Study offers clues to why heavy people and anorexics have higher asthma rates

A new study led by Columbia University researchers has found that leptin, a hormone that plays a key role in energy metabolism, fertility, and bone mass, also regulates airway diameter.

These findings could explain why obese people are prone to asthma and suggest that body-weight–associated-asthma may be relieved with medications which help the body mediate leptin function. The study, conducted in mice, was published in the online edition of the journal Cell Metabolism.

“Our study started with the clinical observation that both obesity and anorexia can lead to asthma,” said Gerard Karsenty MD, PhD, professor and chair of genetics and development and professor of medicine at CUMC, and lead author of the study. “This led us to suspect that there must be a signal coming from fat cells that somehow affects the lungs —directly or indirectly.” The most likely candidate was leptin, a protein made by fat cells that circulates in the bloodstream and travels to the brain.

Extensive evidence shows that obesity can cause narrowing of the airways (bronchoconstriction). When obesity develops in people with asthma, it exacerbates the breathing disorder and hampers its treatment through mechanisms that are poorly understood. The current study was designed to elucidate the genetic and molecular bases of the relationships among obesity, airway diameter, and lung function.

Through mouse studies, the researchers showed that abnormally low or high body weight and fat mass results in bronchoconstriction and diminished lung function. Next, they showed that leptin increases airway diameter independently of, and at a lower threshold than, its regulation of appetite.

Leptin affects the airways by decreasing the activity of the parasympathetic nervous system, a branch of the autonomic nervous system not usually associated with leptin. The researchers also showed that regulation of airway diameter occurs regardless of local inflammation in the bronchi.

The researchers conducted two subsequent experiments to determine if these findings might have bearing on asthma therapy. In one, they took obese, asthmatic mice and administered a substance that increases lung inflammation. When they infused leptin in the brain of these mice for four days, “There was no effect on inflammation, but airway diameter and lung functions were normal,” said Dr. Karsenty. “This showed that, at least in the mouse, you can cure obesity-related asthma without affecting inflammation.” In the second experiment, the researchers treated obese, asthmatic mice with drugs that decrease parasympathetic tone, or rate of neuronal firing. Again, the asthma abated after several days.

“The therapeutic implication is that it may be possible to correct asthma in obese people with drugs that inhibit parasympathetic signaling—and thereby inhibit leptin deficiency-related brain signaling,” said Dr. Karsenty. Such drugs are already available. One is tiotropium bromide, which is used primarily for the treatment of chronic obstructive pulmonary disease. Clinical trials are needed before this or a more active and selective drug can be recommended for the treatment of body weight–associated asthma, Dr. Karsenty added.

U of Florida study uncovers protein key to fighting and preventing obesity

University of Florida researchers and colleagues have identified a protein that, when absent, helps the body burn fat and prevents insulin resistance and obesity.

The discovery could aid development of drugs that not only prevent obesity, but also spur weight loss in people who are already overweight, said Dr. Stephen Hsu, one of the study’s corresponding authors and a principal investigator with the UF Sid Martin Biotechnology Development Institute.

One-third of adults and about 17 percent of children in the United States are obese, according to the Centers for Disease Control and Prevention. Although unrelated studies have shown that lifestyle changes such as choosing healthy food over junk food and increasing exercise can help reduce obesity, people are often unable to maintain these changes over time, Hsu said.

“The problem is when these studies end and the people go off the protocols, they almost always return to old habits and end up eating the same processed foods they did before and gain back the weight they lost during the study,” he said. Developing drugs that target the protein, called TRIP-Br2, and mimic its absence may allow for the prevention of obesity without relying solely on lifestyle modifications, Hsu said.

First identified by Hsu, TRIP-Br2 helps regulate how fat is stored in and released from cells. To understand its role, the researchers compared mice that lacked the gene responsible for production of the protein, with normal mice that had the gene.

They quickly discovered that mice missing the TRIP-Br2 gene did not gain weight no matter what they ate — even when placed on a high-fat diet — and were otherwise normal and healthy. On the other hand, the mice that still made TRIP-Br2 gained weight and developed associated problems such as insulin resistance, type 2 diabetes and high cholesterol when placed on a high-fat diet. The normal and fat-resistant mice ate the same amount of food, ruling out differences in food intake as a reason why the mice lacking TRIP-Br2 were leaner.

“We had to explain why the animals eating so much fat were remaining lean and not getting high cholesterol. Where was this fat going?” Hsu said. “It turns out this protein is a master regulator. It coordinates expression of a lot of genes and controls the release of the fuel form of fat and how it is metabolized.”

