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According to the article titled, “Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis,” “Approximately 20% of KRAS-mutant LUAD tumors carry loss-of-function mutations in the KEAP1 gene encoding Kelch-like ECH-associated protein 1, a negative regulator of nuclear factor erythroid 2-like 2 (NFE2L2; hereafter NRF2), which is the master transcriptional regulator of the endogenous antioxidant response.” This article essentially states that we should look at a glutaminase inhibition approach. After doing some research, I have learned that if we were to remove glutamine from the body then this would mean a reduction in cell growth or prompt cell death. But what if we remove it and it leads to increase in cell death where there shouldn’t be. I remember from lecture it being mention how in some patients they affected red blood cells and then led to high risk patients with anemia. I am having a hard time wrapping my mind in figuring ways where we won’t be affecting other functions and cells. In my research it also mentions how this indicates that these cells are dependent on, or “addicted” to, glutamine. 

The KRAS gene provides instructions for making a protein called K-Ras. It’s part of a signaling pathway known as the RAS/MAPK pathway. In RAS/MAPK we know that an activated RAS activates MAKKK by binding to it. Then activates MAPKK by phosphorylation and then MAPK. Then MAPK activates proteins or transcription regulators in order to either change protein activity or alter gene expression. The protein relays signals which instruct the cell to grow, divide, and differentiate. The K-Ras protein is a GTPase. When the protein is bound to GDP, it does not relay signals to the cell's nucleus and when its bound GTP it does. The KRAS gene belongs to the oncogene class. From lecture we have learned that when mutated, oncogenes have the potential to cause normal cells to become cancerous. 

There are many ideas for downstream experiements that could be utilized in order to delve into remaining questions resulting from this study.  Potential utilization of the more modern idea of optogenetics, which involves the use of light to control the synaptic transmission of neurons that have been genetically modified to express light sensitive ion channels.  The CNO injections used in this experiement take at least an hour to stimulate neuronal activity, which is not a realistic depiction of how memory processes work in real life.  Running the same labeling, training, and retrieval tests using a more realistic method of generating synthetic memories might depict more accurate and applicable results.  Another idea would be to include female mice in a totally separate experimental group that undergoes the same synthetic memory generation.  All male mice were utilized in these experiments in order to rule out any discrepancies that might result from a difference in hormones, and the subsequent affect on memory retrieval.  It would be interesting, however, to actually prove if there is a difference associated with hormones and memory.  This difference might explain why some sexes are more predisposed to experience certain neurological conditions associated with memory, such as women being more likely to experience Alzheimer’s.  

In conclusion, carrying capacity and competition plays a huge role whether it can be seen on the surface or if it’s a hidden motive in certain ideas such as racism. Carrying capacity can limit many species, but humans have found a way to manipulate this concept. For example, humans have developed ways to control food supply in the agricultural industry. If they need more food, they can easily intensify or improve their already massive food supplies. Also humans have developed the ability to expand their habitat, an ability not many species on the earth possess. For example, humans have developed the technology of air conditioning and heating, which allows them to expand their habitat into hotter and colder regions respectively. Competition also was a huge factor in racism, as the whites were given majority of the better supplies. The DVD explained that of the $120 billion the government spent on new houses, less than 2% of those homes went to non-whites. All in all, whether we like to admit it or not subconsciously competition and carry capacity play a significant role in the actions we make.  

A plant leaf is composed of several layers. On the outside of the leaf, both top and bottom, the is a waxy layer called the cuticle. This layer helps to prevent water loss from the leaf so that the plant can have more control over its transpiration rates. The next layer is the epidermis, which is also on the top and bottom of the leaf. This layer serves primarily for protection of the internal structures of the leaf. The next layer from the top is the palisade layer. This layer is denesly packed and is primarily used for photosynthesis. The final layer from the top is the spongy mesophyll layer. This layer is thick, but loosely packed together. While it has some photosynthetic function, its primary purpose is to facilitate the gas exhanges within the leaf.  

Humidity has a major impact on the movement of water in plants. Since water movement is passive in plants, its transfer is largely dependent on outside factors. For instance, the humidity of the outside air has a major impact on how quickly water can move through the plant. Humidity in the air makes evaporation more difficult. With higher concentrations of water in the air, the leaf has a harder time transpiring, thus reducing water movement in the plant.

When I first discovered this article, I did not know what to expect when reading the title. I did not know of the egg based vaccine growth process so that was my first spark of interest, but then with further reading learning about the setbacks of the process also drew me in. I find this predicament to be relatable to the problem of antibiotic resistance, bacteria are becoming resistant and gaining advantageous adaptions in order to survive and beat its competitors. The virus in the same way are gaining mutations due to its exposure, advancing so they can survive longer in certain environment. It is the job of scientists and future scientists to find ways to combat these problems and find other suitable alternatives and reliable sources in keep the human population healthy.

In a recent discovery, the process of growing the components of an influenza vaccine in chicken eggs disrupts the major antibody target site on the surface of the virus, thus causing the vaccine to be less effective in humans. The vaccine is injected into the eggs, allowing for replication and then purification of the fluids to extract the virus. However, as the prevalence of the H3N2 virus increases, only 33% of flu vaccines are effective against it. When H3N2 is grown in eggs a specific mutation named LI94P disrupts the region on the protein that is usually recognized by the immune system. Because of this, a vaccine with the mutated protein cannot generate an efficient immune response. Researchers are still further studying the virus and its response, they are also hoping for a substitute in egg base vaccine inoculation.

Figure 10.8 (A) and (B) illustrated a huge decline before rising back up and then flattening out. Where lambda is eventually beginning to settle to a constant value although we still see smaller increases and decreases throughout the years. Some of the reasons these differences could have occurred could be the difference in the number of newborns present. In addition, we only show data for up to 5 years versus 11 years and we had the low number of three-year olds compared to the graph 10.8. Where we could see the oldest generation had the most abundant members and the newborns had the least.  As we have learned during lecture, if reproduction rates and age-specific survival rates have no change, then the population growth rate will eventually be stable. Based on the graph and what we have learned, in the future years we will see population stabilizing and stay the same that is if the age specific survival rate has no change. 

AATF also referred to as, Apoptosis Antagonizing Transcription Factor, is a regulator of p53 in DNA damage response. It is known to inhibit apoptosis in vivo and be overexpressed in lung cancer. In Kras-driven lung adenocarcinoma if the deletion of AATF occurs then this results in delayed lung cancer formation mainly in a p53 dependent manner. Targeting AATF will be targeting tumor progression and putting a stop to it. AATF through the PI3K/Akt pathway can inhibit Ba. This then results in the activation of BCL-2 leading to immortality of these multiplying cells.  We know that BCL-2 works in the survival pathway. Its job is to stop cell death. When a phosphate is added to Bad it could then prevent it from sequestering Bcl₂, so Bcl₂ can do its function. Bad prevents Bcl₂ from doing its job. When Bad is bound to Bcl₂, the cell will die, however, when Bad is not bound to Bcl₂, Bcl₂ will be active and it will stop cell death. In order to keep Bad inactive, protein 14-3-3 will make sure a phosphate is stuck on Bad.