Consuming low calorie diet leads to ‘longer, healthier life’

Washington, July 10 (ANI): Substantially cutting calories from the diet could slow the ageing process and increase life expectancy, according to a decades-long study of monkeys.

Researchers at the University of Wisconsin-Madison, the Wisconsin National Primate Research Center and the William S. Middleton Memorial Veterans Hospital have found that a nutritious but reduced-calorie diet blunts aging and significantly delays the onset of such age-related disorders as cancer, diabetes, cardiovascular disease and brain atrophy.

“We have been able to show that caloric restriction can slow the aging process in a primate species,” says Richard Weindruch, a professor of medicine in the UW-Madison School of Medicine and Public Health who leads the National Institute on Aging-funded study. “We observed that caloric restriction reduced the risk of developing an age-related disease by a factor of three and increased survival.”

During the 20-year course of the study, half of the animals permitted to eat freely have survived, while 80 percent of the monkeys given the same diet, but with 30 percent fewer calories, are still alive.

Begun in 1989 with a cohort of 30 monkeys to chart the health effects of the reduced-calorie diet, the study expanded in 1994 with the addition of 46 more rhesus macaques. All of the animals in the study were enrolled as adults at ages ranging from 7 to 14 years.

Today, 33 animals remain in the study. Of those, 13 are given free rein at the dinner table, and 20 are on a calorie-restricted diet. Rhesus macaques have an average life span of about 27 years in captivity. The oldest animal currently in the study is 29 years.

Weindruch notes that in terms of overall animal health, the restricted diet leads to longer lifespan and improved quality of life in old age.

“There is a major effect of caloric restriction in increasing survival if you look at deaths due to the diseases of aging,” he said.

The study has been published in the journal Science. (ANI)

Novel MRI technique can lead to less breast biopsies in high-risk women

Washington, June 30 (ANI): Researchers from University of Wisconsin-Madison have suggested a new method, that when applied with MRI scans of the breast, can help rid women with increased breast cancer risk of the pain and stress of having to endure a biopsy of the lump or lesion.

It is recommended that women with certain breast cancer risk factors – including inherited genetic mutations, family or personal history of breast cancer, or previous radiation therapy to the chest should receive an annual MRI screening in addition to their yearly mammogram.

During a breast MRI, which lasts about a half hour, the technician injects a contrast agent into a vein in the patient’s arm.

The contrast agent flows throughout the body, including the breasts.

Because they are growing quickly, cancerous lesions often have immature vasculature, and the contrast agent flows in and “leaks” out quickly. Conversely, benign lesions show more gradual in and out flow.

“The tricky ones are the ones that enhance quickly and then fall off more slowly,” said Wally Block, a UW-Madison associate professor of biomedical engineering and medical physics.

“Many of these lesions turn out to be difficult to classify and lead to biopsy,” Block added.

The researchers suggest that right kind of MRI scan can help identify a cancerous lesion based on characteristics about its shape.

For instance, breaks or interruptions in a lesion can indicate a benign fibroadenoma. Lumps with smooth edges often are benign, while those with jagged edges can signal cancer.

With the new technique, an MRI machine acquires data radially and generates a high-resolution, three-dimensional image that radiologists can turn, slice and view from many perspectives – enabling them to study a lesion’s physical characteristics more carefully.

Machines equipped with the technique also acquire more data in less time. (ANI)

Mechanism behind carbohydrate synthesis may pave way for new TB drugs

Washington, June 23 (ANI): The mechanism behind how carbohydrates are synthesised from small sugar units has shed new light on a promising way to target new medicines against tuberculosis, revealed a new study.

While working with components of the tuberculosis bacterium, researchers from the University of Wisconsin-Madison identified an unusual process by which the pathogen builds an important structural carbohydrate.

The mechanism also offers insight into a widespread but poorly understood basic biological function – controlling the length of carbohydrate polymers.

“Carbohydrate polymers are the most abundant organic molecules on the planet, and it’s amazing that we don’t know more about these are made. There’s not much known about how length is controlled in these carbohydrate polymers,” said Laura Kiessling, a professor of chemistry and biochemistry at UW-Madison.

Most carbohydrates exist as many sugar molecules linked into long chains, or polymers, but the right number of sugars in the chain is vital for them to work properly.

However, Kiessling has said that not much is known about how carbohydrate length is determined.

Unlike some biological chains – such as DNA and proteins – that are built off a template that guides the length of the final product, carbohydrate-synthesizing enzymes work without templates.

The research team focused on an enzyme called GlfT2 that is responsible for building a critical carbohydrate component of the TB bacterial cell wall, and found that a small fatty component at the starting end binds to the enzyme and helps it track the length of the growing polymer.

As the enzyme adds more and more sugar units to the opposite end, the chain becomes increasingly unmanageable.

