Some environmental factors influencing phytoplankton in the Southern Ocean around South Georgia

Data on phytoplankton and zooplankton biomass, and physical and chemical variables, are combined with a published multivariate description of diatom species composition to interpret variation within an area around South Georgia surveyed during an austral summer. Large-scale species distributions could be equated to the different water masses which reflected the interaction of the Antarctic Circumpolar Current with the island and the Scotia Ridge. Small-scale factors were found to act at an interstation scale and imposed local variation on the biogeographic pattern. Nutrient depletion could be related to phytoplankton biomass but no single inorganic nutrient of those measured (NO 3 −N, PO 4 −P and silica) could be identified as important. The ratio Si:P appeared to be more important as an ecological factor. The impact of grazing by krill and other zooplankton could only be resolved as differences in phytoplankton biomass and phaeopigment content. Diatom species composition showed a relation to local krill abundance very different from that suggested by published studies, but could be explained as the effect of earlier grazing outside the study area. The effects of vertical mixing could not account for interstation differences as pycnocline depth was uniformly greater than euphotic depth, and vertical stability very low. Some comparison was made with data collected in 1926–31 by the Discovery Investigations. Significant differences in the distribution of certain taxa such as Chaetoceros criophilum and C. socialis were traced to major differences in hydrology.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/46983/1/300_2004_Article_BF00443379.pd

Perivascular macrophages in health and disease

Macrophages are a heterogeneous group of cells that are capable of carrying out distinct functions in different tissues, as well as in different locations within a given tissue. Some of these tissue macrophages lie on, or close to, the outer (abluminal) surface of blood vessels and perform several crucial activities at this interface between the tissue and the blood. In steady-state tissues, these perivascular macrophages maintain tight junctions between endothelial cells and limit vessel permeability, phagocytose potential pathogens before they enter tissues from the blood and restrict inappropriate inflammation. They also have a multifaceted role in diseases such as cancer, Alzheimer disease, multiple sclerosis and type 1 diabetes. Here, we examine the important functions of perivascular macrophages in various adult tissues and describe how these functions are perturbed in a broad array of pathological conditions

Proliferation of Perivascular Macrophages Contributes to the Development of Encephalitic Lesions in HIV-Infected Humans and in SIV-Infected Macaques

The aim of the present study was to investigate if macrophage proliferation occurs in the brain during simian immunodeficiency virus (SIV) infection of adult macaques. We examined the expression of the Ki-67 proliferation marker in the brains of uninfected and SIV-infected macaques with or without encephalitis. Double-label immunohistochemistry using antibodies against the pan-macrophage marker CD68 and Ki-67 showed that there was a significant increase in CD68+Ki-67+ cells in macaques with SIV encephalitis (SIVE) compared to uninfected and SIV-infected animals without encephalitis, a trend that was also confirmed in brain samples from patients with HIV encephalitis. Multi-label immunofluorescence for CD163 and Ki-67 confirmed that the vast majority of Ki-67+ nuclei were localized to CD163+ macrophages in perivascular cuffs and lesions. The proliferative capacity of Ki-67+ perivascular macrophages (PVM) was confirmed by their nuclear incorporation of bromodeoxyuridine. Examining SIVE lesions, using double-label immunofluorescence with antibodies against SIV-Gag-p28 and Ki-67, showed that the population of Ki-67+ cells were productively infected and expanded proportionally with lesions. Altogether, this study shows that there are subpopulations of resident PVM that express Ki-67 and are SIV-infected, suggesting a mechanism of macrophage accumulation in the brain via PVM proliferation