TAG: "Diabetes"

Graduate student examines use of social media in health care


Post conveying negative emotions generate an increase in user comments, study finds.

Holly Rus, UC Merced

By James Leonard, UC Merced

The use of images and direct questions by health communicators on Facebook tends to increase user engagement, though linking to external websites and videos does not. Posts conveying positive emotions have no clear impact on engagement, while negative ones — including expressions of depression, sadness, doubt, fear, hopelessness, anxiety and anger — generate an increase in user comments.

Those were a few of the results of a study on social media and health communications by UC Merced Ph.D. student Holly Rus, who will present her findings this week during the 36th Annual Meeting & Scientific Sessions of the Society of Behavioral Medicine in San Antonio.

Working with professor Linda Cameron, Rus conducted an analysis of more than 500 posts by diabetes-related support pages on Facebook. The researchers looked for attributes in posts that could be used to predict not just overall user engagement, but specific types of engagement.

Among the study’s findings:

  • Posts with images had more than four times as many likes and 11 times as many shares as those without.
  • Messages of support or encouragement and posts soliciting input both had more than twice as many comments as those without.
  • Emotionally positive posts — including hope, optimism, humor, happiness, benefit finding and gratitude — did not predict any particular engagement, while negative ones generated a roughly threefold increase in comments.
  • Posts about the possible effects of diabetes generated more than twice as many shares as those without, while the use of external links predicted fewer likes and shares.

It’s clear that social media has the potential to be a significant resource for health communicators and for patients and their supporters. Rus said her study is a step toward a better understanding of how to make this growing form of health communication more effective.

“Ultimately we aimed to figure out which ingredients of online health messages were most likely to engage users,” she said. “Doing this will help us better understand if and how social media can best be used in health care.”

Rus’ study received special recognition from SBM, being chosen as a Citation Abstract and a Meritorious Student Abstract. An enlarged version of her abstract will be on display during one of the poster sessions at the San Antonio Marriott Rivercenter.

Cameron’s research focuses on health communications and psychosocial interventions for individuals who have or are at risk for illnesses like cancer, heart disease and diabetes. She’s part of a thriving group of UC Merced professors studying health psychology, a rapidly emerging field examining the interactions between behavior and physical health.

Cameron said this research could have significant implications in an area of ever-increasing importance.

“The big-picture question is how we can best harness social media to improve health care,” Cameron said. “Social media is a huge resource that people are increasingly using to gather health information. How can we shape these messages to increase engagement and encourage better health behaviors? If we want to be effective, we have to attract people to the message and have those people pass it around.”

View original article

CATEGORY: NewsComments (0)

New clues to treat juvenile diabetes


Hartwell Foundation award winners include researchers from UC Davis, UC San Diego.

By Andy Fell, UC Davis

UC Davis assistant professor Mark Huising is a recipient of The Hartwell Foundation 2014 Individual Biomedical Research Award to support his early-stage research toward a cure for juvenile diabetes. Diabetes affects 10 percent of the entire United States population, including approximately a million children. Remarkably, 40 children every day receive the diagnosis of diabetes.

Huising, who works in the Department of Neurobiology, Physiology and Behavior at the UC Davis College of Biological Sciences, also holds an appointment in the Department of Physiology and Membrane Biology at the UC Davis School of Medicine. He joined UC Davis in November 2014 having previously worked at the Salk Institute in La Jolla. He is interested in how certain cells in the pancreas control the body’s response to sugar in diabetes. Achieving a balance between reduction of elevated blood sugar levels and the need to prevent potentially fatal low sugar levels is critical to maintaining health.

The Hartwell Foundation award will provide $300,000 in direct cost over three years to support Huising’s research looking at the biological signals and triggers affecting a small pool of cells in the pancreas that could be essential in regenerating control of blood sugar in this disease. The Individual Biomedical Research Award to Huising represents the ninth time a researcher from UC Davis has won such recognition from The Hartwell Foundation over the last seven years. The 12 Hartwell Foundation 2014 Individual Biomedical Research Award winners also include Shira Robbins, UC San Diego associate clinical professor of ophthalmology, for “Omega-3 Fatty Acids as a Therapy for the Prevention of Retinopathy of Prematurity.”

Islets, insulin and diabetes

Diabetes has been a prevalent health problem since ancient times. Two forms of the disease are known — Type 1, or “insulin-dependent” diabetes, and Type 2 diabetes, caused when the body fails to regulate the level of sugar properly, sending it either soaring high or dropping to very low levels.

In juvenile diabetes, the body’s own immune system causes damage to a specialized region in the pancreas, called the islets of Langerhans, effectively rejecting the tissue. The damage is significant because the beta cells within the islets make insulin. Normally, increasing blood sugar stimulates insulin production, which causes the body’s cells to pull sugar out of circulation. The islets also house alpha cells, which make another hormone, glucagon. When blood sugar falls, alpha cells make more glucagon, which causes the liver to break out stocks of glycogen and turn it into glucose.

