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Stream habitats in Illinois have been fragmented over time by human interference, specifically agriculture and pollution. Stream fragmentation may cause distinct patch formation within a stream and may produce negative effects upon both abiotic and biotic factors of a stream. Therefore, if patch formation exists, we would expect to see changes in algal growth rates within patches, which in turn may lead to changes in growth rates of fish at various trophic levels. In this study, our objectives were to: 1) determine if distinct patch formation occurred within a stream environment; 2) discover if algal growth potential differed between habitat types; and 3) determine if growth rates of fish are affected by differences in algal growth or patch formation. Seven sites were sampled for fish and algal growth potential along Polecat Creek, located in Coles County, Illinois. For all sites, stream habitat quality assessment was conducted using the Stream Habitat Assessment Procedure (SHAP), stream algal growth potential was assessed using biostimulation, and fish growth rates were determined using the back calculation method. We concluded from SHAP scores that distinct patch formation occurred within a stream and resulted in two habitat classes: the good habitat class containing four good sites and the poor habitat class containing three sites. When comparing good and bad site classes no significant difference was observed in algal growth potential or fish growth rates. The reason for the absence of differences in algal growth potential and fish growth rates between site classes may be due to the overall phosphorous deficiency within the stream.
Tumor necrosis factor (TNF) is a mediator of inflammation during immune responses and is produced by activated macrophages and T cells. It is synthesized as a membrane-bound homotrimer that is released from activated cells. Its functions are to inhibit viral replication, cause capillary leakage, induce cell apoptosis, and to recruit other immune cells to the infected area. Many humans infected with Sin Nombre (SN) virus develop an inflammatory pulmonary immunopathology caused by abundant production of TNF. In contrast, infected deer mice, the natural reservoir of SN virus, exhibit no pathology or inflammation in the lungs. Because of this, it is unlikely that deer mice produce appreciable amounts of TNF in response to SN virus infection. To begin to address this issue, we have cloned and sequenced the Tnf gene of deer mice. We obtained all but the final 9 nucleotides of Tnf and have determined that it is highly conserved with orthologous sequences.