Join us Wednesday, September 9th, 2015, 7:30 – 8:30 pm at Terra Linda HS, 320 Nova Albion, San Rafael – Room 207 – to hear Dr. Judge talk about her work. Link to Dr. Judge’s Marin Science Seminar profile.
Join us Wednesday, September 9th, 2015, 7:30 – 8:30 pm at Terra Linda HS, 320 Nova Albion, San Rafael – Room 207 – to hear Dr. Judge talk about her work. Link to Dr. Judge’s Marin Science Seminar profile.
Monkey Flower |
Dr. Katie Ferris, UC Berkley |
Interview with Alex Gunderson Ph.D.
by Isobel Wright, MSS Intern, Tamalpais HS
Alex Gunderson, Ph. D.
1. How did you decide to enter this line of work, as it is so specialized?
I think I gravitated toward biology as a profession because I love being in nature. I grew up in a very rural part of the Midwest where I spent a lot of time outside, on lakes and in the woods. That led me to be interested in how the natural world works.
2. Why did you decide to use the Price is Right as an analogy for the effects of global warming?
The Price is Right was as easy choice for me because it is one of my favorite game shows. When I was in grade school and would get sick and stay home, it was the show I looked forward to watching most. I have always wanted to spin the big wheel!
I have learned a lot! Maybe one of the biggest things is how subtle nature can be. On Puerto Rico there are ten different species of Anolislizard and to most people they all just sort of look like a generic lizard. But when you look closely, you see that they have evolved all of these small differences that allow them to live and thrive in different habitats. It really is amazing!
4. What level of education do you need to do what you do?
It depends on what your ultimate goal is. You can get paid to do biology with a Bachelor’s degree, but many positions require graduate degrees like a Master’s or PhD. My goal is to be a college professor, so a PhD is required.
5. If there was one thing you could tell us to do to prevent climate change, what would it be?
The biggest road-block to making progress on climate change is political inaction, so speak up about it through your vote (if you are 18!), letters to politicians, and outreach activities. On a personal level, there are a lot of things you can do to reduce your contribution to climate change. The Nature Conservancy has a great website where you can calculate your carbon footprint and learn about ways to reduce it: http://www.nature.org/greenliving/carboncalculator/
6. What was your biggest “Aha” moment in life so far, relating to your work?
I think the biggest “Aha” moment I had was when I decided that I wanted to study how animals adapt to different climates. It was my first year as a PhD student, and I was in Puerto Rico for the first time. I thought I wanted to study the evolution of animal signals, or how animals communicate with one another. I had been studying one species in northern Puerto Rico, but I knew the same species also lived in southern Puerto Rico so I decided to drive down there. I was driving south through the mountains with my cousin Neil (he was helping me do my research) and all of a sudden, the landscape changed dramatically. It went from cool, shady tropical rainforest to hot, dry desert in just a few miles. I thought there was no way the same species could live in such different conditions. But sure enough, the same species was there. I wanted to know how they did it, and my fascination with thermal biology was born!
7. What are the best parts of your job? What are the worst parts?
There are two things that I think are best about my job. First, my job takes me amazing places to study amazing animals. Over the years, I have studied lizards in the Caribbean, frogs in the back-country wilderness of Montana, and seabirds in the Galapagos, to name a few. Hard to beat. Second, in many ways, I am my own boss. With some caveats, I get to decide what I study, where I study it, and how I study it. That kind of freedom is hard to come by in many professions.
The worst part of my job? Writing grants. Because most scientific research doesn’t generate profits like a business, you have to convince other people to give you money to do it. Those “other people”are usually government agencies like the National Science Foundation and the National Institutes of Health. It’s fantastic that they give the money, but the grant writing itself is often extremely tedious.
Learn more about Alex Gunderson and his research here. Join us and Learn!
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Fast Fasts about the Harbor Porpoise from the National Geographic Society:
Terra Linda High School graduate Jonathan Stern is a lecturer and adjunct professor in the Biology Department at San Francisco State University. He has studied minke whales since 1980 and currently serves as a Co-Principal Investigator at Golden Gate Cetacean Research, where he studies harbor porpoises, bottlenose dolphins, and minke whales locally in the San Francisco Bay. He has also studied an assortment of whales including gray whales, killerwhales, fin whales, humpback whales, and pilot whales. He was the first volunteer at the Marine Mammal Center when it opened in 1975.
How did you decide to study marine life?
From left: Lloyd Bridges stars in Sea Hunt, Seashell collection, Explorer Jacque Cousteau |
How do you conduct your research?
