if sperm contains only 50% of someone's DNA how can it be used to identify someone? Is DNA so unique that 50% of it is enough to identify a single person?

The comment from @User137 pretty much gets it: the mix of all sperm cells in even a small sample will contain the whole genome on average. So in the hair example in the comments above, there are probably a good number of dead cells hanging onto the hair, enough for analysis. Meiosis will redistribute the DNA sequences inherited from mom and dad randomly, so each sperm is in theory a unique patchwork of that person's genome, but overall the genome will be covered well. Single-cell work, on the other hand, is technically very challenging.

[edit: here is an article describing methods for low-input analysis of forensic samples. Unfortunately paywalled.]

To directly answer the OP on uniqueness: absolutely a single sperm is that unique for each person, in principle. There are lots and lots of genetic variants in each human, and everyone represents a unique mix. It is estimated that 1/1000 places in the genome of each person differ from any other person, on average (for substitutions). there are 3*10^9 places in the genome for this to be the case, which gives you a very large number of differences, ASSUMING that you can actually ascertain all those differences. [edit: for a discussion of these stats see here.]

The technical problem with forensics is that often they only look at a few places in the genome (microsatellites usually), because it is relatively expensive and hard even with recent technology to look at more than that in any detail. This leads to the non-trivial possibility of misidentification with the standard battery of loci. This possibility never goes away entirely, but it becomes very small with more data. I am not a forensic scientist, possibly they have gotten more comprehensive or the methods have changed in recent times.

[edit: here is a document that has what appears to be a readable introduction to DNA forensics, including technical discussions of some drawbacks of marker panels used by for instance the FBI of the USA.]

It would be more difficult to identify someone from a single sperm cell, rather than other cells contained in their semen.

However, if we are just comparing the DNA from any diploid cell in the body, you run electrophoresis to compare DNA samples.

For example, if you wanted to establish the paternity of a child. You would collect a sample of the child's DNA, the mother's DNA and the possible fathers' DNA (usually all from cheek or hair cells).

PCR would be carried out to replicate each sample into a large quantity.
You would then use the same restriction enzyme in each sample to cut the DNA in specific places along the sample.

Each sample is placed in an individual well at one end of agarose gel, immersed in a buffer solution, and a current passed through (cathode at the well-end, anode at the opposite end).

As DNA is negatively charged due to phosphate groups, it travels towards the anode, through the gel. Shorter fragments of DNA travel faster in the set time the electrophoresis is run for.

Southern blotting is then used to establish a banding pattern of the fragments of DNA - you rule out the bands that the child and the mother share. To establish paternity, you identify bands that the child shares with each possible father. The father whom the child shares the most bands is the most likely father.


Is α-keratin a fully functional protein? Is α-keratin before it coils with another polypeptide, makes chains, and build intermediate filaments a fully functional protein?

I mean, is the single monomer of α-keratin a protein or does it have to become a dimer to become a protein?

What we call as protein is the final quaternary structure. Whether it is translated from a single gene or from multiple genes (as in haemoglobin), always the structure with all bonds and interactions taken into account. Similarly here the alpha- Keratin forms Disulfide bonds to form a functional protein.


My dog and I are wondering: is this a biting midge, or another bug? A week or two ago, my dog started scratching, and it only increased. Not long after, I started getting bit by something that itches something awful. I thought it was fleas so got some medication and moved my dog out of my room. He stopped scratching immediately. After deep cleaning, I let him back in my room the next day. He shortly thereafter scratched again, but not intensely or frequently. My bites have continued.
I set out a flea trap (water, dish soap, flashlight on the water) and it caught the bug you see in the pic (it has only caught four of them).
Is that a biting midge, or something else?
Also, I'm in New York City.

https://i.stack.imgur.com/GC0iL.jpg -- close-up pic, color and pattern
https://i.stack.imgur.com/CVgnl.jpg -- several from a distance to show size
https://i.stack.imgur.com/rQqp4.jpg -- same one as in the first pic

The size is maybe as big as the hole a small nail makes in the wall, a very small ant, or a freckle.

