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2013年7月5日星期五

Antifreeze, cheap materials may lead to low-cost solar energy

And when perfected, this approach might also cook up the solar cells in a microwave oven similar to the one in most kitchens.

Engineers at Oregon State University have determined that ethylene glycol, commonly used in antifreeze products, can be a low-cost solvent that functions well in a "continuous flow" reactor -- an approach to making thin-film solar cells that is easily scaled up for mass production at industrial levels.

The research, just published in Material Letters, a professional journal, also concluded this approach will work with CZTS, or copper zinc tin sulfide, a compound of significant interest for solar cells due to its excellent optical properties and the fact these materials are cheap and environmentally benign.

"The global use of solar energy may be held back if the materials we use to produce solar cells are too expensive or require the use of toxic chemicals in production," said Greg Herman, an associate professor in the OSU School of Chemical, Biological and Environmental Engineering. "We need technologies that use abundant, inexpensive materials, preferably ones that can be mined in the U.S. This process offers that."

By contrast, many solar cells today are made with CIGS, or copper indium gallium diselenide. Indium is comparatively rare and costly, and mostly produced in China. Last year, the prices of indium and gallium used in CIGS solar cells were about 275 times higher than the zinc used in CZTS cells.

The technology being developed at OSU uses ethylene glycol in meso-fluidic reactors that can offer precise control of temperature, reaction time, and mass transport to yield better crystalline quality and high uniformity of the nanoparticles that comprise the solar cell -- all factors which improve quality control and performance.

This approach is also faster -- many companies still use "batch mode" synthesis to produce CIGS nanoparticles, a process that can ultimately take up to a full day, compared to about half an hour with a continuous flow reactor. The additional speed of such reactors will further reduce final costs.

"For large-scale industrial production, all of these factors -- cost of materials, speed, quality control -- can translate into money," Herman said. "The approach we're using should provide high-quality solar cells at a lower cost."

The performance of CZTS cells right now is lower than that of CIGS, researchers say, but with further research on the use of dopants and additional optimization it should be possible to create solar cell efficiency that is comparable.

This project is one result of work through the Center for Sustainable Materials Chemistry, a collaborative effort of OSU and five other academic institutions, supported by the National Science Foundation. Funding was provided by Sharp Laboratories of America. The goal is to develop materials and products that are safe, affordable and avoid the use of toxic chemicals or expensive compounds.

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2013年7月4日星期四

Scientists identify genetic cause of 'spongy' skin condition

July 3, 2013 — Scientists have identified the genetic cause of a rare skin condition that causes the hands and feet to turn white and spongy when exposed to water.

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The study, led by researchers from Queen Mary, University of London, has provided scientists with an insight into how the skin barrier functions and could help with research into a variety of conditions.

Diffuse non-epidermolytic palmoplantar keratoderma (NEPPK) is a rare condition in which individuals have thickened, yellowish skin over their palms and soles, thickened nails and suffer from excessive sweating. When their hands and feet are exposed to water, the skin quickly turns white and spongy and individuals are prone to fungal infections.

While prevalence in the general population is estimated at one in 40,000 it is much higher in northern Sweden (up to one in 200 people), where a single ancestral genetic mutation is believed to have originated and then subsequently passed down from generation to generation.

A team led by David Kelsell, Professor of Human Molecular Genetics at Queen Mary studied DNA from a number of families of British and Swedish origin in which the skin condition is present. Using high throughput DNA sequencing methods they were able to pin down the underlying cause of the condition to mutations in the AQP5 gene, which encodes a water channel protein known as aquaporin 5. All individuals who have inherited an AQP5 mutation will present with this rare skin condition.

Professor Kelsell, from the Blizard Institute at Barts and The London School of Medicine and Dentistry, Queen Mary, said: "Aquaporins are a family of proteins known as "the plumbing system for cells" as they form pores which allow water to flow through cells rapidly.

"We knew aquaporin 5 was present in high amounts in the sweat glands, salivary glands and tear ducts -- routes by which the body loses water. Here we've demonstrated it is also found in the skin, with higher amounts in the hands and feet."

Co-author Dr Diana Blaydon, also from the Blizard Institute, explained: "The AQP5 gene mutation appears to result in a protein that has a wider channel than usual, forming a bigger pore in the cell membrane allowing more water to permeate it."

Further work is needed to understand exactly how the mutations identified and the associated changes in the skin barrier lead to NEPPK.

