kaori
last scene
ikimono gakari
avoided quasiparticle decay from strong quantum interactions
ruben verresen et al. 2019
doi.org/10.1038/s41567-019-0535-3
"Until now, the assumption was that quasiparticles in interacting quantum systems decay after a certain time. We now know that the opposite is the case: strong interactions can even stop decay entirely," explains Frank Pollmann, Professor for Theoretical Solid-State Physics at the TUM. Collective lattice vibrations in crystals, so-called phonons, are one example of such quasiparticles.
The concept of quasiparticles was coined by the physicist and Nobel prize winner Lev Davidovich Landau. He used it to describe collective states of lots of particles or rather their interactions due to electrical or magnetic forces. Due to this interaction, several particles act like one single one.
Numeric methods open up new perspectives
Up until now, it wasn't known in detail which processes influence the fate of these quasiparticles in interacting systems," says Pollmann. "It is only now that we possess numerical methods with which we can calculate complex interactions as well as computers with a performance which is high enough to solve these equations."
"The result of the elaborate simulation: admittedly, quasiparticles do decay, however new, identical particle entities emerge from the debris," says the lead author, Ruben Verresen. "If this decay proceeds very quickly, an inverse reaction will occur after a certain time and the debris will converge again. This process can recur endlessly and a sustained oscillation between decay and rebirth emerges."
From a physical point of view, this oscillation is a wave which is transformed into matter, which, according to quantum mechanical wave-particle duality, is possible. Therefore, the immortal quasiparticles do not transgress the second law of thermodynamics. Their entropy remains constant, decay has been stopped.
The reality check
The discovery also explains phenomena which were baffling until now. Experimental physicists had measured that the magnetic compound Ba3CoSB2O9 is astonishingly stable. Magnetic quasiparticles, magnons, are responsible for it. Other quasiparticles, rotons, ensure that helium which is a gas on the Earth's surface becomes a liquid at absolute zero which can flow unrestricted.
abstract Quantum states of matter—such as solids, magnets and topological phases—typically exhibit collective excitations (for example, phonons, magnons and anyons)1. These involve the motion of many particles in the system, yet, remarkably, act like a single emergent entity—a quasiparticle. Known to be long lived at the lowest energies, quasiparticles are expected to become unstable when encountering the inevitable continuum of many-particle excited states at high energies, where decay is kinematically allowed. Although this is correct for weak interactions, we show that strong interactions generically stabilize quasiparticles by pushing them out of the continuum. This general mechanism is straightforwardly illustrated in an exactly solvable model. Using state-of-the-art numerics, we find it at work in the spin-1/2 triangular-lattice Heisenberg antiferromagnet (TLHAF). This is surprising given the expectation of magnon decay in this paradigmatic frustrated magnet. Turning to existing experimental data, we identify the detailed phenomenology of avoided decay in the TLHAF material2 Ba3CoSb2O9, and even in liquid helium3,4,5,6,7,8, one of the earliest instances of quasiparticle decay9. Our work unifies various phenomena above the universal low-energy regime in a comprehensive description. This broadens our window of understanding of many-body excitations, and provides a new perspective for controlling and stabilizing quantum matter in the strongly interacting regime.
the collapse of complex societies
joseph tainter 1988 978-0521386739
diminishing returns
speculation
quotes gregory bateson on flexibility
volney on decline
the ruins; or, meditation on the revolutions of empires and the law of nature
to read next
translated jefferson–barlow
gutenberg.org/ebooks/1397
via en.m.wikipedia.org/wiki/Constantin_François_de_Chassebœuf,_comte_de_Volney
donald trump and the coming fall of american empire
jeremy scahill 2017
theintercept.com/2017/07/22/donald-trump-and-the-coming-fall-of-american-empire/
kohler
antifragile: things that gain from disorder
nassim taleb 2014 9780679645276
hormesis
domain independence
taleb believes variance in “ability” of males is larger than variance in “ability” of females
from his blog:
“Now let us get deeper into the application of the Silver Rule in intellectual debates. You can criticize either what a person said or what the person meant. The former is more sensational, hence lends itself more readily to dissemination. The mark of a charlatan –say the journalist Sam Harris –is to defend his position or attack a critic by focusing on some of his/her specific statement (“look at what he said”) rather than blasting his exact position (“look at what he means” or, more broadly, “look at what he stands for”), the latter of which requires an extensive grasp of the proposed idea. Note that the same applies to the interpretation of religious texts, often extracted from their broader circumstances.”
but in the heat of the moment in a twitter spat against Mary beard, he does exactly what he laments here.
is it the fate of all great thinkers to end up like this? to make the great ideas they need to believe in themselves, but in the end this becomes their downfall as this belief means they no longer respond to reality, a reality that has now moved beyond their idea.
or is this the fate of everyone, and is why we must all eventually die to make room for those who are still malleable?
massimo pigliucchi thinks taleb has fallen for scientism
iainews.iai.tv/articles/beard-nassem-taleb-twitter-feud-and-dangers-of-scientism-auid-868
the true tempo of evolutionary radiation and decline revealed on the hawaiian archipelago
jun y. lim, charles r. marshall 2017
doi.org/10.1038/nature21675
anthropogenic strath terrace formation caused by reduced sediment retention
sarah a. schanz et al. 2019
doi.org/10.1073/pnas.1814627116
"In the last century, we have more river incision in this area than expected. Something caused these rivers to start eroding a lot more," said lead author Sarah Schanz, a former UW doctoral student who is now a postdoctoral researcher at Indiana University. "We know the Teanaway River has eroded into bedrock before, naturally -- it has some terraces that are 1,800 years old. But this current cycle is anthropogenic, or human-driven."
Results show that practices related to logging caused bedrock incision of up to 2 meters (6 feet) along the riverbed. As much as a half of what had been a floodplain was transformed into a new terrace abutting the river.
"This is the first time that we've been able to pinpoint erosion into bedrock due to human action," Schanz said. "Most rivers are eroding at about a tenth of a millimeter per year. This is about 100 times that amount."
The discovery means this beautiful riverbank resulted from human action, not natural forces. It could change how geologists think about landscapes in other parts of the world, such as Taiwan, with its long history of intense human activity.
The study began 20 years ago when co-author Brian Collins, a UW senior lecturer in river geology, was curious why there was so much exposed bedrock in the Teanaway.
Collins also noticed unusual river terraces, the stepped structures along the river bank resulting from cycles of the river flooding and then running more quickly, cutting a new channel deeper into the sediment. He led a 2016 study that calculated short-term changes in the Teanaway's western fork and suggested logging may have caused the river to cut a new channel.
This site in a community forest offered good access for regular visits by the research team and undergraduate assistants to all three forks. By combining newspaper records, material from the UW Libraries Special Collections, Central Washington University and the local Kittitas County historical society, the researchers were able to piece together and confirm the full history.
Before logging roads existed, companies built temporary "splash dams" high up on the slope with all the logs and then broke up the dam with tools or explosives. Released water helped send logs shooting down to the mills.
"It was such an event that schools closed, and newspaper records show it really well," Schanz said. "People who are still alive today, some of their earliest memories are of going to see it."
Key to the process is that loggers would clear away debris to give the logs a clear shot down the river. This removed barriers that held back sediment and cleared out much of the gravel from the riverbed. Such events, the authors believe, caused the erosion to change dramatically.
"If you have too much sediment, you're basically protecting the river from erosion. But if you have not enough sediment, as that sediment is moving along, it starts to hit the bedrock and erode it," Schanz said.
David Montgomery, a UW professor of Earth and space sciences, and the other two co-authors used many techniques to analyze the four youngest terraces on the river's edge, including LIDAR maps, carbon dating of rocks and computer models. In 1999 the team even hammered nails into the bedrock and measured the erosion rates directly.