New insight on insulin from immature cells

At diagnosis of diabetes, the body’s immune system has already destroyed most beta cells and any ability to produce insulin. The remaining alpha cells build up and release glucagon, which causes a serious side-effect of juvenile diabetes. The majority of scientific strategies focus on means to prevent beta cell death and promote beta cell division. However, efforts to restore lost beta cells have been largely unsuccessful.

Huising has discovered that, in laboratory mice, immature beta cells may spontaneously arise from alpha cells. He proposes to identify the biochemical signals that switch alpha cells into beta cells and determine in human tissue whether such beta cells are adequately mature and functional. Huising’s approach represents a shift in the current paradigm that after birth beta cells arise exclusively through the division of existing beta cells.

If successful, Huising will harness the intrinsic potential for beta cell regeneration that exists within pancreatic islets. This approach has the benefit of blocking a serious side effect of juvenile diabetes and represents a potential path to a cure for the disease.

Biomedical research that benefits children

“The Hartwell Foundation has a strong commitment to providing financial support to stimulate discovery in early-stage, innovative biomedical research that has potential to benefit children of the United States,” said Fred Dombrose, president of The Hartwell Foundation. “Mark Huising typifies the innovative, young investigator we seek to fund. We want to make a difference.”

Top Ten Center designation

In addition to the individual award, The Hartwell Foundation designated UC Davis as one of its Top Ten Centers for Biomedical Research for the fifth consecutive year.

In selecting each research center of excellence, The Hartwell Foundation takes into account the shared values the institution has with the foundation relating to children’s health, the presence of an associated medical school and biomedical engineering program, and the quality and scope of ongoing biomedical research.

The foundation also considers the institutional commitment to support collaboration, provide encouragement, and extend technical support to the investigator, especially as related to translational approaches and technology transfer that could promote rapid clinical application of research results.

View original article

Related links:

CATEGORY: NewsComments Off

‘Open’ stem cell chromosomes reveal new possibilities for diabetes


UC San Diego researchers map chromosomal changes over time.

Pancreatic cells derived from embryonic stem cells.

By Heather Buschman, UC San Diego

Stem cells hold great promise for treating a number of diseases, in part because they have the unique ability to differentiate, specializing into any one of the hundreds of cell types that comprise the human body. Harnessing this potential, though, is difficult. In some cases, it takes up to seven carefully orchestrated steps of adding certain growth factors at specific times to coax stem cells into the desired cell type. Even then, cells of the intestine, liver and pancreas are notoriously difficult to produce from stem cells. Writing in Cell Stem Cell today (April 2), researchers at the UC San Diego School of Medicine have discovered why.

It turns out that the chromosomes in laboratory stem cells open slowly over time, in the same sequence that occurs during embryonic development. It isn’t until certain chromosomal regions have acquired the “open” state that they are able to respond to added growth factors and become liver or pancreatic cells. This new understanding, say researchers, will help spur advancements in stem cell research and the development of new cell therapies for diseases of the liver and pancreas, such as type 1 diabetes.

“Our ability to generate liver and pancreatic cells from stem cells has fallen behind the advances we’ve made for other cell types,” said Maike Sander, M.D., professor of pediatrics and cellular and molecular medicine and director of the Pediatric Diabetes Research Center at UC San Diego. “So we haven’t yet been able to do things like test new drugs on stem cell-derived liver and pancreatic cells. What we have learned is that if we want to make specific cells from stem cells, we need ways to predict how those cells and their chromosomes will respond to the growth factors.”

Sander led the study, together with co-senior author Bing Ren, Ph.D., professor of cellular and molecular medicine at UC San Diego and Ludwig Cancer Research member.

Chromosomes are the structures formed by tightly wound and packed DNA. Humans have 46 chromosomes – 23 inherited from each parent. Sander, Ren and their teams first made maps of chromosomal modifications over time, as embryonic stem cells differentiated through several different developmental intermediates on their way to becoming pancreatic and liver cells. Then, in analyzing these maps, they discovered links between the accessibility (openness) of certain regions of the chromosome and what they call developmental competence – the ability of the cell to respond to triggers like added growth factors.

“We’re also finding that these chromosomal regions that need to open before a stem cell can fully differentiate are linked to regions where there are variations in certain disease states,” Sander says.

In other words, if a person were to inherit a genetic variation in one of these chromosomal regions and his or her chromosome didn’t open up at exactly the right time, he or she could hypothetically be more susceptible to a disease affecting that cell type. Sander’s team is now working to further investigate what role, if any, these chromosomal regions and their variations play in diabetes.

Co-authors of this study also include Allen Wang, Ruiyu Xie, Thomas Harper, Nisha A. Patel, Kayla Muth, Jeffrey Palmer, Jinzhao Wang, and Dieter K. Lam, UC San Diego; Feng Yue, The Pennsylvania State University; Yan Li, Yunjiang Qiu, Ludwig Cancer Research; and Jeffrey C. Raum, Doris A. Stoffers, University of Pennsylvania.

This research was funded, in part, by the National Institutes of Health (grants U01-DK089567, U01-DK072473, U01-ES017166, U01-DK089540 and T32-DK7494-27), California Institute for Regenerative Medicine (grants RB5-07236 and TG2-01154, Bridges to Stem Cells Program), Helmsley Charitable Trust and JDRF.

