Date:
August 15, 2016

Source:
University of Pittsburgh Schools of the Health Sciences

Summary:
Neuroscientists have identified the neural networks that connect the cerebral cortex to the adrenal medulla, which is responsible for the body’s rapid response in stressful situations. These findings provide evidence for the neural basis of a mind-body connection. Specifically, the findings shed new light on how stress, depression and other mental states can alter organ function, and show that there is a real anatomical basis for psychosomatic illness.

 

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The findings of this study shed new light on how stress, depression and other mental states can alter organ function, and show that there is a real anatomical basis for psychosomatic illness.
Credit: © llhedgehogll / Fotolia

 

 

Neuroscientists at the University of Pittsburgh have identified the neural networks that connect the cerebral cortex to the adrenal medulla, which is responsible for the body’s rapid response in stressful situations. These findings, reported in the online Early Edition of the journal Proceedings of the National Academy of Sciences (PNAS), provide evidence for the neural basis of a mind-body connection.

Specifically, the findings shed new light on how stress, depression and other mental states can alter organ function, and show that there is a real anatomical basis for psychosomatic illness. The research also provides a concrete neural substrate that may help explain why meditation and certain exercises such as yoga and Pilates can be so helpful in modulating the body’s responses to physical, mental and emotional stress.

“Our results turned out to be much more complex and interesting than we imagined before we began this study,” said senior author Peter L. Strick, Ph.D., Thomas Detre Chair of the Department of Neurobiology and scientific director of the University of Pittsburgh Brain Institute.

In their experiments, the scientists traced the neural circuitry that links areas of the cerebral cortex to the adrenal medulla (the inner part of the adrenal gland, which is located above each kidney). The scientific team included lead author Richard P. Dum, Ph.D., research associate professor in the Department of Neurobiology; David J. Levinthal, M.D., Ph.D., assistant professor in the Department of Medicine; and Dr. Strick.

The scientists were surprised by the sheer number of neural networks they uncovered. Other investigators had suspected that one or, perhaps, two cortical areas might be responsible for the control of the adrenal medulla. The actual number and location of the cortical areas were uncertain. In the PNAS study, the Strick laboratory used a unique tracing method that involves rabies virus. This approach is capable of revealing long chains of interconnected neurons. Using this approach, Dr. Strick and his colleagues demonstrated that the control of the adrenal medulla originates from multiple cortical areas. According to the new findings, the biggest influences arise from motor areas of the cerebral cortex and from other cortical areas involved in cognition and affect.

Why does it matter which cortical areas influence the adrenal medulla? Acute responses to stress include a wide variety of changes such as a pounding heart, sweating and dilated pupils. These responses help prepare the body for action and often are characterized as “fight or flight responses.” Many situations in modern life call for a more thought-out reaction than simple “fight or flight,” and it is clear that we have some cognitive control (or what neuroscientists call “top-down” control) over our responses to stress.

“Because we have a cortex, we have options,” said Dr. Strick. “If someone insults you, you don’t have to punch them or flee. You might have a more nuanced response and ignore the insult or make a witty comeback. These options are part of what the cerebral cortex provides.”

Another surprising result was that motor areas in the cerebral cortex, involved in the planning and performance of movement, provide a substantial input to the adrenal medulla. One of these areas is a portion of the primary motor cortex that is concerned with the control of axial body movement and posture. This input to the adrenal medulla may explain why core body exercises are so helpful in modulating responses to stress. Calming practices such as Pilates, yoga, tai chi and even dancing in a small space all require proper skeletal alignment, coordination and flexibility.

The PNAS study also revealed that the areas of the cortex that are active when we sense conflict, or are aware that we have made an error, are a source of influence over the adrenal medulla. “This observation,” said Dr. Strick, “raises the possibility that activity in these cortical areas when you re-imagine an error, or beat yourself up over a mistake, or think about a traumatic event, results in descending signals that influence the adrenal medulla in just the same way as the actual event.” These anatomical findings have relevance for therapies that deal with post-traumatic stress.

Additional links with the adrenal medulla were discovered in cortical areas that are active during mindful mediation and areas that show changes in bipolar familial depression. “One way of summarizing our results is that we may have uncovered the stress and depression connectome,” says Dr. Strick.

Overall, these results indicate that circuits exist to link movement, cognition and affect to the function of the adrenal medulla and the control of stress. This circuitry may mediate the effects of internal states like chronic stress and depression on organ function and, thus, provide a concrete neural substrate for some psychosomatic illness.


Story Source:

The above post is reprinted from materials provided by University of Pittsburgh Schools of the Health Sciences. Note: Content may be edited for style and length.


Journal Reference:

  1. Richard P. Dum, David J. Levinthal, Peter L. Strick. Motor, cognitive, and affective areas of the cerebral cortex influence the adrenal medulla.Proceedings of the National Academy of Sciences, 2016; 201605044 DOI:10.1073/pnas.1605044113

 

Source: University of Pittsburgh Schools of the Health Sciences. “New insights into how the mind influences the body.” ScienceDaily. ScienceDaily, 15 August 2016. <www.sciencedaily.com/releases/2016/08/160815185555.htm>.

Date:
August 15, 2016

Source:
Scripps Research Institute

Summary:
Scientists have succeeded in creating a ribozyme that can basically serve both to amplify genetic information and generate functional molecules, a big step toward the laboratory re-creation of the ‘RNA world’ generally believed to have preceded modern life forms based on DNA and proteins.

 

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How did life on Earth start?
Credit: Copyright Michele Hogan

 

 

Scientists at The Scripps Research Institute (TSRI) have taken a big step toward the laboratory re-creation of the “RNA world,” which is generally believed to have preceded modern life forms based on DNA and proteins.

“This is probably the first time some of these complex RNA molecules have been synthesized with a ribozyme [a special RNA enzyme] since the end of the RNA world four billion years ago,” said TSRI Professor Gerald F. Joyce, the senior author of the study.

