Culture

Unequal compensation reduces people's motivation to work, even among those who stand to benefit from unfair advantages, finds a new UCL-led study.

The researchers found that large disparities in rewards offered for the same task reduce people's happiness, which in turn reduce their willingness to work, in the study published in PLOS One.

Lead author, Dr Filip Gesiarz (UCL Psychology & Language Sciences) said: "Here we have shown the psychological impacts of inequality of opportunity, and how it can hurt the productivity and well-being of everyone involved.

"Our findings may shed light on how psychological mechanisms, apart from structural barriers, can contribute to higher unemployment and lower university application rates of people from disadvantaged backgrounds. It's more difficult to motivate yourself to work hard if you know that other people will be more generously rewarded for the same effort."

For the study, 810 participants were asked to complete a simple task in exchange for some money. In different scenarios across three experiments, participants were told that other people were being paid more or less than they were for the same task, to varying degrees of inequality. They were given the option of refusing to work on a given task, and in some of the trials, they were also asked how they were feeling.

The researchers found that when people were told there were wide disparities in pay between them and their peers, they were less willing to work, including participants who were told that other people were being paid much less than they were.

The findings show how people are less motivated to work if they are being paid less than others, but also if they perceive the whole system to be unjust.

Dr Gesiarz said: "People who are economically disadvantaged might face a two-fold reduction in motivation and well-being - first due to their lower relative position, and second due to their reaction to the unfair distribution of opportunities."

The findings showed that a large disparity in rewards brought about greater unhappiness, which was in turn associated with lower willingness to work. People were more likely to refuse to work in an unfair scenario, even if they would benefit, and despite their refusal being a private decision that had no impact on other people's rewards.

The researchers speculate that the negative feelings caused by arbitrary disparities may in part explain why disadvantaged people are more likely to experience anxiety and depression.

Co-author Dr Jan-Emmanuel De Neve (University of Oxford) said: "This study documents yet another example of a 'poverty trap': a situation in which being put at a disadvantage by random circumstances decreases a person's motivation to work, further worsening their situation."

Senior author Professor Tali Sharot (UCL Psychology & Language Sciences) said: "Whether inequality will negatively affect those at the top in 'the real world', outside the lab, remains to be studied. One thing to consider is that in our experiment, people were made aware that their position was randomly assigned. In the 'real world' people many times assume that their good fortune is justified by their talent and effort and therefore inequality might not have a negative influence on the motivation and well-being of privileged individuals in those situations. This is an important question that we hope to answer in the future."

Although immune responses are generated by a complex, hierarchical arrangement of immune system organs, tissues, and components, the unit of the cell has a particularly large effect on disease progression and host survival. These cell-level defense mechanisms, known as cell-autonomous immunity, are among the most important determinants of human survival, and are millions to billions of years old, inherited from our prokaryotic and single-celled ancestors.

The authors of a new paper published in the September 2020 issue of The Quarterly Review of Biology argue that understanding how cell-autonomous immunity has evolved in primates is crucial to understanding the human evolution, not only because infectious agents thought to have affected human genomic evolution are excellent manipulators of cell-autonomous immunity, but because these defenses are found in every cell in every body system.

In "Cell-Autonomous Immunity and the Pathogen-Mediated Evolution of Humans: Or How Our Prokaryotic and Single-Celled Origins Affect the Human Evolutionary Story," Jessica F. Brinkworth and Alexander S. Alvarado discuss how the ubiquity of cell-autonomous immunity highlights a biological reality not commonly addressed in human evolutionary studies - pathogens can mediate the evolution of all body cells, and therefore, all human body systems.

The article examines these ancient tactics in light of evolutionarily important human pathogens and illustrates inter-primate differences in their function. The authors posit that, often considered an independent physiological system in human evolutionary biology, the immune system is ubiquitous, integrated into every other aspect of human physiology. "We argue, therefore, that immunity and pathogen-mediated natural selection is a consideration in the examination of the evolution and function of any human physiological system or trait."

The authors show how human pathogens considered important in the evolution of the human genome manipulate cell-autonomous immunity and have shaped primate evolution, including phagosomes like Yersinia pestis (the causative bacteria of plague) and antimicrobial peptides like Toxoplasma gondii, the 1-2 million-year-old obligate intracellular feline-borne parasite.

"The ancient nature of these defenses is an important consideration in human evolutionary studies because their antiquity is both why cell-autonomous immunity exists in every cell, and the pathogens commonly considered the most pernicious and to have exerted the most stringent selective pressure on the human lineage tend to be organisms that bear microbiological innovations that manipulate these tactics," the authors write.

The paper also illustrates that these defenses are diverging in primate immune cells, and present evidence that they are also changing in "nonimmune" tissues. "For decades, it has been understood that microorganisms and cell-autonomous immune responses to them alter human behavior and vice versa. Incorporation of the same biological relationships between pathogens, cell-autonomous defenses, and body system X extended to other physiological systems or traits at the center of the classic questions of human evolutionary biology (e.g., why does skin color vary in humans, why do primate placentae vary in shape and size, how did human bipedal locomotion evolve, how does primate bone and dental microstructure vary) can enrich and improve our understanding of why such features evolved."

For this kind of information to contribute to a better understanding of the gross features of human evolution, however, the authors say researchers in this area must increase integration of molecular and morphological methods or findings in human evolutionary studies. "Any examination of human evolutionary biology, regardless of physiological system and when possible, should consider autonomous immunity of the cells in that system and how microorganisms have shaped them."

A team of scientists, led by researchers at University of California San Diego School of Medicine, report that a class of drugs used for a broad array of conditions, from allergies and colds to hypertension and urinary incontinence, may be associated with an increased risk of cognitive decline, particularly in older adults at greater risk for Alzheimer's disease (AD).

The findings were published in the September 2, 2020 online issue of Neurology, the medical journal of the American Academy of Neurology.

Anticholinergic drugs are widely used for dozens of conditions, minor and major. Some of these medications require a prescription, while others can be purchased over the counter. They work by blocking acetylcholine -- a type of neurotransmitter or chemical messenger known to be critical for memory function -- from binding to receptors on certain nerve cells. The effect is to inhibit parasympathetic nerve impulses, which are involved in a variety of involuntary muscle movements, such as those in the gastrointestinal tract and lungs, and bodily functions like salivation, digestion and urination.

Researchers reported that cognitively normal study participants who were taking at least one anticholinergic drug at baseline were 47 percent more likely to develop mild cognitive impairment (MCI), often a precursor to dementia such as AD, while being tracked over a period of up to a decade compared to participants who did not take such drugs.