View original article

CATEGORY: NewsComments Off

UC researchers awarded stem cell grants


Funding to develop treatments for Huntington’s, spina bifida, chronic diabetic wounds.

Roslyn Rivkah Isseroff, UC Davis

University of California researchers from two campuses received three grants totaling more than $12 million in funding from the state’s stem cell agency to develop stem cell treatments for Huntington’s disease, spina bifida and chronic diabetic wounds.

The funding was part of $25.2 million in Preclinical Development Awards targeting seven deadly or disabling disorders – what the California Institute for Regenerative Medicine considers “the most promising” research leading up to human clinical trials using stem cells to treat disease and injury.

UC Davis researchers were awarded a pair of grants totaling more than $7 million to develop stem cell therapies for spina bifida ($2.2 million) and chronic diabetic wounds ($5 million).

Diana Farmer, professor and chair of surgery at UC Davis Medical Center, is developing a placental stem cell therapy for spina bifida, the common and devastating birth defect that causes lifelong paralysis as well as bladder and bowel incontinence. She and her team are working on a unique treatment that can be applied in utero – before a baby is born — in order to reverse spinal cord damage.

Diana Farmer, UC Davis

Roslyn Rivkah Isseroff, a UC Davis professor of dermatology, and Jan Nolta, professor of internal medicine and director of the university’s Stem Cell Program, are developing a wound dressing containing stem cells that could be applied to chronic wounds and be a catalyst for rapid healing. This is Isseroff’s second CIRM grant, and it will help move her research closer to having a product approved by the U.S. Food and Drug Administration that specifically targets diabetic foot ulcers, a condition affecting more than 6 million people in the country.

Also, Leslie Thompson of the Sue & Bill Gross Stem Cell Research Center at UC Irvine has been awarded $5 million to continue her CIRM-funded effort to develop stem cell treatments for Huntington’s disease. The grant supports her next step: identifying and testing stem cell-based treatments for HD, an inherited, incurable and fatal neurodegenerative disorder. In this project, Thompson and her colleagues will create an HD therapy employing human embryonic stem cells that can be evaluated in clinical trials.

Leslie Thompson, UC Irvine

CIRM’s governing board also approved an application for the Tools and Technology Award that had been deferred from the January meeting. UCLA’s Carla Koehler will now get $1.3 million for research on a small molecule tool for reducing the malignant potential in reprogramming human induced pluripotent stem cells and embryonic stem cells.

Overall, CIRM’s governing board has awarded nearly $1.9 billion in stem cell grants, with half of the total going to the University of California or UC-affiliated institutions.

For more information:

Related links:

CATEGORY: NewsComments Off

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.

View original article

CATEGORY: NewsComments Off

Forging ahead in fight against hemochromatosis


Research advances are improving prognosis for hereditary blood-iron overload disorder.

By Tom Vasich, UC Irvine

Since coming to the UC Irvine School of Medicine in 1998, Christine and Gordon McLaren have been leading the way in the research and treatment of hemochromatosis, a hereditary disease that causes the body to absorb too much iron from ingested food.

The excess iron is stored in various organs – especially the liver, heart and pancreas – and can poison them, precipitating such life-threatening conditions as cirrhosis and liver cancer, heart arrhythmias and diabetes. Once considered a rare disease, hemochromatosis is now recognized as one of the most common inherited disorders, affecting as many as 1 million people in the U.S.

Christine McLaren is a professor of epidemiology, and Dr. Gordon McLaren is a professor of medicine specializing in hematology and oncology who practices in the Veterans Affairs Long Beach Healthcare System.

Over the past few months, the wife and husband have made noteworthy strides: Last September, they received a $2 million grant from the National Institute of Diabetes & Digestive & Kidney Diseases to investigate the genetic modifiers of iron status in hemochromatosis. And a study the McLarens presented in December at the annual meeting of the American Society of Hematology was a “Best of ASH” honoree.

Here, they discuss their work:

How did you both acquire an interest in this field?

Christine: We developed a focus on the disorder independently. Early in my career, I provided statistical consulting for hematologists who had research projects involving iron overload and iron deficiency. Meanwhile, Gordon has had a long-standing interest for over 30 years in the area of iron metabolism, with an emphasis on hemochromatosis.

In 2000, after Gordon and I had joined the faculty at UCI, we were fortunate to receive National Institutes of Health funding to work together and to screen more than 20,000 primary care patients for iron overload and hereditary hemochromatosis at UCI ambulatory care clinics.

The primary goal of that research was to contribute to a national epidemiologic study of iron overload and hereditary hemochromatosis in a multicenter, multiethnic, primary care-based sample of over 100,000 people.

How are people susceptible to hemochromatosis?

Gordon: Generally, iron overload occurs only in people with two copies of the hemochromatosis gene (one copy inherited from each parent). The frequency of having two copies in the European-American population is about 5 per 1,000 persons.

However, not all people with two copies of the gene will develop iron overload. Thus, we think there must be other factors – such as mutations in other genes affecting dietary iron absorption – that are required for the disease to become fully manifest, and this is what we’re studying.

