We currently describe dogs and grey wolves as the same species, Canis lupus.

Dogs didn't evolve from gray wolves specifically, but they definitely evolved from some kind of wolf or wolves.

A snow-slab avalanche is triggered by structural failure in a weak layer of snow beneath the "slab". It takes 200-500 Pascals of pressure change to cause the weak layer to structurally fail and trigger an avalanche—easy enough for explosives or a skier directly atop the snow.

The sound wave of a loud human scream can only achieve a pressure amplitude of about 2 Pa, however, which is two orders of magnitude too weak. Even a passing jet plane would only see a wave amplitude of 20 Pa, although the shockwave of a passing supersonic jet can be enough (the study that proved this, while I don't have a link, was amusingly titled Opération "Bangavalanches".)

So, no, somebody yelling loudly is not going to trigger an avalanche, but a passing supersonic jet shockwave might.

Endless Forms Most Beautiful is an incredible read and I will never stop recommending that people pick it up.

Mounting any one immune response also requires a significant amount of energy...in studies on mice, older mice mounting an antibody response to an injected antigen aren't fully able to maintain their body temperature at the same time. So while I don't have hard numbers for humans, if you were taking dozens or hundreds of different vaccines in a short time you'd probably hit a point where the metabolic load was too much for the rest of the body....

In addition to getting out mineral compounds, the soaking helps loosen any clay "dust" that might be left over from firing/shipping. The soak/dry is basically a way of gently washing the pot (and all of its tiny pores) without scrubbing it.

As to the temperature, vegetable oils can even polymerize at room temperature; heat merely speeds up the process. So choosing a low heat like 350° F, and a long time like 2.5 hours, is basically just a "low and slow" way of achieving the same polymerization as a higher heat for a shorter time. However, I suspect that by staying below the smoke point of the oil, you're going to not get that deep black carbonized look associated with cast-iron seasoning, but a much lighter-colored, low-carbonization seasoning that is nevertheless fully polymerized.

As to the choice of oil, olive oil specifically has one of the highest ratios of monounsaturated fats to polyunsaturated fats, so there's fewer carbon bonds available to cross-link for polymerization (meaning polymerization will be slower than with an oil higher in polyunsaturated fats). However, I suspect that u/Corvis_74 is right that the choice of oil is probably not the result of rigorous terracotta-seasoning research.

The short answer is, it appears that baleen evolved from the system that grew "adult" teeth in baleen whale ancestors, in combination with existing genes used elsewhere in whales for producing keratin as hair or claw sheaths.

The ancestors of whales, like us, had two sets of teeth—what we call "baby teeth" and "adult teeth." As fetuses, baleen whales actually begin to grow their baby teeth! The teeth bud and can even begin to mineralize, but eventually tooth development is halted and the tooth buds reabsorbed, after which baleen forms in the upper gums.

So baleen whales never begin to grow their "adult" set of teeth, but the genetic/protein signals that trigger the development of baleen are very similar to ones that trigger development of teeth in all other mammals, even though the baleen itself is nothing like teeth (instead, baleen is thick sheets of keratin, very similar to hair or fingernails). So what seems to be happening is:

• The whales jaws/gums signal the production of "baby" teeth.
• A different signal then aborts their development and they are reabsorbed rather than rupturing out of the gums.
• The gums then signal the production of "adult" teeth, but with a twist, where hair-like baleen grows out of the gums instead of enameled teeth.

We have several examples—at least in insects—that suggest that "learned" behaviors and "instinctive" behaviors use the exact same "hardware" in the brain. For example, take a fly encountering a smell for the first time. That "smell" goes through a number of structures in the fly's nervous system, from olfactory receptors to other nerve cell networks that identify those different inputs, filter out noise, and ultimately evaluate how to react. This network is capable of changing based on experience...if the is evaluated as "neutral" the first time, but then the fly gets hurt, perhaps the next time the same network will identify the smell as "dangerous," with an evaluation of "run away from that smell!" Running away from this smell based on prior experience would be a "learned" behavior.

Now take the same fly, and expose it to sex pheromones from its own species. The smell of sex pheromones goes through the exact same olfactory system as every other smell...receptors, identification, evaluation. But even the very first time the fly smells it, its identification/evaluation system connects that smell with sex. It doesn't need to experience sex a few times first to "learn" what that smell means...within that plastic, malleable olfactory system, a few connections came already pre-made, and those connections draw a bright line between sex pheromone olfactory receptors and sex, exactly as if the fly had learned to make that connection.

