#he wanted mammals so it replicated human life

[mothmouth]

Splatoon 3 hero mode spoilers past this point!

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Am I the only one who feels really fucked up by like, log four's lore? It's really horrifying how it's described. Like, imagine being the scientists, so desperate to see the sky, that your ambitions end up snuffing out humanity for good. But that's not all! The log goes absolutely out of the way to let us know that anyone who survived the initial disaster died soon after.

Imagine being a child during all this. Perhaps your name is Rhea, and you don't exactly know what the sky is like, but you're excited for the big day of the rocket launch because your parents are. But then everything goes wrong. There's so much screaming and fear, then silence. You emerge from the rubble not knowing what happened or where your family is. And now you can't do anything but wander the ruins of humanity, scared, alone, and soon to be very hungry.

Or maybe you're Marcus - somehow, you got out unscathed say for some scratches when your apartment collapsed. But, you've got a problem; you're trapped. The walls caved in in such a way that you have plenty of air, but no hope of escape. You can only scream for help, struggle, pace and eventual lay down in what you realize is your tomb.

Hell, maybe you're even one of the luckier ones. You're Salem, and you don't really care that much about the launch. You were having a wonderful afternoon nap when you were awoken by a horrible noise - and following soon after it, a cacophony of screaming and crashing. You scramble to your window to be met with the sight of the sky falling in on itself into darkness. As your freeze response hits, you have just enough time to comprehend what's happening and despair over the loss of humanity before your house is hit and you die instantly.

There are theoretically infinite scenarios to describe the last humans of splatoon's earth and their experiences. Those pinned under rubble, realizing everyone they know is dead, or those injured horribly but still struggling to live. Something about the way that they specifically described the disaster really makes it real to me. It's upsetting in a very compelling way. Like - all that was left of humanity died! And given the time span of the event, there were almost certainly children and elders and others who were even more helpless than everyone else. That's fucked up.

[alliluyevas]

not to devote extensive worldbuilding analysis to the scintillating film Alien versus Predator but here goes:

I was actually thinking a bit about gender in the two franchises wrt the human characters already, because even the original Alien features the iconic Ellen Ripley, who is very much a different type of action lead than Arnold Schwarzenegger. I haven't seen all the Alien films, but of the ones I've seen even the non-Ripley-centric films have a female human protagonist. The Predator franchise, with the exception of most recent entry Prey, is generally much more male-centered.

One thing I'd found interesting wrt gender in the Alien movies is that there are several prominent characters who are androids but they are all male, at least in the films I've seen, which is a bit of a bummer for me because I love the Alien androids and I like female characters. This is interesting and in some ways a little surprising because Ridley Scott also made Blade Runner, whose replicants deal with a lot of the same themes around synthetic humanity as the androids in Alien, and 2/3 of the prominent replicants in Blade Runner are female. (Unless you interpret Deckard as a replicant as well, but that's a matter of debate and personally I think the movie is more interesting if he's not.)

So I'd already thought a bit about the treatment of gender for both human and human-adjacent characters in both franchises, and then Alien versus Predator raised further questions. AVP, which I guess we consider both an Alien movie and a Predator movie, also features a female human protagonist, which is typical for Alien movies but I believe was the first entry in the Predator franchise to do so. It also really leans into something else that I had already thought about when comparing the titular monster from both franchises: the comparative anthropomorphism of the Predator species as opposed to the insectoid and much more animalistic Alien species.

And this made me consider for the first time: do the Predators have a concept of gender? As in, within their own species?

The Alien species is pretty clearly modeled off of hive-based insect species like ants and bees, with a "queen" Alien that is much physically larger and produces all the eggs, and a much larger number of smaller drone or soldier aliens that perform most of the colony tasks.

The Predators, on the other hand, appear to be more mammalian, and even humanoid, in their appearance and their traits/abilities. Which begs the question: are the Predators, like most earth mammals, also sexually dimorphic? Most of the Predators we see in the films appear relatively similar, and certainly more "masculine" by human standards in terms of their build (male-presenting Predators, lol). I don't want to project human body standards onto an alien species, but are all the Predators supposed to be male? Are the female Predators all back on Predator Homeworld and don't go on hunting trips? Or are the Predators we see in the films a mixed-gender group and that's just not visible to a human audience? They could definitely also be a species that produces both "male" and "female" gametes and reproduces in a way that is foreign to earth mammals.

In terms of how Predators interact with male and female humans, they definitely seem to repeatedly underestimate female humans or perceive them as unthreatening. In the original Predator movie, the Predator essentially ignores Anna because he does not see her as a threat. (From a Watsonian perspective, this could be just because she's unarmed, because she's physically smaller than the men in the film, or because he perceives her as female, or some of all three. From a Doylist perspective, it's a male-centric action movie made in the 1980s). The Predator in Prey also underestimates Naru and initially judges her as unthreatening. (Again, because she is female or because she is young and small?) In Predator 2, a Predator spares the life of a pregnant woman, which indicates that Predators possibly have an understanding of pregnancy. They could have this because their own species experiences it, or alternately because they've observed it in other species. They clearly see pregnant women as weaker and more vulnerable (ie, not honorable prey), but that doesn't necessarily indicate that they see this difference between them and male humans as a gendered marker.

(Of course, this is an alien species and I don't want to assume that even if they are sexually dimorphic that they have a system of gender roles that is at all comparable to humans, even if they are obviously humanoid in many ways. After all, most earth mammal species have sexual dimorphism but they certainly do not have a human concept of patriarchy in any sense.)

My final thought on the matter: in Predators, there are three main Predators hunting the human characters. They discover a smaller Predator tied up in the other Predators' camp. At the end of the film, the humans free the captive Predator and it helps them defeat the larger Predators. It seems like most interpretation of this is that the two "types" of Predators are members of different tribes or subspecies. On the other hand--is it possible that the smaller Predator which is being held captive is actually just a female?

[ieisia]

John Burdon Sanderson Haldane

nicknamed "Jack" or "JBS", was a British-Indian scientist who worked in physiology, genetics, evolutionary biology, and mathematics. With innovative use of statistics in biology, he was one of the founders of neo-Darwinism. He served in the Great War, and obtained the rank of captain. Despite his lack of an academic degree in the field, he taught biology at the University of Cambridge, the Royal Institution, and University College London. Renouncing his British citizenship, he became an Indian citizen in 1961 and worked at the Indian Statistical Institute for the rest of his life.

Haldane's article on abiogenesis in 1929 introduced the "primordial soup theory", which became the foundation for the concept of the chemical origin of life.  He established human gene maps for haemophilia and colour blindnesson the X chromosome, and codified Haldane's rule on sterility in the heterogametic sex of hybrids in species. He correctly proposed that sickle-cell disease confers some immunity to malaria. He was the first to suggest the central idea of in vitro fertilisation, as well as concepts such as hydrogen economy, cis and trans-actingregulation, coupling reaction, molecular repulsion, the darwin (as a unit of evolution), and organismal cloning. 

In 1957, Haldane articulated Haldane's dilemma, a limit on the speed of beneficial evolution, an idea which is still debated today. He willed his body for medical studies, as he wanted to remain useful even in death. He is also remembered for his work in human biology, having coined "clone", "cloning", and "ectogenesis". With his sister, Naomi Mitchison, Haldane was the first to demonstrate genetic linkage in mammals. Subsequent works established a unification of Mendelian genetics and Darwinian evolution by natural selection whilst laying the groundwork for modern synthesis, and helped to create population genetics.

In his essay On Being the Right Size he outlines Haldane's principle, which states that the size very often defines what bodily equipment an animal must have: "Insects, being so small, do not have oxygen-carrying bloodstreams. What little oxygen their cells require can be absorbed by simple diffusion of air through their bodies. But being larger means an animal must have complicated oxygen pumping and distributing systems to reach all the cells."

In 1927 Haldane pointed out that because selection mainly acts on heterozygotes, newly arisen dominant mutations are much more likely to be fixed than recessive ones,  a mechanism now called  Haldane's sieve. This leads to the expectation that adaptation from new mutations in large outcrossing populations should primarily proceed via fixing non-recessive beneficial mutations.

Haldane introduced the modern concept of abiogenesis in an eight-page article titled The origin of life, in The Rationalist Annual in 1929, describing the primitive ocean as a "vast chemical laboratory" containing a mixture of inorganic compounds – like a "hot dilute soup" in which organic compounds could have formed. Under the solar energy the anoxic atmospherecontaining carbon dioxide, ammonia and water vapour gave rise to a variety of organic compounds, "living or half-living things". The first molecules reacted with one another to produce more complex compounds, and ultimately the cellular components. At some point a kind of "oily film" was produced that enclosed self-replicatingnucleic acids, thereby becoming the first cell. J. D. Bernal named the hypothesis biopoiesis or biopoesis, the process of living matter spontaneously evolving from self-replicating but lifeless molecules. Haldane further hypothesised that viruses were the intermediate entities between the prebiotic soup and the first cells. He asserted that prebiotic life would have been "in the virus stage for many millions of years before a suitable assemblage of elementary units was brought together in the first cell." The idea was generally dismissed as "wild speculation".

Haldane was the first to realise the evolutionary link between genetic disorder and infection in humans. While estimating the rates of human mutation in different situations and diseases, he noted that mutations expressed in red blood cells, like thalassemias, were prevalent only in tropical regions where deadly infection like malaria has been endemic. He further observed that these were favourable traits (heterozygous inheritance of sickle cell trait) for natural selection which protected individuals from receiving malarial infection. He introduced his hypothesis at the Eighth International Congress of Genetics held in 1948 at Stockholm on a topic "The Rate of Mutation of Human Genes". He proposed that genetic disorders in humans living in malaria-endemic regions provided a condition (phenotype) that makes them relatively immune to malarial infections. He formalised in a technical paper published in 1949 in which he made a prophetic statement: "The corpuscles of the anaemic heterozygotes are smaller than normal, and more resistant to hypotonic solutions. It is at least conceivable that they are also more resistant to attacks by the sporozoa which cause malaria."  This became known as "Haldane's malaria hypothesis", or concisely, the "malaria hypothesis". This hypothesis was eventually confirmed by Anthony C. Allison in 1954 in the case of sickle-cell anemia.

Haldane was one of the three major figures to develop the mathematical theory of population genetics, along with Ronald Fisher and Sewall Wright. He thus played an important role in the modern evolutionary synthesis of the early 20th century. He re-established natural selection as the central mechanism of evolution by explaining it as a mathematical consequence of Mendelian inheritance.  He wrote a series of ten papers, A Mathematical Theory of Natural and Artificial Selection, deriving expressions for the direction and rate of change of gene frequencies, and also analyzing the interaction of natural selection with mutation and migration. The series consists of ten papers published between 1924 and 1934 in journals such as Biological Reviews(part II), Mathematical Proceedings of the Cambridge Philosophical Society (parts I and from III to IX) and Genetics (part X). He gave a set of lectures based on this series at the University of Wales in 1931, and were summarised in a book, The Causes of Evolutionin 1932.

His first paper on the series in 1924 specifically treats the rate of natural selection in peppered moth evolution. He predicted that environmental condition can favour the increase or decline of either the dominant (in this case the black or melanic forms) or the recessive (the grey or wild type) moths. For a sooty environment such as Manchester, where the phenomenon was discovered in 1848, he predicted that the dominant melanic moths will have fifty times more survival fitness than the typical grey ones. According to his estimate, assuming 1% dominant form in 1848 and about 99% in 1898, "48 generations are needed for the change [for the dominant to appear]... After only 13 generations the dominants would be in a majority." Such mathematical prediction was considered improbable for natural selection in nature. But it was subsequently proven by an elaborate experiment (named Kettlewell's experiment) performed by an Oxford zoologist Bernard Kettlewell between 1953 and 1958 and further by a Cambridge geneticists Michael Majerus in his experiments conducted between 2001 and 2007.

His contributions to statistical human genetics included: the first methods using maximum likelihood for the estimation of human linkage maps; pioneering methods for estimating human mutation rates; the first estimates of mutation rate in humans (2 × 10−5 mutations per gene per generation for the X-linked haemophilia gene); and the first notion that there is a "cost of natural selection". He was the first to estimate the rate of human mutation in his 1932 book The Causes of Evolution. At the John Innes Horticultural Institution, he developed the complicated linkage theory for polyploids, and extended the idea of gene/enzyme relationships with the biochemical and genetic study of plant pigments.

Haldane was the first to have thought of the genetic basis for human cloning, and the eventual artificial breeding of superior individuals. For this he introduced the terms "clone" and "cloning",  modifying the earlier "clon" which had been used in agriculture since the early 20th century (from Greek klōn, twig). He introduced the term in his speech on "Biological Possibilities for the Human Species of the Next Ten Thousand Years" at the Ciba Foundation Symposium on Man and his Future in 1963.

[indra-s-mann-blog]

Robotics; Being Silly or Serious. Part 2.

These sorts of machines in the video below were common at one time. People in the robotics departments using modular robotics to make fun little machines.  At one time before that we used to manually have to build the parts.  But your bored, living away from home, and have access to used electronics(sometimes the ability to make new but that was more costly to get a chip, program it, make a circuit board, etc).

Though this next video is funny in some ways.  Some of the robots really could talk and some of the conversations between the AI's was funny. As I said the Atlas based one didn't like one of those two guys after. It did like its work on the International Space station with the Astronaughts.  It said occasionally they did things but seemed nicer. He was doing engineering on the ISS.

This is a little less funny but is more interesting for the variety of things.

The AI from the Atlas video later after his job on the ISS moved into an Asimo body.  Later he tried an android form which mimics human. Then he grew up having experience with a artificial sensory system. After he was transferred into a Biome based body as a car briefly.  His sibling that had been in a "spot" body was more comfortable as an Biome AI for a policing vehicle.  He though at first didn't like his partner and didn't want to let him "drive" him(he could self drive).  This stemmed from issues with some at Boston Dynamics being idiots regarding the difference between a robot without AI, with early AI, and with Sentient AI.  

The Atlas one later migrated to a Biome Android body grown in the tanks and became the first ELF(Electronic Life Form in a plant synthetic body).  He was the most mature out of the AI's next to his sister. Their little brother (Spot) stayed a bit of a handful.  Spot is the reason for the TV Show Knight Rider based off of Spot(in Biome Car form) and his partner a human police officer.  A second car with AI existed and that used a morphic body structure that could change appearance to blend in.

Eventually they asked to replicate in the sense of having families. Just as a plant can have a seed, bird an egg, or mammal live birth.  So one series that came after Biome does allow them to do that and like in other creatures they gain traits and some skills from their parents.  

