Insights into Parkinson's balance problems

In PD, disorganized sensorimotor signals cause muscles in the limbs to contract, such that both a muscle promoting a motion and its antagonist muscle are Read more

Cajoling brain cells to dance

“Flicker” treatment is a striking non-pharmaceutical approach aimed at slowing or reversing Alzheimer’s disease. It represents a reversal of EEG: not only recording brain waves, but reaching into the brain and cajoling cells to dance. One neuroscientist commentator called the process "almost too fantastic to believe." With flashing lights and buzzing sounds, researchers think they can get immune cells in the brain to gobble up more amyloid plaques, the characteristic clumps of protein seen in Read more

Research

Blood biomarkers may help predict risk in stroke and TBI


Biomarkers circulating in the bloodstream may serve as a predictive window for recurrent stroke risk and also help doctors accurately assess what is happening in the brains of patients with acute traumatic brain injury (TBI).

Michael Frankel, MD

Researchers at Emory University School of Medicine, led by principal investigator Michael Frankel, MD, Emory professor of neurology and director of Grady Memorial Hospital’s Marcus Stroke & Neuroscience Center, are studying biomarkers as part of two ancillary studies of blood samples using two grants from the National Institutes of Health.

In the $1.47 million, four-year grant called “Biomarkers of Ischemic Outcomes in Intracranial Stenosis” (BIOSIS), Emory researchers are analyzing blood samples from 451 patients from around the country who were enrolled in a study known as SAMMPRIS (Stenting and Aggressive Medical Management for Preventing Recurrent stroke in Intracranial Stenosis), the first randomized, multicenter clinical trial designed to test whether stenting intracranial arteries would prevent recurrent stroke.

Researchers in the SAMMPRIS study recently published their results in the New England Journal of Medicine, showing that medical management was more effective than stenting in preventing recurrent strokes in these patients. Frankel’s BIOSIS research team is using blood samples from these same patients to continue learning more about the molecular biology of stroke to predict risk of a stroke occurring in the future.

“Our goal is to learn more about stroke by studying proteins and cells in the blood that reflect the severity of disease in arteries that leads to stroke. If we can test blood samples for proteins and cells that put patients at high risk for stroke, we can better tailor treatment for those patients,” says Frankel.

Patients with narrowed brain arteries, known as intracranial stenosis, have a particularly high risk of disease leading to stroke. At least one in four of the 795,000 Americans who have a stroke each year will have another stroke within their lifetime. Within five years of a first stroke, the risk for another stroke can increase more than 40 percent. Recurrent strokes often have a higher rate of death and disability because parts of the brain already injured by the original stroke may not be as resilient.

The other study, “Biomarkers of Injury and Outcome in ProTECT III” (BIO-ProTECT)” is a $2.6 million, five-year NIH grant in which Frankel’s team will use blood to determine what is happening in the brain of patients with acute TBI.  The blood samples are from patients enrolled in the multicenter clinical trial ProTECT III (Progesterone for Traumatic brain injury, Experimental Clinical Treatment), led by Emory Emergency Medicine Professor, David Wright, MD, to assesses the use of progesterone to treat TBI in 1,140 patients at 17 centers nationwide.

In the BIO-ProTECT study, Emory is collaborating with the Medical University of South Carolina, the University of Pittsburgh, the University of Michigan and Banyan Biomarkers.

TBI is the leading cause of death and disability among young adults in the US and worldwide. According to the Centers for Disease Control and Prevention, approximately 1.4 million Americans sustain a traumatic brain injury each year, leading to 275,000 hospitalizations, 80,000 disabilities, and 52,000 deaths.

Acute TBI leads to a cascade of cellular events set in motion by the initial injury that ultimately lead to cerebral edema (swelling of the brain), cellular disruption and sometimes death. Tissue breakdown leads to the release of proteins into the bloodstream. These proteins may serve as useful biomarkers of the severity of the injury and perhaps provide useful information about response to treatment.

