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Universal Paid Sick Leave Reduces Spread of Flu, According to Pitt Simulation

Posted by andrewsj3 on Thursday, June 13th 2013     
PITTSBURGH, June 13, 2013 – Allowing all employees access to paid sick days would reduce influenza infections in the workplace, according to a first-of-its-kind analysis by University of Pittsburgh Graduate School of Public Health modeling experts.
The researchers simulated an influenza epidemic in Pittsburgh and surrounding Allegheny County and found that universal access to paid sick days would reduce flu cases in the workplace by nearly 6 percent and estimated it to be more effective for small, compared to large, workplaces. The results are reported in the online version of the American Journal of Public Health and will be in the August print issue.
“The Centers for Disease Control and Prevention recommends that people with flu stay home for 24 hours after their fever breaks,” said lead author Supriya Kumar, Ph.D., M.P.H., a post-doctoral associate in Pitt Public Health’s Department of Epidemiology. “However, not everyone is able to follow these guidelines. Many more workers in small workplaces than in large ones lack access to paid sick days and hence find it difficult to stay home when ill. Our simulations show that allowing all workers access to paid sick days would reduce illness because fewer workers get the flu over the course of the season if employees are able to stay home and keep the virus from being transmitted to their co-workers.”
In addition to investigating the impact of universal access to paid sick days, Dr. Kumar and her colleagues looked at an alternative intervention they termed “flu days,” in which all employees had access to one or two paid days to stay home from work and recover from the flu. The idea behind flu days is that they encourage employees to stay home longer than they currently do, thus reducing the potential for them to transmit illness to colleagues at work.
Giving employees one flu day resulted in more than a 25 percent decrease in influenza infections due to workplace transmission. A two flu-day policy resulted in a nearly 40 percent decrease. The researchers found that flu days were more effective for larger workplaces, defined as having 500 or more employees.
Dr. Kumar and her colleagues used a modeling system developed at Pitt Public Health called “Framework for Reconstructing Epidemic Dynamics” (FRED), which is part of work housed in Pitt’s Modeling of Infectious Disease Agents Study (MIDAS) National Center of Excellence. MIDAS was initiated by the National Institute of General Medical Sciences to investigate novel computational and mathematical models of existing and emerging infectious diseases.
“Our mission is to protect the U.S. and the global community against communicable infectious disease threats,” said senior authorDonald S. Burke, M.D., Pitt Public Health dean and UPMC-Jonas Salk Chair of Global Health. “Our modeling work allows scientists both here and worldwide to investigate strategies to minimize epidemics. At the heart of this effort is free, open data sharing.”
“These findings make a strong case for paid sick days,” said Dr. Kumar. “Future research should examine the economic impacts of paid sick-day policies.”
Additional authors of this study include John J. Grefenstette, Ph.D., David Galloway, M.S., and Steven M. Albert, Ph.D., all of Pitt Public Health.
This work was supported by the National Institute of General Medical Sciences grant U54GM088491.
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Pitt-led Team Describes Molecular Detail of HIV’s Inner Coat, Pointing the Way to New Therapies