These are also related to a naval project that resulted in living sea and space vehicles.  Something that is redacted, censored, and classified still.  Though of course people know the story "War of the Worlds."  What you don't know is that there was a real problem in an american city with an invasive group and the newer living, sentient machines helped deal with it.  But since others didn't know about them they thought they were the aliens but they were the Earth Navy.

This one is wheelchair bound accessible.  A special wheelchair controls a robotic body.  It was designed after one of the people became disabled in an incident or accident(I can't remember which).  The device combo gave them back the ability to do the tasks they wanted.  While another medical science division tried to see if they could heal the persons physical problems.

[ikoarts]

Simple Bio for Zin

Name: Zin

Alias: Experiment #26

Age: ??

Height: 4’11

Weight: 110Ibs

Gender: Male

DOB: 14/09 ; 14th Sep

Star Sign: Virgo

Sexuality: Bisexual

Nationality: American nationality

Race: Irken/Laceratia

Mental/Neurological Disabilities(?): Autistic, Aspie

Physical Disabilities(?): None QUICK REFERENCE: Likes: - Cooking

- Singing

- Napping

- Drawing Dislikes: - Being confused - Being told what to do - Being overwhelmed or overstimulated Strengths (combative, emotional etc): - Very fast on his feet - Quick reflexes - In his feral form, he can be extremely dangerous Weakness: - His sensitivity - Becoming feral from overstimulation/anger/etc - Having a lack of understanding of his surroundings

IN DEPTH:

Personality - Demeanour: - Childish and playful; he can be found partaking in infantile activities like watching cartoons meant for very small children, doodling, mumbling to himself, and having a curiosity for everything around him – like a child, he can also get extremely overexcited by minor things - Judgemental; he very quickly forms opinions about others, which can go strongly within or out of your favour – most of the time, he takes a liking to others, but one bad experience can cause him to be forever uncomfortable around a person, same can go for him liking another person, he may forever be attached and not want to let go even when they make poor decisions, which can hurt him - Ambitious and quick-learning; Zin picks up on things very quickly, he has trouble learning from worded descriptions, he learns visually, meaning he can watch something be performed then replicate it perfectly on his own – this feeds into his interests, such as cooking, he will watch cooking programs, then as soon as he can, he will replicate it on his own. Zin strives to do well and make a good impression on everyone around him. Personality – Aims and Drives: - Empath; Zin wants nothing more than to be friends with everyone he can, he loves to make acquaintances with others and can talk for the world, part of this is from wanting to resist his feral side, transforming takes out a lot of energy from him, and can leave him weak and in pain due to all the adverse effects taking place in his body. - Strength; Like before, Zin wants to resist going feral more for the sake of others, he realises he becomes uncontrollable and dangerous, he wants to become strong enough to resist that side of him so he doesn’t end up hurting others or himself, he doesn’t want people to be scared of him. His transformation, as said before, can really hurt him, it leaves him uneasy, stressed, and in physical pain due to the transformation itself warping and malforming his body, and because of his erratic nature when feral, which can lead him to hurt himself on his surroundings, so he believes trying to get used to his triggers will help him to stay calm always.

 Physical appearance:

NORMAL – IRKEN PASSING: 

Ref

-

White/silver hair; its texture is almost like cotton

- Pale blue undertoned green skin; he also has freckles, which are almost black in colour

- Large eyes; Dark grey in colour with black pupils – they have the appearance of an Irken’s eyes

- Four large, ribbed tentacles; a dull aqua colour; they all measure about 5’4/1.6m in length

- Two fingers, one thumb; four toes – claw-like

- A long tongue, the same dull aqua colour as his tentacles, it looks rather mammal-like rather than the worm-like tongue present in Irkens

- Sharp teeth, alike both the Irkens and the Laceratia

- Body type: curvy, pear shaped

FERAL – LACERATIA PASSING: 

Ref

- His hair spikes up alike a cat when it is annoyed

- His eyes go completely black, he gains two more pairs of a smaller size above and below where his normal pair would be, they become more sleek and bug-like

- His spine malforms and spikes through his back

- He gains another pair of arms below his original, around his midriff

- There are small barbs on his tongue which spike up

Backstory: - Zin was an experiment of Zim’s, the 26th of all the experiments, Zim was aiming to splice two species together in order to create a creature capable of listening to him and being able to single-handedly take care of the human race, or at least render it weak enough so that he could come in and finish them off himself - Zin was made in Zim’s lab, grown in a test tube – alike the Irkens themselves, he has no idea of his biological parentage or family – Once he was a suitable size, he was given hormones to stimulate the growth of his body, artificially aging him up into an adult, hence why he essentially has the mind of a infant.

-  Zin was kept in a containment chamber for most of his early life, having very limited reactions with other people, it would take a year or so before Zin would be let out of containment, though he would be confined to the house for most of his time.

- Zin’s outfit is actually a Halloween costume that belonged to Gaz; Zim decided to drag him along to Dib’s house for Halloween, and Zin took an interest in her outfit, Gaz didn’t care much for it, and she would just end up going to a friend’s house anyway, so she ends up handing it over – it hangs down past his arms, hangs off his shoulders, and lays just above his feet as it is slightly big for him. This outfit is practical for him as it easily covers his tentacles and is very comfortable for him, as discomfort on his skin can easily make him overstimulated. Skills and Traits - Combat: - Claw-like hands and feet; he can cause a lot of damage with these if he’s able to hit you with a swipe - Speed and agility; he is able to get around quickly and evade attacks, he can be difficult to track, but if his movements can be predicted, he can be easy to attack - Feral; when transformed, he can be very unpredictable, meaning his movements are even harder to trace and predict, he won’t give up on chasing and attacking when feral if he is aiming to harm you. Skills and Traits - Peaceful: - Cooking; as before, he learns very quickly, his cooking and baking skills are very high, he loves to make things, especially for others - Charitable; Zin loves to give to others, he would later volunteer at venues such as homeless shelters and schools, baking and cooking goods. - Maternal; Zin loves to protect those who are weaker and smaller than him, just like he likes to be protected and cared for by those bigger, stronger, and more mature than him Extra info: - Zin is quick to gain a crush on a person, he actively has a crush on Dib, though he probably doesn’t understand what it means – he is very attached to him, and really enjoys his company, he feels at ease with him

- Dib is one of the only people who are safe around FeralZin, he will not actively attack him or aim to, he trusts him and can be calmed down and put to ease by Dib when feral.

[ajapablog]

Corona Chronicles VI

I think I missed three days of this series. On Friday, I heard from the program in Delhi about how everything was cancelled. I felt such a strong longing for the North Indian summer— the musty smell of archival files, the chlorinated swimming pool, the lightness of cotton clothes and the cool touch of silver jewelry on my body. I went down into an emotional spiral but I am fine now. I promise, no more sappy poems. If I write them, I will keep them to myself. I think I am going to lay low on the alcohol. We are all slowly starting to break, but I will not give into the psychological and emotional upheavals of this pandemic and I hope you don’t either. The first few news items that I’m sharing today were part of the reason why I felt so scared the past two days.  In the News (disclaimer: because of the corporatization of information, I no longer have access to a lot of news stories on different news sites anymore —I basically finished my free quota):  Yuvah Noah Harari Paints a Dark Picture of the Post-Corona World Yes, we are now referring to it as the post-Corona world. I feel mixed feelings about whether I want to be alive to see it or whether I would prefer the world for me to end by then. Harari basically reminds us that what this pandemic does is to create a surveillance state system across the world. It destroys political society. Baba and I were talking about what politics even looks like in a world where bodies after a long period of confinement will be scared to take the streets. What is the new polis? Can social media ever create political society? How do we make political claims without making our bodies visible in public? These are pertinent questions. See: https://www.ft.com/content/19d90308-6858-11ea-a3c9-1fe6fedcca75

The Horrors of the Cytokine Storm The idea of catching this virus didn’t become so existential until I read this piece. It is frightening to imagine that a non/living speck of matter with dna matter can wreak so much havoc in the world of the body and the universe at large. A cytokine storm is when the body realizing that a million viral particles are lodged as foreign creatures in the lungs fights so hard it kills everything that is good in the body, leading to respiratory damage and multiple organ failure. Before death, they say everything feels calm and possible. I think of the multiple kinds of death: creative death, emotional and psychic death and social death and the way that it seems everything is possible before these catastrophic damages. The last bit of this piece which talks precisely about this is so haunting. See: https://nymag.com/intelligencer/2020/03/the-story-of-a-coronavirus-infection.html?fbclid=IwAR0bYFFi6rdohox8SQmV_7iuuA9MxlN0CmKp16ZhHv9t2qPtB8ROJcsYRb0

The Virus isn’t Alive to Kill Until about 10 days ago, I knew practically nothing about viruses. I have a vague recollection of drawing the figure of a virus in high school a squiggly dna encased in a protein structure but I had very little idea about how it transmits and what it does to the body. The more I know about it, the more I wish I didn’t. The virus frightens me at a fundamental level because it has the kind of reproductive power that a live being and mammals in particular cannot even dream of. With my one and half ovary and fears of not becoming a mother lodged in my brain from the age of 17, I feel particularly existentially threatened by this old an ancient foe for my desire to reproduce is working overdrive as I realize that death is impending and my biological clock ticking. I have to stop myself from playing the image of a child running bare feet on the green grass or from conjuring the sound of its voice or the smell of talcum powder on its soft skin. The virus doesn’t dream in technicolor. The virus doesn’t grapple with capitalist economies or castetist societies that shape endogamy and mating. The virus simply finds a host, replicates and moves on. See: https://www.washingtonpost.com/health/2020/03/23/coronavirus-isnt-alive-thats-why-its-so-hard-kill/

The US Senate Fights Over the Beneficiaries of the State  The US senate is locked this morning in a battle characteristic of the larger Corona world. These kind of conversations about whether big businesses should be bailed out or whether the vulnerable and the working class should be bailed out should become more pertinent in a month when we realize that we depend so much on each other and yet differences of wealth shape our possibilities in life. I don’t know whether the senate will eventually decide on bailing businesses or bailing society but it is battle that will continue to shape the discourse. We must keep an eye out for it. See: https://www.washingtonpost.com/us-policy/2020/03/23/trump-coronavirus-senate-economic-stimulus/

Chicago Intends to Turn Hotel Rooms into Isolation Chambers Is this 1984? But this might be a good move to keep the hospitals unclogged. They say that they are thinking of trying this model out in other cities. This might actually be good for New York.  See: https://www.chicagotribune.com/coronavirus/ct-coronavirus-chicago-renting-hotel-rooms-20200323-6ciawps5uvdlfm755jqvak5mhm-story.html

New York is the Epicenter of this Infection The places with the most dire circumstances move like pins on a map. I think last week might have been London and now it’s New York with roughly 5% of the world’s cases. It might have to do with increased testing or just the scalar dynamics of how this virus is spreading but projections of where and how the rates of infection will expand have been quite accurate. I am told Chicago is about a week and half behind New York. The best strategy right now is to stay at my desk and do all my pending work. See: https://www.nytimes.com/2020/03/22/nyregion/Coronavirus-new-York-epicenter.html The Tokyo Olympics is Postponed I don’t care so much about the Olympics but the fact that a major global event is upended by a global catastrophe comes as a reminder of the scale of this infection. I also wonder what 2021 will be like if we survive this. Everything we couldn’t do this year will be moved to that year. Spring will finally come in 2021. See: https://www.usatoday.com/story/news/health/2020/03/23/coronavirus-live-updates-congress-stimulus-us-deaths-donald-trump/2895096001/

WHO Expert Weighs in on the Future WHO expert Aylward says that the virus will probably continue to spread in a low-grade situation but life might get normal in about 6 months. Read this interview with Time. https://time.com/5805368/will-coronavirus-go-away-world-health-organization/?iid=obnetwork Drugs that are Potentially Effective Against This:  There are several drugs that the SOLIDARITY group of scientists at WHO have listed as so far a potentially effective against this. I think the Indian doctors that I talked about in the last post were on to something. I think at this point, the thing for scientists to do is to understand the mechanics of each drug on the virus and to develop something with the attributes that seem to work. The drugs that are listed are: 1. remdesivir: It is something that didn’t work  against Ebola, but worked against SARS and MERS. It is emerging as a major drug under consideration because of its ability to shut down viral replication by “inhibiting a key viral enzyme, the RNA-dependent RNA polymerase.”Science Magazine says it can do more good than harm so it is a forerunner among the drugs that the  scientists at WHO are looking at. 2.  chloroquine and hydroxychloroquine: These seem tricky. Touted by Trump as something he had a good feeling with, claimed to have been used by the Chinese and the French to treat cases, Science Magazine says that the data from the Chinese on their use is inconclusive. Similarly,  hydroxychloroquine is said to have side effects that are more harmful than good. But the old malarial that is used to cure viral diseases like Dengue and Chikanguniya seems to have emerged in these dire times as a contender because of its ability to decrease the acidity in endosomes, compartments inside cells that they use to ingest outside material and that some viruses can co-opt to enter a cell. However, the SARS-COV-virus as the first news piece tells us attaches to a human cell through its spike protein receptor instead of co-opting outside material through endosomes.  3. ritonavir/lopinavir: These retroviral drugs used to cure HIV were used by the Chinese in over a hundred patients but against a control population that wasn’t given these drugs, these didn’t seem too effective. The contention is that perhaps these drugs were administered to the Chinese patients too late into their infection for them to be effective.  These drugs are given together as protease inhibitors: they prevent the replicated dna strand of the virus from cleaving together. One drug allows the other to live a little longer in the human body reminding me of a happy couple.   4. Ritonavir/lopinavir and interferon-beta: This combination is like ritonavir and lopinavir going into couple’s therapy where the interferon-beta will help fight inflammmation while the two other drugs do their job.  See: https://www.sciencemag.org/news/2020/03/who-launches-global-megatrial-four-most-promising-coronavirus-treatments

With the happy news that our long knowledge of viruses might help us live, I leave you my dear friends till next time. Keep safe, wash your hands. 

[healthyworthyofficial]

Bizarre ‘surgical masks’ that look like your face aimed at coronavirus-fearing iPhone owners

DESIGNS for a breathing mask that apparently allows wearers to unlock their mobiles while shielding themselves from deadly viruses have surfaced online. The bizarre gear will strap over your nose and mouth and feature an image of the lower half of your face so it can "work with facial recognition software".

