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Do Gut Bacteria Rule Our Minds?

 

 In an Ecosystem Within Us, Microbes Evolved to Sway Food Choices       

 

          By Jeffrey Norris on August 15, 2014

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It sounds like science fiction, but it seems that bacteria within us – which outnumber our own cells about 100-fold – may very well be affecting both our cravings and moods to get us to eat what they want, and often are driving us toward obesity.

In an article published this week in the journal BioEssays, researchers from UC San Francisco, Arizona State University and University of New Mexico concluded from a review of the recent scientific literature that microbes influence human eating behavior and dietary choices to favor consumption of the particular nutrients they grow best on, rather than simply passively living off whatever nutrients we choose to send their way.

A Power Struggle Inside the Gut

Bacterial species vary in the nutrients they need. Some prefer fat, and others sugar, for instance. But they not only vie with each other for food and to retain a niche within their ecosystem – our digestive tracts – they also often have different aims than we do when it comes to our own actions, according to senior author Athena Aktipis, PhD, co-founder of the Center for Evolution and Cancer with the Helen Diller Family Comprehensive Cancer Center at UCSF.

Are we at the mercy of our gut bacteria? The above image illustrates how microbes can "pull our strings," driving us to crave foods that give them the nutrients they need, including fat and sugar.

While it is unclear exactly how this occurs, the authors believe this diverse community of microbes, collectively known as the gut microbiome, may influence our decisions by releasing signaling molecules into our gut. Because the gut is linked to the immune system, the endocrine system and the nervous system, those signals could influence our physiologic and behavioral responses.

“Bacteria within the gut are manipulative,” said Carlo Maley, PhD, director of the UCSF Center for Evolution and Cancer and corresponding author on the paper. “There is a diversity of interests represented in the microbiome, some aligned with our own dietary goals, and others not.”

Fortunately, it’s a two-way street. We can influence the compatibility of these microscopic, single-celled houseguests by deliberating altering what we ingest, Maley said, with measurable changes in the microbiome within 24 hours of diet change.

“Our diets have a huge impact on microbial populations in the gut,” Maley said. “It’s a whole ecosystem, and it’s evolving on the time scale of minutes.”

There are even specialized bacteria that digest seaweed, found in humans in Japan, where seaweed is popular in the diet.

The Connection Between Digestive Tract and Brain

Research suggests that gut bacteria may be affecting our eating decisions in part by acting through the vagus nerve, which connects 100 million nerve cells from the digestive tract to the base of the brain.

Athena Aktipis, PhD

Carlo Maley, PhD

“Microbes have the capacity to manipulate behavior and mood through altering the neural signals in the vagus nerve, changing taste receptors, producing toxins to make us feel bad, and releasing chemical rewards to make us feel good,” said Aktipis, who is currently in the Arizona State University Department of Psychology.

In mice, certain strains of bacteria increase anxious behavior. In humans, one clinical trial found that drinking a probiotic containing Lactobacillus casei improved mood in those who were feeling the lowest.

Maley, Aktipis and first author Joe Alcock, MD, from the Department of Emergency Medicine at the University of New Mexico, proposed further research to test the sway microbes hold over us. For example, would transplantation into the gut of the bacteria requiring a nutrient from seaweed lead the human host to eat more seaweed?

The speed with which the microbiome can change may be encouraging to those who seek to improve health by altering microbial populations. This may be accomplished through food and supplement choices, by ingesting specific bacterial species in the form of probiotics, or by killing targeted species with antibiotics. Optimizing the balance of power among bacterial species in our gut might allow us to lead less obese and healthier lives, according to the authors.

“Because microbiota are easily manipulatable by prebiotics, probiotics, antibiotics, fecal transplants, and dietary changes, altering our microbiota offers a tractable approach to otherwise intractable problems of obesity and unhealthy eating,” the authors wrote.

Implications for Obesity, Diabetes and even Cancer

The authors met and first discussed the ideas in the BioEssays paper at a summer school conference on evolutionary medicine two years ago.

Aktipis, who is an evolutionary biologist and a psychologist, was drawn to the opportunity to investigate the complex interaction of the different fitness interests of microbes and their hosts and how those play out in our daily lives. Maley, a computer scientist and evolutionary biologist, had established a career studying how tumor cells arise from normal cells and evolve over time through natural selection within the body as cancer progresses.

In fact, the evolution of tumors and of bacterial communities are linked, points out Aktipis, who said some of the bacteria that normally live within us cause stomach cancer and perhaps other cancers.

“Targeting the microbiome could open up possibilities for preventing a variety of disease from obesity and diabetes to cancers of the gastro-intestinal tract. We are only beginning to scratch the surface of the importance of the microbiome for human health,” she said.

