Archive for the ‘News’ Category
We have Dr. Gil Van Bokkelen, the CEO, Chairman, and Co-Founder of Athersys, coming to speak at 10am, with a Q&A session afterwards. He’ll be speaking about his work in Stem Cells, as well as on his career path. His seminar is titled, “Opportunities in the Field of Regenerative Medicine – Impact on Areas of Substantial Unmet Medical Need” In the afternoon, there are 15 min opportunities for students or faculty to meet with him in small groups (1-3 people) to discuss specific/personal questions. These meetings are available by reservation only.
In the afternoon there is a career fair, which includes 12 scientific companies (see the website for an exact list, including job postings). These companies are specifically interested in grad students in the sciences, but there are plenty of positions for undergrads too and for students of all majors.
UT researchers map genetic code to determine cancer risk, by Rose Zolondek, doctoral student in the Biomedical Science programMonday, April 3rd, 2017
Lung cancer is the leading cause of cancer-related death in the United States and is the most common cancer worldwide. About 160,000 Americans were expected to die from lung cancer in 2016, accounting for 27 percent of all cancer-related deaths.
Identifying and then screening a person at high risk can reduce the likelihood of that person dying from lung cancer. Screening allows doctors to find tumors at an earlier stage when they are more responsive to treatment and potentially curable by surgical removal. About 9 million Americans are at high risk for lung cancer. Based on a large clinical trial, early screening of people at high risk reduced the risk of dying from lung cancer by 20 percent.
How do we identify who is at risk? The risk of lung cancer varies from person to person and depends on both a person’s inherited genetics and on environmental exposures such as smoking, radon, asbestos, and many other toxins that can get into your lungs.
At the University of Toledo college of medicine and life sciences, formerly the Medical College of Ohio, we are investigating the differences in our risk of lung cancer by studying differences in inherited genetic code. Most of the cells in the body, including lung cells, contain chromosomes you inherited from one’s parents. Each chromosome is composed of DNA building blocks in a sequence that defines an individual’s unique genetic code, just like sequences of letters define a word, sequences of musical notes define a song, or sequences of symbols define a computer program.
We now know specific DNA sequences of each human genome that produce different hair and eye color. We also see differences in DNA sequences at certain genetic locations that increase the risk for human diseases such as lung cancer. For example, certain inherited DNA sequence differences can change the way cells in the lung react to environmental exposures such as tobacco smoke.
Differences in DNA sequence are called single nucleotide polymorphisms, or SNPs. Each SNP is a change in a single DNA building block, also called a nucleotide. SNPs are found every 300 nucleotides on average. This means that one’s entire genome contains about 10 million SNPs total. Most SNPs do not have any effect on one’s health. However, some SNPs are within DNA sequences that code for proteins and therefore can affect one’s risk for a specific disease such as lung cancer.
Our research lab studies SNPs in genetic sequences that are responsible for the repair of damaged DNA. This is a very important function within one’s cells. Damaged DNA, if not repaired properly, can result in a population of cells with a DNA mutation that may lead to cancer.
We now know that if certain SNPs occur in specific genetic sequences, they can inhibit DNA from being repaired properly, which increases the chance of lung cancer, especially if you smoke.
We now have machines that can rapidly sequence the entire human genome, which is 3 billion nucleotides long. Our research lab uses these machines to identify the nucleotide sequence of SNPs that are associated with increased risk for lung cancer. My research focus is based on our recent results with genes that are responsible for protecting DNA in lung cells from damage and other genes that repair damage when it occurs.
For example, we are studying genes such as glutathione peroxidase, or GPX1, that protect lung cells from certain toxic effects of cigarette smoke. We are also studying genes called TTC38 and TRMU. Very little is known about the function of TTC38, which makes it exciting to study. We know that TRMU helps to modify letters in the DNA code and SNPs in this gene are associated with deafness, but also appear to have a role in lung cancer.
Identifying the function of SNPs in these genes help us better identify high risk individuals who may have the best benefit from regular screenings in the clinic. This would increase early detection of lung cancer and allow patients to be treated earlier. Earlier treatment often means better outcomes especially for lung cancer.
We continue to increase our understanding of lung cancer risk and to fight against this devastating disease by our ongoing collaborative work with other researchers and pulmonary doctors at the University of Toledo, the Toledo Hospital, the University of Michigan, and many other centers of excellence in lung cancer research. Our research is supported by the National Institutes of Health and the George Isaac Cancer Research Fund.
Rose Zolondek is a student pursuing her doctorate of philosophy in the University of Toledo college of medicine and life sciences biomedical science program. Ms. Zolondek is doing her research in the laboratory of Dr. James Willey. For information, contact email@example.com or go to utoledo.edu/med/grad/biomedical.
Deadline April 3, 2017 at 12:00 noon
UT researchers take new approach in cholera prevention by Cara Deangelis, PhD student in the Department of Medical Microbiology and Immunology UTMonday, March 6th, 2017
How often do you find yourself thinking about the safety of the water you drink?