When functioning normally, TRIP-Br2 restricts the amount of fat that cells burn as energy. But when TRIP-Br2 is absent, a fat-burning fury seems to occur in fat cells. Although other proteins have been linked to the storage and release of fat in cells, TRIP-Br2 is unique in that it regulates how cells burn fat in a few different ways, Hsu said. When TRIP-Br2 is absent, fat cells dramatically increase the release of free fatty acids and also burn fat to produce the molecular fuel called ATP that powers mitochondria — the cell’s energy source. In addition, cells free from the influence of TRIP-Br2 start using free fatty acids to generate thermal energy, which protects the body from exposure to cold.

“TRIP-Br2 is important for the accumulation of fat,” said Dr. Rohit N. Kulkarni, also a senior author of the paper and an associate professor of medicine at Harvard Medical School and the Joslin Diabetes Center. “When an animal lacks TRIP-Br2, it can’t accumulate fat.”

Because the studies were done mostly in mice, additional studies are still needed to see if the findings translate to humans.

“We are very optimistic about the translational promise of our findings because we showed that only human subjects who had the kind of fat (visceral) that becomes insulin-resistant also had high protein levels of TRIP-Br2,” Hsu said.

“Imagine you are able to develop drugs that pharmacologically mimic the complete absence of TRIP-Br2,” Hsu said. “If a patient started off fat, he or she would burn the weight off. If people are at risk of obesity and its associated conditions, such as type 2 diabetes, it would help keep them lean regardless of how much fat they ate. That is the ideal anti-obesity drug, one that prevents obesity and helps people burn off excess weight.”

Pesticides and Parkinson's: Researchers Uncover Further Proof of a Link

For several years, neurologists at UCLA have been building a case that a link exists between pesticide chemical exposure and Parkinson's disease. To date, paraquat, maneb and ziram — common chemicals sprayed in California's Central Valley and elsewhere — have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.

Now, UCLA researchers have discovered a link between Parkinson's and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.

Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson's disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.

Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson's. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual's risk of developing Parkinson's.

The investigators believe their findings concerning benomyl may be generalized to all Parkinson's patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.

The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Parkinson's disease is a debilitating neurodegenerative disorder that affects millions worldwide. Its symptoms — including tremor, rigidity, and slowed movements and speech — increase with the progressive degeneration of neurons, primarily in a part of the mid-brain called the substantia nigra. This area normally produces dopamine, a neurotransmitter that allows cells to communicate, and damage to the mid-brain has been linked to the disease. Usually, by the time Parkinson's symptoms manifest themselves, more than half of these neurons, known as dopaminergic neurons, have already been lost.

While researchers have identified certain genetic variations that cause an inherited form of Parkinson's, only a small fraction of the disease can be blamed on genes, said the study's first author, Arthur G. Fitzmaurice, a postdoctoral scholar in Bronstein's laboratory.

"As a result, environmental factors almost certainly play an important role in this disorder," Fitzmaurice said. "Understanding the relevant mechanisms — particularly what causes the selective loss of dopaminergic neurons — may provide important clues to explain how the disease develops."

Benomyl was widely used in the U.S. for three decades until toxicological evidence revealed it could potentially lead to liver tumors, brain malformations, reproductive effects and carcinogenesis. It was banned in 2001.

The researchers wanted to explore whether there was a relationship between benomyl and Parkinson's, which would demonstrate the possibility of long-lasting toxicological effects from pesticide use, even a decade after chronic exposure. But because a direct causal relationship between the pesticide and Parkinson's can't be established by testing humans, the investigators sought to determine if exposure in experimental models could duplicate some of the pathologic features of the disease.

They first tested the effects of benomyl in cell cultures and confirmed that the pesticide damaged or destroyed dopaminergic neurons.

Next, they tested the pesticide in a zebrafish model of the disease. This freshwater fish is commonly used in research because it is easy to manipulate genetically, it develops rapidly and it is transparent, making the observation and measurement of biological processes much easier. By using a fluorescent dye and counting the neurons, the researchers discovered there was significant neuron loss in the fish — but only to the dopaminergic neurons. The other neurons were left unaffected.

Until now, evidence had pointed to one particular culprit — a protein called α-synuclein — in the development of Parkinson's. This protein, common to all Parkinson's patients, is thought to create a pathway to the disease when it binds together in "clumps" and becomes toxic, killing the brain's neurons. (See UCLA research using "molecular tweezers" to break up these toxic aggregations.)

The identification of ALDH activity now gives researchers another target to focus on in trying to stop this disease.

