News

Dr. Supriya Prasanth, associate professor of cell and developmental biology, awarded the Lynn M. Martin Award for Distinguished Women Teachers

Dr. Prasanth’s primary teaching responsibility has been the creation and delivery of MCB 400 Cancer Cell Biology, one of the most popular undergraduate elective courses. She is consistently ranked as excellent by her students each semester.

In addition to her classroom teaching, Dr. Prasanth has been an outstanding mentor to students engaged in undergraduate research. Training undergraduate research students in the lab involves significant commitments of time, effort, and resources, and the 15 students she has trained demonstrate her commitment to creating opportunities for undergraduates. Currently, her lab has three undergraduate students performing research under her guidance.

Many of her former students are on their way to successful careers- three have gone on to graduate school, four to medical school, two to research positions, and one is a director of private healthcare company in India. Several of her research students have won awards and recognition for their work.

Dr. Prasanth’s lectures are known for their clarity and her ability to explain complex topics. Her lectures noted for being lively, enthusiastic, and engaging, even during a 1.5 hour session.

The Department of Cell and Developmental Biology recognizes her dedication, talent, and effectiveness in teaching.

Named for the founder of the award, the Lynn M. Martin Award for Distinguished Women Teachers is designated to promote exceptional achievement in undergraduate teaching by women. Two awards (one for Teaching Assistants and one for Faculty members) are awarded by the College of Liberal Arts and Sciences.

     
Posted May 09, 2017
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Emad Tajkhorshid named the J. Woodland Hastings Endowed Chair in Biochemistry

One of the highest honors that a faculty member can receive, this endowed chair is named for the late John Woodland “Woody” Hastings (1927-2014), and set up by donors George and Tamara Mitchell. Hastings was a decorated scholar who served as a faculty member at Illinois from 1957-66 and was best known for his innovation in the field of bioluminescence. He was also a founder in the field of circadian biology, focusing on the biological cycles of plants, animals, fungi, and other living things.

Tajkhorshid is a professor of biochemistry, biophysics, and computational biology. He is also professor and head of pharmacology, and interim head of the medical biochemistry. He joined the Department of Biochemistry and pharmacology in 2007, and has since developed an extensive research portfolio. He was chosen for the award by a committee of his senior colleagues who hold endowed positions. He is a member of the Beckman Institute for Advanced Science and Technology.

George W. Mitchell III (1942-2016) earned his master’s degree in chemistry from U of I in 1966 while working under the mentorship of Professor Hastings. He moved with Hastings to Harvard University, where he continued his research to receive a doctoral degree in 1969.

University of Illinois faculty influenced Mitchell greatly throughout his career and entrepreneurial efforts, which revolutionized biomedical research and patient care. Mitchell co-founded SLM Instruments along with David Laker and Dick Spencer (MS, ’67 PhD, ’70; chemistry; MBA, ’92) who also were affiliated with the College of Liberal Arts and Sciences (Laker was a machinist for the department). SLM Instruments designed and built the first commercial instrument to measure biological fluorescence – a groundbreaking advance in medicine and biological research.

Tamara T. Mitchell was employed by Carle Clinic and Carle Foundation Hospital as well as serving as a clinical associate professor with the Regional College of Medicine at U of I from 1970-2001. Her medical and research interests focused on family practice, rural health, and farm safety. At the time of her retirement in 2001, she was serving as a medical director at Carle Clinic. Tamara Mitchell was chosen by her peers as among the Best Doctors in the Midwest in 1996.

Tamara Mitchell spoke at the ceremony, held at the Beckman Institute, and described Hastings as a scientist of passion and generosity who “was never in it for the money, rather for his own curiosity and love of science.”

Tajkhorshid has authored over 180 research articles with over 17,500 citations in high-profile journals such as Nature, Science, eLife, and PNAS. He has delivered nearly 150 invited lectures at international meetings, universities, and research institutes. He serves on the editorial boards of multiple journals, including Biophysical Journal, Journal of Biological Chemistry, and PLoS Computational Biology.

He started his career with pharmacy and doctoral degrees in medicinal chemistry at Tehran University. He then earned a second doctoral degree in molecular biophysics from the University of Heidelberg before he moved to the U of I at Urbana-Champaign, where he completed postdoctoral studies in computational biophysics at the Beckman Institute.