Perhaps you thought about it during the summer of 2014 when the southwest region of Lake Erie had a toxic algae bloom. After that summer though, I am sure many of us returned to using our tap water, without any second thoughts.
Unfortunately, many countries lack the basic resources that we take for granted every day, like clean drinking water. Those without water treatment plants and sewage systems are at risk for numerous diseases. One such disease is cholera, caused by the bacteria Vibrio cholerae.
Vibrio cholerae likes to live in warm, salty waters and can attach to shellfish. If you drink water or eat food contaminated with these bacteria, you can become infected and very sick within a few hours. The bacteria secrete a toxic substance, called cholera toxin, in the intestine of an infected person. The toxin causes a very rapid loss of water, leading to severe dehydration and death if not treated.
The best treatment for cholera is oral rehydration therapy, which replaces the water lost from the body. Such resources are not always available or easily accessible in countries affected by this disease, so other treatments are being investigated.
Luckily for us, cholera is not a problem in industrialized countries like the United States. However, Vibrio cholerae affects more than 50 countries worldwide, causing about 4 million cases of cholera a year and up to 143,000 deaths. Therefore, this disease is a global threat to public health and research is necessary to help save lives.
At the University of Toledo College of Medicine and Life Sciences, formerly the Medical College of Ohio, I am a part of Jyl Matson’s research group that studies Vibrio cholerae. The bacteria has an outer and an inner membrane, which protect them from their environment, whether that is water or the human intestine. For example, these bacteria have to be able to live through large changes in temperature, the acid in our stomachs, and attack from our immune systems.
Picture these bacteria as tiny castles surrounded by two outer walls for defense against outside enemies. If cannons are fired at either wall, soldiers are sent to shield the weak locations and keep out the enemy.
My project in Ms. Matson’s laboratory is focused on learning about a system that the bacteria deploy when their inner membrane is damaged. This response system is called the phage-shock-protein response and has never been studied in Vibrio cholerae. However, it has been studied in several other types of bacteria, which give us clues about what it could do in Vibrio cholerae. We know that in those bacteria, when the inner membrane is damaged, the bacteria turn on their phage-shock-protein response. The bacteria then make specific proteins that are sent to the inner membrane to keep it functioning correctly. This response system makes these other bacteria better at causing disease.
It is likely that the phage-shock-protein response in Vibrio cholerae operates in a similar manner as these other bacteria, but it is also possible that it works in a different way. My research is to figure out exactly what this phage-shock protein response is doing in Vibrio cholerae.
One way I have begun to study this response system is by deleting specific pieces of DNA, or genes, that create phage-shock proteins. The concept behind this is elegantly simple: If we remove a gene from the bacteria and they do not function as well without it in stressful situations, then we know that it was important for the bacteria to survive. So far, I have found that all of the phage-shock-protein genes I have deleted are important for the bacteria to survive in stressful environments.
The next step is to target the proteins made from these genes to cripple the bacterial response system. You would expect that the bacteria would be weaker and therefore more easily defeated without that protection system in place, would you not? This would be like removing the soldiers that help protect the castle wall.
By understanding the phage-shock-protein response in further detail, we hope to contribute to the development of more effective treatments for cholera. If we manage to target and knock down the phage-shock-protein response, other medications might be better able to kill the bacteria. With those two methods of attack combined, we may be able to decrease the number of lives lost to cholera.
Cara DeAngelis is a PhD student in the Department of Medical Microbiology and Immunology in the University of Toledo College of Medicine and Life Sciences Biomedical Science Program. Ms. DeAngelis is doing her research in the laboratory of Jyl Matson. For more information, contact Cara.Deangelis@rockets.utoledo.edu or go to utoledo.edu/med/grad/biomedical.
What nursing degree do you need to advance your career? MSN/DNP/Graduate Certificate? Learn more at the Graduate Nursing Information Session, Tuesday, February 28th 5:00 -6:30 pm, UT Health Science Campus, Collier Building, Room 1200. Click on the flyer for more information.
Call for abstracts for posters for the 4th Annual Symposium on Research in Psychiatry, Psychology and Behavioral ScienceWednesday, February 8th, 2017
Researchers aim to stop progression of kidney disease by Jeffrey Xie, M.D./PhD student in the Department of Medicine UTMonday, February 6th, 2017
Scientists at UT look at one specific molecule that can detect problems early
Both high blood pressure and diabetes can cause damage to the kidneys, which over time, can result in chronic kidney disease. One reason this disease is so widespread is that it is often silent, meaning that many people with chronic kidney disease do not have enough symptoms to diagnose until it is very advanced.
Scientists from around the world, including several of us at the University of Toledo College of Medicine and Life Sciences, formerly the Medical College of Ohio, are working hard to find ways to prevent patients diagnosed with chronic kidney disease from ever progressing to the most severe stage of the disease.
The kidney’s primary job is to filter the blood to remove waste products. Doctors can determine how effective a person’s kidneys are by measuring something called his glomerular filtration rate. Doctors use glomerular filtration rates to determine the progression of chronic kidney disease in their patients. When a patient’s glomerular filtration rate drops to 15 percent of a healthy person’s, that patient has reached end-stage kidney failure.
