Culture

Delivery services have increased rapidly with the expansion of online shopping and, in Japan, failed deliveries that result in redelivery attempts occur 20% of the time. In terms of labor, fuel, and environmental (increased CO2 emissions) costs, empty homes causing redeliveries have become an issue. Until now, long-term trends of households with every member out-of-home has not been fully clarified.

Researchers from Kumamoto University, Japan used a travel behavior survey conducted by local governments, called the Person Trip (PT) Survey, to analyze the movement data of people in the Kumamoto metropolitan area--specifically when every member of a household was out-of-home. The PT survey captures a person's movements over a day to examine their travel behavior. It is basic data that is used to develop transportation plans.

The researchers used PT surveys of the Kumamoto metropolitan area from 1984, 1997, and 2012 to analyze both individual out-of-home rates (IO rates) and the rates of households with every member out-of-home (HEMO rates). Between 1984 and 2012, the IO rate did not change significantly, except for a slight increase in the evening. The relatively unchanging IO rate may be caused by an offset of a decreased high-IO-rate working population by an increase in high-IO-rate active elderly.

In contrast, the HEMO rates at 11:00 am were 41.3% in 1984 and 51.5% in 2012, an increase of 10.2 percentage points. The contributing factors are considered to be a decrease in household size, an increase in single-person households, a decrease in households with full-time housewives, and an increase in the IO rate of active elderly people. The researchers also developed a method to decompose the HEMO rate change into these factors for further analysis.

This is the first study to analyze HEMO rates using PT surveys. Although the research team used Kumamoto data this time, they are currently conducting similar analyses using travel data from both Japan and overseas.

"The issues arising from all household members being out-of-home of are not only related to failed deliveries, but also to difficulties investigators have visiting households during the census and similar visits," said study leader Associate Professor Takuya Maruyama. "We hope that this study leads to the development of efficient redelivery systems and on-site survey methods. It can also be useful for studying methods to deter crimes such as burglary."

Researchers from Tokyo Medical and Dental University (TMDU) discover a novel mechanism by which immunodeficiency viruses evolved over time to evade the protective measures of the host

Tokyo, Japan - When Charles Darwin theorized how the struggle for existence drives natural selection, he laid the cornerstone of modern biology. Now, researchers from Tokyo Medical and Dental University (TMDU) have investigated the process of selection in the context of human immunodeficiency virus (HIV) infection. In a new study published in the Journal of Virology, they showed how certain primate immunodeficiency viruses (PIVs) acquire the ability to survive in a hostile environment in the midst of the host's protective apparatus.

The goal of viruses is to infect cells of a host and to use them to multiply and infect more cells. In contrast, the defense system of animals including immune system protects the host from foreign invaders, such as viruses, by suppressing their proliferation. Many viruses adapt to this constant pressure by the host by finding new ways to circumvent the host's defense system. One of the important players in this system is a protein called BST-2, which ensures that PIVs are not released from the cell where they originate. Many PIVs make a protein called viral protein U (Vpu) to antagonize host BST-2.

"This interaction between BST-2 and Vpu is highly species-specific, meaning that not all BST-2 and Vpu proteins from different species interact with each other," says corresponding author of the study Takeshi Yoshida. "The goal of our study was to understand how PIVs that infect primates learn to evade the human defense system by inactivating human BST-2."

To achieve their goal, the researchers infected human cells with virus expressing Vpu protein from simian immunodeficiency viruses (SIVs) that infect wild chimpanzees or various monkeys, and found that only Vpu from the SIV that infects the greater spot-nosed monkey (SIVgsn) had the ability to neutralizehuman BST-2 and thus to be able to release virus efficiently from human cells.

"We wanted to know what this particular Vpu does differently from the other Vpu proteins to ensure that the SIV can inactivate the human defense system," says lead author of the study Weitong Yao.

The researchers then investigated the molecular interaction between human BST-2 and this particular Vpu, and specifically focused on a certain amino acid sequence, also called a motif, in Vpu that had previously been shown to be important for its interaction with BST-2. Interestingly, they found that Vpu from SIVgsn possesses two such motifs, and that only one of them is required to inactivate BST-2 of its natural host, the greater spot-nosed monkey, but both to inactivate human BST-2.

"These are striking results that implyhow PIVs learn during the course of evolution to adapt to new situations and to survive," says Yoshida.

HIV is responsible for acquired immunodeficiency syndrome (AIDS) and is thought to have been derived from an SIV that infects wild chimpanzees (SIVcpz). While HIV can antagonize human BST-2, SIVcpz cannot. The findings of this study shed new light on the evolution of a virus that is the cause of the worst pandemic in human history.

The red panda (Ailurus fulgens) is an endangered mammal endemic to the Himalaya and Hengduan Mountains, and its distribution spans China, Myanmar, Bhutan, India and Nepal. Prior to 1902, all red pandas were classified as one species. However, in 1902, scientists established two subspecies, based on their morphological differences: the Himalayan subspecies (A. f. fulgens) and the Chinese subspecies (A. f. styani).