Using the large patient group in the ProTECT III trial, the researchers hope to validate promising TBI biomarkers as predictors of clinical outcome and also evaluate the relationship between progesterone treatment, biomarker levels and outcome.

“If we can better determine the amount of brain injury with blood samples, we can use blood to help doctors better assess prognosis for recovery, and, hopefully whether a patient will respond to treatment with progesterone,” says Frankel.

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Redirecting beta-amyloid production in Alzheimer’s

Pharmacologist Thomas Kukar is exploring a strategy to subtly redirect the enzyme that produces beta-amyloid, which makes up the plaques appearing in the brains of Alzheimer’s patients.

Thomas Kukar, PhD

Preventing beta-amyloid production could be an ideal way to head off Alzheimer’s, but the reason why a subtle approach is necessary was illustrated last year by disappointing results from a phase III clinical trial. The experimental drug semagacestat was designed to block the enzyme gamma-secretase, which “chomps” on the amyloid precursor protein (APP), usually producing an innocuous fragment but sometimes producing toxic beta-amyloid.

Gamma-secretase also is involved in processing a bunch of other vital proteins, such as Notch, central to an important developmental signaling pathway. Scientists suspect that this is one of the reasons why trial participants who received semagacestat did worse on cognitive/daily function measures than controls and saw an increase in skin cancer, leading watchdogs to halt the study.

While a postdoc at Mayo Clinic Jacksonville and working with Todd Golde and Edward Koo, Kukar identified compounds – gamma-secretase modulators or GSM’s — that may offer an alternative.

“We are looking at a strategy that’s different from global gamma-secretase inhibition,” he says. “The approach is: don’t inhibit the enzyme overall, but instead modify its activity so that it makes less toxic products.”

Gamma-secretase chomps on amyloid precursor protein, and how it does so determines whether toxic beta-amyloid is produced. It also processes several other proteins important for brain function.

This line of inquiry started when it was discovered that some anti-inflammatory drugs also could reduce beta-amyloid production. Then, the crosslinkable probes Kukar was using to identify which part of the gamma-secretase fish was doing the chomping ended up binding the bait (APP). This suggested that drugs might be able to change how the enzyme acts on one protein, APP, but not others.

Now an assistant professor at Emory, he is examining in greater detail how gamma-secretase modulators work. Two recent papers he co-authored in Journal of Biological Chemistry show 1) how the proteins that gamma-secretase chews up are “anchored” in the membrane and 2) how selective GSM’s can be on amyloid precursor protein.

Although clinical studies of a “first generation” GSM, tarenflurbil, were also stopped after negative results, Kukar says GSM’s still haven’t really been tested adequately, since researchers do not know if the drugs are really having an effect on beta-amyloid levels in the brain. Newer compounds coming through the pharmaceutical pipeline are more potent and more able to get into the brain. While looking for more potent GSM’s is critical, Kukar says it’s equally as important to understand how gamma-secretase works to understand its biology.

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Blue pill or red pill? Brains need both for memory consolidation

In the 1999 film The Matrix, the character Neo is offered a choice between a blue pill (to forget) and a red pill (to remember). If only neuroscience was that simple! It may be that neurons need both red and blue, possibly an elaborate dance of molecules, for a fragile memory to lodge itself in the brain.

Neuroscientists Kimberly Maguschak and Kerry Ressler provide a glimpse into this process with their recent paper in the Journal of Neuroscience.

Ressler is both a psychiatrist and a Howard Hughes Medical Institute-supported researcher with a laboratory at Yerkes National Primate Research Center. Maguschak completed her doctorate at Emory and is now a postdoc with Guoping Feng at MIT.

The research is a follow-up on their work probing the role of beta-catenin in fear memory formation. We previously described this protein as acting “like a Velcro strap”, attaching cells’ internal skeletons to proteins on their external membranes that help them adhere to other cells. If brain cells need to change shape and form new connections for memories to be consolidated, we can see how this kind of molecule would be important.

Beta-catenin is also central to a signaling circuit that maintains stem cells and prods an embryo to separate into front and back or top and bottom. This circuit is called “Wnt” (the name is a fusion of the fruit fly gene wingless and a cancer-promoting gene discovered in mice, originally called Int-1).