Professor Kelsell added: "While we've studied aquaporins in the skin, these results also give us an idea of what might be happening in internal aquaporins, which are found in structures throughout the body, including the kidneys, cornea and lungs."

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New insights into how antibiotics damage human cells suggest novel strategies for making long-term antibiotic use safer

"Clinical levels of antibiotics can cause oxidative stress that can lead to damage to DNA, proteins and lipids in human cells, but this effect can be alleviated by antioxidants," said Jim Collins, Ph.D., who led the study. Collins, a pioneer of synthetic biology and Core Faculty member at the Wyss Institute, is also the William F. Warren Distinguished Professor at Boston University, where he leads the Center of Synthetic Biology.

Doctors often prescribe antibiotics freely, thinking that they harm bacteria while leaving human tissue unscathed. But over the years reports have piled up about the occasional side effects of various antibiotics, including tendonitis, inner-ear problems and hearing loss, diarrhea, impaired kidney function, and other problems.

Collins suspected these side effects occurred when antibiotics triggered oxidative stress -- a condition in which cells produce chemically reactive oxygen molecules that damage the bacteria's DNA and enzymes, as well as the membrane that encloses the cell.

Collins' team had already discovered that antibiotics that kill bacteria do so by triggering oxidative stress in the bacteria. They wondered whether antibiotics caused side effects by triggering oxidative stress in the mitochondria, a bacterium-like organelle that supplies human cells with energy.

Sameer Kalghatgi, Ph.D., a former postdoctoral fellow in Collins' laboratory who is now Senior Plasma Scientist at EP Technologies in Akron, Ohio, and Catherine S. Spina, a M.D./Ph.D. candidate at Boston University and researcher at the Wyss Institute, first tested whether clinical levels of three antibiotics -- ciprofloxacin, ampicillin, kanamycin -- each cause oxidative stress in cultured human cells. They found that all of these drugs were safe after six hours of treatment, but longer-term treatment of about four days caused the mitochondria to malfunction.

Kalghatgi and Spina then did a series of biochemical tests, which showed that the same three antibiotics damaged the DNA, proteins and lipids of cultured human cells -- exactly what one would expect from oxidative stress.

The results mean that "doctors should only prescribe antibiotics when they're called for, and patients should only ask for antibiotics when they have a serious bacterial infection," Collins said.

The team also treated mice with the same three antibiotics in mouse-sized doses similar to what patients receive in the clinic. Long-term treatment with each of the three antibiotics damaged the animal's lipids and caused levels of glutathione, one of the body's natural antioxidants, to fall -- another sign of oxidative stress.

To make a difference in the clinic, however, the scientists still needed a way to prevent antibiotic-induced oxidative stress -- or a way to remediate it as it was occurring. They found both. They were able to prevent oxidative stress by using a bacteriostatic antibiotic -- an antibiotic such as tetracycline that stops bacteria from multiplying but doesn't kill them. They could also ease oxidative stress by mopping up chemically reactive oxygen molecules with an FDA-approved antioxidant called N-acetylcysteine, or NAC, that's already used to help treat children with cystic fibrosis.

The new results come on the heels of two other recent breakthroughs on antibiotic treatment from Collins' group -- a report in Nature showing that viruses in the gut that infect bacteria harbor genes that confer antibiotic resistance, and another report in Science Translational Medicine showing that silver can boost the effectiveness of many widely used antibiotics.

"Jim and his team are moving at lightning speed toward unlocking the medical mysteries that stand in the way of safe and effective antibiotic treatment," said Don Ingber, M.D., Ph.D., Wyss Institute Founding Director. "Doctors have known for years that antibiotics occasionally cause serious side effects, and Jim's new findings offer not one but two exciting new strategies that could address this long-neglected public health problem."

Next, Collins plans more animal studies to work out the best ways to remediate oxidative stress. But since both bacteriostatic antibiotics and NAC are already FDA-approved, doctors might be using this strategy soon.

"We're interested in seeing if this could be moved toward the clinic," Collins said.

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DNA markers in low-IQ autism suggest heredity

July 3, 2013 — Researchers are striving to understand the different genetic structures that underlie at least a subset of autism spectrum disorders. In cases where the genetic code is in error, did that happen anew in the patient, perhaps through mutation or copying error, or was it inherited? A new study in the American Journal of Human Genetics finds evidence that there may often be a recessive, inherited genetic contribution in autism with significant intellectual disability.

