Naturally high total dissolved solids and upstream agricultural runoff often mask the influence of urban land cover on stream chemistry and biology. We examined the influence of headwater urbanization on the water chemistry, microbiology, and fish communities of the Big Brushy Creek watershed, a 96 km 2 drainage basin in the piedmont of South Carolina, USA. Concentrations of most major anions and cations (especially nitrate, sulfate, chloride, sodium, potassium, and calcium) were highest in the urban headwaters and decreased downstream. Generally, the highest concentrations of suspended coliform bacteria occurred in the urban headwaters. In contrast, stream habitat quality and the abundance, species richness, and species diversity of fishes did not differ significantly between urban and rural sites. Discharge of wastewater treatment plant effluent at one rural location caused an increase in concentrations of many solutes and possibly the abundance of benthic algae. We hypothesize that atmospheric dry deposition and domestic animal wastes are important sources of stream solutes and of coliform bacteria, respectively, in the urban headwaters. The lack of significant differences in fish abundance and diversity between urban and rural sites may indicate that urban development in the Big Brushy Creek watershed has not yet degraded habitat conditions greatly for stream fishes. Alternatively, agriculture or other land uses may have degraded stream habitat quality throughout the watershed prior to urbanization.

As the global population ages, and rates of dementia rise, understanding lifestyle factors that play a role in the development and acceleration of cognitive decline is vital to creating therapies and recommendations to improve quality of later life. Obesity has been shown to increase risk for dementia. However, the specific mechanisms for obesity-induced cognitive decline remain unclear. One potential contributor to diet-induced cognitive changes is neuroinflammation. Furthermore, a source of diet-induced inflammation to potentially increase neuroinflammation is via gut dysbiosis. We hypothesized that a high fat diet would cause gut microbe dysbiosis, and subsequently: neuroinflammation and cognitive decline. Using 7-month old male Sprague Dawley rats, this study examined whether 8 weeks on a high fat diet could impact performance on the water radial arm maze, gut microbe diversity and abundance, and microgliosis. We found that a high fat diet altered gut microbe populations compared to a low fat, control diet. However, we did not observe any significant differences between dietary groups on maze performance (a measure of spatial working memory) or microgliosis. Our data reveal a significant change to the gut microbiome without subsequent effects to neuroinflammation (as measured by microglia characterization and counts in the cortex, hippocampus, and hypothalamus) or cognitive performance under the parameters of our study. However, future studies that explore duration of the diet, composition of the diet, age of animal model, and strain of animal model, must be explored.

Wild-type Salmonella typhimurium expresses three proline transport systems : a high-affinity proline transport system encoded by the putP gene, and two glycine betaine transport systems with a lower affinity for proline encoded by the prop and proU genes. Although proline uptake by the Prop and ProU transport systems is sufficient to supplement a proline auxotroph, it is not efficient enough to allow proline utilization as a sole source of carbon or nitrogen. Thus, the PutP transport system is required for utilization of proline as a carbon or nitrogen source. In this study, an overexpression suppressor, designated pmY, which allows proline utilization in a putP genetic background and does not require the function of any of the known proline transport systems, was cloned and characterized. The suppressor gene, designated proY, maps at 8 min on the 5. typhimurium linkage map, distant from any of the other characterized proline transport genes. The DNA sequence of the proY gene predicts that it encodes a hydrophobic integral membrane protein, with strong similarity to a family of amino acid transporters. The suppressor phenotype requires either a multicopy clone of the pmY+ gene or both a single copy of the p r o p gene and a pmZ mutation. These results indicate that the proY gene is the structural gene for a cryptic proline transporter that is silent unless overexpressed on a multicopy plasmid or activated by a proZ mutation.

Proline uptake can be mediated by three different transport systems in wild-type Salmonella typhimurium: a high-affinity proline transport system encoded by the putP gene and two glycine-betaine transport systems with a low affinity for proline encoded by the proP and proU genes. However, only the PutP permease transports proline well enough t allow growth on proline as a sole carbon or nitrogen source. By selecting for mutations that allow a putP mutant to grow on proline as a sole nitrogen source, we isolated mutants (designated proZ) that appeared to activate a cryptic proline transport system. These mutants enhanced the transport of proline and proline analogs but did not require the function of any of the known proline transport genes. The mutations mapped between 75 and 77.5 min on the S. typhimurium linkage map. Proline transport by the proZ mutants was competitively inhibited by isoleucine and leucine, which suggests that the ProZ phenotype may be due to unusual mutations that alter the substrate specificity of the branched-chain amino acid transport system encoded by the liv genes.