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Basketball season tickets on sale

The University of Toledo Athletic Department announced this week that 2018-19 men’s and women’s basketball season tickets are now on sale.

Season ticket plans are available with a variety of pricing options, benefits and new opportunities.

Season ticket options for men’s basketball include the lower level premium blue and gold sections. These premium areas are some of the very best seats in Savage Arena and require a Rocket Fund premium seat payment.

New to the 2018-19 season is the expansion of the premium purple season ticket package to include Section 101 and part of Section 110. Season tickets for this section start at just $180 plus a premium seat payment of $75. Other reserved season ticket options for the men are available in the upper east level starting at $80.

The Rocket men registered a 23-11 record last year, including a trip to the Mid-American Conference Championship Game, and will return four starters for the 2018-19 campaign. Senior guard Jaelan Sanford earned second-team All-MAC honors last year and ranked ninth in the MAC with 16.3 points per game and a 40.3 three-point shooting mark. Senior forward Nate Navigato set a school record last year with 94 three-pointers and ranked second in the MAC with a 42.7 three-point percentage. Also returning will be the junior duo of center Luke Knapke (10.8 points per game, 6.3 rebounds per game) and forward Willie Jackson (7.6 points per game, 5.6 rebounds per game), as well as All-MAC Freshman Team member Marreon Jackson (8.0 points per game, 2.7 assists per game).

Women’s basketball elite reserved season tickets are $150 in sections 108, 109 and the first five rows of section 102 and 103. General admission season tickets for women’s basketball are priced at $95.

The Rocket women made their sixth Postseason WNIT appearance last year. UT defeated Horizon League member Wright State, 64-50, in the first round before falling at Big Ten foe Michigan State, 68-66. Two-time All-MAC honoree senior Mikaela Boyd (12.1 points per game, 8.0 rebounds per game, 4.2 assists per game), 2017-18 third-team All-MAC selection senior Kaayla McIntyre (16.0 points per game, 7.7 rebounds per game) and 2016-17 All-MAC Freshman Team recipient junior Mariella Santucci (6.4 points per game, 4.1 assists per game) will be the focal points of UT’s offense in 2018-19.

Another new option for the 2018-19 basketball season is a youth season ticket price (50 percent discount for 12 and younger) in all areas.

Also, the UT Athletic Department is pleased to announce a ticket exchange program where season ticket members can exchange tickets for games they cannot attend. Season ticket members may exchange a ticket they are not using for a ticket of equal or lesser value to a future home game. Some restrictions may apply, and all ticket exchanges are based upon availability. In addition, exchanges must be made at least 48 hours in advance of the game by the physical ticket in at the UT Ticket Office.

A limited number of club and loge seats also are on sale. Fans may contact the Athletic Development Office at 419.530.4183 for more information or to purchase.

Full-time UT employees and retirees may purchase up to two season tickets at half-price. Additional season tickets may be purchased at the full price.

Fans who order season tickets by the early bird deadline of Friday, Aug. 10, will receive a Glass City Basketball T-shirt (one shirt per account). Additional benefits include:

• Discount to Rocky’s Locker;

• Complimentary general admission parking (Rocket Fund donors receive premium parking);

• Special discounts from corporate partners of the UT Athletic Department;

• Invitations to various Athletic Department special events throughout the year;

• Pre-sales for special events; and

• Rocket Athletic Department emails.

For more information or to purchase season tickets, visit the UT Athletic Ticket Office in the Sullivan Athletic Complex in Savage Arena, contact the UT Athletic Ticket Office at 419.530.GOLD (4653), or go online at utrockets.com/tix.

Reopening of West Rocket Drive delayed

Two-way traffic on West Rocket Drive is expected to resume Wednesday, July 18.

“We apologize for the delay,” Dan Perry, electrical manager with Facilities and Construction, said. “We had a set back with the sloping of the road and need to remove more asphalt to make it right.”

Traffic can still enter lot 12 by the Law Center, lot 26 by the Student Medical Center, and lot 26E by the Horton International House from the north.

