A study in Botswana by Columbia University Mailman School of Public Health scientists finds that spikes in cases of life-threatening diarrhea in young children are associated with La Niña climate conditions. The findings published in the journal Nature Communications could provide the basis for an early-warning system that would allow public health officials to prepare for periods of increased diarrhea cases as long as seven months ahead of time.
In low- and middle-income countries, diarrhea is the second leading cause of death in children younger than five years of age, with 72 percent of deaths occurring in the first two years of life. Rates of under-5 diarrhea in Africa are particularly high, with an estimated incidence of 3.3 episodes of diarrhea per child each year and one-quarter of all child deaths caused by diarrhea.
The El Niño-Southern Oscillation (ENSO) is a coupled ocean-atmosphere system spanning the equatorial Pacific Ocean that oscillates in a 3-to-7-year cycle between two extremes, El Niño (warmer ocean temperatures) and La Niña (cooler ocean temperatures). The ENSO cycle affects local weather patterns around the world, including temperatures, winds, and precipitation.
Researchers analyzed associations between ENSO and climate conditions and cases of under-5 diarrhea in the Chobe region in northeastern Botswana. They found that La Niña is associated with cooler temperatures, increased rainfall, and higher flooding during the rainy season. In turn, La Niña conditions lagged 0-7 months are associated with about a 30-percent increase in incidence of under-5 diarrhea in the early rainy season from December through February
"These findings demonstrate the potential use of the El Niño-Southern Oscillation as a long-lead prediction tool for childhood diarrhea in southern Africa," says first author Alexandra K. Heaney, a former doctoral student in environmental health sciences at Columbia Mailman and now a postdoc at University of California, Berkeley. "Advanced stockpiling of medical supplies, preparation of hospital beds, and organization of healthcare workers could dramatically improve the ability of health facilities to manage high diarrheal disease incidence."
Previously, El Niño events have been linked to diarrhea outbreaks in Peru, Bangladesh, China, and Japan, but until now studies of the effects of ENSO on diarrheal disease in Africa have been limited to cholera -- a pathogen responsible for only a small fraction of diarrheal cases in Africa.
Infectious diarrhea is caused by many different pathogens (viruses, bacteria, and protozoa) and meteorological conditions can have a critical influence on pathogen exposures, in particular, those associated with waterborne transmission. For example, extreme rainfall events may contaminate drinking water by flushing diarrhea-causing pathogens from pastures and dwellings into drinking water supplies, and drought conditions can concentrate animal activity increasing the movement of diarrhea-causing pathogens into surface water resources.
Water Treatment Systems Appear To Be Strained
The researchers speculate that centralized water disinfection processes currently used in the Chobe region may be insufficient to deal with changes in water quality brought on by extremes of wet and dry weather, although they caution that further confirmatory studies are needed.
Earlier research by Columbia Mailman researchers in the Chobe region found that cases of diarrhea in young children spiked during extreme climate conditions, in both the wet and dry seasons. A second study reported on a method to forecast childhood diarrheal disease there. Because climate conditions vary from region to region, forecasts for infectious diseases must be region-specific. In other studies, the scientists have created forecasts for influenza, Ebola, and West Nile Virus. During the influenza season in the United States, they publish weekly regional forecasts with predictions on whether cases are expected to rise or fall and by how much.
Read more at Science Daily
Jan 2, 2020
Learning from the bears
Grizzly bears spend many months in hibernation, but their muscles do not suffer from the lack of movement. In the journal Scientific Reports, a team led by Michael Gotthardt reports on how they manage to do this. The grizzly bears' strategy could help prevent muscle atrophy in humans as well.
A grizzly bear only knows three seasons during the year. Its time of activity starts between March and May. Around September the bear begins to eat large quantities of food. And sometime between November and January, it falls into hibernation. From a physiological point of view, this is the strangest time of all. The bear's metabolism and heart rate drop rapidly. It excretes neither urine nor feces. The amount of nitrogen in the blood increases drastically and the bear becomes resistant to the hormone insulin.
A person could hardly survive this four-month phase in a healthy state. Afterwards, he or she would most likely have to cope with thromboses or psychological changes. Above all, the muscles would suffer from this prolonged period of disuse. Anyone who has ever had an arm or leg in a cast for a few weeks or has had to lie in bed for a long time due to an illness has probably experienced this.
A little sluggish, but otherwise fine
Not so the grizzly bear. In the spring, the bear wakes up from hibernation, perhaps still a bit sluggish at first, but otherwise well. Many scientists have long been interested in the bear's strategies for adapting to its three seasons.
A team led by Professor Michael Gotthardt, head of the Neuromuscular and Cardiovascular Cell Biology group at the Max Delbrueck Center for Molecular Medicine (MDC) in Berlin, has now investigated how the bear's muscles manage to survive hibernation virtually unharmed. The scientists from Berlin, Greifswald and the United States were particularly interested in the question of which genes in the bear's muscle cells are transcribed and converted into proteins, and what effect this has on the cells.
Understanding and copying the tricks of nature
"Muscle atrophy is a real human problem that occurs in many circumstances. We are still not very good at preventing it," says the lead author of the study, Dr. Douaa Mugahid, once a member of Gotthardt's research group and now a postdoctoral researcher in the laboratory of Professor Marc Kirschner of the Department of Systems Biology at Harvard Medical School in Boston.
"For me, the beauty of our work was to learn how nature has perfected a way to maintain muscle functions under the difficult conditions of hibernation," says Mugahid. "If we can better understand these strategies, we will be able to develop novel and non-intuitive methods to better prevent and treat muscle atrophy in patients."
Gene sequencing and mass spectrometry
To understand the bears' tricks, the team led by Mugahid and Gotthardt examined muscle samples from grizzly bears both during and between the times of hibernation, which they had received from Washington State University. "By combining cutting-edge sequencing techniques with mass spectrometry, we wanted to determine which genes and proteins are upregulated or shut down both during and between the times of hibernation," explains Gotthardt.
"This task proved to be tricky -- because neither the full genome nor the proteome, i.e., the totality of all proteins of the grizzly bear, were known," says the MDC scientist. In a further step, he and his team compared the findings with observations of humans, mice and nematode worms.
Non-essential amino acids allowed muscle cells to grow
As the researchers reported in the journal "Scientific Reports," they found proteins in their experiments that strongly influence a bear's amino acid metabolism during hibernation. As a result, its muscle cells contain higher amounts of certain non-essential amino acids (NEAAs).
"In experiments with isolated muscle cells of humans and mice that exhibit muscle atrophy, cell growth could also be stimulated by NEAAs," says Gotthardt, adding that "it is known, however, from earlier clinical studies that the administration of amino acids in the form of pills or powders is not enough to prevent muscle atrophy in elderly or bedridden people."