If we can identify what causes the difference, we may be able to use this information to predict which patients are at greater risk of developing iron overload and when to begin therapy to remove excess iron before it accumulates to toxic levels.

Interestingly, the frequency of the genetic predisposition to hemochromatosis among European-Americans is the same in men and women, but for reasons that are not completely understood, men are more likely to develop the full-blown syndrome.

What do you plan to accomplish with the $2 million in support from the National Institute of Diabetes & Digestive & Kidney Diseases?

Gordon: We’re leading a multidisciplinary team of investigators at eight research institutions in the U.S., Canada and Australia. To better understand the reasons for this variability in disease expression, our group will examine genetic factors in the susceptibility or resistance to iron overload in patients with a genetic predisposition for hemochromatosis across a wide range of geographic areas.

The purpose of this research is to identify other inherited traits that may interact to cause more severe disease in certain patients. It’s important to identify persons at risk because effective iron removal treatment is available, and beginning such therapy before iron overload becomes advanced can prevent disease complications.

Christine: This work can have important clinical applications, including the ability to identify young hemochromatosis patients at risk for potentially severe iron overload later in life, thereby influencing physicians’ recommendations for iron removal therapy and long-term follow-up. We’re hopeful that our findings will lead to new approaches that will inform the development of innovative prevention and treatment strategies tailored to the individual.

View original article

CATEGORY: NewsComments Off

Pens filled with high-tech inks for do-it-yourself sensors


New simple tool is opening door to where anyone will be able to build sensors, anywhere.

By Ioana Patringenaru, UC San Diego

A new simple tool developed by nanoengineers at the University of California, San Diego, is opening the door to an era when anyone will be able to build sensors, anywhere, including physicians in the clinic, patients in their home and soldiers in the field.

The team from the University of California, San Diego, developed high-tech bio-inks that react with several chemicals, including glucose. They filled off-the-shelf ballpoint pens with the inks and were able to draw sensors to measure glucose directly on the skin and sensors to measure pollution on leaves.

Skin and leaves aren’t the only media on which the pens could be used. Researchers envision sensors drawn directly on smart phones for personalized and inexpensive health monitoring or on external building walls for monitoring of toxic gas pollutants. The sensors also could be used on the battlefield to detect explosives and nerve agents.

The team, led by Joseph Wang, the chairman of the Department of NanoEngineering at the University of California, San Diego, published their findings in the Feb. 26 issue of Advanced Healthcare Materials. Wang also directs the Center for Wearable Sensors at UC San Diego.

“Our new biocatalytic pen technology, based on novel enzymatic inks, holds considerable promise for a broad range of applications on site and in the field,” Wang said.

The biggest challenge the researchers faced was making inks from chemicals and biochemicals that aren’t harmful to humans or plants; could function as the sensors’ electrodes; and retain their properties over long periods in storage and in various conditions. Researchers turned to biocompatible polyethylene glycol, which is used in several drug delivery applications, as a binder. To make the inks conductive to electric current they used graphite powder. They also added chitosan, an antibacterial agent which is used in bandages to reduce bleeding, to make sure the ink adhered to any surfaces it was used on. The inks’ recipe also includes xylitol, a sugar substitute, which helps stabilize enzymes that react with several chemicals the do-it-yourself sensors are designed to monitor.

Reusable glucose sensors

Wang’s team has been investigating how to make glucose testing for diabetics easier for several years. The same team of engineers recently developed non-invasive glucose sensors in the form of temporary tattoos. In this study, they used pens, loaded with an ink that reacts to glucose, to draw reusable glucose-measuring sensors on a pattern printed on a transparent, flexible material which includes an electrode. Researchers then pricked a subject’s finger and put the blood sample on the sensor. The enzymatic ink reacted with glucose and the electrode recorded the measurement, which was transmitted to a glucose-measuring device. Researchers then wiped the pattern clean and drew on it again to take another measurement after the subject had eaten.

Researchers estimate that one pen contains enough ink to draw the equivalent of 500 high-fidelity glucose sensor strips. Nanoengineers also demonstrated that the sensors could be drawn directly on the skin and that they could communicate with a Bluetooth-enabled electronic device that controls electrodes called a potentiostat, to gather data.

Sensors for pollution and security

The pens would also allow users to draw sensors that detect pollutants and potentially harmful chemicals sensors on the spot. Researchers demonstrated that this was possible by drawing a sensor on a leaf with an ink loaded with enzymes that react with phenol, an industrial chemical, which can also be found in cosmetics, including sunscreen. The leaf was then dipped in a solution of water and phenol and the sensor was connected to a pollution detector. The sensors could be modified to react with many pollutants, including heavy metals or pesticides.

Next steps include connecting the sensors wirelessly to monitoring devices and investigating how the sensors perform in difficult conditions, including extreme temperatures, varying humidity and extended exposure to sunlight.

“Biocompatible Enzymatic Roller Pens for Direct Writing of Biocatalytic Materials: ‘Do-it-yourself’ Electrochemical Biosensors” is authored by Amay J. Bandodkar, Wenzhao Jia, Julian Ramirez and Wang.

