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Hunger and body weight are negative feedback loops regulated by the brain. The cycles are controlled by leptin and grellin hormones. Leptin POMC neurons signal for satiety by producing alphaMSH. AGRP neurons signals for hunger. The leptin hormone is produced by fat stores and excites the POMC neurons, signals for satiety. Leptin activates AGRP neurons, signaling for hunger. This corresponds with the hunger-sateity curve. When energy is high, fat stores release leptin to signal sateity. When energy is low, the gut releases ghrelin to signal hunger. This allows the brain to regulate when we eat based on energy and food stores.

To accomplish this, we followed the protocol from ThermoFisher titled, “ER-Tracker™ Dyes for Live-Cell Endoplasmic Reticulum Labeling”.  Initially we incubated the plate of cells at 370C for 30 minutes. Following the incubation period, the cells were again rinsed with PBS and given media without CO2. The resultant cells appeared to over-fluoresce in unexpected locations so we repeated the procedure. We decided to incubated for 20 minutes in the staining mixture to prevent the overfluorescense. The cells incubated for 20 minutes appeared to clearly mark parts of the ER. These distinct sections of the ER marked by the tracker did not seem to distinctly overlap with the portions of the ER marked by the plasmid. However, we can confidently say that the plasmid marked the ER, just not the same aspects as the ER tracker did.

We nucleofected Sec61 beta plasmid labeled with mCherry into LLC-Pk1 cells in order to mark the endoplasmic reticulum. To verify that the plasmid marked the ER, we planned to use an ER tracker to stain the ER. Unfortunately, both the ER tracker and our labelled cells fluoresced mCherry. We thus chose to stain parental LLC-Pk1 cells with the ER tracker, with the understanding that if we stained our nucleofected cells with the marker, it would be difficult to distinguish between fluorescence signal from the plasmid or the tracker. We compared the overall ER morphology from each set of cells to determine if they mark relatively the same location.

Chemistry is at the heart of all bodily processes. Understanding these processes and how they work is crucial for finding solutions to medical problems. Even something as minor as heartburn can be broken down into acid-base chemistry. When you take Tums, the active ingredient is calcium carbonate (CaCO3), which can neutralizer the overproduced stomach acids and protect the lining of the esophagus from damage. Pharmaceutical drugs rely on knowledge of chemical processes and biological pathways in order to produce the desired effect. Usually, there are many processes happening at once and sometimes drugs have other, undesired side effects along with the desired ones. Trying to minimize secondary effects plays a major part in designing pharmaceutical drugs, and often can become a big problem when trying to get a drug into production. It is hard to minimize other effects often because the unwanted effects could be happening due to a multitude of reasons. This is why getting a drug to be approved for human consumption and mass-produced can be a very long process.

I have always wondered how the alcohol and tobacco industries promote their products. Is it through person to person? Or social media? Maybe both? These two industries are also largely on social media promoting their topics, and this is where they have a large similarity. In a study called “Booze and Butts”, scientists discovered 14 of 73 (19%) magazine covers featured alcohol; 581 of 1558 (37%) magazine articles mentioned alcohol; 119 of 444 (27%) tobacco ads showed alcohol images; and 57 of 695 (8%) non-tobacco ads portrayed alcohol. There is no better way to enlarge the industries than putting these products on a magazine cover, as psychology has said that a person is more likely to buy it if they have seen it in a famous magazine/movie/show etc. 

The Gospel of Germsis a social history of the implications of the germ theory on Americans. It provides a valuable and absorbing window into how the American society, with the introduction of the germ theory, saw the world with new eyes. Major themes of this book are the measures adopted by Americans to avoid germs and how these radical changes served to fortify societal distinctions. The countless stories of the victims of unseen killers shocked me to the core. In each of them, I found a little of myself. However, a disadvantage of the author’s work is her inability to reflect the subjective thoughts of scientists on the issues covered. Tomes is limited to presenting the facts, but not the essence of the scientific discoveries. Furthermore, another problem with The Gospel of Germsis that it focuses too much on the Progressive Era, downgrading the social movements of the later era as less important. Moreover, Tomes failed to recognize the class differences among women. As history tends to forget that class differences have always affected the lives of women. Furthermore, Tomes does not mention the impact of the germ theory on African American women. The gospel of germs highlights the media as an important actor in the public health system, that can catalyze action at the national and local levels. This was particularly true with respect to diseases. The greatest challenge of the early 20-century germ gospellers was to convince Americans that tuberculosis was a communicable disease. As a result, many anti-tuberculosis societies relied on pamphlets, popular lectures, and newspaper articles to promote public awareness of the disease. Through the media, the germ panics reflected the notion that contact with the diseased and the things they touched was bad, so it helped reinforce feelings of class prejudice and racism. 