"This study, led by Alexandra Weigand, suggests that reducing anticholinergic drug use before cognitive problems appear may be important for preventing future negative effects on memory and thinking skills, especially for people at greater risk for Alzheimer's disease," said senior author Lisa Delano-Wood, PhD, associate professor in the Department of Psychiatry at UC San Diego School of Medicine. Weigand is a graduate student in the San Diego State University/University of California San Diego Joint Doctoral Program in Clinical Psychology.

Six hundred and eighty-eight adults were involved in the study, evenly divided by sex with an average age of 74. None of the participants displayed cognitive or memory problems at the beginning of the study. Each reported whether they were taking anticholinergic drugs. One-third were taking such medications, with an average of 4.7 anticholinergic drugs per person. Participants were given annual comprehensive cognitive tests for up to 10 years.

The scientists also looked at whether participants had biomarkers for AD in their cerebrospinal fluid, such as certain types of proteins, or a well-known genetic risk factor for AD. They found that participants with AD biomarkers who were taking anticholinergic drugs were four times more likely to develop MCI than persons lacking biomarkers and not taking the drugs.

Similarly, persons at genetic risk for AD who took anticholinergic drugs were approximately 2.5 times more likely to develop MCI than those without genetic risk factors and who were not taking the drugs.

"We believe this interaction between anticholinergic drugs and Alzheimer's risk biomarkers acts in a 'double hit' manner," said Weigand, the study's first author. "In the first hit, Alzheimer's biomarkers indicate that pathology has started to accumulate in and degenerate a small region called the basal forebrain that produces the chemical acetylcholine, which promotes thinking and memory. In the second hit, anticholinergic drugs further deplete the brain's store of acetylcholine. This combined effect most significantly impacts a person's thinking and memory."

Study authors noted that, although older persons metabolize anticholinergic drugs differently than younger people, anticholinergic medications were being taken at levels much higher than the lowest effective dose recommended for older adults, with 57 percent taken at twice the recommended dosage and 18 percent at least four times the recommended dosage.

"This points to a potential area for improvement since reducing anticholinergic drug dosages may possibly delay cognitive decline," said Weigand. "It's important for older adults who take anticholinergic medications to regularly consult with their doctors and discuss medication use and dosages."

Delano-Wood noted that more work is needed to examine brain and cognitive effects of anticholinergic medications and whether these medications accelerate age-related cognitive changes or directly lead to neurodegenerative disorders, such as AD. "Clinical 'deprescribing' studies are currently underway at certain research sites across the nation in an effort to investigate whether reducing or stopping use of these drugs does, in fact, lead to reductions in progressive cognitive impairment," Delano-Wood said.

The hemoglobin in the red blood cells ensures that our body cells receive sufficient oxygen. When the blood pigment is broken down, "heme" is produced, which in turn can influence the protein cocktail in the blood. Researchers at the University of Bonn have now discovered in complex detective work that the "activated protein C" (APC) can be commandeered by heme. At the same time, APC can also reduce the toxic effect of heme. Perspectively, the findings may provide the basis for better diagnostic and therapeutic approaches to blood diseases. The study has been published online in advance in the journal "Antioxidants & Redox Signaling". The print version will be published soon.

"Blood is a juice of very special kind," is what Johann Wolfgang von Goethe had his Mephistopheles say. The hemoglobin gives blood its red color and ensures that the erythrocytes (red blood cells) can bind oxygen for breathing. This is managed by the hemoglobin-bound molecule "heme", which is a complex composing of a central iron ion and a porphyrin molecule. "The breakdown of erythrocytes results in a pool of so-called labile, regulatory heme," explains Prof. Dr. Diana Imhof from the Pharmaceutical Institute of the University of Bonn. As it can exert toxic effects in high concentrations, the body tries to keep the amount of heme in check.

It has been known for quite some time that this "labile, regulatory heme" affects the function of biomolecules. The team around Diana Imhof has now discovered in meticulous detective work which of the many proteins in the blood is particularly under the control of heme. "Over the last few years, our research group has established a large database of model peptides," reports Imhof. The peptides are individual protein "snippets" from which the sometimes huge and complex structures are built. Instead of studying the giant molecules, the proteins, in their entirety, the researchers first took a shortcut with the snippets.

Researchers searched like profilers for "suspects"

The pharmacists at the University of Bonn proceeded in a similar way to profilers in thrillers, who draw conclusions about the perpetrator's behavior from crime scene traces, circumstantial evidence and the type of crime. The researchers used an algorithm to systematically search the database for protein fragments that might potentially interact with heme. Using these data, they were able to conclude that the "activated protein C" (APC) is a particular candidate for heme binding. This enzyme is known for its anticoagulant and clot-dissolving effect, but can also take over cell-protective and anti-inflammatory tasks.

"So far, the impact of heme on the function of APC has been unknown," says Imhof's colleague and lead author of the study, Marie-Thérèse Hopp. The researchers investigated the association with pure compounds in the test tube and by using blood plasma samples provided by the Institute of Experimental Hematology and Transfusion Medicine at the University Hospital Bonn. There, Prof. Dr. Bernd Pötzsch and Dr. Nasim Shahidi Hamedani also supported the pharmacists with know-how, APC samples, test systems and access to specific devices. "We demonstrated that the enzymatic and anticoagulant activity of APC is reduced in the presence of heme," reports Hopp. For example, if there is too little APC or its activity is restricted, the risk of a clot forming in the bloodstream increases, thereby causing thrombosis, heart attack or stroke. Indeed, diseases with an increased incidence of labile heme (hemolytic diseases), such as sickle cell disease, are often associated with thrombotic complications.

Greater scope than previously assumed

"For this reason, the influence of heme on the enzyme APC is more significant than has probably been suspected so far," says Imhof. Furthermore, the team discovered that APC might protect the cells of the inner blood vessel wall like a bodyguard against the cytotoxic effect of heme. The researchers cultivated human endothelial cells and exposed them to heme. If APC was present at the same time, the toxic effect of heme on the cells was suppressed.

"We are convinced that this interaction between APC and heme is significant, because many other blood proteins we were looking for did not bind heme," says Imhof. It might be worthwhile to further investigate the impact of labile, regulatory heme on APC in order to also gain new diagnostic and therapeutically relevant insights regarding blood coagulation disorders that occur in hemolytic diseases. Imhof: "The terrain should be explored much more thoroughly than has been the case to date."

