TAG: "Heart"

Necklace and smartphone app can help people track food intake


UCLA-developed app could help battle obesity, heart disease and diabetes.

WearSens rests loosely above the sternum and uses highly sensitive sensors to capture vibrations from the action of swallowing.

By Bill Kisliuk, UCLA

A sophisticated necklace developed by researchers at the UCLA Henry Samueli School of Engineering and Applied Science can monitor food and drink intake, which could help wearers track and improve their dietary habits.

The inventors of the WearSens device say it could help battle obesity, heart disease, diabetes and other problems related to nutrition.

Majid Sarrafzadeh, a distinguished professor of computer science and co-director of UCLA’s Wireless Health Institute, led a team that created the device and an algorithm that translates data from the necklace, and tested it on 30 people who ate a variety of foods.

The researchers found that WearSens can differentiate between solids and liquids with 87 percent accuracy, between hot drinks and room-temperature drinks with 90 percent accuracy, and between food items with different textures with 80 percent accuracy. Researchers say those figures will improve as users calibrate the device based on their eating habits.

The research was published online by the IEEE Sensors Journal.

“Today, many people try to track their food intake with journals, but this is often not effective or convenient,” Sarrafzadeh said. “This technology allows individuals and health care professionals to monitor intake with greater accuracy and more immediacy.”

WearSens rests loosely above the sternum and uses highly sensitive piezoelectric sensors to capture vibrations from the action of swallowing. Piezoelectric sensors produce voltage based on the mechanical stress — or movement or pressure — that is applied to them.

When the wearer eats or drinks, skin and muscle motion from the lower trachea trigger the sensors, and the necklace transmits the signals to a smartphone, where the UCLA-developed algorithm converts the data into information about the food or beverage. The phone displays data about the volume of food or liquid consumed and can offer advice or analysis; for example, that the wearer is eating more than in previous days or that the person should drink more water.

With the WearSens device, the sensor information is translated using a spectrogram, which offers a visual representation of vibrations picked up by the sensors. Spectrograms are often used in speech therapy and seismology, among other applications.

“The breakthroughs are in the design of the necklace, which is simple and does not interfere with daily activity, and in identifying statistical measures that distinguish food intake based on spectrogram images generated from piezoelectric sensor signals,” said Nabil Alshurafa, a graduate student researcher at UCLA who is a co-inventor of the device and the first author of the research.

The study’s other authors are co-inventor Haik Kalantarian, a graduate student researcher; Shruti Sarin and Behnam Shahbazi, also graduate student researchers; Jason Liu, who was a UCLA graduate student at the time he worked on the research; and postdoctoral researcher Mohammad Pourhomayoun.

The team is continuing to refine the algorithms and the necklace’s design. The researchers hope WearSens will be available to the public later this year.

The technology is available for licensing via the UCLA Office of Intellectual Property and Industry-Sponsored Research, which facilitates the conversion of UCLA research to benefit the public.

The research was supported by the National Science Foundation.

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Infant leaves UCLA’s Mattel hospital for home with a transplanted heart


Drayvn is the hospital’s second youngest heart transplant recipient.

Drayvn Johnson got a heart transplant when he was 23 days after he was born with a heart defect and only one coronary artery. Now 5 weeks old, he left Mattel Children's Hospital UCLA for home today with his mother, Nicole Eggleston. (Photo by Reed Hutchinson, UCLA)

By Amy Albin, UCLA

Staff at Mattel Children’s Hospital UCLA witnessed a happy ending today (March 11) instead of what could have easily been a tragic one  when they bid farewell to 5-week-old Drayvn Johnson, who went home with his mother, Nicole Eggleston, and two older brothers after becoming the hospital’s second youngest heart transplant recipient. He was only 23 days old when he received his new heart, which was the size of a strawberry.

“All of our heart transplant patients are special, but I think this one was special because we knew there was a risk we might not find a donor in time,” said Dr. Juan Alejos, professor of pediatric cardiology and director of the Pediatric Heart Transplant Program at Mattel Children’s Hospital UCLA

Dravyn was born with a condition called pulmonary atresia in which the pulmonary valve does not form properly. It was discovered during Eggleston’s pregnancy in a sonogram performed at 22 weeks. Doctors had thought initially that his heart could be repaired with a series of corrective surgeries performed over the first few years of Dravyn’s life.

However, when he was born in early February at an Orange County hospital, doctors found that he had only one coronary artery instead of two and determined that surgery would be too risky for the baby.

