Jenny+Choi

Week 3: T-Cell Redirection This week we took a trip to ** Janssen, a pharmaceutical company of Johnson & Johnson. ** We got a tour of their beautiful campus and learned quite a few things about the research being conducted there.

Seeing all the different labs and hearing about research really made me rethink how I felt about science as a career. Since I had always equated biology to doctors, I was under the assumption that a medical-related job was my only option. ** However, I was really in the wrong **Friday. We were introduced to so many different areas that scientists were currently exploring—immunology and oncology to name a few.

I really enjoyed seeing the autonomy of the different departments there. People could form their own schedules, had a say in the layout during the remodeling of the campus. I could really see the effort Janssen made in creating a positive atmosphere and my experience there really encouraged to exploring a career in the pharmaceutical industry.

The doctor who showed us around told us a lot about what scientists do there, and it changed my viewpoint about a career in pharmacy too. I always thought that pharmacists just made boring drugs all day. ** However, the researchers at Janssen are, as certainly are scientists around the world, actively seeking for cures for diseases and knowledge of unknown and unexplored areas of science. **

One topic she discussed with us that interested me was a current treatment called ** T-cell redirection. **As we’ve learned in class, T-cells and their ability to protect our bodies are extremely important to our immune response and we can see the detrimental effects in alterations of their normal functions in AIDS.

A [|blog] from Penn Medicine discusses ways on how cancer cells, or a mass of them called tumors, have developed ways to evade our immune system. For instance, ** pancreas tumor cells make themselves practically invisible by “produc[ing] a molecule that attracts inflammatory cells to cloak the tumor, thereby preventing other immune cells from killing the cancer cells.” **

 Penn researchers are apparently attempting to “redirect” the powerful activities of the T cells against tumors. How do T cells normally recognize pathogens and other foreign substances? If you don’t remember, Helper T cells have receptors on their surfaces that identify specific substances. A macrophage or dendritic cell, after taking in a foreign substance activates a helper T cell by presenting a piece of the substance attached to a receptor on its cell surface. The ** T cell, after recognizing the foreign substance, proliferates, or rapidly divides, into killer T cells, more helper T cells, and memory T cells. **The T cells then target body cells that have been infected by the foreign substance and destroys them in what is called the cell-mediated response.

Another response carried out by helper T cells is the humoral response. The same process occurs until right after identification by the helper T cell. In this case, the helper T cell activates another type of cell called the B cell. The B cell is unique in that it uses something called antibodies—protein specific molecules that recognize “antigens” or the foreign substances. These antibodies search for the foreign substance recognized by the T cell and immobilizes or destroys it.



According to the blog, “potent antibodies can be made against most surface proteins expressed by tumor cells by immunizing animals such as mice, and such antibodies have been used clinically in a number of cancers.” However, “isolating T cells with potent TCRs[T-cell receptor complex] against proteins expressed by tumor cells is considerably more difficult since this cannot be done in animals, and ** our immune system selectively eliminates potent T cells against self **…”

Researchers want to enable T cells to fight tumors because ** though antibodies are effective against tumors, they must be administered regularly because they are not created by the body in the presence of tumors. Which means that their effectiveness is short-lived. **However, T cells stay in our immune system for a long time after one exposure, and are very powerful.

One approach by Penn researchers is to create a “chimeric antigen receptor,” or CAR, which “combine[s] the potent antibody binding domains that bind to cancer cells with domains that signal T cells to target those cells.” This approach is apparently yielding “** very promising results to treat patients with leukemias **” and is currently being developed to combat other types of cancers.

Hopefully this research will continue to be developed. Injecting a T cell that is able to recognize and eradicate cancers could very well mean an end to cancer itself. Although there will be several obstacles along the way, such as ethical concerns and lack of funding, etc., surely one day cancer will be eradicated.

Week 2: Global Obesity Rate on the Rise This week’s post is about obesity. I got this idea from the movie Wall-E we saw in class last week! I’m sure the jello-like body shapes of future humans were hilarious and amusing, but the movie got me thinking: whether we ruin Earth or not, will we become obese as well? Why, how quickly, and how will that affect humans?

I googled worldwide obesity, and found a bunch of stuff.

[|This] website tells you, in real time, the number of obese people in the world and the money spent in the US for obesity-related diseases.

Roughly one-third of Americans are obese.

Here’s something absolutely crazy. According to [|www.exchangemagazine.com], “** no country ** has witnessed a significant decline in obesity prevalence **over past three decades**.”

According to the World Health Organization, If these facts hasn’t made your jaw drop yet, ** 2.1 billion ** people, as of 2013, are either overweight or obese.


 * Why is this so significant? Obesity is a huge global issue and it is something that is much, much worse than gaining a few pounds over a long winter. Obesity and overweight directly causes some of the leading causes of death in the US, as can be seen in the picture below. **



The article I found, to which the link can be found [|here], discusses “a comprehensive new analysis of the global, regional, and national prevalence” of overweight and obese people between 1980 and 2013 led by Professor Emmanuela Gakidou from the Institute for Health Metrics and Evaluation at the University of Washington.

Some of their findings include: - In Tonga, a small island kingdom in the South Pacific, ** more than 50% of the adult population is obese. ** - In Kuwait, Libya, Qatar, and the Pacific Islands of Kiribati, Federated States of Micronesia, and Samoa, more than 50% of women are obese. - In developed countries, childhood obesity has risen from 17% to 24% in 2013 in boys and from 16% to 23% in girls.