Many rivers, including the Teanaway, have individual features that show evidence of human impact on areas of bedrock. But this is the first time an entire river basin is found to have been transformed by human activity.
"This is a direct topographic signature of the Anthropocene, the 'age of humans' that we now live in," Montgomery said. "The finding that terrace surfaces in the Teanaway are recently-abandoned floodplains suggests that similar landforms around the world may also reflect the influence of human activity."
The UW team recently published an overview paper looking at where river terraces have formed worldwide over the past 4,000 years. The authors showed that in many cases, river terrace formation coincided with deforestation.
"It's sort of a hand-wavey linkage at this point, but I think this could be prevalent worldwide," said Schanz. "It's just not a signal that we've known to look for before."
Schanz will start a faculty position in August at Colorado College, where she plans also to explore what the finding means for how river canyons form through natural processes.
"I think the human part is really interesting, but what has broader implications, for me, is the proof that if you change how sediment moves through a river, you can change erosion rates," Schanz said.
ends of the world
peter brannen 2017
to read next
from dead woods to triumph of nature, 30 years after the Great Storm
dan glaister 2017
theguardian.com/environment/2017/oct/15/british-woodlands-30-years-after-great-storm
The devastating winds of 1987 felled 15 million trees but also prompted a radical change to the way we work with the countryside to let it heal itself
It is remembered as a generation-defining moment, the night when ships ran aground, London endured its first blackout since the Blitz, 18 people died and 15 million trees were toppled. But the devastation wrought by the Great Storm of 1987 also left in its wake a startling woodland recovery, prompting a radical reshaping of the way we work with nature to care for the countryside.
Thirty years ago on Monday the storm hit south-east England after a fierce wind swooped up from the Bay of Biscay, across a corner of northern France before making landfall in the south-west and sweeping through southern England to bring the full force of its 100mph winds to bear on the south-east.
The storm did its work during the early hours of the morning, leaving behind a landscape that looked as if it had been subject to the whim of a particularly malevolent giant. “It seemed as if someone had pulled a curtain to one side to reveal a formless scene that bordered upon the underworld,” wrote the German writer WG Sebald in his 1995 novel The Rings of Saturn. “Entire tracts of woodland were pressed down flat as if they had been cornfields.”
For the then home secretary Douglas Hurd, the storm had produced “the most widespread night of devastation in the south-east since 1945”.
Ray Townsend, like most people living in the south-east at the time, vividly remembers the morning of the storm. “I remember waking up at 5.30 and there was no electricity. So I looked out of the window and it was completely dark. It was quite eerie.”
Townsend eventually arrived at Kew Gardens where he worked, and where he is now the arboretum manager. “The gardens at Kew had been obliterated,” he recalls. “The trees had gone over like dominoes. The wind had come off the river and the trees had gone down like a channel, a tunnel. Within that tunnel there was tremendous devastation. Some of the trees had been corkscrewed by the wind, like twisting the lid off a jar.”
A few miles away, at the National Trust’s Leith Hill site in Surrey, Paul Redsell had just settled into his new job as warden. He was woken at 6.30 by a neighbour asking for help to free a horse trapped in a stable by a fallen tree. Setting off on his motorbike to search for a working telephone, he came across trees laying on tracks and roads that were so obscured by debris that the only way of knowing where they ran was by following the raised banking on each side.
Eventually making his way to the top of Leith Tower, he was able to gain a view of the new landscape. “What was quite clear was that the storm had dipped in and out, there was devastation but not everywhere – there were pockets of destruction,” he says.
Redsell, who is now countryside manager at Leith Hill, followed what was then standard practice after a severe storm: he started to clear up. “Man loves being in control,” he says. “It was a natural event, and at the time there was almost a sense of urgency to go out and clean up. Once we’d gone in with machines and contractors and loading bays and all the rest of it, we were causing more damage than the storm had in some places. The urge was to remove all the fallen trees and then plant new ones with little plastic tubes around them.”
The clearing operations removed trees that might have regenerated and compacted soil that could have provided fertile ground for wild flowers. Intervention and clearing was not practised everywhere, however. At another National Trust site, Toys Hill, near Sevenoaks in Kent – which lost six of its eponymous oaks – 98% of the trees fell, and while clearing work took place across much of the site, an “exclusion zone” was set aside to allow nature the opportunity to repair the damage itself.
“Scords Wood was left alone,” says Tom Hill, the National Trust’s trees and woodlands specialist. “There’s been no intervention at all, and it’s now a thriving woodland in terms of its diversity.”
In nearby Knole Park, most of the trees that fell were also left, benefiting fungi, plants and wildlife, while in the neighbouring Emmetts Garden, where 95% of its surrounding woodland was lost, tree stumps and fallen specimens remain in the formal setting as a reminder of the storm.
Hill says the storm had a profound effect on the way we care for our woodland, with an understanding that decay has a role in promoting new life, and that nature is more than capable of adapting to changed conditions, and might even need them to survive. “There’s a better appreciation of decay as a natural process,” Hill says. “Veteran trees have decay and growth happening at the same time. One of the biggest attitudes that changed was the process of decay being seen as an integrated part of life not just something dirty or rotten.
“Storms mix things up, they allow light to get in, which is a vital factor. Toys Hill is like a mosaic of different habitats and light and shade, and it has a very diverse structure. That’s exactly what you want if you’re seeking to maintain healthy woodland. Destruction is very important, and nature is self-destructive and self-healing at the same time.”
Ed Ikin, head of landscapes and horticulture at Kew Gardens’s Wakehurst estate in West Sussex, where 20,000 trees were lost, says the storm marked a turning point. “It was the end of a chapter that dated back 200 years, the curation of trees knitted into ancient medieval woodland. People were disorientated, they couldn’t navigate, facing three years of tidying up. But in the midst of all of that trauma, what emerged was a grand vision, a desire to do something different with the wild landscape.”
That something was to promote diversity and to understand that we can learn from nature how to protect woodland and to adapt to extreme natural events.
“It’s hardwired into the ecology of some areas to have this moment of violence,” says Ikin. “Pre-1987 we had allowed too much of our tree stock to get to a similar age. The storm generated horizontal tornadoes, and we had created vertical planes of trees. Now we promote ‘shelter belts’ of trees to buffer and filter high winds.”
The lessons learned are starting to bear fruit, says Ikin. “Thirty years gives us the first real opportunity to look at the woodland and see if it’s doing what it was supposed to do. I think we’re starting to achieve something extraordinary.”
the spirit of history: hegel’s search for the universal patterns of history revealed a paradox: freedom is coming into being, but is never guaranteed
terry pinkard 2019
aeon.co/essays/what-is-history-nobody-gave-a-deeper-answer-than-hegel
if
bread
if a picture paints a thousand words
then why can't i paint you?
the words will never show
the you i've come to know
if a face could launch a thousand ships
then where am i to go?
there's no one home but you
you're all that's left me too
and when my love for life is running dry
you come and pour yourself on me
if a man could be two places at one time
i'd be with you
tomorrow and today
beside you all the way
if the world should stop revolving
spinning slowly down to die
i'd spend the end with you
and when the world was through
then one by one the stars would all go out
then you and i would simply fly away
a model-based approach to the tempo of “collapse”: the case of rapa nui (easter island)
robert j. dinapoli et al. 2020
doi.org/10.1016/j.jas.2020.105094
abstract •Collapse hypothesis for Easter Island tested using Bayesian models.
•Tempo plots quantify the onset, rate, and end of monument construction.
•Results contradict ‘collapse’ scenario for Rapa Nui.
•Tempo plots provide means for evaluating collapse hypotheses.
