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UT’s Master’s in Accounting ranked a top online degree program!

UT’s Master of Accountancy has been identified as one of the best 50 Master of Accounting degree programs in 2017-2018!

“Without a doubt, one of the fastest and most cost effective ways to earn CPA licensure in Ohio is through the University of Toledo’s top master’s degree in accounting.” – Online Accounting Degree Programs, please Click Here to know more

UT makes ad­vances in treat­ing sex­ual dys­func­tion

Published on May 1, 2017 | Updated 1:04 a. m.

Erin Semple is an M.D./PhD graduate student at the University of Toledo College of Medicine and Life Sciences.

Sexual dysfunction can be an uncomfortable topic, but if you have experienced it, you are not alone.

Sexual dysfunction occurs in about one-third of men in the United States and worldwide. It is important to understand sexual dysfunction for the purpose of finding treatments.

Erin Semple is an M.D./PhD graduate student at the University of Toledo College of Medicine and Life Sciences.

Men experience sexual dysfunction in many forms. Erectile dysfunction, or the inability to maintain an erection, is common. Some men lack the desire to engage in sexual activity. Others experience premature ejaculation or delayed ejaculation.

Medications such as Viagra are known to help, but in some men, they are ineffective. Viagra and related medications target the blood flow to the penis which is necessary to achieve an erection.

There are not many treatment options for men who have a low desire for sexual activity. Often this problem is secondary to other medications, an unhealthy lifestyle, or mental health problem. Testosterone replacement is used in certain cases for improving sexual desire.

Similarly, men who have either premature or delayed ejaculation have few treatment options. One type of antidepressant known as a selective serotonin reuptake inhibitor has shown promise for treating premature ejaculation in men. Unfortunately, delayed ejaculation is not well-understood, and treatment usually focuses on finding and treating any underlying cause.

Signals from the brain are also known to influence sexual function.

In our lab at the University of Toledo College of Medicine & Life Sciences, formerly the Medical College of Ohio, we study how sexual function is influenced by a hormone in the brain called melanocortin. Melanocortin binds to a protein called the melanocortin 4 receptor (MC4R), which activates many different cells in the brain, called neurons.

Mice also have MC4R in their brains, so they can be used as a model to test how this receptor affects sexual behavior.

When we remove this protein from all neurons of male mice, we find that the mice have difficulty reaching ejaculation. This means that some of the neurons that are activated by melanocortins are important for controlling ejaculation.

 We want to know which neurons are responsible for this behavior, so we selectively restore MC4R in certain populations of neurons in the brain.

We found that restoring these proteins in a very specific region of the brain called the paraventricular nucleus of the hypothalamus (PVN) results in normal ejaculation.

Because sexual function gets worse with age, we also tested these mice as they got older.

We found that older mice without MC4R proteins in their brain are completely unable to reach ejaculation and also have signs of erectile dysfunction.

When we restored these proteins in the PVN, the mice were able to reach ejaculation and no longer had erectile dysfunction.

The results of our studies indicate that melanocortins in the PVN are important for ejaculation, and perhaps erectile function in older mice.

Drugs that increase melanocortins in the brain are being explored as treatments for sexual dysfunction, but there are unwanted side effects such as high blood pressure, increased heart rate, and excessive yawning.

This is because melanocortins act on many different neurons. Imagine a river that flows into multiple smaller streams. This river sends the same water to all of its branches, but only one of the streams leads to the pathway affecting sexual function. If we can increase the flow of that one stream, without affecting the others, we can improve sexual function without unwanted side effects. We have identified that one stream affecting sexual function starts in the PVN of the brain. Now we need to follow that stream to identify even smaller branches that lead to sexual function.

So far, we have found one group of cells in the PVN, called oxytocin neurons, which are involved in sexual behavior. Using the same method as before, we restored MC4R only on oxytocin neurons and found that these mice had normal sexual behavior compared to mice with no MC4R.

Our future goals are to learn how these oxytocin neurons within the PVN are influencing sexual behavior. We may be able to develop therapies with fewer unwanted side effects for men of all ages by continuing our studies to find specific melanocortin cells that are involved in sexual behavior.

Erin Semple is an M.D./​PhD graduate student at the University of Toledo College of Medicine and Life Sciences biomedical science program. She is completing her doctoral studies in the neuroscience and neurological disorders track in the lab of Jennifer Hill. For details email or go to​med/​grad/​biomedical

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Election Results for GSA Officers 2017-2018

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Careers in Science Day on April 6, 2017

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 program

Published on April 3, 2017 | Updated 12:54 a. m.


Rose Zolondek is a student pursuing her doctorate in philosophy at the University of Toledo college of medicine and life sciences biomedical science program.

Do you know someone with cancer? If so, there is a strong chance that this person has lung cancer.

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.


Rose Zolondek is a student pursuing her doctorate in philosophy at the University of Toledo college of medicine and life sciences biomedical science program.

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 or go to​med/​grad/​biomedical.

Voting Open for 2017-2018 GSA Officer Elections! Deadline April 3, 2017 at 12:00 noon

Deadline April 3, 2017 at 12:00 noon

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UT researchers take new approach in cholera prevention by Cara Deangelis, PhD student in the Department of Medical Microbiology and Immunology UT


    Cara DeAngelis is a PhD student of microbiology and immunology in the University of Toledo College of Medicine.

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.


Cholera is commonplace in countries where access to clean water is limited. As many as 143,000 deaths from the disease occur annually. UNIVERSITY OF TOLEDO

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.


Cara DeAngelis is a PhD student of microbiology and immunology in the University of Toledo College of Medicine.

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 or go to​med/​grad/​biomedical.

Graduate Nursing Information Session on February 28, 2017

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 Science

$300 prize for the Best Student Submission! Call for abstracts for posters for the 4th Annual Symposium on Research in Psychiatry, Psychology and Behavioral Science. Click on the flyer for more information.

Researchers aim to stop progression of kidney disease by Jeffrey Xie, M.D./​PhD student in the Department of Medicine UT

Scientists at UT look at one specific molecule that can detect problems early

Published on
It is estimated that 14 percent of the U.S. population has chronic kidney disease, which is an umbrella term for many conditions that can cause ongoing injury to the kidneys.

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.


Jeffrey Xie is a student at the University of Toledo College of Medicine and Life Sciences Biomedical Science.

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 or go to​med/​grad/​biomedical.