Tajkhorshid joined the faculty as a professor of biochemistry and pharmacology in 2007, was promoted to associate professor in 2010, and then again to the rank of professor in 2013. In 2015, Tajkhorshid was named a University of Illinois Scholar, after being nominated by both the Urbana-Champaign and Chicago campuses, and was then awarded the Faculty Excellence Award from the School of Molecular and Cellular Biology in 2016.

Speakers at the ceremony included U of I Provost John Wilkin, Feng Sheng Hu, the Harry E. Preble Dean of the College of LAS, Steve Sligar, director of the School of Molecular and Cellular Biology, and Susan Martinis, head of the Department of Biochemistry. Martinis said Tajkhorshid’s potential was obvious from early in his career.

“We often talk about the powerful legacy of the Department of Biochemistry and the University of Illinois. All aspects of Emad’s career in academia honor that and continue that legacy,” she said.

Martinis added: “Many people in this room know how wonderful a collaborator Emad is, because they work closely with him—that collaborative spirit for Emad extends worldwide.”

Tajkhorshid thanked George and Tamara Mitchell for their “generosity, vision and commitment.” He added that their “contribution is invaluable to research throughout the university and [he is] very glad to be one of the groups that is benefitting from [their] contribution.”

“Most importantly, I would like to acknowledge my students, post-docs and colleagues,” Tajkhorshid said. “They are the reason I’m standing here, presenting what they have been doing for many, many years; I really appreciate and enjoy working with them.”

By Logan Weeter, College of Liberal Arts and Sciences communications

     
Posted May 01, 2017
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Study offers new insight into powerful inflammatory regulator

A new study in mice reveals how a protein called Brd4 boosts the inflammatory response – for better and for worse, depending on the ailment. The study is the first to show that this protein, while problematic in some circumstances, also can protect the body from infection. The findings are reported in the Proceedings of the National Academy of Sciences.

The heat, swelling, redness and pain associated with inflammation are evidence that the immune system is working to protect the body. Once its job is complete, the acute inflammation normally recedes and disappears.

Sometimes inflammation fails to stop, and instead turns against the body, attacking healthy tissues and leading to chronic inflammatory diseases such as asthma, arthritis, diabetes and cancer.

One very powerful protein complex, called NF-kappaB, influences the expression of numerous genes and governs both beneficial and harmful inflammatory responses. When NF-kappaB regulates discriminately, the body heals and survives. When NF-kappaB overreacts, inflammation can become dangerous.

The NF-kappaB protein is a primary target for research looking for a way to stop inflammatory diseases.

The new study, led by University of Illinois biochemistry professor Lin-Feng Chen, reveals how Brd4 influences NF-kappaB and contributes to inflammation.

“Brd4 acts like a turboboost for the NF-kappaB protein that regulates inflammation. For NF-kappaB to be 100 percent productive, it needs the help from Brd4,” Chen said.

Earlier work in Chen’s lab revealed that Brd4 attaches to the NF-kappaB protein by recognizing a chemical tag. If Brd4 or the tag is not present, the potential of NF-kappaB protein to act as inflammation regulator is compromised.

The new study in mice confirmed that Brd4 plays a major role in acute inflammatory responses. The researchers deleted the mouse Brd4 gene in certain types of immune cells, including macrophages, and monitored the immune response of these mice. Many of the NF-kappaB-dependent, inflammation-related genes involved in fighting infection were down-regulated in Brd4-deficient macrophages.

“We found that in the absence of Brd4, the immune system of mice was compromised. They were more resistant to a massive immune response, but more susceptible to bacterial infection,” Chen said.

“Cancers and some inflammatory diseases use Brd4 to boost the expression of genes that lead to the growth or persistence of the disease, but Brd4 has the same effect on inflammation that is needed to kill bacteria and viruses,” he said.

The researchers also discovered a new mechanism for the reduced inflammatory gene expression in cells lacking Brd4. They found that deletion of Brd4 enhanced the protein synthesis of a NF-kappaB inhibitor, preventing the NF-kappaB from stimulating inflammatory gene expression.

“The next step is to test whether the absence of the gene for Brd4 would weaken the strength of the NF-kappaB protein – and inhibit chronic inflammatory diseases – without compromising the body’s ability to fight off bacteria and viruses,” Chen said.

