Potential Direct and Indirect Effects of Climate Change on a Shallow Natural Lake Fish Assemblage

Much uncertainty exists around how fish communities in shallow lakes will respond to climate change. In this study, we modelled the effects of increased water temperatures on consumption and growth rates of two piscivores (northern pike [Esox lucius] and largemouth bass [Micropterus salmoides]) and examined relative effects of consumption by these predators on two prey species (bluegill [Lepomis macrochirus] and yellow perch [Perca flavescens]). Bioenergetics models were used to simulate the effects of climate change on growth and food consumption using predicted 2040 and 2060 temperatures in a shallow Nebraska Sandhill lake, USA. The patterns and magnitude of daily and cumulative consumption during the growing season (April–October) were generally similar between the two predators. However, growth of northern pike was always reduced (–3 to –45% change) compared to largemouth bass that experienced subtle changes (4 to –6% change) in weight by the end of the growing season. Assuming similar population size structure and numbers of predators in 2040–2060, future consumption of bluegill and yellow perch by northern pike and largemouth bass will likely increase (range: 3–24%), necessitating greater prey biomass to meet future energy demands. The timing of increased predator consumption will likely shift towards spring and fall (compared to summer), when prey species may not be available in the quantities required. Our findings suggest that increased water temperatures may affect species at the edge of their native range (i.e. northern pike) and a potential mismatch between predator and prey could exist

CD44 isoforms in human retinal and choroidal endothelial cells

Author version available from PubMed Central (PMC) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609890

Toxoplasma gondii migration within and infection of human retina.

Toxoplasmic retinochoroiditis is a common blinding retinal infection caused by the parasite, Toxoplasma gondii. Basic processes relating to establishment of infection in the human eye by T. gondii tachyzoites have not been investigated. To evaluate the ability of tachyzoites to navigate the human retina, we developed an ex vivo assay, in which a suspension containing 1.5 × 10(7) parasites replaced vitreous in a posterior eyecup. After 8 hours, the retina was formalin-fixed and paraffin-embedded, and sections were immunostained to identify tachyzoites. To determine the preference of tachyzoites for human retinal neuronal versus glial populations, we infected dissociated retinal cultures, subsequently characterized by neuron-specific enolase or glial fibrillary acidic protein expression, and retinal cell lines, with YFP-expressing tachyzoites. In migration assays, retinas contained 110-250 live tachyzoites; 64.5-95.2% (mean  =79.6%) were localized to the nerve fiber layer, but some were detected in the outer retina. Epifluorescence imaging of dissociated retinal cultures 24 hours after infection indicated preferential infection of glia. This observation was confirmed in growth assays, with significantly higher (p ≤ 0.005) numbers of tachyzoites measured in glial verus neuronal cell lines. Our translational studies indicate that, after entering retina, tachyzoites may navigate multiple tissue layers. Tachyzoites preferentially infect glial cells, which exist throughout the retina. These properties may contribute to the success of T. gondii as a human pathogen

<i>T. gondii</i> tachyzoites migrate through human retina.

<p>(A). Representative photomicrographs showing <i>T. gondii</i> tachyzoites within the retina 8 hours following addition of a suspension of 1.5×10⁷ live parasites to a human posterior eyecup. Tachyzoites are identified by immunostaining for the parasite SAG-1 antigen. Fast Red with hematoxylin counter stain. Original magnification: 1000X. Arrows indicate tachyzoites. Negative control sections showed no positive staining. (B). Graph showing number of tachyzoites counted within retinas from eyecups incubated with live or heat-killed tachyzoites. Columns  =  mean. Error bars  =  standard error of mean. (C). Pie chart showing mean percentage of tachyzoites located at different retinal layers. NFL  =  nerve fiber layer; GCL  =  ganglion cell layer; IPL  =  inner plexiform layer; INL  =  inner nuclear layer; OPL  =  outer nuclear layer; ONL  =  outer nuclear layer. Data shown in (B) and (C) were generated in experiments using 3 paired human cadaver posterior eyecups.</p

<i>T. gondii</i> tachyzoites infect human retinal glial cells in preference to neurons.

<p>(A). Immediately prior to infection, dissociated human retinal cultures presented a layer of glial cells with neurons positioned above. Original magnification: 100X. (B and C). Expression of (B) neuron specific enolase (NSE) (red), as detected by rabbit polyclonal anti-human NSE antibody and Alexa Fluor 594-conjugated donkey anti-rabbit immunoglobulin (Ig)G antibody and (C) glial fibrillary acidic protein (GFAP) (red), as detected by sheep polyclonal anti-human GFAP antibody and Alexa Fluor 594-conjugated donkey anti-sheep IgG antibody. <i>T. gondii</i> tachyzoites express YFP (green). Original magnification: 630X. Negative control cultures showed no positive staining. (D). Graph showing percentage growth of tachyzoites in Y79 human retinoblastoma cells and MIO-M1 human Müller glial cells, plus positive control human foreskin fibroblasts (FF), over a 24-hour period. n = 7–8 wells/condition. Columns  =  mean. Error bars  =  standard error of mean. Representative of two independent experiments.</p