And obesity is not slowing down. According to [|www.medicalnewstoday.com], half of **all** Americans will be obese by 2030, if current rates continue. That’s 164 million.Treating obesity related diseases would cost $66 billion more annually by 2030 - a 2.6% rise in overall health spending. Also, There would be ** 7.8 million ** more people with diabetes, ** 6.8 million ** cases of coronary heart disease and stroke, and ** 539,000 ** extra cases of cancer.

What causes obesity? According to the World Health Organization, “the fundamental cause of obesity and overweight is **an energy imbalance between calories consumed and calories expended…** an increased intake of energy-dense foods that are high in fat… an increase in physical inactivity due to the increasingly sedentary nature of many forms of work, changing modes of transportation, and increasing urbanization… lack of supportive policies in sectors such as health, agriculture, transport, urban planning, environment, food processing, distribution, marketing and education.” Currently, the rate of obesity is increasing because low- and middle-income families are facing a “double burden” of disease. They deal with malnutrition **and** obesity from processed or fast foods that poor in micronutrients and are high in fat, sugar, and salt.

But the thing is, ** obesity can be avoidable. **

Below are some sources with plausible solutions and preventions everyone can take to stop obesity!

[] lays out a list of things the individual and the food industry can do as well as suggest a “Global Action Plan for the prevention and control of non-communicable diseases 2013-2020.”

A Ted Talk by famous chef Jamie Oliver below discusses obesity and its deadly consequences and proposes a creative solution for it! (I think you guys will like it; it disses school lunches, because let’s be honest—school food hasn’t been the same since elementary school).

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I hope that global awareness and education will initiate a movement to reduce obesity! It is definitely possible and would save millions, even billions of lives.

To end, here is a cool Ted Talk by Mick Cornett, mayor of Oklahoma City, about how his very overweight town collectively lost **1 million pounds.**

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Week 1: Could Ending Pain Make Us Live Longer? Nowadays, there is more and more research being done to extend life. One such research is a study at UC Berkeley that revealed that genetically engineered mice without a certain pain receptor lived longer—** with more lively metabolism and less diseases. **When you feel pain, the nerves in your body relay messages to the brain to do something to stop the pain, and thus our bodies are protected from further damage. To elaborate, a stimulus, whether it is a paper cut, a punch on the arm, or stepping on a pin, as shown below, is sensed by a nerve ending, which sends a signal to the central nervous system. The brain then receives this information for more processing and action. However, too much pain ** can actually be harmful for us. ** For one, people with chronic pain are more likely to have shorter lifespans. The scientists at UC Berkeley bred mice without the gene for TRPV1, a pain receptor found on the skin, nerve, and joints. It is also found in the nerves that reach the pancreas. TRPV1 provides the sensation of scorching heat and pain. Surprisingly, these mice lived // an average of 14% longer than did normal mice. //Why did these mice live longer? According to Andrew Dillin, the lead researcher of this study, their extended life may be due to TRVP1’s regulation of insulin, a hormone released from the pancreas that promotes glucose uptake by cells from the blood. TRVP1 stimulates the release of CGRP (calcitonin gene-related peptide), a substance that inhibits insulin from being released into the bloodstream. ** With less insulin, the ability to control blood sugar also decreases, which leads to a risk of obesity as well as type II diabetes and other diseases. **According to [|www.sciencedaily.com], from which I discovered Dillin’s research, “ mice lacking TRPV1 are protected against diet-induced obesity, suggesting that this receptor plays a role in metabolism. ” ** Without TRVP1, these mice could regulate their blood glucose levels better despite their advanced age, and sustain their health and lives longer. **  <span style="font-family: Cambria,serif; font-size: 11pt;">On a side note, capsaicin, the spicy compound in chili peppers, activates TRPV1. And according to Dillin, “prolonged exposure to capsaicin can actually kill the neuron [that sends messages to TRVP1].” Then could a diet abundant to capsaicin extend life? Maybe, but you’ll have to eat //a lot// of spicy food over a long period of time. <span style="font-family: Cambria,serif; font-size: 11pt;">Anyway, what does all of this have to do with us? TRPV1 is already a common target of drug companies trying to treat pain, but Dillin thinks that these companies could take their drugs beyond mere pain control. “These drugs might also be useful for treating diabetes and obesity,” he says. Inhibiting TRVP1 in people may imitate the lack of the TRVP1 gene in the genetically engineered mice may treat such diseases and ultimately lead to a longer, healthier life. According to [|www.sciencedaily.com], “Old mice treated with [an] anti-migraine drug, which inhibits the activity of CCRP receptors, **showed a more youthful metabolic profile than untreated old mice** [emphasis added].” <span style="font-family: Cambria,serif; font-size: 11pt;">On the other hand, pain is necessary to our survival and serves as a crucial evolutionary advantage. It stops us from doing things that will injure and kill us, like touching a hot surface. The key, though, is blocking TRPV1 in humans without making the effect too strong. <span style="color: #e46c0a; font-family: Cambria,serif; font-size: 11pt;">What do you think? Do you think ridding ourselves of pain would make us live longer? If anti-aging drugs were released on the market (and worked), how would the human population and the world be affected? <span style="font-family: Cambria,serif; font-size: 11pt;">An article that discusses the research at UC Berkeley and its possible benefits can be found here: []