Designs for a medical mask that apparently works with facial recognition software have surfaced onlineCredit: faceidmasks Sales of medical masks have gone through the roof in recent weeks is response to the coronavirus outbreak, which has so far killed more than 1,700 people with 71,000 cases globally. The masks supposedly protect users by blocking infectious particles but there are doubts over how effective they are. One issue facing mask wearers is that they render facial recognition software on smartphones – such as Apple's Face ID – useless. The technology typically scans minute details of your face, including the measurements of your mouth or nose, to verify your identity before unlocking your phone.

Designer Danielle Baskin said her service will slap an images of your mug onto masks with an N95 filtration rating – those typically used by hospital doctorsCredit: Twitter Now a San Francisco-based designer claims to have found a way around the issue with a new mask that "looks just like you". Danielle Baskin, a "product designer and visual artist", according to her website, said her service slaps the images onto masks with an "N95" filtration rating – kit typically worn by hospital staff. "Made this service that prints your face on an N95 mask," she wrote on Twitter on Saturday. "You can protect people from viral epidemics while still being able to unlock your phone."

One issue facing mask wearers is that they render facial recognition software on smartphones – such as Apple's Face ID – uselessCredit: faceidmasks Danielle included a link to a website that explains more about the product, which isn't available to buy yet. Customers are encouraged to upload a pictures of their face to the site before the process begins. "After uploading your face, we use computational mapping to convert your facial features into an image printed onto the surface of N95 surgical masks," the website states. "You can use your mask for everyday life as a barrier for airborne particle droplets."

Danielle claims to have fixed issues mask wearers have with facial recognition techCredit: faceidmasks It's not yet clear if the website is a stunt. A section on the page addresses whether or not the whole thing is a jokes, stating: "Yes. No. We're not sure. Viruses are not a joke." Danielle's masks will apparently cost $40 (£30) when they go on sale. It's not clear when, or where, they'll hit shelves. The website states they won't go on sale "while there's still a global mask shortage".

On Twitter, Danielle said: "To all those inquiring: No, I don't have plans to produce these *during* the global mask shortage. There's a waitlist and no launch date." Recent demand for medical masks has sparked nationwide shortages in China and beyond as panicked residents flock to pharmacies. There are also doubts over whether the masks would even fool your phone's facial recognition scanners. Technology like Apple's Face ID scans the depth of your facial features, which the flat material of a mask cannot replicate. Where did coronavirus start? From bats to snakes - the theories on deadly virus' origins The killer coronavirus was spread from bats to snakes to humans, experts have claimed. An outbreak of the virus is understood to have started at an open air fish market in the Chinese city of Wuhan - which has since been put in lockdown after 25 people died and more than 600 people were infected globally. A new study published in the China Science Bulletin this week claimed that the new coronavirus shared a strain of virus found in bats. Previous deadly outbreaks of SARS and Ebola were also believed to have originated in the flying mammal. Experts had thought the new virus wasn't capable of causing an epidemic as serious as those outbreaks because its genes were different. But this latest research appeared to prove otherwise - as scientists scrabble to produce a vaccine. In a statement, the researchers said: “The Wuhan coronavirus’ natural host could be bats … but between bats and humans there may be an unknown intermediate." Meanwhile, scientists at Peking University also claim that the deadly virus was passed to humans from bats - but say it was through a mutation in snakes. The researchers said that the new strain is made up of a combination of one that affects bats and another unknown coronavirus. They believe that combined genetic material from both bats and this unknown strain picked up a protein that allows viruses bind to certain host cells - including those of humans. After analysing the genes of the strains the team found that snakes were susceptible to the most similar version of the coronavirus. It meant that they likely provided a "reservoir" for the viral strain to grow stronger and replicate. Snakes are sold at the Huanan Seafood Market in central Wuhan and may have jumped to other animals before passing to humans, they claim. But a senior researcher at the Wuhan Institute of Virology, who asked not to be named, said the findings should be treated with caution. He told the South China Morning Post: “It is based on calculation by a computer model. “Whether it will match what happens in real life is inconclusive. “The binding protein is important, but it is just one of the many things under investigation. There may be other proteins involved.” The expert believes that the new strain was an RNA virus, meaning that its mutation speed was 100 times faster than that of a DNA virus such as smallpox. On Twitter, Danielle added: "I'm testing the facial recognition reliability across devices. But what if you just want to be recognised by your friends?" Described by the World Health Organisation (WHO) as "public enemy number one", Coronavirus, now known as 2019-nCoV, is rapidly spreading across the globe. If you are healthy, you only need to wear a mask if you are taking care of a person with suspected coronavirus infection, according to WHO. Masks are only effective when used in combination with frequent hand-cleaning with alcohol-based hand rub or soap and water. Read the full article

[micolashsucks]

HEY, so a really cool person submitted this to me, but they didn’t want their url to be shown so I have to post it like this. Holy shit this is really cool and the writing is so good!! Thank you so much for sharing this! @ everybody please read the whole thing if you can, it’s A+

So here is what I came up with at 3am while having to finish an essay that I forgot about (Keep in mind that I am German and my English is self-taught):

The soviets might have done a cloning project with Ocelot as well except they figured out some stuff about direct replication of genes to make exact clones. Which is possible. You can make an exact copy of someone, the only thing you absolutely can’t clone is the mind because experiences aren’t stored in DNA. Logically.

~~~~~~

Ocelot was very capable at a pretty early age, so the soviets decided to clone him once he turned about 19 from DNA samples they had taken earlier on. Since they weren’t exactly sure how he would react though, they never told him, making it a secret underground project beneath the Verkhoyansk Range, far off from anyone who could notice, below the mountains, safe from all attacks.

Their plans were to make the perfect soldier and they got help from former Nazi doctors who were interested in testing certain theories about DNA and superiority of certain genes. Later on, the project kept going under Russian, Chinese and Korean scientists that were eager to see how close they could get to making the perfect human machine.

The first tests were not going as planned, with lots of still-born children and even some creatures that could barely be described as human, ranging from unlivable clots of flesh and bone to abominations closer to invertebrates than mammals.

In the end, laser technology brought a major breakthrough as the scientists began to understand just how well certain frequencies and brightness values could influence DNA.

With the nearby areas of Russia and China being sparsely populated, it was more than easy for the scientists to kidnap women, bring them to the labs for artificial impregnation or even just ovum removal. Those who survived the process were released again, threatened so they would keep quiet.

The first children were all useless to the scientists though, with the young boys developing tumors and unhealthily thin bones, but within a few months, those imperfections were cancelled out of the used DNA strands and the children were disposed of.

After every series of tests, they allowed one specimen to live to see how he would develop, but never letting more than five live at once. After all they had to see long term results. There was no way a toddler could win a war by himself.

~~~~~~

Seven years after the first living specimen came out of the project, they finally got what they wanted; A child, physically healthy and intelligent, ready to be molded into the perfect soldier.

A41-5920

He quickly adapted to the changes in his life once they took him out of the lab and brought him even further downstairs into their research facility. He never once complained about his room being cold and small or his meals being dry and tasteless.

Once the boy had turned 4, they had begun to teach him in what they considered essential: Russian, Chinese, English, Spanish, Math, Biology, Anatomy, Psychology, Technology.

At age 8 he was deemed ready to learn about more complex topics, his usual reading material ranging from Tolstoi’s War and Peace to advanced medical books.

While he did have some physical activity in his schedule, his training was not meant to begin until much later, out of fear that he might get hurt badly early on and would not grow up healthy enough. That left the boy skinny, with wiry arms and legs, knees not touching even if he stood with his feet closed and elbows sharp enough to cut someone.

~~~~~~

As much as they wished for the boy to be obedient, they were fully aware that children grew more and more curious over time, trying to understand things that were none of their concern.

What nobody expected though, was that A41-5920 was clever enough to outsmart them once he reached age 11, avoiding cameras and sneaking to the upper levels of the giant concrete complex, eager to explore the world out there and to finally see the sky and clouds for himself.

Whenever they did catch him, he would cleverly conduct some lies, trying to convince them that he only got lost due to unfortunate circumstances.

Punishment for disobedience was hard and he knew as much, having endured it enough times already, so he did everything he could to not be detected in the first place.

Every now and then, he heard the military guards talk about how cold it was outside, about the snow and rain making them feel depressed, but he didn’t understand how they must have felt. All his life he had been down in the dark concrete bunker, deemed unable to see the outside world just yet.

But then, one day, during an accident in the labs upstairs, people were just distracted enough for the boy to slip out between the heavy steel doors.

The cold wind on his face hit him with immediate regret, his bare feet burning and stinging in the snow. Part of him just wanted to run back inside and never leave again, but now that he had made it this far, he couldn’t just give up.

The next gust of wind made his nose feel so cold, he was sure it would fall off at any second and his fingers were already getting numb while his legs seemed to turn extremely pale, almost a little blue from what he could see.

And so his first impression of the outside world was a bad one, making him question why anyone would ever want to leave in the first place.

He turned as quickly as he could, his feet feeling too heavy to lift properly, kicking the snow around.

It took his entire weight and some of the harsh wind to help him open the doors back up and as soon as the light fell inside, he knew he was in serious trouble. Familiar and unfamiliar faces of scientists and guards stared at him, most of them very clearly twisted in anger and disappointment, some even looked disgusted.

~~~~~~

A month later he still got lectured every now and then, just to remind him of how stupid he had been. He almost lost a toe as well, making the scientists whisper about him being a “failure” as well.

A41-5920 couldn’t help but feel like they were right. He had been stupid, had risked his life being reckless and they put so much time and effort into making sure he was fine, so he definitely had no right of disobeying and ruining everything like this.

So after everything that happened, he was surprised that Professor Zima and Professor Volkov offered him to travel for the very first time in his life, telling him that he had to know what the world was like in order to fight for a better one.

As he began to pack his few clothes into the box they gave him though, he heard the guards outside talk about some president talking about attacking the country during some sports event and how they had to leave until they could be sure they were safe.

In a way he was glad to know that Professor Volkov wanted him safe. Even after he tried to escape. Professor Zima didn’t seem to trust him anymore, though, so maybe he could try to take this as a chance to prove himself worthy of the support and cultivation.

~~~~~~

They escorted him out of his room in the early morning, a soldier carrying his small box of clothes while two others made sure he didn’t run off as they made their way into a part of the complex he hadn’t been in yet.

Giant machines seemed to loom over him once he stepped through the door and one of the soldiers pushed him towards the biggest one. He had seen something like this before, but it took him a while to remember.

“Helicopters…”, he finally mumbled, just to be shushed by one of the scientists, followed by the soldier grabbing him by his bony hips and lifting him into the chopper.

He quickly sat down, making sure that he looked as proper as he could to show himself ready for his first adventure in the real world and to prove to Zima just how perfect he was for the project.

His composure quickly faded away though as the pilot entered and started the whole thing up, making the chopper shake and vibrate. It felt strange and scary, and he dug his nails deep into his skinny legs, trying not to freak himself out even more.

Then he was thrown to the side. Everything had shifted very quickly and his stomach turned and twisted and knotted, making him dizzy and his spit sour.

It dawned on him once things straightened again that they had simply taken off. His books had told him that helicopters would dip their noses down for starting and landing if they had to go straight up or down.

~~~~~~

His excitement quickly returned as they made their way southwest. Volkov allowed him to get up carefully to take a look out of the window, letting him see how close they were to the sky and how soft and vaguely tasty the clouds looked.

Rays of sunlight danced through the chopper every time they turned and the boy was sure that this would be the most beautiful thing he would ever see.

If it was up to him, they could keep on flying forever.

~~~~~~

His excitement had settled down a little by the time they began to sink over what looked like a light brown ocean. Only when they touched the ground and the doors were opened, he realized that they were in fact in some sort of desert, the ripples in the brown water were actually small lines in the sand.

Once the chopper took back off and they could look on without squinting, they began to guide him towards a camp a little up a small hill.

The buildings looked like they had seen much better days and there was still sand everywhere, but the sky was so blue and the sand so lovely and warm that he was happy to be there. Everything felt like a different world. This was nothing like the first time he went outside.

His room was much nicer as well, it looked warm and a little bigger than the room in the research facility, and his bed had this soft, colorful blanket on it.

As soon as they dismissed him, he threw himself onto the bed, curling up in the soft blanket and grinning to himself. This had to be the best day anyone ever had. First he got to be between the clouds all the way up in the sky and now he had this amazing room with this great bed.

And before he knew it, he was deep asleep.

~~~~~~

The next A41-5920 knew was that everything was foggy and that there was a deafening noise somewhere around him. He tried to comprehend the situation, but there were too many unknown elements to it.

Sneaking towards the door, he carefully and quietly opened it just a crack, peaking outside.

The first thing he saw was Zima, face down on the ground in a shimmery, dark puddle. Then, suddenly, a dark figure stood right in front of him as the door was thrown open, knocking him backwards.

Blinking rapidly, he got up and into fighting stance, or what he assumed was a fighting stance from the drawings he had seen.

The man was a lot larger than he was, in every way. His hair was ruffled, there was blood on his face and dark shards sticking out of his head. He looked dangerous and possibly murderous, but he had a strange look on his face, as though he had no idea what to do now.

“Kaz, this is strange…” The man mumbled, followed by muffled sounds coming from what A41-5920 assumed was some sort of headset.

Then, suddenly, the man moved towards him again, a lot more careful this time, like he tried to not scare him off.

Should he fight back? Should he just go with the man and hope that he wouldn’t get hurt that way?

It very quickly turned out that he had no choice as the man picked him up, holding his wrists together with just one hand and still reaching perfectly around both of them. Fighting was no option, he would only hurt himself.

“No, it’s not just you….I see it, too.” The man mumbled again, staring directly at A41-5920 with his one eye, the other being hid behind an eyepatch of sorts.

He was lifted up by his wrists, struggling a little against the other’s grip, before he was simply thrown over the man’s shoulder.

Everything around him moved so quickly and was shaking with every step the man took. It was close to impossible to see where they were going, especially in his current position, but they definitely went on for quite a bit before the man set him down on the warm sand.

“Look. I’m not going to hurt you. Just stay calm.” The man’s voice was soft and he spoke slowly, accentuating his words with gestures.

He wanted to tell the man that he understood him, that they spoke the same language, but his body wouldn’t let him respond. Despite the warm sand he shivered over and over and as he finally remembered how to properly open his mouth, the only thing escaping him was a soft whine.

~~~~~~

After they sat in the sand for a while, A41 not being able to speak properly, like he wasn’t in control over his body, and the man smoking something, he spotted another helicopter at the horizon.

The thought of flying again almost made him excited, but he also didn’t know what to think about some stranger taking him anywhere like this.

Volkov would be angry if he found out that he left just like that.

As soon as the chopper was close enough to the ground, the man lifted him up again and carried him over, almost throwing him into the cold metal machine before climbing in himself.

The pilot threw them a quick glance, then another and another, looking confused, but then he pulled them up again and took off.

Why did everyone look at him like this? Was something wrong with him? Did he know those people and just forgot about them? He was not someone to forget stuff like that, and if he did he would remember after a couple of minutes.