"Obviously, it is important for the muscle to produce these amino acids itself -- otherwise the amino acids might not reach the places where they are needed," speculates the MDC scientist. A therapeutic starting point, he says, could be the attempt to induce the human muscle to produce NEAAs itself by activating corresponding metabolic pathways with suitable agents during longer rest periods.
Tissue samples from bedridden patients
In order to find out which signaling pathways need to be activated in the muscle, Gotthardt and his team compared the activity of genes in grizzly bears, humans and mice. The required data came from elderly or bedridden patients and from mice suffering from muscle atrophy -- for example, as a result of reduced movement after the application of a plaster cast. "We wanted to find out which genes are regulated differently between animals that hibernate and those that do not," explains Gotthardt.
However, the scientists came across a whole series of such genes. To narrow down the possible candidates that could prove to be a starting point for muscle atrophy therapy, the team subsequently carried out experiments with nematode worms. "In worms, individual genes can be deactivated relatively easily and one can quickly see what effects this has on muscle growth," explains Gotthardt.
Read more at Science Daily
A grizzly bear only knows three seasons during the year. Its time of activity starts between March and May. Around September the bear begins to eat large quantities of food. And sometime between November and January, it falls into hibernation. From a physiological point of view, this is the strangest time of all. The bear's metabolism and heart rate drop rapidly. It excretes neither urine nor feces. The amount of nitrogen in the blood increases drastically and the bear becomes resistant to the hormone insulin.
A person could hardly survive this four-month phase in a healthy state. Afterwards, he or she would most likely have to cope with thromboses or psychological changes. Above all, the muscles would suffer from this prolonged period of disuse. Anyone who has ever had an arm or leg in a cast for a few weeks or has had to lie in bed for a long time due to an illness has probably experienced this.
A little sluggish, but otherwise fine
Not so the grizzly bear. In the spring, the bear wakes up from hibernation, perhaps still a bit sluggish at first, but otherwise well. Many scientists have long been interested in the bear's strategies for adapting to its three seasons.
A team led by Professor Michael Gotthardt, head of the Neuromuscular and Cardiovascular Cell Biology group at the Max Delbrueck Center for Molecular Medicine (MDC) in Berlin, has now investigated how the bear's muscles manage to survive hibernation virtually unharmed. The scientists from Berlin, Greifswald and the United States were particularly interested in the question of which genes in the bear's muscle cells are transcribed and converted into proteins, and what effect this has on the cells.
Understanding and copying the tricks of nature
"Muscle atrophy is a real human problem that occurs in many circumstances. We are still not very good at preventing it," says the lead author of the study, Dr. Douaa Mugahid, once a member of Gotthardt's research group and now a postdoctoral researcher in the laboratory of Professor Marc Kirschner of the Department of Systems Biology at Harvard Medical School in Boston.
"For me, the beauty of our work was to learn how nature has perfected a way to maintain muscle functions under the difficult conditions of hibernation," says Mugahid. "If we can better understand these strategies, we will be able to develop novel and non-intuitive methods to better prevent and treat muscle atrophy in patients."
Gene sequencing and mass spectrometry
To understand the bears' tricks, the team led by Mugahid and Gotthardt examined muscle samples from grizzly bears both during and between the times of hibernation, which they had received from Washington State University. "By combining cutting-edge sequencing techniques with mass spectrometry, we wanted to determine which genes and proteins are upregulated or shut down both during and between the times of hibernation," explains Gotthardt.
"This task proved to be tricky -- because neither the full genome nor the proteome, i.e., the totality of all proteins of the grizzly bear, were known," says the MDC scientist. In a further step, he and his team compared the findings with observations of humans, mice and nematode worms.
Non-essential amino acids allowed muscle cells to grow
As the researchers reported in the journal "Scientific Reports," they found proteins in their experiments that strongly influence a bear's amino acid metabolism during hibernation. As a result, its muscle cells contain higher amounts of certain non-essential amino acids (NEAAs).
"In experiments with isolated muscle cells of humans and mice that exhibit muscle atrophy, cell growth could also be stimulated by NEAAs," says Gotthardt, adding that "it is known, however, from earlier clinical studies that the administration of amino acids in the form of pills or powders is not enough to prevent muscle atrophy in elderly or bedridden people."
"Obviously, it is important for the muscle to produce these amino acids itself -- otherwise the amino acids might not reach the places where they are needed," speculates the MDC scientist. A therapeutic starting point, he says, could be the attempt to induce the human muscle to produce NEAAs itself by activating corresponding metabolic pathways with suitable agents during longer rest periods.
Tissue samples from bedridden patients
In order to find out which signaling pathways need to be activated in the muscle, Gotthardt and his team compared the activity of genes in grizzly bears, humans and mice. The required data came from elderly or bedridden patients and from mice suffering from muscle atrophy -- for example, as a result of reduced movement after the application of a plaster cast. "We wanted to find out which genes are regulated differently between animals that hibernate and those that do not," explains Gotthardt.
However, the scientists came across a whole series of such genes. To narrow down the possible candidates that could prove to be a starting point for muscle atrophy therapy, the team subsequently carried out experiments with nematode worms. "In worms, individual genes can be deactivated relatively easily and one can quickly see what effects this has on muscle growth," explains Gotthardt.
Read more at Science Daily
Many younger patients with stomach cancer have a distinct disease
Many people under 60 who develop stomach cancer have a "genetically and clinically distinct" disease, new Mayo Clinic research has discovered. Compared to stomach cancer in older adults, this new, early onset form often grows and spreads more quickly, has a worse prognosis, and is more resistant to traditional chemotherapy treatments, the study finds. The research was published recently in the journal Surgery.
While rates of stomach cancer in older patients have been declining for decades, this early onset cancer is increasing and now makes up more than 30% of stomach cancer diagnoses.
"I think this is an alarming trend, as stomach cancer is a devastating disease," says senior author Travis Grotz, M.D., a Mayo Clinic surgical oncologist. "There is little awareness in the U.S. of the signs and symptoms of stomach cancer, and many younger patients may be diagnosed late -- when treatment is less effective."
The research team studied 75,225 cases using several cancer databases to review stomach cancer statistics from 1973 to 2015. Today, the average age of someone diagnosed with stomach cancer is 68, but people in their 30s, 40s and 50s are more at risk than they used to be.