The results from the study, reported this week in the online Early Edition of the Proceedings of the National Academy of Sciences, show the scientists have succeeded in creating a ribozyme that can basically serve both to amplify genetic information and to generate functional molecules.

The new ribozyme can replicate short lengths of RNA efficiently and perform transcription on even longer RNAs to make functional RNA molecules with complex structures — coming close to what scientists imagine in terms of an RNA replicator that could have supported life before modern biology, where protein enzymes now handle gene replication and transcription.

Taking Up a Decades-Old Challenge

In the new study, Joyce and TSRI Research Associate David P. Horning set out to use test-tube evolution techniques to tackle the decades-old challenge of creating an enzyme that could both replicate and transcribe RNA and thus support an RNA world.

The team started with an enzyme that had been developed and improved upon by other researchers since the early 1990s. The class I RNA polymerase ribozyme, as it has come to be known, can perform the basic task of RNA synthesis — required for transcribing an RNA template into a functional RNA molecule — by binding to a strand of RNA and using it as a template to stitch together a complementary RNA strand.

But prior forms of the ribozyme had been very limited in the RNA sequences they could handle, and couldn’t transcribe RNAs that have even moderately complex structures. Because of those limitations, they also could not perform full replication of RNA, which requires the transcription of a complementary strand back into a copy of the original.

Horning and Joyce drew upon several improvements described in previous research and then added random mutations to create a population of roughly 100 trillion distinct variants of the molecule. Mimicking the evolutionary process of natural selection, they set up a system to isolate only the variant ribozymes that could synthesize — from the respective RNA templates — two different and challenging RNA molecules, which have mixed sequences and complex structures, and have functions in the sense that they bind tightly to specific target molecules.

“The selection was based on the ability of these newly synthesized RNAs to actually function by binding to their targets,” said Horning. “To be able to make these functional RNAs, the ribozyme effectively had to evolve to become versatile in terms of the sequence and the structure of the RNA it could handle.”

Best Performer

The best performer after two dozen rounds of selection, polymerase ribozyme 24-3, proved capable of synthesizing not only the two target-binding RNAs but also several other structurally complex RNA molecules that exist in nature — as functional remnants of the ancient RNA world — including a yeast version of a “transfer RNA” molecule that has an essential protein-making role in all cells.

“We found that the new ribozyme can handle most sequences and all but the most difficult structures, so we can use it to make a variety of functional RNA molecules,” Joyce said.

Even when synthesizing the limited RNA sequences that the original class I RNA polymerase ribozyme could handle, ribozyme 24-3 proved capable of stitching them together about 100 times faster than its ancestor could.

Turning to the much harder task of replication, the TSRI researchers found that ribozyme 24-3 could copy RNAs of up to two dozen nucleotides, achieving what biologists call “exponential replication” and creating as many as 40,000 copies of a target RNA within 24 hours.

The 24-3 ribozyme is thus the first ever to combine the two basic capabilities — RNA synthesis and RNA replication — necessary for a pre-protein, pre-DNA world of RNA life.

To generate and sustain a true “RNA world,” the new ribozyme will have to be improved further to enable the replication of longer, more complex RNA molecules — crucially including the polymerase ribozyme itself. The Joyce laboratory is now driving its ribozyme toward that goal with further test-tube evolution experiments.

“A polymerase ribozyme that achieves exponential amplification of itself will meet the criteria for being alive,” Joyce said. “That’s a summit that’s now within sight.”


Story Source:

The above post is reprinted from materials provided by Scripps Research Institute. Note: Content may be edited for style and length.


Journal Reference:

  1. David P. Horning and Gerald F. Joyce. Amplification of RNA by an RNA polymerase ribozyme. PNAS, 2016 DOI:10.1073/pnas.1610103113

 

Source: Scripps Research Institute. “Scientists take big step toward recreating primordial ‘RNA world’ of 4 billion years ago.” ScienceDaily. ScienceDaily, 15 August 2016. <www.sciencedaily.com/releases/2016/08/160815185822.htm>.

Date:
August 11, 2016

Source:
University of Cambridge

Summary:
Study of bee-manipulating plant virus reveals a ‘short-circuiting’ of natural selection. Researchers suggest that replicating the scent caused by infection could encourage declining bee populations to pollinate crops — helping both bee and human food supplies.

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Researcher Dr Alex Murphy releasing bumblebees in the ‘flight area’ of the glasshouse in the Cambridge University Botanic Gardens, surrounded by tomato plants — some infected with Cucumber Mosaic Virus, and some that are healthy.
Credit: John Carr

 

 

Plant scientists at the University of Cambridge have found that the cucumber mosaic virus (CMV) alters gene expression in the tomato plants it infects, causing changes to air-borne chemicals — the scent — emitted by the plants. Bees can smell these subtle changes, and glasshouse experiments have shown that bumblebees prefer infected plants over healthy ones.

Scientists say that by indirectly manipulating bee behaviour to improve pollination of infected plants by changing their scent, the virus is effectively paying its host back. This may also benefit the virus: helping to spread the pollen of plants susceptible to infection and, in doing so, inhibiting the chance of virus-resistant plant strains emerging.

The authors of the new study, published in the journal PLOS Pathogens, say that understanding the smells that attract bees, and reproducing these artificially by using similar chemical blends, may enable growers to protect or even enhance yields of bee-pollinated crops.

“Bees provide a vital pollination service in the production of three-quarters of the world’s food crops. With their numbers in rapid decline, scientists have been searching for ways to harness pollinator power to boost agricultural yields,” said study principal investigator Dr John Carr, Head of Cambridge’s Virology and Molecular Plant Pathology group.

“Better understanding the natural chemicals that attract bees could provide ways of enhancing pollination, and attracting bees to good sources of pollen and nectar — which they need for survival,” Carr said.