“Pharmaceutical companies are currently investing enormous resources – to the tune of hundreds of millions of dollars – seeking molecules that will inhibit the Brd4,” Chen said. “Our findings urge caution and further foundational research before treatments involving the inhibition of Brd4 are used on patients.”

Read the full article here.     
Posted May 01, 2017
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Mobile Summer Institute (MoSI) on Scientific Teaching

Expand and sharpen your teaching skills through workshops facilitated by national science education experts. Participants will develop original, innovative classroom materials ready for immediate implementation. The workshop begins on the afternoon of Monday, June 5, 2017, and ends for participants on the afternoon of Thursday, June 8, with an optional strategic planning meeting in the morning of June 9. More information, including a preliminary schedule for the workshop is attached. Please register by April 30, 2017.

     
Posted April 07, 2017
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Assistant Professor Nien-Pei Tsai’s lab has published a study in PLOS Genetics on how a novel epilepsy-associated gene controls neuronal excitability

Human genetic studies have identified many epilepsy-associated genes, but the mechanisms by which those genes are linked to brain circuit excitability and seizures are largely unknown.

A recent study published in PLOS Genetics by Assistant Professor Nien-Pei Tsai’s lab at the Department of Molecular and Integrative Physiology uncovered how the disruption of a novel epilepsy-associated gene, named ‘neural precursor cell expressed developmentally down-regulated gene 4-like’, or Nedd4-2, leads to neuronal hyperexcitability and seizures.

Nedd4-2 encodes a ubiquitin ligase that is responsible for degrading specific substrate proteins. Dr. Tsai’s lab has previously identified a neurotransmitter receptor, named ‘AMPA receptor’, as a novel substrate of Nedd4-2.

In this current study, using a mouse model in which one of the major forms of Nedd4-2 in the brain is selectively deficient, they found that the spontaneous neuronal activity in cortical neurons is basally elevated and very sensitive to the blockage of AMPA receptor when compared with wild-type neurons.

Most importantly, the elevated seizure susceptibility in this mouse model can be normalized when the AMPA receptors are genetically reduced. When studying the Nedd4-2 that carries one of the three epilepsy-associated mutations, they found that all mutations reduce the affinity of Nedd4-2 to modulate the degradation of AMPA receptors. These findings suggest that impaired AMPA receptor degradation contributes to Nedd4-2-dependent neuronal hyperexcitability and seizures. The pharmacologically targeting of AMPA receptors has already been applied clinically for treating patients with epilepsies. This study suggests a promising therapeutic target and introduces a currently available therapy for alleviating epilepsy symptoms in patients who carry mutations of Nedd4-2.

Read the full article here.     
Posted February 28, 2017
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Kehl-Fie and team discover how bacteria exploit a chink in the body’s armor

Researchers at the University of Illinois at Urbana-Champaign and Newcastle University in the UK are investigating how infectious microbes can survive attacks by the body’s immune system. By better understanding the bacteria’s defenses, new strategies can be developed to cure infections that are currently resistant to treatments.

The study, reported in PLoS Pathogens, focused on the bacterium Staphylococcus aureus (which, in its most pathogenic form, is renowned as the so-called ‘superbug’ methicillin-resistant S. aureus, or MRSA). S. aureus is found on approximately half of the population. While it usually safely coexists with healthy individuals, it has the ability to infect nearly the entire body.

The human body uses a diverse array of weapons to fight off bacteria. “Our immune system is very effective and prevents the majority of microbes we encounter from causing infections,” said U. of I. microbiology professor Thomas Kehl-Fie, who led the study with Kevin Waldron, of Newcastle University. “But pathogens such as S. aureus have developed ways to subvert the immune response.”

S. aureus can overcome one of the body’s key defenses known as “nutritional immunity.” Other, less pathogenic relatives are stopped by this defense, which prevents bacteria from obtaining critical nutrients. It starves S. aureus of manganese, a metal needed by the bacterial enzyme superoxide dismutase, or SOD. This enzyme functions as a shield, minimizing the damage from another weapon in the body’s arsenal, the oxidative burst. Together, the two host weapons usually function as a one-two punch, with nutritional immunity weakening the bacteria’s shields, enabling the oxidative burst to kill the bacterium.