Although there's no clear cutoff age for the definition of early onset and late-onset stomach cancer, the researchers found the distinctions held true whether they used an age cutoff of 60, 50 or 40 years. The researchers found that the incidence of late-onset stomach cancer decreased by 1.8% annually during the study period, while the early onset disease decreased by 1.9% annually from 1973 to 1995 and then increased by 1.5% through 2013. The proportion of early onset gastric cancer has doubled from 18% of all cases in 1995 to now more than 30% of all gastric cancer cases.
"Typically, we see stomach cancer being diagnosed in patients in their 70s, but increasingly we are seeing 30- to 50-year-old patients being diagnosed," Dr. Grotz says.
The increased rate of the early onset disease is not from earlier detection or screening, Dr. Grotz adds. "There is no universal screening for stomach cancer, and the younger patients actually presented with later-stage disease than the older patients," he says.
In addition to being more deadly, early onset stomach cancer is also genetically and molecularly distinct, researchers found. Furthermore, traditional risk factors for developing stomach cancer among older Americans, such as smoking tobacco, did not appear to correlate with its early onset counterpart.
"Hopefully, studies like this will raise awareness and increase physician suspicion of stomach cancer, particularly in younger patients," Dr. Grotz says. Younger patients who feel full before finishing a meal, or have reflux, abdominal pain, unintentional weight loss and difficulty eating should see their health care provider, he adds.
Stomach cancer is the 16th most common cancer in the U.S., according to the American Cancer Society. It has a five-year survival rate of 31.5%, and there will be an estimated 27,510 new cases in 2019, according to the National Cancer Institute. The World Health Organization reports that cancer was the second leading cause of death globally in 2018 and that stomach cancer was the third most common cause of cancer death that year.
Read more at Science Daily
While rates of stomach cancer in older patients have been declining for decades, this early onset cancer is increasing and now makes up more than 30% of stomach cancer diagnoses.
"I think this is an alarming trend, as stomach cancer is a devastating disease," says senior author Travis Grotz, M.D., a Mayo Clinic surgical oncologist. "There is little awareness in the U.S. of the signs and symptoms of stomach cancer, and many younger patients may be diagnosed late -- when treatment is less effective."
The research team studied 75,225 cases using several cancer databases to review stomach cancer statistics from 1973 to 2015. Today, the average age of someone diagnosed with stomach cancer is 68, but people in their 30s, 40s and 50s are more at risk than they used to be.
Although there's no clear cutoff age for the definition of early onset and late-onset stomach cancer, the researchers found the distinctions held true whether they used an age cutoff of 60, 50 or 40 years. The researchers found that the incidence of late-onset stomach cancer decreased by 1.8% annually during the study period, while the early onset disease decreased by 1.9% annually from 1973 to 1995 and then increased by 1.5% through 2013. The proportion of early onset gastric cancer has doubled from 18% of all cases in 1995 to now more than 30% of all gastric cancer cases.
"Typically, we see stomach cancer being diagnosed in patients in their 70s, but increasingly we are seeing 30- to 50-year-old patients being diagnosed," Dr. Grotz says.
The increased rate of the early onset disease is not from earlier detection or screening, Dr. Grotz adds. "There is no universal screening for stomach cancer, and the younger patients actually presented with later-stage disease than the older patients," he says.
In addition to being more deadly, early onset stomach cancer is also genetically and molecularly distinct, researchers found. Furthermore, traditional risk factors for developing stomach cancer among older Americans, such as smoking tobacco, did not appear to correlate with its early onset counterpart.
"Hopefully, studies like this will raise awareness and increase physician suspicion of stomach cancer, particularly in younger patients," Dr. Grotz says. Younger patients who feel full before finishing a meal, or have reflux, abdominal pain, unintentional weight loss and difficulty eating should see their health care provider, he adds.
Stomach cancer is the 16th most common cancer in the U.S., according to the American Cancer Society. It has a five-year survival rate of 31.5%, and there will be an estimated 27,510 new cases in 2019, according to the National Cancer Institute. The World Health Organization reports that cancer was the second leading cause of death globally in 2018 and that stomach cancer was the third most common cause of cancer death that year.
Read more at Science Daily
Dec 31, 2019
Happy New Year
Dec 30, 2019
Mosquitoes can sense toxins through their legs
Researchers at LSTM have identified a completely new mechanism by which mosquitoes that carry malaria are becoming resistant to insecticide.
After studying both Anopheles gambiae and Anopheles coluzzii, two major malaria vectors in West Africa, they found that a particular family of binding proteins situated in the insect's legs were highly expressed in resistant populations.
First author on a paper published today in the journal Nature, Dr Victoria Ingham, explains: "We have found a completely new insecticide resistance mechanism that we think is contributing to the lower than expected efficacy of bed nets. The protein, which is based in the legs, comes into direct contact with the insecticide as the insect lands on the net, making it an excellent potential target for future additives to nets to overcome this potent resistance mechanism."
Examining the Anopheline mosquitoes, the team demonstrated that the binding protein, SAP2, was found elevated in resistant populations and further elevated following contact with pyrethroids, the insecticide class used on all bed nets. They found that when levels of this protein were reduced, by partial silencing of the gene, susceptibility to pyrethroids were restored; conversely when the protein was expressed at elevated levels, previously susceptible mosquitoes became resistant to pyrethroids.
The increase in insecticide resistance across mosquito populations has led to the introduction of new insecticide treated bed nets containing the synergist piperonyl butoxide (PBO) as well as pyrethroid insecticides. The synergist targets one of the most widespread and previously most potent resistance mechanisms caused by the cytochrome P450s. However, mosquitoes are continually evolving new resistance mechanisms and the discovery of this new resistance mechanism provides an excellent opportunity to identify additional synergists that could be used to restore susceptibility
Professor Hilary Ranson is senior author on the paper. She said: "Long-lasting insecticide treated bed nets remain one of the key interventions in malaria control. It is vital that we understand and mitigate for resistance within mosquito populations in order to ensure that the dramatic reductions in disease rates in previous decades are not reversed. This newly discovered resistance mechanism could provide us with an important target for both the monitoring of insecticide resistance and the development of novel compounds able to block pyrethroid resistance and prevent the spread of malaria."
From Science Daily
After studying both Anopheles gambiae and Anopheles coluzzii, two major malaria vectors in West Africa, they found that a particular family of binding proteins situated in the insect's legs were highly expressed in resistant populations.
First author on a paper published today in the journal Nature, Dr Victoria Ingham, explains: "We have found a completely new insecticide resistance mechanism that we think is contributing to the lower than expected efficacy of bed nets. The protein, which is based in the legs, comes into direct contact with the insecticide as the insect lands on the net, making it an excellent potential target for future additives to nets to overcome this potent resistance mechanism."