The future economy based on renewable and sustainable energy sources might utilize battery-powered cars, large-scale solar and wind farms, and energy reserves stored in batteries and chemical fuels. Although there are examples of sustainable energy sources in use already, scientific and engineering breakthroughs will determine the timeline for widespread adoption.

One proposed paradigm for shifting away from fossil fuels is the hydrogen economy, in which hydrogen gas powers society’s electrical needs. To mass produce hydrogen gas, some scientists are studying the process of splitting water — two hydrogen atoms and one oxygen atom — which would result in hydrogen fuel and breathable oxygen gas.

Feng Lin, an assistant professor of chemistry in the Virginia Tech College of Science, is focusing on energy storage and conversion research. This work is part of a new study published in the journal Nature Catalysis that solves a key, fundamental barrier in the electrochemical water splitting process where the Lin Lab demonstrates a new technique to reassemble, revivify, and reuse a catalyst that allows for energy-efficient water splitting. Chunguang Kuai, a former graduate student of Lin’s, is first author of the study with Lin and co-authors chemistry graduate students Zhengrui Xu, Anyang Hu, and Zhijie Yang.

The core idea of this study goes back to a subject in general chemistry classes: catalysts. These substances increase the rate of a reaction without being consumed in the chemical process. One way a catalyst increases the reaction rate is by decreasing the amount of energy needed for the reaction to commence.

Water may seem basic as a molecule made up of just three atoms, but the process of splitting it is quite difficult. But Lin’s lab has done so. Even moving one electron from a stable atom can be energy-intensive, but this reaction requires the transfer of four to oxidize oxygen to produce oxygen gas.

“In an electrochemical cell, the four-electron transfer process will make the reaction quite sluggish, and we need to have a higher electrochemical level to make it happen,” Lin said. “With a higher energy needed to split water, the long-term efficiency and catalyst stability become key challenges.”

In order to meet that high energy requirement, the Lin Lab introduces a common catalyst called mixed nickel iron hydroxide (MNF) to lower the threshold. Water splitting reactions with MNF work well, but due to the high reactivity of MNF, it has a short lifespan and the catalytic performance decreases quickly.

Lin and his team discovered a new technique that would allow for periodic reassembling to MNF’s original state, thus allowing the process of splitting water to continue. (The team used fresh water in their experiments, but Lin suggests salt water – the most abundant form of water on Earth – could work as well.)

MNF has a long history with energy studies. When Thomas Edison tinkered with batteries more than a century ago, he also used the same nickel and iron elements in nickel hydroxide-based batteries. Edison observed the formation of oxygen gas in his nickel hydroxide experiments, which is bad for a battery, but in the case of splitting water, production of oxygen gas is the goal.

“Scientists have realized for a long time that the addition of iron into the nickel hydroxide lattice is the key for the reactivity enhancement of water splitting.” Kuai said. “But under the catalytic conditions, the structure of the pre-designed MNF is highly dynamic due to the highly corrosive environment of the electrolytic solution.”

During Lin’s experiments, MNF degrades from a solid form into metal ions in the electrolytic solution — a key limitation to this process. But Lin’s team observed that when the electrochemical cell flips from the high, electrocatalytic potential to a low, reducing potential, just for a period of two minutes, the dissolved metal ions reassemble into the ideal MNF catalyst. This occurs due to a reversal of the pH gradient within the interface between the catalyst and the electrolytic solution.

“During the low potential for two minutes, we demonstrated we not only get nickel and iron ions deposited back into the electrode, but mixing them very well together and creating highly active catalytic sites,” Lin said. “This is truly exciting, because we rebuild the catalytic materials at the atomic length scale within a few nano-meter electrochemical interface.”

Another reason that the reformation works so well is that the Lin Lab synthesized novel MNF as thin sheets that are easier to reassemble than a bulk material.

Validating findings through X-rays

To corroborate these findings, Lin’s team conducted synchrotron X-ray measurements at the Advanced Photon Source of Argonne National Laboratory and at Stanford Synchrotron Radiation Lightsource of SLAC National Accelerator Laboratory. These measurements use the same basic premise as the common hospital X-ray but on a much larger scale.

“We wanted to observe what had happened during this entire process,” Kuai said. “We can use X-ray imaging to literally see the dissolution and redeposition of these metal irons to provide a fundamental picture of the chemical reactions.”

Synchrotron facilities require a massive loop, similar to the size of the Drillfield at Virginia Tech, that can perform X-ray spectroscopy and imaging at high speeds. This provides Lin high levels of data under the catalytic operating conditions. The study also provides insights into a range of other important electrochemical energy sciences, such as nitrogen reduction, carbon dioxide reduction, and zinc-air batteries.

“Beyond imaging, numerous X-ray spectroscopic measurements have allowed us to study how individual metal ions come together and form clusters with different chemical compositions,” Lin said. “This has really opened the door for probing electrochemical reactions in real chemical reaction environments.”

The work was supported by the Department of Chemistry startup funds and the Institute for Critical Technology and Applied Science.

Journal

Nature Catalysis

DOI

10.1038/s41929-020-0496-z

CAMBRIDGE, MA - September 2, 2020—Rapid Reviews: COVID-19 (RR:C19), is an open-access overlay journal published by the MIT Press that accelerates peer review of COVID-19-related research preprints to advance new and important findings and prevent the dissemination of false or misleading scientific news.

For the month of August, the preprints selected for review covered a wide range of subjects with peer reviewers finding recommendations for new prognostic scores to guide clinical decision making and hospital admissions and a study of estrogen levels and COVID-19 symptoms in women particularly noteworthy and useful.

Peer reviewers also flag as potentially misleading new research on whether beta-coronavirus MHV, a pathogen of mice, uses deacidification of lysosomes to exit cells while avoiding degradation. They caution decision-makers to not act on this research.