S. aureus is particularly adept at causing devastating infections. Differing from other closely related species, S. aureus possesses two superoxide dismutases. The team discovered that the second superoxide dismutase enhances the ability of S. aureus to resist nutritional immunity and cause disease.

“This realization was both exciting and perplexing, as both SODs were thought to utilize manganese and therefore should be inactivated by manganese starvation,” said Dr. Kehl-Fie.
The most prevalent family of SODs, to which both of the S. aureus SOD enzymes belong, has long been thought to come in two flavors: those that are dependent on manganese for function and those that use iron.

In light of their findings, the team tested whether the second staphylococcal SOD was dependent on iron. To their surprise, they discovered that the second SOD was capable of using either metal. While the existence of these “cambialistic” SODs, capable of using both iron and manganese, was proposed decades ago, the existence of this type of enzyme was largely dismissed as a quirk of chemistry, unimportant in real biological systems. The team’s findings dispel this notion, demonstrating that cambialistic SODs critically contribute to infection.

The team found that, when starved of manganese by the body, S. aureus activated the cambialitic SOD with iron instead of manganese, ensuring its critical bacterial defensive barrier was maintained.
“The cambialistic SOD plays a key role in this bacterium’s ability to evade the immune defense,” said Dr. Kevin Waldron of Newcastle University. “Importantly, we suspect similar enzymes may be present in other pathogenic bacteria. Therefore it could be possible to target this system with drugs for future antibacterial therapies.”

The emergence and spread of antibiotic resistant bacteria, such as MRSA, make such infections increasingly difficult, if not impossible, to treat.

This has led leading health organizations, such as the Centers for Disease Control and Prevention and the World Health Organization, to issue an urgent call for new approaches to combat the threat of antibiotic resistance.

Read the full article here.     
Posted January 19, 2017
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Two Molecular and Integrative Physiology Graduate Students Make Final Round of Graduate College’s Research Live! Competition

The competition draws entrants from across the College, and entrants are challenged to explain their graduate work in 3 minutes with only 2 slides. Presentations were scored on delivery, clarity, effectiveness of visual material, and accessibility of language.

Ms. Mapes’ presentation titled, “What Makes Breast Cancer Cells Grow?” focuses on elucidating the mechanisms by which hormones and growth factors control normal breast development and how they are disregulated in breast cancer.

“We have discovered a novel gene, called Cuzd1, that plays an essential role in breast development and is overexpressed in a subset of human breast tumors. This research has allowed for a better understanding the specific pathways that regulate the growth of the breast and enabled us to devise more targeted therapies to treat breast cancer,” she said.

Mapes entered Research Live! “because it seemed like it would be a fun challenge, and it certainly was. It is so important for the general public to understand the research being done at institutions like the University of Illinois and events like this are a great way to get both the graduate students and the community engaged in this process.”

Jessica Saw’s presentation, “Kidney Stones: Exposing Geology Within the Human Body,” explains that even though kidney stones are extremely common, the exact mechanisms of formation are still not understood.

“I presented our hypothesis of microbially-induced formation mechanisms in the kidney stone, showing evidence in high resolution microscopy and 16S rRNA gene sequencing results. Recognizing the similarities between environmental geology and biomineralization in our body, we are applying geological technique and concepts to this interdisciplinary work,” said Saw.

Saw entered the contest “because I really identified with the Research Live! concept. I’ve been to many talks where interesting topics were ruined by poor presenting, and it really shouldn’t be that way. There is a component of performance, and even entertainment, in presenting - it is important not to neglect that!”

Watch the Research Live! Presentations:

Janelle Mapes: What Makes Breast Cancer Cells Grow?

Jessica Saw: Kidney Stones: Exposing Geology Within the Human Body.

     
Posted December 16, 2016
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A study published in PNAS by Prof. Claudio Grosman and Dr. Gisela D. Cymes has revealed the elusive link between amino-acid sequence and charge selectivity in the superfamily of nicotinic acetylcholine receptors.