And drivers can continue to detour around the construction via Secor Road and through lot 25 by Rocket Hall.

Crews have installed a tunnel system between two steam vaults and new steam lines, Perry said, and new sidewalks and roadway are still going in.

UT neuroscientist awarded $1.75 million to develop method to modify traumatic memories, treat PTSD

A neuroscientist at The University of Toledo is creating a new way to help people face their fears.

The National Institute of Mental Health awarded Dr. Jianyang Du, assistant professor in the UT Department of Biological Sciences, a five-year, $1.75 million grant to develop a method to modify fearful memories, which could lead to new treatment options for mental health illnesses, such as post-traumatic stress disorder, anxiety, depression and schizophrenia.

Du

“Excessive fear memories such as war-time trauma or a near-death experience can be crippling,” Du said. “However, fear memories also can be critical for survival. Developing means to either erase or to strengthen fear memory could aid understanding of how memories are formed and may suggest novel therapeutic strategies.” 

Du, who studies how protons regulate brain circuits and behaviors, found in mouse brains that manipulating pH in the amygdala can influence or control fear memories during recollection, creating a short window of increased susceptibility to either erase or enhance the memory.

Du manipulates the pH levels by using carbon dioxide inhalation and activating key molecular components of the central nervous system called acid-sensing ion channels, which spread throughout the body and allow for transmission of signals in the nervous system. The acid-sensing ion channels are important targets for pharmaceutical drug designers because of their importance to learning and memory.

“Our goal is to uncover the cellular and molecular mechanisms by which traumatic memories are stored in the brain and how carbon-dioxide inhalation and acid-sensing ion channels influence or control emotional behaviors, such as anxiety and depression,” Du said. “The ability to rewire the brain to modify existing fearful memories is very important as it relates to mental disorders.”

Study shows overeating during breastfeeding may lead to health problems for offspring

Breastfeeding has many health benefits for children, such as reducing their risk of obesity and strengthening their immune system. However, new mothers who consume a high-fat diet while breastfeeding may undermine some of those advantages, according to new research at The University of Toledo.

When mouse moms ate a high-fat, high-calorie diet while nursing, their offspring developed obesity, early puberty, diabetes and fertility issues.

Wang

Dr. Mengjie Wang, a PhD candidate in the Department of Physiology and Pharmacology, is the lead researcher of a team that used mice as a model to study the impact of excess calories during the breastfeeding stage on the offspring’s metabolism and reproduction.

“All over the world, puberty is starting earlier than it did in the past,” said Wang, who is earning her PhD at UT after graduating from medical school in China at Guangxi Medical University. “Childhood obesity, a common health issue, is one of the risk factors for early puberty. Previous evidence from animals has revealed that post-weaning overeating advances the timing of puberty, but we lack knowledge of how nutrition before weaning influences metabolism and reproduction.”

To determine how excess body fat alters the timing of puberty, Wang’s team gave female mice that are new mothers a high-fat diet from the date they gave birth and started breastfeeding until they weaned their offspring. A second group of mice that also were new mothers were given a regular diet. The onset of puberty was evaluated in the offspring after weaning, and fertility tests were done on the mice in adulthood, as well as an examination of their metabolic function.

“We found that excess calories during the breastfeeding phase can cause early obesity and early puberty and increases the risk of developing diabetes, metabolic dysfunction and subfertility during adulthood,” Wang said. “These results show that the breastfeeding phase is a critical window that influences when puberty happens.”

The study found that offspring of the mothers fed a high-fat diet while breastfeeding suffered from glucose intolerance and insulin insensitivity. They also had decreased litter sizes and impaired pregnancy rates.

“Human studies are needed to know whether these results apply to our species,” Wang said. “Still, I recommend that mothers consume a moderate and healthy diet while breastfeeding to protect their child’s long-term health.”

Wang said the research is significant in the clinical setting because doctors don’t always follow the same patients from puberty to adult life.