"We've known that in animal models and cell cultures, agricultural pesticides trigger a neurodegenerative process that leads to Parkinson's," said Bronstein, who directs the UCLA Movement Disorders Program. "And epidemiologic studies have consistently shown the disease occurs at high rates among farmers and in rural populations. Our work reinforces the hypothesis that pesticides may be partially responsible, and the discovery of this new pathway may be a new avenue for developing therapeutic drugs."

"Tricorders" closer to becoming a reality

Photo: Peter Norgard, University of Missouri

The hand-held scanners, or tricorders, of the Star Trek movies and television series are one step closer to reality now that a University of Missouri engineering team has invented a compact source of X-rays and other forms of radiation.

 The radiation source, which is the size of a stick of gum, could be used to create inexpensive and portable X-ray scanners for use by doctors, as well as to fight terrorism and aid exploration on this planet and others.

“Currently, X-ray machines are huge and require tremendous amounts of electricity,” said Scott Kovaleski, associate professor of electrical and computer engineering at MU. “In approximately three years, we could have a prototype hand-held X-ray scanner using our invention. The cell-phone-sized device could improve medical services in remote and impoverished regions and reduce health care expenses everywhere.”

Kovaleski suggested other uses for the device. In dentists’ offices, the tiny X-ray generators could be used to take images from the inside of the mouth shooting the rays outward, reducing radiation exposure to the rest of the patients’ heads. At ports and border crossings, portable scanners could search cargoes for contraband, which would both reduce costs and improve security. Interplanetary probes, like the Curiosity rover, could be equipped with the compact sensors, which otherwise would require too much energy.

The accelerator developed by Kovaleski’s team could be used to create other forms of radiation in addition to X-rays. For example, the invention could replace the radioactive materials, called radioisotopes, used in drilling for oil as well as other industrial and scientific operations. Kovaleski’s invention could replace radioisotopes with a safer source of radiation that could be turned off in case of emergency.

“Our device is perfectly harmless until energized, and even then it causes relatively low exposures to radiation,” said Kovaleski. “We have never really had the ability to design devices around a radioisotope with an on-off switch. The potential for innovation is very exciting.”

The device uses a crystal to produce more than 100,000 volts of electricity from only 10 volts of electrical input with low power consumption. Having such a low need for power could allow the crystal to be fueled by batteries. The crystal, made from a material called lithium niobate, uses the piezoelectric effect to amplify the input voltage. Piezoelectricity is the phenomenon whereby certain materials produce an electric charge when the material is under stress.

Kovaleski’s team published “Investigation of the Piezoelectric Effect as a Means to Generate X-Rays” in the journal IEEE Transaction on Plasma Science. Kovaleski is interim department chair of the Electrical & Computer Engineering in MU’s Department of Engineering.


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Study Finds Flame Retardant Pollutants Even in Remote Areas like Nepal

Chemicals used as flame retardants are present as environmental pollutants at locations around the globe, including remote sites in Indonesia, Nepal and Tasmania, according to a study by researchers from the Indiana University School of Public and Environmental Affairs.

The study, published this month in the journal Environmental Science and Technology, makes use of a novel but highly effective sampling technique: measuring concentrations of the chemicals in the bark of trees, which absorbs airborne chemical compounds in both vapor and particle phases.

"These findings illustrate further that flame retardants are ubiquitous pollutants and are found all around the world, not only in biota and humans but also in plants," said Amina Salamova, a research associate in the School of Public and Environmental Affairs at IU Bloomington and co-author of the study with Ronald A. Hites, Distinguished Professor in SPEA and in the Department of Chemistry in the College of Arts and Sciences.

The study measured concentrations of brominated and chlorinated flame retardants collected in tree bark samples at 12 locations around the globe: three sites in Canada and single sites in Iceland, Ireland, Norway, Czech Republic, South Africa, Nepal, Indonesia, Tasmania and American Samoa.

The highest concentrations were found at an urban site: Downsview, Ontario, Canada, near Toronto. However, the second-highest concentration of one type of flame retardant, Dechlorane Plus, was found at a remote site at Bukit Kototabang in Indonesia. Researchers don't know the cause of the relatively high concentrations at the site but suspect it may be near a source.

The study was carried out in cooperation with the Global Atmospheric Passive Sampling network, an international monitoring initiative established in 2004 on six continents.

Brominated and chlorinated flame retardants have been used for several decades in consumer products made of plastic, foam, wood and textiles to prevent combustion and slow the spread of fire. They persist in the environment and bio-accumulate in ecosystems and in human tissues. Exposure to the compounds has been associated with thyroid and other endocrine system disruption and with adverse neurological development. As a result, the production and use of certain flame retardants has been restricted in North America and the European Union.