Separately from this, we also know that some species—like mice—can pass certain learned associations to their children and grandchildren through epigenetics. When a mouse makes a traumatic-enough association with a certain smell, that mouse's body is able to make alterations to how certain bits of DNA will be expressed in their offspring. Even when in-vitro fertilization is used (to rule out the mice somehow teaching their children about the truama), offspring show increased behavioral sensitivity to the same smell that traumatized their parent or grandparent, but not to other smells.

So between these lines of evidence (and some others), some scientists hypothesize that all instincts, from insects to mammals, are evolutionary hijacks of our "learned behavior" systems. Essentially, while animal brains (including ours) are often very flexible and adaptable, which lets us learn new behaviors over time, those same "teachable" systems are capable of developing with certain specific "learned" behaviors already built in.

Unfortunately, no. While at least some insects have a limited ability to heal the cuticle in their abdomens or legs, the cuticle of the wings cannot be repaired.. Dragonflies instead have resilient wings with lots of flexible micro-joints and cross-veins to prevent damage, and adjust their flight kinematics if and when damage to the wings eventually does occur.

Unfortunately, the regrown tail portion is all collagen and cartilage. There's no fat or muscle stores for it to provide that kind of value.

The alligator-tail paper authors point out a couple of additional pieces of information you might find interesting:

- A robust, adaptive immune system is seen as an impediment to regeneration, which could be why mammals and birds are both so rubbish at regrowing lost body parts compared to reptiles and amphbibians. In salamanders, limb loss provokes only a weak immune response and regeneration is fairly robust. In the clawed frog Xenopus, regenerative abilities are robust in juveniles but reduce as the immune system matures. Adult crocodilians have robust immune systems like birds and mammals do, and as their only tail regeneration was seen in very juvenile alligators, its possible that their underdeveloped immune systems allows them to (partially) regenerate in a way that wouldn't be possible once the full power of their adult immune system is established.

- We have fossil evidence of partial tail regeneration in the Jurassic marine crocodile Steneosaurus bollensis (unfortunately, the papers the authors link are both in German and I don't understand them). The authors (briefly) speculate that tail regeneration was something all archosaurs inherited from their reptile ancestors, but that this ability was subsequently lost in the dinosaur/bird line (again, possibly and partially because they evolved more adaptive immune systems). So rather than being a new trait that evolved in alligators, it might be a partially-inherited ability that was potentially diminished/lost in some other surviving crocodilians.

Crocodiles actually can also regrow their tails to a limited degree. Both crocodiles and alligators have limited tail regenerative ability though...it seems that crocodilian (including alligator) tail regrowth is limited to a rod of cartilage wrapped in mostly collagen, without even any bone or muscle tissue. Alligator regrowth seems limited to only a few inches, and only when young, and is very slow (something like 15-18 months). Crocodile tail regrowth is not nearly so well studied (although, to be fair, the alligator study was only published 2 years ago and was something of a surprise to researchers at the time.)

Regeneration in general is metabolically expensive, which is probably why young alligators take so long to regrow anything at all, and even then don't bother regrowing the muscle or bones. It seems like the tip of the tail is very vulnerable to damage in crocodilians, and also important enough to propulsion in water that it's worth regrowing something to make up a little of the lost surface area, but that's about the extent of it.

The tobacco ringspot virus—an RNA virus infecting many different kinds of plants—has jumped from the plant kingdom to the animal kingdom, infecting the European honeybee. Various genera of rhabdoviruses are able to infect vertebrates, invertebrates, or plants, implying that both cross-kingdom and cross-phylum jumps have occurred within this virus family. Both groups are RNA viruses that—in their plant-infecting forms—use animals to spread from one plant to another...I imagine (but have no evidence) that this combination helped facilitate the jump between kingdoms.

There was also one documented case of plant-to-fungus virus transmission, where the cucumber ringspot virus was found to infect Rhizoctonia solani, a fungus that causes cucumber belly rot. The linked paper shows that the virus can actually move back and forth from plant to fungus to plant, making it a single multi-Kingdom virus.

There is also research in the last 10 years showing that spider legs are actually covered in a non-stick chemical coating that, combined with adhesive-repellent leg hairs and careful footwork makes spider-web-glue roll right off their legs. When scientists use hexane to wash away the anti-stick coating, their legs were much more likely to get stuck to their webs.