He conducted the study with Professor Beverley Glover, Director of Cambridge University Botanic Garden, where many of the experiments took place, and collaborators at Rothamsted Research.

CMV is transmitted by aphids — bees don’t carry the virus. It’s one of the most prevalent pathogens affecting tomato plants, resulting in small plants with poor-tasting fruits that can cause serious losses to cultivated crops.

Not only is CMV one of the most damaging viruses for horticultural crops, but it also persists in wild plant populations, and Carr says the new findings may explain why: “We were surprised that bees liked the smell of the plants infected with the virus — it made no sense. You’d think the pollinators would prefer a healthy plant. However, modelling suggested that if pollinators were biased towards diseased plants in the wild, this could short-circuit natural selection for disease resistance,” he said.

“The virus is rewarding disease-susceptible plants, and at the same time producing new hosts it can infect to prevent itself from going extinct. An example, perhaps, of what’s known as symbiotic mutualism.”

The increased pollination from bees may also compensate for a decreased yield of seeds in the smaller fruits of virus-infected plants, say the scientists.

The findings also reveal a new level of complexity in the evolutionary ‘arms race’ between plants and viruses, in which it is classically believed that plants continually evolve new forms of disease-resistance while viruses evolve new ways to evade it.

“We would expect the plants susceptible to disease to suffer, but in making them more attractive to pollinators the virus gives these plants an advantage. Our results suggest that the picture of a plant-pathogen arms race is more complex than previously thought, and in some cases we should think of viruses in a more positive way,” said Carr.

Plants emit ‘volatiles’, air-borne organic chemical compounds involved in scent, to attract pollinators and repulse plant-eating animals and microbes. Humans have used them for thousands of years as perfumes and spices.

The researchers grew plants in individual containers, and collected air with emissions from CMV-infected plants, as well as ‘mock-infected’ control plants.

Through mass spectrometry, researchers could see the change in emissions induced by the virus. They also found that bumblebees could smell the changes. Released one by one in a small ‘flight arena’ in the Botanic Gardens, and timed with a stopwatch by researchers, the bees consistently headed to the infected plants first, and spent longer at those plants.

“Bees are far more sensitive to the blends of volatiles emitted by plants and can detect very subtle differences in the mix of chemicals. In fact, they can even be trained to detect traces of chemicals emitted by synthetic substances, including explosives and drugs,” said Carr.

Analysis revealed that the virus produces a factor called 2b, which reprograms genetic expression in the tomato plants and causes the change in scent.

Mathematical modelling by plant disease epidemiologist Dr Nik Cunniffe, also in the Department of Plant Sciences at Cambridge, explored how the experimental findings apply outside the glasshouse. The model showed how pollinator bias for infected plants can cause genes for disease-susceptibility to persist in plant populations over extremely large numbers of generations.

The latest study is the culmination of work spanning almost eight years (and multiple bee stings). The findings will form the basis of a new collaboration with the Royal Horticultural Society, in which they aim to increase pollinator services for cultivated crops.

With the global population estimated to reach nine billion people by 2050, producing enough food will be one of this century’s greatest challenges. Carr, Glover and Cunniffe are all members of the Cambridge Global Food Security Initiative at Cambridge, which is involved in addressing the issues surrounding food security at local, national and international scales.


Story Source:

The above post is reprinted from materials provided by University of Cambridge. The original story is licensed under a Creative Commons Licence. Note: Content may be edited for style and length.


Journal Reference:

  1. Simon C. Groen, Sanjie Jiang, Alex M. Murphy, Nik J. Cunniffe, Jack H. Westwood, Matthew P. Davey, Toby J. A. Bruce, John C. Caulfield, Oliver J. Furzer, Alison Reed, Sophie I. Robinson, Elizabeth Miller, Christopher N. Davis, John A. Pickett, Heather M. Whitney, Beverley J. Glover, John P. Carr. Virus Infection of Plants Alters Pollinator Preference: A Payback for Susceptible Hosts?PLOS Pathogens, 2016; 12 (8): e1005790 DOI: 10.1371/journal.ppat.1005790

 

Source: University of Cambridge. “Virus attracts bumblebees to infected plants by changing scent.” ScienceDaily. ScienceDaily, 11 August 2016. <www.sciencedaily.com/releases/2016/08/160811143524.htm>.

Date:
August 11, 2016

Source:
New Jersey Institute of Technology

Summary:
Batches of sand from a beach on the Delaware Bay are yielding insights into the powerful impact of temperature rise and evaporation along the shore that are in turn challenging long-held assumptions about what causes beach salinity to fluctuate in coastal zones that support a rich network of sea creatures and plants.

 

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Researchers have developed models that show that increases in temperature associated with global warming will not only make inland locations more salty, but would also create drastically different pattern of pore water salinity that will have implications for animals and plants in the intertidal zone.
Credit: © Vladimir Sazonov / Fotolia

 

 

Batches of sand from a beach on the Delaware Bay are yielding insights into the powerful impact of temperature rise and evaporation along the shore that are in turn challenging long-held assumptions about what causes beach salinity to fluctuate in coastal zones that support a rich network of sea creatures and plants.

The findings have implications for the migration and survival of invertebrates such as mussels and crabs as global warming drives temperatures higher.

A first major study of the effects of evaporation on the flow of subsurface water and salinity, or salt content, in the beach intertidal zone — the section of the beach between the low and high tide marks — is being published today in Scientific Reports, an online affiliate of Nature.

The study, by New Jersey Institute of Technology’s Center for Natural Resources Development (CNRDP) and led by two environmental engineers and a coastal geologist, shows that sediments from some sections of Slaughter Beach in Delaware have salt concentrations four times as high as the ocean water that washes over them. The finding came as a surprise.