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The authors also make predictions in the study regarding how far back in the history of the family the disease-associated variants may have occurred. It's far.

The research team led by Eric Morrow, assistant professor of biology in the Department of Molecular Biology, Cell Biology, and Biochemistry at Brown University, made its findings by analyzing the DNA of more than 2,100 children with autism who were born into "simplex" families where neither their parents nor a sibling has an autism disorder -- a Simons Foundation data set known as the Simons Simplex Collection. The researchers combed through the genomes of affected children and their siblings for so-called "runs of homozygosity" -- long strands of DNA in which the genetic material contributed by both the mother and the father turn out to be the same.

Many genetic disorders are recessive, meaning that they won't occur in people who end up with at least one healthy copy of a gene. This may allow disease-associated variants to hide out in the population for generations without causing disease or fizzling out. But children with a high "burden of homozygosity," in which they have received long runs of the same DNA from each parent, might not get any working copies, as both mom and dad gave them the same flawed DNA. These parents may have unwittingly co-inherited these recessive variants from a distant shared relative about which neither parent is aware.

Virtually every participant in the study had small runs of homozygosity in their DNA here and there. For instance, everyone had at least runs of homozygosity adding up to a million DNA letters long. This reflects some degree of distant shared ancestry in the sample of parents who now live in North America. Approximately one-third of the pedigrees also had a least one larger block of homozygosity measured as 2.5 million letters. Parents of children with such larger blocks, the authors said, shared a common ancestor approximately 40 generations or 1,000 years ago.

The researchers found that among the more than 500 children in the sample with autism and intellectual disability -- an IQ of 70 or below -- there were frequently more large runs of homozygosity than in their unaffected siblings. The findings suggest that more deleterious recessive genetic variants were co-inherited from each parent in the affected sibling, the authors said, and these variants were derived from the remote shared ancestor of the parents.

The study does not find runs of homozygosity or recent shared ancestry to be a risk factor for autism across the population, Morrow said. Instead, within a given family, the autism-affected individual generally had more runs of homozygosity than an unaffected sibling, he said, suggesting that these runs may harbor recessive variants that tip the "apple-cart" toward disease in an individual that may already have a high degree of risk.

"At the highest level, the importance of this paper is to refocus on runs of homozygosity as an element of the genetic variation that can contribute to the susceptibility to disease," said Morrow, a geneticist and psychiatrist who sees autism patients at the Bradley Hospital. "This new sort of variant looks like it is important in a subset of autism."

Dissecting heterogeneity

For a minimum run size of 2.5 million DNA letters, the affected siblings had a 1.32 times more runs of homozygosity than their unaffected brother or sister. Moreover, the likelihood of being affected with autism and having an IQ below 70 increased as total length of long runs of homozygosity increased.

The paper shows an association, therefore, in which a higher burden of homozygosity predicted a higher risk of developing autism with intellectual disability compared to a sibling. The study did not find any association between long runs of homozygosity and a risk of autism disorders without intellectual disability.

"Autism is a very broad, heterogeneous condition," Morrow said. "With genomics, we've begun to be able to dissect the heterogeneity into smaller groupings. We find an association between runs of homozygosity and those with co-occuring intellectual disability and autism, but not in so-called 'higher functioning' autism."

The study also found a gender difference. In general girls are much less likely to be affected by autism but they tend to have more severe cases when they are, said study lead author Ece Gamsiz, who holds a Translational Neuroscience Fellowship at Brown and the Lifespan health care system. As has been seen previously, in the new study's data, girls were mysteriously abundant among the intellectual disabled patients, and those affected also showed a higher burden of runs of homozygosity compared to their sisters.

"In simplex families, [affected] females tend to have greater homozygosity compared to their same-gender unaffected siblings. This trend was not observed in same-gender male siblings," Gamsiz said. "Our study presents among the first data to suggest that the genetic susceptibility to the disorder may have some distinct aspects in girls and in 'lower-functioning' autism."

An eventual biomarker?

In their search for genetic explanations of particular autism disorders, researchers have focused mostly on spontaneous mutations and having too many or too few copies of a gene to explain how autism arises in otherwise non-autistic families, Morrow said. Runs of homozygosity appear to be another place to look.

It is too soon to say, however, that homozygosity is a clinically useful biomarker, Morrow said, but with much more work it could prove to be.

