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Science Writing Activity

Homework before the lesson:

Carefully read the following sources, including the introductory information for each source. Considering what you’ve read, create a claim about which you would want to write a persuasive essay. A good claim should be 1-2 sentences and clearly take a position on a topic about which others may or may not agree.

Homework after the lesson:

Synthesize information from at least three of the sources and incorporate it into a coherent, well-developed essay that defends, challenges, or qualifies the claim that was agreed upon during the lesson. Make sure that your argument is the central focus of the essay; use the sources to illustrate and support your reasoning. Avoid merely summarizing the sources. Indicate clearly which sources you are drawing from, whether through direct quotation, paraphrase, or summary. You may cite the sources as Source A, Source B, etc., or by using the descriptions in parentheses.

Source A (Singer) Source C (Koerner)

Source B (Kortagere, Krasowski, and Ekins)* Source D (Hayden)

* To be viewed in class, not read at home

Persuasive Essay Evaluation Grid (How your work will be evaluated)

Item/Rating / Weak / Fair / Good / Strong
Title indicates writer’s attitude toward the topic
The lead attracts the reader’s attention
Writer gives sufficient background on the topic
Writer makes overall purpose clear
Thesis statement is clear and prominent
Each paragraph reveals author’s purpose
Writer identifies relationships between sources
Writer provides support from sources in each paragraph
Writer provides enough commentary in each paragraph
Conclusion does more than summarize main points
Writer includes parenthetical documentation
There is a Works Cited page

Comments:

Source A

Singer, Emily “The Molecule That Tells You When You’ve Used Too Much Sriracha.” Wired.com. February 27, 2014.

Conde Nast. http://www.wired.com/2014/02/pain-sensor/

This excerpt describes how new imaging techniques have allowed research scientists to better understand how the shape of an important protein effects changes in how mammals sense pain.

The fiery sting of a habanero pepper, the scalding heat of a boiling teapot, the excruciating bite of the earth tiger tarantula, and even the heightened sensitivity to touch following a sunburn — all of these painful sensations are made possible by a sophisticated molecular machine operating in nerve fibers in the skin and tongue.

Known as TRPV1, the protein was discovered more than 15 years ago. Although scientists knew that it could sense heat and various chemicals, exactly how it worked remained a mystery. In December, however, scientists reported creating a high-resolution image of the protein’s structure for the first time. Like the blueprint of a motor, that information should help researchers understand how the tiny apparatus can respond to such a wide array of signals — from temperature to toxins — and the role it plays in both acute and chronic pain. The results could ultimately lead to new painkillers, potentially without the troublesome side effects of opiates.

David Julius began hunting for TRPV1 close to 20 years ago. At the time, scientists had for decades been using capsaicin, the molecule that gives chili peppers their heat, to study pain. But little was known about how it triggered that sensation. Other scientists had already tried and failed to find the molecule that binds to capsaicin, known as its receptor, but that only enticed Julius to take on the challenge. He and his team reported hitting the jackpot in 1997, identifying a member of a family of receptors known as TRP (transient receptor potential) ion channels

Mammals have nearly 30 different TRP channels scattered throughout different parts of the body. Six to nine are involved in sensing temperature. TRPV1 is by far the best studied; scientists are learning more about the other TRP channels, but the function of many remains unknown.

The TRPV1 molecule, found in the nerve fibers that suffuse the skin and tongue, forms a channel that acts like a gated passage between the inside and outside of the neuron. When you bite into a chili pepper, capsaicin binds to the channel and opens the gate. Charged particles rush into the cell, triggering electrical activity that sends messages of pain to the brain. The same thing happens when you sip a cup of scalding tea, with heat itself opening the gate.