The nearshore seawater the team measured had salt concentrations of 25 grams per liter (g/L), leading the researchers to expect that the subsurface water in areas of the beach it infiltrated would have similar or even lower levels as seawater mixes with inland groundwater in this zone. However, they discovered that the average salinity in the upper intertidal zone — the high tide line — was 60 g/L, with some values reaching as high as 100.

“These elevated levels can only be caused by evaporation, as there is no other mechanism for increasing the salt in pore water — the water trapped between the grains of sediment,” said Xiaolong Geng, a postdoctoral fellow at NJIT and the principal author of the study, noting that the rates of evaporation — and salinity — are thus mainly determined by temperature and relative humidity, while tide and wave flows dilute a beach’s salt content.

“Previous studies have identified seawater as the primary source of salinity in coastal aquifer systems, thereby concluding that seawater infiltration always increases pore-water salinity by seawater-groundwater mixing dynamics,” said Michel Boufadel, director of the CNRDP, who is also an author of the study. “Based on what we learned, we think this finding should alter the way water management in coastal areas is conducted.”

The team analyzed nearly 400 sediment samples collected during the sequential phases of a complete tidal cycle, from day to night, on seven discontinuous days.

The intertidal, or littoral, zone, is a dynamic habitat, washed by seawater at high tide and uncovered at low tide, that is favored by crabs, mussels and sea anemones, the birds and sea mammals that feed on them, and plants such as kelp. Many of these animals burrow in the beach to find food and to seek protection from predators and the action of waves, and are in near constant contact with pore water.

The researchers have developed models that show that increases in temperature associated with global warming will not only make inland locations more salty, but would also create drastically different pattern of pore water salinity that will have implications for animals and plants in the intertidal zone.

“Evaporation is an important driver of underground water flow and salinity gradients, and animals such as mussels and crabs are affected by changes in salinity. If the concentrations are too high or too low, they will move away,” noted Geng.

Nancy Jackson, a professor of coastal geomorphology in the Department of Chemistry and Environmental Science and the study’s third author, collected the beach samples from Slaughter Beach and provided interpretations of pore water dynamics.


Story Source:

The above post is reprinted from materials provided by New Jersey Institute of Technology. Note: Content may be edited for style and length.


Journal Reference:

  1. Xiaolong Geng, Michel C. Boufadel, Nancy L. Jackson. Evidence of salt accumulation in beach intertidal zone due to evaporation.Scientific Reports, 2016; 6: 31486 DOI: 10.1038/srep31486

 

Source: New Jersey Institute of Technology. “Global warming’s next surprise: Saltier beaches.” ScienceDaily. ScienceDaily, 11 August 2016. <www.sciencedaily.com/releases/2016/08/160811142647.htm>.

Cancer cells kill blood vessel cells so that they can slip through the vascular wall, form metastases

Date:
August 10, 2016

Source:
Max-Planck-Gesellschaft

Summary:
Many cancers only become a mortal danger if they form metastases elsewhere in the body. Now researchers have discovered that cancer cells kill blood vessel cells so that they can slip through the vascular wall and form metastases.

 

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The most common cause of cancer deaths is not the primary tumor itself but metastases that subsequently form.
Credit: © mybaitshop / Fotolia

 

 

Many cancers only become a mortal danger if they form metastases elsewhere in the body. Such secondary tumours are formed when individual cells break away from the main tumour and travel through the bloodstream to distant areas of the body. To do so, they have to pass through the walls of small blood vessels. Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim and Goethe University Frankfurt have now shown that tumour cells kill specific cells in the vascular wall. This enables them to leave the vessels and establish metastases, a process facilitated by a molecule called DR6.

The most common cause of cancer deaths is not the primary tumour itself but metastases that subsequently form. Most tumour cells spread via the bloodstream. To do so, individual tumour cells have to enter blood vessels and leave the bloodstream again at remote locations.

Together with scientists at the universities of Cologne and Heidelberg, the Research Group led by Stefan Offermanns, Director of the Department of Pharmacology at the Max Planck Institute for Heart and Lung Research and professor at Goethe University Frankfurt, has now succeeded in clarifying the underlying mechanism. The researchers, working with cell cultures, first observed how individual tumour cells kill specific cells in the vascular wall, called endothelial cells. This process, known as necroptosis, enabled cancer cells to overcome an endothelial cell layer in the laboratory. “We were then able to show in studies on mice that the same process occurs in living organisms,” says Boris Strilic, first author of the study.

The scientists also found that endothelial cells themselves give the signal for their own death: To do this, the vascular wall cells have a receptor molecule called Death Receptor 6 (DR6) on their surface. “When a cancer cell comes into contact with it, a protein on the cell’s surface, known as APP, activates DR6. This marks the start of the cancer cells’ attack on the vascular wall, which culminates in the necroptosis of wall cells,” Strilic explains.

Death Receptor in the cell membrane

The Max Planck researchers then showed that less necroptosis of endothelial cells and less metastasis occur in genetically modified animals in which Death Receptor 6 is disabled. “This effect was also found after a blockade of DR6 or the cancer-cell protein APP, thus confirming our previous observations,” Strilic says.

It is still not entirely clear whether the cancer cells migrate directly through the resulting gap in the vascular wall or whether there is an indirect effect: “We have evidence that many more molecules are released when the vascular wall cell dies and that they render the surrounding area more permeable to cancer cells,” says Offermanns.

“This mechanism could be a promising starting point for treatments to prevent the formation of metastases,” says Offermanns. First, however, it must be determined whether a blockade of DR6 triggers unwanted side effects. It must also be determined to what extent the observations can be transferred to humans.


Story Source:

The above post is reprinted from materials provided by Max-Planck-Gesellschaft. Note: Content may be edited for style and length.