Posted by andrewsj3 on Wednesday, May 29th 2013     
PITTSBURGH, May 29, 2013 – A team led by researchers at the University of Pittsburgh School of Medicine has described for the first time the 4-million-atom structure of the HIV’s capsid, or protein shell. The findings, highlighted on the cover of the May 30 issue of Nature, could lead to new ways of fending off an often-changing virus that has been very hard to conquer.
Scientists have long struggled to decipher how the HIV capsid shell is chemically put together, said senior author Peijun Zhang, Ph.D., associate professor, Department of Structural Biology, University of Pittsburgh School of Medicine.
“The capsid is critically important for HIV replication, so knowing its structure in detail could lead us to new drugs that can treat or prevent the infection,” she said. “This approach has the potential to be a powerful alternative to our current HIV therapies, which work by targeting certain enzymes, but drug resistance is an enormous challenge due to the virus’ high mutation rate.”
Previous research has shown that the cone-shaped shell is composed of identical capsid proteins linked together in a complex lattice of about 200 hexamers and 12 pentamers, Dr. Zhang said. But the shell is non-uniform and asymmetrical; uncertainty remained about the exact number of proteins involved and how the hexagons of six protein subunits and pentagons of five subunits are joined. Standard structural biology methods to decipher the molecular architecture were insufficient because they rely on averaged data, collected on samples of pieces of the highly variable capsid to identify how these pieces tend to go together.
Instead, the team used a hybrid approach, taking data from cryo-electron microscopy at an 8-angstrom resolution (a hydrogen atom measures 0.25 angstrom) to uncover how the hexamers are connected, and cryo-electron tomography of native HIV-1 cores, isolated from virions, to join the pieces of the puzzle. Collaborators at the University of Illinois then used their new Blue Waters supercomputer to run simulations at the petascale, involving 1 quadrillion operations per second, that positioned 1,300 proteins into a whole that reflected the capsid’s known physical and structural characteristics.
The process revealed a three-helix bundle with critical molecular interactions at the seams of the capsid, areas that are necessary for the shell’s assembly and stability, which represent vulnerabilities in the protective coat of the viral genome.
“The capsid is very sensitive to mutation, so if we can disrupt those interfaces, we could interfere with capsid function,” Dr. Zhang said. “The capsid has to remain intact to protect the HIV genome and get it into the human cell, but once inside it has to come apart to release its content so that the virus can replicate. Developing drugs that cause capsid dysfunction by preventing its assembly or disassembly might stop the virus from reproducing.”
The project was funded by National Institutes of Health grants GM082251, GM085043 and GM104601 and the National Science Foundation.
“By using a combination of experimental and computational approaches, this team of investigators has produced a clearer picture of the structure of HIV’s protective covering,” said the National Institutes of Health’s Michael Sakalian, Ph.D., who oversees this and other grants funded through an AIDS-related structural biology program. “The new structural details may reveal vulnerabilities that could be exploited by future therapeutics.”
Co-authors include Gongpu Zhao, Ph.D., Xin Meng, Ph.D., Jiying Ning, Ph.D., Jinwoo Ahn, Ph.D., and Angela M. Gronenborn, Ph.D., all of the University of Pittsburgh; Juan R. Perilla, Ph.D., and Klaus Schulten, Ph.D., of the University of Illinois at Urbana-Champaign; Ernest L. Yufenyuy, Ph.D., and Christopher Aiken, Ph.D., of Vanderbilt University School of Medicine; and Bo Chen, Ph.D., of theUniversity of Central Florida, in Orlando.
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Pitt Researchers Find Immune Cells May Play Previously Unrecognized Role in Inflammation in HIV/AIDS

Posted by andrewsj3 on Tuesday, May 28th 2013     
PITTSBURGH, May 28, 2013 – Depleted numbers of a specific type of white blood cell in the immune systems of people infected with HIV/AIDS appear to be associated with increased levels of unchecked and often damaging inflammation in the body, University of Pittsburgh researchers have discovered.
The low numbers of white blood cells, known as CD4+CD73+ T cells – named for the expression of certain proteins and enzymes on their surface, persist even when HIV is well-controlled with medications. The results of the National Institutes of Health-funded study, now available online, will be reported in an upcoming issue of the journal AIDS.
“People with well-controlled HIV have been shown to have higher rates of chronic, non-AIDS-related diseases, such as cardiovascular disease. This is believed to be related to the persistent immune activation and inflammation associated with chronic HIV-1 infection,” said corresponding author Bernard J.C. Macatangay, M.D., Division of Infectious Diseases/HIV/AIDS Program, Pitt School of Medicine. “We believe that the depleted CD4+CD73+ T cells may play an important role in this inflammation.”
The study included men from the Pittsburgh Multicenter AIDS Cohort Study, an investigation of the natural history of HIV infection in gay and bisexual men. Blood samples were analyzed from 36 men positive for HIV, some who had consistently taken a medication regimen to suppress the virus and some who had not, along with 10 HIV-negative controls.
The body has ways to decrease and control inflammation through different regulatory mechanisms. One of these is through the production of adenosine, a biochemical compound that may have anti-inflammatory properties. CD73 is an enzyme that is important in the production of adenosine. In the HIV-positive men, the study found that the CD4+CD73+ T cells are depleted and, despite treatment, do not increase to levels seen in uninfected individuals. The Pitt researchers found an association between the low levels of CD4+CD73+ T cells and higher levels of immune activation and inflammation in the study participants.
“This inflammation issue is similar to that seen in cancer patients,” said co-author Theresa Whiteside, Ph.D., professor of pathology, immunology and otolaryngology at Pitt’s School of Medicine and a member of Pitt’s Cancer Institute. “The suppression pathways we explore in this study have similarities to those that we have recently linked to immune suppression in cancer.”
Scientists are not sure why this pathway remains disrupted in people with very well-controlled HIV. One hypothesis is that HIV-positive patients do not completely recover from damage done during the first few weeks of infection in their gut lining, which hosts the body’s largest population of immune cells.
“Significant damage occurs very early in infection, while they are still asymptomatic and do not even know they have the virus,” said Dr. Macatangay. “This is why it is important that we continue to examine the role of CD4+CD73+ T cells and adenosine in increased inflammation among HIV/AIDS patients and look for ways to repair the damage to the natural pathways by which these cells act.”
Additional study co-authors include Patrick J. Schuler, M.D., Ph.D., of the University of Ulm in Germany; Zenichiro Saze, M.D., Ph.D., Edwin K. Jackson, Ph.D., Sharon A. Riddler, M.D., Benedict B. Hilldorfer and John W. Mellors, M.D., all of Pitt’s School of Medicine; and William G. Buchanan, M.M., and Charles R. Rinaldo, Ph.D., both of Pitt’s Graduate School of Public Health.
This study was supported by National Institutes of Health grants PO1 CA109668, U01 AI035041, DK079307, T32 AI065380, and HHSN261200800001E.
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Pitt Team Finds Biologic Mechanism That Causes Noise-Induced Tinnitus and Drug That Can Prevent It