Examining the Anopheline mosquitoes, the team demonstrated that the binding protein, SAP2, was found elevated in resistant populations and further elevated following contact with pyrethroids, the insecticide class used on all bed nets. They found that when levels of this protein were reduced, by partial silencing of the gene, susceptibility to pyrethroids were restored; conversely when the protein was expressed at elevated levels, previously susceptible mosquitoes became resistant to pyrethroids.
The increase in insecticide resistance across mosquito populations has led to the introduction of new insecticide treated bed nets containing the synergist piperonyl butoxide (PBO) as well as pyrethroid insecticides. The synergist targets one of the most widespread and previously most potent resistance mechanisms caused by the cytochrome P450s. However, mosquitoes are continually evolving new resistance mechanisms and the discovery of this new resistance mechanism provides an excellent opportunity to identify additional synergists that could be used to restore susceptibility
Professor Hilary Ranson is senior author on the paper. She said: "Long-lasting insecticide treated bed nets remain one of the key interventions in malaria control. It is vital that we understand and mitigate for resistance within mosquito populations in order to ensure that the dramatic reductions in disease rates in previous decades are not reversed. This newly discovered resistance mechanism could provide us with an important target for both the monitoring of insecticide resistance and the development of novel compounds able to block pyrethroid resistance and prevent the spread of malaria."
From Science Daily
Using deep learning to predict disease-associated mutations
During the past years, artificial intelligence (AI) -- the capability of a machine to mimic human behavior -- has become a key player in high-techs like drug development projects. AI tools help scientists to uncover the secret behind the big biological data using optimized computational algorithms. AI methods such as deep neural network improves decision making in biological and chemical applications i.e., prediction of disease-associated proteins, discovery of novel biomarkers and de novo design of small molecule drug leads. These state-of-the-art approaches help scientists to develop a potential drug more efficiently and economically.
A research team led by Professor Hongzhe Sun from the Department of Chemistry at the University of Hong Kong (HKU), in collaboration with Professor Junwen Wang from Mayo Clinic, Arizona in the United States (a former HKU colleague), implemented a robust deep learning approach to predict disease-associated mutations of the metal-binding sites in a protein. This is the first deep learning approach for the prediction of disease-associated metal-relevant site mutations in metalloproteins, providing a new platform to tackle human diseases. The research findings were recently published in a top scientific journal Nature Machine Intelligence.
Metal ions play pivotal roles either structurally or functionally in the (patho)physiology of human biological systems. Metals such as zinc, iron and copper are essential for all lives and their concentration in cells must be strictly regulated. A deficiency or an excess of these physiological metal ions can cause severe disease in humans. It was discovered that a mutation in human genome are strongly associated with different diseases. If these mutations happen in the coding region of DNA, it might disrupt metal-binding sites of the proteins and consequently initiate severe diseases in humans. Understanding of disease-associated mutations at the metal-binding sites of proteins will facilitate discovery of new drugs.
The team first integrated omics data from different databases to build a comprehensive training dataset. By looking at the statistics from the collected data, the team found that different metals have different disease associations. A mutation in zinc-binding sites has a major role in breast, liver, kidney, immune system and prostate diseases. By contrast, the mutations in calcium- and magnesium-binding sites are associated with muscular and immune system diseases, respectively. For iron-binding sites, mutations are more associated with metabolic diseases. Furthermore, mutations of manganese- and copper-binding sites are associated with cardiovascular diseases with the latter being associated with nervous system disease as well. They used a novel approach to extract spatial features from the metal binding sites using an energy-based affinity grid map. These spatial features have been merged with physicochemical sequential features to train the model. The final results show using the spatial features enhanced the performance of the prediction with an area under the curve (AUC) of 0.90 and an accuracy of 0.82. Given the limited advanced techniques and platforms in the field of metallomics and metalloproteins, the proposed deep learning approach offers a method to integrate the experimental data with bioinformatics analysis. The approach will help scientist to predict DNA mutations which are associated with disease like cancer, cardiovascular diseases and genetic disorders.
Read more at Science Daily
A research team led by Professor Hongzhe Sun from the Department of Chemistry at the University of Hong Kong (HKU), in collaboration with Professor Junwen Wang from Mayo Clinic, Arizona in the United States (a former HKU colleague), implemented a robust deep learning approach to predict disease-associated mutations of the metal-binding sites in a protein. This is the first deep learning approach for the prediction of disease-associated metal-relevant site mutations in metalloproteins, providing a new platform to tackle human diseases. The research findings were recently published in a top scientific journal Nature Machine Intelligence.
Metal ions play pivotal roles either structurally or functionally in the (patho)physiology of human biological systems. Metals such as zinc, iron and copper are essential for all lives and their concentration in cells must be strictly regulated. A deficiency or an excess of these physiological metal ions can cause severe disease in humans. It was discovered that a mutation in human genome are strongly associated with different diseases. If these mutations happen in the coding region of DNA, it might disrupt metal-binding sites of the proteins and consequently initiate severe diseases in humans. Understanding of disease-associated mutations at the metal-binding sites of proteins will facilitate discovery of new drugs.
The team first integrated omics data from different databases to build a comprehensive training dataset. By looking at the statistics from the collected data, the team found that different metals have different disease associations. A mutation in zinc-binding sites has a major role in breast, liver, kidney, immune system and prostate diseases. By contrast, the mutations in calcium- and magnesium-binding sites are associated with muscular and immune system diseases, respectively. For iron-binding sites, mutations are more associated with metabolic diseases. Furthermore, mutations of manganese- and copper-binding sites are associated with cardiovascular diseases with the latter being associated with nervous system disease as well. They used a novel approach to extract spatial features from the metal binding sites using an energy-based affinity grid map. These spatial features have been merged with physicochemical sequential features to train the model. The final results show using the spatial features enhanced the performance of the prediction with an area under the curve (AUC) of 0.90 and an accuracy of 0.82. Given the limited advanced techniques and platforms in the field of metallomics and metalloproteins, the proposed deep learning approach offers a method to integrate the experimental data with bioinformatics analysis. The approach will help scientist to predict DNA mutations which are associated with disease like cancer, cardiovascular diseases and genetic disorders.
Read more at Science Daily
Evolution: Revelatory relationship
A new study of the ecology of an enigmatic group of novel unicellular organisms by scientists from Ludwig-Maximilians-Universitaet (LMU) in Munich supports the idea hydrogen played an important role in the evolution of Eukaryota, the first nucleated cells.