View original article

CATEGORY: NewsComments Off

Molecular link between obesity, type 2 diabetes reveals potential therapy


UC San Diego researchers find that inflammatory molecule LTB4 promotes insulin resistance.

By Heather Buschman, UC San Diego

Obesity causes inflammation, which can in turn lead to type 2 diabetes. What isn’t well established is how inflammation causes diabetes — or what we can do to stop it. Researchers at the UC San Diego School of Medicine have discovered that the inflammatory molecule LTB4 promotes insulin resistance, a first step in developing type 2 diabetes. What’s more, the team found that genetically removing the cell receptor that responds to LTB4, or blocking it with a drug, improves insulin sensitivity in obese mice. The study is published today (Feb. 23) by Nature Medicine.

“This study is important because it reveals a root cause of type 2 diabetes,” said Jerrold M. Olefsky, M.D., professor of medicine, associate dean for scientific affairs and senior author of the study. “And now that we understand that LTB4 is the inflammatory factor causing insulin resistance, we can inhibit it to break the link between obesity and diabetes.”

Here’s what’s happening in obesity, according to Olefsky’s study. Extra fat, particularly in the liver, activates resident macrophages, the immune cells living there. These macrophages then do what they’re supposed to do when activated — release LTB4 and other immune signaling molecules to call up an influx of new macrophages. Then, in a positive feedback loop, the newly arriving macrophages also get activated and release even more LTB4 in the liver.

This inflammatory response would be a good thing if the body was fighting off an infection. But when inflammation is chronic, as is the case in obesity, all of this extra LTB4 starts activating other cells, too. Like macrophages, nearby liver, fat and muscle cells also have LTB4 receptors on their cell surfaces and are activated when LTB4 binds them. Now, in obesity, those cells become inflamed as well, rendering them resistant to insulin.

Once Olefsky and his team had established this mechanism in their obese mouse models, they looked for ways to inhibit it. First, they genetically engineered mice that lack the LBT4 receptor. When that approach dramatically improved the metabolic health of obese mice, they also tried blocking the receptor with a small molecule inhibitor. This particular compound was at one time being tested in clinical trials, but was dropped when it didn’t prove all that effective in treating its intended ailment. Olefsky’s team fed the prototype drug to their mice and found that it worked just as well as genetic deletion at preventing — and reversing — insulin resistance.

“When we disrupted the LTB4-induced inflammation cycle either through genetics or a drug, it had a beautiful effect — we saw improved metabolism and insulin sensitivity in our mice,” Olefsky said. “Even though they were still obese, they were in much better shape.”

Co-authors of this study include Pingping Li, Da Young Oh, Gautam Bandyopadhyay, William S. Lagakos, Saswata Talukdar, Olivia Osborn, Andrew Johnson, Heekyung Chung, Rafael Mayoral, Michael Maris, Jachelle M Ofrecio, Sayaka Taguchi, Min Lu, all at UC San Diego.

This research was funded, in part, by the National Institute of Diabetes and Digestive and Kidney Diseases (DK033651, DK074868, DK063491, DK09062), the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and Merck Inc.

View original article

CATEGORY: NewsComments Off

Tobacco-smoking parents increase diabetes risk for children exposed in utero


“Smoking of parents is by itself a risk factor for diabetes, independent of obesity or birth weight.”

Credit: iStock

By Michele La Merrill and Kat Kerlin, UC Davis

Children exposed to tobacco smoke from their parents while in the womb are predisposed to developing diabetes as adults, according to a study from the University of California, Davis, and the Berkeley nonprofit Public Health Institute.

In the study, published today (Feb. 9) in the Journal of Developmental Origins of Health and Disease, women whose mothers smoked while pregnant were two to three times as likely to be diabetic as adults. Dads who smoked while their daughter was in utero also contributed to an increased diabetes risk for their child, but more research is needed to establish the extent of that risk.

“Our findings are consistent with the idea that gestational environmental chemical exposures can contribute to the development of health and disease,” said lead author Michele La Merrill, an assistant professor of environmental toxicology at UC Davis.

The study analyzed data from 1,800 daughters of women who had participated in the Child Health and Development Studies, an ongoing project of the Public Health Institute. The CHDS recruited women who sought obstetric care through Kaiser Permanente Foundation Health Plan in the San Francisco Bay Area between 1959 and 1967. The data was originally collected by PHI to study early risk of breast cancer, which is why sons were not considered in this current study.

In previous studies, fetal exposure to cigarette smoke has also been linked to higher rates of obesity and low birth weight. This study found that birth weight did not affect whether the daughters of smoking parents developed diabetes.

“We found that smoking of parents is by itself a risk factor for diabetes, independent of obesity or birth weight,” said La Merrill. “If a parent smokes, you’re not protected from diabetes just because you’re lean.”

The study was supported through funding from the National Institute of Environmental Health Sciences, the Eunice Kennedy Shriver National Institute of Child Health and Human Development, and the California Breast Cancer Research Program Special Research Initiative.

View original article

CATEGORY: NewsComments Off

A gamechanger for pediatric diabetes


UC Santa Barbara scientists are developing a pediatric artificial pancreas.