The co-authors’ BioEssays study was funded by the National Institutes of Health, the American Cancer Society, the Bonnie D. Addario Lung Cancer Foundation and the Institute for Advanced Study, in Berlin.

UC San Francisco (UCSF), now celebrating the 150^th anniversary of its founding, is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care. It includes top-ranked graduate schools of dentistry, medicine, nursing and pharmacy, a graduate division with nationally renowned programs in basic, biomedical, translational and population sciences, as well as a preeminent biomedical research enterprise and two top-ranked hospitals, UCSF Medical Center and UCSF Benioff Children’s Hospital San Francisco.

What a 66-million-year-old forest fire reveals about the last days of the dinosaurs

Bet there was evidence of C60 in the charcoal after the forest fire-66 million year old fullerenes -COOL-Walter Derzko

Remains of an ancient forest fire preserved in stone

This news release is available in French.

		IMAGE:   A McGill field crew is collecting fossils as part of a field course in Grasslands National. Click here for more information.

As far back as the time of the dinosaurs, 66 million years ago, forests recovered from fires in the same manner they do today, according to a team of researchers from McGill University and the Royal Saskatchewan Museum.

During an expedition in southern Saskatchewan, Canada, the team discovered the first fossil-record evidence of forest fire ecology - the regrowth of plants after a fire - revealing a snapshot of the ecology on earth just before the mass extinction of the dinosaurs. The researchers also found evidence that the region's climate was much warmer and wetter than it is today.

"Excavating plant fossils preserved in rocks deposited during the last days of the dinosaurs, we found some preserved with abundant fossilized charcoal and others without it. From this, we were able to reconstruct what the Cretaceous forests looked like with and without fire disturbance", says Hans Larsson, Canada Research Chair in Macroevolution at McGill University.

The researchers' discovery revealed that at the forest fire site, the plants are dominated by flora quite similar to the kind that begin forest recovery after a fire today. Ancient forests recovered much like current ones, with plants like alder, birch, and sassafras present in early stages, and sequoia and ginkgo present in mature forests.

"We were looking at the direct result of a 66-million-year old forest fire, preserved in stone," says Emily Bamforth, of the Royal Saskatchewan Museum and the study's first author. "Moreover, we now have evidence that the mean annual temperature in southern Saskatchewan was 10-12 degrees Celsius warmer than today, with almost six times as much precipitation".

"The abundant plant fossils also allowed us for the first time to estimate climate conditions for the closing period of the dinosaurs in southwestern Canada, and provides one more clue to reveal what the ecology was like just before they went extinct", says Larsson, who is also an Associate Professor at the Redpath Museum.

Forest fires can affect both plant and animal biodiversity. The team's finding of ancient ecological recovery from a forest fire will help broaden scientists' understanding of biodiversity immediately before the mass extinction of dinosaurs. "We won't be able to fully understand the extinction dynamics until we understand what normal ecological processes were going on in the background". says Larsson.

###

To access the full article:

"Paleoclimate estimates and fire ecology immediately prior to the end-Cretaceous mass extinction in the Frenchman Formation (66 Ma), Saskatchewan, Canada" Palaeogeography, Palaeoclimatology, Palaeoecology: Emily L. Bamforth, Christine L. Button, Hans C.E. Larsson, Volume 401, 1 May 2014 http://www.sciencedirect.com/science/article/pii/S0031018214000947#

This release is also available on the McGill University Facebook page.

Study on flu evolution may change textbooks, history books says Michael Worobey

Study on flu evolution may change textbooks, history books

A new study reconstructing the evolutionary tree of flu viruses challenges conventional wisdom and solves some of the mysteries surrounding flu outbreaks of historical significance

		IMAGE:   This is the influenza virus under the electron microscope. Click here for more information.

A new study reconstructing the evolutionary tree of flu viruses challenges conventional wisdom and solves some of the mysteries surrounding flu outbreaks of historical significance.

The study, published in the journal Nature, provides the most comprehensive analysis to date of the evolutionary relationships of influenza virus across different host species over time. In addition to dissecting how the virus evolves at different rates in different host species, the study challenges several tenets of conventional wisdom, for example the notion that the virus moves largely unidirectionally from wild birds to domestic birds rather than with spillover in the other direction. It also helps resolve the origin of the virus that caused the unprecedentedly severe influenza pandemic of 1918.

The new research is likely to change how scientists and health experts look at the history of influenza virus, how it has changed genetically over time and how it has jumped between different host species. The findings may have implications ranging from the assessment of health risks for populations to developing vaccines.

"We now have a really clear family tree of theses viruses in all those hosts – including birds, humans, horses, pigs – and once you have that, it changes the picture of how this virus evolved," said Michael Worobey, a professor of ecology and evolutionary biology at the University of Arizona, who co-led the study with Andrew Rambaut, a professor at the Institute of Evolutionary Biology at the University of Edinburgh. "The approach we developed works much better at resolving the true evolution and history than anything that has previously been used."