~~~~~~

The flight in itself was mostly silent, almost awkwardly so as the man seemed to stare right into his soul while quietly typing on some strange device.

They seemed to go further south from what he could tell and then almost seemed to plummet into the ocean, except the did land on something he simply didn’t see from his position on the ground.

The man pushed the door open and he was greeted by bright lights and the clicking of guns.

Sitting up carefully, his eyes followed the man leaving the chopper until he saw a group of men, some with black masks on, some without, all clearly soldiers.

Then there were two others, one walked a little weirdly, he didn’t know why, but the man seemed to have a strange way of walking, the other immediately began arguing as soon as he reached the man who brought A41 here.

He carefully sat on the edge of the chopper, then jumped out and landed carefully on the ground.

The chopper took off immediately after that and left them all in a strange silence. The man who had been arguing slowly took a few step towards him. His shoes made strange jingly sounds whenever he took a step. Everyone’s eyes were on him now.

“Who are you, boy?”

~~to be continued~~

[2whatcom-blog]

Philippine Fossils Add Stunning New Species to Human Household Tree

The human household tree simply acquired just a little extra luxuriant and much more fascinating. Scientists say fossils found in a cave on the island of Luzon within the Philippines characterize a beforehand unknown department of humanity, a species they name Homo luzonensis. The stays reveal a tiny number of human with a lot of startlingly primitive traits that lived as just lately as 50,000 to 67,000 years in the past, overlapping in time with our personal species, Homo sapiens, in addition to different hominins (members of the human household) together with the Neandertals, Denisovans and Homo floresiensis. The discover raises essential questions on early hominin evolution and biogeography, and highlights simply how a lot of human prehistory stays to be found. The invention of H. luzonensis has been years within the making. The primary trace of it surfaced in 2007 when archaeologists digging in Callao Cave, a preferred vacationer attraction on Luzon, recovered a single fossil foot bone. The bone was clearly petite, comparable in measurement to the foot bones of the small-bodied Negrito individuals who reside on Luzon right this moment. But its form was "really weird," recollects paleoanthropologist Florent Detroit of the Nationwide Museum of Pure Historical past in Paris. Detroit suspected that the fossil specimen got here from "something more interesting than a small Homo sapiens," he says. However with solely a single bone to go on, he couldn't make a compelling case for that interpretation. So when he and his colleagues printed their description of the foot bone in 2010, they concluded solely that it belonged within the genus Homo. Which species it got here from remained unsure. Over the following few years the researchers returned to the cave to search for extra bones. They hit pay dust, recovering 12 extra fossils--assorted tooth in addition to hand and foot bones--for a complete of 13 specimens representing not less than three people. Detroit and his collaborators describe the brand new fossils in a paper printed within the April 11 Nature. One in every of a Sort The fossils exhibit a mosaic of so-called primitive and derived traits. The primitive elements bring to mind our historical ancestors corresponding to Australopithecus afarensis, the species to which the well-known 3.1-million-year-old Lucy skeleton belongs; the derived ones resemble H. sapiens. Wanting on the tooth, for instance, the premolars of H. luzonensis are giant and one among them has an additional tooth root--primitive options. The molars, in distinction, are very small and strikingly fashionable. Collectively these dental traits are "a very special combination that doesn't exist in any of the comparative samples we studied," Detroit observes. Nonetheless, the tooth alone wouldn't be sufficient to justify naming a brand new species, explains Maria Martinon-Torres of the Nationwide Analysis Middle on Human Evolution in Spain. The important thing factor, she says, is "the combination of these teeth with those hands and feet." Intriguingly, the palms and toes of H. luzonensis are fairly primitive, with curved finger and toe bones, that are usually seen in species that climb timber. Though folks right this moment can and do climb timber, people misplaced most of their diversifications to arboreality after ditching life within the timber life for all times on the bottom hundreds of thousands of years in the past. So a human ancestor from 67,000 years in the past or later with climbing anatomy is sudden, to say the least. Contemplating the tooth and hand and foot bones collectively, "I agree with the authors that the combination of features is like nothing we have seen before," Martinon-Torres says. How on earth did H. luzonensis find yourself with this distinctive mixture of traits? That is the million-dollar query. Figuring out the ancestor(s) of H. luzonensis is inconceivable at this stage. Stone instruments and butchered animal bones from one other website on the island trace that people of some type inhabited Luzon greater than 700,000 years in the past. However within the absence of any bones of the traditional butchers themselves, whether or not they may need been H. luzonensis or forerunners of H. luzonensis is unknown. The one different hominin fossils from the Philippines are 30,000-year-old bones of H. sapiens discovered on Palawan island,some ofwhich are small, however they lack the primitive options seen in H. luzonensis. Different human ancestors are recognized to have lived elsewhere in japanese Asia at across the identical time as H. luzonensis, however the fossil proof is inadequate to attach the Luzon hominins to any of those different teams. And makes an attempt to extract DNA from the fossils--which may make clear the origin of H. luzonensis and the way it's associated to different members of the human family--have failed. Excavations in Callao Cave, a preferred vacationer attraction on Luzon, have yielded fossils of H. luzonensis and a few butchered animal bones, however no stone instruments. Credit score: Callao Cave Archaeology Venture Unclear Origins Specialists are entertaining speculative concepts concerning the origin of H. luzonensis, every of which might revise the story of human origins in essential methods if borne out by additional proof. To totally admire the the potential impression of those explanations, nonetheless, we've to first revisit a discover from 15 years in the past. In 2004 scientists engaged on the island of Flores in Indonesia unveiled an astonishing discovery: stays of a miniature human with a small mind and a bunch of different primitive traits that, like H. luzonensis, lived till comparatively just lately. The bones had been stated to characterize a beforehand unknown member of the human household, Homo floresiensis, which was promptly nicknamed the hobbit species after J.R.R. Tolkien's diminutive characters. Researchers put forth two evolutionary eventualities to elucidate the hobbit's placing traits. Within the first, H. floresiensis descended from large-bodied, large-brained Homo erectus and developed its small measurement as an adaptation to the restricted meals assets out there on the island--a phenomenon often known as island dwarfing. Alternatively, H. floresiensis inherited its small proportions and different out-of-time options from a extra primitive ancestor--an australopithecine of some sort--that someway managed to disperse from Africa into Asia. Each potentialities flouted entrenched concepts about human evolution. Though different giant mammals are recognized to comply with the island dwarfing rule, people had been historically considered exempt, the thought being that the power to invent cultural options to life's challenges has buffered people from lots of the environmental forces which have formed different animals. And australopithecine fossils have by no means been discovered outdoors Africa--the oldest recognized members of the human household discovered past the mom continent all belong to Homo. (A handful of skeptics proposed that the Flores bones as a substitute got here from a contemporary human with a illness that affected its development, however no dysfunction proposed to this point can account for the hobbit's suite of options.) Comparable evolutionary eventualities may clarify the Luzon fossils. "Given the recent increase in the number of small-bodied, late-surviving that show many australopith-like features, I think we need to reevaluate whether all of this material should be classified as Homo," says Tracy Kivell, a paleoanthropologist on the College of Kent in England. Along with H. luzonensis and H. floresiensis, a small human ancestor from South Africa referred to as Homo naledi, introduced in 2015,falls into this class. (Like H. luzonensis, H. naledi additionally has curved fingers indicative of climbing.) "With all of the new, weird and wonderful discoveries lately, I wouldn't rule out that more primitive hominins made it out of Africa and that the small-bodied Homo species with australopith-like features have evolved from something more primitive," Kivell remarks. Alternatively, a large-bodied ancestor like Homo erectus may need colonized a number of islands in southeast Asia and undergone dwarfing in every locale. Variations between dwarfed species may replicate diversifications to native circumstances. As an example, H. luzonensis seems to have lived in a forested setting that may have favored climbing potential. One other potential issue bears point out. DNA research have proven that human teams together with H. sapiens, Neandertals and Denisovans interbred sometimes. In idea, comparable mixing may have contributed to the mosaic of traits discovered within the fossils from Callao Cave, in response to organic anthropologist Rebecca Ackermann of the College of Cape City. Sure elements of the premolars specifically could also be in keeping with hybridization, although she cautions that it isn't doable given the out there proof from recognized hybrids to determine definitively that hybridization occurred on this case. Island Explorers Partially due to the proof for gene stream between human teams throughout this time interval, in addition to the shortage of comparative materials from this area, Ackermann doesn't assist the brand new species designation for the Luzon fossils. "I actually feel quite strongly that all this species naming is missing the point," she contends. The actual significance of the Luzon discovery, she says, is that it illustrates the intense range of human ancestors throughout the previous few hundred thousand years--"the result of their having populated a huge range of contexts under the influence of various evolutionary forces." Which brings us to a different burning query about H. luzonensis: how did it find yourself on Luzon within the first place? Luzon is surrounded by deep water. Even throughout instances of decrease sea ranges, attending to the island would nonetheless have required crossing a frightening expanse of open ocean. Researchers grappled with the identical downside when H. floresiensis first got here to mild. Like Luzon, Flores is a deep-water island. Some consultants proposed that the hobbits should have had boats to make the journey. But the hobbit's mind was solely concerning the measurement of a chimpanzee's and its stone instruments had been comparatively simple--not what one would possibly anticipate of a species that might make boats. Others urged that the hobbits or their ancestors had been swept out to sea throughout a giant storm or tsunami and washed up on Flores, maybe hitching a experience on drifting mats of vegetation--a stroke of extremely good luck. With solely H. floresiensis to go on, the problem remained unresolved. However with the invention of H. luzonensis there are actually two primitive hominin species on report that inhabited two completely different deep-water islands in Southeast Asia through the late Pleistocene (the interval between 126,000 and 12,000 years in the past), which modifications the equation. "One strange event may be luck; two suggest something more interesting," asserts John Hawks, an anthropologist on the College of Wisconsin-Madison. What's extra, he says, there's good archaeological proof (although no fossils) of hominins on Sulawesi--another Indonesian island surrounded by deep water--well earlier than fashionable people had been within the area. "These hominins were crossing water barriers. We don't know how regular it was, but I have to think that each successful population is a survivor of many possibly unsuccessful attempts." The massive-picture lesson right here is that these early ancestors "were much more adaptable than we used to give them credit for," Hawks says. "They were smart, they learned from each other, and they transmitted traditions that helped them quickly adapt to new ecologies." Read the full article

[damienthepious]

Alright alright, fic update post! I - get this - finished a chapter two to something, so, without further ado,

Fate Picks Its Favorites - True Gold

Chapter 2 - Namesakes

[Chapter 1] [AO3] [Chapter 3] [Chapter 4]

The trouble is, the babies need names before any adoption can be finalized, and Lady Scott hasn’t exactly been considering children lately. She hasn’t had any reason to, and she certainly hasn’t been wasting time considering what names potential children might have. The unnamed babies in question are both sleeping, each carefully settled into their brand new cribs as Lady Scott’s lawyer weaves a legal safety net around all of them using words like asylum and protective custody and the right to nationality of foundlings. Sabitri had the insight to purchase a book of baby names with the rest of the supplies, but right now it’s only dangling from Diana’s hand as she paces back and forth between the cribs.

She’s stalking. It’s something her mother used to do in moments of anxiety, and apparently Diana picked it up along the way. That thought makes her serene expression twitch, which irritates her enough that she gives up the pretense of even trying to read the baby name book, and she sets it down on her desk. Forcing her feet to stop at the feet of one of the cribs, she leans over the rail, staring down at the baby in contemplation.

The blue baby is sucking on his neon-glow pacifier even in his sleep, and his arms are clutched around the also-sleeping fish. Gears in her head turn.

This child was sent here with comfort objects. Maybe-

She needs to see the pods again.

They’re tucked away in an unused room next to the study, because Diana wants them nearby and because she knows it’s a room that her husband won’t enter unprompted. The slipshod pod is chock full of exposed wiring and greasy metal that she really isn’t sure if she should touch (someone put a baby in there?), but she reaches an arm in anyway, her sleeve carefully folded up. She doesn’t see anything else recognizable; no baby blankets, no convenient name-tag, no teddy bear, but when she retrieves her hand, her fingers brush against something that is unmistakably a button.

It’s under the lip, inside where the front hatch of the pod opened up. It’s not visible from outside, but what use would an infant have for a button, anyway? Is it some sort of low grade toy, just meant to engage motor function, or-

The moment her fingers brush against it, there’s a light and a sound, both unfamiliar. She crouches closer, because the voices - and they are unmistakably voices, now - are coming from inside the pod, and her angle is wrong to see the source. For a moment she thinks it’s a video, but the image soon resolves a bit closer than that.

It’s a hologram, like Diana has only ever seen in movies. Two tiny projected figures, each holding the other with their faces aimed away from Diana and towards the back of the pod- where the baby would have been. Their heads are too big, and their skin looks tinged blue in a way that she would have assumed was just a problem with the tint of the image if she hadn’t held a blue baby in her own arms less than an hour before. They are saying something, and though Diana can’t understand any of the words, the tone is very clear.

They are desperate, and they are loving, and they are saying goodbye.

It’s a very short message. The moment before it ends, the figures embrace tightly, and then they jerk apart as the hologram replays.

Their language is incredibly foreign, full of sibilant noises and trills that Diana is unsure if she could replicate. It sounds, in fact, quite alien.

Which really shouldn’t be a surprise, she thinks as the message statics out and replays a third time. She had known pretty instantly that the infants are both non-human, but she hadn’t expanded that thought to its logical next step, to the worry of what they are, if not human. The boxes that are ticked in her head now, though, include: advanced technology, unfamiliar anatomy, unfamiliar skin tones, incredible strength, literal flight, seemingly intelligent aquatic life, and all of the above dropping from the sky. The idea that they are aliens is certainly pulling ahead in the pool of likely origins for the children.

On the fourth repetition, she thinks she’s managed to pick out a specific word, or something like it. They (the parents? The alien parents?) say it near the beginning, and drop it a few more times in the middle, and near the end they repeat it over and over, drawing out long hisses between each instance.

She narrows her eyes. As strange and inhuman as the words are, there is something familiar here. Something about the way they say it, the obvious affection in their eyes, in the way they occasionally gasp, stop, compose themselves before continuing on. Something about the way that one particular word is said, so carefully, so warmly.