UC Santa Barbara chemical engineers Frank Doyle (left) and Eyal Dassau with a model of their artificial pancreas for adults.

By Sonia Fernandez, UC Santa Barbara

Anyone who lives with Type 1 diabetes is all too familiar with the sheer amount of effort — and often round-the-clock attention — required to manage the disease. Food intake is closely monitored, as is physical activity, and the period between meals is carefully tracked in order to calculate appropriate insulin dosages, which have to be delivered at the right time.

All this to keep blood glucose levels within a healthy range.

For parents of children with Type 1 diabetes, the stress is amplified. Children’s unpredictable eating habits and food preferences, spontaneous physical activity and sensitivity to insulin require parents to be extra vigilant. The dreaded overnight hypoglycemia — a condition in which glucose levels drop to dangerously low levels between dinner and breakfast — requires parents to interrupt their own sleep habits so they can check their children’s blood sugar and give the child a snack if needed. Conversely, if the glucose reading is too high, they would need to administer insulin. And those eagerly anticipated birthday parties (complete with cake and ice cream), sleepovers and playdates? Only if the other parents involved can be trusted to monitor the child closely and respond to emergencies.

But with a $1.8-million, three-year grant from the National Institutes of Health, UC Santa Barbara chemical engineers Frank Doyle and Eyal Dassau and Yale University’s Dr. Stuart Weinzimer could make such hands-on care a thing of the past. And it could happen within a decade. The researchers and their teams are embarking on the development of artificial pancreas (AP) for children. The grant is the UC Santa Barbara researchers’ first award for a pediatric closed-loop study.

“I think one of the most important things we can do is alleviate parents’ fears of overnight hypoglycemia,” said Dassau, a research engineer in UC Santa Barbara’s Department of Chemical Engineering and the principal investigator on this study. “As a result, parents can get a full night’s sleep without having to worry what might happen at 4 a.m., or who’s awake to check their child’s glucose. That would be a big success.”

Over the past 12 years, Doyle, director of the Institute for Collaborative Biotechnologies at UC Santa Barbara, and his research group have developed the artificial pancreas, a combination of sensor technology and insulin pump, which, thanks to a control algorithm, reads levels of glucose and injects the appropriate amount of insulin based on the data, and the patient’s individual characteristics.

Thus far, the researchers have made great strides in developing UCSB’s AP for use in adults. In a collaboration with the William Sansum Diabetes Research Center in Santa Barbara, and in local and international clinical trials, the AP’s multinational team of researchers has been refining the device based on input from engineering, clinical and behavioral aspects of diabetes management.

Tailoring the device to manage pediatric diabetes, however, requires the researchers to consider an additional set of factors.

“Children have unpredictable eating habits,” said Dassau. “You can put a certain amount of food in front of them, but you don’t know whether they’re going to eat it all.” Additionally, they may graze throughout the day, and tend to be more spontaneous than adults with their physical activity. Also coming into play are the children’s general lack of awareness about their condition and their limited ability to inform parents and caregivers of any immediate health situations.

The protocols for diabetes management vary by age as well. With adults and teenagers who can predict their meals and mealtimes, insulin can be delivered subcutaneously about 15 minutes before eating to ensure an adequate amount of the hormone has reached the bloodstream by the time they eat. This “pre-meal bolus” is an ideal way to manage meal glucose control, as it allows insulin to be absorbed when the glucose surge arrives with the meal, and mimics as closely as possible the way a healthy individual’s body regulates blood sugar.

However, in younger children with Type 1 diabetes, because of unpredictable eating habits and higher sensitivity to insulin, the hormone must be delivered after the meal, which creates both a delay and the chance of a swing to the hypoglycemic extreme of the blood sugar range, due to the tendency to overcompensate.

According to the researchers, the first phase of research for the pediatric AP involves data collection. With clinical expertise from Weinzimer, a pediatric endocrinologist, professor at Yale School of Medicine and a leading expert on Type 1 diabetes in children, the researchers will tune the AP’s Zone MPC (model predictive control) algorithm to meet the specific challenges of managing pediatric diabetes.

“I would look for the following things in a pediatric version of an AP: safety above all; efficacy; reliability; and ease of use,” said Weinzimer. In addition to protecting against constant wild swings in blood sugar, which would in turn alleviate the high rates of anxiety, depression and burnout in parents, and prevent the additional problem of disrupted psychosocial development in children with Type 1 diabetes, he said. The device itself must perform in a predictable manner and not be overly complicated or burdensome to use.

“One of the things I appreciate most about Drs. Doyle and Dassau is that they are, above all, scientists. They are extremely knowledgeable about control systems for the artificial pancreas, world experts in fact, and they approach this field with scientific rigor and balance,” Weinzimer continued. “We have to be very careful as investigators not to minimize the potential risks and shortcomings in our systems as we test them. We have a moral duty to protect our patients. I firmly believe that these systems will be transformative in diabetes care, but we should not lose our scientific objectivity and skepticism. Frank and Eyal have always struck me as very balanced and circumspect in how they approach this field, and I am looking forward to working with them.”