Kiessling said that “if the chain gets too long, it gets hard to hold on to both of the ends, so the chain falls off” the synthesizing enzyme, forming a completed carbohydrate polymer.

The researchers believe that the enzymes responsible for building different types of carbohydrates exceed their comfort level at different points, leading to molecules of different prescribed lengths.

He said that the report was the first description of this “tethering” mechanism – named for the fatty lipid that tethers the start of the polymer to the enzyme – in carbohydrate synthesis, though it may prove to be common among other organisms as well.

The work gives significant insight into developing new therapeutics against TB.

The GlfT2 enzyme has two binding sites – one for each end of the growing carbohydrate – that make it an especially appealing candidate.

“Our mechanism provides a blueprint for strategies to block a new anti-mycobacterial target,” said Kiessling.

The new study has appeared in the online Early Edition of the Proceedings of the National Academy of Sciences. (ANI)

Skin cells may help mend your broken heart

Washington, February 13 (ANI): Having demonstrated in their previous studies that skin cells could be turned back into stem cells, University of Wisconsin-Madison scientists have now shown that such “induced” cells can actually form the specialized cells that make up heart muscle.

Reporting their findings in the journal Circulation Research, the researchers claimed that that they were able to grow working heart-muscle cells from induced pluripotent stem cells, known as iPS cells.

Tim Kamp, UW-Madison School of Medicine and Public Health professor of medicine, revealed that the heart cells were originally reprogrammed from human skin cells by his co-authors on the study, James Thomson and Junying Yu.

“It’s an encouraging result because it shows that those cells will be useful for research and may someday be useful in therapy. If you have a heart failure patient who is in dire straits – and there are never enough donor hearts for transplantation – we may be able to make heart cells from the patient’s skin cells, and use them to repair heart muscle. That’s pretty exciting,” said Kamp, who is also a cardiologist with UW Health.

The researchers used a virus to insert four transcription factors into the genes of the skin cell, reprogramming it back to an embryo-like state.

However, since the virus is taken up by the new cell, the researchers fear that it may eventually cause cancer.

Considering this, they suggest that therapies from reprogrammed skin cells will have to wait until new methods are perfected.

Kamp, however, still calls his team’s findings to be significant, saying that the speed at which knowledge is progressing is very encouraging.

His latest research, proving that iPS cells can become functional heart cells, is just one step along the way to better understanding and treatment of disease.

“We’re excited about it, because it’s the some of the first research to show it can be done, but in the future, we’ll probably say, ‘Well, of course it can be done.’ But you don’t know until you do it. It’s a very mysterious and complicated dance to get these cells to go from skin cells to stem cells to heart cells,” he says. (ANI)

Empathy may lie in the genes

Washington, Feb. 11 (ANI): The ability to identify and act on another’s emotions is partially determined by genes, says a new study on mice.

In the University of Wisconsin-Madison and Oregon Health and Science University (OHSU) study, a highly social strain of mice learned to associate a sound played in a specific cage with something negative simply by hearing a mouse in that cage respond with squeaks of distress.

A genetically different mouse strain with fewer social tendencies did not learn any connection between the cues and the other mouse’s distress, showing that the ability to empathise may have a genetic basis.

The study has been published in the Public Library of Science ONE journal.

Like humans, mice can automatically sense and respond to others’ positive and negative emotions, such as excitement, fear or anger.

Understanding empathy in mice may lead to important discoveries about the social interaction deficits seen in many human psychosocial disorders, including autism, schizophrenia, depression and addiction, the researchers say.

“The core of empathy is being able to have an emotional experience and share that experience with another,” says UW-Madison graduate student Jules Panksepp, who led the work along with undergraduate QiLiang Chen.

“We are basically trying to deconstruct empathy into smaller functional units that make it more accessible to biological research,” the researcher added.

In the experiments, one mouse observed as another mouse was placed in a test chamber and trained to associate a 30-second tone with a mild foot shock. Upon experiencing the shock, the test mouse emitted a short distress call or squeak.

Though having no direct knowledge of the foot shock, observers from a very social mouse strain learned from the distress calls to associate the test chamber and tone with something negative.

When later placed in the test chamber and presented with the tone, they exhibited clear physiological signs of aversion, such as freezing in place, even though no shock was delivered.

In contrast, observer mice from a less gregarious strain – less likely to seek the company of other mice – showed no response to the tone when they were placed in the test chamber. (ANI)

Early childhood stress leads to long-term health problems

Washington, Jan 27 (ANI): Early childhood stress can have lifelong impact on kids’ health, according to a new study.

The researchers found that adolescents who as youngsters have experienced either physical abuse or time in an orphanage are likely to have impaired immune function.