One of the most consequential developments in the history of biological evolution occurred approximately 2 billion years ago with the appearance of the first eukaryotes -- unicellular organisms that contain a distinct nucleus. This first eukaryotic lineage would subsequently give rise to all higher organisms including plants and animals, but its origins remain obscure. Some years ago, microbiologists analyzed DNA sequences from marine sediments, which shed new light on the problem. These sediments were recovered from a hydrothermal vent at a site known as Loki's Castle (named for the Norse god of fire) on the Mid-Atlantic Ridge in the Arctic Ocean. Sequencing of the DNA molecules they contained revealed that they were derived from a previously unknown group of microorganisms.
Although the cells from which the DNA originated could not be isolated and characterized directly, the sequence data showed them to be closely related to the Archaea. The researchers therefore named the new group Lokiarchaeota.
Archaea, together with the phylum Bacteria, are the oldest known lineages of single-celled organisms. Strikingly, the genomes of the Lokiarchaeota indicated that they might exhibit structural and biochemical features that are otherwise specific to eukaryotes. This suggests that the Lokiarchaeota might be related to the last common ancestor of eukaryotes. Indeed, phylogenomic analysis of the Lokiarchaeota DNA from Loki's Castle strongly suggested that they were derived from descendants of one of the last common ancestors of Eukaryota and Archaea. Professor William Orsi of the Department of Earth and Environmental Sciences at LMU, in cooperation with scientists at Oldenburg University and the Max Planck Institute for Marine Microbiology, has now been able to examine the activity and metabolism of the Lokiarchaeota directly. The results support the suggested relationship between Lokiarchaeota and eukaryotes, and provide hints as to the nature of the environment in which the first eukaryotes evolved. The new findings appear in the journal Nature Microbiology.
The most likely scenario for the emergence of eukaryotes is that they arose from a symbiosis in which the host was an archaeal cell and the symbiont was a bacterium. According to this theory, the bacterial symbiont subsequently gave rise to the mitochondria -- the intracellular organelles that are responsible for energy production in eukaryotic cells. One hypothesis proposes that the archaeal host was dependent on hydrogen for its metabolism, and that the precursor of the mitochondria produced it. This "hydrogen hypothesis" posits that the two partner cells presumably lived in an anoxic environment that was rich in hydrogen, and if they were separated from the hydrogen source they would have become more dependent on one another for survival potentially leading to an endosymbiotic event. "If the Lokiarchaeota, as the descendants of this putative ur-archaeon, are also dependent on hydrogen, this would support the hydrogen hypothesis," says Orsi. "However, up to now, the ecology of these Archaea in their natural habitat was a matter of speculation."
Orsi and his team have now, for the first time, characterized the cellular metabolism of Lokiarchaeota recovered from sediment cores obtained from the seabottom in an extensive oxygen-depleted region off the coast of Namibia. They did so by analyzing the RNA present in these samples. RNA molecules are copied from the genomic DNA, and serve as blueprints for the synthesis of proteins. Their sequences therefore reflect patterns and levels of gene activity. The sequence analyses revealed that Lokiarchaeota in these samples outnumbered bacteria by 100- to 1000-fold. "That strongly indicates that these sediments are a favorable habitat for them, promoting their activity," says Orsi.
Read more at Science Daily
One of the most consequential developments in the history of biological evolution occurred approximately 2 billion years ago with the appearance of the first eukaryotes -- unicellular organisms that contain a distinct nucleus. This first eukaryotic lineage would subsequently give rise to all higher organisms including plants and animals, but its origins remain obscure. Some years ago, microbiologists analyzed DNA sequences from marine sediments, which shed new light on the problem. These sediments were recovered from a hydrothermal vent at a site known as Loki's Castle (named for the Norse god of fire) on the Mid-Atlantic Ridge in the Arctic Ocean. Sequencing of the DNA molecules they contained revealed that they were derived from a previously unknown group of microorganisms.
Although the cells from which the DNA originated could not be isolated and characterized directly, the sequence data showed them to be closely related to the Archaea. The researchers therefore named the new group Lokiarchaeota.
Archaea, together with the phylum Bacteria, are the oldest known lineages of single-celled organisms. Strikingly, the genomes of the Lokiarchaeota indicated that they might exhibit structural and biochemical features that are otherwise specific to eukaryotes. This suggests that the Lokiarchaeota might be related to the last common ancestor of eukaryotes. Indeed, phylogenomic analysis of the Lokiarchaeota DNA from Loki's Castle strongly suggested that they were derived from descendants of one of the last common ancestors of Eukaryota and Archaea. Professor William Orsi of the Department of Earth and Environmental Sciences at LMU, in cooperation with scientists at Oldenburg University and the Max Planck Institute for Marine Microbiology, has now been able to examine the activity and metabolism of the Lokiarchaeota directly. The results support the suggested relationship between Lokiarchaeota and eukaryotes, and provide hints as to the nature of the environment in which the first eukaryotes evolved. The new findings appear in the journal Nature Microbiology.
The most likely scenario for the emergence of eukaryotes is that they arose from a symbiosis in which the host was an archaeal cell and the symbiont was a bacterium. According to this theory, the bacterial symbiont subsequently gave rise to the mitochondria -- the intracellular organelles that are responsible for energy production in eukaryotic cells. One hypothesis proposes that the archaeal host was dependent on hydrogen for its metabolism, and that the precursor of the mitochondria produced it. This "hydrogen hypothesis" posits that the two partner cells presumably lived in an anoxic environment that was rich in hydrogen, and if they were separated from the hydrogen source they would have become more dependent on one another for survival potentially leading to an endosymbiotic event. "If the Lokiarchaeota, as the descendants of this putative ur-archaeon, are also dependent on hydrogen, this would support the hydrogen hypothesis," says Orsi. "However, up to now, the ecology of these Archaea in their natural habitat was a matter of speculation."
Orsi and his team have now, for the first time, characterized the cellular metabolism of Lokiarchaeota recovered from sediment cores obtained from the seabottom in an extensive oxygen-depleted region off the coast of Namibia. They did so by analyzing the RNA present in these samples. RNA molecules are copied from the genomic DNA, and serve as blueprints for the synthesis of proteins. Their sequences therefore reflect patterns and levels of gene activity. The sequence analyses revealed that Lokiarchaeota in these samples outnumbered bacteria by 100- to 1000-fold. "That strongly indicates that these sediments are a favorable habitat for them, promoting their activity," says Orsi.
Read more at Science Daily
How cells learn to 'count'
One of the wonders of cell biology is its symmetry. Mammalian cells have one nucleus and one cell membrane, and most humans have 23 pairs of chromosomes. Trillions of mammalian cells achieve this uniformity -- but some consistently break this mold to fulfill unique functions. Now, a team of Johns Hopkins Medicine researchers have found how these outliers take shape.