"It's an exciting possibility," said Morrow, who is also affiliated with the Brown Institute for Brain Science. "It could be in the picture where, if you have a person with autism and who has some degree of intellectual disability, and you see also they have large runs of homozygosity, then together you could say that constellation of symptoms might help us predict that they'd be less responsive to conventional treatments and we'd have to discern a new treatment pathway."

In addition to Gamsiz and Morrow, the paper's other authors from Brown are Emma Viscidi, Abbie Frederick, Shailender Nagpal, Michael Schmidt, Elizabeth Triche and Sorin Istrail; Stephan Sanders, Michael Murtha and Matthew State at Yale; Daniel Geschwind at the University of California-Los Angeles; Edwin Cook at the University of Illinois-Chicago; and Bernie Devlin at the University of Pittsburgh.

The Simons Foundation supported the research with grant SFARI 124827EM. Morrow is also supported by the Burroughs Wellcome Fund and the National Institutes of Health. Gamsiz's fellowship is supported by Lifespan, the Brown Institute for Brain Science, and the Norman Prince Neurosciences Institute.

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Device physics: Simulating electronic smog

A research team from A*STAR and Samsung Electronics has developed a fast and accurate way to estimate the electromagnetic emissions from printed circuit boards that could help designers to ensure that devices meet regulatory standards.

Circuits that carry rapidly changing electrical currents can generate unwanted electromagnetic waves, wasting energy, causing interference with other electrical equipment, and potentially posing health risks to users. To ensure that such emissions are within acceptable limits, electronic products such as mobile phones and laptops must undergo tests for this 'electronic smog' before they can be marketed.

Those tests have traditionally been done in large rooms designed to capture all the electromagnetic waves emitted from the device, explains Wei-Jiang Zhao of A*STAR's Institute of High Performance Computing, Singapore, who led the study. An alternative to this costly process involves scanning the electromagnetic field very close to the device's circuit boards (the near field), and then calculating the resulting radiation at a distance (the far field). But those calculations can take powerful computers many hours to complete.

The mathematical model developed by Zhao and co-workers translates near-field measurements into an accurate estimate of far-field radiation in less than 10 minutes on a standard desktop computer. "Our simulation technique could help to shorten the product design cycle, save laboratory space, and reduce product development cost," says Zhao.

The researcher's model mathematically mimics the readings from a scan of the near-field above a printed circuit board. Their simulation relies on a series of virtual magnetic dipoles -- effectively tiny, imaginary bar magnets -- that collectively replicate the variations in the measured magnetic field.

The simulation runs iteratively, each time altering the magnetic dipoles so that they fit the data better. This process of 'differential evolution' eventually produces a solution that is a sufficiently close match to the circuit-board's near field. The researchers then use those magnetic dipoles to simplify their calculation of the far-field radiation produced by the device.

The researchers tested their model using simulated near-field data from a thin, L-shaped metal strip laid on a small circuit board. The data contained 1,273 sample points, each 10 millimeters above the board. The model could approximate this magnetic field using just a few virtual magnetic dipoles. The match improved as they added more dipoles, until they reached very good agreement at nine dipoles -- adding a tenth did not significantly improve the match. The team is now working to refine the system to make it suitable for use by the electronics industry.

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Graphene provides efficient electronics cooling

"This discovery opens the door to increased functionality and continues to push the boundaries when it comes to miniaturising electronics," said Chalmers Professor Johan Liu who heads the international research project.

Modern electronic systems generate a great deal of heat, above all due to the constantly increasing demand for more and more functionality. It is important to be able to remove the heat generated in an efficient way to maintain the long life of the system. One rule of thumb is that a 10-degree Celsius increase in working temperature halves the working life of an electronics system.

During the study, the researchers focused on reducing the temperature in the small area where the electronics work most intensively -- such as inside a processor, for instance. These tiny hotspots are found in all electronics. Size wise, they are on a micro or nano scale, in other words a thousandth of a millimetre or smaller.

"The normal working temperature in the hotspots we have cooled with a graphene layer has ranged from 55 to 115 degrees Celsius. We have been able to reduce this by up to 13 degrees, which not only improves energy efficiency, it also extends the working life of the electronics."

Efficient cooling is a major challenge in many different applications, such as automotive electronics, power electronics, computers, radio base stations and in various light emitting diodes, or LED lights. In automotive electronics systems, any single device in the ignition system can pump out up to 80 W continuously and in transient stage up to 300 W (within 10 nanoseconds). LED devices can have a thermal intensity almost on a par with the sun, up to 600 W/cm² due to their extremely small size.