Maguschak and Ressler wanted to assess the role Wnt signals play in learning and memory. The model system was the same as in their previous work: if mice are electrically shocked just after they hear a certain tone, they gradually learn to fear that tone, and they show that fear by freezing.

Kerry Ressler, MD, PhD

Maguschak saw that in the amygdala, a part of the brain important for fear responses, Wnt genes are turned down during the learning process temporarily but then come back on. If the mice only hear the tone or only get the shock, the genes’ activities don’t change significantly.

She then introduced proteins that perturb Wnt signaling directly into the amygdala. Extra Wnt injected before training, while it didn’t stop the mice from learning to fear the tone, made that training less likely to “stick.” Two days later, the mice that received Wnt didn’t seem to fear the tone as much.

Here’s the possibly confusing part: a Wnt inhibitor also impaired fear memory consolidation. In effect, both blue and red pills actually interfered with how well memories endured. The authors suggest this is because Wnt signals have to be turned down during fear memory formation but then turned back up so those memories can solidify. The Wnt signals seem to go along with the adhesive interactions of beta-catenin. It looks like beta-catenin’s stickiness also needs to be tuned down and then back up.

The off-then-on-again requirement Maguschak and Ressler observe is reminiscent of results from cell biologist James Zheng’s lab. He and his colleagues saw that the actin cytoskeleton needed to be weakened and then stabilized during long-term potentiation, an enhancement of connections between neurons thought to lie behind learning and memory.

Several laboratories have identified potential drugs that modify beta-catenin/Wnt. These new results suggest that the timing of when and how to use such drugs to enhance memory may critically important to consider, Ressler says.

“To interfere with memory formation after trauma or enhance memory formation in people with dementia, researchers will clearly need to attend to the full complexity of the dynamics of synaptic plasticity and memory,” he says.

A nifty link to an animation of Wnt signaling

 

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Personalized Medicine Day in Georgia

Governor Nathan Deal was joined by Ambassador Andrew Young, Georgia State Representative Calvin Smyre and Leroy Hood, founder of the Institute of Systems Biology, in formally proclaiming September 1, 2011 Personalized Medicine Awareness Day in the State of Georgia.

Georgia Governor Nathan Deal presents Morehouse School of Medicine’s Dean and Executive Vice President, Valerie Montgomery Rice, MD, with a state proclamation declaring Sept. 1, 2011 Personalized Medicine Awareness Day in Georgia.

The event at Morehouse School of Medicine (MSM) was sponsored by Georgia Bio; the Atlanta Clinical & Translational Science Institute (ACTSI, which is funded by the NIH and led by Emory University with partners MSM and Georgia Tech); and Iverson Genetics, Inc.

“The collaboration within the ACTSI between these three research universities is an important undertaking and an example of how it should be done,” remarked Governor Deal as he kicked off the day’s program.

A visionary in the personalized medicine field, Dr. Hood developed the DNA gene sequencer and synthesizer and the protein synthesizer and sequencer – four instruments that paved the way for the successful mapping of the human genome.

During his keynote address he proposed a revolution in medicine.  P4 Medicine – Predictive, Preventive, Personalized and Participatory – is a proactive (instead of a reactive) approach to medicine. The paradigm change will drive radical changes in science.

For P4 medicine to succeed, a cross-disciplinary culture with team science and new approaches to educating scientists, as is done through the ACTSI, has to take place. Dr. Hood predicts the human genome will be part of individual medical records in 10 years.

Leroy Hood, MD, PhD

“The vision of P4 medicine is that each patient will be surrounded by a virtual cloud of billions of data points. Advances in science and technology will reduce this enormous data dimensionality to simple hypotheses about human health and disease,” says Hood.

“The ultimate outcome is to create individualized patient disease models that are predictive and actionable. The shift to P4 Medicine will also require societal changes.”