More recent research on their morphological differences and geographical distribution, however, led the taxonomist Colin Groves to reclassify the two subspecies as two distinct species: the Himalayan red panda (A. fulgens) and the Chinese red panda (A. styani). Despite this change, the evolutionary histories of Himalayan and Chinese red pandas have remained unclear and controversy has persisted about whether they should be classified as two distinct species or not.

In order to help clarify these questions, a research team led by Prof. WEI Fuwen from the Institute of Zoology of the Chinese Academy of Sciences, used population genomics methods to analyze the genome resequencing data of 65 wild red pandas (including both Himalayan and Chinese red pandas) from seven geographical populations; mitochondrial genomes of 49 red pandas; and Y chromosome single-nucleotide polymorphism (SNP) data from 49 male individuals.

All results from these three types of markers found substantial genetic divergence between the two species, and no sharing was found for the haplotypes of mitochondrial genome and Y chromosome SNPs.

These findings clearly support Groves' classification of red pandas into two phylogenetic species. Further analysis also found that the Yalu Zangbu River, rather than the Nujiang River, is most likely the geographical boundary between the two species. This explains previous observations that the discriminating morphological characteristics were inconsistent with their geographical distributions.

Furthermore, the research team reconstructed the demographic and divergence histories of the two species based on the genome resequencing data. The results revealed clearly different demographic histories for the two species: The Chinese red panda had experienced two population bottlenecks and one large population expansion, whereas the Himalayan red panda had experienced three bottlenecks and one very small expansion. These two species started to diverge after the serious population bottleneck caused by the Penultimate Glaciation (0.3 to 0.13 Mya).

In contrast to the Chinese red panda, the Himalayan red panda has less genetic diversity, higher linkage disequilibrium and a higher genetic load, thus highlighting the urgency of protecting this endangered species. These findings have important conservation implications for wild red panda conservation, pedigree construction and interbreeding avoidance for captive red pandas.

Researchers identified an increased prevalence of five traits associated with previous extinction-survival responses among corals.

Human-driven climate change is rapidly increasing stressors on coral communities, such that 75% of species could become extinct within the next few centuries.

NEW YORK, March 3, 2020 -- A study published Tuesday in Scientific Reports shows that stony corals, which provide food and shelter for almost a quarter of all ocean species, are preparing for a major extinction event.

The research team--which includes scientists from The Graduate Center, CUNY; Baruch College; Scripps Institution of Oceanography; University of Haifa; University of Leeds; and GEOMAR Helmholtz Centre for Ocean Research--found that corals are currently exhibiting a suite of dynamic survival responses that correspond with their last major extinction 66 million years ago. These coral traits include increased prevalence of deep-water residing, cosmopolitan distributions, non-symbiotic relationship to algae, solitary or small colonies, and bleaching resistance.

Scientists were able to trace these behaviors due to excellent fossil records that coral skeletons leave behind. This study compared those fossil records to the modern International Union for Conservation of Nature (IUCN) Red List data. The IUCN Red List of threatened species is world's most comprehensive information source on the global conservation status of animal, fungi, and plant species.

"It was incredibly spooky to witness how corals are now exhibiting the same traits as they did at the last major extinction event," said Professor David Gruber, a researcher and marine biologist with The Graduate Center, CUNY and Baruch College. "Corals seem to be preparing to jump across an extinction boundary, while we are putting our foot further on the pedal."

The study highlights how primates do not possess survival characteristics or have a record of mass extinction survival as some corals do.

The researchers examined 250 million years of fossil coral data from the Paleobiology Database and then compared this to modern data. They noted striking similarities in the corals’ recorded survival behaviors between the Cretaceous-Tertiary (KT) extinction event 66 million years ago (when the dinosaurs disappeared) and the current Anthropocene time period. Using the data, they were able to infer relevant traits, including an 18% decrease in coloniality, an 18% decrease in photosymbiosis, and a 12% decrease in the occupation of shallow habitats. Scientists also noted an evolutionary selection toward slower-growing coral, which may increase their chances of survival.

"This study reminds us that corals are diverse and flexible organisms with a demonstrated success facing the most extreme environmental crisis in Earth's history: mass extinction," said the study's first author Gal Dishon, a marine biologist with the Scripps Institution of Oceanography at the University of California. "Nevertheless, based on the lessons we learned from fossil data, the surviving corals will not be those reef builders we know from hyper-diverse tropical coral reefs, but rather small, solitary, slow-growing, and deep-dwelling corals."

The authors note that while slow recovery time (2-10 million years) of coral reefs following a mass extinction is distressing, they also call attention that primates (the order that also includes humans) are also increasingly becoming threatened with extinction.

“There is something very powerful about this message coming from the corals,” said Gruber. “Corals are such a sensitive group of marine creatures, they are essentially the canary in the coal mine.”