“Our findings can alert doctors and patients with early puberty that other health problems may arise after they become adults,” Wang said.

Former men’s basketball team manager passes away

Former UT Basketball Manager Bobby Graney of Dunedin, Fla., died June 30. He was 58.

Graney served as head ball boy for the men’s basketball team from 1979 to 2000, and could always be found in his seat at the end of the scorer’s table next to the Rocket bench at every home basketball game. He also worked with the football and women’s basketball teams.

Graney

In the late 1980s, Graney increased his duties and began attending every UT men’s and women’s basketball practice where he would run the scoreboard and the clock. He also helped out in the equipment room.

In 2000, Graney, who had Down syndrome, retired with his family to Florida, where the climate was better suited to his condition.

He was inducted into The University of Toledo Varsity ‘T’ Hall of Fame in 2000.

“All of us who knew and worked with Bobby came to love him,” said UT Deputy Athletic Director Dave Nottke, who worked with Graney during his time as a basketball manager in the 1990s. “He was a fixture at UT basketball games and practices. The UT Athletic Department extends its deepest sympathies to Bobby’s family during this difficult time.”

Graney is survived by parents, Bonnie and Mike; brother, Tim (June); sister, Michelle (Andrew); brother, Chris; nephews, Zach (Sarah) and Brandon; and niece, Emily.

Services will be private. The family gives special thanks to all their friends who knew Bobby, to the UT basketball staff, coaches, players, and everyone who made his life normal and complete.

Memorials are suggested to the UT Foundation for the basketball program.

UT researcher cures high blood pressure in rats

A University of Toledo researcher recently won a prestigious award for his cutting-edge hypertension study that cured high blood pressure in rats.

Dr. Xi Cheng, a UT College of Medicine postdoctoral fellow, won the Physiological Genomics Group New Investigator Award from the American Physiological Society and presented his research in April at the Experimental Biology meeting in San Diego.

Cheng

In his trailblazing research, Cheng identified a gene responsible for inherited high blood pressure in rats, and then he genetically engineered that gene to cure hypertension in the rats. Both were firsts in the field of genomic science that is focused on essential hypertension.

About one in three U.S. adults suffers from essential hypertension, or high blood pressure, which is a complex condition with no clear cause. Blood pressure can be affected by environmental factors such as diet and weight, but hypertension also runs in families with no identifiable, pre-existing cause. This kind of hypertension is what interests the UT researchers.

Cheng also discovered that another kind of genetic material — circular RNA — also seems to play a role in hypertension. His paper, published last fall in Physiological Genomics, was chosen as an APSselect article, an award given to authors of the most exciting original research articles published by the American Physiological Society.

Cheng has been studying hypertension since 2013, when he came to UT as a doctoral student in molecular medicine. He continues to work with his mentor, Dr. Bina Joe, Distinguished University Professor and chair of the Department of Physiology and Pharmacology, and director of the Center for Hypertension and Personalized Medicine. Their research focuses on how to correct and, if possible, permanently cure hypertension.

Scientists believe patients with hypertension inherit multiple genetic defects, which are difficult for researchers to find on strands of DNA that are millions of base pairs long. It’s also difficult to prove whether the defects “cause” or are “associated” with high blood pressure.

Cheng identified a new gene that regulates blood pressure in rats and pinpointed the mutation that is inherited and causes high blood pressure. He found a 19-base sequence of DNA in rats with lower blood pressure that was missing in rats with higher blood pressure.

Using a new technology, he extracted that critical DNA sequence from the rats with normal blood pressure and inserted it into the genome of hypertensive rats to see if correcting the mutation would cause their blood pressure to decrease. It was the first time anyone had used the new technique, called CRISPR/​Cas9 technology, to perform genome surgery in rats for correcting mutations for hypertension.

The embryos with the edited gene were implanted into surrogate mother rats. When the rodents were born, they became the world’s first genetically altered rats created to pinpoint the area on their DNA that caused them to inherit hypertension. More importantly, Cheng’s new rat strain no longer had high blood pressure. The “cure” had worked.