But TRPV1 doesn’t simply sense chemicals or temperature. It acts like a tiny computer, collecting information about the environment to help protect us from further injury. It can make certain sensations feel more painful, warning us to take care. Scientists know from previous experiments that the channel can act like a volume knob to amplify pain; dousing it with capsaicin, for example, lowers its threshold for heat. That’s why hot tea feels even hotter after eating a chili pepper. Damage to the skin, such as sunburn, has a similar effect. It releases inflammatory molecules that act like capsaicin, making the channel easier to open and the skin hypersensitive to additional dangers, like heat or chemicals.

The newly resolved structure helps to explain how the channel changes shape in response to different chemicals, revealing a sophisticated system for how different triggers open the gate. Rather than a simple entrance, the TRPV1 channel is guarded by two sets of doors, similar to a double airlock, according to the new findings, published in Nature in December. The channel has two gates — one faces the inside of the cell and one faces the outside. Both have to open for ions to flow through.

Some chemical triggers, such as capsaicin or the inflammatory molecules that the immune system releases after an injury, seem to act like WD-40, encouraging the gates to swing open more frequently. Others, such as spider toxins, act more like a doorstop to keep them open. In one of the new studies, researchers captured images of TRPV1 in action using three different triggers: capsaicin, a capsaicin-like molecule from succulents, and a spider toxin. They found that capsaicin and the similar molecule both bound near the inner gate, while the spider toxin bound near the outer gate. Exposure to these chemicals increases the likelihood that both gates will be open, which makes it more sensitive to heat or other chemicals.

Scientists are now trying to figure out how heat changes the shape of the channel—they already know hot temperatures can open it, but they don’t know exactly how. They also want to examine how molecules produced by our body in response to injury affect the sophisticated sensor and, in turn, our perception of pain.

Source B

Kortagere, Sandhya; Krasowski, Matthew D. and Ekins, Sean. “The Importance of Discerning Shape in Molecular Pharmacology.” Trends in Pharmacological Science. March 2009.

National Center for Biotechnology Information.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2854656/

* This source will be made available during the lesson due to its visual nature.

Source C

Koerner, Brendan I. “One Doctor’s Quest to Save People by Injecting Them With Scorpion Venom.” Wired.com. June 24, 2014.

Conde Nast. http://www.wired.com/2014/06/scorpion-venom/

This excerpt describes how one doctor has found a way to dye tumor cells by attaching a specially shaped molecule to a fluorescent dye, helping to reduce the possibility that cancerous cells are left in the patient unintentionally after surgery. It also discusses his fundraising methods which are innovative, but controversial.

Because it’s so late on a Monday afternoon, there is a listless vibe inside the University of Washington lecture hall where Jim Olson is about to speak. The audience consists of a few dozen grad students struggling with end-of-day fatigue. Olson’s first slide wakes them up. It is a pixelated photograph of an adorable 6-year-old boy named Hayden Strum, who sports a white Quiksilver T-shirt and a pirate-style eye patch. Hayden, who suffered from a pernicious brain tumor, came to Olson in 1995, back when Olson was just starting his career as a pediatric oncologist and cancer researcher. For four years, the doctor treated Hayden with successive rounds of chemotherapy and major surgeries, but nothing could save the boy’s life. Olson tells the audience that while sitting in the back row at Hayden’s memorial service, listening to the speakers express their pain, he had an epiphany about his scientific priorities.

“I decided that I would never design an experiment just to get grants or publications or promotions,” says the 51-year-old Olson. “Every experiment I ever did was going to be to make sure that other boys and girls didn’t have to go through what Hayden had gone through.” Having been caught off guard by the emotional wallop of his opening story, Olson’s audience stays rapt as he goes on to describe a decade-long quest to solve one of the most vexing problems in oncology: the fact that a tumor’s precise boundaries are nearly impossible to define during surgery. A preoperative MRI provides only a rough guide to a tumor’s fuzzy edges; the scans often miss slivers of cancer that seamlessly blend into the surrounding tissue. Surgeons often face a brutal catch-22: Either cut out any suspicious tissue, an approach that can lead to debilitating side effects, or risk leaving behind malignant cells that will eventually kill the patient.