Journal Reference:

  1. Boris Strilic, Lida Yang, Julián Albarrán-Juárez, Laurens Wachsmuth, Kang Han, Ulrike C. Müller, Manolis Pasparakis, Stefan Offermanns.Tumour-cell-induced endothelial cell necroptosis via death receptor 6 promotes metastasis. Nature, 2016; 536 (7615): 215 DOI:10.1038/nature19076

 

Source: Max-Planck-Gesellschaft. “Loophole for cancer cells found: Cancer cells kill blood vessel cells so that they can slip through the vascular wall, form metastases.” ScienceDaily. ScienceDaily, 10 August 2016. <www.sciencedaily.com/releases/2016/08/160810104248.htm>.

Women in parts of Africa without dairy farming far less likely to develop osteoporosis than women in dairy farming areas of Africa, research shows

Date:
August 9, 2016

Source:
University of North Texas

Summary:
An evolutionary historian has determined that the region of origin of ancestors contributes to descendants’ risk of developing certain medical conditions.

 

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The medical community “needs to look at hereditary history and not put all races in a few categories,” say authors of a new report.
Credit: © filipefrazao / Fotolia

 

 

Research from a University of North Texas historian supports the idea that the nation and region of origin of your ancestors contributes to your risk of developing, or not developing, a growing list of medical conditions.

Constance Hilliard, professor of history specializing in pre-colonial African history, discovered that West African women living in regions infested by tsetse flies, which attack cattle and so prevent dairy farming, have a much lower rate of postmenopausal hip fractures caused by osteoporosis than their East African peers. The West African women, however, have diets low in calcium, which prevents bone loss that leads to osteoporosis. The research was recently published in the Bonekey edition of Nature.

Using data for women from 40 nations, including Cameroon and Nigeria in West Africa and Kenya in East Africa, on the amount of hip fractures, annual dairy consumption and prevalence of a genetic mutation that leads to lactose intolerance, Hilliard determined that the West African women were “essentially immune” to osteoporosis, with only three hip fractures per 100,000 people.

The East African women, who were living in regions with dairy farming, suffered 243 hip fractures — still far lower than the rate for U.S. women of 595 fractures, and residents of other nations with much larger dairy farming and much larger calcium consumption.

Both ethnic groups, Hilliard notes, lack the genetic alleles, or variations, needed to process the lactose in milk, and also have little access to other foods high in calcium.

“Osteoporosis appears to have entered the human genome approximately 10,000 years ago with the advent of dairy farming. In a genetic trade off, those humans who received evolutionary advantages through expansion of the food supply with readily available dairy protein might also have genetically adapted their own calcium homeostasis in ways that disadvantage bone strength,” Hilliard said.

She said the medical community “needs to look at hereditary history and not put all races in a few categories.”

“You may think those in certain races look the same, but their genetics are not necessarily the same,” she said. “For example, during my research, I found out that people in India were categorized as Asians and had high rates of osteoporosis, despite living in a dairy culture that considers cows as sacred and not to be slaughtered.”

The findings, she said, resolve a longstanding paradox in the public health community: While African-Americans are generally low consumers of dietary calcium, as compared to other racial and ethnic groups in the U.S., they are also at far less risk for developing osteoporosis than the other groups.

“Eighty-five percent of European populations have the genetic variant that allow them to drink milk, but Americans of European descent have higher rates of osteoporosis,” Hilliard said.

She is now researching androgen-resistant prostate cancer, the often fatal form of this cancer, in African Americans. African Americans have 2.5 times the rate of this form of cancer than males of European descent.

“Past research has determined a powerful correlation between cancer and high dairy consumption, but African Americans are getting prostate cancer with lower levels of dairy consumption,” she says.


Story Source:

The above post is reprinted from materials provided by University of North Texas. Note: Content may be edited for style and length.


Journal Reference:

  1. Constance B Hilliard. High osteoporosis risk among East Africans linked to lactase persistence genotype. BoneKEy Reports, 2016; 5: 803 DOI: 10.1038/bonekey.2016.30

 

Source: University of North Texas. “Heredity explains African-American paradox, researcher says: Women in parts of Africa without dairy farming far less likely to develop osteoporosis than women in dairy farming areas of Africa, research shows.” ScienceDaily. ScienceDaily, 9 August 2016. <www.sciencedaily.com/releases/2016/08/160809145300.htm>.

Modifier appears to dissolve crystals of the most common kidney stone

Date:
August 8, 2016

Source:
University of Houston

Summary:
Researchers have found evidence that a natural fruit extract is capable of dissolving calcium oxalate crystals, the most common component of human kidney stones. This finding could lead to the first advance in the treatment of calcium oxalate stones in 30 years.

 

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Engineer Jeffrey Rimer and collaborators have discovered a new molecule that has the potential to be a more effective inhibitor of kidney stone formation.
Credit: University of Houston

 

 

Researchers have found evidence that a natural fruit extract is capable of dissolving calcium oxalate crystals, the most common component of human kidney stones. This finding could lead to the first advance in the treatment of calcium oxalate stones in 30 years.

Jeffrey Rimer, associate professor of chemical engineering at the University of Houston, was lead author of the study, published Aug. 8 in the online edition of Nature. The work offers the first evidence that the compound hydroxycitrate (HCA) is an effective inhibitor of calcium oxalate crystal growth that, under certain conditions, is actually able to dissolve these crystals. Researchers also explain how it works.

The findings are the result of a combination of experimental studies, computational studies and human studies, Rimer said.

Kidney stones are small, hard mineral deposits that form inside the kidneys, affecting up to 12 percent of men and seven percent of women. High blood pressure, diabetes and obesity can increase the risk, and the reported incidence is on the rise.

Preventive treatment has not changed much over the last three decades. Doctors tell patients who are at risk of developing stones to drink lots of water and avoid foods rich in oxalate, such as rhubarb, okra, spinach and almonds. They often recommend taking citrate (CA), in the form of potassium citrate, a supplement that can slow crystal growth, but some people are unable to tolerate the side effects.