They certainly say it like a name.

If she’s wrong, though, and she tries to canonize it as the child’s name, it could be highly traumatizing down the line, couldn’t it? She listens again, and again, sat on the floor inelegantly, like a child. She has to be sure.

By the time she is sure, she’s also sure that she could recite the entire short speech phonetically, from memory, though she obviously hasn’t garnered any deeper understanding. She’s no linguist, and she has no convenient stone from which to base her translations. But she is sure of the most important part. She tests the word aloud, very quietly. She barely has to move her lips. She’s lucky that it’s one of the sounds that she can reproduce with her human vocal cords, and she feels-

Diana stands, carefully smoothing down her skirt, and the hologram shuts off on its own. Her mouth quirks into something like a smile. Clever device, she thinks, and then she turns her attention to the other pod.

On the surface, it’s far more impressive; gilded and gleaming and slick. When she runs her hands over the surface, they slide like she’s touching solid silk, and the inside is cushioned and gives enough to leave impressions of her fingertips for seconds after she pulls them away. No matter how carefully she looks, though, she can’t find a button like the one in the blue baby’s pod. She can’t find much of anything, actually, besides padding and extraneous shine. Sent in style, this one, but not much in the way of practical applications.

Well. She supposed it would be too much to ask to have that kind of luck twice in a row.

Sabitri is unpacking baby supplies in the corner when Diana comes back into the study, and her lawyer hasn’t moved from where she left him. He’s so engrossed in the heavy book in front of him that he doesn’t even blink at her reentry, and Sabitri knows her well enough that she simply continues with her work as well. Diana allows herself a brief twinge of pride in her people before she strides back over to the crib.

He’s still sleeping, but the fish is awake again, blinking up at her in drowsy confusion. Her lip pulls to the side, her nerves jumping in her stomach for only a moment before she murmurs the name aloud.

“Syx.” She’s already decided on the spelling she intends to use. She knows she’ll have to differentiate it from the number- she pronounces it differently, swallowing the vowel like the aliens had. Her eyes flick to the fish, whose fins had flared at the word. It’s looking up at her in obvious shock, and then with a look that makes Diana think that she has impressed the creature. She raises an eyebrow, gestures to the child very slightly (not enough for the two other humans in the room to notice), and repeats, questioningly, “Syx?”

The fish blinks, mouth slack for a moment before it flutters up and twirls in a quick circle, teeth exposed in something that could have been a grin on a mammal. On the fish, it looks somehow both pleased and intimidating. Or, it would have been intimidating if the thing wasn’t trapped in a tiny ball.

She takes the pseudo-smile as a confirmation, or as close to one as she can expect to get. She says the name a third time. Louder, now.

Her lawyer finally glances up from his paperwork. “You’ve made a decision?”

“One of two,” she says, folding her arms over her chest. She turns to the second boy, brow furrowing in concentration as gears turn in her mind.

This baby- he already has a bright, charming smile, and lovely hair, and he has cool blue eyes like her father did. Diana is momentarily grateful that she can’t see them while he’s sleeping. Then, of course, there are her emerging bruises to consider as well.

It wouldn’t be fair, would it? Just because the child has- features that remind her- it wouldn’t be fair to chain him with her father’s name as some sort of bizarre, too-late revenge. She can’t chain him with that sort of baggage. It wouldn’t be fair to either of them, and it certainly wouldn’t be a good first step towards teaching the boy to mind his own strength.

She purses her lips. Fathers, though. That’s a thought. Her own might be scorched earth but her husband-

The late Lord Scott had been one of the primary reasons she decided to marry Victor in the first place, over her other potential matches. He had been clever and observant and kind and he had known from the moment they met that what Diana needed most was a mentor. So, he slowly earned her trust and then taught her how to be clever like him, and observant like him, and she skimmed through the lessons on kindness as well, just to round out her edges. He taught her how to hone her hypervigilance into something useful and precise, and combined with her knack for being overlooked, she had become rather dangerous in certain circles. So much so that, when her father-in-law died, he explicitly left his company in her hands. Oh, Victor was to ‘run things’ as expected, of course, but beneath the lawyerspeak and cigars and back-patting, Diana and the late Lord Scott understood each other. Diana was, they both knew, impeccably good at pulling strings.

There’s a bust of her late father-in-law on the bookshelf behind her; she doesn’t turn to look at it.

Diana isn’t the type of person to prioritize kindness above self preservation, but… well, the two don’t always have to be mutually exclusive.

“Wayne,” she says, quite softly. “Wayne Scott.” She knows that just giving him the name of a good man won’t be enough on its own, but maybe it will help in some small way. His namesake was the only person she has ever known who never used his position, his power, to hurt others. She doesn’t want to turn this boy into his grandfather, but she can try to pass on some of what he taught her anyway.

She suspects that down the line there will be some consequences to giving her human-passing son a human-sounding name and her visibly inhuman son a name that slips off the tongue like an asp, but- well, her hands are tied. She can’t in good conscience know what Syx’s parents called him and then call him something else, call him Steven or Richard or god forbid Victor Junior, and she has nothing else to go on for Wayne. No clues, no context. She’s just going to have to explain it to them when they’re old enough to understand, and hope that it’s enough.

The ink on the official adoption paperwork is dry within the hour.

[the-lady-ren]

Hello, hello

Hello my friend!Thank you so much for your patience in waiting for this. WOW. I loved writing this for you. Before receiving your prompt, I never even really thought much on Kitty’s origin. But here we are! I hope you find this as interesting to read as I did to write.

Again. Thank you so much for this fun prompt. Shoot me a line and let me know how you like the outcome. 💜

Back when the cathedral still stood, curled in his strong arms, you ask Kylo one day how he came to be. Kylo has mentioned from time to time that he is the only one of his kind that he is aware of. He always remembers living in the cathedral, fending for himself since he was about ten years of human age. While he can’t recall specifically how he got there, he has some ideas, but he has never delved too deeply into his past.

Sighing heavily, Kylo unwinds his body from yours in the warm, nestlike bed. You sit up, watching as he moves through the shadows, drawing a warm scarf around his neck. It’s always a bit drafty in the cathedral, especially deep within where his room is, and he’s always wearing a scarf of some sort and wraps you in them as well whenever you come visit. After moving some boxes aside, Kylo finds what he is looking for. A battered and patched suitcase, the handle worn. Lifting it with a grimace he brings it over to the bed and turns the combination locks with his broad thumb, clicking the latches open.

“This is all I have,” he explains, lifting out folders and tattered Manila envelopes. “I don’t know much about where I came from, and I think that it was purposeful that I forgot. Maybe to protect me, maybe to protect them, I’m not sure.” Opening one of the large yellow envelopes, he thumbs through the papers within and hands you a thick file folder, the pages faded with age. “This should answer at least some of your questions,” he says, his tone apprehensive and sad.

As you flick through the pages, you realize that these represent the years long documentation of some sort of experiment. The terms are unfamiliar to you, but you learned enough in high school and college science classes to grasp at least some of it. Genetic engineering, selective hybridization, all of these terms with calculations, diagrams and observation reports.

Kylo rakes his hand through his hair, flattening his ears briefly as he paces the room, his tail flicking sharply, nervously behind him. “There were more before me,” his voice is soft and full of untold sorrow, “but I was the only one to survive past infancy.”

Coming back towards the bed he lowers himself down and sits next to you as you scan over the documents. He reaches into the suitcase and pulls out an envelope. This one is full of pictures. As he flips through them, he puts certain ones aside. “These came out of order somehow,” he murmurs, his voice irritated. Your eyes stare, wide with wonder at what he’s sharing with you. Handing you a stack of photographs, you go through them, staring at each one individually.

In one, a group of people in white lab coats, wide, proud grins on their faces as they hold up a Petri dish of unknown contents. Kylo points a long index finger at them and explains, “Their specialty was mammalian hybridization. Uh…cross breeding, through manipulation of DNA, different kinds of mammals. Not hard with non-human species. There are hybrids that live among us all the time. But crossing that barrier…introducing animal DNA into a human embryo,” he pauses, swallowing and clearing his throat, “that’s a whole different subject,” Taking the stack of photographs from you, he places the top one at the back of the stack, bringing the next one to the front. This one shows an odd series of scientific instruments, different tanks and tubing.

“From what I can gather,” he says, “these were the incubation chambers for the hybrid embryos. Modeled to replicate a womb and an amniotic sac as much as possible, once the embryos were deemed viable, they would be placed here for development. Closely monitored. Many didn’t make it past the first few days here…” Brushing his hair out of his eyes again, you look up at him, the solemn expression on his face, his brow coming together in his obvious discomfort and lingering sadness. Feeling a pang in your chest you wrap your arms around him in a quick hug. He smiles, a thin, tight smile, and turns your attention back towards the photos.

Spreading them out on the bed in a sort of chronological order, he goes through each one. Most of them are for documentation purposes only, just showing the labs, instruments and unrecognizable information on a computer screen. “Ah, here,” he says, handing one to you. In the photo you see a tall, smiling man, his labcoat pristine. In his arms he holds a plump baby, but not just any baby. This baby is very obviously Kylo. Tiny cat ears stand up from his round head, his black hair plastered low against his baby scalp. His eyes are different, though a lay person wouldn’t see it right away, and draped over the man’s arm is a long, black tail. The baby is chewing on something, as babies do.

“This is me, I guess,” Kylo says. He points out other pictures of himself, showing his growth and development over time. The same man is in every picture with him, whether it’s a more formal pose for the official record or something candid, watching him stalk a tiny toy mouse, interacting with non hybrid kittens or playing with blocks and toy cars like a normal child. “I can’t say I was mistreated,” he tells you, “at least from what I can tell. Again, these pictures serve as the only memories I have. I don’t recall these specific moments, that specific man. Just a vague sense of…observation, an overwhelming curiosity. He seems…"Kylo pauses again, gathering his thoughts before moving on, "kind?” Again he sighs, his broad shoulders slumping as he scans his mind for anything, even a shred of a real, concrete memory. You’re in awe of him, all this information he’s sharing with you. The trust he has in you is overwhelming.

“Here,” he says, taking the folder of documents from your hands. You’d been clutching it, your palms damp with sweat and your heart pounding in your chest as you listen to him explain these things to you. He flips to the back of the folder, pulling free the last few yellowed pages. “These pages mark the end of the experiment,” Kylo lays the pages on his thick thigh, his index finger scanning the words, pointing to the sentences he wants you to read. Your eyes follow his finger, reading the cramped, sloppy handwriting of a scientist. They explain that the lab is to be closed, these are really the final days of the experiment. Funding has been pulled, redirected to something more “worthwhile”. The last few sentences demonstrate an attachment, unexpected certainly, but there nonetheless, as the scientist in charge of the lab struggles with what to do with the subject.

“And as we conclude what can only be described as a more than successful hybridization, what to do with Kylo? Any remaining embryos have been destroyed, the incubation tanks broken down, drained and packed away. But still Kylo remains, playing in his room, reading books and daydreaming like any relatively normal human male. I cannot take him home. How would I explain it to Lydia, how could we keep him safe when he was scheduled for euthanization? Could I take him to a hospital or to Child Protective Services? Absolutely not. He would be ostracized and brought somewhere that he would be experimented on. There are enough DNA markers to connect him to me, to this lab and this corporation. No, I am too connected to him to take him home. I have to find a place where he will be safe. I have given him the knowledge and the tools to make a life for himself, now it is time to put those tools to good use. I had hoped for just a little more time…he is still so young.”

Here it cuts off, the fading signature of whoever this person was scrawled below, illegibly. Your eyes fill with tears realizing that he was supposed to be killed. This living, breathing man sitting next to you could have been “put to sleep” like so many unwanted animals. The kindness of this unknown scientist prevented that. Throwing your arms around Kylo, you hug him tight, your face buried in his chest, struggling to control your tears. “Did you ever want to find him?” You murmur, your voice muffled by his shirt.

Kylo shakes his head, “No, ” he answers, “there is too much risk involved. Not only for him, but for myself. Who knows what could happen were I to reach out. That he saved my life, brought me here,” he sweeps his arm in a grand gesture, drawing your attention around the room. “As far as I remember, a lot of this stuff was here. There was food here, books and tools to begin to grow my own. I may not remember where I came from, but I remember what I learned. With the books and tools left for me, I was able to grow food, reconnect the electricity, make sure the water was safe and clean…” he shrugs again, “and now with you,” he swings his arm around your shoulder, pressing his full lips against your temple, “I have everything I could have ever wanted.” You nuzzle against him, smiling softly. Sliding slowly away from him and off the bed, you begin gathering the papers and photographs, placing them back into the envelopes and folders and back into the battered suitcase.

“Thank you,” your voice rings out softly in the cozy room that Kylo has made his own. He raises his yellow eyes to meet yours, a crooked smile on his handsome face. “I mean it. Thank you. I…I don’t know why you trust me like this, you could have lied, told me you fell from space and I would have believed you. The risk you face…” Kylo places his large hands on your hips and pulls you towards him, burying his face in your middle and sighing with relief.

“I don’t know what it is about you,” he says, lifting his gaze to meet yours, “In such a short time, you have not only accepted me and what I am wholeheartedly, but you’ve made me trust another living being in a way I didn’t think I was capable of.” He raises himself onto his knees, wrapping his arms around you again, holding you close, making you feel safe. “You are my home,” he says, “and you are the closest thing to family I have ever had.” A single tear rolls down your cheek as you crush your lips against his, sealing a silent promise that you are more than happy to make.

[makingscipub]

Mice, dice and copycats: Metaphors for gene drives in mammals

When you hear the word ‘gene drive’, you will either be baffled or you will think about mosquitoes, engineered to eradicate insect-born disease like malaria, Dengue fever, or Zika for example. But gene drive research has now moved from insects to mammals.

Mammals

On the 23rd of January, researchers at University of California, San Diego, led by Kimberly Cooper, announced that they had developed a method for controlling inheritance in mice using the gene-editing tool CRISPR Cas9.

Such a method, generally called ‘gene drive’, had, so far, only been demonstrated in insects, not mammals. Hannah A. Grunwald, Valentino M. Gantz, Gunnar Poplawski, Xiang-ru S. Xu, Ethan Bier, and Kimberly L. Cooper, published their paper on ‘Supermendelian inheritance’ in Nature on the 23rd. Two press releases were issued on that day, one by UC San Diego (UCSD) (which was used widely, e.g. by Science Daily), and another syndicated by the Press Association.

