overestimates the rate to agonists like carbachol because it includes an primary rate of transiently high secretion

Quantifying all chytrids that infect Planktothrix is an estimate of this pressure. A decrease in host diversity at a constant parasitic pressure is either showing that the Red Queen theory is not applicable or that the host is increasingly better protected. Our findings indicate that the hypothesis of De Bruin et al. using the Red Queen theory is not upheld in our sediment study. Other factors might have played a role in maintaining chemotype1 dominance over other chemotypes and chytrids. The disease triangle presented by Gsell describes the relationship not only as between parasite-host but also including environmental pressures. Gsell describes the potential environmental stressors that affect both host and parasite but where adaptation to environmental stressors by either parasite or host can lead to increased relative fitness of one over the other. For example, low temperatures in the spring can be used as an advantage by diatoms enabling them a window of opportunity to bloom at a time when chytrids are limited by temperature constraints. The result is to release the diatoms from chytrid infection pressure. Light is another environmental stressor for both chytrids and phytoplankton hosts. Bruning found that there was a significant decrease in zoospore production on a light limited host. In the 1990s Kolbotnvannet Planktothrix changed habitat from the epilimnion to the metalimnion, at a time when nutrient and chlorophyll a concentrations in the lake had decreased allowing light to penetrate deeper into the water column. This shift downward by Planktothrix during periods of increasing light penetration is a common and a routinely found event around the world and not indicative of light limitation. Planktothrix in the metalimnion can take advantage of the environmental constraints of low light and lower temperatures on chytrid infection rates to increase growth. The ability to utilize low light levels could then be also viewed as a positive environmental adaptation by Planktothrix to avoid chytrid infection. One noted difference between Planktothrix and Asterionella is the presence of intracellular oligopeptides found in Planktothrix. These oligopeptides are responsible for internal defense against chytrid infection by inhibiting the chytrid proteases that are produced by the rhizoids as they extend through the cell. They do not, however, protect the cell from cell death caused by chytrid parasitism. Instead they interfere with the life cycle or nutrient accumulation that would result in a decrease in production or maturation of zoospores and therefore a decrease in chytrid fitness. Rohrlack et al. clearly showed in laboratory studies using wild type and mutant knock out strains of Planktothrix that the oligopeptides are a natural defense system used by the host against its chytrid predator. Table 2 presents the differences in cellular oligopeptides between the common Norwegian chemotypes 1, 5, 7 and 9. If chemotypes have adapted by increasing their internal defense system against parasitism then our study in Kolbotnvannet suggests that chemotype 1 shows a better defense against the chytrid infection than chemotype 9 in this lake. It might be considered that chemotype 5 and chemotype 7 were PR-957 960374-59-8 unable to present sufficient defense against resident parasites to support populations in this lake. It is possible that the internal oligopeptide diversity found in chemotype 1 could present chytrids with such a diverse internal environment that would challenge to chytrid adaption. Multiple oligopeptides in a cell could be considered similar to the multi-clonal population results found by De Bruin et al.. While this study is unable to answer those questions, use of multiple oligopeptides for the protection of Planktothrix chemotypes against chytrid infection should be further researched. Influenza-like illness, a subset of acute respiratory infections, represents approximately 62% of acute respiratory infections. Viral pathogens are the most significant contributors.ARI is caused by many viruses, including the following: influenza viruses, respiratory syncytial virus,rhinovirus, human parainfluenza viruses 1-4, human metapneumovirus, human coronaviruses NL63,229E, OC43, and HKU1, human enterovirus and adenovirus.The similar clinical presentations of patients infected by various respiratory viruses make etiological diagnoses difficult when physicians simply make decisions based only on physical symptoms.

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