“We’ve already proved in previous clinical trials that our medically inspired artificial pancreas design can handle unannounced meals and physical activity,” said Dassau, adding that bringing this design to the younger population of Type I diabetes patients would ease the burden on parents who worry about the extra cookie or surprise sugary treat. “We’ve already developed safety algorithms for hypo- and hyperglycemia that can be adjusted for young children.”

Because insulin requirements change as the child gets older, the algorithm will be adjusted and refined according to different age groups, the researchers noted.

The second phase of the project involves developing and in-clinic testing of an advisory system and an alert system for parents that both provides insight on strategies for the management of their children’s conditions in general, and informs them of impending hypo- or hyperglycemia.

At every phase, the researchers will conduct repeated evaluations and refinements to the algorithm as well as to the alert and advisory systems. The goal is to give parents and children the ability to be involved in the management of diabetes to the extent that they can be, while safeguarding against extremes when unexpected circumstances arise. Snacking, unscheduled naps, spur-of-the-moment activities or missed meals will no longer result in increased stress levels for both parents and children.

According to Doyle, who holds the Mellichamp Chair in Process Control at UC Santa Barbara, when his group started work on the artificial pancreas over a decade ago, the researchers found that subjects using the conventional multiple daily injection method of controlling blood sugar were able to keep their glucose level in a safe range for only slightly over 50 percent of the time.

“In our most recent trials, we have demonstrated that our algorithms can keep subjects in a safe range for 80 percent or more of the time,” he said. The UC Santa Barbara AP’s Health Monitoring System sends user alerts in the form of messages and audible signals when problems arise, such as blood sugars that are trending low. Additionally, Doyle’s AP researchers have two other active grants funding research to examine how the device can monitor its own operations and alert users to potential malfunctions.

In future studies, pediatric AP testing will move to an outpatient component, in which subjects are given free rein over what they eat and do, but at locations near the clinic, with supervision from technical staff.

“But the home is where we want to get,” said Doyle, “with the normal routine, with no interference or intrusion. The true end-game is at home.”

Research for the development of this artificial pancreas is supported by the National Institutes of Health, award number DP3DK104057.

View original article

CATEGORY: SpotlightComments Off

Temporary tattoo offers needle-free way to monitor glucose


‘Proof-of-concept’ tattoo could pave way for UC San Diego to explore others uses of device.

Nanoengineers at UC San Diego have tested a temporary tattoo that both extracts and measures the level of glucose in the fluid in between skin cells.

By Ioana Patringenaru

Nanoengineers at UC San Diego have tested a temporary tattoo that both extracts and measures the level of glucose in the fluid in between skin cells. This first-ever example of the flexible, easy-to-wear device could be a promising step forward in noninvasive glucose testing for patients with diabetes.

The sensor was developed and tested by graduate student Amay Bandodkar and colleagues in professor Joseph Wang’s laboratory at the NanoEngineering Department and the Center for Wearable Sensors at the Jacobs School of Engineering at UC San Diego. Bandodkar said this “proof-of-concept” tattoo could pave the way for the center to explore other uses of the device, such as detecting other important metabolites in the body or delivering medicines through the skin.

At the moment, the tattoo doesn’t provide the kind of numerical readout that a patient would need to monitor his or her own glucose. But this type of readout is being developed by electrical and computer engineering researchers in the Center for Wearable Sensors. “The readout instrument will also eventually have Bluetooth capabilities to send this information directly to the patient’s doctor in real-time or store data in the cloud,” said Bandodkar.

The research team is also working on ways to make the tattoo last longer while keeping its overall cost down, he noted. “Presently the tattoo sensor can easily survive for a day. These are extremely inexpensive — a few cents — and hence can be replaced without much financial burden on the patient.”

The center “envisions using these glucose tattoo sensors to continuously monitor glucose levels of large populations as a function of their dietary habits,” Bandodkar said. Data from this wider population could help researchers learn more about the causes and potential prevention of diabetes, which affects hundreds of millions of people and is one of the leading causes of death and disability worldwide.

People with diabetes often must test their glucose levels multiple times per day, using devices that use a tiny needle to extract a small blood sample from a fingertip. Patients who avoid this testing because they find it unpleasant or difficult to perform are at a higher risk for poor health, so researchers have been searching for less invasive ways to monitor glucose.

In their report in the journal Analytical Chemistry, Wang and his co-workers describe their flexible device, which consists of carefully patterned electrodes printed on temporary tattoo paper. A very mild electrical current applied to the skin for 10 minutes forces sodium ions in the fluid between skin cells to migrate toward the tattoo’s electrodes. These ions carry glucose molecules that are also found in the fluid. A sensor built into the tattoo then measures the strength of the electrical charge produced by the glucose to determine a person’s overall glucose levels.

“The concentration of glucose extracted by the non-invasive tattoo device is almost hundred times lower than the corresponding level in the human blood,” Bandodkar explained. “Thus we had to develop a highly sensitive glucose sensor that could detect such low levels of glucose with high selectivity.”

A similar device called GlucoWatch from Cygnus Inc. was marketed in 2002, but the device was discontinued because it caused skin irritation, the UC San Diego researchers note. Their proof-of-concept tattoo sensor avoids this irritation by using a lower electrical current to extract the glucose.