In experiments with genetically engineered mice, a research team has ruled out a mechanism that scientists have long believed controls the number of hairlike structures, called cilia, protruding on the outside of each mammalian cell. They concluded that control of the cilia count might rely instead on a process more commonly seen in non-mammalian species.
The experiments, described Dec. 2 in Nature Cell Biology and led by Andrew Holland, Ph.D., associate professor of molecular biology and genetics at the Johns Hopkins University School of Medicine, may eventually help scientists learn more about human diseases related to cilia function, such as respiratory infections, infertility and hydrocephaly.
Cilia are ancient structures that first appeared on single-celled organisms as small hairlike "fingers" that act as motors to move the cell or antennae to sense the environment. Nearly all human cells have at least one cilium that senses physical or chemical cues. However, some specialized cell types in humans, such as those lining the respiratory and reproductive tracts, have hundreds of cilia on their surface that beat in waves to move fluids through the system.
"Our main question was how these multicilliated cells become so dramatically different than the rest of the cells in our body," says Holland. "Most cells make exactly one cilium per cell, but these highly specialized cells give up on this tight numerical control and make hundreds of cilia."
In an effort to answer the question, Holland and his team took a closer look at the base of cilia, the place where the organelles attach and grow from the surface of the cell. This base is a microscopic, cylinder-shaped structure called a centriole.
In single-ciliated cells, Holland says, centrioles are created before a cell divides. A cell contains two-parent centrioles that each duplicate so that both new cells gets one pair of centrioles -- the oldest of these two centrioles then goes on to form the base of the cilium. However, multicilliated cells create unique structures, called deuterosomes, that act as a copy machine to enable the production of tens to hundreds of centrioles, allowing these cells to create many cilia.
"Deuterosomes are only present in multicilliated cells, and scientists have long thought they are central for determining how many centrioles and cilia are formed," says Holland.
To test this, Holland and his team developed a mouse model that lacked the gene that creates deuterosomes. Then, they analyzed the tissues that carry multicilliated cells and counted their cilia.
The researchers were surprised to find that the genetically engineered mice had the same number of cilia on cells as the mice with deuterosomes, ruling out the central role of deuterosomes in controlling the number of cilia. For example, the multicilliated cells lining the trachea all had 200-300 cillia per cell. The researchers also found that cells without deuterosomes could make new centrioles just as quickly as cells with them.
With this surprising result in hand, the researchers engineered mouse cells that lacked both deuterosomes and parent centrioles, and then counted the number of cilia formed in multicilliated cells.
"We figured that with no parent centrioles and no deuterosomes, the multicilliated cells would be unable to create the proper number of new cilia," says Holland.
Remarkably, Holland says, even the lack of parent centrioles had no effect on the final cilia number. Most cells in both normal and genetically engineered groups created between 50 and 90 cilia.
"This finding changes the dogma of what we believed to be the driving force behind centriole assembly," explains Holland. "Instead of needing a platform to grow on, centrioles can be created spontaneously."
While uncommon in mammals, the so-called de novo generation of centrioles is not new to the animal kingdom. Some species, such as the small flatworm planaria, lack parent centrioles entirely, and rely on de novo centriole generation to create the cilia they use to move.
In further experiments on genetically engineered mice, Holland found that all the spontaneously created centrioles were assembled within a region of the cell rich with fibrogranular material -- the protein components necessary to build a centriole.
He says he suspects that proteins found in that little-understood area of the cell contain the essential elements necessary to construct centrioles and ultimately control the number of cilia that are formed. Everything else, the deuterosomes and even the parent centrioles, are "not strictly necessary," he says.
"We think that the deuterosomes function to relieve pressure on the parent centrioles from the demands of making many new centrioles, freeing up parent centrioles to fulfill other functions," says Holland.
Read more at Science Daily
In experiments with genetically engineered mice, a research team has ruled out a mechanism that scientists have long believed controls the number of hairlike structures, called cilia, protruding on the outside of each mammalian cell. They concluded that control of the cilia count might rely instead on a process more commonly seen in non-mammalian species.
The experiments, described Dec. 2 in Nature Cell Biology and led by Andrew Holland, Ph.D., associate professor of molecular biology and genetics at the Johns Hopkins University School of Medicine, may eventually help scientists learn more about human diseases related to cilia function, such as respiratory infections, infertility and hydrocephaly.
Cilia are ancient structures that first appeared on single-celled organisms as small hairlike "fingers" that act as motors to move the cell or antennae to sense the environment. Nearly all human cells have at least one cilium that senses physical or chemical cues. However, some specialized cell types in humans, such as those lining the respiratory and reproductive tracts, have hundreds of cilia on their surface that beat in waves to move fluids through the system.
"Our main question was how these multicilliated cells become so dramatically different than the rest of the cells in our body," says Holland. "Most cells make exactly one cilium per cell, but these highly specialized cells give up on this tight numerical control and make hundreds of cilia."
In an effort to answer the question, Holland and his team took a closer look at the base of cilia, the place where the organelles attach and grow from the surface of the cell. This base is a microscopic, cylinder-shaped structure called a centriole.
In single-ciliated cells, Holland says, centrioles are created before a cell divides. A cell contains two-parent centrioles that each duplicate so that both new cells gets one pair of centrioles -- the oldest of these two centrioles then goes on to form the base of the cilium. However, multicilliated cells create unique structures, called deuterosomes, that act as a copy machine to enable the production of tens to hundreds of centrioles, allowing these cells to create many cilia.
"Deuterosomes are only present in multicilliated cells, and scientists have long thought they are central for determining how many centrioles and cilia are formed," says Holland.
To test this, Holland and his team developed a mouse model that lacked the gene that creates deuterosomes. Then, they analyzed the tissues that carry multicilliated cells and counted their cilia.
The researchers were surprised to find that the genetically engineered mice had the same number of cilia on cells as the mice with deuterosomes, ruling out the central role of deuterosomes in controlling the number of cilia. For example, the multicilliated cells lining the trachea all had 200-300 cillia per cell. The researchers also found that cells without deuterosomes could make new centrioles just as quickly as cells with them.
With this surprising result in hand, the researchers engineered mouse cells that lacked both deuterosomes and parent centrioles, and then counted the number of cilia formed in multicilliated cells.
"We figured that with no parent centrioles and no deuterosomes, the multicilliated cells would be unable to create the proper number of new cilia," says Holland.
Remarkably, Holland says, even the lack of parent centrioles had no effect on the final cilia number. Most cells in both normal and genetically engineered groups created between 50 and 90 cilia.