At 5 days old, Drayvn was airlifted to Mattel where doctors confirmed that the only hope for his survival was an urgent heart transplant. Miraculously, within two days after Drayvn’s name went on a list for a transplant, a donor was found. And Drayvn got his new heart. The hospital’s youngest heart recipient was a 16-day-old infant who received a transplanted heart in 1994.

The UCLA Pediatric Heart and Heart-Lung Transplant Program is one of the major referral centers for the western United States. The team has performed more than 300 pediatric heart transplants since 1984 when it did its first such surgery. The program is a coordinated effort among pediatric cardiologists, cardiothoracic surgeons, dentists, nurse practitioners, transplant coordinators, nutritional specialists, social workers and child developmental specialists. For more information, visit http://transplants.ucla.edu/heart.

The family has set up a website to help raise funds for Drayvn’s care.

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Bioengineers put human hearts on chip to aid drug screening


Chips ultimately could replace use of animals to screen drugs for safety, efficacy.

By Sarah Yang, UC Berkeley

When UC Berkeley bioengineers say they are holding their hearts in the palms of their hands, they are not talking about emotional vulnerability.

Instead, the research team led by bioengineering professor Kevin Healy is presenting a network of pulsating cardiac muscle cells housed in an inch-long silicone device that effectively models human heart tissue, and they have demonstrated the viability of this system as a drug-screening tool by testing it with cardiovascular medications.

This organ-on-a-chip, reported in a study published today (March 9) in the journal Scientific Reports, represents a major step forward in the development of accurate, faster methods of testing for drug toxicity. The project is funded through the Tissue Chip for Drug Screening Initiative, an interagency collaboration launched by the National Institutes of Health to develop 3-D human tissue chips that model the structure and function of human organs.

“Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy,” said Healy.

The study authors noted a high failure rate associated with the use of nonhuman animal models to predict human reactions to new drugs. Much of this is due to fundamental differences in biology between species, the researchers explained. For instance, the ion channels through which heart cells conduct electrical currents can vary in both number and type between humans and other animals.

“Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans,” said Healy. “It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market.”

The heart cells were derived from human-induced pluripotent stem cells, the adult stem cells that can be coaxed to become many different types of tissue.

The researchers designed their cardiac microphysiological system, or heart-on-a-chip, so that its 3-D structure would be comparable to the geometry and spacing of connective tissue fiber in a human heart. They added the differentiated human heart cells into the loading area, a process that Healy likened to passengers boarding a subway train at rush hour. The system’s confined geometry helps align the cells in multiple layers and in a single direction.

Microfluidic channels on either side of the cell area serve as models for blood vessels, mimicking the exchange by diffusion of nutrients and drugs with human tissue. In the future, this setup also could allow researchers to monitor the removal of metabolic waste products from the cells.

“This system is not a simple cell culture where tissue is being bathed in a static bath of liquid,” said study lead author Anurag Mathur, a postdoctoral scholar in Healy’s lab and a California Institute for Regenerative Medicine fellow. “We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs.”

Within 24 hours after the heart cells were loaded into the chamber, they began beating on their own at a normal physiological rate of 55 to 80 beats per minute.

The researchers put the system to the test by monitoring the reaction of the heart cells to four well-known cardiovascular drugs: isoproterenol, E-4031, verapamil and metoprolol. They used changes in the heart tissue’s beat rate to gauge the response to the compounds.

The baseline beat rate for the heart tissue consistently fell within 55 to 80 beats per minute, a range considered normal for adult humans. They found that the responses after exposure to the drugs were predictable. For example, after half an hour of exposure to isoproterenol, a drug used to treat bradycardia (slow heart rate), the beat rate of the heart tissue increased from 55 to 124 beats per minute.

The researchers noted that their heart-on-a-chip could be adapted to model human genetic diseases or to screen for an individual’s reaction to drugs. They also are studying whether the system could be used to model multi-organ interactions. A standard tissue culture plate could potentially feature hundreds of microphysiological cell culture systems.

“Linking heart and liver tissue would allow us to determine whether a drug that initially works fine in the heart might later be metabolized by the liver in a way that would be toxic,” said Healy.

The engineered heart tissue remained viable and functional over multiple weeks. Given that time, it could be used to test various drugs, Healy said.

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Researchers discover protein’s key role in heart failure


Better understanding of molecular mechanism could lead to new drug targets.

By Bonnie Ward, UC San Diego

Researchers at the UC San Diego School of Medicine have identified a key piece in the complex molecular puzzle underlying heart failure – a serious and sometimes life-threatening disorder affecting more than 5 million Americans.