New August peer reviews from RR:C19, in order of the evidence scale rating (strong, reliable, potentially informative, not informative, or misleading) as provided by each of the two reviewers:

The utility of established prognostic scores in COVID-19 hospital admissions: a multicentre prospective evaluation of CURB-65, NEWS2, and qSOFA by Freddy Frost, et al. Preprint | Reviews

Evidence Scale Rating: Strong/Strong

Summary: This robust analysis is novel and of high interest for the medical community. This study informs how new prognostic scores should be created to more accurately guide clinical decision-making in patients with COVID-19. Reviewers: Michael Meisner and Kapil Gururangan

Progenitor identification and SARS-CoV-2 infection in long-term human distal lung organoid cultures by Ameen A. Salahudeen, et al. Preprint | ReviewsEvidence Scale Rating: Reliable/Strong

Summary: This study offers a chemically-defined human lung organoid culture system and employs this model to identify club cells as a novel target in SARS-CoV-2 infection. The findings reported are reliable for informing future COVID-19 research. Reviewers: Jaymin Kathiriya and Jeffrey A. Whitsett

Estrogen and COVID-19 symptoms: associations in women from the COVID Symptom Study by Ricardo Costeira, et al. Preprint | Reviews

Evidence Scale Rating: Reliable/Reliable

Summary: This is a reliable study that shows the protective role of estrogens against COVID-19 severe complications among 1.6 million UK women. Novel findings show potential increased risk amongst postmenopausal women and a potentially protective role of COCP in premenopausal women. Reviewers: Giovanni Grandi and Azure Grant

Anti-SARS-CoV-2 IgG from severely ill COVID-19 patients promotes macrophage hyper-inflammatory responses. Preprint | ReviewEvidence Scale Rating: Reliable/Reliable

Summary: This study introduces a novel therapeutic approach to treating COVID-19. Study motivates further investigation of whether selectively inhibiting FcR receptor-driven inflammation could result in more targeted and effective COVID-19 interventions. Reviewers: Sarah Stanley, Scott Biering, and Saumendra N. Sarkar

Intestinal receptor of SARS-CoV-2 in inflamed IBD tissue is downregulated by HNF4A in ileum and upregulated by interferon regulating factors in colon by Bram Verstockt, et al. Preprint | Review

Evidence Scale Rating: Reliable/Potentially Informative

Summary: Study claims increased susceptibility of IBD patients to SARS-CoV-2 infection. Study lacks sufficient evidence to support the authors’ claims concerning the importance of IBD medication in COVID-19 risk management. Claims are not actionable except to prompt further research. Reviewers: Girija Goyal, Cicely Fadel, Donald Ingber, and Magdalena Kasendra

Medical Costs of Keeping the US Economy Open During COVID-19 by Jiangzhuo Chen, et al. Preprint | Reviews

Evidence Scale Rating: Reliable/Potentially Informative

Summary: A major benefit of this analysis is that it presents a credible,flexible model for estimating the costs of COVID-19, although models will require updating with valid evidence. Sufficient compliance with lockdown guidelines could substantially reduce the medical costs of COVID-19. Reviewers: Christine Eibner, Raffaele Vardavas, and Mehdi Shiva

The infection fatality rate of COVID-19 inferred from seroprevalence data by John Ioannidis. Preprint | Reviews

Evidence Scale Rating: Potentially informative/Potentially informative

Summary: This study finds substantial heterogeneity in the infection fatality rate (IFR)across different locations. Data are useful and add to the emerging picture on IFR, however, substantial conclusions cannot be drawn. Reviewers: Timothy Hallett, Kenji Mizumoto, and Gerardo Chowell

Predicted success of prophylactic antiviral therapy to block or delay SARS-CoV-2 infection depends on the drug’s mechanism of action by Peter Czuppon, et al. Preprint | Review

Evidence Scale Rating: Reliable/Not informative

Summary: Authors claim that stochastic modeling can be used to predict the efficacy of repurposed drugs to prevent or treat SARS-CoV-2 infections. Readers and decision makers should assess results with some caution. Reviewers: Anna Bershteyn and Praveen P Nekkar Rao

Clinical validation of innovative, low cost, kit-free, RNA processing protocol for RT-PCR based COVID-19 testing by Nikhil Shri Sahajpal, et al. Preprint | Reviews

Evidence Scale Rating: Potentially informative/Not Informative

Summary: While informative, there are many flaws in the protocol testing if SARS-CoV2 RNA can be amplified from nasopharyngeal swab samples. The protocol does not appear to support claims that authors have made that this approach will decrease assay time, reduce cost, and instrumentation. Reviewers: Aditi Bhargava Bhargava and Mohamed Sharafeldin

β-Coronaviruses use lysosomal organelles for cellular egress by S Ghost, et al. Preprint | Reviews

Evidence Scale Rating: Misleading/Potentially informative

Summary: This study claims β-coronaviruses utilize a lysosome-mediated egress mechanism. In its current form, this pre-print includes numerous unsubstantiated, misleading, or poorly supported claims and is unreliable for informing future COVID-19 research. Reviewers: David Avram Sanders and Cristina Risco Ortiz

Researchers from Florida State University are shedding light on nutrient levels in the Gulf of Mexico with new findings published this month in the Journal of Geophysical Research - Oceans.

The Gulf of Mexico receives considerable levels of nutrients from the rivers that empty into it, especially the Mississippi River, which causes the Gulf's northern shelf waters to become overly enriched and more susceptible to algae growth. But scientists have remained unsure whether a significant portion of those nutrients ever leave the Gulf to potentially impact the chemistry of the North Atlantic Ocean.

"The Gulf of Mexico is an economically important body of water, as the surrounding areas rely on it for tourism, fisheries and oil production, and it also has significant ecological diversity," said Samantha Howe, a graduate student in the College of Arts and Sciences' Department of Earth, Ocean and Atmospheric Science, who led the research. "It is important to track the nutrient input from the Mississippi and Atchafalaya River System to the Gulf as those nutrients contribute to harmful algal blooms on the Northern Gulf Shelf."

Researchers found no evidence that nitrate from the Mississippi-Atchafalaya River System is mixing across the Northern Gulf shelf into the open waters of the Gulf of Mexico. The findings are consistent with recent modeling work by fellow scientists that indicates 90 percent of Mississippi River nutrients are retained in the near-shore ecosystem, which implies that nutrients from the Mississippi River do not leave the Gulf.

"In order to assess and manage ecological challenges in the Gulf, it is critical to understand whether the nutrients are processed and retained nearshore or whether they are transported to the North Atlantic," Howe said. "This finding is valuable to know, as these ecosystems must harbor the nutrient burden."

To conduct the study, the team collected and analyzed water samples taken during four different research cruises to the Gulf and the Florida Straits from 2011 to 2018.

The research is the first ever to provide isotopic composition measurements of nitrate in the Gulf of Mexico, as well as a new isotopic profile from the Florida Straits. These new water column profiles were then compared with prior measurements from the North and South Atlantic and with the magnitude of nitrogen inputs to the Gulf.

Howe, who earned her bachelor's degree in environmental science from FSU in Spring 2019, is now pursuing her master's in aquatic environmental science. She began the nutrient research as part of her honors undergraduate thesis while working in the research lab of study co-author, Associate Professor of Oceanography Angela Knapp.