Posted by andrewsj3 on Monday, May 27th 2013     
PITTSBURGH, May 27, 2013 – An epilepsy drug shows promise in an animal model at preventing tinnitus from developing after exposure to loud noise, according to a new study by researchers at the University of Pittsburgh School of Medicine. The findings, reported this week in the early online version of the Proceedings of the National Academy of Sciences, reveal for the first time the reason the chronic and sometimes debilitating condition occurs.
An estimated 5 to 15 percent of Americans hear whistling, clicking, roaring and other phantom sounds of tinnitus, which typically is induced by exposure to very loud noise, said senior investigator Thanos Tzounopoulos, Ph.D., associate professor and member of the auditory research group in the Department of Otolaryngology, Pitt School of Medicine.
“There is no cure for it, and current therapies such as hearing aids don’t provide relief for many patients,” he said. “We hope that by identifying the underlying cause, we can develop effective interventions.”
The team focused on an area of the brain that is home to an important auditory center called the dorsal cochlear nucleus (DCN). From previous research in a mouse model, they knew that tinnitus is associated with hyperactivity of DCN cells — they fire impulses even when there is no actual sound to perceive. For the new experiments, they took a close look at the biophysical properties of tiny channels, called KCNQ channels, through which potassium ions travel in and out of the cell.
“We found that mice with tinnitus have hyperactive DCN cells because of a reduction in KCNQ potassium channel activity,” Dr. Tzounopoulos said. “These KCNQ channels act as effective “brakes” that reduce excitability or activity of neuronal cells.”
In the model, sedated mice are exposed in one ear to a 116-decibel sound, about the loudness of an ambulance siren, for 45 minutes, which was shown in previous work to lead to the development of tinnitus in 50 percent of exposed mice. Dr. Tzounopoulos and his team tested whether an FDA-approved epilepsy drug called retigabine, which specifically enhances KCNQ channel activity, could prevent the development of tinnitus. Thirty minutes into the noise exposure and twice daily for the next five days, half of the exposed group was given injections of retigabine.
Seven days after noise exposure, the team determined whether the mice had developed tinnitus by conducting startle experiments, in which a continuous, 70 dB tone is played for a period, then stopped briefly and then resumed before being interrupted with a much louder pulse. Mice with normal hearing perceive the gap in sounds and are aware something had changed, so they are less startled by the loud pulse than mice with tinnitus, which hear phantom noise that masks the moment of silence in between the background tones.
The researchers found that mice that were treated with retigabine immediately after noise exposure did not develop tinnitus. Consistent with previous studies, 50 percent of noise-exposed mice that were not treated with the drug exhibited behavioral signs of the condition.
“This is an important finding that links the biophysical properties of a potassium channel with the perception of a phantom sound,” Dr. Tzounopoulos said. “Tinnitus is a channelopathy, and these KCNQ channels represent a novel target for developing drugs that block the induction of tinnitus in humans.”
The KCNQ family is comprised of five different subunits, four of which are sensitive to retigabine. He and his collaborators aim to develop a drug that is specific for the two KCNQ subunits involved in tinnitus to minimize the potential for side effects.