Actin filaments have several important functions inside cells. For one, they support the cell membrane by binding to it. However, scientists did not know exactly how the actin interacts with the membrane lipids. Simulations performed at the University of Groningen, supported by experiments, provide a molecular view on this very fundamental process. The results were published in the journal Proceedings of the National Academy of Sciences on 2 March.

Actin filaments are involved in many important processes in eukaryotic cells, from motility to division to the contraction of muscle fibers. Actin can also form a network underneath the lipid bilayer. Here, it provides additional support for this structure, while curved filaments also play a role in cell division, when the membrane needs to constrict. Despite its importance, the molecular processes underlying the binding of actin to cell membranes is still not clear.

Simulations

'The literature provides conflicting results,' says University of Groningen Professor of Molecular Dynamics Siewert-Jan Marrink. 'All agree that actin, which is negatively charged, could bind to positively charged lipids and some say that they can even bind to membranes with no positive or even a negative charge.' The latter is relevant for the biological situation as normal cell membranes carry a negative charge on the inside.

Marrink and his colleagues, therefore, performed molecular dynamics simulations of the interaction between lipids and actin. They used the Martini coarse-grained forcefield, which was developed by Marrink and is now used worldwide.

Molecular glue

By varying the components in the simulation, the scientists discovered that the ions that are present define the binding process. Marrink: 'Actin could only bind to negatively charged lipids in the presence of calcium ions. The two positive charges of calcium act as a kind of molecular glue.' In contrast, in the presence of positively charged lipids, calcium ions inhibited the binding of actin. The results of this simulation were confirmed by experiments performed in Professor Gijsje Koenderink's lab at Delft University of Technology.

'The concentrations of calcium that were required in the simulations are higher than you would find inside cells,' says Marrink. 'However, calcium ions tend to bind to membrane lipids, so the local concentration could be high enough.'

Synthetic cell

The results provide the first clear picture of actin-binding to membrane lipids. 'We want to use this in a national effort to build an artificial cell,' Marrink explains. The Dutch BaSyC (Building a Synthetic Cell) project involves many different steps and one of them is constructing membranes. 'These need to be reinforced with actin, so we have to understand how to control the interaction between the filaments and the lipid membrane. And we need to guide division of the artificial cell, where actin is needed for constriction.'

University of Kent research suggests that men can distinguish between the scents of sexually aroused and non-aroused women.

The detection of sexual arousal through smell may function as an additional channel in the communication of sexual interest and provide further verification of human sexual interest.

This research by Dr Arnaud Wisman, a Psychologist at the University of Kent, expands on previous studies which have concluded that humans can communicate and detect emotions such as fear or sadness through scent. Sexual arousal is also identified as an emotional physical state.

Findings were established through three different experiments where men processed the scents of axillary sweat samples from anonymous sexually aroused and non-aroused women. Men evaluated the scent of sexually aroused women as relatively more attractive and this increased their sexual motivation. This suggests that the chemical signals of scent alone can elicit a sexual response in recipients.

Dr Arnaud Wisman said: 'The present studies suggest that men are sensitive to the olfactory signals of sexual arousal released by women. This research suggests that these signals released along with corresponding visual and auditory expressions of sexual interest can produce a stronger overall signal that increases sexual motivation. Sexual interest may entail more than meets the eye and we hope that the current findings encourage further research to examine the role of sexual olfactory signals in human communication.'

Scientists at the Laboratoire des Maladies Neurodégénératives (CNRS/CEA/Université Paris-Saclay) and the Neurocentre Magendie (INSERM/Université de Bordeaux) have just shown that a metabolic pathway plays a determining role in Alzheimer's disease's memory problems. This work, published on 3 March 2020 in Cell Metabolism, also shows that supplying a specific amino acid as a nutritional supplement in a mouse model of Alzheimer's restores spatial memory affected early. This is a promising path for reducing memory loss related to that disease.

The brain uses a large part of the energy available to our body. To work properly, neurons and the surrounding cells, particularly astrocytes, must cooperate. The early phase of Alzheimer's disease is characterized by a reduction in this energy metabolism, but until now we did not know whether this deficit contributed directly to the cognitive symptoms of Alzheimer's disease.

A collaborative study has shown in a mouse model of Alzheimer's disease that a decrease in the use of glucose by astrocytes reduces L-serine production. This amino acid is mainly produced by these brain cells and its biosynthesis path is altered in patients. L-serine is the precursor of D-serine, known to stimulate NMDA receptors, essential for brain function and to the establishment of memory. So by producing less L-serine, astrocytes cause reduced activity in these receptors, which alters neuronal plasticity and the associated memorization capacities. Scientists have also demonstrated that memorization functions in mice were restored by supplying nutritional L-serine.

With the identification of the role of L-serine in memory disorders and the experimental efficacy of nutritional supplementation, new strategies appear that may complement medical treatment, to combat early symptoms of Alzheimer's disease and other diseases that display metabolic deficits, like Parkinson's and Huntington's. Since L-serine is available as a nutritional supplement, this compound should be rigorously tested in humans, through controlled clinical trials.