Researchers measured a variety of flame retardants, including widely used polybrominated diphenyl ethers, or PBDE, as well as nonregulated compounds such as Dechlorane Plus and "older" flame retardants that were used in the 1980s. Findings included:

-- Most of the compounds were detected at all the locations, with concentrations varying widely.
-- Concentrations were associated with population density, suggesting the compounds most likely entered the environment through their use in nearby homes and offices.
-- Concentrations found in tree bark are correlated with those measured in previous atmospheric sampling at the sites by the Global Atmospheric Passive Sampling network.

Higher concentrations of flame retardants in bark and the atmosphere have been found by Hites and others in previous studies of the Great Lakes region, especially urban areas near Chicago and Cleveland, and also at cities in China. Even higher concentrations were found in southern Arkansas and at Niagara Falls, N.Y., near the sites of manufacturing facilities for PBDE and Dechlorane Plus, respectively.

The study also confirms the effectiveness of using tree bark as a sampling medium, a technique that Hites and colleagues have used in previous studies of persistent organic pollutants such as flame retardants.

Bark makes an effective sampling medium because of its large surface area and high lipid content. The samples are easy and inexpensive to collect, an advantage in developing countries that lack funding for extensive environmental monitoring programs. Tree bark also collects both vapor and particle phase pollutants, while other samplers collect one or the other.

Modern parenting may hinder brain development, research shows

Social practices and cultural beliefs of modern life are preventing healthy brain and emotional development in children, according to an interdisciplinary body of research presented recently at a symposium at the University of Notre Dame.

“Life outcomes for American youth are worsening, especially in comparison to 50 years ago,” says Darcia Narvaez, Notre Dame professor of psychology who specializes in moral development in children and how early life experiences can influence brain development.

“Ill-advised practices and beliefs have become commonplace in our culture, such as the use of infant formula, the isolation of infants in their own rooms or the belief that responding too quickly to a fussing baby will ‘spoil’ it,” Narvaez says.

This new research links certain early, nurturing parenting practices — the kind common in foraging hunter-gatherer societies — to specific, healthy emotional outcomes in adulthood, and has many experts rethinking some of our modern, cultural child-rearing “norms.”

“Breast-feeding infants, responsiveness to crying, almost constant touch and having multiple adult caregivers are some of the nurturing ancestral parenting practices that are shown to positively impact the developing brain, which not only shapes personality, but also helps physical health and moral development,” says Narvaez.

Studies show that responding to a baby’s needs (not letting a baby “cry it out”) has been shown to influence the development of conscience; positive touch affects stress reactivity, impulse control and empathy; free play in nature influences social capacities and aggression; and a set of supportive caregivers (beyond the mother alone) predicts IQ and ego resilience as well as empathy.

The United States has been on a downward trajectory on all of these care characteristics, according to Narvaez. Instead of being held, infants spend much more time in carriers, car seats and strollers than they did in the past. Only about 15 percent of mothers are breast-feeding at all by 12 months, extended families are broken up and free play allowed by parents has decreased dramatically since 1970.

Whether the corollary to these modern practices or the result of other forces, an epidemic of anxiety and depression among all age groups, including young children; rising rates of aggressive behavior and delinquency in young children; and decreasing empathy, the backbone of compassionate, moral behavior, among college students, are shown in research.

According to Narvaez, however, other relatives and teachers also can have a beneficial impact when a child feels safe in their presence. Also, early deficits can be made up later, she says.

“The right brain, which governs much of our self-regulation, creativity and empathy, can grow throughout life. The right brain grows though full-body experience like rough-and-tumble play, dancing or freelance artistic creation. So at any point, a parent can take up a creative activity with a child and they can grow together.”

Cornell University: Conditions right for outbreak of new virus in NYC, Atlanta, Miami

Global travel and climate warming could be creating the right conditions for outbreaks of a new virus in this country, according to a new Cornell University computer model.

The model predicts that outbreaks of "chikungunya", a painful virus transported by travelers and spread by the invasive Asian tiger mosquito, could occur in 2013 in New York City during August and September, in Atlanta from June through September, and year-round in Miami. The probability of a disease outbreak is correlated with temperature, as warmer weather allows the Asian tiger mosquito to breed faster and grow in numbers, according to the study published in PLOS Neglected Tropical Diseases.

According to the simulation, there is a high probability of a chikungunya outbreak if a single infected person arrives in New York in July or August and is bitten by an Asian tiger mosquito. The risks are the same, but with wider time frames, for transmission in Atlanta and Miami, according to the paper.

Asian tiger mosquitoes were introduced to the United States in Texas in the 1980s; they are established up the East Coast into New Jersey and are rising in numbers in New York City. The aggressive mosquito outcompetes local varieties and transmits more than 20 pathogens, including chikungunya and dengue, said Laura Harrington, associate professor of entomology and the study’s senior author.