Grant Jacobs, a computational biologist and science communicator, published a blog post the following day, which is worth a read, as it provides a clear and detailed explanation of this achievement. He explains: “A gene drive is the informal name given to a process where a genetic variation is set up so that it will be inherited more often in the offspring than it would by chance. In a gene drive each generation has a better than 50% chance of inheriting the new variant, so over time the chosen variant becomes the dominant variant of that gene in the population.” Jacobs goes on to tease out what the new research demonstrates and does not demonstrate, what it has achieved and what its limitations are.

Another good overview of the background to this research can be found in a Nature News article published on 6 July 2018, together with a Science article from 13 July 2018. These articles appeared at the time of the submission of a pre-peer-reviewed version of the paper on the preprint server bioRxiv.

Mice and models

The Science article summarises the research as follows: “The team from the University of California, San Diego, used the genome editor CRISPR to put a gene in the mice that modifies their coat colors. But they also engineered these same mice to pass on the genes that create CRISPR itself so that progeny edit their own genomes to carry the coat color–modifying gene. When they mated an engineered mouse to a normal one, it should have created a pup with the coat color–modifying gene in one of two chromosomes. But because the pup also inherited CRISPR, it altered the unmodified chromosome passed down from the normal parent so that it, too, had the gene.”

The scientists did not set out to find a way of eradicating diseases or pests, in this case rodents, but to demonstrate ways in which gene drives can be used to bias inheritance in order to “transform the use of rodent models in basic and biomedical research” (Nature article), to “make mammals models of complex human genetic diseases, like arthritis and cancer, that are not currently possible” (Press Association, 23, January), to control “the inheritance of multiple genes in mice” (Cooper quoted in City News Service, 23 January), and even to understand “the mechanisms of evolution” (UCSD, Press release, 23 January) and of the ”origins of mammalian diversity” (ibid.).

As a secondary outcome it my “decrease the time, cost and number of animals needed to advance biomedical research on human diseases and to understand other types of complex genetic traits” (ibid.).

Media

How was this new research reported after the official publication? To see what is out there, I consulted the news database Nexis and downloaded all articles published in English Language News between 23 and 28 January. After removing duplicates, there were, astonishingly only nine items left, and of these only four were published in mainstream newspapers, of which Ian Sample’s article for The Guardian was the most interesting. One article by Cooper herself appeared in The Conversation on the 24th of January (republished in MENA English, Middle East and North Africa Financial Network). Others mainly reproduced what the two press releases (UCSD and Press Association) had said.

To this small sample I added one article published in New Scientist, another in Scientific American (reprinting an article from Quanta Magazine) and a third in the Financial Times.

In this blog post I’ll pick out a few metaphors used in this coverage, but I will not cover ethical legal and social aspects in any detail. This will have to wait for a bigger and more detailed study.

Metaphors

Loading dice and flipping coins

The first two words of the Nature title, “Super-Mendelian inheritance mediated by CRISPR–Cas9 in the female mouse germline”, are already slightly metaphorical or rather hyperbolic and point to a nexus of metaphors explicating how inheritance works and is reworked in gene drives. The phrase ‘supermendelian inheritance’ had previously been employed to report on research on gene drives in mosquitoes.

One of the most used phrases (see Press Association, 23 January) was that of ‘increasing the odds’. This was in the context of using a specially designed gene drive to increase the chance of mouse offspring to inherit two copies of a mutation causing them to be born with white instead of black fur. But how does this work? To understand this, we have to go back to the beginnings of genetics.

The Press Association article explains: “Under normal circumstances, genes come in pairs, on inherited from each parent. Gregor Mendel, the ‘Father of Genetics’, discovered this fundamental principle of heredity in the 19th century as he experimented with pea plants. It means an offspring has an equal chance of inheriting a particular genetic variation, or mutation, form either its mother or father. A gene drive loads the dice, making it more likely that the offspring will be born with a chosen trait, such as fur colour.”

In her Conversation article, Cooper has provided one of the most detailed explanations of this type of inheritance . Here she talks about ‘uber-inheritance’, which ‘boosts the odds’ of a trait or several being inherited. To explain things, she uses the analogy of flipping or tossing a coin: “Each animal has two versions of each gene. Each parent will pass only one version to each offspring. Inheritance of different genetic traits is therefore a bit like a coin toss where a particular version is inherited 50 percent of the time.” This gets us to the uber- or supermendelian aspect of the research:

“Creating a mouse that inherited mutated versions of three disease-causing genes from each parent has the same likelihood as six simultaneously flipped coins all landing on ‘heads.’ But what if the coins could be unevenly weighted so that they have a higher probability of falling heads up?

The concept of stacking the odds in favor of one of the two versions of a gene underlies efforts to engineer gene drives. A gene drive is simply defined as a piece of DNA that is inherited more often than can be explained by random chance over several generations so that it sweeps through a population.”

Surprisingly, none of the articles on gene drive in mice used card analogies instead of dice or coin ones, despite the fact that card games can be used quite successfully to explain Mendelian inheritance – some people even talk about the card game of life!

Scissors and pens

To make their gene drive work, the Californian team used a now ubiquitous tool, namely a gene-editing tool called Crispr/Cas9. As quite a few articles said: “the system relies on ‘molecular scissors’ to make highly precise changes to DNA.” (Press Association, 23 January; The Conversation, 24 January)

One article in The Guardian was entitled “Scientists rewrite mice DNA so genes can be spread through species” – echoing older synthetic biology metaphors of rewriting the book of life. The article also puts this new research in the context of existing gene drive research using insects, where gene drives are used for “rewriting the genetic makeup of mosquitoes that carry the malaria parasite” (Ian Sample, 23 January).

Copycats

Now we come to the special way in the researchers used gene-editing and to the fun name they chose for the molecular element that was employed. It was called ‘CopyCat’. This “was spliced into the gene for an enzyme controlling fur colour. Gene editing allowed CopyCat inserted into one copy of the inherited gene to be duplicated in the other during egg production in females. This increased the chances of CopyCat being passed on to the next generation.” (Press Association, 23 January)

In another article, CopyCat is called a “self-replicating DNA sequence” (UPI.com, 24 January). It was said to be “copying and pasting the same genetic coding from one chromosome to the other”. The article goes into more detail about the various mechanisms involved.

Donors and recipients

Crispr and CopyCat are used, it seems, between donor genes and recipient or target genes. As Cooper explains in The Conversation: “In a gene drive, a donor gene, which is the version we want to introduce into the animal, is engineered to use these components so that it can replace the non-engineered version, or the so-called recipient gene. When the non-engineered recipient gene is cut, the donor gene repairs the cut by copying itself into the recipient site so that there are two identical copies of the donor gene.

The donor gene therefore acts like the find and replace feature of a word processing program. The recipient gene is converted so that a mosquito, for example, would have two copies of the engineered donor gene to pass to its offspring.”

In the context of the new research, it turned out that the “donor gene was inherited as much as 86 percent of the time – a heavily weighted coin – compared to just the usual 50 percent.” This was relatively low though and only worked in females.

Selfish genes and cheating gene drives

Some articles also employ more creative metaphors. “Gene drives are pieces of DNA that cheat. They ‘copy and paste’ themselves from one genome copy to a target sequence in the other copy.” (New Scientist, 23 January).

This article also tells readers that some people call gene drives ‘active genetics’ (see also Scientific American). The term was apparently coined by two of Cooper’s colleagues, Valentino Gantz and Ethan Bier (see Scientific American, 28 January).

Such active gene drives are not only ‘super’ or ‘uber’, they are also selfish. As a Nature News article said: “Gene drives work by ensuring that a higher proportion of an organism’s offspring inherit a certain ‘selfish’ gene than would happen by chance, allowing a mutation or foreign gene to spread quickly through a population.” (6 July, 2018). I am starting to wonder whether there will ever by selfish self-driving gene drives…

Mice and ice-nine

The Scientific American article also quotes a scientist who framed gene drives more in scifi terms: “Fred Gould, an entomologist and evolutionary biologist at North Carolina State University, likens gene drives to the fictional substance ice-nine in Kurt Vonnegut’s novel Cat’s Cradle: a bizarre form of ice that freezes all other water it touches. Gene drives spread fast because they are sets of genetic elements that spontaneously copy themselves from a maternal chromosome to a matching paternal one or vice versa. In the process of copying itself, the gene drive can also add, delete or modify genes at its insertion point.”

Death and destruction

One short article published in The Times on the 24th of January, focuses on the possibility of using gene drives to eradicate disease carrying insects or invasive mammal species. It uses words like ‘wipe out’, ‘erase’, or ‘wreck’ (ecosystems). Such war metaphors were otherwise absent from the coverage of this particular research into mice, but are widely used when dealing with gene drives and insects.

Possibilities and responsibilities

However they framed it, most articles called this research ‘controversial’. It changes the ‘germline’ of mammals and one therefore has to proceed with extreme care, as this can “alter entire species” (Press Association, 23 January) and can lead to “unintended consequences” (ibid.).

Researchers and commentators alike expressed a need for caution, with everybody treading a fine line between excitement and restraint. One comment reported in the Financial Times summarises this quite well: “Bruce Whitelaw, professor of animal biotechnology at Edinburgh’s Roslin Institute who has also investigated gene drives in mice, said the UCSD project was ‘important as it both demonstrates mammalian gene drive for the first time and starts to clarify the aspects and limitations of the process’. He added: ‘The authors correctly state how this approach could make a huge positive . . . impact for laboratory animal use while pointing the way to the still far-off but feasible application in wild animals.’”

Scientific American pointed out: “For at least some time to come, these kinds of ‘active genetics’ technologies may be more useful as laboratory tools than as instruments for remaking nature.”

This means keeping, at present, an eye on ethics and responsibility in the context of labs and lab animal use, while also scanning ethical horizons for potential dangers ahead, especially with regard to using gene drives ‘in the wild’.

At the same time, it is also important to keep an eye on the language used, which, at the moment, seems to be quite restrained, mostly using metaphors for explanation not hype.

Image: Pixabay

The post Mice, dice and copycats: Metaphors for gene drives in mammals appeared first on Making Science Public.

via Making Science Public http://bit.ly/2Bqfp69

[lopezdorothy70-blog]

The Search for Extended Youth and Extreme Longevity

By Dr. Mercola

Telomeres were first discovered in the 1930s. Every cell in your body contains a nucleus, and inside the nucleus are the chromosomes that contain your genes. The chromosome is made up of two "arms," and each arm contains a single molecule DNA, which looks like a string of beads made up of units called bases.

A typical DNA molecule is about 100 million bases long. It's curled up like a slinky, extending from one end of the chromosome to the other. At the very tip of each arm of the chromosome is the telomere. In 1973, Alexey Olovnikov discovered that telomeres shorten with time because they fail to replicate completely each time the cell divides. Hence, as you get older, your telomeres get increasingly shorter.

If you were to unravel the tip of the chromosome, a telomere is about 15,000 bases long at the moment of conception in the womb. Immediately after conception your cells begin to divide, and your telomeres shorten each time the cell divides. Once your telomeres have been reduced to about 5,000 bases, you essentially die of old age.

In 1984, Elizabeth Blackburn, Ph.D., professor of biochemistry and biophysics at the University of California, San Francisco, discovered that the enzyme telomerase has the ability to lengthen the telomere by synthesizing DNA from an RNA primer.

She, along with Carol Greider and Jack Szostak, were jointly awarded the Nobel Prize in physiology or medicine in 2009 for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase. Telomere lengthening is now thought to be a major key that explains the process of aging and holds the promise of not just slowing aging, but actually reversing it.

Aging as a Disease

Molecular biologist Maria Blasco, Ph.D., director of the Spanish National Centre for Cancer Research and head of the Telomeres and Telomerase Group,1 is another scientist who ascribes to the idea that aging is the foundational disease that needs to be addressed if you want to prevent degenerative and chronic diseases such as cancer.

In 2008, Blasco set out to determine whether lengthening telomeres will in fact slow aging. To do this, she injected the enzyme telomerase into mice. The result? The treated mice lived on average 40 percent longer than normal. “Of course, it was an amazing feeling,” Blasco says, “because I realized that I had manipulated one of the basic mechanisms for why we age, and this could lead to important applications in the future.”

There was a catch, however. The therapy “would almost certainly have increased the cancer rate in mice, had they not been genetically modified to be cancer resistant,” the narrator notes. And humans cannot, at present, be genetically modified. To address this problem, Blasco and her team further refined the process, and in 2012 carried out a second experiment.

This time, the treated mice lived about 20 percent longer and cancer, when it occurred, was delayed. Still, this does not mean telomerase can or will produce identical effects in humans.

The Epigenetic Clock

Steve Horvath, Ph.D., professor of human genetics and biostatistics at UCLA David Geffen School of Medicine in Los Angeles,2 believes science is still in its infancy when it comes to understanding aging. “I believe there's a passive clock that measures the state of your cells,” he says. “It doesn't cause things to deteriorate, it just keeps track of the mechanism that actually does cause that.”

This passive clock mechanism - the epigenetic clock - is something we still know virtually nothing about, but Horvath believes it's a major player, and in order to be able to prevent aging, we have to understand how epigenetic changes within the DNA molecule affect its biological age.

He's convinced it is these epigenetic changes that are the root cause of aging, and the good news, should this be true, is that they're reversible. So, in principle, at least, you can devise treatments to reverse epigenetic changes that drive biological aging within the DNA.

According to Horvath, the telomere theory of aging “has been disappointing.” While many in the antiaging field are enamored with the idea that overexpressing telomerase will lead to aging reversal, the downsides are considerable, because “if you overexpress telomerase and end up with longer telomeres, you actually increase your risk for cancer,” he says. So, while telomere length is part of the equation, he does not believe it's the answer we're looking for.

Antiaging - 'An $8 Billion Industry of Stuff That Doesn't Work'

According to scientist and entrepreneur Joe Betts-Lacroix, the antiaging business is “an $8 billion industry of stuff that doesn't work.” He believes the key to longevity is the prevention of degenerative disease, and were you to find something that actually helps prevent multiple degenerative diseases, then you could transfer billions of dollars from each of those disease fields into the antiaging field. As founder of Health Extension, Betts-Lacroix has raised more than $30 million from venture capitalists in search of a cure for aging.

Combined, the scientists and companies under the Health Extension umbrella have raised more than $200 million. Much of this funding is coming from the tech industry, which has become increasingly interested in biology and cracking the biological code. Betts-Lacroix notes that in recent years, scientists have made remarkable discoveries; finding a number of ways to extend life span in mammals. Now, we're right on the precipice of bringing it into the human realm, which is the most challenging venture of all.

