A particulate threat to diabetics

In a new study of people with diabetes, blood pressure rose in rough lockstep with short-term increases in soot and other microscopic air pollutant particles. Such transient increases in blood pressure can place the health of the heart, arteries, brain and kidneys at risk, particularly in people with chronic disease.

In contrast, when ozone levels climbed, blood pressure tended to fall among these people, independent of particulate levels. "And that was certainly not what we expected," notes study coauthor Barbara Hoffmann of the Leibniz Research Institute for Environmental Medicine in Düsseldorf, Germany.

Temperature also had an independent effect: A five-day average increase of 11.5 degrees Celsius, for instance, was associated with a small drop in blood pressure, Hoffmann and her colleagues report online October 21 in Environmental Health Perspectives.

Earlier studies suggested that particulates of the size measured in this study — just 2.5 micrometers in diameter — can hike blood pressure, particularly in people with diabetes.

To further investigate, Hoffman and her colleagues followed 70 Boston-area men and women, ages 40 to 85, with long-standing type 2 diabetes. All lived within 25 kilometers of a major air pollution monitoring station. Each participant submitted to repeated health tests at intervals of several weeks, which the researchers matched up with air pollution values from the preceding five days.

The team found pollution-related changes primarily in systolic blood pressure, the pressure exerted by the pumping action of each heartbeat. Systolic pressure is the top number in a blood pressure reading.

Since levels of particulates and ozone don’t necessarily track, one type of air pollutant cannot be expected to cancel out blood pressure alterations posed by the other, the researchers say. And ozone-associated drops in blood pressure aren’t necessarily beneficial. In fact, Hoffmann says, they offer additional evidence of a diabetes-related impairment in the ability of blood vessels to quickly adjust to changing environmental conditions by relaxing or constricting.

Changes in ozone and air pollution levels had no effect on people whose blood sugar was well controlled. Similarly, people with healthy baseline blood pressure readings exhibited little vulnerability to pollution.

"So especially if you want to positively influence your risk from air pollution," Hoffmann says, "it seems a very good idea to tightly control your blood pressure and your blood sugar."

The fact that a rise in concentrations of near-nanoscale particulates as small as 3.5 micrograms per cubic meter of air could raise systolic blood pressure “corroborates that current levels of particulate matter disrupt blood pressure control,” says physician Robert Brook of the Division of Cardiovascular Medicine at the University of Michigan Medical School in Ann Arbor. The new data, he maintains, confirm that short-term inhalation of fine airborne particulates at ambient levels — and perhaps traffic-related soot in particular — "have small but potentially clinically meaningful effects."

Found in: Body & Brain, Earth and Environment

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Greenland’s ice sheets face new threat

DEEP TROUBLESubsurface warming of ocean waters threatens to undercut and accelerate calving of Greenland’s ice sheets, which serve as vast water reservoirs. Shown is West Greenland’s Store Glacier, which is losing mass rapidly.E. Rignot/NASA JPL

Scientists have uncovered a potentially potent risk to Greenland’s ice sheets during the next century and beyond: rapidly warming deep water. The subsurface ocean off Greenland is now expected to warm at roughly double the rate that is projected for such waters globally, including off the coast of Antarctica.

Calling the ocean “the 900-pound gorilla of global warming and climate change,” oceanographer Josh Willis of NASA’s Jet Propulsion Laboratory in Pasadena, Calif., says he’s excited to finally see long-term climate projections homing in on the ocean’s role. “How the oceans affect the great ice sheets in Greenland and Antarctica could mean the difference between getting two feet and six feet of sea level rise in the coming century,” observes Willis, who had no role in the new analysis. “So this is a big deal.”

Until now, “no one had noticed that the ocean surrounding Greenland and Antarctica will warm very differently during this century and the next,” says climate modeler Jianjun Yin of the University of Arizona in Tucson, who led the new study, published online July 3 in Nature Geoscience. Although his group’s conclusions come from computer analyses, Yin notes that the study’s projections “are quite consistent with recent observations of subsurface ocean temperatures around Greenland.”

Yin’s team ran 19 computer programs to project the effects of global climate change on the world’s great bodies of water, many for periods through 2200. These analyses consistently turned up surprises, Jin says, including signs of substantial warming during the next 90 years and beyond in waters off Greenland at depths of 200 to 500 meters.

The increase, projected to total about 2° Celsius, could erode the base of glaciers in fjords, where the ice can reach as deep as 1,000 meters below the ocean surface. And unlike the glacial surface, which remains frozen in winter, the deeply submerged portions of tidal glaciers can melt year-round, Yin says, greatly accelerating their underwater calving.

In contrast to projections for Greenland’s waters, deep-ocean warming globally will probably increase by only about 0.5° C, the researchers reported.

Antarctica’s ice sheets are expected remain relatively insulated throughout the next century because of a circumpolar current that effectively keeps warm waters from penetrating beyond 60° S latitude. “Multiple projections show that this current will become stronger during this century and to the end of the next,” adds Yin, based on his study. That’s good news, he says, because although Greenland’s ice sheets in total contain enough water to increase global sea level by 7 meters, or about 23 feet, Antarctica’s ice sheets contain roughly 10 times that much water.

