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Evolution may occur overtime through a succession of mutations or a gene that might be used for a different purpose than originally expressed. With that in mind, mountain goats with horns may have evolved from an ancestral population without horns through the following process. A goat that had a mutation for slight nubs where horns are located and due to genetic drift or selection that goat passed on that trait. Again another mutation might occur where the nubs grow more into smaller horns and that goat may pass on that trait due to drift or selection. This repeats until goats have full horns. Again this trait may be selected for due to mating reasons, influencing natural selection and making the trait have higher fitness. The trait may have also been influenced by genetic drift and been under no selection.

    Another possible theory in terms of genetics is that there could be a mutation in the promoter region specifically that codes for small horns resulting in over expression. Again the theory could be overexpression increased over time due to mutations until the fitness decreased when a goat had horns that were too large.

Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID). It works by reducing hormones that cause inflammation and pain in the body. One of these hormones, prostaglandin, is inhibited when taking the medication. The synthesis of prostaglandin results in dilation of afferent arterioles. Because ibuprofen inhibits the formation of prostaglandin, our afferent arteriole’s begin to constrict without a signal to dilate due to the absence of the hormone. As a result, there is a decrease of blood flow in the kidney and therefore filtration is also reduced.

When we exercise, our vessels constrict in the kidney and slow down blood flow so that our bodies can focus more pumping blood to the muscles as we are using them when we exercise. From the information just learned, taking ibuprofen for a cramp during physical exercise would only have negative effects on the body. This would increase stress on the kidney inducing further constriction and reduced blood flow to the arterioles.

Chirp structure and EOD frequency differs across wave-type fish and can be sexually dimorphic, though to different extents. In Apteronotids, EOD frequency - males often have lower EOD frequency than females - and chirping can be sexually dimorphic, but appears in a number of different ways (Smith 2013, 2422; Ho et al. 2013, 335; Ho et al. 2010, 1050). For example, A. albifrons males have lower EOD frequencies than females while A. leptorhynchus males have a higher EOD frequency than females (Smith 2013, 2422). Additionally, in A. leptorhynchus, males chirp more than females and in A. bonapartii and A. devenanzii chirp complexity is higher in males than in females (Smith 2013, 2428; Ho et al. 2010, 1059). However, another Apteronotid Sternarchogiton nattereri shows no sexual dimorphism, as males and females show no discernible difference in EOD frequency, chirp rate, and chirp form (Ho et al. 2013,337). Instead, S. nattereri shows differences in EOD frequency that are dependent on male morphology, with toothed males showing higher EOD frequency than toothless males (Fernandes et al. 2010, 660). In the wave-type Gymnotiform Gymnotus omarorum, and unlike in many of the aforementioned Apteronotids, electric signalling is sexually monomorphic (Batista et al. 2012, 398). Sexually monomorphic electrocommunicative behaviour has also been observed in other non-Apteronotid genera such Eigenmannia and Sternopygus (Smith 2013, 2422).

The conclusion of the study is that the method of AAV9-PHPB delivery and CRISPR/Cas9 treatment combination resulted in the most effective disruption of the mutant gene, indicating that this method of the treatment may be the most effective and is likely to be successful in human studies. The study also indicates that the treatment was done successfully in a human cell, with high efficiency using the CRISPR/CAS9 treatment. The researchers also tested the method in mice, which indicates that not only does the treatment works on human cells, but it also works at a larger scale and is unlikely to affect other organ systems.  Specifically, of all of the treatments and delivery, it has been noted by the scientists that the mice that were given treatment through an injection into the eye, had a higher level of damage compared to the untreated eye, but had less damage compared to other methods of delivering the AAV virus. By indicating that a method of treatment that has worked in the human cell and mice. If the treatment has worked in both human cells and mice it is an indication that it is also likely to work in a human patient. Using data that is published in this paper it would be possible to go to human trial, which if it works, will be able to have permanent treatment for the retinitis prigmentosa, which takes away the sight of those that are affected. 