Superior cooling of electronics can deliver tremendous advantages. According to a study in the USA based on data from 2006, around 50 percent of the total electricity used to run data servers goes on cooling the systems.

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2013年7月3日星期三

Why do we gesticulate?

July 2, 2013 — If you rely on hand gestures to get your point across, you can thank fish for that! Scientists have found that the evolution of the control of speech and hand movements can be traced back to the same place in the brain, which could explain why we use hand gestures when we are speaking.

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Professor Andrew Bass (Cornell University), who will be presenting his work at the meeting of the Society for Experimental Biology on the 3rd July, said: "We have traced the evolutionary origins of the behavioural coupling between speech and hand movement back to a developmental compartment in the brain of fishes."

"Pectoral appendages (fins and forelimbs) are mainly used for locomotion. However, pectoral appendages also function in social communication for the purposes of making sounds that we simply refer to as non-vocal sonic signals, and for gestural signalling."

Studies of early development in fishes show that neural networks in the brain controlling the more complex vocal and pectoral mechanisms of social signalling among birds and mammals have their ancestral origins in a single compartment of the hindbrain in fishes. This begins to explain the ancestral origins of the neural basis for the close coupling between vocal and pectoral/gestural signalling that is observed among many vertebrate groups, including humans.

Professor Bass said: "Coupling of vocal and pectoral-gestural circuitry starts to get at the evolutionary origins of the coupling between vocalization (speech) and gestural signalling (hand movements). This is all part of the perhaps even larger story of language evolution."

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Atmospheric CO2 has big consequences for the tiny bacteria that are foundation of most of life in the sea

In climate change, as in everything, there are winners and losers. As atmospheric carbon dioxide levels and temperature rise globally, scientists increasingly want to know which organisms will thrive and which will perish in the environment of tomorrow.

The answer to this question for nitrogen-fixing cyanobacteria (bacteria that obtain energy through photosynthesis, or "blue-green algae") turns out to have implications for every living thing in the ocean. Nitrogen-fixing is when certain special organisms like cyanobacteria convert inert -- and therefore unusable -- nitrogen gas from the air into a reactive form that the majority of other living beings need to survive. Without nitrogen fixers, life in the ocean could not survive for long.

"Our findings show that CO₂ has the potential to control the biodiversity of these keystone organisms in ocean biology, and our fossil fuel emissions are probably responsible for changing the types of nitrogen fixers that are growing in the ocean," said David Hutchins, professor of marine environmental biology at the USC Dornsife College of Letters, Arts and Sciences and lead author of an article about this research that appeared in Nature Geoscience on June 30.

"This may have all kinds of ramifications for changes in ocean food chains and productivity, even potentially for resources we harvest from the ocean such as fisheries production," Hutchins said.

Hutchins and his team studied two major groups of nitrogen-fixing cyanobacteria: Trichodesmium, which forms large floating colonies big enough to see with the naked eye and makes vast "blooms" in the open ocean, and Crocosphaera, which is also very abundant but is a single-celled, microscopic organism.

Previous research showed that these two types of cyanobacteria should be some of the biggest "winners" of climate change, thriving in high CO₂ levels and warmer oceans. However, those previous studies only examined one or two strains of the organisms.

That's where USC's unique resource comes into play -- the university is home to a massive culture library of strains and species of the organisms assembled by USC Associate Professor Eric Webb.

Using the culture library, the team was able to show that some strains grow better at CO₂ levels not seen since the start of the Industrial Revolution, while others will thrive in the future "greenhouse" Earth.

"It's not that climate change will wipe out all nitrogen fixers; we've shown that there's redundancy in nature's system. Rather, increasing atmospheric carbon dioxide changes specifically which nitrogen fixers are likely to thrive," Hutchins said. "And we're not entirely certain how that will change the ocean of tomorrow."

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New catalyst could cut cost of making hydrogen fuel

July 2, 2013 — A discovery at the University of Wisconsin-Madison may represent a significant advance in the quest to create a "hydrogen economy" that would use this abundant element to store and transfer energy.

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Theoretically, hydrogen is the ultimate non-carbon, non-polluting fuel for storing intermittent energy from the wind or sun. When burned for energy, hydrogen produces water but no carbon dioxide. Practically speaking, producing hydrogen from water, and then storing and using the gas, have proven difficult.