Olson tells the students that he finally has a solution. His lab has developed a compound that appears to pinpoint all of the malignant cells in a patient’s body. It gives those cells a bright fluorescent sheen, so that surgeons can easily spot them in the operating room. Olson calls the product Tumor Paint, and it comes with a surprising twist: The compound’s main ingredient is a molecule that is found in the stinger of Leiurus quinquestriatus, a potent little animal more popularly known as the deathstalker scorpion.

A scorpion-venom concoction that makes tumors glow sounds almost too outlandish to be true. In fact, Olson explains, that’s what troubled the big grant-making organizations when he came to them for funding. But when those organizations dismissed his ideas as too bizarre, Olson started accepting donations from individuals—particularly the families of current and former patients—quickly raising $5 million for his research. It was a bold and unprecedented tactic: Though patients and their families are often asked to donate to foundations with broad goals, Olson raised money for one specific, untested technology—a much riskier gamble. But thanks to his efforts, Olson’s fluorescent scorpion toxin is now in Phase I clinical trials, an impressive accomplishment for a compound with such a peculiar lineage.

Olson always ends his talks by urging his audience to visit his crowdfunding platform, Project Violet, where they can make direct donations to his lab. Both his idea and his approach to funding it make Olson something of a maverick in the field of cancer research. There are critics who worry that the oncologist might be offering more hope than he can deliver—particularly to the desperate loved ones of his patients. But Olson’s mission is to prevent more kids from suffering Hayden Strum’s fate, and to do that, he says, he must rely on families who possess intimate knowledge of what’s at stake. “Without them,” he says, “Tumor Paint wouldn’t exist. Simple as that.”

Scorpion venoms are cocktails of numerous individual toxins, which attack different targets within a victim’s body. The initial American research on the deathstalker’s venom focused on these toxins’ ability to block electrical signals generated by the movement of sodium ions. Then, in 1993, a team at Harvard Medical School identified a new L.quinquestriatus toxin that appeared to block the channels that cells use to pass chloride ions across their membranes. The researchers noted that this molecule, which they dubbed chlorotoxin, consists of a short chain of amino acids—a peptide, in biochemical parlance. At the center of this particular 36-amino-acid peptide is a tightly packed structure consisting of four disulfide bonds, which gives the molecule a knot at its core. Despite its ominous name, pure chlorotoxin is harmless to humans; its sole evolutionary purpose seems to be to paralyze the muscles of the cockroaches that the deathstalker likes to eat.

The most incredible revelation came when Olson began to inject fluorescent-tipped chlorotoxin into mice—the compound lit up cancer cells that no other technology could identify. In one instance, the chlorotoxin illuminated a clump of just 200 malignant cells that were burrowed deep within a wad of fat. “That was the point we learned that the technology was far more sensitive than an MRI,” Olson says. To advance his chlorotoxin research, Olson applied for grants from the National Cancer Institute and other eminent organizations. But not a single one agreed to back his cause. “The rejections were based on comments like ‘This is highly speculative’ or ‘This is highly ambitious,’ which is grant code for ‘They are proposing more than I think they can accomplish,’” Olson says. But Olson had supreme confidence in chlorotoxin’s value. The series of rejections just led him to conclude that creative research such as his required creative funding.

(Olson’s) … steady bedside manner has always been much appreciated by the families of Olson’s patients, and they’ve long expressed their gratitude by supporting his research. Shortly after Olson founded his Fred Hutchinson lab in 2000, for example, a few parents banded together to host chili cook-offs and golf tournaments to raise money for staff salaries. And so when they heard that none of his chlorotoxin grants came through, parents upped their fundraising efforts. “I embraced their generosity,” Olson says. He began to reach out to more families after the earliest group of donors assured him that they would go to any length “to make sure you have the funding you need when you have a good idea.”