In a study published in today’s (March 5) online issue of Cell Reports, Xiang-Dong Fu, Ph.D., and colleagues explored the heart’s progression from initial weakening to heart failure, and found that a protein, known as RBFox2, plays a critical role in this process.

Contrary to its name, heart failure does not mean the heart completely stops working, but rather that the heart muscle becomes weakened to the point that it can no longer pump enough blood for the body’s needs. Coronary artery disease, high blood pressure and heart defects are among various factors that can lead to heart failure, which has no cure and is currently treated with medications, lifestyle changes, oxygen and cardiac devices. In some cases, a heart transplant is required.

Fu and his team studied the cellular changes that occur during the weakened heart muscle’s transition from working harder to maintain proper blood flow, known as the compensatory stage, to failing to sustain adequate blood supplies, known as decompensation.

“Numerous signaling molecules have been shown to be part of the compensatory program, but relatively little was known about the transition to decompensation that leads to heart failure,” said Fu.

To answer this question, the research team explored RBFox2, a gene splicing protein known to be involved in the heart’s early development and ongoing function.

“We wanted to know how RBFox2 might contribute to decompensation, given its vital role in heart functions,’’ said Fu.

In their studies, the researchers restricted blood flow in mice to induce a condition similar to heart failure and then tested their RBFox2 protein levels over a period of weeks.

“Strikingly, we found that RBfox2 protein was largely diminished in the hearts of live mice five weeks after the procedure,” he said.

Fu and colleagues also tested the reduction of the RBFox2 protein in mice specially engineered to lack the protein. In these experiments, the mice lacking the RBFox 2 protein developed heart failure symptoms similar to those in the blood-restricted mice, suggesting a functional connection between the reduction of RBFox2 and decline of the heart muscle.

The research team then sought to determine why, from a mechanistic point of view, the loss of RBFox2 would weaken the heart. To study this, they examined RBFox2-controlled changes in gene expression, which refers to the biological actions taken by genes, during various scenarios of heart development in mice. Specifically, the scientists compared changes detected in the hearts of RBFox2-deleted or blood-restricted mice to those that occur during post-natal heart “remodeling.” Remodeling is the process of heart strengthening that begins at birth and continues throughout childhood.

“The RBFox2 deletion-induced genetic changes are similar to those that occurred during blood restriction-induced heart failure, but opposite to those taking place during heart remodeling,” said Fu. “This indicates that the normal developmental program for strengthening heart performance is reversed during heart failure.”

Fu said the finding could lead to new drug targets for heart failure.

“We’ve learned that the RBFox2 protein is very important in keeping the heart muscle strong,” he said.  “Our research shows its diminished expression coincides with the weakening of the heart muscle. This strongly suggests a causal role for this protein in heart failure. By understanding these mechanisms, we may be able to find a way to prevent the decreased expression of RBFox2, which may help in preventing heart failure.”

Co-authors include Chaoliang Wei, Jinsong Qiu, Yu Zhou, Yuanchao Xue, Jing Hu, Kunfu Ouyang, Indroneal Banerjee, Hairi Li, Ju Chen, all at UC San Diego; and Caimei Zhang, Biyi Chen and Long-Sheng Song, all at the University of Iowa Carver College of Medicine.

Funding for this research came, in part, from the National Institutes of Health (grants GM049369, HG004659, and HG007005).

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UC Irvine first in Orange County to use remote heart failure monitoring system


Implanted CardioMEMS sensor helps reduce heart failure-related hospital readmissions.

Pranav Patel, UC Irvine

UC Irvine Health is the first medical center in Orange County to offer heart failure patients a wireless system that allows cardiologists to remotely monitor their pulmonary artery pressure and heart rate measurements.

Real-time access to this data enables doctors to proactively manage a patient’s condition, helping to reduce the rate of hospital readmission related to heart failure, the leading cause of hospitalization among adults 65 and older in the U.S., according to the American College of Cardiologists.

Heart failure refers to the progressive weakening of the heart muscle until it no longer pumps enough blood to meet the body’s needs. Advances in treatment allow more patients to survive hospitalization for heart failure, but more than 50 percent of them experience a new onset of symptoms and end up being readmitted within six months. Cardiologists hope the CardioMEMS Heart Failure System will help break this cycle.

Dr. Pranav Patel, chief of the UC Irvine Health Division of Cardiology, implanted the sensor in an 84-year-old male patient on Feb. 6.