Performing this experiment could lead us to results that will benefit farmers and society from an agricultural standpoint. If the results turn out as predicted and seeds with no seed coat germinate faster, we could apply this information to crop production. The application of the seed coat removal technique in agriculture could benefit people economically and environmentally. If the results do not turn out as predicted, i.e. the seeds fail to germinate or it has no effect on germination rates, this will help us understand crop production further to make better decisions in the future. We could then conclude if the seed coat is or is not important for success rates of plants and crops, and use this information to our advantage in the future of agriculture.

When you order live ants, they come in a little tube with only one small carrot piece. It is important to put them in a suitable enclosure as soon as they are delivered to increase their chances of survival. An ant farm ordered online usually comes with all the necessary pieces as well as some small bags of the sand. The ant farm must be turned upside down, with the bottom removed, in order to add the sand, and as much as possible should be added to give the ants more room to roam. Once all the sand is added to the ant farm, the bottom piece can be placed back on and the farm can be turned upright. Next, water must be added to the sand, around 60 mL, by pouring it through the top. All the sand should be dampened, but not soaked, so that the ants have water to survive as well as dig stable tunnels. A small cotton ball is usually blcoking the entry way to the ant farm, so a long probe is provided to poke the cotton through as well as push it halfway down into the sand to encourage them to burrow. Lastly, before adding your ants, small pieces of food should be placed inside. Cut up carrots or apples are easily inserted into the farm, and they are better to place right on top of the sand to encourage the ants to go down there and start digging. Always make sure your ants have plenty of food and water, and the farm is kept at a suitable temperature. 

The presymptomatic phase of kuru lasts, on average, 10 to 13 years but incubation time can range from 5 years to 50 years (Collinge et al., 2008). The mean clinical duration of the disease is 12 months but may be as short as 3 months, as long as 2 years, or even longer in some atypical cases (Collinge et al., 2008). Kuru infection progresses through three general stages: ambulatory, sedentary, and terminal (Alpers, 2005). Throughout all of these stages, the primary physiological symptom of the disease is progressive cerebellar ataxia (Gajdusek, 1957). In the ambulatory stage, patients demonstrate involuntary tremors, and a lack of coordination, though they are still capable of speaking and moving themselves around (Gajdusek, 1957). In the sedentary stage, an infected individual shows strong ataxia, they cannot move around without assistance, show major dysarthria, and are prone to excessive bursts of laughter (Gajdusek, 1957). At the terminal stage, infected individuals can no longer sit without support, speech is completely lost, urinary and fecal incontinence appear, dysphagia occurs and eventually, many develop ulcerated wounds that are prone to infection (Gajdusek, 1957). Death occurs shortly thereafter either due to wound infection or terminal static bronchopneumonia (Gajdusek, 1957). 

At the neuropathological level, kuru shows similar features to other diseases caused by prions. PrPSC accumulates in grey matter regions throughout the cerebrum, cerebellum, brainstem, and spinal cord, leading to an atrophied brain overall (Hainfellner et al., 1997). PrPSC deposits in two ways: fine, granular deposits that occur perineuronally and periaxonally, and in dense plates with a homogeneous centre surrounded by radiating spikes (Hainfellner et al., 1997). Though PrPSC aggregates resist proteolysis, they are relatively inert. The danger comes as they self-propagate because they create a byproduct called PrPL that is neurotoxic and is directly responsible for neurodegeneration (Collinge & Clarke, 2007). This neurodegeneration presents itself, in part, as fibrillary astrogliosis most apparent in the parasagittal and interhemispheric areas of the frontal, central, and parietal cortex, as well as the cingulate cortex, striatum, and thalamus (Hainfellner et al., 1997). Loss of neurons due to PrPSC accumulation is most prominent in the: dorsomedial frontal cortex, dorsomedial central cortex, pre/parasubiculum of the hippocampus, striatum, thalamus, and inferior olivary nuclei of the medulla (Hainfellner et al., 1997). Though less severely, some PrPSC plates introgress into the white matter of both the cerebrum and the cerebellum (Hainfellner et al., 1997). The brainstem suffers from some neurodegeneration and astrogliosis caused by periaxonal and perineuronal PrPSC deposits rather than plaques (Hainfellner et al., 1997). Lastly, there are accentuated periaxonal and perineuronal PrPSC aggregates in the substantia gelatinosa of the spinal cord (Hainfellner et al., 1997).

Gliding assays are in vitro methods to examine the movement of microtubule motors. To perform a gliding assay, a cover slip is placed on a slide and you add purified kinesin motors. The motors stick to the bottom of the cover slip, and you add microtubules and taxol. You can then observe the motors moving the microtubules around the slide. Taxol is important because it binds to and stabilizes the microtubules, preventng them from depolymerizing.