Worobey explained that "if you don't account for the fact that the virus evolves at a different rates in each host species, you can get nonsense – nonsensical results about when and from where pandemic viruses emerged."

"Once you resolve the evolutionary trees for these viruses correctly, everything snaps into place and makes much more sense," Worobey said, adding that the study originated at his kitchen table.

"I had a bunch of those evolutionary trees printed out on paper in front of me and started measuring the lengths of the branches with my daughter's plastic ruler that happened to be on the table. Just like branches on a real tree, you can see that the branches on the evolutionary tree grow at different rates in humans versus horses versus birds. And I had a glimmer of an idea that this would be important for our public health inferences about where these viruses come from and how they evolve."

"My longtime collaborator Andrew Rambaut implemented in the computer what I had been doing with a plastic ruler. We developed software that allows the clock to tick at different rates in different host species. Once we had that, it produces these very clear and clean results."

The team analyzed a dataset with more than 80,000 gene sequences representing the global diversity of the influenza A virus and analyzed them with their newly developed approach. The influenza A virus is subdivided into 17 so-called HA subtypes – H1 through H17 – and 10 subtypes of NA, N1-N10. These mix and match, for example H1N1, H7N9, with the greatest diversity seen in birds.

Using the new family tree of the flu virus as a map showed which species moved to which host species and when. It revealed that for several of its 8 genomic segments avian influenza virus is not nearly as ancient as often assumed.

"What we're finding is that the avian virus has an extremely shallow history in most genes, not much older than the invention of the telephone," Worobey explained.

The research team, which included UA graduate student Guan-Zhu Han and Andrew Rambaut, a professor from the University of Edinburgh who is also affiliated with the U.S. National Institutes of Health, found a strong signature in the data suggesting that something revolutionary happened to avian influenza virus, with the majority of its genetic diversity being replaced by some new variant in a selective sweep in an extremely synchronous event.

Worobey said the timing is provocative because of the correlation of that sudden shift in the flu virus' evolution with historical events in the late nineteenth century.

"In the 1870s, an immense horse flu outbreak swept across North America," Worobey said, "City by city and town by town, horses got sick and perhaps five percent of them died. Half of Boston burned down during the outbreak, because there were no horses to pull the pump wagons. Out here in the West, the U.S. Cavalry was fighting the Apaches on foot because all the horses were sick. This happened at a time when horsepower was actual horse power. The horse flu outbreak pulled the rug out from under the economy."

According to Worobey, the newly generated evolutionary trees show a global replacement of the genes in the avian flu virus coinciding closely with the horse flu outbreak, which the analyses also reveal to be the closest relative to the avian virus.

"Interestingly, a previous research paper analyzing old newspaper records reported that in the days following the horse flu outbreak, there were repeated outbreaks described at the time as influenza killing chickens and other domestic birds," Worobey said. "That's another unexpected link in the history, and the there is a possibility that the two might be connected, given what we see in our trees."

He added that the evolutionary results didn't allow for a definitive determination of whether the virus jumped from horses to birds or vice versa, but a close relationship between the two virus species is clearly there.

With regard to humans, the research sheds light on a longstanding mystery. Ever since the influenza pandemic of 1918, it has not been possible to narrow down even to a hemisphere the geographic origins of any of the genes of the pandemic virus.

"Our study changes that," Worobey said. "It is now clear that most of its genome jumped from birds very close to 1918 in the Western Hemisphere, and there is a suggestion that it was North America in particular."

The results also challenge the accepted wisdom of wild birds as the major reservoir harboring the flu virus, from where it jumps to domestic birds and other species, including humans. Instead, the genetic diversity across the whole avian virus gene pool in domestic and wild birds often appears to trace back to earlier outbreaks of the virus in domestic birds, Worobey explained.

"People tend to think of wild birds as the source of everything, but we see a very strong indication of spillover from domestic birds to wild birds," he said. "It turns out the animals we keep for food and eggs may be substantially shaping the diversity of these viruses in the wild over time spans of decades. That is a surprise."

###

Poison-breathing bacteria may be boon to industry, environment

Athens, Ga. - Buried deep in the mud along the banks of a remote salt lake near Yosemite National Park are colonies of bacteria with an unusual property: they breathe a toxic metal to survive. Researchers from the University of Georgia discovered the bacteria on a recent field expedition to Mono Lake in California, and their experiments with this unusual organism show that it may one day become a useful tool for industry and environmental protection.

The bacteria use elements that are notoriously poisonous to humans, such as antimony and arsenic, in place of oxygen, an ability that lets them survive buried in the mud of a hot spring in this unique saline soda basin.

