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Dr. Brown Immune Experiment Summary

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Dr. Brown Immune Experiment Summary
Dr. Brown conducted three distinctive experiments in order to understand how an individual’s immunological phenotype is the result of its genotype, the environment, and development. For the first experiment, Dr. Brown’s research was testing how selection on basal and maximal metabolic rates affect immune function. In addition, Dr. Brown had four hypotheses for this particular experiment, two were for basal metabolic rate and two were for maximal metabolic rate. Moreover, trade-off with BMR decreases as basal metabolic rate increases, and assimilation increases as basal metabolic rate increases. Furthermore, trade-off with MMR decreases as maximal metabolic rate decreases as well as energetic capacity increases as maximal metabolic rate increases. …show more content…

The selection treatment consisted of mass-independent metabolic rates, basal and maximal. The sample size for the mice is n=12 which means that there are 4 replicates. BMR measurements were made using mouse treadmills. Each mouse had an hour to run on the treadmill, and the speed was increased incrementally. Selection treatments worked as the mice that have the lowest MMR (control) do not have the lowest BMR (antagonistic). Dr. Brown did innate immune experiment to measure BMR and MMR, where the mice were inoculated with sham or LPS, LPS essentially initiates immune response. In addition, quantified plasma TNF- was measured because LPS > macrophage response. BMR wasn’t related to inflammation as TNF-: LR= 12.31, p<0.01. Selection for high-MMR suppressed innate immunity and Dr. Brown wanted to determine what is the potential mechanism? The determination was changes in signaling networks, specifically, glucocorticoids, as well as selection for an exercise phenotype. Overall, Dr. Brown believes that MMR may be an important architect for immune function and correlates of MMR should be studied when considering the evolution of metabolic …show more content…

Brown conducted an experiment on was how population density affects investment in immune function. Female elk were largely used in the experiment; elk were used for the experiment as they exhibit slow-paced life histories consisting of long life spans and large body size. Elk trade-off current reproduction for future reproduction, which means they will forego reproduction for the next time if not able to survive and it is facilitated by the body condition in the elk. Additionally, one male elk will reproduce with many female elk. The hypothesis is that there will be a positive relationship between immune function and max fat up to a threshold. Complement Cascade consisted of an invading cell where it was tagged by antibodies and complement activated. Dr. Brown measured the complement pathway through the bacteria killing ability using a serum that was mixed with the bacteria which in turn allowed to measure the percentage of bacteria killed. Hemolytic-complement activity was also measured through serum mixing with SRBC and anti-SRBC antibodies which allowed for the percentage of cells lysed to be able to be recorded. Dr. Brown aimed to see if population density had an effect on the parasite load, and she concluded it does. Additionally, she came to the conclusion that not just density has an effect, but age as well. Furthermore, Dr. Brown concluded the duration of individuals that infectious has a direct correlation to the frequency of the spread

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