“The virus is moving in people, and resident mosquito populations are picking it up,” Harrington said.

The model estimates that with typical regional temperatures, a chikungunya outbreak in New York would infect about one in 5,000 people, said Diego Ruiz-Moreno, a postdoctoral associate and the paper’s lead author

“However, this number would increase drastically as temperatures rise due to climate change,” Ruiz-Moreno said.

Chikungunya symptoms include a fever, severe joint pain, achiness, headache, nausea and fatigue, as well as “debilitating and prolonged” pain in the small joints of the hands and feet, according to the paper. The virus originated in Central Africa and is endemic in Southeast Asia.

Since no chikungunya vaccine exists, U.S. residents can help prevent an outbreak by removing standing water, wearing long sleeves and repellent during the day when the mosquitoes feed, and knowing the risk and symptoms when traveling, Harrington said.

The study was funded by a National Institute for Food and Agriculture Hatch grant and Cornell’s Atkinson Center for a Sustainable Future Climate Change and Disease Program.

Toys and Training Batons May Expose Dogs to Dangerous Chemicals

Sometimes orange, sometimes white, dog trainers often use plastic fetching batons called bumpers to teach dogs how to retrieve. But researchers at Texas Tech University have discovered that the dogs also may fetch a mouthful of potentially dangerous chemicals at the same time.

Researchers also found these chemicals, though at significantly lower concentrations, in a multitude of plastic chew toys purchased from a pet store.

The research was conducted by Kimberly Wooten, a master’s student using the project as her thesis, and Phil Smith, an associate professor of terrestrial ecotoxicology at The Institute of Environmental and Human Health at Texas Tech. Though unpublished, Wooten presented the results at the Society of Environmental Toxicology and Chemistry conference held in California.

“I raise and train Labrador retrievers and hunt with them as well,” Smith said, explaining what inspired him and Wooten to conduct the experiments. “In the process of training a lab, you do a lot of work with these plastic bumpers. I have a lot of bumpers in my garage, and they spend a lot of time in the mouths of my retrievers. Well, lots of attention has been given to chemicals in plastics lately regarding their effects on humans. Since we all care about our dogs, and we want them to be as healthy and smart and well-behaved as possible, we decided to look into this.”

Wooten and Smith said they predicted the possibility that the bumpers could leach phthalates and bisphenol A (BPA), which are used to give elasticity to plastic and vinyl and are known endocrine disruptors that mimic estrogen or act as anti-androgens and could lead to negative health effects. However, both said the findings have created more questions than answers because hardly any data exists on long-term effects of these chemicals on man’s best friend.

“The whole end goal was to answer the questions, ‘What does this mean for my pet? Is this a concern for our health?’” Wooten said. “We don’t have a good answer yet because there’s no good data to compare to our findings.”

To test for the chemicals, Wooten and Smith created simulated dog saliva, then simulated chewing by squeezing the bumpers and dog toys with stainless steel salad tongs.

Some bumpers and toys were weathered outside as well to see if older toys gave off more chemicals, Smith said.

“We found that the aging or weathering the toys increased concentrations of BPA and phthalates,” Smith said. “The toys had lower concentrations of phthalates than the bumpers, so that’s good news. But they also had some other chemicals that mimicked estrogen. We need to find out what those are.”

Wooten said BPA and phthalates can have effects on developing fetuses and can have a lifelong effect on offspring on lab animals. Some studies on humans conclude that BPA poses no health risks while others cite a number of adverse effects. Because of this, the U.S. government banned the use of BPA in baby bottles in 2012.

Wooten said questions still remain also as to how much of a dose a dog may get from playing with the bumpers, since it was difficult to say how much of these chemicals may actually leach out into a dog’s mouth.

“The interaction of pet health and environmental chemicals is understudied,” Wooten said. “What may be a safe dose for one species isn’t always a good measure for another species. But the amount of BPA and phthalates we found from the bumpers would be considered on the high end of what you might find in children’s toys.”

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Survey Shows That Nearly 1 in 3 Children with Food Allergies Experience Bullying

Photo: Stuart Miles

Nearly a third of children diagnosed with food allergies who participated in a recent study are bullied, according to researchers at the Icahn School of Medicine at Mount Sinai. Almost eight percent of children in the U.S. are allergic to foods such as peanuts, tree-nuts, milk, eggs, and shellfish.

Nearly half of parents surveyed (47.9 percent) were not aware of the bullying—although both the bullied children and their parents reported experiencing higher stress levels and lower quality of life.

