However, to visualize a quantum object or phenomenon where the illumination is weak, or emanating from nonvisible infrared or far infrared wavelengths, scientists need far more sensitive tools. For example, they have developed single-pixel imaging in the spatial domain as a way to pack and spatially structure as many photons as possible onto a single pixel detector and then create an image using computational algorithms.

Similarly, in the time domain, when an unknown ultrafast signal is either weak, or in the infrared or far infrared wavelengths, the ability of single-pixel imaging to visualize it is reduced. Based on the spatio-temporal duality of light pulses, University of Rochester researchers have developed a time-domain single-pixel imaging technique, described in Optica, that solves this problem, detecting 5 femtojoule ultrafast light pulses with a temporal sampling size down to 16 femtoseconds. This time-domain analogy of the single-pixel imaging shows similar advantages to its spatial counterparts: a good measurement efficiency, a high sensitivity, robustness against temporal distortions and the compatibility at multiple wavelengths.

Lead author Jiapeng Zhao, a PhD student in optics at the University of Rochester, says possible applications include a highly accurate spectrographic tool, demonstrated to achieve 97.5 percent accuracy in identifying samples using a convolutional neural network with this technique.

The technique can also be combined with single-pixel imaging to create a computational hyperspectral imaging system, says Zhao, who works in the Rochester research group of Robert Boyd, professor of optics. The system can greatly speed up the detection and analysis of images at broad frequency bands. This could be especially useful for medical applications, where detection of nonvisible light emanating from human tissue at different wavelengths can indicate disorders such as high blood pressure.

“By coupling our technique with single pixel imaging in the spatial domain, we can have good hyperspectral image within a few seconds. That’s much faster than what people have done before,” Zhao says.

Other coauthors include Boyd and Xi-Cheng Zhang at Rochester, Jianming Dai at Tianjin University, and Boris Braverman at the University of Ottawa.

This project was supported with funding from the Office of Naval Research, the National Natural Science Foundation of China and the National Key Research and Development Program of China.

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Now, a new study of car use in Japan shows that, even with gasoline vehicles, keeping and using cars with good fuel efficiency longer could reduce CO₂ emissions significantly more than an accelerated transition to alternative fuel vehicles.

“The faster you replace a car, the more CO₂ it emits. It’s no different with electric cars, because when the demand for new cars increases, it shoots up manufacturing emissions,” says Shigemi Kagawa, professor of Kyushu University’s Faculty of Economics and leader of the study.

Car replacement is especially rapid in Japan, where people enjoy longevity but cars do not. The average life expectancy of a car, from its birth in a factory to its end in a scrapyard, is around thirteen years. Moreover, the average length of ownership of a new car by its first owner is seven years.

These trends are largely attributed to the island nation’s mass-production, mass-consumption economy and its costly vehicle inspection system. While these might help to get more fuel-efficient vehicles on the road, Kagawa explains that we need to diligently look at the supply chain to maximize carbon reductions.

“The carbon footprint of a car goes far beyond just the fuel it uses. To produce alternative fuel cars intended to reduce emissions from driving, you need iron, nuts, and bolts for construction, factories for assembly, and mega-containerships for transport. All these points in the supply chain produce CO₂.”

Of the about nine percent of Japan’s total greenhouse gas emissions attributed to cars, about forty percent is due to gasoline combustion from driving new cars and twenty-four percent due to their manufacturing.

“Our hypothesis is that driving current internal combustion engine vehicles a little longer during the transition to green vehicles is a viable strategy to help the environment,” says Kagawa.

Using economic statistics, Kagawa’s group conducted a case study of newly registered and used cars in Japan between 1990 and 2016. The group modeled how replacement behavior of car owners affects their carbon footprint.

Their modeling shows that, if cars had been kept on the road ten percent longer before being scrapped, the cumulative carbon footprint from cars would have decreased by 30.7 million tonnes, or one percent, during this period.

This is because the decrease in manufacturing emissions more than offsets additional emissions produced by existing cars.

Moreover, the study finds a similar one percent decrease in carbon footprint would be realized if owners of new cars had used their cars ten percent longer.