“Such a medication could be a very helpful preventive strategy for soldiers and other people who work in situations where exposure to very loud noise is likely,” Dr. Tzounopoulos said. “It might also be useful for other conditions of phantom perceptions, such as pain in a limb that has been amputated.”

Co-authors of the paper are Shuang Li and Veronica Choi, both of Pitt’s Department of Otolaryngology. The project was funded by U.S. Department of Defense grant PR0934050, National Institutes of Health/National Institute on Deafness and Other Communication Disorders grant DC007905, UPMC and The Eye and Ear Foundation of Pittsburgh.

 

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Drug Reverses Alzheimer’s Disease Deficits in Mice, Pitt Research Confirms

Posted by andrewsj3 on Friday, May 24th 2013     
PITTSBURGH, May 23, 2013 – An anti-cancer drug reverses memory deficits in an Alzheimer’s disease mouse model, University of Pittsburgh Graduate School of Public Health researchers confirm in the journal Science.
 
The research, funded by the National Institutes of Health’s National Institute on Aging and Alzheimer’s Association, reviewed previously published findings on the drug bexarotene, approved by the U.S. Food and Drug Administration for use in cutaneous T cell lymphoma. The Pitt Public Health researchers were able to verify that the drug does significantly improve cognitive deficits in mice expressing gene mutations linked to human Alzheimer’s disease, but could not confirm the effect on amyloid plaques.
 
“We believe these findings make a solid case for continued exploration of bexarotene as a therapeutic treatment for Alzheimer’s disease,” said senior author Rada Koldamova, M.D., Ph.D., associate professor in Pitt Public Health’s Department of Environmental and Occupational Health.
 
Dr. Koldamova and her colleagues were studying mice expressing human Apolipoprotein E4 (APOE4), the only established genetic risk factor for late-onset Alzheimer’s disease, or APOE3, which is known not to increase the risk for Alzheimer’s disease, when a Case Western Reserve University study was published last year stating that bexarotene improved memory and rapidly cleared amyloid plaques from the brains of Alzheimer’s model mice expressing mouse Apolipoprotein E (APOE). Amyloid plaques consist of toxic protein fragments called amyloid beta that seem to damage neurons in the brain and are believed to cause the associated memory deficits of Alzheimer’s disease and, eventually, death.
 
Bexarotene is a compound chemically related to vitamin A that activates Retinoic X Receptors (RXR) found everywhere in the body, including neurons and other brain cells. Once activated, the receptors bind to DNA and regulate the expression of genes that control a variety of biological processes. Increased levels of APOE are one consequence of RXR activation by bexarotene. The Pitt researchers began studying similar compounds a decade ago.
 
“We were already set up to repeat the Case Western Reserve University study to see if we could independently arrive at the same findings,” said co-author Iliya Lefterov, M.D., Ph.D., associate professor in Pitt Public Health’s Department of Environmental and Occupational Health. “While we were able to verify that the mice quickly regained their lost cognitive skills and confirmed the decrease in amyloid beta peptides in the interstitial fluid that surrounds brain cells, we did not find any evidence that the drug cleared the plaques from their brains.”
 
The Pitt researchers postulate that the drug works through a different biological process, perhaps by reducing soluble oligomers which, like the plaques, are composed of the toxic amyloid beta protein fragments. However, the oligomers are composed of smaller amounts of amyloid beta and, unlike the plaques, are still able to “move.”
 
“We did find a significant decrease in soluble oligomers,” said Dr. Koldamova. “It is possible that the oligomers are more dangerous than the plaques in people with Alzheimer’s disease. It also is possible that the improvement of cognitive skills in mice treated with bexarotene is unrelated to amyloid beta and the drug works through a completely different, unknown mechanism.”
 