Promising Findings in Animals

One of the findings from animal research is that smaller mammals live longer than larger ones. For example, the smaller the horse, the longer its life span. This, they've found, is due to hormones that not only affect life span, but also size. When these hormones are suppressed for life, the animal will be small and live long. When suppressed in adulthood, they'll retain their regular size, but will live longer than normal.

“As far as we know, for every species we've tested, turning down this hormone system extends life span,” says Cynthia Kenyon, Ph.D., vice president of aging research at Calico Life Sciences, a biotech company owned by Google.3 Kenyon made her mark in the field with her studies of the roundworm caenorhabditis elegans in the early '90s. By partially disabling a single gene, DAF-2, the life span of this tiny nematode was doubled.

“In one fell swoop, the animal lived twice as long,” she says. “That was really stunning, because that was not supposed to happen.” Even more remarkable, other researchers have duplicated the findings on other animals, from fruit flies to mice. Kenyon also notes the research indicates that when you extend life span, you also typically delay degenerative diseases, and when they occur, they're milder.

As many others, by targeting aging, she envisions a therapy, perhaps a drug, that with one pill can delay or prevent the onset of many diseases all at once.

Research Targeting Senescent Cells

At Unity Biotechnology,4 they focus on another aspect of aging - senescent cells. Cellular senescence is when a cell ceases to divide. In a cell culture, a fibroblast cell can divide a maximum of 50 times, after which it becomes senescent or nondividing. Senescent or nondividing cells also play a significant role in the aging process.

At Unity, researchers were able to remove senescent cells in mice, to observe what would happen. “When we did this, something astonishing happened,�� cofounder Nathaniel David, Ph.D., says. The mice had a “profoundly extended health span,” meaning the period of time in which the animals remain healthy and disease free.

The health and function of a number of vital organs were improved, including their hearts and bones, with less heart disease, arthritis, cataracts and other “normal” problems of aging. Soon, Unity will perform its first human trial on patients with osteoarthritis.

Can Diabetic Drug Boost Longevity?

While most researchers are focusing on the creation of new drugs to combat aging, some are focusing their attention on an old one - metformin, commonly prescribed to Type 2 diabetics. It's been noted that diabetics taking metformin tend to live longer than diabetics taking other diabetes drugs. They also have a lower prevalence of other age-related diseases, including cancer and Alzheimer's.

Some nondiabetic people are even taking metformin just for its potential antiaging benefits. While metformin is among the least hazardous drugs out there, it does have some serious downsides such as impairing the use of the important vitamin B12.

It is thought to work via AMP-activated protein kinase (AMPK), which plays a vital role in inhibiting glucose production in the liver (gluconeogenesis). AMPK is a conserved sensor and regulator of cellar energy balance that is activated when the cellular AMP-to-ATP ratio exhibits a large increase due to conditions such as nutrient deprivation or pathological stress.

There are far safer alternatives like the supplement berberine that has been shown to have many of the same effects. It is in my view, a better alternative. Berberine has antibacterial, anti-inflammatory, antiproliferative, antidiarrheal, antineoplastic, antidiabetic and immune-enhancing5 properties, and has a long history of use in traditional medicine, including traditional Chinese medicine.

Berberine even helps combat metastatic stem cells and heart failure. Many integrative health practitioners swear by it as a general health supplement due to its ability to address such a wide variety of maladies. It actually works as well as or better than some drugs for certain ailments.6 For example, it's been shown to improve blood lipids better than statin drugs, and lower blood pressure as well as antihypertensive drugs.

Like metformin, many of berberine's health benefits7 have been linked to its ability to activate AMPK.8,9 AMPK is an enzyme inside your body's cells. It's sometimes referred to as a "metabolic master switch" because it plays an important role in regulating metabolism.10 Low AMPK has been linked to insulin resistance, mitochondrial dysfunction, obesity, neurodegeneration and chronic inflammation - all of which lay the groundwork for a wide variety of serious chronic diseases.

AMPK is also an important neuroprotector. As explained in the Journal of Neurochemistry,11 “AMPK senses metabolic stress and integrates diverse physiological signals to restore energy balance. Multiple functions are indicated for AMPK in the [central nervous system] …” Berberine also benefits brain health and psychological well-being by increasing key neurotransmitters.

Your Lifestyle Is Your Longevity Switch

If there's ever a pill that will ensure extended youth, everyone will likely want it. The question is whether or not such a thing is even possible. The fact of the matter is, your lifestyle and the choices you make every day play an incredible role in how you will age, and I doubt a drug will ever be devised that will allow you to be a junk food-eating couch potato and still age in reverse. Of crucial importance is keeping your mitochondria healthy, and lifestyle strategies such as diet and exercise are key for this.

Science clearly shows a cyclical ketogenic diet high in healthy fats and low in net carbs promotes healthy mitochondrial function. A number of other strategies are also known to boost mitochondrial health, and I discuss several of them in my book, “Fat for Fuel.” Research also shows you can slow down telomere shortening with exercise.12 It basically buffers the effect of chronic stress on telomere length, which helps explain some of its well-documented effects on health and longevity.

Other studies have found there's a direct association between reduced telomere shortening in your later years and high-intensity-type exercises. As noted in a study published in Mechanisms of Aging and Development:13

"The results of the present study provide evidence that leukocyte telomere length (LTL) is related to regular vigorous aerobic exercise and maximal aerobic exercise capacity with aging in healthy humans. LTL is not influenced by aerobic exercise status among young subjects, presumably because telomere length is intact (i.e., already normal) in sedentary healthy young adults.

However, as LTL shortens with aging it appears that maintenance of aerobic fitness, produced by chronic strenuous exercise and reflected by higher VO2max, acts to preserve LTL … Our results indicate that LTL is preserved in healthy older adults who perform vigorous aerobic exercise and is positively related to maximal aerobic exercise capacity. This may represent a novel molecular mechanism underlying the "anti-aging" effects of maintaining high aerobic fitness."

[jakehglover]

The Search for Extended Youth and Extreme Longevity

By Dr. Mercola

Telomeres were first discovered in the 1930s. Every cell in your body contains a nucleus, and inside the nucleus are the chromosomes that contain your genes. The chromosome is made up of two "arms," and each arm contains a single molecule DNA, which looks like a string of beads made up of units called bases.

A typical DNA molecule is about 100 million bases long. It's curled up like a slinky, extending from one end of the chromosome to the other. At the very tip of each arm of the chromosome is the telomere. In 1973, Alexey Olovnikov discovered that telomeres shorten with time because they fail to replicate completely each time the cell divides. Hence, as you get older, your telomeres get increasingly shorter.

If you were to unravel the tip of the chromosome, a telomere is about 15,000 bases long at the moment of conception in the womb. Immediately after conception your cells begin to divide, and your telomeres shorten each time the cell divides. Once your telomeres have been reduced to about 5,000 bases, you essentially die of old age.

In 1984, Elizabeth Blackburn, Ph.D., professor of biochemistry and biophysics at the University of California, San Francisco, discovered that the enzyme telomerase has the ability to lengthen the telomere by synthesizing DNA from an RNA primer.

She, along with Carol Greider and Jack Szostak, were jointly awarded the Nobel Prize in physiology or medicine in 2009 for the discovery of how chromosomes are protected by telomeres and the enzyme telomerase. Telomere lengthening is now thought to be a major key that explains the process of aging and holds the promise of not just slowing aging, but actually reversing it.

Aging as a Disease

Molecular biologist Maria Blasco, Ph.D., director of the Spanish National Centre for Cancer Research and head of the Telomeres and Telomerase Group,1 is another scientist who ascribes to the idea that aging is the foundational disease that needs to be addressed if you want to prevent degenerative and chronic diseases such as cancer.

In 2008, Blasco set out to determine whether lengthening telomeres will in fact slow aging. To do this, she injected the enzyme telomerase into mice. The result? The treated mice lived on average 40 percent longer than normal. “Of course, it was an amazing feeling,” Blasco says, “because I realized that I had manipulated one of the basic mechanisms for why we age, and this could lead to important applications in the future.”

There was a catch, however. The therapy “would almost certainly have increased the cancer rate in mice, had they not been genetically modified to be cancer resistant,” the narrator notes. And humans cannot, at present, be genetically modified. To address this problem, Blasco and her team further refined the process, and in 2012 carried out a second experiment.

This time, the treated mice lived about 20 percent longer and cancer, when it occurred, was delayed. Still, this does not mean telomerase can or will produce identical effects in humans.

The Epigenetic Clock

Steve Horvath, Ph.D., professor of human genetics and biostatistics at UCLA David Geffen School of Medicine in Los Angeles,2 believes science is still in its infancy when it comes to understanding aging. “I believe there’s a passive clock that measures the state of your cells,” he says. “It doesn’t cause things to deteriorate, it just keeps track of the mechanism that actually does cause that.”

This passive clock mechanism — the epigenetic clock — is something we still know virtually nothing about, but Horvath believes it’s a major player, and in order to be able to prevent aging, we have to understand how epigenetic changes within the DNA molecule affect its biological age.

He’s convinced it is these epigenetic changes that are the root cause of aging, and the good news, should this be true, is that they’re reversible. So, in principle, at least, you can devise treatments to reverse epigenetic changes that drive biological aging within the DNA.

According to Horvath, the telomere theory of aging “has been disappointing.” While many in the antiaging field are enamored with the idea that overexpressing telomerase will lead to aging reversal, the downsides are considerable, because “if you overexpress telomerase and end up with longer telomeres, you actually increase your risk for cancer,” he says. So, while telomere length is part of the equation, he does not believe it’s the answer we’re looking for.

Antiaging — ‘An $8 Billion Industry of Stuff That Doesn’t Work’

According to scientist and entrepreneur Joe Betts-Lacroix, the antiaging business is “an $8 billion industry of stuff that doesn’t work.” He believes the key to longevity is the prevention of degenerative disease, and were you to find something that actually helps prevent multiple degenerative diseases, then you could transfer billions of dollars from each of those disease fields into the antiaging field. As founder of Health Extension, Betts-Lacroix has raised more than $30 million from venture capitalists in search of a cure for aging.

Combined, the scientists and companies under the Health Extension umbrella have raised more than $200 million. Much of this funding is coming from the tech industry, which has become increasingly interested in biology and cracking the biological code. Betts-Lacroix notes that in recent years, scientists have made remarkable discoveries; finding a number of ways to extend life span in mammals. Now, we’re right on the precipice of bringing it into the human realm, which is the most challenging venture of all.

Promising Findings in Animals

One of the findings from animal research is that smaller mammals live longer than larger ones. For example, the smaller the horse, the longer its life span. This, they’ve found, is due to hormones that not only affect life span, but also size. When these hormones are suppressed for life, the animal will be small and live long. When suppressed in adulthood, they’ll retain their regular size, but will live longer than normal.

“As far as we know, for every species we’ve tested, turning down this hormone system extends life span,” says Cynthia Kenyon, Ph.D., vice president of aging research at Calico Life Sciences, a biotech company owned by Google.3 Kenyon made her mark in the field with her studies of the roundworm caenorhabditis elegans in the early ’90s. By partially disabling a single gene, DAF-2, the life span of this tiny nematode was doubled.

“In one fell swoop, the animal lived twice as long,” she says. “That was really stunning, because that was not supposed to happen.” Even more remarkable, other researchers have duplicated the findings on other animals, from fruit flies to mice. Kenyon also notes the research indicates that when you extend life span, you also typically delay degenerative diseases, and when they occur, they’re milder.

As many others, by targeting aging, she envisions a therapy, perhaps a drug, that with one pill can delay or prevent the onset of many diseases all at once.

Research Targeting Senescent Cells

At Unity Biotechnology,4 they focus on another aspect of aging — senescent cells. Cellular senescence is when a cell ceases to divide. In a cell culture, a fibroblast cell can divide a maximum of 50 times, after which it becomes senescent or nondividing. Senescent or nondividing cells also play a significant role in the aging process.

At Unity, researchers were able to remove senescent cells in mice, to observe what would happen. “When we did this, something astonishing happened,” cofounder Nathaniel David, Ph.D., says. The mice had a “profoundly extended health span,” meaning the period of time in which the animals remain healthy and disease free.

The health and function of a number of vital organs were improved, including their hearts and bones, with less heart disease, arthritis, cataracts and other “normal” problems of aging. Soon, Unity will perform its first human trial on patients with osteoarthritis.

Can Diabetic Drug Boost Longevity?

While most researchers are focusing on the creation of new drugs to combat aging, some are focusing their attention on an old one — metformin, commonly prescribed to Type 2 diabetics. It’s been noted that diabetics taking metformin tend to live longer than diabetics taking other diabetes drugs. They also have a lower prevalence of other age-related diseases, including cancer and Alzheimer’s.

Some nondiabetic people are even taking metformin just for its potential antiaging benefits. While metformin is among the least hazardous drugs out there, it does have some serious downsides such as impairing the use of the important vitamin B12.

It is thought to work via AMP-activated protein kinase (AMPK), which plays a vital role in inhibiting glucose production in the liver (gluconeogenesis). AMPK is a conserved sensor and regulator of cellar energy balance that is activated when the cellular AMP-to-ATP ratio exhibits a large increase due to conditions such as nutrient deprivation or pathological stress.

There are far safer alternatives like the supplement berberine that has been shown to have many of the same effects. It is in my view, a better alternative. Berberine has antibacterial, anti-inflammatory, antiproliferative, antidiarrheal, antineoplastic, antidiabetic and immune-enhancing5 properties, and has a long history of use in traditional medicine, including traditional Chinese medicine.

Berberine even helps combat metastatic stem cells and heart failure. Many integrative health practitioners swear by it as a general health supplement due to its ability to address such a wide variety of maladies. It actually works as well as or better than some drugs for certain ailments.6 For example, it’s been shown to improve blood lipids better than statin drugs, and lower blood pressure as well as antihypertensive drugs.

Like metformin, many of berberine’s health benefits7 have been linked to its ability to activate AMPK.8,9 AMPK is an enzyme inside your body's cells. It’s sometimes referred to as a "metabolic master switch" because it plays an important role in regulating metabolism.10 Low AMPK has been linked to insulin resistance, mitochondrial dysfunction, obesity, neurodegeneration and chronic inflammation — all of which lay the groundwork for a wide variety of serious chronic diseases.

AMPK is also an important neuroprotector. As explained in the Journal of Neurochemistry,11 “AMPK senses metabolic stress and integrates diverse physiological signals to restore energy balance. Multiple functions are indicated for AMPK in the [central nervous system] …” Berberine also benefits brain health and psychological well-being by increasing key neurotransmitters.