Willis cautions, however, that computer analyses of climate lack the resolution to evaluate the impact of eddies that might weaken the insulating Antarctic current. Recent studies have suggested such eddies could dampen that current enough to let warm water breach it and approach the continent’s ice sheets. “So,” Willis says, “it might be that the scenario painted by Yin and company for Antarctica is a bit too rosy.”

Found in: Earth and Environment

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Researchers see a 'picture' of threat in the brain: Work may lead to new model of neuroinflammation

ScienceDaily (May 3, 2011) — A team of researchers is beginning to see exactly what the response to threats looks like in the brain at the cellular and molecular levels.

This new information, including the discovery that a model of social stress can increase inflammation among brain cells, should provide new insight into how the stress response affects inflammatory and behavioral responses.

It may also provide new targets for drugs treatments in the continuing struggle to curtail depression and anxiety.

Scientists from Ohio State University's Institute of Behavioral Medicine Research reported their results in the latest issue of the Journal of Neuroscience.

John Sheridan, professor of oral biology, and Jonathan Godbout, an assistant professor of molecular virology, immunology and medical genetics, turned to colonies of mice to make their discoveries.

Groups of mice living together quickly adopt a hierarchy ranging from dominant to subordinate. This vaguely political system controls the interaction among the animals. Once these patterns had been established, the researchers then added an additional, highly aggressive mouse to the mix for a two-hour period each day to disrupt the social hierarchy.

With no place to retreat, the mice were forced into conflicts with the new aggressor. After as few as three episodes with the aggressor, the original mice showed distinct signs of what the researchers considered "anxiety-like behaviors." This kind of experiment creates a "social disruption" within the group of mice and is widely used to mimic psychological stress.

"These animals can't flee, so they have to stand and fight," Sheridan explained. "In doing so, they're repeatedly defeated, creating a condition called "learned helplessness," a condition closely linked to depression.

What Sheridan and Godbout saw was that the animals' anxiety continued for a long time after the termination of the stressful episodes of defeat. "For two weeks or more after we stopped the stressor, we could still see this anxiety-like behavior," Sheridan said.

The real discoveries came when the researchers analyzed what was happening in the animals' brains and in their immune response.

"We found that in the stressed animals, a certain type of immune cell (myeloid progenitor cell, or MPC), produced in the bone marrow, entered the circulatory system and migrated to the brain," explained Godbout.

These MPCs might normally relocate in this way to deal with an infection or an injury in the brain, but in this case, they moved solely because of the response to a social stressor, he said. The experiments showed that the number of these cells more than tripled in the brain following the stress.

Other immune cells called microglia, normally residing in the brain, also triggered an inflammatory response because of the stress. The researchers also noted that the stressor caused a particular activation pattern of neurons, or nerve cells, within the brain.

The response to social stress also caused an increase in the amounts of some inflammatory cytokines in the brain, including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-a) which are linked to inflammation. These cytokine responses correlated with an insensitivity of MPCs to glucocorticoids, hormones that normally inhibit inflammation in the body.

So the research team saw these and other cellular changes occurring in the brain following the stress, at the same time they were seeing the behavioral changes -- the anxiety-like behavior.

The findings are evidence of a two-way communication that's existing between the body and the brain in times of stress, Sheridan said.

To test that apparent connection, they gave the mice injections of propranolol -- a so-called "beta-blocker" drug often used for cardiac conditions -- before they encountered the more aggressive mouse. In this case, the researchers saw no increase in IL-1 or TNF-a, no glucocorticoid insensitivity, and no long-lasting anxiety-like behavior in the test animals.

"If we treated the animal with a beta-blocker each night before we put the intruder in, it completely blocked the signal. The anxiety-like behavior never developed," Godbout said.

"What this basically argues is that we may now have a new target for individuals who have extended anxiety-like behavior," Sheridan said. "We may have a new target cell to think about in terms of new therapies.

"And since that cell (the MPCs traveling from the bone marrow) is coming from the periphery of the body, we might not need to resort to psychoactive drugs that can have adverse effects on the brain."

Proving that, however, will take more animal studies and subsequent large studies using humans before this approach could be used clinically, he said.

The research was supported in part by the National Institute of Mental Health, the National Institute on Aging and the National Institute of Dental and Craniofacial Research.

Working with Sheridan and Godbout on the research were Eric Wohleb, Mark Hanke, Angela Corona, Nicole Powell, LaTonia Stiner, Michael Bailey and Randy Nelson, all of Ohio State.

Story Source:

The above story is reprinted (with editorial adaptations by ScienceDaily staff) from materials provided by Ohio State University. The original article was written by Earle Holland.

Journal Reference:

E. S. Wohleb, M. L. Hanke, A. W. Corona, N. D. Powell, L. M. Stiner, M. T. Bailey, R. J. Nelson, J. P. Godbout, J. F. Sheridan.  -Adrenergic Receptor Antagonism Prevents Anxiety-Like Behavior and Microglial Reactivity Induced by Repeated Social Defeat. Journal of Neuroscience, 2011; 31 (17): 6277 DOI: 10.1523/JNEUROSCI.0450-11.2011

Note: If no author is given, the source is cited instead.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of ScienceDaily or its staff.

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