Cheng’s first-of-its-kind research proved that genome surgery — editing genes — can permanently cure a genetically inherited cause of hypertension in rats.

Allen Cowley, an internationally renowned hypertension researcher at the Medical College of Wisconsin, remarked in his review of Cheng’s work that “the work represents a technical tour de force and illustrates the critically important role of animal models that can mimic human traits of a complex disease to advance our understanding of the polymorphic associations that have been defined in human populations.”

Human patients can’t throw out their blood pressure meds just yet, though.

“Additional research will determine the possibility of this approach to cure hypertension in humans as we work to identify all the genetic pieces within the human genome that contribute to hypertension,” Cheng said.

The particular region that controls blood pressure in rats is similar to a region on a chromosome in humans in which scientists have reported associations with cardiac dysfunction and high blood pressure.

It’s much more difficult, though, to test this in humans, whose genes vary in millions of ways from person to person. To pinpoint the piece of genetic material that causes high blood pressure is like finding that proverbial needle in a haystack.

But the researchers are hopeful about the future of the research being conducted at the Center for Hypertension and Personalized Medicine.

“Here in Toledo, we are contributing to a piece of the puzzle,” Joe said. “When Xi and I were born, we didn’t have genome sequencing ability. Now we do.”

In the future, she said, scientists will use artificial intelligence and machine learning to predict who will get what diseases. And those scientists will rely on researchers like Joe and Cheng for data and to understand the blueprint of the genome.

Cheng has been accepted into a highly competitive online master’s program in computer science and machine learning at the Georgia Institute of Technology and will apply what he learns in the program to his research in Toledo.

UT astronomer part of NASA mission that discovered famously furious star system shoots cosmic rays

The average person encounters cosmic rays when the fast, tiny particles shoot through the clouds and cause bright pixels on photos. Very few actually reach the ground, and they are not known to be harmful.

Astrophysicists long believed those lightweight protons or electrons moving close to the speed of light reach Earth’s atmosphere after supernova explosions, deflecting off electromagnetic fields in their scrambled path through space that ultimately masks their origin.

The left panel shows the Hubble image of Eta Carinae, and the right shows an X-ray image from the Chandra X-ray Observatory on the same scale. The green contours show where NuSTAR detected the very high-energy source, which also proves that it is Eta Carinae and not another source in the region. The images are courtesy of NASA.

However, a groundbreaking new study involving NASA’s NuSTAR space telescope shows the most luminous and massive stellar system within 10,000 light years also is a source of cosmic rays that sometimes reach Earth, no explosion necessary.

The Eta Carinae discovery, which was published this week in the journal Nature Astronomy, was made by an international team, which includes an astronomer at The University of Toledo.

Dr. Noel Richardson, postdoctoral research associate in the UT Department of Physics and Astronomy, analyzed data from NuSTAR observations of Eta Carinae acquired between March 2014 and June 2016. The space telescope, which was launched in 2012 and can focus X-rays of much greater energy than any previous telescope, detects a source emitting X-rays above 30,000 electron volts at a rate of motion approaching the speed of light.

Richardson

“Most stars can’t produce that much energy,” Richardson said. “Eta Carinae is one of only three star systems NuSTAR has been able to observe. The new technology allowed us to push what we understand about the high-energy universe. And we discovered that we don’t always need an exploding star, but rather two stars with massive winds pushing out cosmic rays.”

The raging winds from Eta Carinae’s two tightly orbiting stars smash together at speeds of more than six million miles per hour approximately every five years. Temperatures reach many tens of millions of degrees — enough to emit X-rays.

“Both of Eta Carinae’s stars drive powerful outflows called stellar winds,” Dr. Michael Corcoran, team member at NASA’s Goddard Space Flight Center, said. “Where these winds clash changes during the orbital cycle, which produces a periodic signal in low-energy X-rays we’ve tracked for more than two decades.”