Among neurotransmitter-gated ion channels, the superfamily of pentameric ligand-gated ion channels (pLGICs) is unique in that its members display opposite permeant-ion charge selectivities despite sharing the same structural fold. Although much effort has been devoted to the identification of the mechanism underlying the cation-versus-anion selectivity of these channels, a careful analysis of past work reveals that discrepancies exist, that different explanations for the same phenomenon have often been put forth, and that no consensus view has yet been reached. Here, the authors present compelling evidence for the critical involvement of ionized side chains—whether pore-facing or buried—rather than backbone atoms and propose a mechanism whereby not only their charge sign, but also, their conformation determines charge selectivity.

Read the full article here.     
Posted November 02, 2016
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Dr. Ting Fu, a recently graduated MCB doctoral student from Prof. Jongsook Kemper's lab, has received the Salk Alumni award to support her postdoctoral research at Salk Institute.

     
Posted October 14, 2016
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MCB Faculty Named Directors of LAS Graduate Programs

Professor Satish Nair of the Department of Biochemistry has been appointed Director of the Center for Biophysics and Quantitative Biology. Professor Nair has been serving as Interim Director since November 2015.

The Center for Biophysics and Quantitative Biology serves physical and computer science students who are interested in applying their knowledge to biology, as well as students with a biological background interested in instrumentation, computation, and physical aspects of biology. The cooperation and cross-training of scientists with engineering, physical sciences, and life sciences backgrounds has infused biology with powerful technologies and exciting new paradigms. Close interactions between theory and experiments have led to fundamental advances in our understanding of the physical basis of life. Now biology is undergoing a transformation with application of modern computational methods and advanced experimental tools to solve problems of unprecedented complexity.

The Center for Biophysics and Quantitative Biology is interdisciplinary, consisting of over 40 faculty members who have their home departments in Biochemistry, Physics, Chemistry, Chemical Engineering, Bioengineering, Computer Engineering, Molecular and Integrative Physiology, Cell and Developmental Biology, Microbiology, and the Medical School. The Center serves as the interface between faculty research programs in experimental biophysics and quantitative and computational biology, with common interests in elucidating the physical basis of biological phenomena. The graduate degree program of the Center offers training in all aspects of this rapidly growing area.

Professor Martha Gillette of the Department of Cell and Developmental Biology has been appointed Director of the Neuroscience Program as of August 2015.

The Neuroscience Program is an interdisciplinary program of study and research leading to the doctoral degree. It offers a rigorous yet flexible program designed to foster the growth of the student through research activities, close interactions with the faculty, and exposure to top neuroscientists through seminars and attendance at professional meetings.

Recognizing that there are many paths to success in neuroscience, the program imposes few specific requirements. Students design their own programs leading to the Ph.D., with oversight by faculty committees ensuring appropriate depth and breadth of training.

The Neuroscience Program currently has over 85 affiliated faculty from more than 20 departments, and 70 students, studying the brain from a broad range of perspectives.

     
Posted September 27, 2016
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Force triggers gene expression by stretching chromatin

How genes in our DNA are expressed into traits within a cell is a complicated mystery with many players, the main suspects being chemical. However, a new study by University of Illinois researchers and collaborators in China has demonstrated that external mechanical force can directly regulate gene expression. The study also identified the pathway that conveys the force from the outside of the cell into the nucleus.

Identifying the ways mechanical forces send signals within cells has applications not only in fundamental cell biology, but also for cancer, stem cells and regenerative medicine, said mechanical science and engineering professor Ning Wang, who led the study with cell and developmental biology professor Andrew Belmont. The researchers published their work in the journal Nature Materials.

“Each cell in your body has the same DNA, but tissues behave very differently because genes are expressed differently,” Wang said. “There is so much we don’t know about gene expression. I think this work is the beginning to unravel some of the unknowns.”

Researchers have long known that forces, both external and internal, can affect cell behavior. But the question loomed as to whether the forces themselves triggered changes in gene expression, or if the forces triggered a chemical-signaling pathway within the cell.

“Cells only have two ‘senses’ to interact with their environment,” Wang said. “They cannot see or hear, but they can ‘feel’ mechanical forces and ‘taste’ chemical signals. Many studies have detailed chemical-signaling pathways, but it’s important to understand how the mechanical forces affect the cell as well. Mechanical signaling is as important as chemical signaling, and this study shows it’s a direct pathway.”

