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If 3 UV active spots were in the crude material and co-spot TLC plate, and only one spot had the same R_f as the starting material and the other 2 are very different, predictions for the 2 non-starting material spots could be something in the middle of the mechanisms. There are four parts to the mechanism, the one in the middle are the ones that alter the mechanisms. So the second and third part of the mechanism would be the 2 non-starting material spots. This is because of the rate of the hydride attack on the carbon double bonded to the oxygen. It depends heavily on the R group present, and the more electron deficient it is, the faster the hydride can attack. But because they are different from the starting material spot, it would mean that it was caught between and could not fully reduced and go to completion. If it were to be the 1st and 4th instead of the two in the middle steps of this mechanism, it would go through but it will not be full.

If 3 UV active spots were in the crude material and co-spot TLC plate, and only one spot had the same R_f as the starting material and the other 2 are very different, predictions for the 2 non-starting material spots could be something in the middle of the mechanisms. There are four parts to the mechanism, so the second and third part of the mechanism would be the 2 non-starting material spots. This is because of the rate of the hydride attack on the carbon double bonded to the oxygen. It depends heavily on the R group present, and the more electron deficient it is, the faster the hydride can attack. But because they are different from the starting material spot, it would mean that it was caught between and could not fully reduced and go to completion.

            First, add benzoin (0.5g) and ethanol (4mL) to an Erlenmeyer flask (25mL) swirling at room temperature until it is all dissolved. Add sodium borohydride (0.1g) using a micro spatula in small amounts for 5 minutes (swirl for addition 20 minutes at room temperature). Cool the mixture using ice bath, add water (5mL) after and 6M HCl (0.3mL). Wait 15 minutes to add more water (2.5mL). Then collect the product using vacuum filtration (reserve 1-2mg for TLC analysis) after 15 minutes. Recrystallize from acetone, using 25 mL flask. Let it all dry and come back for evening hours. MP, yield %, and mass needs to be determined. Dissolve a small amount of benzoin, using recrystallized product and reserved crude product in ethyl acetate. Spot 2 TLC plates, with starting material, reserved crude product, recrystallized product, and a spot that contains both in the middle. Run the TLC plates in 9:1 CH­­₂Cl₂: ethanol. Add eluent to TLC developing chamber, use tweezers to carefully put the TLC plate in the chamber and screw the cap. Allow the solvent to run from the baseline to about 1cm from the top. Remove the TLC plate when it is ready marking the solvent from it and allow it to dry. Use UV light and mark them once it is all dry. Tape the plates on a sheet of the lab notebook paper or take a picture and draw into the lab notebook. 

The three known substances naphthalene, urea, and sulfanilamide were all provided with its relative MP ranges. Naphthalene was 79 degrees and I found it to be 80 degrees. Urea was given 132-134 but mine did not completely melt until it hit 137. Lastly, sulfanilamide was 165-167 but mine was 1 degree higher to be 168. For the two unknowns, I wasn't given the MP range so I had to start from 0 degrees and slowly raise the temperature. Unkown 8 that I was given which I did for my first unknown came out to have melting point of 95 which is why I thought it was acenaphthene with melting point of 94-96. Unkown #7 which I used for my second unknown came out to have MP 166 which is why I concluded that it was sulfanilamide once again because it had 165-167 degrees.

The kidneys of the stellar river otter look very similar to the American river otter Lutra Canadensis. This is a multi-lobed kidney which is commonly found in many marine and aquatic mammals. The kidneys are multi-lobed and are fully equipped to remove toxins however they are not specialized for water conservation. Because the stellar river otter lives in a freshwater environment it does not need kidneys adapted for the conservation of water. Water is extremely prevalent in the habitat of the river otter and it has little need to conserve it when there is a river just outside its back door. The river otter also has a large multi-lobed liver, which supports the idea that its body is more adapted to purify toxins than it is to conserve water.

When looking at the male stellar river otter it possesses the morphology of a powerful predator. The two long pairs of canines and huge forelimbs make this mammal an intimidating predator. The mane of the stellar river otter can be erected and lowered to accommodate for the situation. When swimming the mane is lowered to make their body more streamline. However, there is evidence suggesting that the mane may be used when P. hydrobyothynus is turning and uses the mane like a sail. When walking around on land P. hydrobothynus keeps its mane erect at all times. P. hydrobothynus is able to erect and lower its mane by contracting and relaxing its arrectorus pilorum muscles. The arrectorus pilorum is the muscle responsible for causing goose bumps in humans. One of the other most distinguishing factors that the male’s skeleton has is its large olecranon process, while this does aid in swimming it is also very common in mammals that specialize in fossorial locomotion. 