Harbor Porpoise sighting near the Golden Gate Bridge |
Report your porpoise sightings! Golden Gate Cetacean Research’s page for Porpoise, Dolphins & Whale sightings in SF Bay & the NorCal coast. http://www.ggcetacean.org/
To learn more about the return of the harbor porpoise and its ecological implications, attend the Marin Science Seminar presentation “San Francisco Bay Has a Renewed Sense of Porpoise” with Jonathan Stern Ph.D. of San Francisco State University, January 29, 2014, 7:30 – 8:30 pm, Terra Linda High School, San Rafael, Room 207. See the flyer here
Want more information? Check out the websites below.
National Wildlife Federation California
Golden Gate Cetacean Research
National Geographic
NPR
SF Gate Article
~Claire Watry
When you hear the term public health, ideas that may come to mind might be about immunizations or food recalls. However, many of us don’t realize how big of a role public health plays in our everyday lives. From the faucets that we fill our drinking cups with to the seat belts that we wear in our cars, almost all aspects of our well being relate to Public Health in some way. On October 16th, 2013 Julie Pettijohn did an exemplary job of explaining the topic of public health and talked about what being in the field really involves. As an industrial hygienist, a typical work day for Julie is not just filling out paperwork in an office. Wearing a full outfit of protective gear, Julie often goes to a site to detect possible lead amounts in a work environment. Her job keeps us safe by enforcing the proper health requirements. The work and service of people like Julie in the public health field may often be taken for granted. Nevertheless, by attending the seminar many of us learned that being in the field is not just a job, it is establishing safe and healthy ways of life. I had the honor of asking Julie some questions about both herself and her field. Our interview is below.
While it could be considered cliché to compare cancer cells to supervillains, the similarities are undeniable. Supervillains are cunning, deeply rooted within their far-reaching schemes, and fearsome to the extreme. Cancer cells are just as sly, difficult to remove from the human body and terrifying to the afflicted and their loved ones. It’s not hard to visualize cancer cells as the shady criminal syndicate of the human body; their reach extends to the lungs, bones, tissue and bloodstream, and their tactics are ruthless. Make no mistake—cancer cells have long been antagonists to the scientists fighting for a cure and the patients fighting for their life.
But when it comes down to the science of it, cancer cells differ from many classic villains in that they aren’t innately evil. Rather, cancer cells and their dangerous properties originate from chance mutations during the division of normal cells. Mutations explain a lot of strange phenomena, from unexpected eye colors to increased resistance to diseases. These unexpected changes in gene sequences can be harmless, or even beneficial. However, they have an equal chance of damaging DNA, mutating it in such a way that the cell distorts into fast-splicing cancer cells.
Usually, mitosis—the process in which a cell divides—takes precautions against such mutations. “Checkpoints” during a cell’s growth period scan for identity-changing DNA mishaps, ensuring things are running as expected. If something is wrong, the cell will stop growing; if the damage to the DNA can’t be repaired, the cell will kill itself in a process called apoptosis. Through such self-sacrificing vigilance, cells that are mutated beyond repair never get the chance to multiply into a runaway number of damaged cells. But sometimes cell mutations go undetected, due to the sheer number of cells within the human body, with its trillions of constantly dividing cells, each with their own double-helix sequences and enzyme and lysosomes. In such a rush, a handful of mutations can slip by even the strict quality standards cells hold to themselves. Many of these mutations go undetected because they’re harmless to the identity of that cell—but some aren’t so benign.
When a cell with damaged DNA successfully slips by and divides, it creates the first two in a series of cells that will rapidly divide and spread incorrect DNA, beginning the first rapidfire stages of cancer. The speed of growth and division of cancer cells is unmatched, and unyielding; a cancer cell’s daunting ability to keep multiplying without ever dying, as normal cells do, is often referred to as ‘immortality’. This trait is due to two substances within the cell in particular: telomere and telomerase.
Telomere is a repeating DNA sequence that essentially acts as a cap for the chromosome it’s on. The sequence acts as a buffer between valuable DNA sequences within the chromosome and the often messy process of dividing a cell. Without the telomere, the ends of the chromosome would lose important base pairs much like a rope fraying at the ends. The more a cell divides, the more telomere is lost in protecting the chromosome. Once all of the telomere is gone, the chromosome reaches “critical length” and no longer replicates. When this happens, the cell doesn’t divide and dies through apoptosis. The erosion of telomere thus measures the age of a cell, with long telomere sequences indicating young cells and short sequences indicating old ones.