In this case, by keeping more cars in the hands of their original owners longer, the number of used cars on the road decreases. Accordingly, emissions from the driving of new, relatively fuel-efficient cars increase while those of used, relatively fuel-inefficient cars decrease.

“What this means is that we can reduce CO₂ emissions just by keeping and driving cars longer,” concludes Kagawa. “Moreover, if the car we keep is relatively new and fuel-efficient, the effect is greater. So the next time you are thinking of getting a new car, perhaps consider if your current car has a few more kilometers left in it.”

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Based at WSU Vancouver, lead author Deepti Singh, assistant professor in the School of the Environment, drew on hundreds of studies of climate change, air quality, agriculture, and public health to propose a “systems lens,” or scientific approach, that connects health risks with simultaneous environmental changes driven by human practices.

“The health consequences of air pollution, climate change, and transformations in agriculture are often discussed separately,” Singh said. “But these issues are all related — they have similar sources, and each one affects the others. Agricultural activities contribute to air pollution and affect regional climate patterns, while farm production and quality of crops are sensitive to air quality and climate conditions.”

Collaborating with researchers at Columbia University, the Indian School of Business, Boston University, and the University of Delaware, Singh studied the situation in South Asia, where rapid industrialization and modern farming practices have aided economic development and increased food production, but also compromised multiple dimensions of human health.

“We’re offering a framework to assess the overall health impacts from multiple parts of Earth’s natural systems, which are all changing simultaneously because of human activities,” Singh said. “The research could help identify policies and solutions that will have multiple co-benefits for the environment and human health.”

“Our work sheds new light on the ways that food systems affect, and are affected by, climate change and air pollution,” said Kyle Davis, co-author and assistant professor at the University of Delaware.

The scientists reviewed multiple examples of health impacts from changes in climate, air quality, and agricultural output, as well as co-benefits and unintended consequences of efforts to curb emissions and save water, for example. They found these examples share the need for better tools and local, high-resolution data on health, weather, emissions, air pollution, and land use to better measure human and environmental impacts.

“This study points out how useful and effective policy responses need to take multiple factors and interactions into account, and highlights the problem with simplistic explanations,” said Ashwini Chhatre, co-author and associate professor of public policy at the Indian School of Business.

Use of fossil fuels, burning of crop residue, and changes to the landscape from expansion and intensification of agriculture have contributed to extremely poor air quality in South Asia, changed the main source of rainfall, the summer monsoon, and also increased health risks for nearly a quarter of the world’s population living in the region.

“Late autumn is ‘pollution season’ in north India, and also brings vicious debates in our society about who and what are contributing to it,” Chhatre said.

Additionally, more frequent and intense heat waves and floods have killed thousands, displaced millions, lowered labor productivity, and caused disease outbreaks. Severe air pollution has contributed to increased heart and lung diseases as well as millions of premature deaths and weakened monsoonal rains. At the same time, air pollution and climate change have reduced yields of important food crops.

“While the climate benefits of reductions in greenhouse gas emissions we make today may not be felt for decades, our approach shines a light on some of the immediate health benefits, as well as unintended consequences, of policies that aim to minimize human impacts on climate and the environment,” Singh said.

In a preclinical study published in the journal Glia, Peter King, M.D., and Burt Nabors, M.D., show that their small molecule drug, SRI-42127, can potently attenuate the triggers of neuroinflammation. These experiments in glial cell cultures and mice now open the door to testing SRI-42127 in models of acute and chronic neurological injury.

Glial cells are the non-neuronal cells of the central nervous system, or CNS, that help support and protect neurons. One of the types, microglia, are brain macrophages that respond to injury or infection. “Microglia and astroglia are key cells in the central nervous system that — when activated — drive neuroinflammation by secreting toxic inflammatory mediators, including cytokines and chemokines,” King and Nabors said.

King and Nabors, both professors in the University of Alabama at Birmingham Department of Neurology, have collaborated for 25 years to study the mechanisms that trigger neuroinflammation and the role of neuroinflammation in neurological injury, degenerative disease and cancer. They say this current study builds on their prior findings that microglia and astroglia cells rely on a key RNA-binding protein called HuR that protects the messenger RNAs encoding inflammatory mediators from degradation and promotes their translation into proteins.