The researchers stuck tiny magnetic beads to proteins attached to the external membranes of hamster cells. They were able to change the direction and angle of the force the beads exerted while maintaining a consistent magnitude of the force, and found that the external force directly caused regions of chromatin in the nucleus to stretch out. Chromatin is the condensed DNA and protein mixture that makes up chromosomes. Using advanced imaging techniques, the researchers found an increase in transcription of the genes in the stretched regions.

“Work extending back decades has correlated chromosome decondensation with increased gene expression, but it has been extremely difficult to distinguish cause and effect,” Belmont said. “Does gene activity cause chromatin to decondense, or does decondensation actually drive increased gene expression? Here, we saw chromatin stretching directly drive increased gene expression, which provides a mechanically based mechanism for cells to sense their environment.”

The degree of stretching and therefore gene expression varied based on the direction of the force in relation to the cell’s cytoskeleton, the internal framework of protein tubes that supports the cell.

“The actin in the cytoskeleton forms bundles. When the force is perpendicular to the bundles, it’s like plucking violin strings,” Wang said. “It’s incredibly tense, and the signal is transferred through the cytoskeleton to the nucleus and stretches the chromatin. Doing it the other way, along the string direction, there isn’t much vibration, so a force of the same magnitude has less effect. The effect gets stronger the closer the angle gets to 90 degrees.”

The researchers were able to follow the force and identify the pathway that it travels along the cytoskeleton to the chromatin in the nucleus. Knowing the pathway is important, Wang said, because researchers can now explore mechanical signaling in more detail and perhaps develop ways to harness it for gene regulation or identify targets for cancer therapies.

For example, Wang’s group has published several studies detailing the unique mechanical properties of tumor-repopulating cells – cancer cells that evade standard drug therapies and tend to slip away to metastasize in new locations. He hopes that this study opens new avenues of attack to disable tumor-repopulating cells with fewer side effects than traditional cancer treatments.

Now that they’ve detailed how forces affect stretching of the chromatin, the researchers are beginning to look at how forces affect chromatin compression and what that means for gene expression. They are also probing further into other factors regulating gene expression when the chromatin is stretched.

“When we apply these forces, why are some genes activated while some are not? We think there are factors that inhibit, so that some genes are not ready to be force-activated,” Wang said.

The National Institutes of Health supported this work.

Story by Liz Ahlberg Touchstone, News Bureau
Photo by L. Brian Stauffer

Read the full article here.     
Posted August 26, 2016
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Unexpected function of nucleoporin RanBP2 maintains BA homeostasis, protecting against liver toxicity.

Link to full article.     
Posted August 01, 2016
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2016 MCB Convocation Address by Dr. Deborah A. Paul





Thank you Dr. Sligar for the invitation to speak at the convocation, and thank you graduates for graduating so that I could have the opportunity to come back to one of my favorite places. I’m sure that most of you are here today with friends & family that have supported you in reaching this achievement. I want to talk to you today about someone who supported me, my brother Tim.

I was the shy, introverted scientist; Tim was the extroverted, artistic type. He wrote stories and poetry, and was quite a musician – playing many different instruments, though excelling at piano. He could walk into a room full of strangers and make everyone his friend. He was younger than me, but he supported me in so many ways, for example:

1. He was my date for 10 year high school class reunion – since he knew all my friends anyway;

2. He went with me when, in my mid-twenties, I was able to buy my 1st pair of toe shoes – having taken up ballet, which I always loved, a bit late in life. He knew how much it meant to me to have achieved this, and he wanted to be there.

3. He was also one of my biggest boosters for going back to get my PhD. After I had received my Masters in Biology here at Illinois, I wanted to go on for a PhD but I didn’t know what area of science I wanted to focus on. So I took a job at Abbott working on the Development side of R & D in Diagnostics, working on tests to detect Hepatitis B infection. After working a few years, I decided what I wanted to do for a PhD and took a leave of absence from Abbott to go back to grad school – combining biochemistry, virology and immunology to study Hepatitis B. Tim was so proud, and would introduce me as “my sister who’s working on her PhD.”

A few weeks before I left for grad school, Tim ended up in the hospital. He hadn’t been feeling well, and all of the lymph nodes all over his body had become enlarged. They ran all sorts of tests, but never figured out the problem. He started feeling better and was released.