The project grew out of preliminary work done by collaborator John Asplin, a nephrologist at Litholink Corporation, who suggested HCA as a possible treatment. HCA is chemically similar to CA and is also available as a dietary supplement.

“HCA shows promise as a potential therapy to prevent kidney stones,” the researchers wrote. “HCA may be preferred as a therapy over CA (potassium citrate).”

In addition to Rimer and Asplin, authors on the paper include Giannis Mpourmpakis and his graduate student, Michael G. Taylor, of the University of Pittsburgh; Ignacio Granja of Litholink Corporation, and Jihae Chung, a UH graduate student working in Rimer’s lab.

The head-to-head studies of CA and HCA determined that while both compounds inhibit the growth of calcium oxalate crystals, HCA was more potent and displayed unique qualities that are advantageous for the development of new therapies.

The team of researchers then used atomic force microscopy, or AFM, to study interactions between the crystals, CA and HCA under realistic growth conditions. According to Rimer, the technique allowed them to record crystal growth in real time with near-molecular resolution.

Chung noted that the AFM images recorded the crystal actually shrinking when exposed to specific concentrations of HCA. Rimer suspected the initial finding was an abnormality, as it is rare to see a crystal actually dissolve in highly supersaturated growth solutions. The most effective inhibitors reported in the literature simply stop the crystal from growing.

It turned out that Chung’s initial finding was correct. Once they confirmed it is possible to dissolve crystals in supersaturated solutions, researchers then looked at reasons to explain why that happened.

Mpourmpakis and Taylor applied density functional theory (DFT) — a highly accurate computational method used to study the structure and properties of materials — to address how HCA and CA bind to calcium and to calcium oxalate crystals. They discovered HCA formed a stronger bond with crystal surfaces, inducing a strain that is seemingly relieved by the release of calcium and oxalate, leading to crystal dissolution.

HCA was also tested in human subjects, as seven people took the supplement for three days, allowing researchers to determine that HCA is excreted through urine, a requirement for the supplement to work as a treatment.

While Rimer said the research established the groundwork to design an effective drug, questions remain. Long-term safety, dosage and additional human trials are needed, he said.

“But our initial findings are very promising,” he said. “If it works in vivo, similar to our trials in the laboratory, HCA has the potential to reduce the incidence rate of people with chronic kidney stone disease.”


Story Source:

The above post is reprinted from materials provided by University of Houston. The original item was written by Jeannie Kever. Note: Content may be edited for style and length.


Journal Reference:

  1. Jihae Chung, Ignacio Granja, Michael G. Taylor, Giannis Mpourmpakis, John R. Asplin, Jeffrey D. Rimer. Molecular modifiers reveal a mechanism of pathological crystal growth inhibition. Nature, 2016; 1 DOI: 10.1038/nature19062

 

Source: University of Houston. “Researchers propose new treatment to prevent kidney stones: Modifier appears to dissolve crystals of the most common kidney stone.” ScienceDaily. ScienceDaily, 8 August 2016. <www.sciencedaily.com/releases/2016/08/160808115447.htm>.

Pluripotency factor primes genes involved in differentiation

Date:
August 4, 2016

Source:
Sanford-Burnham Prebys Medical Discovery Institute

Summary:
Scientists have made a major advance in understanding how the cells of an organism, which all contain the same genetic information, come to be so diverse. A study shows that a protein called OCT4 narrows down the range of cell types that stem cells can become. The findings could impact efforts to produce specific types of cells for future therapies to treat a broad range of diseases.

 

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Fluorescence microscopic view of human skin cells (stock image).
Credit: © Vshyukova / Fotolia

 

 

Scientists at Sanford Burnham Prebys Medical Discovery Institute (SBP) have made a major advance in understanding how the cells of an organism, which all contain the same genetic information, come to be so diverse. A study published today in Molecular Cell shows that a protein called OCT4 narrows down the range of cell types that stem cells can become. The findings could impact efforts to produce specific types of cells for future therapies to treat a broad range of diseases, as well as aid the understanding of which cells are affected by drugs that influence cell specialization.

“We found that the stem cell-specific protein OCT4 primes certain genes that, when activated, cause the cell to differentiate, or become more specialized,” said Laszlo Nagy, M.D., Ph.D., professor and director of the Genomic Control of Metabolism Program and senior author of the study. “This priming customizes stem cells’ responses to signals that induce differentiation and makes the underlying genetic process more efficient.”

Differentiation matters

As an organism — such as a human — develops from its simplest, earliest form into maturity, its cells transition from a highly flexible state — stem cells — to more specialized types that make up its tissues. Many labs are trying to recapitulate this process to generate specific types of cells that could be transplanted into patients to treat disease. For example, pancreatic beta cells could treat diabetes, and neurons that produce dopamine could treat Parkinson’s.

What OCT4 does

OCT4 is a transcription factor — a protein that regulates gene activity — that maintains stem cells’ ability to give rise to any tissue in the body. OCT4 works by sitting on DNA and recruiting factors that either help initiate or repress the reading of specific genes.

The new study shows that, at certain genes, OCT4 also collaborates with transcription factors that are activated by external signals, such as the retinoic acid (vitamin A) receptor (RAR) and beta-catenin, to turn on their respective genes. Vitamin A converts stem cells to neuronal precursors, and activation of beta-catenin by Wnt can either support pluripotency or promote non-neural differentiation, depending on what other signals are present. Recruitment of these factors ‘primes’ a subset of the genes that the signal-responsive factors can activate.

The big picture

“Our findings suggest a general principle for how the same differentiation signal induces distinct transitions in various types of cells,” added Nagy. “Whereas in stem cells, OCT4 recruits the RAR to neuronal genes, in bone marrow cells, another transcription factor would recruit RAR to genes for the granulocyte program. Which factors determine the effects of differentiation signals in bone marrow cells — and other cell types — remains to be determined.”

