that Pb induces migration of DC and activate a T helper (Th) response

More than a century of bathymetric observations and present-day shallow sediment characterization in Belfast Bay, Maine, USA: implications for pockmark field longevity

This paper is not subject to U.S. copyright. The definitive version was published in Geo-Marine Letters 31 (2011): 237-248, doi:10.1007/s00367-011-0228-0.Mechanisms and timescales responsible for pockmark formation and maintenance remain uncertain, especially in areas lacking extensive thermogenic fluid deposits (e.g., previously glaciated estuaries). This study characterizes seafloor activity in the Belfast Bay, Maine nearshore pockmark field using (1) three swath bathymetry datasets collected between 1999 and 2008, complemented by analyses of shallow box-core samples for radionuclide activity and undrained shear strength, and (2) historical bathymetric data (report and smooth sheets from 1872, 1947, 1948). In addition, because repeat swath bathymetry surveys are an emerging data source, we present a selected literature review of recent studies using such datasets for seafloor change analysis. This study is the first to apply the method to a pockmark field, and characterizes macro-scale (>5 m) evolution of tens of square kilometers of highly irregular seafloor. Presence/absence analysis yielded no change in pockmark frequency or distribution over a 9-year period (1999–2008). In that time pockmarks did not detectably enlarge, truncate, elongate, or combine. Historical data indicate that pockmark chains already existed in the 19th century. Despite the lack of macroscopic changes in the field, near-bed undrained shear-strength values of less than 7 kPa and scattered downcore 137Cs signatures indicate a highly disturbed setting. Integrating these findings with independent geophysical and geochemical observations made in the pockmark field, it can be concluded that (1) large-scale sediment resuspension and dispersion related to pockmark formation and failure do not occur frequently within this field, and (2) pockmarks can persevere in a dynamic estuarine setting that exhibits minimal modern fluid venting. Although pockmarks are conventionally thought to be long-lived features maintained by a combination of fluid venting and minimal sediment accumulation, this suggests that other mechanisms may be equally active in maintaining such irregular seafloor morphology. One such mechanism could be upwelling within pockmarks induced by near-bed currents.Graduate support for Brothers came from a Maine Economic Improvement Fund Dissertation Fellowship

The Road Less Traveled: Regulation of Leukocyte Migration Across Vascular and Lymphatic Endothelium by Galectins

Leukocyte entry from the blood into inflamed tissues, exit into the lymphatics, and migration to regional lymph nodes are all crucial processes for mounting an effective adaptive immune response. Leukocytes must cross two endothelial cell layers, the vascular and the lymphatic endothelial cell layers, during the journey from the blood to the lymph node. The proteins and cellular interactions which regulate leukocyte migration across the vascular endothelium are well studied; however, little is known about the factors that regulate leukocyte migration across the lymphatic endothelium. Here, we will summarize evidence for a role for galectins, a family of carbohydrate-binding proteins, in regulating leukocyte migration across the vascular endothelium and propose that galectins are also involved in leukocyte migration across the lymphatic endothelium