Studying the inner ear of apes and humans could uncover new information on our species' evolutionary relationships, suggests a new study published today in eLife.

Humans, gorillas, chimpanzees, orangutans and gibbons all belong to a group known as the hominoids. This 'superfamily' also includes the immediate ancestors and close relatives of these species, but in many instances, the evolutionary relationships between these extinct ape species remain controversial. The new findings suggest that looking at the structure (or morphology) of the inner ears across hominoids as a whole could go some way to resolving this.

"Reconstructing the evolutionary history of apes and humans and determining the morphology of the last common ancestor from which they evolved are challenging tasks," explains lead author Alessandro Urciuoli, a researcher at the Institut Català de Paleontologia Miquel Crusafont (ICP) in Barcelona, Spain. "While DNA can help evolutionary biologists work out how living species are related to one another, fossils are typically the principle source of information for extinct species, although they must be used with caution."

The bony cavity that houses the inner ear, which is involved in balance and hearing and is fairly common in the fossil record, has proven useful for tracing the evolution of certain groups of mammals. But until now, no studies have explored whether this structure could provide insights into the evolutionary relatedness among living and extinct hominoids.

To address this, Urciuoli and his team used a 3D imaging technique to capture the complex shapes of the inner ear cavities of 27 species of monkeys and apes, including humans and the extinct ape Oreopithecus and fossil hominin Australopithecus. Their results confirmed that the shape of these structures most closely reflected the evolutionary relationships between the species and not, for example, how the animals moved.

The team next identified features of these bony chambers that were shared among several hominoid groups, and estimated how the inner ears of these groups' ancestors might have looked. Their findings for Australopithecus were consistent with this species being the most closely related to modern humans than other apes, while those for Oreopithecus supported the view that this was a much older species of ape related in some respects with other apes still alive today.

"Our work provides a testable hypothesis about inner ear evolution in apes and humans that should be subjected to further scrutiny based on the analysis of additional fossils, particularly for great apes that existed during the Miocene," says senior author David Alba, Director of the ICP. The Miocene period, which extends from about 23 to five million years ago, is when the evolutionary path to hominoids became distinct.

Urciuoli adds that, in years to come, disentangling the kinship relationships between Miocene apes will be essential for improving our understanding of the evolution of hominoids, including humans and our closest living relatives, the chimpanzee and bonobo.

A black hole, ejecting material at close to the speed of light, has been observed using e-MERLIN, the UK's radio telescope array based at Jodrell Bank Observatory.

A research team based at Oxford University used e-MERLIN, as well as the VLA and MeerKAT telescopes based in the US and South Africa respectively, to track the ejecting material over a period of months.

The observations have allowed a deeper understanding into how black holes feed energy into their environment. Co-lead of the project, and author on the paper appearing in Nature Astronomy, Rob Fender said "We've been studying these kind of jets for over 20 years and never have we tracked them so beautifully over such a large distance."

The group successfully tracked these ejections of this particular system, known as MAXI J1820+070, after it went into outburst in the summer of 2018. The extreme distances from the black hole and the final angular separation is among the largest seen from such systems.

The ejections are moving so fast that they appear to be moving faster than the speed of light - they are not, rather this is a phenomenon known as apparent superluminal motion.

Dr Rob Beswick, Head of e-MERLIN science operations at Jodrell Bank stated: "This work shows the power of world-class instruments such as e-MERLIN, MeerKAT and the VLA working in tandem.

"e-MERLIN's unique combination of resolution, sensitivity and rapid response made it the perfect instrument for this sort of study".

"Using our radio observations we were able to better estimate how much energy is contained in these ejections using a novel method for this type of system." explains Joe Bright, DPhil student at Oxford University's Department of Physics.

"Galactic black holes, such as MAXI J1820+070, are thought to be miniature versions of the supermassive black holes that are found at the centre of galaxies. The feedback from these black holes is thought to be a vital component regulating the growth of galaxies".

New insight on the neural processes that drive a desire for revenge during conflict between groups has been published today in the open-access journal eLife.

The study suggests that the 'love hormone' oxytocin is increased during conflict between groups and influences the medial prefrontal cortex, the section of the brain associated with our decision-making activity. This leads to a greater feeling of love and empathy among a group and the desire to seek revenge when attacked by an outside group. The findings may help explain how a process called 'conflict contagion' can occur, where a conflict that starts between a few individuals ends up spreading among entire groups.

"The desire to seek revenge for an attack during conflict is universal among humans, but the neurobiological processes that drive it are still unclear," says lead author Xiaochun Han, Doctor of Psychology and Neuroscience at the School of Psychological and Cognitive Sciences, PKU-IDG/McGovern Institute for Brain Research, Peking University, China. "Building upon previous studies, we suggest there may be a neurobiological mechanism that links pain within a group, known as the 'ingroup', caused by an outside group, or 'outgroup', with the tendency to seek revenge upon the outgroup."