“Even though these children’s environments have changed, physiologically they’re still responding to stress,” said senior author Seth Pollak, a professor of psychology and pediatrics at UW-Madison.

That can affect their learning and their behavior, and having a compromised immune system is going to affect these children’s health,” Pollak added.

As director of the Child Emotion Laboratory in the UW-Madison Waisman Center, Pollak focuses on how experiences early in life affect children’s subsequent development. In the current work, he and fellow Wisconsin psychology professor Chris Coe, an expert on the links between stress and immunity, turned to the immune system as a way to isolate the consequences of early events.

“The immune system is not preset at birth. The cells are there, but how they will develop and how well they’ll be regulated is very much influenced by your early environment and the type of rearing you have,” said said Wisconsin psychology professor Chris Coe.

In the study led by Elizabeth Shirtcliff of the University of New Orleans when she was a postdoctoral fellow at UW-Madison, the authors evaluated immune-system strength among adolescents who have had stressful experiences either typical or unusually stressful childhoods.

The researchers looked for high levels of antibodies against the common and usually latent herpes simplex virus type 1 (HSV-1).

“We can use the control of latent viruses as one way of assessing the competence of the immune system,” Coe explains.

“During times of stress or if the immune system is not appropriately regulated, the herpes virus is more likely to reactivate,” he added.

They found that adolescents with a history of physical abuse and stressful home environments had higher levels of HSV-1 antibodies, showing that their immune systems were compromised.

“That is very unfortunate, but it was not surprising,” Pollak said, since stress is widely known to have negative impacts on immune function.

“It suggests that children’s emotional environments are having widespread repercussions on their health,” the researcher added.

Moreover, another group of adolescents in the study, who spent time in orphanages in Romania, Russia or China before being adopted by U.S. families, showed a similar impairment of immune regulation.

“These children began their lives in a stressful environment, but they’re now adolescents, and for a decade, they’ve been living in stable, affluent, loving environments. And yet, their immune systems are compromised as well. In fact, they look just like the physically abused kids,” said Pollak.

“The bottom line is that these early stressors can really have long-term implications,” Pollak added.

The study appears online in the Proceedings of the National Academy of Sciences. (ANI)

Protein that control hormones critical to women’s health found in pituitary gland

London, Jan 12 (ANI): Researchers at the University of Wisconsin-Madison have uncovered the location of a protein, called on Syt IV, which regulates hormones critical to women’s health- the pituitary gland.

Scientists found that the “rogue protein,” whose main location and function were unknown until now, is located in a specific area of the pituitary gland.

The puzzling protein acts as control knob and may adjust the release of the two hormones that come almost exclusively from the posterior pituitary: oxytocin, which controls many reproductive functions, and vasopressin, which controls fluid balance.

“The findings raise very interesting possibilities for women’s health, in which rising and falling hormone levels play a key role in many biological processes,” Nature magazine quoted senior author Meyer Jackson, a professor of physiology at the UW-Madison School of Medicine and Public Health (SMPH), as saying.

The research focused on Syt IV, which is a member of the synaptotagmin family of 17 proteins, present in both mice and humans.

Synaptotagmins are usually embedded in the membranes of small sacs, or vesicles, filled with neurotransmitters and hormones within nerve terminals.

At the time when an electrical impulse from one cell reaches a nerve terminal, Syt IV triggers the release of calcium.

Calcium, in its turn triggers the spilling out of the vesicle’s contents – neurotransmitters and hormones – so they can act on other cells.

“Most synaptotagmins are triggering molecules that drive a vesicle’s membrane into the membrane that surrounds a neighboring cell so that chemicals inside the vesicle can come out,” said Jackson.

However, Syt IV is different as it doesn’t bind to calcium and is found only sparsely in most parts of the brain.

But the researchers were shocked a few years ago after they discovered large amounts of it in the posterior pituitary, one of the three primary parts of the gland.
For the study, the researchers conducted high-powered biophysical measurements, and then compared the pituitaries from normal mice and mice in which Syt IV had been knocked out.

It was found that like other members of the synaptotagmin family, Syt IV resides on vesicles. But unlike the others, Syt IV doesn’t trigger neurotransmitter or hormone release.

“It does not simply translate a calcium signal into a command for hormone release. Unlike other synaptotagmins, Syt IV tunes the triggering command and determines whether the same electrical impulse will let a large or small amount of hormone out of the nerve terminal,” said Jackson

This ability to modulate hormone release may have important implications for pregnancy, birth, lactation and the menstrual cycle, all of which are linked to fluctuations in oxytocin levels.

“Any change in the body that entails releasing more or less of this hormone into the bloodstream could well be a result of the brain’s making more or less of this protein,” said Jackson.

He further added that more studies will be needed to better understand the protein.

The study appeared in the recent issue of Nature Neuroscience. (ANI)