The study, titled, “Child and Parental Reports of Bullying in a Consecutive Sample of Children with Food Allergy,” appears in the online issue of Pediatrics on December 24. The study was led by Eyal Shemesh, MD, Associate Professor of Pediatrics and Psychiatry at the Icahn School of Medicine at Mount Sinai. Dr. Shemesh and his team surveyed 251 pairs of parents and children. The patient and parent pairs were consecutively recruited during allergy clinic visits to independently answer questionnaires. Bullying due to food allergy or for any cause, quality of life, and distress in both the child and parent were evaluated using validated questionnaires.

“Parents and pediatricians should routinely ask children with food allergy about bullying,” said Dr. Shemesh. “Finding out about the child’s experience might allow targeted interventions, and would be expected to reduce additional stress and improve quality of life for these children trying to manage their food allergies.” Dr. Shemesh is Director of EMPOWER (Enhancing, Managing, and Promoting Well-being and Resiliency), a program within Mount Sinai’s Jaffe Food Allergy Institute. Dr. Shemesh is also Chief of the Division of Behavioral and Developmental Health in the Department of Pediatrics at The Mount Sinai Medical Center.

“When parents are aware of the bullying, the child’s quality of life is better,” said the senior author, Scott H. Sicherer, MD, Professor of Pediatrics, Chief, Division of Pediatric Allergy, Co-Director, EMPOWER program. “Our results should raise awareness for parents, school personnel, and physicians to proactively identify and address bullying in this population.”

The work for the study was supported by the EMPOWER program, a program funded by a generous donation from the Jaffe Family Foundation, that is devoted to understanding and enhancing the quality of life of persons with food allergy.

Infants with Severe RSV Disease May Be Immunosuppressed

Infants with severe lower respiratory tract infection caused by respiratory syncytial virus (RSV) may have a dysfunctional innate immune response that relates to the severity of their disease. These are the findings from a Nationwide Children’s Hospital study appearing in a recent issue of the Journal of Infectious Diseases.

RSV is the leading cause of lower respiratory tract infection in young children worldwide. The majority of children hospitalized with this condition are previously healthy with no known risk factors for serious disease. Of these infants, up to 20 percent will develop a disease severe enough to require admission to the pediatric intensive care unit (PICU).

It’s suggested that viral factors and the host immune response both contribute to the severity of RSV disease. A child’s functional innate immune response is increasingly being recognized as contributing to disease severity, but few studies have examined this phenomenon.

“For a long time we thought that children with severe RSV disease had higher concentrations of innate immunity cytokines, but it seems to be the opposite,” said the study’s senior author Asuncion Mejias, MD, PhD, physician scientist in Infectious Diseases at Nationwide Children’s Hospital. “When we stimulate the blood of these infants the production of innate immunity cytokines is severely impaired, and more importantly, this weakened response correlates with the more severe forms of the disease.”

To investigate the relationship between innate immunity and RSV disease severity, Dr. Mejias and Octavio Ramilo, MD, chief of Infectious Diseases at Nationwide Children’s in collaboration with Cesar Mella, MD, and Mark Hall, MD, from Critical Care at Nationwide Children’s, sought to determine whether patients with bronchiolitis admitted to the PICU had decreased whole blood functional innate immune responses. They also examined the relationships between innate immune dysfunction and disease outcomes.

The team evaluated 66 previously-healthy children less than two years old who were hospitalized with a first episode of RSV bronchiolitis during the 2010 – 2011 respiratory season. A nasal wash sample and a blood sample were obtained from each patient within 24 hours of admission to confirm RSV infection, and to measure cytokine concentrations before and after LPS stimulation. The team also enrolled healthy infants for control comparison.

They found that critically ill children with RSV admitted to the PICU had a significantly lower production capacity of innate cytokines compared with healthy controls and infants with less severe RSV bronchiolitis hospitalized in the Infectious Diseases unit.

“Whether children who develop severe RSV disease are born with an already impaired immune response, and RSV just uncovers their abnormal immune system will require further studies,” says Dr. Mejias, who is also a faculty member at The Ohio State University (OSU) College of Medicine. “Our study clearly suggests the presence of an inadequate, rather than excessive, functional innate immune response in children with RSV. This inadequate functional innate immune response is directly associated with the severity of the disease.”

Dr. Hall, also with OSU College of Medicine, said that immune monitoring of RSV patients at the time of hospitalization could have important clinical implications.

“Our data suggest that children with the most severe forms of RSV disease may already be immunosuppressed when we meet them in the ICU, raising the possibility of worsening this immunosuppression with the addition of commonly prescribed corticosteroids used to blunt the pro-inflammatory response to RSV,” said Dr. Hall.