To restore and keep the cycle of cells replicating in our body, telomerase is needed to extend the eroding telomeres. Telomerase is an enzyme made of proteins and RNA. As an enzyme, telomerase enables certain reactions that couldn’t happen without it—in this case, rebuilding and elongating telomeres to a longer sequence again. Telomerase is sparingly used in somatic, or body, cells, which comprise most of the human body. As a result, humans age without much interference from telomerase.
While telomerase is rarely active in normal body cells, the enzyme becomes ten to twenty times more active in cancer cells. The abundance of telomerase gives cancer cells an endless supply of telomere, and with it, the ability to multiply indefinitely.
In addition to ‘immortality,’ cancer cells have several additional unique properties that explain why finding a cure is proving so difficult. In addition to fast replication, cancer cells don’t undergo apoptosis easily; high levels of survivin, a protein, inhibits the usual method of cell death. Cancer cells need neither the physical space nor the same amount of nourishing chemicals, known as growth factors, that normal cells need. Instead, they pile freely on top of each other, and remain undeterred by a diet on growth factors. The clusters cancer cells often find themselves in form the lumps within the breasts and testes that doctors and outreach campaigns warn about. Despite their ability to clump, cancer cells have unfortunately high mobility, too. While normal cells anchor themselves onto neighboring cells, cancer cells can break away and travel through the body, infecting other organs. Their ability to invade and infect other areas is made possible through the ability to break through the lamina. The lamina is a noncellular shield that protects the tissues, organs and surfaces within the human body, deflecting normal cells with ease. Cancer cells don’t have the same limitation, and spread to different organs with relative ease.
With its unique properties, cancer remains frustratingly difficult to cure. Treating cancer needs to somehow overcome the mobility and speed of replication cancer cells exhibit. Current treatments for cancer actually do better than that—the chemotherapy method of treatment uses the cancer cells’ speedy multiplication against it. Chemotherapy sends chemicals throughout the body that kill fast-replicating cells. Cancer cells are efficiently targeted and wiped out through this method, being some of the fasted replicating cells in the body.
However, chemotherapy has serious faults in its accuracy; by targeting fast-replicating cells, chemotherapy hits hair and blood cells particularly hard. A broad swath of helpful cells get caught in the crossfire between chemotherapy and the cancer cells it’s meant to target. As a treatment for cancer, chemotherapy can cause hair loss, amongst other more painful side-effects.
Other treatments are available, when cancer cells are concentrated in specific parts of the body. Radiation focuses on a single area, maybe one organ, to destroy cancer cells. When cancer cells are concentrated in a single area, forming a tumor, surgery can excise the infected part. Sometimes, a mixture of the three treatments are required to treat a patient.
There is still no way to accurately target and eradicate cancer cells without collateral damage. For that reason, and for the growing number people with breast cancer, leukemia, and other forms of cancer, research for better treatment and ultimately a cure is incredibly important. Cancer is internal, deadly in its silent machinations and intimidating with its arsenal of lethal properties. It’s up to the bright minds and generous hearts of every scientist, doctor, donor and activist to combat, quite literally, the enemy within.
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Interested in cancer cells and what scientists are doing to treat it? Come see Dr. Brad A. Stohr present “Why do Cancer Cells Grow Forever and Can we Stop Them?” Dr. Stohr will be presenting this Wednesday, April 17th, at the Marin Science Seminar. The Marin Science Seminar takes place during 7:30 to 8:30 p.m., in rm. 207 of Terra Linda High School. Come check out the Marin Science Seminar on our website and Facebook!
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Sources:
- Gregory, Michael J. The Biology Web, Clinton Community College.
- “What Is Cancer?” Cancer.org, The American Cancer Society.
- Zaidan, George. “How do cancer cells behave differently from healthy ones?” Getting Under Our Skin, TED-Ed.
- “Facts about telomeres and telomerase.” Shay/Wright Laboratory, Southwestern University.
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Sandra Ning
Susan Fisher, Ph.D. is the Director of Translational Research in Perinatal Biology and Medicine at UCSF. She is also a Professor in the Departments of Oral Biology, Pharmaceutical Chemistry, and Anatomy and Faculty Director at the Biomolecular Resource Center, UCSF. She is also a member of the UCSF Biomedical Sciences Graduate Program (BMS).
RSVP on FaceBook |
with Jane Gitschier, Ph.D. of UCSF’s Institute of Human Genetics
What makes us male or female? What makes us susceptible to disease? What makes us different from each other? And what makes us different from other animals? Come learn the answer to these questions. It’s all in our genes! Download the flyer. (September 28, 2011)