To explore this possible mechanism further, the team developed a new neural-behavioural experiment that simulates real-life revenge during conflict between groups. As oxytocin is known to play a role in empathy within a group and in regulating intergroup conflict, they wanted to examine the oxytocin and neural responses to ingroup suffering caused by an outgroup, and to see how these responses predicted a desire for revenge.

For the experiment, participants watched an ingroup and an outgroup member receive an electric shock that was caused either mutually (for the 'revenge' group) or respectively by a computer (for the 'control' group). The team then combined a brain imaging technique called functional magnetic resonance imaging with measurements of oxytocin levels in the members of both groups.

They found that the conflict encountered by the revenge group was associated with an increased level of oxytocin compared to the control group. Additionally, they saw that these increased levels of oxytocin predicted the medial prefrontal activity associated with ingroup pain. This activity in turn predicted the desire to seek revenge upon the outgroup, regardless of whether some of the individuals were directly involved in the conflict.

"Our experiment allowed us to investigate how harm to an ingroup member caused by an outgroup member inspires an uninvolved ingroup member to seek revenge," explains senior author Shihui Han, Professor at the Department of Psychology and Principle Investigator at PKU-IDG/McGovern Institute for Brain Research, Peking University. "The results highlight an important neurobiological process underpinning the desire for revenge, which may be implicated in conflict contagion during conflict among groups."

Han adds that there are various motivations for seeking revenge within a group, such as feeling threatened, feeling empathy towards a harmed group member, and feeling pressure to avenge the individual or group as a whole. "Further studies will be needed to examine these motivations and associated emotions if we are to fully understand the processes that can drive humans to seek revenge," he concludes.

Netherton syndrome, a rare skin disease caused by a single genetic mutation, is exacerbated by the presence of two common Staphylococcal bacteria living on human skin, one of which was previously thought to only offer protective properties, report University of California San Diego School of Medicine researchers.

"Our study shows how closely tied the human genome is to the genetic information in our skin microbiome. This rare disease is due to a mutation in a human gene. But, in adults, the symptoms of the disease are driven by the skin microbiome," said senior author Richard Gallo, MD, PhD, Irma Gigli Distinguished Professor and chair of the Department of Dermatology at UC San Diego School of Medicine.

"The two genomes work closely together. When one is off, even by a single gene, the other genome reacts."

In a multi-institutional study published online in Cell Reports on March 3, 2020, Gallo and collaborators identified how Staphylococcus aureus and Staphylococcus epidermidis can act as a catalyst for skin inflammation and barrier damage in mouse models.

S. aureus is a pathogenic bacteria known to aggravate skin conditions, such as atopic dermatitis. When it becomes resistant to antibiotics, it is known as methicillin-resistant Staphylococcus aureus or MRSA. It is a leading cause of death resulting from infection in the United States.

Conversely, S. epidermidis is common on healthy human skin and presumed benign. In a previous study, Gallo reported that a specific strain of this bacterium seemed to hold a protective property by secreting a chemical that kills several types of cancer cells but does not appear to be toxic to normal cells. S. epidermidis was also known to promote wound repair, skin immunity and limit pathogen infections. It was not known that, in some cases, S. epidermidis can have pathogenic effects.

Netherton syndrome is a result of a mutation in the SPINK5 gene, which normally provides instructions for making a protein called LEKT1. This protein is a type of protease inhibitor.

With the loss of LEKT1, excess proteases are stimulated by Staphylococcal bacteria on people with Netherton syndrome. This protease activity leads to a breakdown of proteins and skin inflammation.

"This is a major breakthrough for these patients as it describes how we can treat a human genetic mutation by targeting the microbiome," said Gallo, who is also a faculty member in the Center for Microbiome Innovation at UC San Diego. "Altering bacterial gene expression is much easier than trying to fix a mutation in humans."

Researchers swabbed the skin of 10 people with Netherton syndrome and found that their skin microbiome had an abundance of certain strains of S. aureus and S. epidermidis. However, unlike the skin of normal subjects, the excess bacteria produced genes that could not be controlled due to the gene mutation in Netherton syndrome.

According to the National Institutes of Health, most people with this recessive inherited genetic disorder have immune system-related problems, such as food allergies, hay fever, asthma, or an inflammatory skin disorder called eczema. It is estimated that 1 in 200,000 newborns are affected.

"In addition to demonstrating how an abnormal skin microbiome promotes inflammation in Netherton syndrome, this study provides one of the most detailed genomic descriptions to date of the skin microbiome," said Gallo.

Mangroves account for only 0.7 per cent of the Earth's tropical forest area, but they are among the world's most productive and important ecosystems. They provide a wealth of ecological and socio-economic benefits, such as serving as nursery habitat for fish species, offering protection against coastal surges associated with storms and tsunamis, and storing carbon.