“This technology will help change the way we manage heart failure patients,” said Patel. “Once the patient returns home, they must pay careful attention to changes in weight, ankle or abdominal swelling and shortness of breath. CardioMEMS monitors their heart rate and artery pressure daily, and transmits that information to a secure database at the hospital or clinic for review by a physician or a nurse. We can identify early warning signals before the patient feels any symptoms.”

The implantable sensor is about the size the size of a dime, with thin loops at each end, and is placed in the pulmonary artery during a right heart catheterization procedure. Once implanted, the patient cannot feel the sensor, and it does not interfere with other devices such as a pacemaker or defibrillator. The system wirelessly captures and transmits the patient’s data to a secure database for analysis.

CardioMEMS received FDA approval in May 2014 and is designed for use with patients who have been hospitalized the previous year with New York Heart Association Class III heart failure. The American Heart Association uses this classification system, which is based on how much a patient’s physical activity is limited by their heart condition.

“If the patient is experiencing rising pressure or any deterioration of their heart failure condition, we can immediately make changes to their medication, diet and daily activities,” Patel said. “Early detection is the key to preventing more serious complications, avoiding another emergency room visit or hospital stay, and enhancing the patient’s overall well-being.

The UC Irvine Health Heart Failure Program uses state-of-the-science equipment and technologies to identify the cause of heart failure, or cardiomyopathy. A multidisciplinary team then works with patients to stabilize their condition and develops a comprehensive treatment plan.

In each of the last four years, the program has received the American Heart Association’s Get With The Guidelines – Heart Failure Gold Plus Quality Achievement Award. The recognition signifies that UC Irvine Health has achieved the goal of treating heart failure patients according to prevention guidelines recommended by the American Heart Association/American College of Cardiology.

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Nerve regeneration therapy has potential to prevent arrythmias after heart attack


Findings could help in development of therapeutics for post-heart attack care.

A therapy currently under development for spinal cord injuries stimulates nerve regeneration in the heart and provides resistance to arrhythmias following a heart attack, according to a new study published today (Feb. 2) in the journal Nature Communications by researchers at Oregon Health & Science University (OHSU), Case Western Reserve University and UC Davis.

Millions of people have heart attacks each year, and those who survive have increased risks of arrhythmias — or abnormal heart rhythms — and sudden cardiac death. Recent clinical trials showed that the severity of nerve degeneration in the heart caused by heart attack predicts increased arrhythmia susceptibility. Surgical implantation of a cardioverter defibrillator (ICD), a device that tracks and restores heart rate, is one of the only effective therapies for treating arrhythmias following a heart attack.

“Our study initially sought a therapy that would stimulate nerve regeneration after a heart attack. It was a surprising and thrilling discovery that not only could this regeneration be achieved through both genetic and pharmaceutical approaches, but that it also decreases the heart’s susceptibility to arrhythmias,” said Beth Habecker, senior author and professor of physiology and pharmacology in the OHSU School of Medicine. “We are excited to use these findings to pursue the development of therapeutics for post-heart attack care.”

Habecker led a team of researchers in determining why nerves were excluded from cardiac scars after a heart attack. OHSU graduate student Ryan Gardner found that factors preventing nerve regrowth after a spinal cord injury were also present in the heart and that by blocking their actions in mice, via genetic knockout or pharmaceutical therapy, nerve regeneration occurred and arrhythmia susceptibility decreased. The therapy that proved successful was a chemical compound known as intracellular sigma peptide, which was developed for traumatic spinal cord injury by Jerry Silver and colleagues at Case Western Reserve University.

Crystal Ripplinger and Lianguo Wang of UC Davis used high-speed optical imaging of whole mouse hearts in action to assess the effects of nerve regeneration on electrical activity, calcium handling and arrhythmia susceptibility. This technique, available at just a handful of labs in the U.S., allowed the investigators to precisely visualize the cellular events that triggered lethal rhythms and was key to understanding why nerve regeneration prevented arrhythmia.

“Arrhythmia is one of the most unpredictable and life-threatening outcomes of a heart attack,” said Ripplinger,  assistant professor of pharmacology at the UC Davis School of Medicine. “Until now, we had always assumed that arrhythmias were mainly due to damage and death of heart cells. Our study is the first to suggest that treatments targeting nerve regeneration can normalize electrical activity and prevent arrhythmias in heart attack survivors. This finding opens the door to an entirely new avenue of anti-arrhythmic therapy.”

Habecker and Ripplinger hope their research will be applied to future studies in humans and may one day lead to an alternative treatment to ICD therapy.