In the Pitt experiments, mice with the Alzheimer’s gene mutations expressing human APOE3 or APOE4 were able to perform as well in cognitive tests as their non-Alzheimer’s counterparts 10 days after beginning treatment with bexarotene. These tests included a spatial test using cues to find a hidden platform in a water maze and a long-term memory test of the mouse’s ability to discriminate two familiar objects following introduction of a third, novel object.
 
Bexarotene treatment did not affect the weight or general behavior of the mice. The drug was equally effective in male and female mice.
 
First author on this study, Nicholas F. Fitz, Ph.D., and co-author Andrea A. Cronican, Ph.D., both of Pitt Public Health.
 
This work was supported by NIH grants R01AG037481, R01AG037919, R21ES021243 and F32AG034031 and the Alzheimer’s Association.
 
More information, including a copy of the paper, can be found online in the Science press package. A user ID and password are required to access this information.
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AGA Award Given to Fellow From the Division of Gastroenterology, Hepatology, and Nutrition

Posted by UPMC Physician Resources on Thursday, May 23rd 2013     

Jana Al Hashash, MD, a Year III gastroenterology fellow with the Division of Gastroenterology, Hepatology and Nutrition, has been awarded a 2013 American Gastroenterological Association (AGA)-Horizon Pharma Fellow Abstract Prize from the AGA Research Foundation.

Dr. Al Hashash will receive this honor at the 2013 Digestive Disease Week (DDW) international GI research meeting in May 2013. This award will be presented in recognition of her DDW Research Forum oral presentation in the Confocal Endomicroscopy, Enhanced Endoscopy, and Other Emerging Technologies II session, Nuclear Nano-Morphology Markers from Rectal Tissue Predict Colonic Dysplasia/Neoplasia in Ulcerative Colitis Patients. Dr. Al Hashash’s sponsor for this project is Miguel D. Regueiro, MD.

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Experts to Present at Digestive Disease Week 2013

Posted by UPMC Physician Resources on Monday, May 20th 2013     

Experts from the Division of Gastroenterology, Hepatology, and Nutrition will have a strong presence at Digestive Disease Week 2013, with UPMC physicians and researchers making 16 oral presentations and 35 poster presentations. Preview of the key findings to be presented at the conference:

Uncontrolled Therapeutic Observations in IBD

Confocal Endomicroscopy, Enhanced Endscopy, and Other Emerging Technologies II

Upper GI Small Bowel Imaging: Polyps, Biopsies, Endoscopy Histology

Nutrient Digestion, Absorption, and Metabolism

Are you attending DDW?

To learn more about our clinical programs, research efforts, and fellowship opportunities, visit us at DDW booth 1533, May 18 to 21.

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Pitt Transplant Experts Challenge Assumption, Describe Biological Pathway That Leads To Organ Rejection

Posted by andrewsj3 on Wednesday, May 15th 2013     
PITTSBURGH, May 15, 2013 – Transplant researchers at the University of Pittsburgh School of Medicine challenge a long-held assumption about how biologic pathways trigger immune system rejection of donor organs in a report published online today in the Journal of Clinical Investigation. Their study, sponsored by the National Institutes of Health, suggests a different paradigm is needed to develop better anti-rejection therapies.
Immune system troops called T-cells migrate to transplanted organs, fighting the foreign tissue, explained senior author Fadi Lakkis, M.D., Frank & Athena Sarris Chair in Transplantation Biology, professor of surgery, Pitt School of Medicine, and scientific director of theThomas E. Starzl Transplantation Institute. Until now, scientists have thought these T-cells were beckoned to the site by chemokines, proteins secreted by cells in the lining of the blood vessels, or endothelium, of the organ when it becomes inflamed.
“The prevailing view was that when the endothelium gets inflamed, it gets a little sticky, so T-cells that are zipping by in the bloodstream begin to slow down and bind to chemokines that trigger their arrest and migration into the affected tissue,” Dr. Lakkis said. “We decided to test that hypothesis and found out to everyone’s surprise that’s not the way it works.”
If the chemokine receptors on T-cells were blocked, the researchers reasoned, the cascade of immune events would not happen, stalling rejection. So two days after mice received a heart or kidney transplant, they received T-cells treated with pertussis toxin, which irreversibly binds to a key molecule in the receptor to inhibit its activity, and presumably prevent the migration of memory and effector T-cells already sensitized to recognize the foreign proteins of the donor tissue.
Using a technique called two-photon microscopy, which allows real-time visualization of living tissue, they found that pertussis-treated T-cells invaded the donor organs just as they did if they were untreated, leading to organ rejection.
“This showed us that chemokines are not necessary to start the rejection response,” Dr. Lakkis said. “So then we wondered which cells were sounding the alarm to the immune system.”
The sophisticated microscopy technique revealed that  the donor kidney’s dendritic cells, which identify antigens or foreign proteins and present them on their cell surfaces to be recognized by other immune cells, “stick their feet,” as Dr. Lakkis put it, in the bloodstream, thereby exposing donor surface antigens to the recipient’s immune system.
“So, anti-rejection therapies that target chemokine responses have very little effect,” he said. “But novel drugs that interfere with antigen presentation by the endothelium or the dendritic cells could be very helpful.”
Co-authors include lead author and M.D./Ph.D. student Jeff Walch, and researchers from the Starzl Transplantation Institute and the departments of Surgery, Immunology and Medicine at Pitt School of Medicine; and Yale University School of Medicine.
The project was funded by NIH grants AI064343, AI049466 and AI74490.
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UPMC Launches First-Ever Gastrointestinal Dermatology Clinic