Personalized Medicine Awareness Day celebrated the first-of-its-kind personalized medicine study, approved by the Centers for Medicare and Medicaid Services. The study will determine the utility of genetic testing in calculating doses and reducing the incidence of adverse events associated with the initiation of Warfarin therapy. Warfarin is the world’s leading anti-blood clotting drug.

Researchers hope the study will provide data to demonstrate that individualizing treatment can improve patient safety and reduce healthcare costs, says Dean Sproles, CEO of Iverson Genetics, Inc., which is collaborating in the study with MSM and the ACTSI.

Governor Deal congratulated the ACTSI for leading the landmark Warfarin study with Iverson and is “proud that Georgia will be leading the effort.”

The Warfarin Study is led by ACTSI Senior Co-Principal Investigator Elizabeth Ofili, MD, MPH, director of the Clinical Research Center, chief of cardiology and associate dean for clinical research at MSM, and will engage 50 sites across the country and 7,000 participants. The first participant was recently enrolled at Grady Memorial Hospital.

“This study should help us understand how to use each patient’s genetic information to deliver a safer and more effective dose,” says Ofili.

Sproles noted, “The study is evidence of the growing role of genetics in helping doctors to develop optimal individual treatments for their patients.”

A panel including Emory medical leaders David Stephens, Fred Sanfilippo and Kenneth Brigham discussed and addressed questions like how to communicate ‘big science’ to the individual, how to move genetic testing to medical outcomes and who owns genome data.

“Personalized Medicine is the future,” stated Governor Deal. The presence of Governor Deal, Ambassador Young and Representative Smyre is a sign that policymakers are beginning to recognize that personalized medicine is not just a vision for better healthcare; it has the power to improve health and reduce healthcare costs.

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Magnanimous magnolias keep on giving

Honokiol, the versatile compound found by Emory dermatologist Jack Arbiser in the cones of magnolia trees, makes a surprise appearance in a recent paper in Nature Medicine.

Jack Arbiser, MD, PhD, and colleagues originally isolated honokiol from magnolia cones. It can also be found in herbal teas.

The paper, from Sabrina Diano, Tamas Horvath and colleagues at Yale, probes the role of reactive oxygen species (ROS) in the hypothalamus, a part of the brain that regulates appetite. In the paper, Horvath’s laboratory uses honokiol as a super-antioxidant, mopping up ROS that suppress appetite. Arbiser initiated the collaboration with Horvath after finding, while working with Emory free radical expert Sergei Dikalov, how effective honokiol is at neutralizing ROS.

The paper is intriguing partly because it’s an example of a situation where ROS, often thought to be harmful because of their links to aging and several diseases, are actually beneficial. In this case, they provide a signal to stop eating. A recent paper from Andrew Neish’s lab at Emory provides another example, where probiotic bacteria stimulate production of ROS, which promote healing of the intestine.

Arbiser notes that since honokiol can increase appetite, the compound may be helpful in situations where doctors want patients to eat more.

“This might be particularly valuable in patients who are nutritionally deficient due to chemotherapy and provides a rationale for adding honokiol to chemotherapy regimens,” he writes.

Satiety producing neurons in the hypothalamus

A note of caution: in the Nature Medicine paper, honokiol is infused directly into the brain.

Honokiol has been shown to counteract inflammation and slow the growth of blood vessels (important in fighting cancer). Collaborating with Arbiser, Emory endocrinologist Neale Weitzmann has recently found that honokiol stimulates osteoblasts, the cells that build bone, suggesting that it could reduce bone loss in osteoporosis.

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Neuroinflammation: a different way to look at Parkinson’s disease

Emory physiologist Malu Tansey and her colleagues are using recent insights into the role of inflammation in Parkinson’s disease to envision new treatments. One possible form this treatment strategy could take would be surprisingly simple, and comparable to medications that are approved for rheumatoid arthritis.

Malu Tansey, PhD

Understanding the role of inflammation in Parkinson’s requires a shift in focus. Many Parkinson’s researchers understandably emphasize the neurons that make the neurotransmitter dopamine. They’re the cells that are dying or already lost as the disease progresses, leading to tremors, motor difficulties and a variety of other symptoms.