It seems to be a Yellow-banded polybia wasp (Polybia occidentalis), a species of Potter wasp.

my doubts with this conclusion is that the abdomen of the insect in your photo is quite large compared to other observations of the species. Also, Polybia occidentalis is a species that exists in South and Central America, not up north in New York, Perhaps it is able to exist there due to the warm summer weather though I am not entirely sure.
It might be another species of potter wasp. Potter wasps are able to sting but rarely do so to large organisms and their stings don't hurt much. They usually prey on caterpillars and beetle larvae and use those to feed their own. They create these nests that look like a ceramic pot. each of these "pots" contains one larva of the wasp (along with all the food the wasp has collected for their larva when it hatches).
here's a photo of the pots (wasps seem to be willing to create these pots on pretty much any solid surface including under leaves):

Wasps are not parasites, they are hunters of other insects, if my identification of this species is correct, then you and your dog are likely not going to suffer any direct harm from this species let alone parasitic behaviour.


What makes humans omnivores, and not herbivores? Some vegans claim that humans are herbivores, not omnivores, and that we are not physiologically designed to eat meat (see here: http://www.peta.org/living/food/natural-human-diet/).

  "According to biologists and anthropologists who study our anatomy and our evolutionary history, humans are herbivores who are not well suited to eating meat. Humans lack both the physical characteristics of carnivores and the instinct that drives them to kill animals and devour their raw carcasses.
  Although many humans choose to eat a wide variety of plant and animal foods, earning us the dubious title of “omnivore,” we’re anatomically herbivorous."

They go onto claim that we don't have tiger claws and teeth for catching and eating meat, that our jaws and teeth are designed for grinding plants not meat, that our stomach acid is too week to break down meat, that our intestinal tract is long like a herbivore for digesting plants and that it takes so long for meat to pass through that it rots and poisons us causing cancer, that we lack a hunting drive, that meat with it's cholesterol and protein is the cause of all disease so obviously its poison that we are not supposed to eat, that we get food poisoning from meat (like that never happens with vegetables...) and that the only reason humans started eating meat was to survive in times when there was a lack of plant foods available but according to our anatomy it's clear we're actually herbivores not designed for eating meat.

Can this be debunked?

As the answers given already point out, humans are generally considered omnivores that are able to use food sources available to them opportunistically. Apart from that, there actually is not much to debunk in the PETA statement - it is just a slightly one sided view on the history of human diet. Just as one sided as the claims that humans would not have evolved a really big brain without consuming animal products. Especially the canine teeth cannot be seen as evidence for prehistoric hunting, as in great apes the size of canine teeth is ridiculously well explained not only by defensive but mostly by mating behaviour; apart from that, humans do not even have those, and that most likely is caused by the trend towards monogamy which reduces inter-male aggression.

However, coming back to the actual question, in the relative short history (approx. 200-300ky) of our species there is evidence for 'several transitions towards or away from a vegetarian diet in humans' (Nielsen et al., 2017).

And in fact, there even is a human-specific evolutionary derived haplotype (younger than the Human-Neandertal split) that shows signatures of positive selection and is associated with increased efficiency in the synthesis of long chain fatty acid from plant precursor molecules - which would not really be necessary for meat eaters, as these fatty acids are readily available in animal products (Ameur et al., 2012). More specifically, the genes lying on that haplotype belong to the FADS cluster that seemed to have had adaptive value - also for synthesising long chain fatty acids from medium chain plant precursor fatty acids - in African populations even more recently (approx. 85 kya, Mathias et al. 2012).

This finding has been supported by a more recent study by Kothapalli et al. (2016). They investigated a 22bp-indel allele in the FADS2 gene that is associated with both higher blood levels of long chain fatty acids and exhibits high frequency (signature of positive selection) especially in South Asia and Africa where there is long tradition for plant-based diet.