P. hydrobothynus is a sexually dimorphic species of otter. The male otters have very large and colorful mane made of orange, yellow, and red and a dark brown body with a white underside. They have a short stocky body, a short fat tail, and a much more robust pectoral girdle. Males are usually only 1 meter long, and 0.35 meters tall. The female otters are dark brown in color with a white underside and are camouflaged in the murky water and muddy banks. The female stellar river otters are built like a traditional river otter and are very streamline with a long wing-like tail, and a longer skinnier body. Females tend to be roughly 1.2 meters long, and are 0.2 m tall. The male and female both have very thick fur to stay dry and for insulation. The two sexes are so morphologically different they were first thought to be different species; however, a distinct red diamond pattern on the chest of this species was the first clue that the discoverers had in determining they were the same species. 

Using the gene sequence from Sanger sequencing, we compared our gene sequence with several related species. Five species were used, including B. distachyon, and well explored genomes such as O. sativa, which like B. distachyon is a grass species. We also compared our gene with the eudicots A. thaliana and S. lycopersicum.  A. thaliana’s genome is very well studied, and its genes are closely related to B. distahcyon’s. A. trichopoda is considered a sister of flowering plants and was also used. Once again, we used NCBI to align these species; a PSI-BLAST compared our genes amino acid sequence with genes in these five species.  We then used a program called MAFFTA. We took the PSI-BLAST results and used the MAFFTA software to create a phylogenetic tree of our gene and related genes from those five species.  Here we could explore our genes evolutionary relationship with similar species’ genes and using closely related genes, find further clues about our genes function. Finally, we will use two histochemical stains, T-blue and Ph-HCL to observe the polysaccharide and lignin content of our mutant and wildtype stems. We will select regions of the stem which have been predicted to be of high expression in our gene of interest to find if the mutant histology differs from that of wild type.

Retinitis pigmentosa is an inherited disease of the retina that affects 1 in 3,500 people and is one of the leading causes of blindness. It was first discovered and diagnosed by According to an NHGRI article “Learning About Retinitis Pigmentosa” (2013), the disease can be diagnosed at age of 10 in most cases. There are different stages of retinitis pigmentosa. Generally, one of the first common signs is the degeneration of the rod cells. This causes the patient to lose their peripheral vision and acquire tunnel vision. On the other hand, some patients’ first symptoms of retinitis pigmentosa include lose of central vision. In both instances, the progressive cone and rod breakdown causes disruption in color perception, night blindness, peripheral and/or central vision. Because of the variability presented by retinitis pigmentosa, not all patients experience these symptoms during their lifetime, and not all patients become completely blind. Unfortunately, this disease cannot be corrected with corrective lenses and there are no known cures (Learning, 2013).

“Learning about Retinitis Pigmentosa.” National Human Genome Research Institute (NHGRI), 27 Dec. 2013, www.genome.gov/13514348/learning-about-retinitis-pigmentosa/#al-5.

Retinitis pigmentosa is an inherited disease of the retina that affects 1 in 3,500 people and is one of the leading causes of blindness. It was first discovered and diagnosed by According to an NHGRI article “Learning About Retinitis Pigmentosa” (2013), the disease can be diagnosed at age of 10 in most cases. There are different stages of retinitis pigmentosa. Generally, one of the first common signs is the degeneration of the rod cells. This causes the patient to lose their peripheral vision and acquire tunnel vision. On the other hand, some patients’ first symptoms of retinitis pigmentosa include lose of central vision. In both instances, the progressive cone and rod breakdown causes disruption in color perception, night blindness, peripheral and/or central vision. Because of the variability presented by retinitis pigmentosa, not all patients experience these symptoms during their lifetime, and not all patients become completely blind. Unfortunately, this disease cannot be corrected with corrective lenses and there are no known cures (Learning, 2013).

“Learning about Retinitis Pigmentosa.” National Human Genome Research Institute (NHGRI), 27 Dec. 2013, www.genome.gov/13514348/learning-about-retinitis-pigmentosa/#al-5.