Rapa Nui (Easter Island, Chile) presents a quintessential case where the tempo of investment in monumentality is central to debates regarding societal collapse, with the common narrative positing that statue platform (ahu) construction ceased sometime around AD 1600 following an ecological, cultural, and demographic catastrophe. This narrative remains especially popular in fields outside archaeology that treat collapse as historical fact and use Rapa Nui as a model for collapse more generally. Resolving the tempo of “collapse” events, however, is often fraught with ambiguity given a lack of formal modeling, uncritical use of radiocarbon estimates, and inattention to information embedded in stratigraphic features. Here, we use a Bayesian model-based approach to examine the tempo of events associated with arguments about collapse on Rapa Nui. We integrate radiocarbon dates, relative architectural stratigraphy, and ethnohistoric accounts to quantify the onset, rate, and end of monument construction as a means of testing the collapse hypothesis. We demonstrate that ahu construction began soon after colonization and increased rapidly, sometime between the early-14th and mid-15th centuries AD, with a steady rate of construction events that continued beyond European contact in 1722. Our results demonstrate a lack of evidence for a pre-contact ‘collapse’ and instead offer strong support for a new emerging model of resilient communities that continued their long-term traditions despite the impacts of European arrival. Methodologically, our model-based approach to testing hypotheses regarding the chronology of collapse can be extended to other case studies around the world where similar debates remain difficult to resolve.
rapid colonization and turnover of birds in a tropical forest treefall gap
henry s. pollock et al. 2020
doi.org/10.1111/jofo.12328
When the tree fell that October in 2015, the tropical giant didn't go down alone. Hundreds of neighboring trees went with it, opening a massive 2.5-acre gap in the Panamanian rainforest.
Treefalls happen all the time, but this one just happened to occur in the exact spot where a decades-long ecological study was in progress, giving University of Illinois researchers a rare look into tropical forest dynamics.
"I've been walking around that tree for 30 years now. It was just humongous," says Jeff Brawn, Professor and Stuart L. and Nancy J. Levenick Chair in Sustainability in the Department of Natural Resources and Environmental Sciences at Illinois. "Here we are, running around on this plot for years and all of a sudden I couldn't even find my way around. We just lucked into it."
What's lucky is that Brawn and his colleagues had amassed decades of data on the bird community in that exact spot, meaning they had a clear before-and-after view of what a treefall could mean for tropical birds.
This particular gap meant hummingbirds. Lots and lots of hummingbirds.
"After the treefall, we saw a very large spike in the total number of hummingbird species," says Henry Pollock, a postdoctoral scholar working with Brawn and lead author on a study published in the Journal of Field Ornithology. "Within the previous 25 years of the study, we had only documented three or four hummingbird species, and they were usually present in low numbers. There was one species, the snowy-bellied hummingbird, which we had never captured on either of our two plots in 25 years of sampling. The year after the treefall happened, we got 16 unique individuals of this one species, and total diversity of hummingbirds more than doubled."
The gap also attracted fruit-eating birds. The researchers documented a doubling of this group compared to pre-treefall numbers, with certain species being more than three times as abundant. Other species, including the thick-billed seed-finch, which typically inhabits grasslands, appeared as if out of thin air.
"They just swooped in," Brawn says. "It's analogous to a backyard bird feeder. As soon as you put one in, you'll see species you've never seen before."
And then, almost as quickly, the birds disappeared.
Within one to four years, depending on the species, the birds returned to pre-treefall numbers or were not detected again.
"What that suggests is these birds are incredibly mobile and opportunistic," Pollock says. "They are probably just cruising around the landscape prospecting for their preferred food sources and habitats. Given the sheer size of this gap, it acted as a sort of magnet, pulling in species from potentially kilometers away. I mean, 16 snowy-bellied hummingbirds and we've never caught one before? It's pretty astounding."
Treefalls are a common and necessary occurrence in forests all over the world. As sunshine streams in from above, trees hunkered down in the understory finally get their chance to rise. Basking in the suddenly resource-rich environment, tropical trees and other plants produce nectar-filled flowers and fruit, important food sources for birds and other animals.
Previous research has hinted at how important these food sources are for tropical birds, but no one had documented before-and-after differences until now. Instead, researchers typically compared treefall gaps with intact forest areas at a single time point. That approach has its uses, but it can't capture what Brawn and Pollock found: just how quickly the birds arrived on the scene, and how quickly they left.
"I was just really just astonished at how quickly and how efficiently these birds seem to be able to find and exploit a new source of food," Brawn says.
Gaps don't stay open long in the tropics. Understory trees shoot up, elbowing each other out of the way to take the top spot. Soon, there's no evidence a gap -- or its riotous array of feathered occupants -- was there at all.
As short-lived as they may be, treefall gaps represent critical opportunities for species turnover, especially in the tropics where forest fires are comparatively rare.
"This kind of periodic disturbance is probably necessary for these birds to persist in the landscape matrix," Pollock says. "That's true for many organisms and ecosystems; our study provides evidence to back that up in these birds."
abstract Ecological disturbance is an important factor that influences the abundance and distribution of species. Treefalls are a prominent source of disturbance in tropical forests, but robust characterization of community change after treefalls requires baseline data that are often not available. We capitalized on 25 yr of avian mark–recapture data from a lowland moist forest in central Panama to investigate the timescale of colonization and persistence of birds in a newly formed treefall gap. We compared bird species assemblages pre‐ and post‐treefall to explore how the disturbance affected specific foraging guilds and overall assemblage structure (abundance and alpha diversity). We documented rapid colonization (i.e., within five months post‐treefall) of the treefall gap by birds. Abundance and alpha diversity increased following the treefall, but both remained relatively constant in a nearby control plot. At the guild level, frugivores spiked in abundance and nectarivores (i.e., hummingbirds) increased in alpha diversity following the treefall. These results are in agreement with those of previous spatial studies of gap dynamics and suggest that certain tropical frugivores and nectarivores have a remarkable ability to rapidly find and exploit preferred resources and microhabitats embedded in a landscape matrix. Assemblage abundance and alpha diversity decreased back to pre‐treefall levels within 1 and 4 yr of the treefall, respectively. Thus, even large gaps may provide only ephemeral benefits, highlighting the importance of periodic disturbance for landscape‐level persistence of species that use gaps.
quantifying greenhouse gas emission of asphalt pavement preservation at construction and use stages using life-cycle assessment
hao wang et al. 2018
doi.org/10.1080/15568318.2018.1519086
The researchers found that extending the life of pavement through preventive maintenance can reduce greenhouse gases by up to 2 percent; transportation agencies can cut spending by 10 percent to 30 percent; and drivers can save about 2 percent to 5 percent in fuel consumption, tire wear, vehicle repair and maintenance costs because of smoother surfaces.
The research will help transportation agencies choose appropriate maintenance strategies that consider environmental impacts in decision-making.
"When pavement is in its early failure stage, preventive maintenance can restore performance and extend pavement life with lower costs," said study lead author Hao Wang, an associate professor who focuses on infrastructure engineering in the Department of Civil and Environmental Engineering at Rutgers University-New Brunswick. "Pavement preservation leads to significant environmental benefits due to the improved surface condition, which results in smooth pavement, saves energy and reduces user costs."
The transportation sector is the largest source of greenhouse gas emissions, primarily carbon dioxide from cars, trucks and buses. The researchers used the long-term pavement performance (LTPP) database maintained by Federal Highway Administration of U.S. Department of Transportation to measure the environmental impact of roadway repairs, especially preserving asphalt pavement, in terms of carbon dioxide emissions linked to global warming.
The study used a full life-cycle approach to look at the carbon footprint of common ways to preserve pavement. Treatments include thin overlay (placing up to 2 inches of asphalt on roads), chip seal (spraying asphalt emulsion on pavement and laying aggregate), slurry seal (spreading a slurry over pavement) and crack seal (filling cracks with rubberized asphalt or polymer-modified asphalt with some filler).