Conclusion:

Modern humans (and this is relevant, as diet varies strongly between species and therefore the species comparison does not need to be very informative) appear to have changed diet frequently but there is evidence for human-specific molecular adaptations towards plant-based diets.

It is physiologically possible for a human to be an omnivore, carnivore or herbivore. It's not what we are, but what we can be or what we want to be.

Strictly speaking, it seems that humans can not be strict herbivores, because natural plant foods do not contain enough of the essential nutrient vitamin B12 and they are vegan/vegetarian websites that tell you that (Vegan Health, Vegetarian Nutrition Dietetic Practice Group).


Why are so few foods blue? Although blue foods exist, they're rare enough compared to other foods for food preparers to use blue plasters as a convention. The natural colour of a given food is due to pigments that have some biological origin. Is there any evolutionary reason why these are rarely blue?

Short answer
Blue color is not only rare in edible organisms - Blue color is rare in both the animal and plant Kingdoms in general. In animals, blue coloring is generated through structural optic light effects, and not through colored pigments. In the few blue-colored plants, the blue color is generated by blue pigment, namely anthocyanins. The reason for the scarcity of blue pigments remains unknown as far as I know.

Background
The vast majority of animals are incapable of making blue pigments, but the reason appears to be unknown, according to NPR. In fact, not one vertebrate is known to be able to. Even brilliantly blue peacock feathers or a blue eye, for example, don't contain blue pigment. Instead, they all rely on structural colors to appear blue. Structural colors are brought about by the physical properties of delicately arranged micro- and nanostructures.

Blue morpho butterflies are a great example of a brilliant blue color brought about by structural colors. Morphos have a 6-inch wingspan — one side a dull brown and the other a vibrant, reflective blue. The butterflies have tiny transparent structures on the surface of their wings that scatter light in just the right way to make them appear a vibrant blue. But if you grind up the wings, the dust — robbed of its reflective prism structures — would just look gray or brown.

Similarly, the poison dart frog is blue because of the iridiphores in its skin, which contain no pigment but instead feature mirror-like plates that scatter and reflect blue light (source: By Bio).

Morpho and poison dart frog. sources: Wikipedia & LJN Herpetology

Similarly, in the Kingdom of plants less than 10 percent of the 280,000 species of flowering plants produce blue flowers. In fact, there is no true blue pigment in plants and blue is even more rare in foliage than it is in flowers. Blue hues in plants are also generated by floral trickery with the common red anthocyanin pigments. Plants tweak, or modify, the red anthocyanin pigments to make blue flowers, including pH shifts and mixing of pigments, molecules and ions. These complicated alterations, combined with reflected light through the pigments, create the blue hue (source: Mother Nature Network).

But why the blue pigments are so scarce, seems to be unknown as far as I know (MNN, NPR, Science blogs)

Sources
- MNN
- NPR
- Photobiology

It is not that there are no blue foods, it is that the English language does not like calling foods "blue".

There are no natural borders between "colors" in a colorspace, all colors we name (and learn to distinguish) are culturally defined. So, an important thing to recognize is that, a color somebody calls "blue" can be called "purple", "red" or "maroon" or "green" or something else.

With that in mind, we can take a look at foods. Animal foods on the inside are protein, and cooked protein is usually a pale greyish goo (although muscle cooked medium still has reddish coloring). One of the rare examples would be some eggs with blue shells. In plants, basically all leaves we eat are colored by chlorophyl. So they are out of the equation.

Other plant parts, especially fruits, tend to be colored by one of a few other groups of pigments. And a major group of those pigments, the anthocyanins, ranges from blue to purple to red (they also change with pH). So a ton of foods have a somewhat purplish blue color, and are also named "blue" in other languages. Plums, aubergines, red grapes, red cabbage, and many berries are good examples for that. Then you have some plants which come in many colors, but the major cultivars happen to not be blue - potatoes and maize are the first to come to mind.