"Just like humans breathe oxygen, these bacteria respire poisonous elements to survive," said Chris Abin, author of a paper describing the research published recently in the journal Environmental Science & Technology and a doctoral candidate in microbiology.  "It is particularly fond of arsenic, but it uses other related elements as well, and we think it may be possible to harness these natural abilities to make useful products out of different elements."

Antimony, for example, is a naturally occurring silver-colored metal that is widely used by numerous industries to make plastics, vulcanized rubber, flame retardants and a host of electronic components including solar cells and LEDs. To make these products, antimony must be converted into antimony trioxide, and this bacterium is capable of producing two very pure kinds of crystalline antimony trioxide perfectly suited for industry.

Traditional chemical methods used to convert antimony ore into antimony trioxide can be expensive, time-consuming and they often create harmful byproducts. But the bacteria discovered by UGA researchers make antimony trioxide naturally as a consequence of respiration, creating a useful industrial product without creating noxious byproducts or requiring legions of specialized equipment.

"The antimony trioxide crystals produced by this bacterium are far superior to those that are currently produced using chemical methods," said James Hollibaugh, UGA Franklin College of Arts and Sciences Distinguished Research Professor of Marine Sciences and principal investigator for the project. "We tested the crystals we made alongside commercially available products that are 99 percent pure, and ours is either of identical or superior quality."

Hollibaugh and Abin think it might be possible for industry to maintain large cultures of their bacteria in simple holding tanks, feed it oxidized antimony and collect the antimony trioxide crystals as they form naturally. After harvesting the crystals, manufacturers would need only to feed more oxidized antimony into the tanks to keep the predominantly self-sustaining process going.

But the bacteria's usefulness is not restricted to refining antimony. It possesses a number of different enzymes that allow it to use other dangerous elements that accumulate in wastewaters near mines or refineries and pose serious threats to humans and animals. For example, the bacteria are capable of reducing other contaminants including selenium and tellurium.

Preliminary tests suggest that the bacteria could be used to remove these pollutants from the wastewater and protect the surrounding ecosystems.

"It might be used in one of two ways," said Hollibaugh. "The bacteria could be used simply to clean up the water, but it might also be possible for the bacteria to help humans recover and recycle the valuable elements in the water."

This way, says Hollibaugh, the water stays clean and industry doesn't waste a valuable strategic resource.

Both Abin and Hollibaugh caution that more research must be done before any of these applications are ready to deploy. UGA has applied for patents to protect these unique processes as well as the bacterium itself, and they are currently testing the bacteria's efficacy in different environments and conditions to discover how the bacteria react when they are exposed to a variety of metals simultaneously.

"UGA is currently seeking partners interested in licensing this technology and also partnering with professor Hollibaugh toward the development of additional industrial uses for the invention," said Gennaro Gama, senior technology licensing manager at UGA. "We believe this technology represents a feasible solution to many kinds of environmental contamination, but it also is useful for producing important commodities such as antimony trioxide, elemental selenium and tellurium."

For licensing information, please contact Gennaro Gama, [email protected], 706-583-8088.

 

Writer:

James  Hataway     

James  Hataway

Public Relations Specialist

Recent and archived articles by James  Hataway

OVPR                                         Research, Office of the Vice President for (OVPR)                                                                                                     

Work: 706/542-5222                                         Email: [email protected]               

 

Contact:

James T. Hollibaugh     

James Hollibaugh

Professor

Department of Marine Sciences                     Marine Science Building 325 Sanford Dr. Athens, GA                                                                                                                       

                                                            Email: [email protected]               

 

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• 

  James Hollibaugh is a Distinguished Research Professor of Marine Sciences in the Franklin College of Arts and Sciences.

• 

  Mountain ranges surround Mono Lake in California.

• 

  Tufa towers made of limestone adorn the shores of Mono Lake in California.

• 

  Chris Abin, doctoral candidate in microbiology, taking samples at Mono Lake in California.

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Animals Walking the Tightrope Between Stability and Change: Addressing a Grand Challenge in Organismal Biology

Animals Walking the Tightrope Between Stability and Change: Addressing a Grand Challenge in Organismal Biology

Released: 1/1/2014 6:00 PM EST Embargo expired: 1/5/2014 12:00 AM EST Source Newsroom:   Society for Integrative and Comparative Biology (SICB)  

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2014 Society for Integrative and Comparative Biology annual conference

 

 

Byline: Dianna Padilla, State University of New York at Stony Brook Billie J. Swalla, University of Washington Brian Tsukimura, California State University at Fresno

Newswise — Why can some animals respond to climate change, while others cannot?  How do animals develop properly when conditions change?  How do animals respond quickly or build new neural pathways but maintain past abilities and function?  These questions have perplexed biologists for decades.  The challenge in addressing these questions is that biological systems are complex, and they operate at many different spatial scales and time scales simultaneously.  Thus, the conventional tools of biologists limit the advances that can be made.  New approaches are needed to make progress in answering these important questions for animal biology.