The study found that thin overlay leads to the greatest overall reduction in carbon dioxide emissions -- 2 percent -- because of a large decrease in road roughness. The crack seal method led to the lowest emission reduction -- 0.5 percent -- but all preventive maintenance methods reduce emissions overall. The researchers further developed the life-cycle assessment tool for evaluating the environmental impact of roadway projects
abstract This article focused on quantifying environmental impact of asphalt pavement preservation at construction and use stage using life-cycle assessment (LCA) approach. Preservation treatments considered in the analysis include thin overlay, chip seal, and crack seal that are typically used by highway agencies. At construction stage, there are significant differences in emissions caused by various preservation treatments mainly due to different raw material components and manufacturing processes. At use stage, fuel consumptions vary significantly depending on tire rolling resistance that is affected by pavement surface characteristics. The Carbon Dioxide (CO2) emissions at the use stage were predicted using the Motor Vehicle Emission Simulator (MOVES) and pavement roughness models obtained from Long-Term Pavement Performance (LTPP) program. The results show that pavement preservation brings significant environmental benefit in reduction of CO2 emission due to the improved pavement surface condition despite the emission generated at construction stage. Thin overlay produces the highest life-cycle reduction in CO2 emission due to the large International Roughness Index (IRI) jump after treatment; while crack seal has the lowest reduction of CO2 emission. The optimum application timing of preservation treatment was determined for chip seal and thin overlay assuming one-time treatment applied before reaching the IRI threshold.
明日があるさ
ASHITAgaaru
坂本九
the k-core as a predictor of structural collapse in mutualistic ecosystems
flaviano morone et al. 2018
doi.org/10.1038/s41567-018-0304-8
women live longer than men even during severe famines and epidemics
virginia zarulli et al. 2018
doi.org/10.1073/pnas.1701535115
three centuries of historical records show that women don't just outlive men in normal times: They're more likely to survive even in the worst of circumstances, such as famines and epidemics, researchers report.
Most of the life expectancy gender gap was due to a female survival advantage in infancy rather than adulthood, the researchers found. In times of adversity, newborn girls are more likely to survive.
The fact that women have an edge in infancy, when behavioral differences between the sexes are minimal, supports the idea that explanation is at least partly biological, the researchers say.
Led by Virginia Zarulli, an assistant professor at the University of Southern Denmark, and James Vaupel, a research professor at Duke University, the team analyzed mortality data going back roughly 250 years for people whose lives were cut short by famine, disease or other misfortunes.
The data spanned seven populations in which the life expectancy for one or both sexes was a dismal 20 years or less. Among them were working and former slaves in Trinidad and the United States in the early 1800s, famine victims in Sweden, Ireland and the Ukraine in the 18th, 19th and 20th centuries, and Icelanders affected by the 1846 and 1882 measles epidemics.
In Liberia, for example, freed American slaves who relocated to the West African country in the 1800s experienced the highest mortality rates ever recorded. More than 40 percent died during their first year, presumably wiped out by tropical diseases they had little resistance to. Babies born during that time rarely made it past their second birthday.
Another group of people living in Ireland in the 1840s famously starved when a potato blight caused widespread crop failure. Life expectancy plummeted by more than 15 years.
Overall the researchers discovered that, even when mortality was very high for both sexes, women still lived longer than men by six months to almost four years on average.
Girls born during the famine that struck Ukraine in 1933, for example, lived to 10.85, and boys to 7.3 -- a 50 percent difference.
When the researchers broke the results down by age group, they found that most of the female survival advantage comes from differences in infant mortality. Newborn girls are hardier than newborn boys.
The results suggest that the life expectancy gender gap can't be fully explained by behavioral and social differences between the sexes, such as risk-taking or violence.
Instead, the female advantage in times of crisis may be largely due to biological factors such as genetics or hormones. Estrogens, for example, have been shown to enhance the body's immune defenses against infectious disease.
"Our results add another piece to the puzzle of gender differences in survival," the researchers said.
Women live longer than men in nearly all populations today. Some research focuses on the biological origins of the female advantage; other research stresses the significance of social factors. We studied male–female survival differences in populations of slaves and populations exposed to severe famines and epidemics. We find that even when mortality was very high, women lived longer on average than men. Most of the female advantage was due to differences in mortality among infants: baby girls were able to survive harsh conditions better than baby boys. These results support the view that the female survival advantage is modulated by a complex interaction of biological environmental and social factors.
Abstract
Women in almost all modern populations live longer than men. Research to date provides evidence for both biological and social factors influencing this gender gap. Conditions when both men and women experience extremely high levels of mortality risk are unexplored sources of information. We investigate the survival of both sexes in seven populations under extreme conditions from famines, epidemics, and slavery. Women survived better than men: In all populations, they had lower mortality across almost all ages, and, with the exception of one slave population, they lived longer on average than men. Gender differences in infant mortality contributed the most to the gender gap in life expectancy, indicating that newborn girls were able to survive extreme mortality hazards better than newborn boys. Our results confirm the ubiquity of a female survival advantage even when mortality is extraordinarily high. The hypothesis that the survival advantage of women has fundamental biological underpinnings is supported by the fact that under very harsh conditions females survive better than males even at infant ages when behavioral and social differences may be minimal or favor males. Our findings also indicate that the female advantage differs across environments and is modulated by social factors.
if tomorrow never comes
garth brookes soundcloud
sometimes late at night
i lie awake and watch her sleeping
she’s lost in peaceful dreams
so i turn out the lights and lay there in the dark
and the thought crosses my mind
if i never wake in the morning
would she ever doubt the way i feel
about her in my heart
☆if tomorrow never comes
will she know how much i loved her
did i try in every way to show her every day
that she’s my only one
and if my time on earth were through
and she must face the world without me
will the love i gave her in the past
be enough to last
if tomorrow never comes
for i’ve lost loved ones in my life
who never knew how much i loved them
now i live with the regret
that my true feelings for them never were revealed
so i made a promise to myself
to say each day how much she means to me
and avoid that circumstance
where there’s no second chance
to tell her how i feel
☆repeat
so tell that someone that you love
just what you’re thinking of
if tomorrow never comes
stanford accelerated intelligent neuromodulation therapy for treatment-resistant depression
eleanor j. cole et al. 2020
doi.org/10.1176/appi.ajp.2019.19070720
A new form of magnetic brain stimulation rapidly relieved symptoms of severe depression in 90% of participants in a small study conducted by researchers at the Stanford University School of Medicine.
The researchers are conducting a larger, double-blinded trial in which half the participants are receiving fake treatment. The researchers are optimistic the second trial will prove to be similarly effective in treating people whose condition hasn't improved with medication, talk therapy or other forms of electromagnetic stimulation.
The treatment is called Stanford Accelerated Intelligent Neuromodulation Therapy, or SAINT. It is a form of transcranial magnetic stimulation, which is approved by the Food and Drug Administration for treatment of depression. The researchers reported that the therapy improves on current FDA-approved protocols by increasing the number of magnetic pulses, speeding up the pace of the treatment and targeting the pulses according to each individual's neurocircuitry.
Before undergoing the therapy, all 21 study participants were severely depressed, according to several diagnostic tests for depression. Afterward, 19 of them scored within the nondepressed range. Although all of the participants had suicidal thoughts before the therapy, none of them reported having suicidal thoughts after treatment. All 21 participants had previously not experienced improvements with medications, FDA-approved transcranial magnetic stimulation or electroconvulsive therapy.
The only side effects of the new therapy were fatigue and some discomfort during treatment, the study reported. The results will be published online April 6 in the American Journal of Psychiatry.