But thinking about the role of inflammation in Parkinson’s means getting familiar with microglia, the immune system’s field reps within the brain. At first, it was thought that the profusion of microglia in the brains of Parkinson’s patients was just a side effect of neurodegeneration. The neurons die, and the microglia come in to try to clean up the debris.

Now it seems like microglia and inflammation might be one of the main events, if not the initiating event.

“Something about the neurons’ metabolic state, whether it’s toxins, oxidative stress, unfolded proteins, or a combination, makes them more sensitive. But inflammation, sustained by the presence of microglia, is what sends them over the edge,” Tansey says.

She says that several recent studies have led to renewed attention to this area:

  1. In vivo PET imaging using a probe for microglia has allowed scientists to see inflammation starting early in the progression of Parkinson’s (see figure below)
  2. Epidemiology studies show that taking ibuprofen regularly is linked to lower incidence of Parkinson’s
  3. Experiments with animal models of genetic susceptibility demonstrate that inflammatory agents like endotoxin can accelerate neurodegeneration
  4. Genomics screens have identified HLA-DR, an immune system gene, as a susceptibility marker for Parkinson’s (Emory’s Stewart Factor was a co-author on this paper)

Popping a few ibuprofen pills everyday for prevention and possibly damaging the stomach along the way is probably not going to work well, Tansey says. It should be possible to identify a more selective way to inhibit microglia, which may be able to inhibit disease progression after it has started.

Activated microglia in the midbrain and striatum of a Parkinson's patient

Targeting TNF (tumor necrosis factor), an important inflammatory signaling molecule, may be one way to go. Anti-TNF agents are already used to treat rheumatoid arthritis and inflammatory bowel disease. This January, Tansey and her co-workers published a paper showing that a gene therapy approach using decoy TNF can reduce neuronal loss in a rat model of Parkinson’s. More recently, her lab has also shown that targeting the gene RGS10 is another way to inhibit microglia and reduce neurodegeneration in the same models.

It is important to note that in the rat studies, they do surgery and put the gene therapy viral vector straight into the brain. She says it might possible to perform peripheral gene therapy with the microglia, or even anti-TNF medical therapy. In terms of mechanism, decoy (technically, dominant negative) TNF is more selective and may avoid the side effects, such as opportunistic infections, of existing anti-TNF agents.

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Brain tumor patient gives back and moves forward

Jennifer Giliberto

Don’t sweat the small stuff.

That’s the motto 36-year-old Jennifer Giliberto now lives by after recently welcoming a third child into the world. Late night feedings, diaper changes, mounds of dirty laundry and caring for two older boys (ages six and eight) would certainly be a challenge for most moms. But this mom is different.

Four years ago, Giliberto was diagnosed with a brain tumor – a slow growing Grade II astrocytoma located in her posterior right temporal lobe. The shocking diagnosis left Giliberto and her family with many choices and decisions to make.

Giliberto’s inspiring story was profiled on CNN on Aug. 16, 2011 in a special “Human Factor” segment, which takes a look at people accomplishing something significant after overcoming the odds.

The Long Road Ahead

After her second child was born in 2005, Giliberto began noticing a pattern of problems with her fine motor skills. Neurological testing revealed little, but an MRI (magnetic resonance imaging) revealed a lesion and possible tumor in the brain. Follow-up MRIs over the next year showed no new growth, but in June 2007, a definite brain tumor was detected by MRI.

While taking the watch and wait approach to determine if the tumor would grow, she became involved with the Southeastern Brain Tumor Foundation (SBTF) as a volunteer. She focused her efforts on raising money to support critical brain and spinal tumor research. She also met Emory neurosurgeon Costas Hadjipanayis, MD, PhD.

Hadjipanayis, an assistant professor in Emory’s Department of Neurosurgery, would soon become Giliberto’s physician. He confirmed her diagnosis and recommended surgical removal of the tumor.