Other shades of blue are less common just because they don't happen to be covered by the major pigment groups, but if you go down into shade level, then "royal blue" is just one of many on the spectrum which is missing. Also note that there are still plants which have other shades of blue and are consumed, they are just not commonly thought of as "food". Lavender, chicoree, gentian and pansies all have blue flowers of various shades and are traditionally used in recipes.

So there is no special evolutionary reason why plants or animals should not be blue - many of them are blue, and we eat some of the blue ones. It is simply a cultural or linguistic trend for English speaking people to not see their food as blue.


Do Schwann cells have Na+/K+ ATPase pump? I was studying "Action Potential" and this question crossed my mind.
Another question is that, "Why does the action potential not occur in Schwann cells, or if it does, how does it occur?"
I know that many animal cell membranes have this pump, but I was not sure about this one.

Yes. Although utilizing the action potential is not in their function, Schwann cells do have Na/K ATPases. In fact all animal cells do. It contributes to the resting membrane potential in neural networks, with regards to Schwann cells, and prevent differences in osmotic pressure from disrupting the cells.

As for your second question, action potentials do not occur in Schwann cells as there is nowhere for this "impulse" to travel to. A localized depolarization is not an action potential. Papers such as this, and this suggest that voltage-gated ion channels in Schwann cells serve complex and specific purposes such as inducing myelin formation.

Sorry put simply yes. Schwann cell, also called neurilemma cell, any of the cells in the peripheral nervous system that produce the myelin sheath around neuronal axons. Schwann cells are named after German physiologist Theodor Schwann, who discovered them in the 19th century. As such of it function an action potential is needed.

The principal primary active transport system in neurons, as in most other animal cells, is a P-type pump that concurrently extrudes Na+ and accumulates K+. For brevity, we will refer to it as the Na,K-ATPase. Depending on their functions, different tissues have vastly different requirements for pumping Na+ and K+. Transport by Na,K-ATPases is specifically inhibited by cardiac glycosides, such as ouabain.

http://study.com/academy/lesson/the-myelin-sheath-schwann-cells-nodes-of-ranvier.html

enter link description here


What is the primary cause of death for small animals in urban and suburban areas? Small birds (sparrows, robins, jays, finches) and mammals (squirrels, rats, opossums, raccoons) are a common sight in many urban and suburban communities with green space. However, I observe carcasses of these animals relatively infrequently.
I imagine that the following are some of the most common causes of death:

Predation (the species I mention are small, and somewhere in the middle of the food chain)
Age-associated decline in foraging ability, leading to starvation
Disease
Fatal contact with infrastructure (collisions with buildings or wind turbines, contact with electricity lines)

I can think of two reasons why we don't see carcasses very often:

predation is the most common cause of death
individuals that succumb to disease/starvation end up in their nests/dens

Is this plausible? Has this been studied systematically, e.g. in populations of birds with tracking bands?

Cats, windows, and cars appear to be the leading causes of avian (bird) deaths:

 Major sources of anthropogenic bird mortality in the USA [from Fig 2b, Loss et al. (2015)]
Cats and vehicles are likely leading causes of death for many small non-avian animals as well.

Loss et al. (2013) estimated that 6.3–22.3 billion mammals are killed by free-ranging domestic cats in the USA each year.

The Wikipedia article for roadkill provides the following discussion of vehicular deaths:

In 1993, 25 schools throughout New England, United States participated in a roadkill study involving 1,923 animal deaths. By category, the fatalities were: 81% mammals, 15% bird, 3% reptiles and amphibians, 1% indiscernible. Extrapolating these data nationwide, Merritt Clifton (editor of Animal People Newspaper) estimated that the following animals are being killed by motor vehicles in the United States annually: 41 million squirrels, 26 million cats, 22 million rats, 19 million opossums, 15 million raccoons, 6 million dogs, and 350,000 deer.

I welcome others to corroborate these claims with a more reputable source in the comments. (I will try to do so myself and will update as I find them.)