Neuroinflammation occurs when activated microglia and astrocytes in the brain or spinal column secrete cytokines and chemokines like IL1β, IL-6, TNF-α, iNOS, CXCL1 and CCL2. The messenger RNAs for those pro-inflammatory signaling proteins contain adenine- and uridine-rich elements, or AREs, that govern their expression.

King, Nabors and UAB colleagues have previously shown that HuR, an RNA regulator protein that binds to AREs, plays a major positive role in regulating the inflammatory cytokine production, making it a major control point in neuroinflammation.

HuR normally concentrates in the nuclei of glial cells. However, when glial cells are activated, HuR translocates out of the nucleus and into the cell cytoplasm, where it can boost production of neuroinflammatory cytokines and chemokines.

In previous work, the UAB researchers showed that HuR translocates out of the nucleus of astrocytes in the acute CNS diseases spinal column injury and stroke. They also showed that it translocates out of the nucleus in microglia in the chronic CNS disease ALS, or amyotrophic lateral sclerosis.

Importantly, monomer HuR cannot pass through the nuclear envelope that acts as a regulatory membrane barrier between the nucleus and the cytoplasm. Only HuR dimers — made up by the coupling of two single HuR molecules — are able to translocate from nucleus to cytoplasm. This knowledge permitted collaborative research by Southern Research, of Birmingham, Alabama, and UAB, using high-throughput screening, to identify the small molecule drug SRI-42127 that inhibits dimerization of HuR.

In the current study, King, Nabors, Natalia Filippova, Ph.D., and UAB colleagues tested the biological relevance of SRI-42127, using lipopolysaccharide, or LPS, to activate glial cells to initiate the inflammatory cascade. The UAB researchers found that treatment with SRI-42127 suppressed HuR translocation from the nucleus to the cytoplasm in LPS-activated glial cells, both in tissue culture and in mice. SRI-42127 also significantly attenuated the production of proinflammatory mediators, including the cytokines IL1β, IL-6, TNF-α and iNOS, and the chemokines CXCL1 and CCL2.

Furthermore, SRI-42127 suppressed microglial activation in mouse brains, and it attenuated the recruitment of immune-cell neutrophils and monocytes into the CNS from outside the blood-brain barrier. Such an entry of neutrophils and monocytes can exacerbate inflammation in the brain or spinal cord. In summary, SRI-42127 penetrated the blood-brain barrier and quickly suppressed neuroinflammatory responses.

“Our findings,” King and Nabors said, “underscore HuR’s critical role in promoting glial activation and the potential for SRI-42127 and other HuR inhibitors to treat neurological diseases driven by this activation.”

In unpublished work in collaboration with Robert Sorge, Ph.D., associate professor in the Department of Psychology, UAB College of Arts and Sciences, King and Nabors have found potential beneficial effects of SRI-42127 to reduce neuropathic pain, a condition that is triggered by microglial-induced neuroinflammation. “This would be a non-opioid approach to treating pain,” they said.

Any future potential clinical treatments will require finesse.

“Therapeutic targeting of glia in CNS disease is a balancing act since these cells also exert neuroprotective and neuroplastic effects, depending on the phase of recovery from CNS injury or stage of neurodegenerative disease,” King and Nabors said. “In the initial phases after spinal cord injury, traumatic brain injury or stroke, the pro-inflammatory activation of glia worsens secondary tissue injury and triggers pathways of chronic neuropathic pain, in contrast to the more chronic phases where glia become protective. In neurodegenerative processes like ALS and Alzheimer’s, glia also play changing roles during the course of the disease.”

Co-authors with King, Nabors and Filippova in the current study, “SRI-42127, a novel small molecule inhibitor of the RNA regulator HuR, potently attenuates glial activation in a model of lipopolysaccharide-induced neuroinflammation,” are Rajeshwari Chellappan, Abhishek Guha, Ying Si, Thaddaeus Kwan, Xiuhua Yang, Anish S. Myneni, Shriya Meesala and Ashley S. Harms, UAB Department of Neurology.