A few years passed, and I was working on finishing up my PhD when I got the call that Tim had developed Pneumocystis carinii pneumonia – a type of pneumonia typically only found in immunosuppressed people. The doctors said this was consistent with a new disease that was popping up around the country – AIDS. Two weeks in ICU and a month in the hospital later, Tim survived the pneumonia that killed the majority of AIDs patients, but a few months later he developed cancer and started chemotherapy.

As I was finishing my PhD at this time, I had to decide what I wanted to do next. They had recently discovered the virus that causes AIDS – HIV, and Abbott was one of 5 companies that was to receive viral cultures from NIH to work on tests to protect the blood supply. All my work on Hepatitis B was the perfect set up to work on HIV – and I obviously had a lot of personal reasons to want to work on this virus. So I returned to Abbott, now in the research department, to do research for diagnostics tests for HIV. Unfortunately, Tim died 1 month later; he was 28 years old.

The other people in the department had already started work on an HIV Ab test that would be used to protect blood supply. I wanted to develop a test for the virus itself, and see if it was circulating in the bloodstream – even though the prevailing school of thought was that this would not be the case. I developed an ultrasensitive immunoassay and was able to demonstrate that HIV was indeed present in the bloodstream at various times throughout the disease, and this was significant because you could then:

1. Detect initial infection, which would have been useful for Tim’s 1st hospitalization when they could not determine what was wrong with him.

2. Detect viral re-emergence - since most patients, after becoming infected, entered an asymptomatic phase; but later something would trigger the virus to begin reproducing, which was a poor prognostic indicator, usually signaling the start of AIDS related diseases.

3. Monitor therapy – initial therapies were nucleoside analogues, and you could determine if the therapy was working by watching whether the level of circulating virus declined. However, most people also eventually developed drug resistance, so through monitoring for rising viral levels, you would then know to switch to a different therapy.

Abbott also had a Pharmaceutical division, and they were using computer-assisted drug design to develop small molecules that would inhibit the active site of the viral protease. However they needed a way to know which compounds were working. So we collaborated with them – since we were growing virus in culture and monitoring our cultures with the test I developed. We looked for compounds that would kill the virus in culture but leave the human cells healthy. This led to the initial protease inhibitors that were FDA approved and marketed. Though they were not in time for Tim, they changed the tide in the war against HIV infection so that AIDS was not a death sentence but a disease you could live with.

I spent 15 more years in the lab working on HIV and Hepatitis, then moved to business-side of things – though still supporting the work on HIV and Hepatitis. Later this also included work on the next generation nucleic acid tests using PCR to detect HIV, Hepatitis and other infectious diseases.

My career success then enabled me to honor Tim’s memory and his support of me by providing support to others through endowing a chair that will reside in the School of Molecular and Cellular Biology, with a joint appointment in the new College of Medicine, in the field of Infectious Disease and Immunology, in Tim’s name. I cannot tell you how happy it makes me to be able to do this.

In closing I would like to leave you with these thoughts: Do something that means something to you; that you are passionate about. If you do that, it will, by definition, make you personally successful. When you are able to, honor the support that you have received to achieve that success by giving back – and continue the circle of support.

Now – Go do great things ! Thank you.

~~ Deborah A. Paul, Ph.D. received her Masters in Biology from the University of Illinois in 1979.

     
Posted June 14, 2016
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Emad Tajkhorshid receives Department of Defense Multidisciplinary University Research Initiative grant

In all, the Department of Defense awarded 23 studies a total of $162 million over the next five years for experimentation and analysis. Selected studies will benefit one of the Army Research Office, the Air Force Office of Scientific Research, or the Office of Naval Research.

“Over the past 30 years, the DoD’s MURI program has resulted in significant capabilities for our military forces and opened up entirely new lines of research,” Melissa L. Flagg, deputy assistant secretary of defense for research, said in a press release. “Examples include advances in laser frequency combs that have become the gold standard in frequency control for precision in navigation and targeting; atomic and molecular self-assembly projects that have opened new possibilities for nano-manufacturing; and the field of spintronics, which emerged from a MURI award on magnetic materials and devices research.”

LAS faculty receive Department of Defense grants     
Posted June 12, 2016
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