While many countries have established legal protection for mangroves, their value for sustainable ecosystem services face strong competition from converting the land to other more lucrative uses, particularly for agriculture. In the past decade, studies have shown that mangrove deforestation rates are higher than the deforestation of inland terrestrial forests.

New research from the National University of Singapore (NUS) provided additional support for this, with results showing that mangroves deforestation rates in Myanmar, an important country for mangrove extent and biodiversity, greatly exceed previous estimates.

The research, led by Associate Professor Edward Webb and Mr Jose Don De Alban from the Department of Biological Sciences at the NUS Faculty of Science, was published online in the journal Environmental Research Letters on 3 March 2020.

Drastic mangrove deforestation

Using satellite images and multiple analytical tools, the NUS team was able to assess the extent of mangrove in 1996. The researchers then followed the fate of every 30-metre x 30-metre mangrove image pixel for 2007 and 2016.

The team's estimates revealed that in 1996, Myanmar had substantially more mangroves than previously estimated. However, over the 20-year period, more than 60 per cent of all mangroves in Myanmar had been permanently or temporarily converted to other uses. These include the growing of rice, oil palm, and rubber, as well as for urbanisation.

"Although fish and prawn farms accounted for only a minor amount of mangrove conversion, this may change in the near future. These competing land cover types are commercially important, but incompatible with mangrove persistence," said Mr De Alban.

Urgent need for mangrove protection in Myanmar

With the loss of nearly two-thirds of its mangroves, there is a need for the Myanmar government to develop holistic strategies to conserve this important habitat. This is particularly important as Myanmar strives to become more integrated into the regional and global markets for agriculture and aquaculture products.

"The fate of mangroves in the country will be tied to the strength of policies and implementation of conservation measures. Through proper long-term planning, management and conservation, this resilient ecosystem can recover and be maintained for the future," shared Assoc Prof Webb.

Air pollution is responsible for shortening people's lives worldwide on a scale far greater than wars and other forms of violence, parasitic and vector-born diseases such as malaria, HIV/AIDS and smoking, according to a study published in Cardiovascular Research [1] today (Tuesday).

Professors Jos Lelieveld and Thomas Münzel, of the Max Planck Institute for Chemistry and the Department of Cardiology of the University Medical Centre Mainz in Mainz, Germany, who led the research, say the findings suggest the world is facing an air pollution "pandemic".

Using a new method of modelling the effects of various sources of air pollution on death rates, the researchers estimated that globally air pollution caused an extra 8.8 million premature deaths a year in 2015. This represents an average shortening of life expectancy of nearly three years for all persons worldwide.

In comparison, tobacco smoking shortens life expectancy by an average of 2.2 years (7.2 million deaths), HIV/AIDS by 0.7 years (1 million deaths), diseases like malaria that are carried by parasites or insects such as mosquitoes, ticks and fleas by 0.6 years (600,000 deaths), and all forms of violence (including deaths in wars) by 0.3 years (530,000 deaths). [2]

The researchers looked at the effect of air pollution on six categories of disease: lower respiratory tract infection, chronic obstructive pulmonary disease, lung cancer, heart disease, cerebrovascular disease leading to stroke, and other, non-communicable diseases, which include conditions such as high blood pressure and diabetes. They found that cardiovascular diseases (heart disease and cerebrovascular disease combined) are responsible for the greatest proportion of shortened lives from air pollution: 43% of the loss in life expectancy worldwide.

They also found that air pollution had a greater effect on shortening lives in older people, with the exception of deaths in children aged under five in low income countries, such as Africa and South Asia. Globally, about 75% of deaths attributed to air pollution occur in people aged over 60 years.

This is the first study to show the effects of air pollution on deaths according to age, type of disease and also its effect on life expectancy at the level of individual countries and regions.

Professor Jos Lelieveld, who is also from the Cyprus Institute Nicosia, Cyprus, said: "It is remarkable that both the number of deaths and the loss in life expectancy from air pollution rival the effect of tobacco smoking and are much higher than other causes of death. Air pollution exceeds malaria as a global cause of premature death by a factor of 19; it exceeds violence by a factor of 16, HIV/AIDS by a factor of 9, alcohol by a factor of 45, and drug abuse by a factor of 60."

Prof Münzel said: "Since the impact of air pollution on public health overall is much larger than expected, and is a worldwide phenomenon, we believe our results show there is an 'air pollution pandemic'. Policy-makers and the medical community should be paying much more attention to this. Both air pollution and smoking are preventable, but over the past decades much less attention has been paid to air pollution than to smoking, especially among cardiologists.

"In this paper we distinguished between avoidable, human-made air pollution and pollution from natural sources such as desert dust and wildfire emissions, which cannot be avoided. We show that about two-thirds of premature deaths are attributable to human-made air pollution, mainly from fossil fuel use; this goes up to 80% in high-income countries. Five and a half million deaths worldwide a year are potentially avoidable.