Support came from National Institutes of Health grants NS092651 and NS111275-01, and United States Department of Veterans Affairs grant BX001148.

In their long collaboration, King and Nabors have used glioblastoma, a primary brain cancer, as a disease model to study HuR because many of the factors that drive neuroinflammation also promote glioblastoma growth. Nabors has focused on the tumor-suppressive properties of SRI-42127 and its potential use in the treatment of glioblastoma and other cancers.

Our closest animal relatives face a precarious future: Half of the world’s roughly 500 primate species are at risk of extinction due to human activities such as hunting, trapping and deforestation. But the demise of the world’s threatened primates could trigger even more species extinctions for the parasites that lurk on and in them, according to a Duke University-led study.

“If all the primates that are threatened with extinction really do die out, they won’t be the only species that go extinct,” said first author James Herrera of the Duke Lemur Center. “It could also be twice that many parasites.”

“That’s a whole realm of biodiversity that could be going extinct without us even noticing,” Herrera said. “There’s so little that we know about what they do in the body, that we don’t even know what we’re losing.”

One previous study suggests that some 85% to 95% of the parasitic worms of animals aren’t even known to science yet, much less evaluated by the authoritative extinction ‘Red List’ kept by the International Union for Conservation of Nature (IUCN).

Herrera admits this may seem like an odd thing to get worked up about, given all our efforts to deworm and delouse ourselves and our pets. To most people, parasites are “something we want to eradicate, rather than conserve,” Herrera said.

The thought of alien creatures biting, wriggling, squirming, and nestling into the warm wet folds of the intestines makes most people shudder. But parasites don’t always cause noticeable symptoms or make their hosts sick, Herrera said. Parasites can even have some surprising benefits, such as when worms in the gut help the body ward off other infections, or keep autoimmune disorders in check.

To gauge the potential loss of biodiversity if primates go extinct, Herrera and Duke professors Charlie Nunn and James Moody used network analysis techniques to measure the potential ripple effects on the parasites that set up camp in or on primate bodies. Their work appeared Sept. 20 in the journal Philosophical Transactions B.

In their model, species are connected in complex webs of interactions involving 213 primates — monkeys, apes, lemurs and galagos — and 763 worms, mites, protists, and other parasites known to infect them. When one primate host disappears, the parasites connected to it can no longer depend on it for survival. Sever enough of these connections, and their loss sets off a deadly cascade where one extinction begets another.

It’s a bit like the classic kids’ game, KerPlunk, Herrera said. You have a clear tube filled with marbles, which are resting on top of a web of crisscrossing sticks. Removing one or two sticks — or in this case, primate hosts — from the network does little harm, because the marbles are still supported by the remaining sticks. But as the game goes on and fewer sticks remain, it gets harder to keep the marbles from crashing down.

Currently, 108 of the 213 primate species in their dataset are considered threatened by the IUCN. The team found that if all those species were to go kaput, an additional 250 parasites could be doomed as well, and that 176 of these parasite species have no other suitable hosts.

The extinction cascade will likely be worse in isolated places like the island of Madagascar, the study revealed. There, shrinking forests, illegal hunting and collection for the pet trade are pushing 95% of lemur species ever closer to the brink, and more than 60% of lemur parasites inhabit a single host.

For instance, at least two species of nematode worms depend on the aye-aye, a long-fingered, bushy-tailed lemur with beaver-like teeth. If the aye-aye dies out, so too will the worms it carries.

The researchers say they aren’t able to predict, from their analyses, how many of the parasites in their dataset could potentially avert extinction by jumping ship and adapting to new hosts that are more abundant. But some of the most notorious diseases in humans, such as malaria, AIDS caused by HIV and yellow fever, got their start in other primates before spilling over to people, for instance when we share a watering hole, or when we butcher them for meat.

“It’s not that hard to imagine,” Herrera said.

The study is part of a special issue of Philosophical Transactions B devoted to infectious disease macroecology.

This research was supported by grants from the National Institutes of Health (NIH R25HD079352), the National Science Foundation (DEB-0211908, EF-0723939/0904359, BCS-1355902) and Duke University.