"Samantha's thesis looked for distinct geochemical signatures of nitrate from the Mississippi River and whether this nitrate made it off the Northern Gulf of Mexico shelf into the deep waters of the Gulf that mix with the Loop Current and leave via the Florida Straits to enter the North Atlantic," Knapp said.

Howe's collaborators on the study include co-authors Knapp and Carlos Miranda, a 2017 graduate of the FSU Department of Chemistry and Biochemistry and the FSU Department of Biological Science, and colleagues from the University of Southern Mississippi and the University of New Hampshire.

"This work has important implications for understanding the fate of nutrients from the Mississippi Atchafalaya River System and how to manage human inputs to coastal ecosystems," Knapp said.

A team of researchers from the Max Planck Institute for Chemical Ecology in Jena, Germany, and the University of Virginia, USA, has studied the impact of high ozone air pollution on the chemical communication between flowers and pollinators. They showed that tobacco hawkmoths lost attraction to the scent of their preferred flowers when that scent had been altered by ozone. This oxidizing pollutant thus disturbs the interaction between a plant and its pollinator, a relationship that has evolved over millions of years. However, when given the chance, hawkmoths quickly learn that an unpleasantly polluted scent may lead to nutritious nectar (Journal of Chemical Ecology, September 2020, DOI: 10.1007/s10886-020-01211-4).

Pollination in the Anthropocene

Pollination is a critical ecosystem service, one that is performed mainly by insects. Flowers attract insects using floral scents, which are chemical signals that the pollinators can have an innate preference for. This preference is the result of the co-evolutionary relationship between flowers and their pollinators that has evolved over millions of years.

For about 20 years, the term "Anthropocene" has been used in the scientific community to refer to the geological epoch in which humans are responsible for many changes in biological and atmospheric processes. However, until recently, little has been known about the effects of anthropogenic climate change and atmospheric pollution on natural environmental odors that drive chemical communication between organisms.

A team of researchers from the Max Planck Institute for Chemical Ecology and the University of Virginia has investigated whether human-driven ozone pollution in the air influences the attraction of a pollinating moth to the scent of one of their favorite flowers. Ozone is an oxidant, a highly reactive chemical and pollutant known to cause respiratory diseases in humans. Now, ozone is also thought to change the floral scents that flowers emit to attract their pollinators.

For their experiments, the scientists used the tobacco hawkmoth Manduca sexta. "The hawkmoth Manduca sexta is the perfect model for our study. Although it is highly attracted by flower odors, it also uses its visual system to locate flowers. Flowers that usually attract hawkmoth often share specific compounds in their blend and are visually very conspicuous due to their bright white color," says study leader Markus Knaden, who heads a research group in the Department of Evolutionary Neuroethology at the Max Planck Institute.

The research team first determined the exact compositions of the flower odors - with and without increased ozone content - and the respective concentrations of individual odor components using gas chromatography. For the ozone-altered odors, the researchers used ozone concentrations that can be measured on hot days in the natural habitat of tobacco hawkmoths. They tested the responses of the moths in behavioral assays in a wind tunnel, allowing the insect to investigate both the original floral odor and to the ozone-altered floral odor.

"We were surprised, even shocked, that the innate attraction to the odor of tobacco flowers was completely lost in the presence of increased ozone levels," said Knaden, describing what was observed during the experiments.

Tobacco hawkmoths are able to learn

The question remained whether ozone in the air would spoil the appetite of hungry and foraging tobacco hawkmoths, or whether it would prevent insects from finding their food source. Would insects be able to figure out that even polluted flower odors can offer rewards? To answer this question, researchers tested whether tobacco hawkmoths could learn to accept an initially unattractive scent as a food cue if they smelled it while simultaneously being offered a sugar solution reward. The researchers assessed several different ways in which the moth could learn to recognize flowers based on the ozone-altered floral scent. This was critical to relating these experiments to real-world learning. In the real world, a floral scent only becomes ozone-altered as it moves downwind of the flower and mixes with ozone. To see if moths could learn ozone-altered floral scents even when they are decoupled from the sugar reward at the flower, the researchers developed an experiment where the moth had to follow the ozone-altered odor to the flower, but were presented with the original scent at the flower containing the sugar reward.

"While we anticipated that Manduca sexta could learn new floral scents and hoped that they would be able to learn the polluted floral scent of their host flower, we were amazed to see that Manduca sexta could learn the polluted floral blend in a number of different ways, including learning a polluted scent that was decoupled from a sugar reward. This type of learning, which we were surprised to find in Manduca sexta, could be very important in insects' ability to use learning to cope with their rapidly changing environments," says first author Brynn Cook from the University of Virginia. What is especially noteworthy and pertinent about this kind of responsiveness to a changing environment is that it occurs in real time and not over evolutionary timescales.

Learning ability of Manduca sexta is not an all-clear

Although the study shows that tobacco hawkmoths can learn to rely on ozone-altered and initially unattractive plumes to recognize their flowers, air pollution still poses a serious risk to pollination and pollinators. "Learning may be key to insects recognizing their host plants in polluted environments, but one of the major questions remaining from our study is whether pollinators will be able to find their flowers in the first place. Without initially recognizing smells, will pollinators only have visual cues to help them locate host flowers in order to learn the pollution-altered floral scent? Another important aspect to consider is that other pollinators may not have the same facility to learn new smells that Manduca sexta has. Specialist pollinators, for instance, may not have that flexibility in learning. Our study is just a starting point. Field studies are going to be critical to understanding which flowers and insects are most affected by which pollutants, and likely why," says Cook.

Air pollution and climate change have far-reaching consequences for our ecosystem; by no means have all of these been studied and understood. For example, we still know little about the impact of atmospheric changes on the chemical communication between plants and insects. Not only are plant odors altered, but also the sex pheromone female insects use to attract males. Atmospheric changes have the potential to cause alterations in pheromones that could lead to mating failure. Insect mortality has risen dramatically in recent years, and researchers worldwide are searching for the causes. Since 2020, the Max Planck Center next Generation Insect Chemical Ecology, a cooperation between the Max Planck Society and two Swedish universities in which the Max Planck Institute for Chemical Ecology and the co-authors of the study, Bill Hansson and Markus Knaden, play a major role, has been dedicated to this field of research.