"This finding changes the dogma of what we believed to be the driving force behind centriole assembly," explains Holland. "Instead of needing a platform to grow on, centrioles can be created spontaneously."
While uncommon in mammals, the so-called de novo generation of centrioles is not new to the animal kingdom. Some species, such as the small flatworm planaria, lack parent centrioles entirely, and rely on de novo centriole generation to create the cilia they use to move.
In further experiments on genetically engineered mice, Holland found that all the spontaneously created centrioles were assembled within a region of the cell rich with fibrogranular material -- the protein components necessary to build a centriole.
He says he suspects that proteins found in that little-understood area of the cell contain the essential elements necessary to construct centrioles and ultimately control the number of cilia that are formed. Everything else, the deuterosomes and even the parent centrioles, are "not strictly necessary," he says.
"We think that the deuterosomes function to relieve pressure on the parent centrioles from the demands of making many new centrioles, freeing up parent centrioles to fulfill other functions," says Holland.
Read more at Science Daily
Dec 29, 2019
'Lost crops' could have fed as many as maize
Make some room in the garden, you storied three sisters: the winter squash, climbing beans and the vegetable we know as corn. Grown together, newly examined "lost crops" could have produced enough seed to feed as many indigenous people as traditionally grown maize, according to new research from Washington University in St. Louis.
But there are no written or oral histories to describe them. The domesticated forms of the lost crops are thought to be extinct.
Writing in the Journal of Ethnobiology, Natalie Muellert, assistant professor of archaeology in Arts & Sciences, describes how she painstakingly grew and calculated yield estimates for two annual plants that were cultivated in eastern North America for thousands of years -- and then abandoned.
Growing goosefoot (Chenopodium, sp.) and erect knotweed (Polygonum erectum) together is more productive than growing either one alone, Mueller discovered. Planted in tandem, along with the other known lost crops, they could have fed thousands.
Archaeologists found the first evidence of the lost crops in rock shelters in Kentucky and Arkansas in the 1930s. Seed caches and dried leaves were their only clues. Over the past 25 years, pioneering research by Gayle Fritz, professor emerita of archaeology at Washington University, helped to establish the fact that a previously unknown crop complex had supported local societies for millennia before maize -- a.k.a. corn -- was adopted as a staple crop.
But how, exactly, to grow them?
The lost crops include a small but diverse group of native grasses, seed plants, squashes and sunflowers -- of which only the squashes and sunflowers are still cultivated. For the rest, there is plenty of evidence that the lost crops were purposefully tended -- not just harvested from free-living stands in the wild -- but there are no instructions left.
"There are many Native American practitioners of ethnobotanical knowledge: farmers and people who know about medicinal plants, and people who know about wild foods. Their knowledge is really important," Mueller said. "But as far as we know, there aren't any people who hold knowledge about the lost crops and how they were grown.
"It's possible that there are communities or individuals who have knowledge about these plants, and it just isn't published or known by the academic community," she said. "But the way that I look at it, we can't talk to the people who grew these crops.
"So our group of people who are working with the living plants is trying to participate in the same kind of ecosystem that they participated in -- and trying to reconstruct their experience that way."
That means no greenhouse, no pesticides and no special fertilizers.
"You have not just the plants but also everything else that comes along with them, like the bugs that are pollinating them and the pests that are eating them. The diseases that affect them. The animals that they attract, and the seed dispersers," Mueller said. "There are all of these different kinds of ecological elements to the system, and we can interact with all of them."
Her new paper reported on two experiments designed to investigate germination requirements and yields for the lost crops.
Mueller discovered that a polyculture of goosefoot and erect knotweed is more productive than either grown separately as a monoculture. Grown together, the two plants have higher yields than global averages for closely related domesticated crops (think: quinoa and buckwheat), and they are within the range of those for traditionally grown maize.
"The main reason that I'm really interested in yield is because there's a debate within archeology about why these plants were abandoned," Mueller said. "We haven't had a lot of evidence about it one way or the other. But a lot of people have just kind of assumed that maize would be a lot more productive because we grow maize now, and it's known to be one of the most productive crops in the world per unit area."
Mueller wanted to quantify yield in this experiment so that she could directly compare yield for these plants to maize for the first time.
But it didn't work out perfectly. She was only able to obtain yield estimates for two of the five lost crops that she tried to grow -- but not for the plants known as maygrass, little barley and sumpweed.
Read more at Science Daily
But there are no written or oral histories to describe them. The domesticated forms of the lost crops are thought to be extinct.
Writing in the Journal of Ethnobiology, Natalie Muellert, assistant professor of archaeology in Arts & Sciences, describes how she painstakingly grew and calculated yield estimates for two annual plants that were cultivated in eastern North America for thousands of years -- and then abandoned.
Growing goosefoot (Chenopodium, sp.) and erect knotweed (Polygonum erectum) together is more productive than growing either one alone, Mueller discovered. Planted in tandem, along with the other known lost crops, they could have fed thousands.
Archaeologists found the first evidence of the lost crops in rock shelters in Kentucky and Arkansas in the 1930s. Seed caches and dried leaves were their only clues. Over the past 25 years, pioneering research by Gayle Fritz, professor emerita of archaeology at Washington University, helped to establish the fact that a previously unknown crop complex had supported local societies for millennia before maize -- a.k.a. corn -- was adopted as a staple crop.
But how, exactly, to grow them?
The lost crops include a small but diverse group of native grasses, seed plants, squashes and sunflowers -- of which only the squashes and sunflowers are still cultivated. For the rest, there is plenty of evidence that the lost crops were purposefully tended -- not just harvested from free-living stands in the wild -- but there are no instructions left.
"There are many Native American practitioners of ethnobotanical knowledge: farmers and people who know about medicinal plants, and people who know about wild foods. Their knowledge is really important," Mueller said. "But as far as we know, there aren't any people who hold knowledge about the lost crops and how they were grown.
"It's possible that there are communities or individuals who have knowledge about these plants, and it just isn't published or known by the academic community," she said. "But the way that I look at it, we can't talk to the people who grew these crops.
"So our group of people who are working with the living plants is trying to participate in the same kind of ecosystem that they participated in -- and trying to reconstruct their experience that way."
That means no greenhouse, no pesticides and no special fertilizers.
"You have not just the plants but also everything else that comes along with them, like the bugs that are pollinating them and the pests that are eating them. The diseases that affect them. The animals that they attract, and the seed dispersers," Mueller said. "There are all of these different kinds of ecological elements to the system, and we can interact with all of them."
Her new paper reported on two experiments designed to investigate germination requirements and yields for the lost crops.