Next steps

“In a sense, we’ve found the code for stem cells that links the input — signals like vitamin A and Wnt — to the output — cell type,” said Nagy. “Now we plan to explore whether other transcription factors behave similarly to OCT4 — that is, to find the code in more mature cell types.

“If other factors also have this dual function — both maintaining the current state and priming certain genes to respond to external signals — that would answer a key question in developmental biology and advance the field of stem cell research.”

This research was performed in collaboration with scientists at the University of Debrecen in Hungary, the University of Leicester in the United Kingdom, the Max Planck Institute for Molecular Genetics, the University of Würzburg and the Max Delbrück Center for Molecular Medicine in Germany, the Institut de Génomique in France, and Weill Cornell Medical College, and supported by grants from the Hungarian Scientific Research Fund, the Hungarian Brain Research Program, and the U.S. National Institutes of Health.


Story Source:

The above post is reprinted from materials provided by Sanford-Burnham Prebys Medical Discovery Institute. The original item was written by Jessica Moore. Note: Content may be edited for style and length.


Journal Reference:

  1. Zoltan Simandi, Attila Horvath, Lyndsey C. Wright, Ixchelt Cuaranta-Monroy, Isabella De Luca, Katalin Karolyi, Sascha Sauer, Jean-Francois Deleuze, Lorraine J. Gudas, Shaun M. Cowley, Laszlo Nagy. OCT4 Acts as an Integrator of Pluripotency and Signal-Induced Differentiation. Molecular Cell, 2016; DOI:10.1016/j.molcel.2016.06.039

 

Source: Sanford-Burnham Prebys Medical Discovery Institute. “Breakthrough in understanding how stem cells become specialized: Pluripotency factor primes genes involved in differentiation.” ScienceDaily. ScienceDaily, 4 August 2016. <www.sciencedaily.com/releases/2016/08/160804140503.htm>.

Technology could lead to the development of neuromorphic computers

Date:
August 4, 2016

Source:
IBM Research

Summary:
Scientists have created randomly spiking neurons using phase-change materials to store and process data. This demonstration marks a significant step forward in the development of energy-efficient, ultra-dense integrated neuromorphic technologies for applications in cognitive computing.

 

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Phase-change neurons. A chip with large arrays of phase-change devices that store the state of artificial neuronal populations in their atomic configuration. In the photograph, individual devices are accessed by means of an array of probes to allow for precise characterization, modeling and interrogation. The tiny squares are contact pads that are used to access the nanometer-scale phase-change cells (not visible). The sharp probes touch the contact pads to change the phase configuration stored in the cells in response to the neuronal input. Each set of probes can access a population of 100 cells. The chip hosts only the phase-change devices that are the “heart” of the neurons. There are thousands to millions of these cells on one chip and we access them (in this particular photograph) by means of the sharp needles (probe card).
Credit: IBM Research

 

 

IBM scientists have created randomly spiking neurons using phase-change materials to store and process data. This demonstration marks a significant step forward in the development of energy-efficient, ultra-dense integrated neuromorphic technologies for applications in cognitive computing.

Inspired by the way the biological brain functions, scientists have theorized for decades that it should be possible to imitate the versatile computational capabilities of large populations of neurons. However, doing so at densities and with a power budget that would be comparable to those seen in biology has been a significant challenge, until now.

“We have been researching phase-change materials for memory applications for over a decade, and our progress in the past 24 months has been remarkable,” said IBM Fellow Evangelos Eleftheriou. “In this period, we have discovered and published new memory techniques, including projected memory, stored 3 bits per cell in phase-change memory for the first time, and now are demonstrating the powerful capabilities of phase-change-based artificial neurons, which can perform various computational primitives such as data-correlation detection and unsupervised learning at high speeds using very little energy.”

The results of this research are appearing today on the cover of the peer-reviewed journal Nature Nanotechnology.

The artificial neurons designed by IBM scientists in Zurich consist of phase-change materials, including germanium antimony telluride, which exhibit two stable states, an amorphous one (without a clearly defined structure) and a crystalline one (with structure). These materials are the basis of re-writable Blu-ray discs. However, the artificial neurons do not store digital information; they are analog, just like the synapses and neurons in our biological brain.

In the published demonstration, the team applied a series of electrical pulses to the artificial neurons, which resulted in the progressive crystallization of the phase-change material, ultimately causing the neuron to fire. In neuroscience, this function is known as the integrate-and-fire property of biological neurons. This is the foundation for event-based computation and, in principle, is similar to how our brain triggers a response when we touch something hot.

Exploiting this integrate-and-fire property, even a single neuron can be used to detect patterns and discover correlations in real-time streams of event-based data. For example, in the Internet of Things, sensors can collect and analyze volumes of weather data collected at the edge for faster forecasts. The artificial neurons could be used to detect patterns in financial transactions to find discrepancies or use data from social media to discover new cultural trends in real time. Large populations of these high-speed, low-energy nano-scale neurons could also be used in neuromorphic coprocessors with co-located memory and processing units.

IBM scientists have organized hundreds of artificial neurons into populations and used them to represent fast and complex signals. Moreover, the artificial neurons have been shown to sustain billions of switching cycles, which would correspond to multiple years of operation at an update frequency of 100 Hz. The energy required for each neuron update was less than five picojoule and the average power less than 120 microwatts — for comparison, 60 million microwatts power a 60 watt lightbulb.

“Populations of stochastic phase-change neurons, combined with other nanoscale computational elements such as artificial synapses, could be a key enabler for the creation of a new generation of extremely dense neuromorphic computing systems,” said Tomas Tuma, a co-author of the paper.

To read more about this research, please go to:https://www.ibm.com/blogs/research/2016/08/unsupervised-learning-artificial-neurons


Story Source:

The above post is reprinted from materials provided by IBM Research. Note: Materials may be edited for content and length.