What new insights might be gleaned when engineers and mathematicians work with biologists to answer these fundamental questions?  A special symposium at the 2014 Society for Integrative and Comparative Biology annual conference brings together biologists, mathematicians and engineers, who will investigate the potential and power of a new, quantitative organismal systems biology to address these questions.

Speakers include a mix of biologists from different fields, including physiology, neural biology, development, genetics, functional morphology, and ecological and evolutionary biology.  They join with mathematicians and engineers and will present work that illustrates the potential power of cross-disciplinary approaches for answering these complex questions.  The speakers will also explore how organismal biology can be used to help solve questions that have daunted mathematicians and engineers.  Talks will include a wide range of questions from locomotion, physiology, development, networks, and ecology, from the level of genomics to whole organism responses to change.  Talks in this symposium will illustrate the power of engineering and quantitative approaches to address and test complex questions, and lead us to a new organismal systems biology. 

The symposium will be held Sunday, January 5.  Ten speakers will present examples of research and modeling that illustrates how new approaches can help us investigate important questions about complex biological systems, as well as the big questions that remain to be tackled.  Immediately following the symposium, complementary posters will be presented.  On Monday, January 6 there will be a session of additional complementary papers. 

This is an exciting time for organismal biology, and approaching complex systems in new ways.  Come and see what all the excitement is about! http://www.sicb.org/meetings/2014/symposia/organismal.php

For further information, please contact: Dianna K. Padilla [email protected] Billie Swalla [email protected] Brian Tsukimura [email protected]

Odor receptors discovered in lungs

Odor receptors discovered in lungs

They’re just like those in your nose, but instead of conjuring up a cup of coffee, they might make you cough

January 2, 2014

 

Article Body 2010

 

 

 

 

 

Your nose is not the only organ in your body that can sense cigarette smoke wafting through the air. Scientists at Washington University in St. Louis and the University of Iowa have shown that your lungs have odor receptors as well.

Unlike the receptors in your nose, which are located in the membranes of nerve cells, the ones in your lungs are in the membranes of neuroendocrine cells. Instead of sending nerve impulses to your brain that allow it to “perceive” the acrid smell of a burning cigarette somewhere in the vicinity, they trigger the flask-shaped neuroendocrine cells to dump hormones that make your airways constrict.

The newly discovered class of cells expressing olfactory receptors in human airways, called pulmonary neuroendocrine cells, or PNECs, were found by a team led by Yehuda Ben-Shahar, PhD, assistant professor of biology, in Arts & Sciences, and of medicine at Washington University in St. Louis, and including colleagues Steven L. Brody, MD, and Michael J. Holtzman, MD, of the Washington University School of Medicine, and Michel J. Welsh, MD, of the University of Iowa Carver College of Medicine.

“We forget,” said Ben-Shahar, “that our body plan is a tube within a tube, so our lungs and our gut are open to the external environment. Although they’re inside us, they’re actually part of our external layer. So they constantly suffer environmental insults,” he said, “and it makes sense that we evolved mechanisms to protect ourselves.”

In other words, the PNECs, described in the March issue of the American Journal of Respiratory Cell and Molecular Biology, are sentinels, guards whose job it is to exclude irritating or toxic chemicals.

The cells might be responsible for the chemical hypersensitivity that characterizes respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and asthma. Patients with these diseases are told to avoid traffic fumes, pungent odors, perfumes and similar irritants, which can trigger airway constriction and breathing difficulties.

The odor receptors on the cells might be a therapeutic target, Ben-Shahar suggests. By blocking them, it might be possible to prevent some attacks, allowing people to cut down on the use of steroids or bronchodilators.

Every breath you take When a mammal inhales, volatile chemicals flow over two patches of specialized epithelial tissue high up in the nasal passages. These patches are rich in nerve cells with specialized odorant-binding molecules embedded in their membranes.

If a chemical docks on one of these receptors, the neuron fires, sending impulses along the olfactory nerve to the olfactory bulb in the brain, where the signal is integrated with those from hundreds of other similar cells to conjure the scent of old leather or dried lavender.

Aware that airway diseases are characterized by hypersensitivity to volatile stimuli, Ben-Shahar and his colleagues realized that the lungs, like the nose, must have some means of detecting inhaled chemicals.

Earlier, a team at the University of Iowa, where Ben-Shahar was a postdoctoral research associate, had searched for genes expressed by patches of tissue from lung transplant donors. They found a group of ciliated cells that express bitter taste receptors. When offending substances were detected, the cilia beat more strongly to sweep them out of the airway. This result was featured on the cover of the Aug. 28, 2009, issue of Science.