Mueller discovered that a polyculture of goosefoot and erect knotweed is more productive than either grown separately as a monoculture. Grown together, the two plants have higher yields than global averages for closely related domesticated crops (think: quinoa and buckwheat), and they are within the range of those for traditionally grown maize.
"The main reason that I'm really interested in yield is because there's a debate within archeology about why these plants were abandoned," Mueller said. "We haven't had a lot of evidence about it one way or the other. But a lot of people have just kind of assumed that maize would be a lot more productive because we grow maize now, and it's known to be one of the most productive crops in the world per unit area."
Mueller wanted to quantify yield in this experiment so that she could directly compare yield for these plants to maize for the first time.
But it didn't work out perfectly. She was only able to obtain yield estimates for two of the five lost crops that she tried to grow -- but not for the plants known as maygrass, little barley and sumpweed.
Read more at Science Daily
Powder, not gas: A safer, more effective way to create a star on Earth
Scientists have found that sprinkling a type of powder into fusion plasma could aid in harnessing the ultra-hot gas within a tokamak facility to produce heat to create electricity without producing greenhouse gases or long-term radioactive waste.
A major issue with operating ring-shaped fusion facilities known as tokamaks is keeping the plasma that fuels fusion reactions free of impurities that could reduce the efficiency of the reactions. Now, scientists at the U.S. Department of Energy's (DOE) Princeton Plasma Physics Laboratory (PPPL) have found that sprinkling a type of powder into the plasma could aid in harnessing the ultra-hot gas within a tokamak facility to produce heat to create electricity without producing greenhouse gases or long-term radioactive waste.
Fusion, the power that drives the sun and stars, combines light elements in the form of plasma -- the hot, charged state of matter composed of free electrons and atomic nuclei -- that generates massive amounts of energy. Scientists are seeking to replicate fusion on Earth for a virtually inexhaustible supply of power to generate electricity.
"The main goal of the experiment was to see if we could lay down a layer of boron using a powder injector," said PPPL physicist Robert Lunsford, lead author of the paper reporting the results in Nuclear Fusion. "So far, the experiment appears to have been successful."
¬The boron prevents an element known as tungsten from leaching out of the tokamak walls into the plasma, where it can cool the plasma particles and make fusion reactions less efficient. A layer of boron is applied to plasma-facing surfaces in a process known as "boronization." Scientists want to keep the plasma as hot as possible -- at least ten times hotter than the surface of the sun -- to maximize the fusion reactions and therefore the heat to create electricity.
Using powder to provide boronization is also far safer than using a boron gas called diborane, the method used today. "Diborane gas is explosive, so everybody has to leave the building housing the tokamak during the process," Lunsford said. "On the other hand, if you could just drop some boron powder into the plasma, that would be a lot easier to manage. While diborane gas is explosive and toxic, boron powder is inert," he added. "This new technique would be less intrusive and definitely less dangerous."
Another advantage is that while physicists must halt tokamak operations during the boron gas process, boron powder can be added to the plasma while the machine is running. This feature is important because to provide a constant source of electricity, future fusion facilities will have to run for long, uninterrupted periods of time. "This is one way to get to a steady-state fusion machine," Lunsford said. "You can add more boron without having to completely shut down the machine."
There are other reasons to use a powder dropper to coat the inner surfaces of a tokamak. For example, the researchers discovered that injecting boron powder has the same benefit as puffing nitrogen gas into the plasma -- both techniques increase the heat at the plasma edge, which increases how well the plasma stays confined within the magnetic fields.
The powder dropper technique also gives scientists an easy way to create low-density fusion plasmas, important because low density allows plasma instabilities to be suppressed by magnetic pulses, a relatively simple way to improve fusion reactions. Scientists could use powder to create low-density plasmas at any time, rather than waiting for a gaseous boronization. Being able to create a wide range of plasma conditions easily in this way would enable physicists to explore the behavior of plasma more thoroughly.
Read more at Science Daily
A major issue with operating ring-shaped fusion facilities known as tokamaks is keeping the plasma that fuels fusion reactions free of impurities that could reduce the efficiency of the reactions. Now, scientists at the U.S. Department of Energy's (DOE) Princeton Plasma Physics Laboratory (PPPL) have found that sprinkling a type of powder into the plasma could aid in harnessing the ultra-hot gas within a tokamak facility to produce heat to create electricity without producing greenhouse gases or long-term radioactive waste.
Fusion, the power that drives the sun and stars, combines light elements in the form of plasma -- the hot, charged state of matter composed of free electrons and atomic nuclei -- that generates massive amounts of energy. Scientists are seeking to replicate fusion on Earth for a virtually inexhaustible supply of power to generate electricity.
"The main goal of the experiment was to see if we could lay down a layer of boron using a powder injector," said PPPL physicist Robert Lunsford, lead author of the paper reporting the results in Nuclear Fusion. "So far, the experiment appears to have been successful."
¬The boron prevents an element known as tungsten from leaching out of the tokamak walls into the plasma, where it can cool the plasma particles and make fusion reactions less efficient. A layer of boron is applied to plasma-facing surfaces in a process known as "boronization." Scientists want to keep the plasma as hot as possible -- at least ten times hotter than the surface of the sun -- to maximize the fusion reactions and therefore the heat to create electricity.
Using powder to provide boronization is also far safer than using a boron gas called diborane, the method used today. "Diborane gas is explosive, so everybody has to leave the building housing the tokamak during the process," Lunsford said. "On the other hand, if you could just drop some boron powder into the plasma, that would be a lot easier to manage. While diborane gas is explosive and toxic, boron powder is inert," he added. "This new technique would be less intrusive and definitely less dangerous."
Another advantage is that while physicists must halt tokamak operations during the boron gas process, boron powder can be added to the plasma while the machine is running. This feature is important because to provide a constant source of electricity, future fusion facilities will have to run for long, uninterrupted periods of time. "This is one way to get to a steady-state fusion machine," Lunsford said. "You can add more boron without having to completely shut down the machine."
There are other reasons to use a powder dropper to coat the inner surfaces of a tokamak. For example, the researchers discovered that injecting boron powder has the same benefit as puffing nitrogen gas into the plasma -- both techniques increase the heat at the plasma edge, which increases how well the plasma stays confined within the magnetic fields.
The powder dropper technique also gives scientists an easy way to create low-density fusion plasmas, important because low density allows plasma instabilities to be suppressed by magnetic pulses, a relatively simple way to improve fusion reactions. Scientists could use powder to create low-density plasmas at any time, rather than waiting for a gaseous boronization. Being able to create a wide range of plasma conditions easily in this way would enable physicists to explore the behavior of plasma more thoroughly.
Read more at Science Daily
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