Additional authors of the study, titled ”Targeting Protein Tyrosine Phosphatase After Myocardial Infarction Restores Cardiac Sympathetic Innervation and Prevents Arrhythmias,” were Jared Cregg and Bradley Lang of Case Western Reserve University, and Cassandra Dunbar and Bill Woodward of OHSU.

This work was supported by the National Heart, Lung, and Blood Institute of the National Institutes of Health under award numbers HL093056, HL068231 and HL111600; the National Institute of Neurological Disorders and Stroke of the National Institutes of Health under award number NS25713; the American Heart Association under award number 12SDG9010015; and an Oregon Brain Institute Neurobiology of Disease Fellowship.

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Tiny infant has big impact on his community


Tiny Smiles Half Marathon is scheduled for Feb. 7.

By Tricia Tomiyoshi, UC Davis

“Miles” Keiser, though nicknamed “Tiny” by his family, an infant treated at UC Davis Children’s Hospital in 2011, is having a big effect on the lives of children with congenital heart disease in Sacramento and on his community.

Born in Northern California in June 2011, Tiny would undergo the first of three planned surgeries to correct hypoplastic left heart syndrome 10 days after birth, and would be treated afterward in the UC Davis Children’s Hospital Pediatric Intensive Care Unit/Pediatric Cardiac Intensive Care Unit.

The infant received his diminutive nickname from his pre-adoptive parents, Rick and Jean Keiser of Galt, who already had adopted two of Tiny’s siblings and were in the process of adopting their brother.

Tiny would spend most of his young life with his family at the hospital, punctuated by short visits in the Keiser home. The Keiser family was always by his side. Despite the best efforts of his physicians, chief among them associate professor of surgery and pediatrics Gary Raff, in December of 2011 Tiny lost his struggle to survive at just 6 months of age.

“We made some great friends in the hospital, including Dr. Raff and his team, all of the physicians in the PICU/PCICU and his cardiologists Michael Choy and Mark Parrish,” Rick Keiser said. “Everyone was amazing, from the housekeeping staff to Dr. Raff. They were incredible.”

After struggling with the loss of their child, the Keisers decided to establish a commemorative race in Tiny’s honor, the Tiny Smiles Half Marathon – “the tiny half,” to give back to the Children’s Hospital and other pediatric cardiac organizations. This year, 2015, Tiny Smiles has made the Children’s Heart Foundation one of its beneficiaries.

The Tiny Smiles Half Marathon is scheduled for Saturday, Feb. 7. On-site registration starts at 6 a.m. and the event ends at noon. It will combine a half-marathon of 13.1 miles starting at 8 a.m.; a 5 kilometer and 10 kilometer race starting at 8:15 a.m.; and a kids’ fun run starting at 9 a.m.

The race starts at Civic Drive and Chabolla Avenue in Galt; it ends at the Galt Fairgrounds. The half-marathon registration fee is $70; the 5k and 10k registration fee is $40. Registration closes on Thursday, Feb. 7, and is available through this link.

Tiny Smiles already has had some fundraising successes, including holding multiple blood drives and raising more than $10,000 for the UC Davis Children’s Hospital Pediatric Intensive Care Unit/Pediatric Cardiac Intensive Care Unit. Race sponsors include Fleet Feet Sports of Stockton; Central Valley Physical Therapy; SMUD, UC Davis Children’s Hospital, The City of Galt, Pro Transport Ambulance, The Taylor Family Foundation, Spaans Cookies and more.

For additional information about the race, please contact Rick Keiser at rick@tinysmilesrace.org, or (209) 329-4692.

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Project ADAM’s first California affiliate established at UC Davis


Program helps prevent sudden cardiac arrest in children and teens.

Stuart Berger, UC Davis

By Tricia Tomiyoshi, UC Davis

A life-saving program that helps to prevent sudden cardiac arrest in children and teens has now arrived in California.

UC Davis Children’s Hospital in Sacramento has become the first California affiliate for Project ADAM (Automated Defibrillators in Adam’s Memory), a nonprofit organization dedicated to establishing comprehensive defibrillation programs in schools across the country. The program’s mission is to reach out to schools to ensure that automated external defibrillators (AEDs) are installed and that staff, faculty, students and families are trained how to use them and to perform CPR.

Stuart Berger, chief of the Division of Pediatric Cardiology at UC Davis Children’s Hospital, founded Project ADAM while he was working at the Children’s Hospital of Wisconsin in 1999. The program has since expanded to 10 states in its 15 years of operation and more than 85 lives have been saved in children and adolescents as well as adults.