"There's never been a therapy for treatment-resistant depression that's broken 55% remission rates in open-label testing," said Nolan Williams, MD, assistant professor of psychiatry and behavioral sciences and a senior author of the study. "Electroconvulsive therapy is thought to be the gold standard, but it has only an average 48% remission rate in treatment-resistant depression. No one expected these kinds of results."
Calming the brain chatter
When Deirdre Lehman, 60, woke up the morning of June 30, 2018, she said she was hit by "a tsunami of darkness." Lehman had struggled with bipolar disorder all her adult life, but with medications and psychotherapy her mood had been stable for 15 years.
"There was a constant chattering in my brain: It was my own voice talking about depression, agony, hopelessness," she said. "I told my husband, 'I'm going down and I'm heading toward suicide.' There seemed to be no other option."
Lehman's psychiatrist had heard of the SAINT study and referred her to Stanford. After researchers pinpointed the spot in her brain that would benefit from stimulation, Lehman underwent the therapy.
"By the third round, the chatter started to ease," she said. "By lunch, I could look my husband in the eye. With each session, the chatter got less and less until it was completely quiet.
"That was the most peace there's been in my brain since I was 16 and started down the path to bipolar disorder."
In transcranial magnetic stimulation, electric currents from a magnetic coil placed on the scalp excite a region of the brain implicated in depression. The treatment, as approved by the FDA, requires six weeks of once-daily sessions. Only about half of patients who undergo this treatment improve, and only about a third experience remission from depression.
Stanford researchers hypothesized that some modifications to transcranial magnetic stimulation could improve its effectiveness. Studies had suggested that a stronger dose, of 1,800 pulses per session instead of 600, would be more effective. The researchers were cautiously optimistic of the safety of the treatment, as that dose of stimulation had been used without harm in other forms of brain stimulation for neurological disorders, such as Parkinson's disease.
Other studies suggested that accelerating the treatment would help relieve patients' depression more rapidly. With SAINT, study participants underwent 10 sessions per day of 10-minute treatments, with 50-minute breaks in between. After a day of therapy, Lehman's mood score indicated she was no longer depressed; it took up to five days for other participants. On average, three days of the therapy were enough for participants to have relief from depression.
"The less treatment-resistant participants are, the longer the treatment lasts," said postdoctoral scholar Eleanor Cole, PhD, a lead author of the study.
Strengthening a weak connection
The researchers also conjectured that targeting the stimulation more precisely would improve the treatment's effectiveness. In transcranial magnetic stimulation, the treatment is aimed at the location where most people's dorsolateral prefrontal cortex lies. This region regulates executive functions, such as selecting appropriate memories and inhibiting inappropriate responses.
For SAINT, the researchers used magnetic-resonance imaging of brain activity to locate not only the dorsolateral prefrontal cortex, but a particular subregion within it. They pinpointed the subregion in each participant that has a relationship with the subgenual cingulate, a part of brain that is overactive in people experiencing depression.
In people who are depressed, the connection between the two regions is weak, and the subgenual cingulate becomes overactive, said Keith Sudheimer, PhD, clinical assistant professor of psychiatry and a senior author of the study. Stimulating the subregion of the dorsolateral prefrontal cortex reduces activity in the subgenual cingulate, he said.
To test safety, the researchers evaluated the participants' cognitive function before and after treatment. They found no negative side effects; in fact, they discovered that the participants' ability to switch between mental tasks and to solve problems had improved -- a typical outcome for people who are no longer depressed.
One month after the therapy, 60% of participants were still in remission from depression. Follow-up studies are underway to determine the duration of the antidepressant effects.
The researchers plan to study the effectiveness of SAINT on other conditions, such as obsessive-compulsive disorder, addiction and autism spectrum disorders.
'Resilient and stable'
The depression Lehman woke up to almost two years ago was the worst episode she had ever experienced. Today, she said, she is happy and calm.
Since undergoing SAINT treatment, she has completed a bachelor's degree at the University of California-Santa Barbara; she had dropped out as a young woman when her bipolar symptoms overwhelmed her studies.
"I used to cry over the slightest thing," she said. "But when bad things happen now, I'm just resilient and stable. I'm in a much more peaceful state of mind, able to enjoy the positive things in life with the energy to get things done."
abstract New antidepressant treatments are needed that are effective, rapid acting, safe, and tolerable. Intermittent theta-burst stimulation (iTBS) is a noninvasive brain stimulation treatment that has been approved by the U.S. Food and Drug Administration for treatment-resistant depression. Recent methodological advances suggest that the current iTBS protocol might be improved through 1) treating patients with multiple sessions per day at optimally spaced intervals, 2) applying a higher overall pulse dose of stimulation, and 3) precision targeting of the left dorsolateral prefrontal cortex (DLPFC) to subgenual anterior cingulate cortex (sgACC) circuit. The authors examined the feasibility, tolerability, and preliminary efficacy of Stanford Accelerated Intelligent Neuromodulation Therapy (SAINT), an accelerated, high-dose resting-state functional connectivity MRI (fcMRI)–guided iTBS protocol for treatment-resistant depression.
Methods:
Twenty-two participants with treatment-resistant depression received open-label SAINT. fcMRI was used to individually target the region of the left DLPFC most anticorrelated with sgACC in each participant. Fifty iTBS sessions (1,800 pulses per session, 50-minute intersession interval) were delivered as 10 daily sessions over 5 consecutive days at 90% resting motor threshold (adjusted for cortical depth). Neuropsychological testing was conducted before and after SAINT.
Results:
One participant withdrew, leaving a sample size of 21. Nineteen of 21 participants (90.5%) met remission criteria (defined as a score <11 on the Montgomery-Åsberg Depression Rating Scale). In the intent-to-treat analysis, 19 of 22 participants (86.4%) met remission criteria. Neuropsychological testing demonstrated no negative cognitive side effects.
Conclusions:
SAINT, an accelerated, high-dose, iTBS protocol with fcMRI-guided targeting, was well tolerated and safe. Double-blinded sham-controlled trials are needed to confirm the remission rate observed in this initial study.
validation and diagnostic accuracy of predictive curves for age-associated longitudinal cognitive decline in older adults
patrick j. bernier et al. 2017
doi.org/10.1503/cmaj.160792
aging and neurodegeneration are associated with increased mutations in single human neurons
michael a. lodato et al. 2017
doi.org/10.1126/science.aao4426
scam awareness related to incident alzheimer dementia and mild cognitive impairment
patricia a. boyle et al. 2019
doi.org/10.7326/m18-2711
Identifying predictors of dementia and mild cognitive impairment is critically important, but which aspects of behavior to target remains unclear. Older adults frequently are targeted by con-artists and are highly vulnerable to scams and fraud, particularly those that are financial in nature. However, little is known about whether scam awareness predicts transitions from normality to mild cognitive impairment and dementia.
Researchers from Rush Alzheimer's Disease Center in Chicago asked 935 older persons to complete a "scam awareness questionnaire" when all were free from dementia to ascertain a scam awareness score. Over an average of 6 years of follow up, participants also completed traditional neuropsychological tests every year, and the 264 participants who died had an autopsy of the brain to look for the hallmarks of Alzheimer disease. The researchers found that low scam awareness was a harbinger of adverse cognitive outcomes. Low scam awareness was also associated with Alzheimer disease pathology in the brain. According to the researchers, these findings suggest that low scam awareness is an early sign of impending mild cognitive impairment and dementia. Further, they conclude that evaluation of behaviors such as scam awareness may help to identify individuals at risk for dementia before cognitive symptoms manifest.