Costas Hadjipanayis, MD, PhD and patient Jennifer Giliberto

On August 18, 2008, at Emory University Hospital Midtown, Hadjipanayis removed Giliberto’s brain tumor. “Jennifer underwent a craniotomy and had a gross total resection of the tumor, with no complications,” explains Hadjipanayis, who is chief of neurosurgery at the hospital. “She spent one night in the neurosurgical ICU and her recovery afterwards went well.”

Then he encouraged her to embrace life and live it to the fullest. Giliberto has taken her doctor’s orders to heart, and lives life with a new purpose than before.

Giving Back

To support and encourage other brain tumor patients, Giliberto serves as a patient and family advisor at Emory University Hospital Midtown. She visits with hospitalized patients and their families who are in similar situations as the young mother of three.

“This has been a very fulfilling experience and an outlet to give back,” says Giliberto. “Being a patient is lonely, even when you know you have support. Working to assist other patients and families and improve a system goes a long way to ease that lonely journey of the patient experience.”

Patient and family advisors also work to improve hospital processes and procedures from a patient perspective.

She also serves as vice president of the Southeastern Brain Tumor Foundation, continuing the mission to raise funds for research. The SBTF consistently funds innovative brain tumor research at Emory’s Winship Cancer Institute.

And she is a devoted wife and mother.

Moving Forward

Last year, when Giliberto and her husband decided they would like to expand their family of four, she consulted with Hadjipanayis. He, once again, encouraged her to live life and move forward. They did, and their youngest child was born in July 2011.

While Giliberto has remained stable since her surgery in 2008, she continues to have MRI’s every six to nine months to check for any tumor recurrence. Astrocytomas, even once removed, can recur and can also become cancerous.

But for now, it’s on with life as she knows it – stable, moving ahead and enjoying every day with a new sense of hope.

And as for the small stuff – Giliberto’s learned there’s just no reason to sweat it at all.

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Americans cutting sugar – but it’s still not enough

In America’s battle against obesity, there is some good news. According to a study conducted by Emory researchers, Americans consumed nearly a quarter less added sugars in 2008 than they did 10 years earlier.

The study, published in the American Journal of Clinical Nutrition in July 2011, found that the consumption of added sugars, such as those found in sodas, sports drinks, juices and sweetened dairy products, decreased among all age groups over a decade. The largest decrease came in the consumption of sodas, traditionally the largest contributor to added sugar consumption, according to Jean Welsh, MPH, PhD, RN, study author and post-doctoral fellow in pediatric nutrition at Emory University School of Medicine.

“While we were hopeful this would be the case, we were surprised when our research showed such a substantial reduction in the amount of added sugar Americans are consuming,” said Welsh. “We’re hopeful this trend will continue.”

So, why the change? One of Welsh’s partners in the study, Miriam Vos, MD, MSPH, an assistant professor of pediatrics in the Emory University School of Medicine, and a physician on staff at Children’s Healthcare of Atlanta, attributes much of the shift to public education.

“Over the past decade, there has been a lot of public health awareness about obesity and nutrition, and I think people are starting to get the message about sugar,” says Vos. “We’re not trying to send a message that sugar is inherently bad. It’s more that the large amounts of sugar we consume are having negative effects on our health, including increasing our risk of obesity, diabetes and cardiovascular disease.”

The study interpreted data of 40,000 people’s diets collected by the Centers for Disease Control and Prevention (CDC) over 10 years.  From the surveys, researchers were able to calculate how much added sugar – that is sugar that is not originally part of a food – that Americans are consuming. In 1999-2000, the typical person’s daily diet included approximately 100 grams of added sugar, a number that had dropped to 77 grams by 2007 and 2008.

While the study shows that the amount of added sugar Americans are consuming is lower, it doesn’t mean the amount is low enough.

“The American Heart Association recommends that we get about five percent of our calories from added sugars,” says Vos. “In 1999 to 2000, people were consuming about 18 percent of their calories from added sugars. Over 10 years, that amount decreased to 14.5 percent of our daily calories, which is much better. But, clearly, 14.5 percent is still three times more than what is considered a healthy amount. We’re on the right track, but we still have room for improvement.”