Despite all of the advances in modern medicine, the only two treatment options for end-stage kidney failure are repeated dialysis, which often lead to a number of bad side effects, or a kidney transplant, where the estimated wait time for a kidney can be three to five years.
Changes to a patient’s kidney that have occurred by the time he has reached end-stage kidney failure are not reversible. Because of such extensive kidney damage, it is unlikely that a drug will be found to treat end-stage kidney failure for the foreseeable future.
At UT, we are focused on finding better ways to identify chronic kidney disease at earlier stages to give doctors a better chance to slow down or even stop chronic kidney disease in its tracks. Under the direction of professors Steven Haller and Jiang Tian, I research one specific molecule called Cluster of Differentiation 40, or CD40, which we believe could be useful in detecting chronic kidney disease at earlier stages.
Interestingly, scientists have actually known about CD40 for years. It plays a central role in activating an immune response and helping the body fight infection.
However, CD40 has recently been identified as also having an important role in chronic kidney disease.
Through a collaborative effort with other scientists from UT, we have recently shown that blocking CD40 can be helpful in treating chronic kidney disease in the laboratory. We demonstrated that animal models without CD40 were more resistant to chronic kidney disease.
We are working to convert these research findings into real-world benefits for patients with chronic kidney disease. There is still a lot that remains unknown about the function of CD40 in the kidneys, and I have worked hard to unravel these mysteries. However, much more work needs to be done before doctors can apply our research findings in the hospital.
As a result of working alongside a large, multidisciplinary research team that includes statisticians, mathematicians and doctors who specialize in treating patients with kidney disorders, we have made and will continue to strive to make important contributions in our fight against chronic kidney disease.
Jeffrey Xie is an M.D./PhD student in the department of medicine in the University of Toledo College of Medicine and Life Sciences Biomedical Science Program. Mr. Xie is doing his research in the laboratory of Drs. Jiang Tian and Steven Haller. For more information, contact Jeffrey.Xie@rockets.utoledo.edu or go to utoledo.edu/med/grad/biomedical.
UT Leadership Conference
- Saturday, February 11, 2017
- Memorial Field House
- Free to all UT Students!
Registration open until Feb. 3rd: https://orgsync.com/130102/forms/236670
Do you want to develop your leadership ability with the help of experts from campus and the community? The 2017 Leadership Conference will embrace The University of Toledo’s next generation of leaders with its theme of “Next Generation Leadership.” College students today are comprised of a mixture of generation groups. What do the unique characteristics of your generation mean for your leadership style and experience? Campus and community experts will help you discover the importance of being a leader who utilizes technology to showcase your leadership, learns from the advice of experienced leaders, and acquires fundamental leadership skills.
The 2017 Leadership Conference keynote speaker is Frank Kitchen, “The Life and Leadership Connoisseur.” Kitchen will share his FRESH recipes on life and leadership to educate, elevate, and empower students. Other conference speakers include UT faculty and staff as well as community professionals employed in a variety of fields such as marketing, business, and healthcare. Session topics include “Why Cultural Competency Matters for 21st Century Leadership” and “Leverage Leadership on LinkedIn.”
The conference will take place on Saturday, February 11, 2017 (9:00am-3:30pm). Registration is open until February 3rd and can be accessed on OrgSync at https://orgsync.com/130102/forms/236670.
Space is limited, so please register as soon as possible!
Conference t-shirts are available for purchase until January 27th at www.slicustom.com/web-stores.
For more information, please call the Office of Student Involvement & Leadership at 419.530.4944 or email firstname.lastname@example.org.
Welcome to 2017! The New Year always provides an impetus to start fresh! As the new semester begins think of it as your opportunity to freshen your view and sow new seeds to make your path greener and plant new flowers to add the joy and variety you desire in your present and your future.
In our effort to freshen our garden in the College of Graduate Studies, we will announce several changes over the next month. We will see personnel changes, a request for proposals for new graduate programs and new professional and personal development options for our students and mentors. As the university strives to develop its new strategic directions, it is important that graduate education remain actual, relevant and the highest of quality. That is what you demand and that is what we strive to deliver. If you have a graduate program in mind that you would like to see the University of Toledo offer, please respond to the request for proposals that will be announced within the next few weeks. This proposal will be accessible to graduate students as well as faculty and we encourage collaborative proposals between all constituents.
As for professional and personal development, we want to offer what you need. A survey will arrive in your email box soon requesting your input on the areas that you would like to see offered in this domain. If you would like to send me a personal communication instead, please feel free to contact me at Amanda.email@example.com.
I wish you all the best in the new semester and in the new year. We will strive TOGETHER to create the future that we desire for our university, community, nation and world, one step at a time!
Amanda Bryant-Friedrich, Dr. rer. Nat
Dean, College of Graduate Studies
Associate Professor of Medicinal and Biological Chemistry