According to the author of an accompanying editorial, this study provides new information about social cognition as it relates to aging. The author provides an example of a patient who was scammed out of the majority of his life savings by a slick fraudster who tricked him into thinking he had won the lottery. Diminished financial capacity, financial abuse, and exploitation are major economic and public health problems. An older adult who is defrauded may end up unable to pay for medications, food, and long-term care, the author wrote. As such, the findings from this study should be a call to action for health care systems, the financial services industry, and their regulators to protect the health and wealth of our aging population.
bank fraud: couple lose £43,000 but can’t get a refund
miles brignall 2020
theguardian.com/money/2020/feb/08/bank-couple-lose-43000-but-cant-get-a-refund
a non-infectious virus to engineer cells…
reversing a model of parkinson’s disease with in situ converted nigral neurons
hao qian et al. 2020
doi.org/10.1038/s41586-020-2388-4
Fu and his team at University of California San Diego School of Medicine studied a protein called PTB, which is well known for binding RNA and influencing which genes are turned “on” or “off” in a cell. To study the role of a protein like PTB, scientists often manipulate cells to reduce the amount of that protein, and then watch to see what happens.
Several years ago, a postdoctoral researcher working in Fu’s lab was taking that approach, using a technique called siRNA to silence the PTB gene in connective tissue cells known as fibroblasts. But it’s a tedious process that needs to be performed over and over. He got tired of it and convinced Fu they should use a different technique to create a stable cell line that’s permanently lacking PTB. At first, the postdoc complained about that too, because it made the cells grow so slowly.
But then he noticed something odd after a couple of weeks — there were very few fibroblasts left. Almost the whole dish was instead filled with neurons.
In this serendipitous way, the team discovered that inhibiting or deleting just a single gene, the gene that encodes PTB, transforms several types of mouse cells directly into neurons.
More recently, Fu and Hao Qian, PhD, another postdoctoral researcher in his lab, took the finding a big step forward, applying it in what could one day be a new therapeutic approach for Parkinson’s disease and other neurodegenerative diseases. Just a single treatment to inhibit PTB in mice converted native astrocytes, star-shaped support cells of the brain, into neurons that produce the neurotransmitter dopamine. As a result, the mice’s Parkinson’s disease symptoms disappeared.
The study is published June 24, 2020 in Nature.
“Researchers around the world have tried many ways to generate neurons in the lab, using stem cells and other means, so we can study them better, as well as to use them to replace lost neurons in neurodegenerative diseases,” said Fu, who is a Distinguished Professor in the Department of Cellular and Molecular Medicine at UC San Diego School of Medicine. “The fact that we could produce so many neurons in such a relatively easy way came as a big surprise.”
There are several different ways to mimic Parkinson’s disease in mice. In this case, the researchers applied a dopamine look-a-like molecule to poison neurons that produce dopamine. As a result, the mice lose dopamine-producing neurons and develop symptoms similar to Parkinson’s disease, such as movement deficiencies.
The treatment works like this: The researchers developed a noninfectious virus that carries an antisense oligonucleotide sequence — an artificial piece of DNA designed to specifically bind the RNA coding for PTB, thus degrading it, preventing it from being translated into a functional protein and stimulating neuron development.
Antisense oligonucleotides, also known as designer DNA drugs, are a proven approach for neurodegenerative and neuromuscular diseases — study co-author, Don Cleveland, PhD, pioneered the technology, and it now forms the basis for a Food and Drug Administration (FDA)-approved therapy for spinal muscular atrophy and several other therapies currently in clinical trials. Cleveland is chair of the Department of Cellular and Molecular Medicine at UC San Diego School of Medicine and member of the Ludwig Institute for Cancer Research, San Diego.
The researchers administered the PTB antisense oligonucleotide treatment directly to the mouse’s midbrain, which is responsible for regulating motor control and reward behaviors, and the part of the brain that typically loses dopamine-producing neurons in Parkinson’s disease. A control group of mice received mock treatment with an empty virus or an irrelevant antisense sequence.
In the treated mice, a small subset of astrocytes converted to neurons, increasing the number of neurons by approximately 30 percent. Dopamine levels were restored to a level comparable to that in normal mice. What’s more, the neurons grew and sent their processes into other parts of brain. There was no change in the control mice.
By two different measures of limb movement and response, the treated mice returned to normal within three months after a single treatment, and remained completely free from symptoms of Parkinson’s disease for the rest of their lives. In contrast, the control mice showed no improvement.
“I was stunned at what I saw,” said study co-author William Mobley, MD, PhD, Distinguished Professor of Neurosciences at UC San Diego School of Medicine. “This whole new strategy for treating neurodegeneration gives hope that it may be possible to help even those with advanced disease.”
What is it about PTB that makes this work? “This protein is present in a lot of cells,” Fu said. “But as neurons begin to develop from their precursors, it naturally disappears. What we’ve found is that forcing PTB to go away is the only signal a cell needs to turn on the genes needed to produce a neuron.”
Of course, mice aren’t people, he cautioned. The model the team used doesn’t perfectly recapitulate all essential features of Parkinson’s disease. But the study provides a proof of concept, Fu said.
Next, the team plans to optimize their methods and test the approach in mouse models that mimic Parkinson’s disease through genetic changes. They have also patented the PTB antisense oligonucleotide treatment in order to move forward toward testing in humans.
“It’s my dream to see this through to clinical trials, to test this approach as a treatment for Parkinson’s disease, but also many other diseases where neurons are lost, such as Alzheimer’s and Huntington’s diseases and stroke,” Fu said. “And dreaming even bigger — what if we could target PTB to correct defects in other parts of the brain, to treat things like inherited brain defects?
abstract Parkinson’s disease is characterized by loss of dopamine neurons in the substantia nigra. Similar to other major neurodegenerative disorders, there are no disease-modifying treatments for Parkinson’s disease. While most treatment strategies aim to prevent neuronal loss or protect vulnerable neuronal circuits, a potential alternative is to replace lost neurons to reconstruct disrupted circuits. Here we report an efficient one-step conversion of isolated mouse and human astrocytes to functional neurons by depleting the RNA-binding protein PTB (also known as PTBP1). Applying this approach to the mouse brain, we demonstrate progressive conversion of astrocytes to new neurons that innervate into and repopulate endogenous neural circuits. Astrocytes from different brain regions are converted to different neuronal subtypes. Using a chemically induced model of Parkinson’s disease in mouse, we show conversion of midbrain astrocytes to dopaminergic neurons, which provide axons to reconstruct the nigrostriatal circuit. Notably, re-innervation of striatum is accompanied by restoration of dopamine levels and rescue of motor deficits. A similar reversal of disease phenotype is also accomplished by converting astrocytes to neurons using antisense oligonucleotides to transiently suppress PTB. These findings identify a potentially powerful and clinically feasible approach to treating neurodegeneration by replacing lost neurons.
enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity
vincenzo sorrentino et al. 2017
doi.org/10.1038/nature25143
immortals
fall out boy
they say we are what we are
but we don't have to be
i'm bad behavior but i do it in the best way
i'll be the watcher (watcher) of the eternal flame
i'll be the guard dog of all your favorite dreams
(ooh)
i am the sand in the bottom half of the hourglass (glass, glass)
(ooh)
i try to picture me without you but i can't
'cause we could be immortals, immortals
just not for long, for long
and live with me forever now
pull the blackout curtains down
just not for long, for long
we could be immor- immortals
immor- immortals
immor- immortals
immor- immortals
sometimes the only pay off for having any faith
is when it's tested again and again everyday
i'm still comparing your past to my future
it might be your wound but they're my sutures
(ooh)
i am the sand in the bottom half of the hourglass (glass, glass)
(ooh)
i try to picture me without you but i can't
'cause we could be immortals, immortals
just not for long, for long
and live with me forever now
pull the blackout curtains down
just not for long, for long
we could be immor- immortals
immor- immortals
(immortals)
and live with me forever now
and pull the blackout curtains down
we could be immortals, immortals
just not for long, for long
we could be immor- immortals
immor- immortals
immor- immortals
immor- immortals
(immortals)
impaired immune surveillance accelerates accumulation of senescent cells and aging
yossi ovadya et al. 2018
doi.org/10.1038/s41467-018-07825-3
chemically clearing senescent cells appears to promote youthful appearing tissues
The research began with an investigation into the way that the immune system is involved in a crucial activity: clearing away old, senescent cells that spell trouble for the body when they hang around. Senescent cells -- not completely dead but suffering loss of function or irreparable damage -- have been implicated in diseases of aging by promoting inflammation. The researchers used mice in which a crucial gene for this immune activity was missing. At two years (elderly, for mice), the bodies of these mice had a greater accumulation of senescent cells compared with the mice in which the gene for removing these cells was intact. The mice missing the gene suffered from chronic inflammation, and various functions in their bodies appeared to be diminished. They also looked older -- and died earlier -- than their normal counterparts.