“I’m very excited to bring Project ADAM to the Sacramento region,” said Berger. ”This has been such a wonderful community outreach project. It has brought the community together at multiple levels and it has saved livesIt would be wonderful to institute this program in every school in the state of California as well as in the entire country.”

The Sacramento Kings will host a night dedicated to heart health awareness on Feb. 20. A portion of proceeds from tickets purchased through this ticket link (using passcode: Kings) will be donated to the Sacramento Project ADAM.

Project ADAM was named in honor of 17-year-old Wisconsin high school basketball player, Adam Lemel, who died on the court due to an undiagnosed genetic heart condition. According to Berger, at least 100 to 200 children and teens experience sudden non-traumatic cardiac death each year in the U.S., although the exact number is unclear and this number could be an underestimate of the true incidence. Multiple studies, including the new National Institutes of Health and Centers for Disease Control and Prevention’s Sudden Death in the Young registry, have been designed to get more specific data about the incidence of this devastating problem.

Schools, organizations and community members interested in being a part of Sacramento Project ADAM are welcome to attend the next community meeting on Thursday, Jan. 29, at 5:30 p.m. at the UC Davis Health System Facilities Support Services Building, 4800 2nd Ave., Sacramento in Room 2030.

For more information, please contact Amber Lindgren, administrator for the Sacramento Project ADAM, at (916) 734-2460 or amber.lindgren@ucdmc.ucdavis.edu.

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UC Davis heart surgeon publishes his model for medical humanitarian aid


J. Nilas Young details a quarter century of establishing cardiac surgery sites in Russia.

J. Nilas Young, UC Davis

By Karen Finney, UC Davis

J. Nilas Young, UC Davis chief of cardiothoracic surgery, has published a landmark article on medical humanitarian aid, detailing his 25 years of experience establishing six cardiac surgery sites in Russia.

The article appears in the December 2014 issue of the prestigious Journal of Thoracic and Cardiovascular Surgery and is also available online.

Young’s UC Davis co-authors were pediatric cardiac surgeon Gary Raff and pediatric critical care physician James Marcin, and his collaborators included colleagues at the Mayo Clinic, Emory University, Childrens Hospital of Wisconsin, Nationwide Childrens Hospital and the Siberian Branch of the Russian Academy of Medical Science.

The article emphasizes the approach of Heart to Heart International Children’s Medical Alliance in developing sustainable medical aid programs with high-quality outcomes, scalability and efficacy. Although focused on a specific class of diseases (congenital heart diseases), the authors believe the model is applicable to other medical humanitarian projects, particularly those that involve complex surgical interventions.

In 2012, Young received the the World of Children Health Award — hailed as the “Nobel Prize for child advocates” — for his international humanitarian efforts to improve pediatric heart care (read the press release).

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Traffic’s toll on the heart


Clogged interstates aggravate clogged arteries, according to UC Irvine research.

Credit: Jess Wheelock, UC Office of the President

By Nicole Freeling, UC Newsroom

Anyone who has experienced Los Angeles gridlock likely can attest that traffic may cause one’s blood pressure to rise. But UC Irvine researchers have found that, beyond the aggravation caused by fellow drivers, traffic-related air pollution presents serious heart health risks — not just for rush hour commuters, but for those who live and work nearby.

Research by UC Irvine joint M.D./Ph.D. student Sharine Wittkopp contributes to evidence that the increased air pollution generated by vehicle congestion causes blood pressure to rise and arteries to inflame, increasing incidents of heart attack and stroke for people who reside near traffic-prone areas.

“While the impact of traffic-related pollution on people with chronic lung diseases is well known, the link to adverse heart impacts has been less described,” said Wittkopp.

UC Irvine M.D./Ph.D. student Sharine Wittkopp is investigating genetic factors that make some people more vulnerable to pollution’s negative effects. (Photo courtesy of Sharine Wittkopp)

Her research project, funded by the National Institute of Environmental Health Sciences, focused on residents of a Los Angeles senior housing community who had coronary artery disease.

Study participants spend the vast majority of their time at home, which meant they had prolonged exposure to traffic-related air pollution at the site. Because of their age and pre-existing heart conditions, they were thought to be more vulnerable to small, day-to-day variations in air quality.

“They are really in the thick of it,” Wittkopp said. “They are the ones that are going to suffer the most, and who are the least likely to be resilient.”

Up to now, most studies on the impacts of air pollution have focused on its effects over much larger populations, with difficulty capturing accurate exposures and short-term changes. Wittkopp and her team wanted to look at how daily fluctuations in traffic and air quality would affect those residing in the immediate vicinity of congested roadways.