https://www.ncbi.nlm.nih.gov/pubmed/29281027

Figure 3 shows the same pattern as those seen in our experiment. The two markers that the researchers that were used to measure cell proliferation are Ki67 and BrdU. Ki67 is a protein that is highly expressed in cells that are proliferating. Ki67 labels cells that are in M, G1,S, and G2 phases. However, because the only cells that do not express the protein are cells in G0, there are many cells that would be positive for this marker. BrdU is extremely similar to EdU in how they mark cells that are proliferating. Unlike Ki67, BrdU and EdUmarkers only mark's cells that are undergoing S phase, as a result, it is more specific. However, BrdU is an antibody compared to EdU which is a click it reaction and incorporates thymidine analog into the DNA.  In hyperthyroid conditions, A2B5 was upregulated in the mitral cell layer compared to the control, and also had a positive cell in other layers of the olfactory bulb. There is a decrease in MBP protein expression in the optic nerve of hypothyroid rats. The conclusion that I can draw about the effect of thyroid hormone on oligodendrocyte progenitors and mature oligodendrocytes is thyroid hormones regulate something upstream of pre oligodendrocyte and mature oligodendrocyte. This conclusion can be drawn because the thyroid hormone is increasing preoligodendroctyes in hyperthyroid conditions which indicates that there are more preoligodendrocytes in hyperthyroid conditions. The decrease in MBP protein suggests that there is a decrease in mature oligodendrocytes.  From these two pieces of information, no conclusion can be drawn since they are in different parts of the brain and indicate two different types of cell regulation. However, since the paper mentions that there is an increase in MBP protein in hyperthyroid condition and a decrease or no change in hypothyroid condition, as well as that A2B5 is not observed in hypothyroid brains. Using this information, I can predict that the thyroid hormone regulates something that is upstream of pre oligodendrocyte. However, using the information that is just given, no conclusion can be reached because a decrease of thyroid hormone should have an opposite effect and that is not seen as clearly here.  

The goal of this study is to determine whether the effects of T3 on progenitor cell proliferation and oligodendrocyte maturation are causally related or instead are independent. O-2A are biopotential glial progenitor cells. A2B5+ marker for presence of O-2A (biopotential glial progenitor) cells. GC+ is a marker that is expressed by mature oligodendrocytes.Table 1 shows the percentage of glial progenitor cells and mature oligodendrocytes that are present in the cell cultures that has the T3 added and the control.  The control numbers mean that when there is no T3 present, there are around 75% glial progenitor cells and 6.8 mature dendrocytes 6 days after incubation. The T3 numbers means that 6 days after the T3 was added there were 24 percent glial progenitor cells and 57 mature oligodendrocytes, indicating that the presence of T3 causes the cells to mature into mature oligodendrocytes. Table 2 indicates that T3 blocks proliferation. The data is showing that T3 blocks the proliferation by marking the glial progenitor cells that have taken up BrdU. Because the percentage of BrdU in A2B5 labeled cell was twice as much in control as compared to the T3 treated cells. This indicates that the amount of A2B5 that are going under S phase, and as a result also indicates cell proliferation. Because the proliferation is twice as high in the control, the data is demonstrating that the proliferation is lower in the T3 cells. Because all other factors are kept constant, this table shows that T3 is what is causing the cells to stop proliferating.

Facilitation: When there us facilitation, earlier colonizing species facilitate the growth of future species in some way. If there was a removal of earlier colonizing species, then the species that they facilitate may have a harder time existing. Inhibition: When inhibition is taking place earlier colonizing species are inhibiting the growth of future species. If the earlier successional species are removed, then the species that they were inhibiting would be more likely to grow. Tolerance: If neither inhibition or facilitation are occurring then tolerance is occuring. This means that species are tolerating condition. Their survival depends more on their life history strategies than on facilitation or inhibition of earlier species. Thus, if earlier successional species were removed, then only species that can tolerate the ecological conditions will survive there.

The thyroid hormone results in an increase in cyclin kinase inhibitors, p27 in particular. With this upregulation of p27 inhibitors, the cell cycle is arrested at the G2/S restriction point. In order for spindles to form for division to occur, the cyclin-CDK2 complex must be activated. Since thyroid hormones play a role in an increase in cyclin inhibitors, cyclin-CDK2 complex cannot become phosphorylated in order to become active.

(from the paper)

Figure 2A shows that her2 is regulated by the delta-notch pathway. The authors came up with this conclusion by seeing what the figure was showing them. The figure shows her2 was significantly downregulated in mib^ta52bembryos compared with the wild-type embryos. They were also able to conduct another experiment to further analyze their results. In this experiment, they either treated embryos with DAPT at 6 hpf and harvested at 8 hpf, 8 hpf and harvested at 10 hpf, or at 10 hpf and harvested at 24 hpf. They analyzed the embryos and found the embryos treated with DAPT at 8 hpf and harvested at 10 hpf experienced a downregulation of her2 expression, which was what they found in the mib^ta52bmutant embryos. With this experiment and results from Figure 2A, the authors were able to determine that her2 is regulated by the delta-notch pathway.

Neurogenesis occurs 24 to 72 hours post fertilization in zebrafish. This is when neural stem cells differentiate to form neurons. The zebrafish that we are using in our experiment are 7 days post fertilization. Before conducting the first experiment, we hypothesized that we should see an increase in neural stem cell differentiation in T4 treated zebrafish due to an upregulation of her2. Since this study shows that her2 is not affected by Notch signaling after neurogenesis, it makes sense as to why not just one group, but most of the class saw a decrease in neural stem cell differentiation in T4 treated zebrafish.