The new study, now published online at the Journal of the American Chemical Society, introduces a new catalyst structure that can facilitate the use of electricity to produce hydrogen gas from water.

Significantly, the catalyst avoids the rare, expensive metal platinum that is normally required for this reaction. (Catalysts speed up chemical reactions without themselves being consumed.)

The material under study, molybdenum disulfide, contains two common elements, notes Mark Lukowski, a Ph.D. student working with associate professor Song Jin in the UW-Madison chemistry department. "Most people have tried to reduce the cost of the catalyst by making small particles that use less platinum, but here we got rid of the platinum altogether and still got reasonably high performance."

The research group has produced milligram quantities of the catalyst, "but in principle you could scale this up," says Lukowski. "Molybdenum disulfide is a commercially available product. To control purity and structure, we go through the trouble of synthesizing it from the bottom up, but you could buy it today."

To make the new material, Lukowski and Jin deposit nanostructures of molybdenum disulfide on a disk of graphite and then apply a lithium treatment to create a different structure with different properties.

Just as carbon can form diamond for jewelry and graphite for writing, molybdenum disulfide can be a semiconductor or a metallic phase, depending on structure. When the compound is grown on the graphite, it is a semiconductor, but it becomes metallic after the lithium treatment. Lukowski and Jin discovered that the metallic phase has far greater catalytic properties.

"Like graphite, which is made up of a stack of sheets that easily separate, molybdenum disulfide is made up of individual sheets that can come apart, and previous studies have shown that the catalytically active sites are located along the edges of the sheets," says Lukowski.

"The lithium treatment both causes the semiconducting-to-metallic phase change and separates the sheets, creating more edges. We have taken away the limitation from molybdenum disulfide and made the active sites both more pervasive and more reactive."

The experiment, supported by the U.S. Department of Energy's Basic Energy Sciences program, is a proof of concept for a new approach for improving these catalysts, says Jin.

"Even though the efficiency of producing hydrogen has been greatly improved, it is still not as good as what platinum can achieve," he says. "The next steps include finding ways to further improve the performance by optimizing all aspects of the process and exploring related compounds. There are many hurdles to achieving a hydrogen economy, but the advantages in efficiency and pollution reduction are so significant that we must push ahead."

As technological advances put further strain on the supply of platinum and other rare elements, using common elements is a major advantage, Jin stresses. "The elements we use are cheap and abundant in earth's crust, and the raw material is already commercially available at low cost. Building on this discovery and new understanding, we would like to further improve these materials to achieve the efficient production of hydrogen without using precious metals."

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People show more humorous creativity when primed with thoughts of death

A new article by Christopher R. Long of Ouachita Baptist University and Dara Greenwood of Vassar College is titled Joking in the Face of Death: A Terror Management Approach to Humor Production. Appearing in the journal HUMOR, it documents research on whether the activation of thoughts concerning death influences one's ability to creatively generate humor. As humor is useful on a fundamental level for a variety of purposes, including psychological defense against anxiety, the authors hypothesized that the activation of thoughts concerning death could facilitate the production of humor.

For their study, Long and Greenwood subdivided 117 students into four experimental groups. These groups were confronted with the topics of pain and death while completing various tasks. Two of the test groups were exposed unconsciously to words flashed for 33 milliseconds on a computer while they completed tasks -- the first to the word "pain," the second to the word "death." The remaining two groups were prompted in a writing task to express emotions concerning either their own death or a painful visit to the dentist. Afterward, all four groups were instructed to supply a caption to a cartoon from The New Yorker.

These cartoon captions were presented to an independent jury who knew nothing about the experiment. The captions written by individuals who were subconsciously primed with the word death were clearly voted as funnier by the jury. By contrast, the exact opposite result was obtained for the students who consciously wrote about death: their captions were seen as less humorous.

Based on this experiment, the researchers conclude that humor helps the individual to tolerate latent anxiety that may otherwise be destabilizing. In this connection, they point to previous studies indicating that humor is an integral component of resilience.

In light of the finding that the activation of conscious thoughts concerning death impaired the creative generation of humor, Long and Greenwood highlight the need for additional research, not only to explore the effectiveness of humor as a coping mechanism under various circumstances, but also to identify its emotional, cognitive, and/or social benefits under conditions of adversity.

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