Journal Reference:

  1. Tomas Tuma, Angeliki Pantazi, Manuel Le Gallo, Abu Sebastian, Evangelos Eleftheriou. Stochastic phase-change neurons. Nature Nanotechnology, 2016; 11 (8): 693 DOI: 10.1038/nnano.2016.70

 

Source: IBM Research. “Phase-change device imitates the functionality of neurons: Technology could lead to the development of neuromorphic computers.” ScienceDaily. ScienceDaily, 4 August 2016. <www.sciencedaily.com/releases/2016/08/160804093327.htm>.

Method to reinforce these materials could help make airplane frames lighter, more damage-resistant

Date:
August 3, 2016

Source:
Massachusetts Institute of Technology

Summary:
Aerospace engineers have designed carbon nanotube ‘stitches’ that strongly bind composites, which could produce lighter, more damage-resistant airplanes.

 

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MIT aerospace engineers have found a way to bond composite layers, producing a material that is substantially stronger and more resistant to damage than other advanced composites. The improvement may lead to stronger, lighter airplane parts.
Credit: Illustration: Christine Daniloff/MIT

 

 

The newest Airbus and Boeing passenger jets flying today are made primarily from advanced composite materials such as carbon fiber reinforced plastic — extremely light, durable materials that reduce the overall weight of the plane by as much as 20 percent compared to aluminum-bodied planes. Such lightweight airframes translate directly to fuel savings, which is a major point in advanced composites’ favor.

But composite materials are also surprisingly vulnerable: While aluminum can withstand relatively large impacts before cracking, the many layers in composites can break apart due to relatively small impacts — a drawback that is considered the material’s Achilles’ heel.

Now MIT aerospace engineers have found a way to bond composite layers in such a way that the resulting material is substantially stronger and more resistant to damage than other advanced composites. Their results are published this week in the journal Composites Science and Technology.

The researchers fastened the layers of composite materials together using carbon nanotubes — atom-thin rolls of carbon that, despite their microscopic stature, are incredibly strong. They embedded tiny “forests” of carbon nanotubes within a glue-like polymer matrix, then pressed the matrix between layers of carbon fiber composites. The nanotubes, resembling tiny, vertically-aligned stitches, worked themselves within the crevices of each composite layer, serving as a scaffold to hold the layers together.

In experiments to test the material’s strength, the team found that, compared with existing composite materials, the stitched composites were 30 percent stronger, withstanding greater forces before breaking apart.

Roberto Guzman, who led the work as an MIT postdoc in the Department of Aeronautics and Astronautics (AeroAstro), says the improvement may lead to stronger, lighter airplane parts — particularly those that require nails or bolts, which can crack conventional composites.

“More work needs to be done, but we are really positive that this will lead to stronger, lighter planes,” says Guzman, who is now a researcher at the IMDEA Materials Institute, in Spain. “That means a lot of fuel saved, which is great for the environment and for our pockets.”

The study’s co-authors include AeroAstro professor Brian Wardle and researchers from the Swedish aerospace and defense company Saab AB.

“Size matters”

Today’s composite materials are composed of layers, or plies, of horizontal carbon fibers, held together by a polymer glue, which Wardle describes as “a very, very weak, problematic area.” Attempts to strengthen this glue region include Z-pinning and 3-D weaving — methods that involve pinning or weaving bundles of carbon fibers through composite layers, similar to pushing nails through plywood, or thread through fabric.

“A stitch or nail is thousands of times bigger than carbon fibers,” Wardle says. “So when you drive them through the composite, you break thousands of carbon fibers and damage the composite.”

Carbon nanotubes, by contrast, are about 10 nanometers in diameter — nearly a million times smaller than the carbon fibers.

“Size matters, because we’re able to put these nanotubes in without disturbing the larger carbon fibers, and that’s what maintains the composite’s strength,” Wardle says. “What helps us enhance strength is that carbon nanotubes have 1,000 times more surface area than carbon fibers, which lets them bond better with the polymer matrix.”

Stacking up the competition

Guzman and Wardle came up with a technique to integrate a scaffold of carbon nanotubes within the polymer glue. They first grew a forest of vertically-aligned carbon nanotubes, following a procedure that Wardle’s group previously developed. They then transferred the forest onto a sticky, uncured composite layer and repeated the process to generate a stack of 16 composite plies — a typical composite laminate makeup — with carbon nanotubes glued between each layer.

To test the material’s strength, the team performed a tension-bearing test — a standard test used to size aerospace parts — where the researchers put a bolt through a hole in the composite, then ripped it out. While existing composites typically break under such tension, the team found the stitched composites were stronger, able to withstand 30 percent more force before cracking.

The researchers also performed an open-hole compression test, applying force to squeeze the bolt hole shut. In that case, the stitched composite withstood 14 percent more force before breaking, compared to existing composites.

“The strength enhancements suggest this material will be more resistant to any type of damaging events or features,” Wardle says. “And since the majority of the newest planes are more than 50 percent composite by weight, improving these state-of-the art composites has very positive implications for aircraft structural performance.”


Story Source:

The above post is reprinted from materials provided by Massachusetts Institute of Technology. Note: Materials may be edited for content and length.


Journal Reference:

  1. R. Guzman de Villoria, P. Hallander, L. Ydrefors, P. Nordin, B.L. Wardle.In-plane strength enhancement of laminated composites via aligned carbon nanotube interlaminar reinforcement. Composites Science and Technology, 2016; 133: 33 DOI:10.1016/j.compscitech.2016.07.006

 

Source: Massachusetts Institute of Technology. “Carbon nanotube ‘stitches’ make stronger, lighter composites: Method to reinforce these materials could help make airplane frames lighter, more damage-resistant.” ScienceDaily. ScienceDaily, 3 August 2016. <www.sciencedaily.com/releases/2016/08/160803111753.htm>.

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