Prospective immune monitoring may be helpful to identify children with bronchiolitis at high-risk for severe disease.

The findings also suggest the potential for the use of immune stimulant drugs that have been used with some success in reversing innate immune suppression in critically ill adults and children.

“Further studies are needed to explain the mechanisms responsible for innate immune suppression observed in critically-ill RSV-infected children,” said Dr. Ramilo, also with OSU College of Medicine.

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How Excess Holiday Eating Disturbs Your ‘Food Clock’

If the sinful excess of holiday eating sends your system into butter-slathered, sugar-soaked overload, you are not alone: People who are jet-lagged, people who work graveyard shifts and plain-old late-night snackers know just how you feel.

All these activities upset the body’s “food clock,” a collection of interacting genes and molecules known technically as the food-entrainable oscillator, which keeps the human body on a metabolic even keel. A new study by researchers at UCSF is helping to reveal how this clock works on a molecular level.

Published this month in the journal Proceedings of the National Academy of Sciences, the UCSF team has shown that a protein called PKCγ is critical in resetting the food clock if our eating habits change.

The study showed that normal laboratory mice given food only during their regular sleeping hours will adjust their food clock over time and begin to wake up from their slumber, and run around in anticipation of their new mealtime. But mice lacking the PKCγ gene are not able to respond to changes in their meal time – instead sleeping right through it.

The work has implications for understanding the molecular basis of diabetes, obesity and other metabolic syndromes because a desynchronized food clock may serve as part of the pathology underlying these disorders, said Louis Ptacek, MD, the John C. Coleman Distinguished Professor of Neurology at UCSF and a Howard Hughes Medical Institute Investigator.

It may also help explain why night owls are more likely to be obese than morning larks, Ptacek said.

“Understanding the molecular mechanism of how eating at the “wrong” time of the day desynchronizes the clocks in our body can facilitate the development of better treatments for disorders associated with night-eating syndrome, shift work and jet lag,” he added.
Resetting the Food Clock

Look behind the face of a mechanical clock and you will see a dizzying array of cogs, flywheels, reciprocating counterbalances and other moving parts. Biological clocks are equally complex, composed of multiple interacting genes that turn on or off in an orchestrated way to keep time during the day.

In most organisms, biological clockworks are governed by a master clock, referred to as the “circadian oscillator,” which keeps track of time and coordinates our biological processes with the rhythm of a 24-hour cycle of day and night.

Life forms as diverse as humans, mice and mustard greens all possess such master clocks. And in the last decade or so, scientists have uncovered many of their inner workings, uncovering many of the genes whose cycles are tied to the clock and discovering how in mammals it is controlled by a tiny spot in the brain known as the “superchiasmatic nucleus.”

Scientists also know that in addition to the master clock, our bodies have other clocks operating in parallel throughout the day. One of these is the food clock, which is not tied to one specific spot in the brain but rather multiple sites throughout the body.

The food clock is there to help our bodies make the most of our nutritional intake. It controls genes that help in everything from the absorption of nutrients in our digestive tract to their dispersal through the bloodstream, and it is designed to anticipate our eating patterns. Even before we eat a meal, our bodies begin to turn on some of these genes and turn off others, preparing for the burst of sustenance – which is why we feel the pangs of hunger just as the lunch hour arrives.

Scientist have known that the food clock can be reset over time if an organism changes its eating patterns, eating to excess or at odd times, since the timing of the food clock is pegged to feeding during the prime foraging and hunting hours in the day. But until now, very little was known about how the food clock works on a genetic level.

What Ptacek and his colleagues discovered is the molecular basis for this phenomenon: the PKCγ protein binds to another molecule called BMAL and stabilizes it, which shifts the clock in time.

The article, “PKCγ participates in food entrainment by regulating BMAL1” is authored by Luoying Zhang, Diya Abrahama, Shu-Ting Lin, Henrik Oster, Gregor Eichele, Ying-Hui Fu, and Louis J. Ptácek and appears in the Proceedings of the National Academy of Sciences.

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Looking to improve your health in 2013? Start by improving your air quality. An air purifier with activated carbon + HEPA can remove airborne chemicals, gases, odors and 99.97% of particles.

FAQ: Air Purifiers for Odor Control and Second-Hand Tobacco Smoke That Really Work

Have you tried numerous cleaners, fresheners, sprays ---even air purifiers to get rid of smoke odor only to be disappointed with the poor results? Smoke is easily one of the most stubborn odor problems that will often persist even in the presence of the most expensive HEPA air purifiers. That’s because HEPA air purifiers are designed to remove solid particles which account for only a small part of the composition of second-hand smoke. The most extensive by-products of smoking are gases and chemical vapours. 