DISCALIMER: I was previously only aware of Loss et al.'s work, so the emphasis of my post is on their papers. I did not otherwise search exhaustively for data. Noticeably absent from my post is mention of deaths caused by pest control (trapping and poisoning). I may update this post with more info as I come across it.

 Citations
Loss, S.R., Will, T. and Marra, P.P., 2013. The impact of free-ranging domestic cats on wildlife of the United States. Nature communications, 4(1), pp.1-8.
 Loss, S.R., Will, T. and Marra, P.P., 2015. Direct mortality of birds from anthropogenic causes. Annual Review of Ecology, Evolution, and Systematics, 46, pp.99-120.

The overwhelming cause of death of small animals ( and deer) that I see is that fearsome predator , the Toyota, Ford, Chevy, etc; AKA roadkill. I am in suburban E.TX. Other than that ,Coopers Hawks are common here and take many small birds. Also barred Owls are common and they are eating something. I think it is politically incorrect to estimate how many birds and bats are killed by wind turbines so those will be difficult numbers to get and they are not located in suburban areas. There are individual studies such as the local college studied the life cycle of Carolina Wrens ; but I doubt you will find anything covering  the range you are asking about.


T7 Tagging Next to Met Will a T7 tag still work if it is placed next to a start codon? Meaning, will it still work with a Met attached to it in the amino acid sequence?

Thank you!

By "still work" I assume you are asking if it will still be recognized by an antibody? It might. Internal T7 tag fusions are done, though they may require different antibodies than terminally tagged fusions.

That said, do you have a reason for inserting the the tag after methionine? The T7 tag already starts with methionine and naturally functions to initiate translation of T7 gene10. pET based vectors also contain it for this purpose.

[source]

In this vector, your gene of interest is typically inserted after the tag to create a fusion protein (using BamHI) or immediately after the start codon (using NheI). In either case, the T7 tag start codon is used.

You need a ribosomal binding site before the initial codon.


How do platelets produce proteins (if they do)? I'm aware that platelets don't contain a nucleus, but do contain mitochondria (so have mtDNA) and rough endoplasmic reticulum / Golgi. Since platelets require many important cell surface proteins (such as aIIb b3 for ECM binding), are these proteins (1) synthesized de novo in the mitochondria using mtDNA, and then somehow shuttled to the ER / Golgi for secretion, (2) remnants from proteins that were synthesized in their megakaryocyte precursors and not actually created anew, or (3) synthesized via some other mechanism I'm not aware of? Online sources weren't clear on this question. Thanks!

it seems that megakaryocytes, while nucleated, create a large dormant reserve of mRNA and ribosomes, which can be used by platelets later, upon their activation. So platelets can synthesize only certain proteins already transcribed by their megakaryocyte predecessors. The reserve of mRNA decline with the platelet age.


How many mosquitoes would it take to "drain" enough blood to put a person into shock? I'm just curious, how many mosquito "bites" (mosquitoes which have removed blood from a person) would it take to remove enough blood to put a person into shock? (Putting aside all reasons why it wouldn't happen, how many would it take?)

This question falls into different subquestions:

1. How much blood does a mosquito take when feeding?

This is not so easy to answer, but there are publications which measure the volume of different mosquito species. Reference 1 lists volumes between 2.85 and 11.99µL per meal and mosquito. Reference 2 lists 3.07 and 5.71µL. To make the approximation a bit easier, let's assume that mosquitoes drink about 5µL per bite (which should be near enough).

2. How much blood does a human have?

According to Wikipedia, humans have around 77mL blood per kilogram of body weight. If we take a 70kg human, we get around 5L of blood.

3. How many mosquitos does it take to get a human into shock, and how many to suck him out completely?

According to the Medline, Hypovolemic shock occurs when a human loses about 1/5 (or more) of his blood volume. 1/5th of 5L is one litre. Since each mosquito sucks 5µL, this would take about 200.000 mosquitoes. To suck out all blood would take 1 million mosquitoes. (This is not possible since mosquitoes depend on an existing blood pressure, as reference 3 shows. If a capillary is empty due to massive blood sucking, they change to another.)