Next, the researchers gave the mice a drug that inhibits the function of certain proteins that help the aging cells survive in their senescent state, to see if this would contribute to the removal of these cells from the body. The drugs were administered to mice whose aging was a result of the malfunctions the group had uncovered in the immune system as well as those suffering premature aging from a different genetic error. The treated mice responded exceptionally well to the drug: Their blood tests and activity tests showed improvement, and their tissues appeared to be much closer to those of young mice. The scientists counted senescent cells, finding many fewer of them remaining in the treated mice's bodies; and when they looked for signs of inflammation, they found that this, too, was significantly lower. The mice treated with the drug were more active and their median lifespan rose.
The scientists intend to continue exploring ways to prompt the human body to remove its old senescent cells, particularly to find means of activating the immune system to do this job. That is, if future experimentation proves their theories correct, they could end up creating truly "anti-aging" therapies.
abstract Cellular senescence is a stress response that imposes stable cell-cycle arrest in damaged cells, preventing their propagation in tissues. However, senescent cells accumulate in tissues in advanced age, where they might promote tissue degeneration and malignant transformation. The extent of immune-system involvement in regulating age-related accumulation of senescent cells, and its consequences, are unknown. Here we show that Prf1−/− mice with impaired cell cytotoxicity exhibit both higher senescent-cell tissue burden and chronic inflammation. They suffer from multiple age-related disorders and lower survival. Strikingly, pharmacological elimination of senescent-cells by ABT-737 partially alleviates accelerated aging phenotype in these mice. In LMNA+/G609G progeroid mice, impaired cell cytotoxicity further promotes senescent-cell accumulation and shortens lifespan. ABT-737 administration during the second half of life of these progeroid mice abrogates senescence signature and increases median survival. Our findings shed new light on mechanisms governing senescent-cell presence in aging, and could motivate new strategies for regenerative medicine.
translational regulation of non-autonomous mitochondrial stress response promotes longevity
jianfeng lan et al. 2020
doi.org/10.1016/j.celrep.2019.06.078
equivalent of a human living for 400 or 500 years, according to one of the scientists.
The research draws on the discovery of two major pathways governing aging in C. elegans, which is a popular model in aging research because it shares many of its genes with humans and because its short lifespan of only three to four weeks allows scientists to quickly assess the effects of genetic and environmental interventions to extend healthy lifespan.
Because these pathways are “conserved,” meaning that they have been passed down to humans through evolution, they have been the subject of intensive research. A number of drugs that extend healthy lifespan by altering these pathways are now under development. The discovery of the synergistic effect opens the door to even more effective anti-aging therapies.
The new research uses a double mutant in which the insulin signaling (IIS) and TOR pathways have been genetically altered. Because alteration of the IIS pathways yields a 100 percent increase in lifespan and alteration of the TOR pathway yields a 30 percent increase, the double mutant would be expected to live 130 percent longer. But instead, its lifespan was amplified by 500 percent.
“Despite the discovery in C. elegans of cellular pathways that govern aging, it hasn’t been clear how these pathways interact,” said Hermann Haller, M.D., president of the MDI Biological Laboratory. “By helping to characterize these interactions, our scientists are paving the way for much-needed therapies to increase healthy lifespan for a rapidly aging population.”
The elucidation of the cellular mechanisms controlling the synergistic response is the subject of a recent paper in the online journal Cell Reports entitled “Translational Regulation of Non-autonomous Mitochondrial Stress Response Promotes Longevity.” The authors include Jarod A. Rollins, Ph.D., and Aric N. Rogers, Ph.D., of the MDI Biological Laboratory.
“The synergistic extension is really wild,” said Rollins, who is the lead author with Jianfeng Lan, Ph.D., of Nanjing University. “The effect isn’t one plus one equals two, it’s one plus one equals five. Our findings demonstrate that nothing in nature exists in a vacuum; in order to develop the most effective anti-aging treatments we have to look at longevity networks rather than individual pathways.”
The discovery of the synergistic interaction could lead to the use of combination therapies, each affecting a different pathway, to extend healthy human lifespan in the same way that combination therapies are used to treat cancer and HIV, Pankaj Kapahi, Ph.D., of the Buck Institute, has said. Kapahi is a corresponding author of the paper with Rogers and Di Chen, Ph.D., of Nanjing University.
The synergistic interaction may also may explain why scientists have been unable to identify a single gene responsible for the ability of some people to live to extraordinary old ages free of major age-related diseases until shortly before their deaths.
The paper focuses on how longevity is regulated in the mitochondria, which are the organelles in the cell responsible for energy homeostasis. Over the last decade, accumulating evidence has suggested a causative link between mitochondrial dysregulation and aging.
abstract •Longevity of daf-2 rsks-1 is mediated by translational repression of cyc-2.1
•Germline inhibition of cyc-2.1 activates intestinal UPRmt and AMPK to extend lifespan
•Increased GLD-1 represses germline cyc-2.1 translation in the daf-2 rsks-1 mutant
•Translational regulation of cyc-2.1 and UPRmt contribute to longevity of daf-2 rsks-1
Reduced mRNA translation delays aging, but the underlying mechanisms remain underexplored. Mutations in both DAF-2 (IGF-1 receptor) and RSKS-1 (ribosomal S6 kinase/S6K) cause synergistic lifespan extension in C. elegans. To understand the roles of translational regulation in this process, we performed polysomal profiling and identified translationally regulated ribosomal and cytochrome c (CYC-2.1) genes as key mediators of longevity. cyc-2.1 knockdown significantly extends lifespan by activating the intestinal mitochondrial unfolded protein response (UPRmt), mitochondrial fission, and AMP-activated kinase (AMPK). The germline serves as the key tissue for cyc-2.1 to regulate lifespan, and germline-specific cyc-2.1 knockdown non-autonomously activates intestinal UPRmt and AMPK. Furthermore, the RNA-binding protein GLD-1-mediated translational repression of cyc-2.1 in the germline is important for the non-autonomous activation of UPRmt and synergistic longevity of the daf-2 rsks-1 mutant. Altogether, these results illustrate a translationally regulated non-autonomous mitochondrial stress response mechanism in the modulation of lifespan by insulin-like signaling and S6K.