"It is important that policy-makers and the medical community realise that air pollution is an important risk factor for heart and blood vessel disease. It should be included as risk factor, along with smoking, diabetes and high blood pressure and cholesterol, in the guidelines of the European Society of Cardiology and the American Heart Association on the prevention of acute and chronic heart syndromes and heart failure."

The researchers estimate that if air pollution was reduced by removing fossil fuel emissions, the average life expectancy worldwide would increase by just over a year, and by nearly two years if all human-made emissions were removed.

However, there are large differences between regions due to the diversity in emissions. In East Asia, which has the highest loss of life expectancy due to avoidable air pollution, three of the average of four years of lost life expectancy could be prevented by the removal of human-made emissions; whereas in Africa, where population growth is rapid and pollution from dust predominates, only 0.7 of 3.1 years lost could be prevented. In Europe, there is an average of 2.2 years of lost life expectancy, 1.7 of which could be prevented, and in North America there is an average of 1.4 years of lost life expectancy, of which 1.1 could be prevented, mostly by phasing out fossil fuels.

Prof Lelieveld said: "In Africa, air pollution represents a health risk that is comparable to HIV/AIDS and malaria. However, in most of the rest of the world air pollution is a much greater health risk. When we looked at how pollution played a role in several diseases, its effect on cardiovascular disease was by far the largest - very similar to the effect of smoking. Air pollution causes damage to the blood vessels through increased oxidative stress, which then leads to increases in blood pressure, diabetes, stroke, heart attacks and heart failure."

The researchers used exposure data from a model that simulates atmospheric chemical processes and the way they interact with land, sea and chemicals emitted from natural and human-made sources such as energy generation, industry, traffic and agriculture. They applied these to a new model of global exposure and death rates [3] and to data from the Global Burden of Disease [2], which included information on population density, geographical locations, ages, risk factors for several diseases and causes of death. They estimated the death rates and loss of life expectancy from different causes of air pollution compared to other causes of premature death for countries and regions around the world.

Limitations of the study include the fact there is uncertainty surrounding the estimates, so the size of the effect of air pollution on deaths could be larger or smaller. Nevertheless, such uncertainty also applies to other health risk factors, including smoking. More research is needed to understand fully the mechanisms involved in the associations seen between air pollution and a variety of diseases.

As the Affordable Care Act turns 10 years old, a new study shows it has narrowed racial and ethnic gaps in access to health insurance and health care - but definitely not eliminated them.

Just before the ACA's insurance programs took effect, nearly 25% of African-American adults under 65 and 40% of Hispanic adults in the same age group lacked health insurance, compared with 15% of white adults under 65.

But over the next three years, those numbers had dropped dramatically. So did the size of the gap in insurance rates between whites and the other two groups, according to the new University of Michigan analysis. From 2013 to 2017, the insurance gap between blacks and whites narrowed 45%, and the difference between Hispanics and whites narrowed 35%.

In states that expanded Medicaid, the insurance gap between whites and blacks closed completely when population differences were taken into account.
Even so, more than 27 million Americans still lacked health insurance by 2017. The researchers show this includes 14% of blacks, 25% of Hispanics and 8.5% of whites in the 19-64 age range.

Writing in the March issue of the journal Health Affairs, the researchers also report smaller changes over time in the percentage of adults who said they had gone without health care because of cost. The gaps between whites, blacks and Hispanics in this measure also began to close, but still remained by 2017.

"This is a glass half-full, glass half-empty story," says Thomas Buchmueller, Ph.D., one of two U-M health economists who authored the study. "The half full aspect is that coverage increased and disparities declined, and those with the greatest need tended to benefit. But we still have large disparities, particularly for Hispanic non-citizens. And lack of insurance means lower access to care and poorer health outcomes."

Buchmueller, a professor in U-M's Ross School of Business, and Helen Levy, Ph.D., a research professor at the U-M Institute for Social Research, did the study as a follow-up to their 2016 work tracking the effects of the ACA's programs on insurance disparities after its first year. Buchmueller will present the results March 10 at an ACA anniversary event in Washington, D.C. organized by the journal.

More about the study and the ACA

The new paper is based on data from 2008 to 2017, from nationally representative federal surveys. The researchers focused on adults aged 19 to 64, the age group most affected by the ACA coverage expansions, and limited their analysis to white, black and Hispanic adults due to smaller sample sizes for Asian-Americans and Native Americans.

The ACA was signed into law in March 2010, but its provisions for individuals and businesses to buy insurance directly on state or federal Marketplaces, for individuals to get financial assistance to buy insurance, and for states to choose to expand Medicaid programs for low-income adults, didn't take effect until 2014.

The researchers note that if Medicaid work requirements survive legal challenges, they will disproportionately affect blacks and Hispanic citizens who could potentially lose coverage if they do not meet the requirement. Meanwhile, the Supreme Court may decide the fate of the ACA as a whole, including its insurance programs.

Further results: Medicaid expansion and adjusted data

The new study shows that disparities between groups changed at about the same pace in states that did or didn't implement the ACA Medicaid expansion.