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Fertility: a new frontier in treating those with HIV

HIV

Not long ago, physicians who treated those with HIV focused only on helping their patients stay well. Today some physicians are also beginning to focus on helping those patients conceive.

“Most of the patients who are now diagnosed with HIV are in their reproductive years, and as many as a third express a desire to have children,” says Emory reproductive endocrinologist Vitaly Kushnir, MD.

This emerging area of treatment has been made possible thanks to the growing effectiveness of a combination of drugs known as Highly Active Antiretroviral Therapy, or HAART, used for years to treat retroviruses, including HIV.

“Now that people with HIV are living longer, fertility and HIV is an emerging area of interest,” says Kushnir. “Several studies have indicated that HIV drugs if given early in the course of the disease can reduce the risk of transmission from an HIV-positive person to an HIV-negative person.”

But researchers and physicians know very little yet about how treatments for HIV, the virus itself, and the comorbidities associated with HIV affect fertility. So, Kushnir and his colleague, Emory pathologist William Lewis, MD, decided it was time to explore existing data on how HIV and its treatment affect fertility, especially in women. Their review paper on the subject appears in the August 2011 issue of Fertility and Sterility.

Because there are safety concerns and legal restrictions on fertility treatments in couples in which one partner is HIV positive and the other is not, treatment options often are limited.

“This is becoming more and more of an issue,” says Kushnir. “It’s probably time for us to have a more open discussion about the access these patients have to fertility treatment. I think the current system probably discourages these patients from pursuing treatments that are a lot safer than trying to get pregnant on their own.”

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Emory experts weigh in on obesity at AACC Annual Meeting

The obesity epidemic took center stage at this year’s American Association of Clinical Chemistry (AACC) Annual Meeting. Several Emory experts took the podium to further explore obesity not only as a public health problem, but also as an issue that is changing the way we diagnose diseases and treat health issues in children.

Jeffrey Koplan, MD, MPH

Jeffrey Koplan, MD, MPH, director of the Emory Global Health Institute, led one of the meeting’s plenary sessions, emphasizing that obesity must be fought with changes in both public policy and personal decision-making. Koplan also noted that strategies to address obesity must be localized to fit each community because eating and exercise habits are often culturally specific.

Rising rates of obesity also are changing the way physicians and researchers define and diagnose certain diseases, including metabolic syndrome, a cluster of risk factors including insulin resistance, high blood pressure, cholesterol abnormalities and an increased risk for clotting. The common thread among patients with metabolic syndrome is that they are often overweight or obese.

Ross Molinaro, PhD

Pathologist Ross Molinaro, PhD, medical director of the Core Laboratory at Emory University Hospital Midtown and co-director of the Emory Clinical Translational Research Laboratory, presented insights into the important role of lab testing in the definition and diagnosis of metabolic syndrome.  In addition to new markers, Molinaro addressed the global prevalence of metabolic syndrome and the evolving criteria for diagnosis.

Miriam Vos, MD, MSPH

Responding to their members’ demand for more information on how obesity affects children, the AACC hosted a full-day symposium on pediatric obesity and related health complications such as diabetes and high blood pressure.  Miriam Vos, MD, MSPH, assistant professor of pediatrics in  Emory School of Medicine and a physician at Children’s Healthcare of Atlanta described non-alcoholic fatty liver disease as an increasingly common complication of childhood obesity that can cause inflammation and scarring of the liver.

Stephanie Walsh, MD

Stephanie Walsh, MD, assistant professor of pediatrics in Emory School of Medicine and medical director of child wellness at Children’s Healthcare of Atlanta, leads Children’s efforts in preventing and treating childhood obesity in Georgia, which currently has the second highest rate of childhood obesity in the country. Walsh addressed the effect of Children’s wellness initiative, called Strong4Life, on childhood obesity prevention in Georgia.

“From those in the lab, to those in clinic, to those who strategize and implement public health campaigns, we’re all going to need to work together to protect our children’s future,” says Walsh.

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