Artificial intelligence, machine learning and neural networks are terms that are increasingly being used in daily life. Face recognition, object detection, and person classification and segmentation are common tasks for machine learning algorithms which are now in widespread use. Underlying all these processes is machine learning, which means that computers can capture the essential properties or the key characteristics of processes in which the relationships between objects are really complex. The learning process involves good and bad examples with no previous knowledge about the objects or the underlying laws of physics.

However, since it is a blind optimization process, machine learning is like a black box: computers take decisions they regard as valid but it is not understood why one decision is taken and not another so the internal mechanism of the method is still unclear. As a result, the predictions made by machine learning for critical situations are risky and by no means reliable because the results can be deceptive.

In this study, the research group made up of Vladimir Baulin, from the URV's Department of Chemical Engineering, Marc Werner (Leibniz Institute of Polymer Research in Dresden) and YachongGuo (University of Nanjing, China) has tested the predictions of a neural network to check whether they coincide with actual results. To this end, they chose a well defined practical example: the neural network had to design a polymer molecule that would cross the lipid membrane in as short a time as possible. The lipid membrane is a natural barrier that protects cells from damage and external components. To monitor the neural network's prediction, the researchers developed a novel numerical method that uses an exhaustive enumeration system that determines all the possibilities of polymer composition by directly programming the high-performance graphic cards in parallel calculations. "The traditional processor of a computer can contain a maximum of 12-24 nuclei for calculations, but graphic cards are designed to make parallel calculations of image and video pixels, and they have thousands of calculation cores optimized for parallel calculations," explains Vladimir Baulin. This enormous computational power generates thousands of millions of polymer combinations in just a few seconds or minutes. In this way a map can be generated that contains all the possible combinations and, therefore, how the neural network chooses the correct result can be monitored.

"What is surprising is that such a simple, minimum network as the neural network can find the composition of a molecule," Baulin points out. "This is probably due to the fact that physical systems obey the laws of nature, which are intrinsically symmetrical and self-similar. This drastically reduces the number of possible parameter combinations that are then captured by the neural networks."

Therefore, comparing the result of the neural network with the actual result not only makes it possible to check the prediction but also shows how the predictions evolve if the task is changed. And, in turn, this shows how neural networks take decisions and how they "think".

New homes are increasingly being outfitted with solar panels, heat pumps, rechargeable batteries and other means of producing and storing heat, electricity and gas, all of which interconnect with the electrical grid. At the level of an entire neighborhood, these decentralized, intermittent energy sources form a complex network, which can also include energy-consuming installations such as electric vehicle charging stations.

Managing these multi-energy systems and optimizing energy costs raises a number of questions. Should energy be consumed when it is produced, sold to the grid, or stored for later use? And how should various energy sources be distributed if there are groups of consumers generating their own energy?

Orchestrating the production and consumption of energy

CSEM has developed smart, predictive software capable of providing real-time answers to these questions. Designed for non-specialists, it makes use of weather forecasts, data from local infrastructure, residents' consumption habits and market energy costs. As its name indicates, Maestro is like an orchestra conductor that automatically manages resources and keeps costs down. An online simulator, based on a building with eight family apartments, is available here.

Determining the best time to consume energy

"All of Maestro's decisions are based on cost management," says Tomasz Gorecki, one of CSEM's engineers behind the system. "When a solar panel is in use, for example, the software can tell you whether it's more advantageous to charge your electric vehicle, store the energy, or sell it to the grid. The system works for individual homes, but it could also prove to be very useful for a self-sufficient community, sharing various renewable energy sources across several homes," he adds. The system has already been successfully installed in two private homes and in an apartment building in collaboration with Soleco. Negotiations are underway to fit out an entire neighborhood currently under construction in Zurich. Maestro was also presented at the IFAC World Congress in Berlin.

How Maestro works

The software is easy to use and can be quickly adapted to individual neighborhoods. To start with, parameters such as solar panel size, buildings' surface area, battery storage capacity and user preferences and priorities are fed into a planning tool.

Production data from energy installations, provided by sensors, are then sent to the cloud, where Maestro automatically compares possible consumption decisions and identifies the most cost-effective one. Instructions are sent back to the computer, which carries them out on site.

Maestro can incorporate boilers, heat pumps and electric vehicle charging stations, as well as electric batteries, renewable energy sources such as solar panels and wind turbines, power-to-gas facilities, thermal storage tanks, and more.

To learn more and test the online simulator, go to: https://www.csem.ch/page.aspx?pid=126438

Specific questions

What sets Maestro apart from other energy management systems?

Other systems on the market are designed only for individual homes and often employ a very simple mechanism of increasing power consumption whenever solar energy is produced. Maestro, on the other hand, can be used just as well for an entire neighborhood, where the network is more complex. It can also accommodate other energy-consuming installations such as electric vehicle charging stations and home heating and cooling systems. What's more, Maestro looks at weather forecasts for the coming days, which means that it can factor future needs into its consumption decisions. More broadly, the system is designed to keep costs down.

Could this focus on cost actually lead to increased energy consumption?

No, that shouldn't happen. Whenever surplus energy is produced, for example, the system will sell it to the grid if storing it for later use wouldn't be possible or cost-efficient. In making this decision, the system takes into account the losses that would be incurred by storing the energy in batteries. It's all about determining the best time and most rational way to use the energy.

What sort of cost savings are possible?

The cost savings will vary from home to home and user to user. A preliminary study on the first house running Maestro revealed an approximately 20% reduction in heating costs alone.

Researchers in France have discovered that patients suffering from severe COVID-19 show changes in a class of immune cells known as unconventional T cells. The study, published today in the Journal of Experimental Medicine (JEM), suggests that monitoring the activity of these cells in the blood of patients could predict the severity and course of the disease.

While most people infected with the SARS-CoV-2 virus experience relatively mild symptoms, some patients mount an aberrant inflammatory response that can damage the lungs and cause acute respiratory distress syndrome (ARDS), potentially resulting in the patient’s death. However, the immune cells and inflammatory molecules responsible for ARDS associated with COVID-19 remain unclear.

Unconventional T cells are a diverse class of immune cells that help control the response to viral infection and are commonly found in the lungs and other mucosal tissues in the body. “Despite this, the role of unconventional T cells in the pathophysiological process of SARS-CoV-2–driven ARDS has not yet been explored,” says Christophe Paget, a researcher at the INSERM Research Center for Respiratory Diseases, University of Tours.

Paget and colleagues, including co-lead author Youenn Jouan, an intensivist at the academic hospital of Tours, examined 30 patients admitted to intensive care with severe COVID-19 and compared the immune cells in their blood and lungs to those found in healthy volunteers or patients admitted to the ICU for reasons other than COVID-19.

