MAKING OLD LUNGS LOOK YOUNG AGAIN WITH IBUPROFEN

New research shows that the lungs become more inflammatory with age and that ibuprofen can lower that inflammation

In fact, immune cells from old mouse lungs fought tuberculosis bacteria as effectively as cells from young mice after lung inflammation was reduced by ibuprofen. The ibuprofen had no effect on the immune response to TB in young mice.

This was a rare look at inflammation in the aging lung environment by Ohio State University scientists who study the immune response to TB. The researchers already knew that old mice had a harder time clearing TB from the lungs than young mice, but had not investigated the role of lung inflammation in that response.

"Very few researchers have linked inflammation to infectious disease in old age, even though TB in particular will drive that inflammation even further," said Joanne Turner, associate professor of microbial infection and immunity at Ohio State and senior author of the study.

"The inflammation-associated changes that we saw in the lung were a small finding, but an important finding because the implications are great," Turner said. "We should be able to modify the environment in the lung. If we can reverse the inflammatory environment in a very straightforward way, that is a positive."

The research is published in the Journal of Leukocyte Biology.

Most previous research establishing inflammation's links to aging and disease has tested blood for elevated proteins that signal an inflammatory environment. These researchers found the same proteins in the lungs of old mice. Research has already established that the inevitable inflammation that comes with aging is linked to such conditions as Type 2 diabetes and heart disease.

Though this line of work might someday support the use of ibuprofen as an adjunct therapy for elderly people with TB, Turner emphasized that she and colleagues are not recommending use of the drug for the purposes of lowering inflammation.

"You can actually reduce your inflammation as you age by being lean, eating well and exercising. And we know that in the elderly, people who are fitter live longer," she said. "Inflammation is associated with sickness and frailty."

Though the research was conducted in mice, Turner co-led a previous study indicating that both mouse and human lungs develop the same profile of pro-inflammatory proteins and fatty molecules with age, creating an environment that impairs the immune response to infection.

More than 9 million people worldwide are estimated to have active TB infections, and about 1.4 million people die of tuberculosis each year. "The elderly are most likely to die of TB. They get sicker. They're not the biggest population that gets infected with TB, but they can develop the worst cases," said Turner, also an associate director of Ohio State's Center for Microbial Interface Biology (CMIB).

In this new study, the researchers compared lung cells from old and young mice and found that in the old mice, genes that make three classic pro-inflammatory proteins, called cytokines, were more active in the lungs of old mice. The cytokines are interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-a). In addition, immune system cells called macrophages in the lungs from old mice were in an advanced state of readiness to fight an infection -- a status that signals inflammation. Macrophages in young mouse lungs were in a normal, resting state.

In test tubes, the scientists exposed mouse lung macrophages to TB bacteria. The macrophages from old mouse lungs were quicker to absorb the bacteria than were immune cells from young mice, but that initial robust immune response from the cells of old mice could not be sustained.

"A primed macrophage in an old mouse has lots of receptors on its surface that can bind to TB, taking it up and trying to kill it. But what it lacks is the ability to increase the response further," Turner said. "A resting macrophage in a young mouse takes up TB and then can be activated to do something even more effective at killing the bacteria."

Though some elements of the elderly response to TB remain a mystery, this finding suggested that the inflammation in the lungs of elderly mice had the direct effect of reducing the long-term effectiveness of their immune response to TB infection, Turner said.

Old mice in the study were 18 months old -- equivalent to about 65 in human years -- and young mice were 3 months old, a similar age to human young adults.

The researchers gave old and young mice ibuprofen in their food for two weeks and then examined their lung cells. After this diet modification, several pro-inflammatory cytokines in the lungs of old mice had been reduced to levels identical to those in the lungs of young mice, and the macrophages in old mouse lungs were no longer in a primed state.

"There's a trend toward reduced inflammation. Essentially, ibuprofen made the lungs of old mice look young. Putting young mice on ibuprofen had no effect because they had no lung inflammation, which implies the ibuprofen reduced the inflammation and changed the immune response in the old mice," Turner said.

"It might be that ibuprofen works on specific pathways to lower inflammation, and that might help with control of TB."

Turner and colleagues have extended the work to test whether ibuprofen affects the elderly mouse immune response to TB infection.