“We know the blast waves of exploded stars can accelerate cosmic ray particles to speeds comparable to that of light, an incredible energy boost,” said Dr. Kenji Hamaguchi, astrophysicist at NASA’s Goddard Space Flight Center in Greenbelt, Md., and lead author of the study. “Similar processes must occur in other extreme environments. Our analysis indicates Eta Carinae is one of them.”

Eta Carinae’s primary star is almost 100 times more massive and five million times more luminous than the sun. That star also is famous for losing 10 suns worth of material — huge amounts of gas and dust — into space in an enormous explosion in the 1830s that briefly made it the second-brightest star in the sky.

Richardson studies massive stars and also was part of the international team that captured the first sharp image of Eta Carinae’s violent wind collision zone and discovered new and unexpected structures in 2016.

In addition to UT and NASA’s Goddard Space Flight Center, researchers from the University of Maryland in Baltimore County, Catholic University of America, California Institute of Technology, University of Leeds, Hiroshima University, University of Utah and San Jose State University contributed to the new study.

Read more and see a video here.

UT professor to be promoted by Army to lieutenant colonel

Maj. Michael Penney, professor and chair of the UT Military Science and Leadership Department, will be promoted by the U.S. Army to lieutenant colonel Friday, July 6.

The ceremony will take place at 11 a.m. in Thompson Student Union Room 2592.

Penney

Penney is originally from North Texas and received a BBA from Midwestern State University in Wichita Falls, Texas. Since then, he has earned master’s degrees from both Webster University and the Army’s School of Advanced Military Science.

He was commissioned by the Army’s Officer Candidate School in 2002.

Penney came to UT from Carson, Colo., where he served from 2014 to 2017. His time there included two operational deployments — to Europe and to Afghanistan.

Last July, Penney joined the UT faculty as professor and chair of military science and leadership.

Through his department chair position, Penney oversees recruiting, retention, preparation and leadership development of cadets along their path toward their goal of being awarded a commission as an officer in the U.S. Army, Army Reserves or the Army National Guard.

He also instructs Military Science and Leadership Level Four Cadets throughout their transition from Cadet to Army Officer and works directly with UT’s University College and its ROTC program.

“My role as head of the ROTC program here at UT is one of the most important and rewarding jobs the Army has given to me to this point,” Penney said. “Leader development is crucial in the Army of today, and having some impact on the lives of future Army leaders is one of the best jobs.”

Penney will remain at UT for one more year and then take command of a battalion in South Carolina.

“This promotion to lieutenant colonel is an important one along the path to reaching my ultimate Army career goals,” Penney said. “But when I think about my nearly 16 years of commissioned service, I think more of those who have helped me along the way; specifically, those who I have served alongside and those who I have had the honor to lead at some point, and, most importantly, my family.”

‘Handwritten Dreams Project’ exhibit closes

The UT Department of Art has announced Leslie Adams’ solo exhibition, “The Handwritten Dreams Project,” has closed.

The artist’s reception and accompanying lecture scheduled for Friday, July 6 (rescheduled from June 1), at the Toledo Museum of Art’s Little Theater also has been canceled.

As a result of the continuing air conditioning and ventilation issues in the Center for the Visual Arts on the University’s Toledo Museum of Art Campus, the exhibition, organized and curated by Gallery Director and Assistant Professor Brian Carpenter, was removed recently due to extreme temperature and humidity conditions in the building. An expert in the field of conservation was consulted and recommended that the work be moved to a safer, climate-controlled environment.

According to Barbara WF Miner, professor and chair of the UT Department of Art, “The Handwritten Dreams Project” is a tour de force and the department is committed to working with Adams to find a time and venue to present the interactive exhibition in Toledo.

Adams said, “It was an incredible honor to be invited by my alma mater to exhibit ‘The Handwritten Dreams Project’ at the Center for the Visual Arts. I am disappointed that it cannot happen at this time — particularly as the debate on the teaching of cursive is unfolding in our state legislature. However, I am committed to and look forward to sharing my love of handwriting, drawing, and dreams with my community in the future.”