But since people are sensitive to many inhaled substances, not just bitter ones, Ben-Shahar decided to look again. This time he found that these tissues also express odor receptors, not on ciliated cells but instead on neuroendocrine cells, flask-shaped cells that dump serotonin and various neuropeptides when they are stimulated. 

 

Ben-Shahar

“They’re beautiful cells,” said Ben-Shahar, of the pulmonary neuroendocrine cells he has been studying in lung tissues. The flask-like cells that are full of serotonin (stained green here) and other chemicals extend processes up through the epithelial cells (purple) lining the airways to monitor the chemical makeup of each breath. The top part of the image is a plan view of the airway lining and the bottom part is a section through the lining.

 

This made sense. “When people with airway disease have pathological responses to odors, they’re usually pretty fast and violent,” said Ben-Shahar. “Patients suddenly shut down and can’t breathe, and these cells may explain why.”

Ben-Shahar stresses the differences between chemosensation in the nose and in the lung. The cells in the nose are neurons, he points out, each with a narrowly tuned receptor, and their signals must be woven together in the brain to interpret our odor environment.

The cells in the airways are secretory, not neuronal, cells, and they may carry more than one receptor, so they are broadly tuned. Instead of sending nerve impulses to the brain, they flood local nerves and muscles with serotonin and neuropeptides. “They are possibly designed,” he said, “to elicit a rapid, physiological response if you inhale something that is bad for you.”

 

Ben-Shahar

A diagram of the airway lining suggests how the pulmonary neuroendocrine cells (red) trigger a response to inhaled chemicals. When a chemical (orange triangle) docks on a receptor (black) they dump secretory chemicals (thin orange arrows), which have an immediate but localized effect on muscles (blue) and nerves (pink), possibly triggering responses such as a cough.

 

The different mechanisms explain why cognition plays a much stronger role in taste and smell than in coughing in response to an irritant. It is possible, for example, to develop a taste for beer. But nobody learns not to cough; the response is rapid and largely automatic.

The scientists suspect these pulmonary neuroscretory cells contribute to the hypersensitivity of patients with COPD to airborne irritants. COPD is a group of diseases, including emphysema, that is characterized by coughing, wheezing, shortness of breath and chest tightness.

When the scientists looked at the airway tissues from patients with COPD, they discovered that they had more of these neurosecretory cells than airway tissues from healthy donors.

Of mice and men As a geneticist, Ben-Shahar would like to go farther, knocking out genes to make sure that the derangement of neurosecretory cells isn’t just correlated with airway diseases but instead suffices to produce it.

But there is a problem. “For example, a liver from a mouse and a liver from a human are pretty similar, they express the same types of cells. But the lungs from different mammalian species are often very different; you can see it at a glance,” Ben-Shahar said. 

“Clearly, primates have evolved distinct cell lineages and signaling systems for respiratory-specific functions.”

This makes it challenging to unravel the biomolecular mechanisms of respiratory diseases. 

Still, he is hopeful that the PNEC pathways will provide targets for drugs that would better control asthma, COPD and other respiratory diseases. They would be welcome. There has been a steep rise in these diseases in the past few decades, treatment options have been limited, and there are no cures.

Odor receptors discovered in lungs

Odor receptors discovered in lungs

They’re just like those in your nose, but instead of conjuring up a cup of coffee, they might make you cough

January 2, 2014

 

Article Body 2010

 

 

 

 

 

Your nose is not the only organ in your body that can sense cigarette smoke wafting through the air. Scientists at Washington University in St. Louis and the University of Iowa have shown that your lungs have odor receptors as well.

Unlike the receptors in your nose, which are located in the membranes of nerve cells, the ones in your lungs are in the membranes of neuroendocrine cells. Instead of sending nerve impulses to your brain that allow it to “perceive” the acrid smell of a burning cigarette somewhere in the vicinity, they trigger the flask-shaped neuroendocrine cells to dump hormones that make your airways constrict.

The newly discovered class of cells expressing olfactory receptors in human airways, called pulmonary neuroendocrine cells, or PNECs, were found by a team led by Yehuda Ben-Shahar, PhD, assistant professor of biology, in Arts & Sciences, and of medicine at Washington University in St. Louis, and including colleagues Steven L. Brody, MD, and Michael J. Holtzman, MD, of the Washington University School of Medicine, and Michel J. Welsh, MD, of the University of Iowa Carver College of Medicine.

“We forget,” said Ben-Shahar, “that our body plan is a tube within a tube, so our lungs and our gut are open to the external environment. Although they’re inside us, they’re actually part of our external layer. So they constantly suffer environmental insults,” he said, “and it makes sense that we evolved mechanisms to protect ourselves.”