The researchers found that two types of unconventional T cells—known as mucosal-associated invariant T (MAIT) and invariant natural killer T (iNKT) cells—were dramatically reduced in the blood of patients with severe COVID-19. However, the number of MAIT cells increased in the patients’ airways, suggesting that these cells might move from the blood to the lungs to control the response to SARS-CoV-2 infection.

The MAIT and iNKT cells of COVID-19 patients appeared to be highly activated and produced distinct sets of inflammatory molecules. The researchers found that patients whose circulating MAIT and iNKT cells were particularly active at the time of their admittance to the ICU were less susceptible to hypoxemia (low blood oxygen levels) and were discharged sooner than patients whose MAIT and iNKT cells were less active.

“This suggests that MAIT and iNKT cells might play a beneficial role during severe COVID-19, although their precise functions and associated mechanisms require further investigation,” says Jouan.

“Altogether, our findings should encourage further studies on MAIT and iNKT cells in SARS-CoV-2–induced ARDS to assess their potential as biomarkers and/or targets for immune intervention strategies,” adds Paget.

Rather than a slow build-up of plaque over time, a heart attack caused by spontaneous coronary artery dissection strikes suddenly, often in younger women who didn't seem to be at risk for a cardiac event.

SCAD is poorly understood, and it's so far impossible to predict which combination of genes and environmental triggers will lead coronary arteries to spontaneously tear, or dissect, leading to a heart attack that requires emergency, life-saving medical care.

Researchers have now uncovered additional genetic clues to better understand SCAD, which are desperately needed, says senior author Santhi Ganesh, M.D., from the Michigan Medicine Frankel Cardiovascular Center. The genes Ganesh and colleagues have identified further illustrate the difference between SCAD and the more common heart attack, when plaque builds up in the artery and limits blood flow, called atherosclerosis.

"The SCAD risk alleles were inversely associated with coronary disease and myocardial infarction due to atherosclerotic disease, suggesting very different underlying biology in the artery causing each type of heart attack," Ganesh says.

"It is especially intriguing that many of the same genetic markers are involved, but in different ways, in both SCAD-induced heart attack and atherosclerotic heart attack."

The researchers performed a genome-wide association study, analyzing millions of genetic markers in patients with SCAD and healthy controls. They found a significant association of several specific genetic regions associated with SCAD, which further implicated specific genes influenced by the identified genetic variants, Ganesh says.

In addition, researchers report that the genetic risk factors for SCAD also predict SCAD among individuals with fibromuscular dysplasia, or FMD, a vascular disease that may affect any artery in the body and is found in some patients with SCAD. Many people with FMD also lack traditional risk factors underlying atherosclerosis, like high blood pressure and diabetes, researchers say, but still may be at risk for vascular complications such as arterial aneurysms and dissections.

"As a physician caring for patients with both FMD and SCAD, it is gratifying to see results from our research that are beginning to uncover the genetic architecture and risk for these diseases about which so little is known," Ganesh says.

"This unbiased and large-scale analysis has provided us with new clues for where to focus our next steps of research, which is urgently needed. We are grateful for the participation of our patients, without whom these studies and new insights would not be possible."

Finally, the SCAD risk alleles were positively associated with migraine headache, which highlights a shared genetic basis for migraine headache and SCAD. Ganesh says more research is needed to precisely define the biological relationship of SCAD to vascular diseases such as FMD and migraine headache, as well as its implications for clinical care.

"Identifying these genetic risk alleles helps further advance our understanding of risks of SCAD," says co-lead author Jacqueline Saw, M.D., from Vancouver General Hospital/University of British Columbia. "Whether these findings have implications for SCAD in high-risk populations, such as those with peripartum SCAD, is an important next step of this research."

The team's work relied upon international large-scale collaborations including the Canadian SCAD Study, the University of Michigan Genetic Study of Arterial Dysplasia, the UK Biobank, the Million Veteran's Program and the Michigan Genomics Initiative, from which thousands of healthy controls boosted the team's ability to detect genetic associations.

The next step is to conduct studies on larger groups of patients with SCAD, and to conduct further in-depth studies of the genetic and biologic relationship between SCAD and FMD, and related dysplasia-associated arterial diseases, Ganesh says. The group is launching a clinical and genetic study of peripartum, or postpartum, SCAD.

Researchers at Karolinska Institutet in Sweden have identified a small neutralizing antibody, a so-called nanobody, that has the capacity to block SARS-CoV-2 from entering human cells. The researchers believe this nanobody has the potential to be developed as an antiviral treatment against COVID-19. The results are published in the journal Nature Communications.

"We hope our findings can contribute to the amelioration of the COVID-19 pandemic by encouraging further examination of this nanobody as a therapeutic candidate against this viral infection," says Gerald McInerney, corresponding author and associate professor of virology at the Department of Microbiology, Tumor and Cell Biology at Karolinska Institutet.

The search for effective nanobodies--which are fragments of antibodies that occur naturally in camelids and can be adapted for humans--began in February when an alpaca was injected with the new coronavirus' spike protein, which is used to enter our cells. After 60 days, blood samples from the alpaca showed a strong immune response against the spike protein.

Next, the researchers cloned, enriched and analysed nanobody sequences from the alpaca's B cells, a type of white blood cell, to determine which nanobodies were best suited for further evaluation. They identified one, Ty1 (named after the alpaca Tyson), that efficiently neutralizes the virus by attaching itself to the part of the spike protein that binds to the receptor ACE2, which is used by SARS-CoV-2 to infect cells. This blocks the virus from slipping into the cells and thus prevents infection.

"Using cryo-electron microscopy, we were able to see how the nanobody binds to the viral spike at an epitope which overlaps with the cellular receptor ACE2-binding site, providing a structural understanding for the potent neutralisation activity," says Leo Hanke, postdoc in the McInerney group and first author of the study.

Nanobodies offer several advantages over conventional antibodies as candidates for specific therapies. They span less than one-tenth the size of conventional antibodies and are typically easier to produce cost-effectively at scale. Critically, they can be adapted for humans with current protocols and have a proven record of inhibiting viral respiratory infections.

"Our results show that Ty1 can bind potently to the SARS-CoV-2 spike protein and neutralize the virus, with no detectable off-target activity" says Ben Murrell, assistant professor in the Department of Microbiology, Tumor and Cell Biology and co-senior author of the publication. "We are now embarking on preclinical animal studies to investigate the neutralizing activity and therapeutic potential of Ty1 in vivo".