The research team, led by adviser Ralph Delfino, associate professor and vice chair for research and graduate studies in the Department of Epidemiology at UC Irvine’s School of Medicine, set up air quality monitors at the residences of the study participants. They looked for daily and weekly changes in traffic-related pollution such as nitrogen oxides, carbon monoxide, and particulate matter.

What they found: “Blood pressure went up with increased traffic pollutants, and EKG changes showed decreased blood flow to the heart,” Wittkopp said.

Uncovering a genetic link

Just how susceptible a person is to these negative impacts appears to depend not just upon age and proximity to traffic, but also upon genetics, the research team found.

They uncovered what they believe is the first epidemiological evidence that a person’s mitochondrial DNA could affect their susceptibility to adverse health effects related to air pollution.

“When our cells are exposed to toxins, they respond by making more proteins that enable them to detoxify pollutants,” Wittkopp said. “We can actually monitor how the protein levels are going up and down and how the gene readouts change as people are exposed.” Looking at traffic-related pollution, they discovered that a person’s ability to produce the proteins that combat pollutants varied dramatically based on their DNA.

By identifying the genetic variables that place people at greater risk, health care providers could help account for these impacts and prescribe proactive treatments — such as antioxidants that reduce inflammation — that would make people less vulnerable.

But Wittkopp also stresses such treatment would simply be a Band-Aid on the greater problem.

Impetus to improve infrastructure, lessen exposure

“Understanding the health problems that traffic-related pollution causes helps us understand why we need to change things and improve our infrastructure to reduce exposure,” said Wittkopp, who believes this research can provide policymakers and the public with a fuller picture of the impact of pollution.

“This kind of information can help us quantify the cost of traffic-related air pollution in terms of health care costs, lives lost and quality of life diminished.”

While genetic factors may make some more vulnerable than others, Wittkopp points out, “There’s no one who’s not susceptible in some way. No one gets better when they are exposed to these pollutants.”

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Obese kids burdened by more than weight


UC San Diego study finds higher risk for liver disease, high blood pressure, heart problems.

High blood pressure and nonalcoholic fatty liver disease (NAFLD) are two emerging health problems related to the epidemic of childhood obesity. In a recent study, researchers at the UC San Diego School of Medicine sought to determine the prevalence of high blood pressure in children with NAFLD, which places them at risk for premature cardiovascular disease.

The study, published in today’s (Nov. 24) edition of PLOS ONE, found that children with NAFLD are at substantial risk for high blood pressure, which is commonly undiagnosed.

“As a result of our study, we recommend that blood pressure evaluation, control and monitoring should be included as an integral component of the clinical management of children with NAFLD, especially because this patient population is at greater risk for heart attacks and strokes,” said Jeffrey Schwimmer, M.D., in the Department of Pediatrics at UC San Diego School of Medicine and principal investigator of the study. “Hypertension is a main cause of preventable death and disability in the United States in adults, but much of the origin occurs in childhood.”

NAFLD – the inappropriate storage of fat droplets inside liver cells – is the most common cause of chronic liver disease in the United States and affects nearly 10 percent of all children. Although children with chronic liver disease often have no symptoms, some children with NAFLD will have fatigue and/or abdominal pain. The initial evaluation for NAFLD is via a blood test and diagnosis is ultimately based upon a liver biopsy. The disease is most common in children and teenagers who are overweight and can develop in conjunction with other health problems, such as diabetes.

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Global dietary choices show disturbing trends


UC Santa Barbara professor co-authors paper that examines global impact of what we eat.

David Tilman

The world is gaining weight and becoming less healthy, and global dietary choices are harming the environment.

Those are among the findings of a paper co-authored by David Tilman, a professor in the UC Santa Barbara Bren School of Environmental Science & Management, and Michael Clark, a graduate student at the University of Minnesota, where Tilman also is a professor. In “Global Diets Link Environmental Sustainability and Human Health,” published today (Nov. 12) in the journal Nature, the researchers find that rising incomes and urbanization around the world are driving a global dietary transition that is, in turn, diminishing the health of both people and the planet.

“These dietary shifts,” they write, “are greatly increasing the incidence of Type 2 diabetes, coronary heart disease and other chronic non-communicable diseases that lower global life expectancies.”

The paper is the first to show the global links among the elements of what Tilman refers to as the “tightly linked diet–environment–health trilemma.”

“Previous analyses have looked at the effects of diet in individual countries, but we are the first to examine the global impacts on both human health and the environment of diet as it is now and as it is becoming,” he says. “We gathered information on dietary trends and environmental impacts for 90 percent of the global population. Our data let us see how diets, health and the environment have been changing and where they are going.”