collapse: how societies choose to fail or survive
jared diamond 2005
upheaval: turning points for nations in crisis
jared diamond 2019 not yet read
resource wars: the new landscape of global conflict
michael t. klare 2001
too much magic: wishful thinking, technology, and the fate of the nation
james howard kunstler 2012
the long emergency: surviving the converging catastrophes of the twenty-first century
james howard kunstler 2006
reinventing collapse: the soviet example and american prospects
dmitry orlov 2008
the five stages of collapse: survivors’ toolkit
dmitry orlov 2013
the demise of angkor: systemic vulnerability of urban infrastructure to climatic variations
dan penny et al. 2018
doi.org/10.1126/sciadv.aau4029
radical transformation: oligarchy, collapse, and the crisis of civilization
kevin mackay 2017
the strange order of things: life, feeling, and the making of cultures
antonio damasio 2018
the origin of feces: what excrement tells us about evolution, ecology, and a sustainable society
david waltner-toews 2013
adapt: how humans are tapping into nature’s secrets to design and build a better future
amina khan 2017
the long descent: a user’s guide to the end of the industrial age
john michael greer 2008
the ecotechnic future: envisioning a post-peak world
john michael greer 2009
decline and fall: the end of empire and the future of democracy in 21st century america
john michael greer 2014
after progress: reason and religion at the end of the industrial age
john michael greer 2015
dark age america: climate change, cultural collapse, and the hard future ahead
john michael greer 2016
the retro future: looking to the past to reinvent the future
john michael greer 2017
seasteading: how floating nations will restore the environment, enrich the poor, cure the sick, and liberate humanity from politicians
joe quirk & patri friedman 2017
active hope: how to face the mess we’re in without going crazy
joanna macy, chris johnstone 2012
in praise of forgetting: historical memory and its ironies
david rieff 2016
b(older): making the most of our longer lives
carl honoré 2019 unread
how everything can collapse
pablo servigne, raphaël stevens 2020
the precipice: existential risk and the future of humanity
toby ord 2020
notes from an apocalypse: a personal journey to the end of the world and back
mark o’connell 2020
scatter, adapt, and remember: how humans will survive a mass extinction
annalee newitz 2013
ten thousand years of inequality: the archaeology of wealth differences
timothy a. kohler and michael e. smith, editors. 2018
1177 b.c.: the year civilization collapsed
eric h. cline 2015
Link: 04085-609b9c15e25fd23ad4d05a307ab1f5e5.html
七色シンフォニー
NANAIROshinfonii
rainbow symphony
coalamode
Link: 02085-f75a100cd84759c1c8c7c0deb06aa842.html
光るなら
HIKArunara
if you will shine
goose house
漢字
雨上がりの虹も 凛と咲いた花も 色づき溢れ出す
茜色の空 仰ぐ君に あの日 恋に落ちた
瞬間のドラマチックフィルムの中の１コマも
消えないよ 心に刻むから
君だよ 君なんだよ 教えてくれた
暗闇も光るなら 星空になる
悲しみを笑顔に もう隠さないで
煌めくどんな星も 君を照らすから
眠りも忘れて迎えた朝日が やたらと突き刺さる
低気圧運ぶ 頭痛だって 忘れる 君に会えば
静寂はロマンティック 紅茶に溶けたシュガーのように
全身に巡るよ 君の声
君だよ 君なんだよ 笑顔をくれた
涙も光るなら 流星になる
傷付いたその手を もう離さないで
願いを込めた空に 明日が来るから
導いてくれた 光は 君だよ
つられて僕も 走り出した
知らぬ間に クロスし始めた
ほら 今だ ここで 光るなら
君だよ 君なんだよ 教えてくれた 暗闇は終わるから
君だよ 君なんだよ 教えてくれた
暗闇も光るなら 星空になる
悲しみを笑顔に もう隠さないで
煌めくどんな星も 君を照らすから
答えはいつでも 偶然？必然？
いつか選んだ道こそ 運命になる
握りしめたその希望も不安も
きっと２人を動かす 光になるから
eng
雨上がりの虹も 凛と咲いた花も 色づき溢れ出す
AMEAgarinoNIJImo RINtoSAitaHANAmo IROzukiAFUreDAsu
a rainbow after rain, and a flower that bloomed with the cold, abundantly changing colour
茜色の空 仰ぐ君に あの日 恋に落ちた
AKANE-IROnoSORAAOguKIMIni anoHI KOIniOchita
that day, i fell in love with you who looked up at the blazing red sky
瞬間のドラマチックフィルムの中の１コマも
SHUNKANnodoramachikkufirumunoNAKAnohito-komamo
that one instant in a scene of the dramatic film
消えないよ 心に刻むから
KIenaiyo KOKOROniKIZAmukara
won’t disappear, because it’s etched into my heart
君だよ 君なんだよ 教えてくれた
KIMIdayo KIMInandayo OSHIetekureta
it’s you, you who taught me
暗闇も光るなら 星空になる
KURAYAMImoHIKArunara HOSHIZORAninaru
if the darkness shines too, then it’ll become a night of stars
悲しみを笑顔に もう隠さないで
KANAshimiwoEGAOni mouKAKUsanaide
don’t hide your sadness behind a laughing face anymore
煌めくどんな星も 君を照らすから
KIRAmekudonnaHOSHImo KIMIwoTErasukara
because all the twinkling stars will shine on you
眠りも忘れて迎えた朝日が やたらと突き刺さる
NEMUrimoWASUreteMUKAetaASAHIga yataratoTSUkiSAsaru
i forgot to sleep, and the sun that came out to meet me pierced me so much
低気圧運ぶ 頭痛だって 忘れる 君に会えば
TEIKIATSUHAKObu ZUTSUUdatte WASUreru KIMIniAeba
if i see you, i even forget the headache that carries my foul mood
静寂はロマンティック 紅茶に溶けたシュガーのように
SEIJAKUwaromantikku KOUCHAniTOketashugaanoyouni
this romantic stillness like sugar dissolving in tea
全身に巡るよ 君の声
ZENSHINniMEGUruyo KIMInoKOE
your voice, it goes around my whole body
君だよ 君なんだよ 笑顔をくれた
KIMIdayo KIMInandayo EGAOwokureta
it’s you, you who gave me a smiling face
涙も光るなら 流星になる
NAMIDAmoHIKArunara RYUUSEIninaru
if tears shine too, then it’ll become a falling star
傷付いたその手を もう離さないで
KIZUTSUitasonoTEwo mouHANAsanaide
don’t separate those injured hands anymore
願いを込めた空に 明日が来るから
NEGAiwoKOmetaSORAni ASHITAgaKUrukara
because tomorrow will come to the sky filled with wishes
導いてくれた 光は 君だよ
MICHIBIitekureta HIKARIwa KIMIdayo
the light that guided me is you
つられて僕も 走り出した
tsurareteBOKUmo HASHIriDAshita
i was drawn, and i broke into a run
知らぬ間に クロスし始めた
SHIranuMAni kurosushiHAjimeta
while unaware, we started to cross
ほら 今だ ここで 光るなら
hora IMAda kokode HIKArunara
hey, it’s now if it shines here
君だよ 君なんだよ 教えてくれた 暗闇は終わるから
KIMIdayo KIMInandayo OSHIetekureta KURAYAMIwaOwarukara
it’s you, you who taught me the darkness will end
君だよ 君なんだよ 教えてくれた
KIMIdayo KIMInandayo OSHIetekureta
it’s you, you who taught me
暗闇も光るなら 星空になる
KURAYAMImohikarunara HOSHIzoraninaru
if the darkness shines too, then it’ll become a night of stars
悲しみを笑顔に もう隠さないで
KANAshimiwoEGAOni mouKAKUsanaide
don’t hide your sadness behind a laughing face anymore
煌めくどんな星も 君を照らすから
KIRAmekudonnaHOSHImo KIMIwoTErasukara
because all the twinkling stars will shine on you
答えはいつでも 偶然？必然？
KOTAewaitsudemo GUUZEN?HITSUZEN?
is the answer at any time by chance? is it necessary?
いつか選んだ道こそ 運命になる
itsukaERAndaMICHIkoso UNMEIninaru
some day the road that you choose will be your destiny
握りしめたその希望も不安も
NIGIrishimetasonoKIBOUmoFUANmo
the hope and the anxiety you grasped tightly
きっと２人を動かす 光になるから
kittofutariwoUGOkasu HIKARIninarukara
will surely move you and me, because it will become a light
live mv
Link: m.youtube.com/watch
mv
Link: m.youtube.com/watch