This project is the first arising from the CoroNAb consortium, which is coordinated by Karolinska Institutet, and funded by the European Union's Horizon 2020 research and innovation programme. Additional funding for this project was obtained from the Swedish Research Council, and KI Development Office.

The sequence of Ty1 is available in the scientific article and will also be posted on the NCBI GenBank sequence data base under the accession code MT784731.

What's the risk of different human populations to develop a disease? To find out, a team led by Université de Montréal professor Guillaume Lettre created an international consortium to study the blood of hundreds of thousands of people worldwide.

In one of the largest studies of its kind, published today in Cell, close to 750,000 participants from five major populations -- European, African, Hispanic, East Asian and South Asian -- were tested to see the effect of genetic mutations on characteristics in their blood.

These characteristics include such things as hemoglobin concentration and platelet counts.

"Each human population is subject to different environments," said Lettre, a researcher at the Montreal Heart Institute.

"Over thousands of years," he said, "these environmental pressures have resulted in the progressive appearance of variations in DNA, called genetic mutations, which can influence our physical characteristics, such as skin size or color, but also our risk of getting certain diseases."

He added: "This observation (of how the environment affects how people's appearance and health vary in different parts of the world) represents the cornerstone of the theory of evolution by natural selection proposed by Charles Darwin in 1859."

The consortium founded by Lettre and his colleagues chose to study 15 characteristics of blood cells because previous studies had already uncovered mutations whose consequences were limited to certain populations.

45 million genetic mutations

By testing more than 45 million genetic variations in each participant, Lettre and his collaborators have found more than 5,000 mutations in human DNA that affect the blood characteristics of populations around the world.

Done in conjunction with another study focusing exclusively on individuals of European origin, the new study shows that the vast majority of mutations associated with blood cells were common to all five major population groups.

But aside from these, the researchers also found about 100 mutations whose effect was restricted to certain populations and which, it turns out, are not found in people of European descent.

For example, in individuals of South Asian origin, the researchers identified a mutation in the interleukin-7 gene that stimulates the secretion of this molecule and thus increases the levels of lymphocytes (a type of white blood cell in the immune system) circulating in their blood.

"Of course, this kind of mutation can affect the health of people of South Asian origin," Lettre noted. "It's thought that this mutation could influence their capacity to resist certain infections or develop diseases like blood cancer."

However, he cautioned, "these are, at present, only hypotheses, as researchers do not have the capacity to test them, given the immense costs and the difficulty of finding participants for this type of study."

Improving ways of predicting

By comparing the genetic results obtained in each population, the researchers were able to prioritize certain genes that appear to have an overall effect on blood cell production.

This will make it possible, over the long term, to improve ways of predicting the risk of suffering from certain diseases and to develop new, more effective treatments.

Here again, however, major investments in research will be required to analyze the consequences of these mutations on the health of these population groups.

Another major obstacle will be to convince researchers how important it is for all population groups globally to be included in these types of genetic studies.

"Despite the size of our study, the vast majority of participants -- about 560,000 out of 740,000 individuals -- were of European origin," Lettre noted. "This necessarily introduces a bias into the study."

In the future, he said, "we hope to work with populations that have been little studied so far -- for example, East African populations or indigenous peoples -- in order to shed light on new genes that regulate blood cells."

One thing is clear, he concluded: in order to better understand human diseases and to ensure that everyone, regardless of ethnic origin, is able to benefit from advances in genetics and precision medicine, diseases will have to be studied in all populations worldwide.

The path to global sustainability isn't a one-way street and scientists at Michigan State University and in China use the world's adoration of pandas to show new ways to figure out how not to get lost.

The group scrutinized the complex, vast enterprises that feed the boundless love of giant pandas that bring tourists to the Wolong Nature Reserve and other reserves in remote southwestern China, and the successful operations that loan the cuddly bears to zoos all over the world. The goal: understand how achieving one of the 17 United Nations' Sustainable Development Goals (SDGs) spins off more SDG success - or sabotages progress on another goal across spatial and administrative boundaries, as well as unforeseen consequences.

But that's only the beginning, says the group writing in Science of the Total Environment. They employ a new integrated framework to systematically and comprehensively examine human-nature interactions across space. The metacoupling framework integrates how humans and nature interact within a specific place, between adjacent places, and between distant places around the world.

"Previous research indicates that efforts towards the SDGs have an inherent tendency to achieve one at the cost or benefit of others in a specific place," said senior author Jianguo "Jack" Liu, Rachel Carson Chair in Sustainability and director of the Center for Systems Integration and Sustainability. "but it is not clear how SDGs interact across boundaries although the world is increasingly interconnected among different places and the SDGs need to be achieved everywhere. To fill such an important knowledge gap, we have developed new ways to understand SDG tradeoffs and synergies within and across boundaries. Interactions between pandas and people are very useful for exploring this new interdisciplinary frontier."

To find the synergies and tradeoffs that swell around panda endeavors, the group examined a wide range of information surrounding tourism in and around Wolong, as well as 19 other panda reserves in Sichuan Province who were visited by more than 8.2 million tourists annually. They discovered that tourism brought nine synergies amongst the SDGs, with various aspects of economic growth being promoted, which in turn alleviated poverty, raised incomes, improved infrastructures. One SDG took a hit, as hiking trails for tourists disturbed crucial panda habitat.

From 1996 to 2017, Wolong implemented international collaboration agreements with 14 zoos in 12 countries andSDGs_Panda_tourism_2020 sent 28 pandas to those zoos, and that effort created win-win situations for SDGs, both providing economic boosts as well as funding scientific research and supporting training bases for panda reintroduction.

The authors further revealed that the benefits spilled over beyond the reserves' borders, as people who live outside created businesses and made money supporting the tourism effort. Hitting one SDG had the domino effect of providing progress for other goals as people found jobs and improved their lives. The industry that took a chunk out of another goal was the collection of medicinal herbs. While that provided economic benefits to people, that activity damaged natural habitat.

The panda loans, they found, have generated income that has enhanced scientific research - and then generated positive results that have spilled over into benefits for other reserves to have more resources for conservation, which in turn allowed more pandas to be reintroduced in the wild and boost genetic diversity.

"We have found many more synergies than trade-offs when it comes to striving for Sustainable Development Goals," said Zhiqiang Zhao, lead author of the paper. "It is important to cast a wide net when understanding what battles we are winning in sustainability, and what wins may be at a cost of another important goal. Only then can we make necessary adjustments."