Posted by andrewsj3 on Monday, May 13th 2013     
PITTSBURGH, May 13, 2013 – Today, UPMC opened the nation’s first-ever gastrointestinal dermatology clinic to provide coordinated care to inflammatory bowel disease (IBD) and celiac disease patients with associated dermatologic conditions.
Up to 30 percent of patients with IBD and celiac disease have cutaneous (skin-related) manifestations of their disease, yet until now there has not been a specialty clinic devoted specifically to these patients.
IBD, which affects as many as 1.4 million people in the U.S., primarily includes Crohn’s disease and ulcerative colitis. Crohn’s is a severe and chronic disease that causes inflammation, ulcers and bleeding in the digestive tract. Crohn’s often affects the end portion of the small intestine, but can affect any part of the gastrointestinal tract. Ulcerative colitis is another type of IBD which affects the colon (large intestine) and rectum. IBD differs from irritable bowel syndrome, which does not cause ulcers or inflammation and does not damage the bowel. Celiac disease is a digestive disorder which damages the small intestine and interferes with the absorption of nutrients from food. People with celiac cannot tolerate gluten, a protein found in wheat, barley and rye.
The clinic, located on the fifth floor of the Falk Medical Building in the Oakland area of Pittsburgh, will initially be open the first Monday of each month, though hours may change depending on demand. Patients must first be referred from UPMC-based gastroenterology departments.
“This is a novel service that we can provide to our patients,” said Lisa Grandinetti, M.D., assistant professor of dermatology at theUniversity of Pittsburgh and dermatologist at UPMC, who will be leading the new clinic. “We’re excited to open the first-ever specialty clinic to address the needs of IBD patients.”
Dermatologic manifestations of gastrointestinal (GI) diseases can occur as both the skin and the GI tract can be affected by the same conditions. Making the correct diagnosis of these conditions requires the ability of physicians to recognize the dermatological presentations of certain GI diseases. For example, dermatitis herpetiformis, or severely itchy small blisters on the elbows, knees and buttocks, is diagnostic for the GI condition known as celiac disease.
Other conditions that will be addressed by this clinic include, but are not limited to:

 

  • Erythema nodosum
  • Pyoderma gangrenosum
  • Aphthous ulcers/aphthous stomatitis
  • Dermatitis herpetiformis and celiac disease
  • TNFα associated psoriasiform dermatoses
  • Nutritional deficiency dermatoses

Dr. Grandinetti joined UPMC in 2009, and has since been receiving referrals from gastroenterologists for patients with IBD who have skin-related problems. Her interest in cutaneous manifestations of GI disease began after medical school, during her residency at the Cleveland Clinic.

“I saw firsthand how patients’ quality of life was significantly affected by their skin condition, often when their GI disease was under control,” noted Grandinetti. “With time, experience and a growing number of patients with cutaneous manifestations of GI diseases, I felt it was a good time to create a specialized clinic that would provide dermatologic and gastroenterologic coordinated care to patients with IBD and other GI issues.”

 

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