HUMAN FACES ARE SO VARIABLE BECAUSE WE EVOLVED TO LOOK UNIQUE

The amazing variety of human faces -- far greater than that of most other animals -- is the result of evolutionary pressure to make each of us unique and easily recognizable, according to a new study by University of California, Berkeley, scientists.

Our highly visual social interactions are almost certainly the driver of this evolutionary trend, said behavioral ecologist Michael J. Sheehan, a postdoctoral fellow in UC Berkeley's Museum of Vertebrate Zoology. Many animals use smell or vocalization to identify individuals, making distinctive facial features unimportant, especially for animals that roam after dark, he said. But humans are different.

"Humans are phenomenally good at recognizing faces; there is a part of the brain specialized for that," Sheehan said. "Our study now shows that humans have been selected to be unique and easily recognizable. It is clearly beneficial for me to recognize others, but also beneficial for me to be recognizable. Otherwise, we would all look more similar."

"The idea that social interaction may have facilitated or led to selection for us to be individually recognizable implies that human social structure has driven the evolution of how we look," said coauthor Michael Nachman, a population geneticist, professor of integrative biology and director of the UC Berkeley Museum of Vertebrate Zoology.

The study will appear Sept. 16 in the online journal Nature Communications.

In the study, Sheehan said, "we asked, 'Are traits such as distance between the eyes or width of the nose variable just by chance, or has there been evolutionary selection to be more variable than they would be otherwise; more distinctive and more unique?'"

As predicted, the researchers found that facial traits are much more variable than other bodily traits, such as the length of the hand, and that facial traits are independent of other facial traits, unlike most body measures. People with longer arms, for example, typically have longer legs, while people with wider noses or widely spaced eyes don't have longer noses. Both findings suggest that facial variation has been enhanced through evolution.

Finally, they compared the genomes of people from around the world and found more genetic variation in the genomic regions that control facial characteristics than in other areas of the genome, a sign that variation is evolutionarily advantageous.

"All three predictions were met: facial traits are more variable and less correlated than other traits, and the genes that underlie them show higher levels of variation," Nachman said. "Lots of regions of the genome contribute to facial features, so you would expect the genetic variation to be subtle, and it is. But it is consistent and statistically significant."

Using Army data

Sheehan was able to assess human facial variability thanks to a U.S. Army database of body measurements compiled from male and female personnel in 1988. The Army Anthropometric Survey (ANSUR) data are used to design and size everything from uniforms and protective clothing to vehicles and workstations.

A statistical comparison of facial traits of European Americans and African Americans -- forehead-chin distance, ear height, nose width and distance between pupils, for example -- with other body traits -- forearm length, height at waist, etc. -- showed that facial traits are, on average, more varied than the others. The most variable traits are situated within the triangle of the eyes, mouth and nose.

Sheehan and Nachman also had access to data collected by the 1000 Genome project, which has sequenced more than 1,000 human genomes since 2008 and catalogued nearly 40 million genetic variations among humans worldwide. Looking at regions of the human genome that have been identified as determining the shape of the face, they found a much higher number of variants than for traits, such as height, not involving the face.

Prehistoric origins

"Genetic variation tends to be weeded out by natural selection in the case of traits that are essential to survival," Nachman said. "Here it is the opposite; selection is maintaining variation. All of this is consistent with the idea that there has been selection for variation to facilitate recognition of individuals."

They also compared the human genomes with recently sequenced genomes of Neanderthals and Denisovans and found similar genetic variation, which indicates that the facial variation in modern humans must have originated prior to the split between these different lineages.

"Clearly, we recognize people by many traits -- for example their height or their gait -- but our findings argue that the face is the predominant way we recognize people," Sheehan said.

Neuropathy A Close Look At How The Nerves In The Foot Work

Today's video (11 minutes) comes from Dr Michael Graham DPM and is a fascinating look at how the nerves in the foot work and what the problems, causes and results of nerve damage are. It may leave you bewildered because of the amount of medical and scientific terms you've never met before but because of the series of clear images, it's not too difficult to follow. What it does show is how complex the nerve system and surrounding muscles and blood vessels in the foot are and how important it is to look after your feet, irrespective of whether you have neuropathy or not. Using the pause button at each new image may help you take in the information at your own pace.
(There is no sound track)




Uploaded on 1 Mar 2011

Nerves on the bottom of the foot have to make it through 2 tunnels in order to make it to the spine. Faulty foot mechanics and severely affect these nerves. Watch this video to learn more about this very condition and to find out about what additional factors can taken to help