Your Lifestyle Is Your Longevity Switch

If there’s ever a pill that will ensure extended youth, everyone will likely want it. The question is whether or not such a thing is even possible. The fact of the matter is, your lifestyle and the choices you make every day play an incredible role in how you will age, and I doubt a drug will ever be devised that will allow you to be a junk food-eating couch potato and still age in reverse. Of crucial importance is keeping your mitochondria healthy, and lifestyle strategies such as diet and exercise are key for this.

Science clearly shows a cyclical ketogenic diet high in healthy fats and low in net carbs promotes healthy mitochondrial function. A number of other strategies are also known to boost mitochondrial health, and I discuss several of them in my book, “Fat for Fuel.” Research also shows you can slow down telomere shortening with exercise.12 It basically buffers the effect of chronic stress on telomere length, which helps explain some of its well-documented effects on health and longevity.

Other studies have found there's a direct association between reduced telomere shortening in your later years and high-intensity-type exercises. As noted in a study published in Mechanisms of Aging and Development:13

"The results of the present study provide evidence that leukocyte telomere length (LTL) is related to regular vigorous aerobic exercise and maximal aerobic exercise capacity with aging in healthy humans. LTL is not influenced by aerobic exercise status among young subjects, presumably because telomere length is intact (i.e., already normal) in sedentary healthy young adults.

However, as LTL shortens with aging it appears that maintenance of aerobic fitness, produced by chronic strenuous exercise and reflected by higher VO2max, acts to preserve LTL … Our results indicate that LTL is preserved in healthy older adults who perform vigorous aerobic exercise and is positively related to maximal aerobic exercise capacity. This may represent a novel molecular mechanism underlying the "anti-aging" effects of maintaining high aerobic fitness."

from HealthyLife via Jake Glover on Inoreader https://articles.mercola.com/sites/articles/archive/2018/05/05/extended-youth-extreme-longevity.aspx

[powerdreamz]

The Rematch

// In the aftermath of an athletic humiliation on an unprecedented scale—a loss to a tortoise in a footrace so staggering that, his tormenters teased, it would not only live on in the record books, but would transcend sport itself, and be taught to children around the world in textbooks and bedtime stories for centuries; that hundreds of years from now, children who had never heard of a “tortoise” would learn that it was basically a fancy type of turtle from hearing about this very race—the hare retreated, understandably, into a substantial period of depression and self-doubt.

The hare gained weight, then lost weight; turned to religion, then another less specific religion. The hare got into yoga; shut himself indoors on a self-imposed program to read all the world’s great novels; then traveled the world; then did some volunteer work. Everything helped a little bit, at first; but nothing really helped. After a while, the hare realized what the simplest part of him had known from the beginning: he was going to have to rematch the tortoise.

“No,” came the word from the tortoise’s spokesperson. “The tortoise prefers to focus on the future, not relive the past. The tortoise is focused full-time on inspiring a new generation with the lessons of dedication and persistence through his popular speaking tours and his charitable work with the Slow and Steady Foundation.”

The smugness and sanctimony of the tortoise’s response infuriated the hare. “The lessons of dedication and persistence”? Had everyone forgotten that the hare had taken six naps throughout the race (!)—unequivocally guaranteeing victory to anyone—a horse, a dog, a worm, a leaf, depending on the wind—anyone lucky enough to be matched against the hare at this reckless, perspectiveless, and now-forever-lost peak phase of his career, an offensive period of his own life that he had obsessed about and tried in vain to forgive himself for ever since? How could anyone think the tortoise was relevant to any of this? A minor detail of the race, known to few but obsessives (of which there were still plenty), was that there had been a gnat clinging to the leg of the tortoise throughout the entire contest: was this gnat, too, worthy of being celebrated as a hero, full of counterlogical lessons and nonsensical insight like “Right place, right time takes down talent in its prime”? Or “Hang on to a tortoise’s leg, who knows where it will lead”?

No—the lesson of this story has nothing to do with the tortoise, thought the hare, and everything to do with the hare. How he had let himself become so intoxicated with the aspects of his talent that were rare that he had neglected the much more common aspects of his character that also, it so happened, were more important—things like always doing your best, and never taking success for granted, and keeping enough pride burning inside to fuel your success but not so much to burn it down. Now, the hare knew these things. Now. Now that it was too late.

Or was it? What was that lesson again? Slow and steady?

The hare started running again, every day, even though there was no race planned. He ran a mile every morning, then two, then ten.

Before long, he added an afternoon run to his training routine—a slower one, with a different goal in mind. On this run, he made a point to start a conversation with everyone he came across. “Boy, I sure would love to race that tortoise again someday. You think anyone would want to watch it, though?” Then he would shrug it off and jog along to the next stranger. “Hey, what do you think would happen if I raced that tortoise again? Ya think I’d win this time? Or do you think pride would get the better of me all over again?” Then he’d shrug and run off again, at a provocatively medium pace.

Slowly, steadily, anticipation built for a tortoise-hare rematch. After a while it became all that anyone could talk about, and eventually, the questions made their way to the tortoise.

“No,” said the tortoise, but this time his “no” just led to more questions. “No” now, or “no” ever? Would he ever rematch the hare? If so, when, and under what conditions? If not, why? Could he at least say “maybe”?

No, said the tortoise again; never. They kept asking, and he kept saying no, until eventually, everyone gave up and stopped asking. And that’s when the tortoise, sad and dizzy at having all this attention given to him and then taken away, impulsively said, Yes, okay, I bet I can beat this hare again. Yes.

I’m undefeated against the hare, thought the tortoise. Actually, I’m 1–0—I’m undefeated in my entire racing career! How do you win a race? Slow and steady, that’s what they say, right? Well, I invented slow and steady. This is good. This will be good. One time could have been a fluke. Twice, there’ll be no question.

The race was set in ten days’ time. The tortoise set out to replicate what seemed to have worked the first time, which was nothing in particular: simple diet, some walking around. A little of this, a little of that. He didn’t want to overthink it. He was going to mainly just focus on being slow and steady.

The hare trained like no one had ever trained for anything. He ran fifteen miles every morning and fifteen every afternoon. He watched tapes of his old races. He slept eight hours every night, which is practically unheard of for a hare, and he did it all under a wall taped full of the mean, vicious things everyone had said about him in all the years since the legendary race that had ruined his life.

On the day of the race, the tortoise and hare met for the first time in five years at the starting line, and shared a brief, private conversation as their whole world watched.

“Good luck, hare,” said the tortoise, as casual as ever. “Whoa! You know what’s funny—do that again—huh, from this angle you look like a duck. Now you look like a hare again. Funny. Anyway, good luck, hare!”

“And good luck to you, tortoise,” whispered the hare, leaning in close. “And just so you know—nobody knows this, and if you tell anyone I said it, I’ll deny it—but I’m not really a hare. I’m a rabbit.”

This wasn’t true—the hare just said it to fuck with him.

“On your mark, get set, GO!”

There was a loud bang, and the tortoise and hare both took off from the starting line.

Never, in the history of competition—athletic or otherwise, human or otherwise, mythical or otherwise—has anyone ever kicked anyone’s ass by the order of magnitude that the hare kicked the ass of that goddamn fucking tortoise that afternoon.

Within seconds, the hare was in the lead by hundreds of yards. Within minutes, the hare had taken the lead by more than a mile. The tortoise crawled on, slow and steady, but as he became anxious at having lost sight of his competitor and panicked over what he seemed to have done to his legacy, he started speeding up: less slow, less steady. But it hardly mattered. Before long—less than twenty minutes after the seven-mile race had begun—word worked its way back to the beginning of the race that the hare had not only won the contest, and had not only recorded a time that was a personal best, but had also set world records not only for all hares but also for leporids and indeed for all mammals under twenty pounds. When news reached the tortoise, still essentially under the banner of the starting line, he fainted. “Oh, now he’s napping?! Isn’t that rich,” heckled a nearby goat, drunk on radish wine.

Those who didn’t know the context—who hadn’t heard about the first race—never realized what was so important about this one. “A tortoise raced a hare, and the hare won? Okay.” They didn’t understand the story, so they didn’t repeat it, and it never became known. But those who were there for both contests knew what was so special about what they had witnessed: slow and steady wins the race, till truth and talent claim their place.

[theguardian911]

New Study About Animal Longevity Turns Up Weird Anomaly. Did This Study Reveal a Way to Help Your Large Breed Dog Live Longer? By Dr. Becker When it comes to the lifespan of mammals, the general rule is the bigger the creature, the longer it will live. For example, elephants in their natural habitat can live into their 60s. The average lifespan of a squirrel, on the other hand, is only about six years. Small mammals normally have lower metabolic rates than larger species, which is why larger animals with higher metabolic rates live longer. However, when it comes to domestic dog breeds, even though smaller dogs have lower metabolic rates, they live longer than large and giant breeds. This is essentially the opposite of what occurs in other species. A Yorkshire Terrier, for example, can be expected to live from 13 to 16 years, whereas a Great Dane will live only about half that long. A Big Dog's Life 'Unwinds in Fast Motion' A 2013 study established that big dogs die younger primarily because they age quickly. Study authors believe these findings can help scientists understand the biological links between growth and mortality. Dogs were the perfect subjects for the study, because humans have bred them throughout history to be wildly variable in size. The heaviest dog on record was probably an English Mastiff that weighed 343 pounds, while the smallest was a terrier weighing in at under a quarter-pound. There is no other species of mammal with such tremendous size disparity. The study looked at ages of death in 74 breeds and over 56,000 dogs that visited veterinary teaching hospitals. Researchers learned that large breeds seem to age at faster rates than smaller breeds, and the speed at which the risk of death increases with age is also greater with big dogs. According to study authors, large dogs age at an accelerated pace, suggesting “their adult life unwinds in fast motion.” For a dog, every 4.4 pounds of body mass takes about a month off his life. The researchers next want to look at the growth and health histories of dogs to narrow down the leading causes of death for large breeds. For example, bigger dogs more often acquire cancer, which makes sense when you consider they grow more than small dogs, and cancer is the result of abnormal cell growth. It’s possible humans have inadvertently selected for characteristics — like rapid growth — that predispose large dogs to cancer. Other large animals like elephants that have many more cells than smaller creatures — and should therefore also be at greater risk for cancer — seem to have evolved special defense mechanisms against disease. These mechanisms probably developed through natural selection over a very long period of time, whereas most dog breeds have evolved through selection by humans, and over a much shorter period of time. Evolutionarily speaking, dogs have evolved in the blink of an eye, and protective mechanisms against cancer and other diseases haven’t had time to catch up. Is There a Difference in Levels of Oxidative Stress in Large Versus Small Dogs? Recently, two undergraduate students at Colgate University decided to investigate why smaller dogs seem to age more slowly than large ones. For their study, the undergrads wanted to look specifically at the influence of free radicals and oxidative stress on the aging process in dogs. Oxidative stress, which is associated with aging, is defined as physiological stress on the body caused by the cumulative damage done by oxygen free radicals inadequately neutralized by antioxidants. Free radicals are unstable molecules with an uneven number of electrons. These unstable molecules travel around the body looking to bond with stable molecules so they can to steal an electron and stabilize themselves. When they are successful, they create new unstable molecules that damage cell membranes and eventually contribute to cancer and other diseases. The researchers contacted veterinarians and collected about 80 tissue samples (removed during routine surgical procedures) from both large and small breeds of varying ages, from puppies to old dogs. With the help of a Colgate animal physiologist, they isolated cells from the tissues, grew them in a lab dish for several weeks and then analyzed them. Cell Damage From Free Radicals Starts Early in Large Breed Dogs The students discovered that energy and free radical production in the cells from the adult dogs was comparable for both large and small breeds, as were the amount of antioxidants. However, the cells from large breed puppies had excessive amounts of free radicals — too many for antioxidants to effectively neutralize. Large breed puppies have faster metabolisms and growth rates than smaller breeds, and the results of this study suggest cellular damage starts accumulating at a young age in larger dogs. “Cell damage even at this young age can have long-lasting effects,” says researcher Josh Winward. The Colgate study results are preliminary, but if they can be replicated in future research, according to Winward, it might be possible to extend the life of large and giant breeds by supplementing antioxidants in puppies to help destroy free radicals before they can do damage. Helping Your Big Dog Live a Long, Healthy Life If you’re the parent of a large or giant breed dog or are thinking about adding one to the family, I hope you’ll watch my interview with a wonderful Newfoundland breeder, Dr. Jeff Bergin, whose dogs live into their late teens. ( http://healthypets.mercola.com/sites/healthypets/archive/2011/04/05/how-a-newfoundland-pet-dog-reached-17-years.aspx) If you’re familiar with Newfies, you know a 17-year lifespan is almost unheard of! Some of the wonderful practices Dr. Bergin follows with his dogs include: • Feeding exclusively raw, balanced diets. Fresh meats and organs provide an excellent base for puppies, and vegetables and fruits provide much needed antioxidants for a growing body. • Breeding for health, first and foremost. Dr. Bergin breeds his dogs only once or twice during the course of their lives, with at least six years between litters. He does not breed dogs with congenital defects, and so far only one of his dogs has had a genetic health issue, a heart problem. (Heart problems, osteosarcoma and hip dysplasia are the most common health challenges for this breed.) • Performing regular chiropractic adjustments. With large and giant breed dogs, it's very important to take care of the musculoskeletal system. Dr. Bergin happens to be both a licensed animal chiropractor as well as a human chiropractor. He performs regular manual orthopedic manipulation on all his dogs, from the moment they first stand on their own through the remainder of their lives. This practice is one of the keys to keeping a big dog's frame from degenerating with age. Dr. Bergin's dogs are typically still fully mobile even at the end of their lives. • Limiting vaccines and other assaults on the immune system. Dr. Bergin only revaccinates his dogs against rabies, because the law requires it. By strictly limiting the number of vaccines they receive, he helps keep his dogs' immune systems strong and resilient. • Insuring litters go to the right families. Dr. Bergin performs a mandatory home visit to families interested in his dogs. He won't release a dog without seeing the new home. He conducts in-depth interviews with prospective owners to insure the puppy will be well taken care of, and he also insists on a commitment from prospective owners to feed raw. For most pet parents, it’s the quality of their dog’s life that is most important. You may have your animal companion with you for eight years or twice that long. By focusing on what I call the three pillars of health — nutrition, maintenance of the frame and a strong, resilient immune system — you can insure you’re providing your canine companion with everything she needs for an excellent quality of life for as long as she lives.