“Some of what we found is not surprising, but the global implications are frightening,” Tilman adds. “Most of us have heard that some diets are healthier, that eating too many calories is bad for you and that red meat harms the environment. We were surprised at how rapidly and consistently diets were changing around the world, how massively this would impact global health and how much it would increase global greenhouse gas emissions and the destruction of tropical forests and other ecosystems.”

Unhealthful diets linked to urbanization

The links between urbanization, increased wealth and unhealthful diets are clear, Tilman explains. When a country industrializes, the transition from a traditional rural diet to one that includes more processed meats and more empty calories can occur quickly. “People move to cities, leaving behind their own gardens where they grew fruits and vegetables,” Tilman said. “They’re working in a factory 12 hours a day, six or seven days a week, so they need food that’s cheap and fast. The cheapest, fastest food you can get is filled with starch, sugar, fat and salt. Almost overnight, they go from a healthy diet to one that has way too many calories and leads to diabetes and heart disease.”

Also, because people tend to eat more meat as they become wealthier, much of the expected 100-percent increase in crop production that will be required by 2050 would be used to feed not humans but livestock. To do that, much more land will need to be cleared, with the result that more habitat will be lost, more species will likely become extinct and increased runoff of agricultural fertilizers and pesticides will degrade streams, rivers, lakes, groundwater and oceans.

Alternative diets offer health benefits

Tilman suggests that hope — and help — lie in the widespread adoption of alternative diets that offer substantial health benefits and could reduce global agricultural greenhouse gas emissions, reduce land clearing and resultant species extinctions and help prevent a variety of diet-related chronic noncommunicable diseases.

Comparing conventional American omnivorous diets to the Mediterranean diet, a pescetarian diet (in which fish is the only animal protein) and a vegetarian diet, the compiled research showed that the three alternatives to the omnivorous diet decreased Type 2 diabetes by 16 to 41 percent, cancer by 7 to 13 percent and morality rates from coronary heart disease by 20 to 26 percent. Moreover, the authors show that these alternative diets could reduce global greenhouse gas emissions from food production by about 40 percent below what they would be if dietary trends continued.

To reach their conclusions, the researchers gathered all published life-cycle assessments covering “cradle to farm gate” greenhouse gas emissions for production systems of food crops, livestock, fisheries and aquaculture — some 500 studies, of which about 220 were useful. They also gathered 50 years of data for 100 of the world’s more populous nations to analyze global dietary trends and their drivers, using that information to forecast future diets should past trends continue.

To quantify the effects of alternative diets on mortality and on Type 2 diabetes, cancer and chronic coronary heart disease, they summarized results of eight major long-term studies on diet and health. Finally, they combined those relationships with projected increases in global population to forecast global environmental implications of current dietary trajectories and calculate the environmental benefits of diets associated with reduced rates of chronic noncommunicable diseases.

“Better diets are the solution to these big problems,” Tilman says. “Only better diets can prevent a massive global epidemic of chronic noncontagious disease. These same diets would also protect the environment. Since big food companies produce so much of what is eaten, we need them to be part of this solution. By developing, producing and advertising foods that are healthy and tasty, these companies can help their customers, the earth and their bottom line. It is a niche waiting to be filled.”

Tilman wonders if unhealthy foods laden with fats or sugars might grow into a health issue somewhat like smoking. “Throughout history, foods that tasted good were almost always healthy but scarce. Now we have thousands of inexpensive manufactured foods that taste good because of an overabundance of sugar, fat or salt but are bad for us. What is the ethics of selling such foods now that we know how bad they are for heath and the environment?”

The research generated a number of nuanced findings about the environmental impacts of various dietary choices. The following are among them:

  • While the difference in greenhouse gas emissions for animal-based versus plant-based foods is well known, emissions per gram of protein for beef and lamb are about 250 times those of legumes; pork, chicken, dairy, and fish have much lower emissions;
  • Twenty servings of vegetables have fewer greenhouse gas emissions than one serving of beef.
  • Fish caught by trawling, which involves dragging fishnets along the ocean floor, can have three times the emissions of fish caught by traditional methods.
  • And among cereal grains, rice has five times the emissions per gram of protein as wheat.

These and other facts demonstrate that there are many diets that are both good for the environment and healthy.

While Tilman does not expect to see quick societal changes in diet, he hopes that the paper will be seen by the right people who can influence the food supply and that it “can encourage people to think about this challenge and have a dialogue it.”

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