Wang and colleagues applied the tattoo to seven men and women between the ages of 20 and 40 with no history of diabetes. None of the volunteers reported feeling discomfort during the tattoo test, and only a few people reported feeling a mild tingling in the first 10 seconds of the test.

To test how well the tattoo picked up the spike in glucose levels after a meal, the volunteers ate a carb-rich meal of a sandwich and soda in the lab. The device performed just as well at detecting this glucose spike as a traditional finger-stick monitor.

The researchers say the device could be used to measure other important chemicals such as lactate, a metabolite analyzed in athletes to monitor their fitness. The tattoo might also someday be used to test how well a medication is working by monitoring certain protein products in the intercellular fluid, or to detect alcohol or illegal drug consumption.

Bandodkar was joined on the study by UC San Diego nanoengineers Wenzhao Jia, Ceren Yardımcı, Xuan Wang, Julian Ramirez and Wang, director of the Center for Wearable Sensors and SAIC Endowed Chair and distinguished professor in the NanoEngineering Department.

The publication is “Tattoo-Based Noninvasive Glucose Monitoring: A Proof-of-Concept Study,” published Dec. 12 in the journal Analytical Chemistry.

View original article

CATEGORY: NewsComments (1)

Drug reduces diabetes symptoms in mice


Research involves a potent enzyme inhibitor discovered at UC Davis.

Bruce Hammock, UC Davis

Can diabetes be prevented and even reversed?

Yes, it can — at least in genetically obese mice, according to a newly published study by led by researchers Bruce Hammock at the University of California, Davis, and Joan Clària at the University of Barcelona. The research involves a potent enzyme inhibitor discovered by Hammock’s laboratory that dramatically reduces inflammation, inflammatory pain and neuropathic pain.

In the study, published in the Proceedings of the National Academy of Sciences, an enzyme called soluble epoxide hydrolase, or sEH, inhibitor both prevented the onset of diabetes and reversed the effects of diabetes in obese mice.

“Our previous studies show the drug we are working on will reduce the symptoms of diabetes in mice by itself,” Hammock said, “but the excitement about Joan Clària’s work is that if the mice have a genetically increased level of omega-3 fatty acids — the drug offers prevention or cure in mice.”

The Centers for Disease Control and Prevention estimates that 29.1 million Americans, or 9.3 percent of the population, have diabetes, which is characterized by abnormal blood glucose levels. This includes 8.1 million undiagnosed cases.

The new drug apparently works by stabilizing metabolites of an omega-3 fatty acid called DHA. These metabolites are thought to contribute to the beneficial effects of a diet high in omega-3 fatty acids, Hammock said. Previous UC Davis research in the laboratories of Hammock, Nipavan Chiamvimonvat, Robert Weiss, Anne Knowlton and Fawaz Haj showed that the enzyme reduces or reverses such diabetes-linked medical issues as renal failure, hypertension, diabetic pain, hardening of the arteries and heart failure.

“This exciting research brings mechanistic detail to understanding how omega-3 fatty acids in the diet exert important health effects,” said J. Bruce German, director of the UC Davis Foods for Health Institute, Department of Food Science and Technology, who was not involved in the diabetes-based research.

Clària is an associate professor at the Barcelona University School of Medicine and a senior consultant at the Biochemistry and Molecular Genetics Service of the Hospital Clínic of Barcelona.

In the paper, titled “Inhibition of Soluble Epoxide Hydrolase Modulates Inflammation and Autophagy in Obese Adipose Tissue and Liver: Role for Omega-3 Epoxides,” Clària described the administration of the sEH inhibitor as “a promising strategy to prevent obesity-related co-morbidities.”

Clària said the study also sheds more light on the role of sEH and omega-3 epoxides in insulin-sensitive tissues, especially the liver.

In addition to Clària and Hammock, the publication was first-authored by Cristina López-Vicario and co-authored by José Alcaraz-Quiles, Verónica García-Alonso, Bibiana Rius, Aritz Lopategi, Ester Titos  and Vicente Arroyo,  all of the Clària lab or associates; and Sung Hee Hwang of the Hammock Lab, UC Davis Department of Entomology and Nematology, and the UC Davis  Comprehensive Cancer Center.

Hammock is the founder and CEO of a start-up company, EicOsis, which is putting the new compounds into clinical trials for companion animals and the Pre-Investigational New Drug Application, or Pre-IND, Consultation Program for neuropathic pain in human diabetics.

The study was funded by Clària’s Spanish-initiated grants and by Hammock’s Research Project Grant (R01) and Superfund grants from the National Institutes of Health.

More information about the Hammock lab and about the Clària lab.

View original article

CATEGORY: NewsComments Off

Fresno Bee: UCSF Fresno pediatric residency program

Click video for closed captions, larger view

Connect with UC

UC for California   Follow UC News on Twitter   Follow UC on Facebook   Subscribe to UC Health RSS feed

Facebook leads to lifesaving surgery at UC San Diego

Click video for closed captions, larger view

Contact

We welcome your ideas and feedback. To subscribe or send comments or suggestions, please email alec.rosenberg@ucop.edu.