In other words, the PNECs, described in the March issue of the American Journal of Respiratory Cell and Molecular Biology, are sentinels, guards whose job it is to exclude irritating or toxic chemicals.

The cells might be responsible for the chemical hypersensitivity that characterizes respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and asthma. Patients with these diseases are told to avoid traffic fumes, pungent odors, perfumes and similar irritants, which can trigger airway constriction and breathing difficulties.

The odor receptors on the cells might be a therapeutic target, Ben-Shahar suggests. By blocking them, it might be possible to prevent some attacks, allowing people to cut down on the use of steroids or bronchodilators.

Every breath you take When a mammal inhales, volatile chemicals flow over two patches of specialized epithelial tissue high up in the nasal passages. These patches are rich in nerve cells with specialized odorant-binding molecules embedded in their membranes.

If a chemical docks on one of these receptors, the neuron fires, sending impulses along the olfactory nerve to the olfactory bulb in the brain, where the signal is integrated with those from hundreds of other similar cells to conjure the scent of old leather or dried lavender.

Aware that airway diseases are characterized by hypersensitivity to volatile stimuli, Ben-Shahar and his colleagues realized that the lungs, like the nose, must have some means of detecting inhaled chemicals.

Earlier, a team at the University of Iowa, where Ben-Shahar was a postdoctoral research associate, had searched for genes expressed by patches of tissue from lung transplant donors. They found a group of ciliated cells that express bitter taste receptors. When offending substances were detected, the cilia beat more strongly to sweep them out of the airway. This result was featured on the cover of the Aug. 28, 2009, issue of Science.

But since people are sensitive to many inhaled substances, not just bitter ones, Ben-Shahar decided to look again. This time he found that these tissues also express odor receptors, not on ciliated cells but instead on neuroendocrine cells, flask-shaped cells that dump serotonin and various neuropeptides when they are stimulated. 

 

Ben-Shahar

“They’re beautiful cells,” said Ben-Shahar, of the pulmonary neuroendocrine cells he has been studying in lung tissues. The flask-like cells that are full of serotonin (stained green here) and other chemicals extend processes up through the epithelial cells (purple) lining the airways to monitor the chemical makeup of each breath. The top part of the image is a plan view of the airway lining and the bottom part is a section through the lining.

 

This made sense. “When people with airway disease have pathological responses to odors, they’re usually pretty fast and violent,” said Ben-Shahar. “Patients suddenly shut down and can’t breathe, and these cells may explain why.”

Ben-Shahar stresses the differences between chemosensation in the nose and in the lung. The cells in the nose are neurons, he points out, each with a narrowly tuned receptor, and their signals must be woven together in the brain to interpret our odor environment.

The cells in the airways are secretory, not neuronal, cells, and they may carry more than one receptor, so they are broadly tuned. Instead of sending nerve impulses to the brain, they flood local nerves and muscles with serotonin and neuropeptides. “They are possibly designed,” he said, “to elicit a rapid, physiological response if you inhale something that is bad for you.”

 

Ben-Shahar

A diagram of the airway lining suggests how the pulmonary neuroendocrine cells (red) trigger a response to inhaled chemicals. When a chemical (orange triangle) docks on a receptor (black) they dump secretory chemicals (thin orange arrows), which have an immediate but localized effect on muscles (blue) and nerves (pink), possibly triggering responses such as a cough.

 

The different mechanisms explain why cognition plays a much stronger role in taste and smell than in coughing in response to an irritant. It is possible, for example, to develop a taste for beer. But nobody learns not to cough; the response is rapid and largely automatic.

The scientists suspect these pulmonary neuroscretory cells contribute to the hypersensitivity of patients with COPD to airborne irritants. COPD is a group of diseases, including emphysema, that is characterized by coughing, wheezing, shortness of breath and chest tightness.

When the scientists looked at the airway tissues from patients with COPD, they discovered that they had more of these neurosecretory cells than airway tissues from healthy donors.

Of mice and men As a geneticist, Ben-Shahar would like to go farther, knocking out genes to make sure that the derangement of neurosecretory cells isn’t just correlated with airway diseases but instead suffices to produce it.

But there is a problem. “For example, a liver from a mouse and a liver from a human are pretty similar, they express the same types of cells. But the lungs from different mammalian species are often very different; you can see it at a glance,” Ben-Shahar said. 

“Clearly, primates have evolved distinct cell lineages and signaling systems for respiratory-specific functions.”

This makes it challenging to unravel the biomolecular mechanisms of respiratory diseases. 

Still, he is hopeful that the PNEC pathways will provide targets for drugs that would better control asthma, COPD and other respiratory diseases. They would be welcome. There has been a steep rise in these diseases in the past few decades, treatment options have been limited, and there are no cures.