Adams received a bachelor of fine arts degree from UT in 1989.

Researchers discover molecule that could stop movement of cancer cells

Researchers at The University of Toledo have designed a first-of-its-kind gene-targeting molecule that could serve as a therapy to stop cancer growth and to help cancer patients who are resistant to current drugs.

Dr. Terry Hinds, assistant professor in the UT Department of Physiology and Pharmacology, and Lucien McBeth, a second-year medical student, received a full international patent last fall for “Sweet-P,” a new type of anti-cancer molecule.

Dr. Terry Hinds, right, is quick to credit his research team for helping to discover Sweet-P, a new type of anti-cancer molecule. Team members are, from left, Maggie Wong, Vikram Sundararaghavan, Darren Gordon, Charles Hawk, Justin Spear, Lucien McBeth, Abdul-Rizaq Ali Hamoud, Jonathan Demeter, Kari Neifer-Sadhwani and Jonnelle Edwards.

“When cancer cells are moving to other parts of the body, Sweet-P stops the migration,” Hinds said. “There’s nothing like it out there.”

Sweet-P has the potential to be a unique anti-cancer therapy, Hinds said, but more research is needed. It first needs to be used in preclinical investigations in mice before it can be tested in human patients.

Like many scientific discoveries, this one came about as Hinds and his team were studying something else — obesity.

Their work centered on GR beta, one of two proteins that originate from a gene called the glucocorticoid receptor (GR). Hinds genetically modified stem cells to have a higher level of GR beta and hypothesized based on other studies that the stem cells would change into large fat cells.

But they didn’t. They rapidly proliferated instead.

“GR beta was driving the growth phase of the cells,” Hinds said.

This discovery led Hinds and his team to ask more questions about GR beta, which is known to cause cancer cells to grow, proliferate and migrate.

Hinds’ team focused on the place on a gene where small RNAs, in this case microRNA-144, bind on the GR beta gene. Very little is known about microRNA-144 or what it specifically controls, but reports show that levels of it are significantly higher in patients with bladder cancer.

“Typically, microRNAs suppress genes. But this microRNA activates GR beta, especially during migration,” Hinds said. “We’d never seen this before.”

No one had ever created a drug to target microRNA-specific interaction with a gene. So Hinds got to work.

The end result is Sweet-P, a peptide nucleic acid molecule that resembles DNA.

Hinds tested the molecule on bladder cancer cells and found that it did indeed suppress GR beta. It latches on to the microRNA binding site of the GR beta gene and stops the microRNA from activating the protein. If the GR beta doesn’t work properly, the cancer cells don’t migrate.

Think of it as a basketball game. GR beta is the point guard, the playmaker. It sends the basketball (a signal) to other players (the cancer cells) to move and drive to the basket (other parts of the body). MicroRNA-144, then, is the coach screaming at GR beta to go faster. Sweet-P is akin to the referee giving a technical foul to silence the “coach” and slow down the game.

Because Sweet-P targets just one specific gene interaction — between the microRNA and the GR beta gene — it could significantly reduce side effects of potential treatments created with it, Hinds said.

“It’s precision medicine at its best,” he said.

Sweet-P’s ability to target GR beta could have implications for treating other cancers in which GR beta is highly expressed, including glioblastoma, an aggressive brain cancer, and prostate and lung cancers.

Sweet-P also could be a potential treatment for other diseases, like asthma, Hinds said.

Glucocorticoid hormones (GCs), the most commonly prescribed anti-inflammatory drugs, are often used to treat asthma, as well as cancer and other diseases. A high level of GR beta can cause those hormones to become ineffective, a condition known as GC resistance. Asthma patients often have high GR beta in their airways.

“When Sweet-P inhibited the GR beta, it increased the responsiveness of GCs, so Sweet-P may reverse GC-resistant diseases,” Hinds said.

If Sweet-P someday becomes an approved therapy, Hinds, who has asthma, might be able to get rid of the EpiPen on his desk.