Besides this theoretical (but interesting) calculation, there are some real problems about getting biten by so many mosquitos. First, this is a question of available skin. The human skin is about 2 square meters in size, which would require 100.000 bites per square meter. To break this down further, a square meter has 10.000 square centimeters, so there would be 10 mosquitos which need to bite you per square centimeter. Rather unlikely.

Then each mosquito injects a mix of anti-coagulants, pain killers etc. prior to sucking to keep the blood from clotting and also to make sure you won't notice the bite immediately. As pointed out in the comments, this would already cause a lot of trouble and probably cause massive bleeding, since the effect of the anti-coagulants would sum up when biten by thousands of mosquitos. Additionally the body reacts by releasing histamines and since the amount would also be massive, this would cause real trouble and probably kill you.

References:

Regulation of blood meal size in the mosquito
La Crosse Virus Infection Alters Blood Feeding Behavior in Aedes
triseriatus and Aedes albopictus (Diptera: Culicidae)
Visualizing Non Infectious and Infectious Anopheles gambiae Blood
Feedings in Naive and Saliva-Immunized Mice

Everyone seems to forget that the human body replaces blood that is lost quite rapidly. When I donate blood to blood bank they take half a liter or something and I was informed my body will replace it within 30 minutes, I just need to drink plenty of fluid after.

I think it would take a fairly concentrated effort by mosquitoes to do any damage from blood loss.


I found this strange tooth in Galveston, Texas. What does it belong to? I found this on May 7, 2017, on Bolivar Peninsula in Galveston, Texas. What's not visible are the treelike rings inside the tooth and what looks like a tiny interior porous center. It looks like it was considerably larger but broken off.

We're all taking bets on what it is!

This is a cow tooth. Your image matches above image.
https://www.flickr.com/photos/61377404@N08/12300347505

Most likely a horse tooth. Check out this image from Wikipedia.


Is there a purpose for nucleated red blood cells in reptile, avian and fish blood? I have read, and read, and read documents on this subject but still have no conclusions.

Everything I have read explains why mammals don't have a nucleus (to make more room for the haemoglobin and allow for more oxygen to bind as well as making it easier for the RBC to fit through capillaries) but the reports don't explain why birds, reptiles and fish may still have nucleus in a red blood cell.

Is there really any other function a nucleus has within a red blood cell apart from being the 'brain of the cell?

It's doing my head in, all I've gained from this research is the understanding that birds have a far more advanced respiratory system and their capillaries are bigger than mammals, this still doesn't explain the need for a nucleus, it's actually suggesting they don't need one!

Any enlightenment will be great,

Thanks.

http://onlinelibrary.wiley.com/doi/10.1002/iub.490/pdf

It's difficult for vertebrates to aquire/evolve enucleated cells, that's why they are very rare previous to the mammalian adaptation. Salamanders have evolved enucleated cells. Research suggests that it may be due to a salamanders big genome and big cell nucleus, compared to the salamanders small body size.

Mammals may have acquired the trait because they evolved from small animals with miniaturized capillaries and blood cells and large genomes, and the advantage was kept afterwards. Large genomes inhibit flow and flex of nucleated blood cells.

The smallest bird genomes are found in the most miniturized clades of birds at 1 Gb. Mammals of a similar size can have carry 2-3 Gb of chromosomes.

Lizards have lower energy than mammals.

Fish are most active in highly oxygenated water, i.e. salmon, which allows them to be very energetic, water is a more efficient breathing medium than air, hence the small size of gills. fish and humans both contain 6-7 percent blood by volume.

Birds have smaller haemoglobin including the nucleus, and have a different kind of capillary size and structure with advantages and disadvantages, and lighter hollow bones with less marrow. Birds didn't radiate to new shapes as well as mammals did.