"Medicaid expansion made a big difference for low-income Americans in the states that chose to opt in, but it did so for all racial and ethnic groups, so it did not make a significant difference in how much the gap between whites and blacks or Hispanics closed," says Levy.

She points to work by other U-M researchers including the team that is evaluating Michigan's Medicaid expansion, and U-M's Sarah Miller, Ph.D., who showed a decline in disease-related deaths in Medicaid expansion states.

The study also looks at what percentage of adults in each group said they had gone without some form of medical care in the past year because of its cost, and what percentage said they had a health care provider they considered their usual source of care.

Consistent with differences in health insurance status, whites were less likely to have skipped care because of cost, and more likely to have a usual source of care than blacks or Hispanics before the ACA went into effect.

Starting soon after the ACA's main provisions began taking effect, the gaps between whites and the two other groups began to close, though this trend was modest compared to insurance gains. The percentage of black American adults who reported cost-related avoidance of care actually ticked up slightly from 2016 to 2017.

Older adults with irregular sleep patterns--meaning they have no regular bedtime and wakeup schedule, or they get different amounts of sleep each night--are nearly twice as likely to develop cardiovascular disease as those with more regular sleep patterns, according to a new study funded in part by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health.

The five-year study suggests that an irregular sleep pattern may be a novel and independent risk factor for cardiovascular disease (CVD), and that maintaining regular sleep patterns could help prevent heart disease just as physical activity, a healthy diet, and other lifestyle measures do, the researchers said.

Findings from the prospective study--the first believed to link sleep irregularity to the development of CVD--were published online on March 2 in the Journal of the American College of Cardiology.

"We hope that our study will help raise awareness about the potential importance of a regular sleep pattern in improving heart health. It is a new frontier in sleep medicine," said lead study author Tianyi Huang, Sc.D, an epidemiologist with the Channing Division of Network Medicine at Brigham and Women's Hospital in Boston.

"Research has linked irregular sleep schedules to a constellation of disease-causing abnormalities in body function, including changes in blood sugar and inflammation," said Michael Twery, Ph.D., director of the NHLBI's National Center on Sleep Disorders Research. "This study is Important because it is among the largest of its kind, and it specifically associates these irregular sleep patterns with an increased risk for cardiovascular disease."

Previous studies have linked insufficient amounts of sleep to a higher risk of obesity, diabetes, and heart disease, which is among the reasons doctors emphasize the importance of getting seven to eight hours of sleep per night. Although researchers have suspected that high day-to-day variability in sleep duration and timing might also have negative effects on heart health, its effect remained unclear.

In the current study, the researchers followed 1,992 men and women, 45-84 years old, who did not have CVD at the start of the study. The participants, who were part of the NHLBI-funded Multi-Ethnic Study of Atherosclerosis (MESA), lived in communities across the United States. Of the participants, about 38% were white, 28% African American, 22% Hispanic, and 12% Chinese American. They were followed for about five years (2010-2016) after having a sleep examination.

To measure sleep irregularity, the participants wore actigraph devices on their wrists to closely track sleep and wake activity for seven consecutive days, including weekends. The actigraphs resemble smart watches but are designed to specifically measure whether a person is active or at rest, which correlates to wakefulness and sleep. They also underwent a one-night at-home polysomnography--a comprehensive sleep test--at the beginning of the study and took a questionnaire-based sleep assessment.

During the five-year follow-up period, 111 participants developed CVD events, including heart attack and stroke, or died from CVD-related causes. The researchers found that participants with the most irregular sleep duration or timing had more than double the risk of developing a CVD event over the follow-up period compared to those with the most regular sleep patterns. The associations remained strong even after adjusting for known cardiovascular risk factors and other sleep variables such as obstructive sleep apnea and average sleep duration, the researchers said.

The association between irregular sleep and CVD appeared stronger among racial/ethnic minority populations, particularly African Americans, than among whites, the researchers said. This finding is consistent with recent studies that show racial minorities tend to have a higher risk of sleep disorders than whites. Although past studies suggest that women are more likely than men to be affected by unhealthy sleep, the current study did not find significant gender differences.

The researchers said they are still unclear about the exact biological mechanisms behind the sleep irregularity and CVD link, but they suspect that multiple factors, including harmful disturbances in the body's circadian rhythm--the 24-hour internal body clock which controls the sleep-wake cycle--may be in play. Recent studies by the same researchers linked irregular sleep patterns to harmful metabolic changes associated with obesity, diabetes, and high cholesterol, and they suspect similar processes might also influence CVD risk.

In future studies, the researchers said they will look for blood biomarkers that may help explain the apparent link. Larger studies with longer follow-up will also be important to confirm these findings. A better understanding of the root causes could lead to new interventions that could help people better regulate their sleep patterns, such as wearing devices or using specialized mobile apps designed to reduce irregular sleep, the researchers said. Medicinal interventions also may be possible, they noted.