Drafts

To further back up this claim the authors performed a parameter study to assess the sensitivity of their prediction. Mass was not the only important factor in determining their hypothesis. They also looked into limb orientation, and muscle fiber lengths. Since these data points cannot be determined for sure the authors used conservative assumptions leading to an underestimated value of required muscle mass. They used T as the minimum extensor muscle mass per leg and determined that if T  is 5-25% body mass per leg than the biped could not run fast due to the lack of necessary muscle force. Hutchinson and Garcia’s model predicted that the T value for Tyrannosaurus was between 10-21% per leg which is not adequate enough for it to be considered a fast runner.

Hutchinson and Garcia used data from extant animals to help support their claim. They looked at the muscle anatomy of different animal’s hips, knees, ankles, and toes in order to come up with a sufficient comparison to Tyrannosaurus. Also due to fossilized footprints they had data present for small tyrannosaurs. Other animals that were used in comparison include: alligators, chickens, and the extinct Colelophysis. In comparing the muscle percent of the alligator and the chicken they found that the chicken has a larger percent of muscle mass per body mass than alligators which allow them to run faster. This is due to scaling principles predicting that animals of larger body mass have a more restricted locomotor performance. In order for the Tyrannosaurus to be a fast runner it would need enough muscle mass to support its body the authors argue. The authors calculated that the dinosaur would need about 43% of its body mass to be muscles in each leg alone in order to be a fast runner.

The threshold in a membrane potential is reached when there is a significant depolarization which opens the voltage gated Na+ channels a the axon hillock. The diffusion of sodium causes the membrane to have a positive membrane potential. The Nernst potential is then reached at +50 mV, causing the Na channels to inactivate and the K+ voltage gated channels to open as they are triggered by a delayed depolarization. K+ ions will exit until the potential overshoots the resting potential before returning to roughly the K+ Nernst potential.

In the reading by John R. Hutchinson and Mariano Garcia, the two authors propose a controversial concept that large theropod dinosaurs such as Tyrannosaurus were not actually fast runners. They use a method for gauging running through a model system that works for estimating the speed of living species such as alligator and chickens.The authors point out that this concept of Tyrannosaurus being a slow runner is not a new idea. There were earlier assessments based off of biomechanics that suggested the dinosaur was limited in locomotive performance. These early ideas were not widely accepted due to the uncertainty of the dinosaur’s anatomy, physiology, and overall behavior. However other previous studies estimate that Tyrannosaurus was able to run in the range of 11-20 m/s.

An initial step in identifying DNA as the source of genetic information came with the discovery of a phenomenon called transformation. This phenomenon was first observed in 1928 by Fred Griffith, an English physician whose special interest was the bacterium that causes pneumonia: Streptococcus pneumoniae. Griffith had succeeded in isolating several different strains of S. pneumoniae (type I, II, III, and so forth). In the virulent (disease-causing) forms of a strain, each bacterium is surrounded by a polysaccharide coat, which makes the bacterial colony appear smooth (S) when grown on an agar plate. Griffith found that these virulent forms occasionally mutated to nonvirulent forms, which lack a polysaccharide coat and produce a rough-appearing colony (R).

To a 10 mL round bottom flask, tert-butyl methyl ether (TBME) (3mL) and nutmeg (1.000 g) were added in addition to boiling chips. For ten minutes, the solution was refluxed. The solution was filtered into a tared 25 mL Erlenmeyer flask after the solution had settled. To the round bottom flask, TBME (2 mL) was added and briefly refluxed and then filtered as before. Air was passed over the solution to evaporate the solvent. The crude product (0.578 g) and acetone (7 mL) were added in a 25 mL Erlenmeyer flask to recrystalize. After cooling in an ice bath, the crystals were dried and obtained via suction filtration and were rinsed with cold acetone (~1 mL). A small portion was set aside for the melting point. Trimyristin (0.60 g). 6 M NaOH (2 mL), ethanol (2 mL), and boiling chips were added to clean round bottom flask and refluxed for 45 minutes. The remaining trimyristin was then recrystallized for the second time and was cooled at room temperature for 10 minutes before cooling on ice for an additional 10 minutes. After 45 minutes of hydrolysis, the contents were poured into a clean 50 mL beaker that contained 8 mL of water and 2 mL of concentrated HCl, which was added dropwise. After all the contents were well stirred in the beaker, the solid was collected via suction filtration. The product was rinsed three times with 1 mL water and then allowed to dry overnight.

Our method was to study two feeders; one feeder is in an area that experiences a moderate level of human traffic while the other is on a trail that experiences relatively low human traffic on a daily basis. We wanted to test out whether human traffic would affect the number of birds that were coming to each feeder; we tried to do our data collections around the same time in order to ensure that time would not be a determining factor; however, there was a margin of human error in the form that we all went when we were able to fit the visit into our schedule. Our experimental sites were at the Silvan parking lots forest bird feeder and the forest bird feeder at the path that leads to Orchard Hill. We chose those sites because they are within walking distance from where everyone lives. We plan on conducting our experiments at least four times a week until April 11,  a week before the project is due. We plan on observing bird competition on different days and different times in order to avoid pseudoreplication. We have two sites; they are not that far apart so we will most likely have to find another site because if we use our current two we run a high risk of pseudoreplication. We will also do a variety of individuals and pairs when it comes to data collection; during the pair collection ideally, you collect data individually just to ensure randomization of data.

We hypothesize that there is a strong correlation between the presence and number of perch-feeding birds and the number and presence of ground-foraging birds. We also hypothesize that within interspecific feeding competition between perch-feeding birds as well as the interspecific feeding competition between ground-feeding birds that size and innate behavior will determine dominance, and therefore access to the feeder. Our hypothesis is that size will be the biggest factor in terms of feeding success. It is expected that the species that have a larger body mass, girth, or height and exhibits more aggressive behaviors, such as displaying wings and bills, pecking, or mobbing will be capable of outcompeting smaller and more docile species between the two groups that we are studying.

As a group we became intrigued with the dynamics between perching birds that use feeders as their source of food and foraging birds that rely on food that they find on the ground. The main question that continued to arise was whether there was a competitive relationship between these two groups, the first question being whether perching birds attracted foraging birds. As birds perch on a feeder and eat, seed will be dropped from the feeder to the ground. Understanding that, our first goal was to examine if there was a correlation between a bird being at a feeder and the appearance of a ground forager or if they were unrelated and both groups operated individually from one another. Our next question was whether there was a level of competition present among each group and between each group.  As a result, our group decided to analyze the interspecific feeding competition between perch-feeding birds as well as the interspecific feeding competition between ground-feeding birds.

It is essential for the three monoclonal antibodies for CD44, CD24, and ESA to bind to only PaCSCs. Although these antigens are overabundant in PaCSCs, variants may also be expressed in healthy pancreatic cells. As a result, the liposomes will be engineered so the antibodies will only bind to CD44, CD24, and ESA when these antigens are present in high enough concentrations. Titration assays can determine significant thresholds for these effective antigen concentrations. The liposomes will be administered weekly via intravenous infusion in an aqueous or hydrophilic solution to the patient due to their polar exteriors. Dosage efficiency can be evaluated through repeated titrations for a standardized therapeutic threshold of 95% or greater based on liposomal binding and delivery of contents. After approximately five rounds of treatment, 99.99% of PaCSCs should be eliminated, allowing for a relatively short duration of stem cell therapy.