 

Why Smoke Poses a Significant Challenge for Traditional Air Purifiers

Over 4,000 different chemicals have been identified in second-hand smoke.  Solid particles make up about 10 percent of the composition of tobacco smoke and include "tar" and nicotine. These particles are sticky and tend to clog traditional mass-market air purifiers. Gases and chemicals make up about 90 percent of tobacco smoke and include carbon monoxide, formaldehyde and ammonia. These dangerous and complex gases cannot be trapped by a dust filter, even a high efficiency filter like HEPA. Therefore, to successfully reduce the concentration of second-hand smoke and odor the most effective air purifiers must have multiple levels of filtration including an industrial strength filter for heavy chemical and odor control.

Air Purifiers with Activated Carbon

The most widely used filtration method for chemicals, gases and odors is activated carbon. It was first developed by military researchers for use in gases masks and is now used extensively in industrial air and water purification. Activated carbon is essentially charcoal that has been treated with oxygen to open up millions of tiny pores and fissures. It’s in these openings that pollutants are trapped. The surface area created by the activation is so extensive that if you could spread out all of the microscopic openings found in one teaspoon of carbon, it would cover an entire football field.  In home air purifiers specifically designed for tobacco smoke, polluted air is pulled through a deep bed of granular activated carbon where the chemicals, gases and odors are permanently trapped.  

AllerAir Air Purifiers for Smoke Odor Control

Known widely as experts in chemical and odor air filtration, AllerAir manufactures industrial-strength home air purifiers that use multiple filtration methods to better control tough tobacco odor.  Polluted air first passes through a special tar-trapping particle filter. This filter helps prolong the life of the main filters by preventing the sticky airborne tar from clogging the filtration system. The air then travels though an extra-deep bed of activated carbon where chemicals, gases and odors are trapped. Finally the air passes through a micro-HEPA particle filter which removes airborne particles. This multi-stage filtration approach offers superior odor reduction and cleaner air than traditional dust-collecting air purifiers.

To learn more about AllerAir air purifiers for smoke odor or other air purifiers for Multiple Chemical Sensitivities, allergies or mold contact an AllerAir air quality expert today at 1-888-852-8247 or connect via live chat or Twitter.

How Does an Air Purifier Work?

Depending on the type of technology used, an air purifier can remove airborne dust, allergens, chemicals, gases, and odors. Owning an air purifier has become increasingly popular as indoor pollution levels have climbed. Here’s a brief overview of how various air purifier technologies work.

 

Furnace Filters

The most basic of air purifier filters can be used in your home’s heating and cooling system. It’s usually placed between the air return duct and the furnace. This box-like filter slides into a slot so that all air flowing to the furnace passes through a mesh of fibers. It traps large dust and other particles that could otherwise build up and damage the components inside the HVAC system.  This type of filter cannot remove chemicals, gases or odors.

A Room Air Purifier with a HEPA Filter

To be accepted as HEPA (high efficiency particulate air) filter, this type of cleaning technology must remove 99.97% of airborne particles 0.3 micrometers in size or larger. It’s generally made up of a densely fibrous type material that works by trapping passing dust and allergens. It is highly recommended and very effective on particles, but cannot trap chemicals, gases and odors. 

An Air Purifier with Ionizing Technology

This type of air purifier creates a small but intense electrical field. It works by charging air particles and pulling them to metal plates that have an opposite charge. This technology has come under fire for generating ozone, a potentially dangerous pollutant even in small quantities. Some experts, including doctors with the American College of Allergy, Asthma & Immunology don’t recommend this type of air purifier. They say that without fans, these units cannot collect airborne particles from more than a few feet away and as a result do not significantly improve indoor air quality.

Ozone Generators
An ozone generator works like an ionizing purifier, but purposely produces ozone. Ozone is made up of three oxygen molecules one of which can detach and apply itself to other substances altering their make-up. Manufacturers of these units claim that their air purifier technology cleans the air, however most world health agencies believe there is strong evidence that ozone is not only inefficient, but dangerous to human health. These types of devices have actually been banned in the State of California. There is also concern that ozone may react with chemicals in the air and form new pollutants with unknown health effects.

An Air Purifierwith Activated Carbon

The most complete and effective air purifier contains a HEPA filter and an adsorbent material like activated carbon to remove chemicals, gases and odors. Activated carbon is extremely porous and has millions of tiny nooks and crannies that trap passing pollutants. Only an air purifier with this type of “adsorbent” (not absorbent) can remove the airborne pollutants left behind by HEPA dust filters.

Learn More

For more information on how an air purifier works or for a personalized recommendation, chat live with an AllerAir Air Quality Expert at www.allerair.com.