Crude oil from algae in 30 minutes

“Scientists at the Pacific Northwest National Laboratory said they have successfully perfected a new method that can transform a pea-soupy solution of algae into crude oil by pressure cooking in just 30 minutes. The crude oil created is lightweight and low in sulfur and can be “dropped in” to refineries that process fossil crudes.”
Further Details :
L#1 : http://is.gd/cSyLL8

L#2 : http://is.gd/8MGdbn

L#3 : http://is.gd/OTW42a

 

 

Environmental toxins linked to heart defects

 

Abstract: 15332 (Hall F, Core 2, Poster Board: 2092)

Children's congenital heart defects may be associated with their mothers' exposure to specific mixtures of environmental toxins during pregnancy, according to research presented at the American Heart Association's Scientific Sessions 2013.

Congenital heart defects occur when the heart or blood vessels near the heart don't develop normally before birth. Defects may be caused by chromosomal abnormalities, but the cause is unknown in most cases.   

Researchers examined patterns of congenital heart defects incidence and presence of environmental toxicants in Alberta, Canada. The ongoing research seeks to determine if pregnant women's proximity to organic compounds and metals emitted in the air impacts the risk of heart defects in their children.

"Although still in the early stage, this research suggests some chemical emissions — particularly, industrial air emissions — may be linked to heart abnormalities that develop while the heart is forming in the womb," said lead researcher Deliwe P. Ngwezi, M.D., a Ph.D., student and research fellow in pediatric cardiology at the University of Alberta in Canada.

The study is based on congenital heart defects diagnosed in 2004-11 and chemical emissions recorded by a Canadian agency tracking pollutants.

Researchers looked at three chemical categories, but only one group showed a strong correlation with rates of congenital heart defects. According to Ngwezi, the group of chemicals consists of a mixture of organic compounds and metals namely: benzene, butadiene, carbon disulphide, chloroform, ethylene oxide, hexachlorobenzene, tetrachloroethane, methanol, sulphur dioxide, toluene, lead, mercury and cadmium.

Congenital heart defect rates have gradually decreased in Canada since 2006, which is about  the time the government tightened regulations to reduce industrial air emissions, Ngwezi said. The heart defect decreases were mainly associated with heart defects resulting in holes between the upper and lower heart chambers (septal defects) and malformations of the cardiac outflow tracts (conotruncal defects), according to Ngwezi. 

"For now, consumers and healthcare providers should be educated about the potential toll of pollutants on the developing heart," she said. "As we have observed in the preliminary results, when the emissions decrease, the rates of congenital heart defects also decrease." This study, she said, should draw attention to the increasing evidence about the impact of environmental pollution on birth defects. Limitations of the study include that researchers' observations were made at a group level, not according to individual risk and the self-reported industry data which is monitored and collected annually by government, according to Ngwezi. 

###

Co-authors are Lisa K. Hornberger, M.D.; Brad Saretsky, B.Sc.; Sujata Chandra, M.D., M.Sc.; Deborah Fruitman, M.D., F.R.C.P.C.; and Alvaro Osornio-Vargas, M.D., Ph.D. Author disclosures are on the abstract.

The study was funded by the Women and Children's Health Research Institute, University of Alberta; Hamilton-Naki Foundation of South Africa; and an Emerging Research Team Grant from the University of Alberta's Faculty of Medicine and Dentistry and Alberta Health Services.

Learn more about Congenital Heart Defects.

For more news from AHA Scientific Sessions 2013 follow us on Twitter @HeartNews #AHA13.

Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at http://www.heart.org/corporatefunding.

Note: Actual presentation time is from 3 p.m. CT/4 p.m. ET Sunday, Nov. 17, 2013.

Downloadable video/audio interviews, B-roll, animation and images related to this news release are on the right column of the release link at http://newsroom.heart.org/news/environmental-toxins-linked-to-heart-defects?preview=176456a4352eb666d9efa2edb9f0edf2. Video clips with researchers/authors of the studies will be added to the release link after embargo

Fracking Operations Triggered 100 Quakes in a Year – (New Scientist – August 19, 2013)

Fracking Operations Triggered 100 Quakes in a Year – (New
Scientist – August 19, 2013)
The Ohio quakes, centred around Youngstown,  were triggered by the disposal of wastewater from fracking operations in the  neighbouring state of Pennsylvania rather than by the fracking process itself.
The new geophysical research, by Won-Young Kim at Columbia University in  Palisades, New York, is the latest to suggest that the main risk of earthquakes  associated with fracking relates to the way the water used in the operations is  disposed of afterwards. In Ohio, the wastewater was injected into a deep well.
This raised the pressure of water within the rock and triggered 109 small quakes between January 2011 and February 2012. The largest, on 31 December 2011, had a  magnitude of 3.9.