Enucleate cells are fairly rare in the plant and animal world, so they perhaps have a hidden expense. Maybe it's not just a factor of shedding the nucleus, and in fact there is a cost of adapting the primary circulation system's immunity against paramecia and pathogens without a nucleus. various viruses can take advantage of enucleate cells.

Perhaps that is the reason why birds did not evolve backwards into dinosaurs. some factor made their genome comparatively small. It could be the lack of enucleated bloodcells that forced them to shed genes as an alternative. Perhaps that's why they lost the dinosaur genes which held code for quadrupeds, arms, jaws, horns and teeth and the things that birds don't have.

Good discussion, very complex topic.
I’m not sure we know/understand all variables and interactions at play in circulatory/respiratory physiology(not to mention aspects of the RBC involved).
That said:
Without a nucleus(and mitochondria), the red cell has less tendency to metabolize whatever O2 is available, as well as many of other well stated advantages of the enucleated state for increasing O2 availability at the cellular level.
Camels, with nucleated RBCs, are an exception to the mammals enucleated RBC, implying the capacity for DNAs response to environmental pressures.
Balancing advantages and disadvantages of fundamental physiological and cellular changes will direct the path of an organisms success (i.e. adaptive evolutionary experimentation with organisms reproductive success or failure being the final arbiter).
The camel “giving up” the well established mammalian enucleated RBC (gaining adaptive physiological advantages) might be an apt example of the DNA biochemical feedback loop required to coordinate significant cellular changes within a species.
Evolution is not a one way street, u-turns are available(which is why there’s no such thing as “junk” DNA, a story for another time).
Keep cooking baby!


Snail species identification from the United Kingdom Can anybody identify the species of this snail?

From this website, it looks like a Common Snail.

Could it be the dextral type of Cornu aspersum?

These snails have been found in a garden, have survived a month on lettuce in a home environment, retreat in their shell sometimes. Their shell measures about 2 cm diameter.

This snail is Cornu aspersum its common name is garden snail, it belongs to Helicidae family click here for more information


How are presynaptic burst firing signals transmitted post-synaptically? Neurons can exhibit burst firing and this presynaptic process basically results in a flurry of action potentials being fired in a short time window.

I'm, however, wondering how these signals are further relayed once they synapse onto other neurons? Specifically, does each action potential in the burst volley generate another post-synaptic action potential, or is the bursting somehow averaged to then transmit either one or no action potential post-synaptically depending on long the burst train was?

Short answer
It depends.

Background
It all depends on the neuronal circuit and neurotransmitter system under investigation. For example, raphe neurons release 5-HT in a burst-like fashion onto cortical dendrites. However, the postsynaptic effect is inhibitory, so no action potentials there (Gartside, 2000).

Intracortical recordings in the rat have shown that each action potential in a burst resulted in neurotransmitter (glutamate) release and subsequent excitatory postsynaptic currents (EPSCs) and potentials (EPSPs) (Williams & Stuart, 1999). So that would positively answer your question, at least in this specific neuronal circuit.

Reference
- Gartside, Neurosci (2000); 98(2): 295-300
- Williams & Stuart, J Physiol (1999); 521(2): 467–82

This is just my personal opinion and impression:

First, it's not at all clear which effects burst firing of action potentials of a pre-synaptic neuron do have at the synaptic end bulbs: Does it cause a burst of fusions of vesicles and thus a burst of releases of neurotransmitters? Or isn't the intricate firing pattern completely smeared and blurred at the synapse?

Second: Each neuron's synaptic input to another neuron takes a long way (along the dendrite and so on) to get part of the effect at the axon hillock where post-synaptic action potentials are created. The firing pattern of the pre-synaptic neuron (which is one of thousands) will hardly be visible and mirrored here.


If a mother had a child with her own son, could a paternity test yield positive result for the son's father? Let's imagine a family composed of Mr A and Mrs B, who have a son named John.

Now, if for whatever twisted reason, John had a child with Mrs B, could a paternity test yield positive result for Mr A ?

Since John's genes all come from Mr A and Mrs B, the child's genes would all come originally from Mr A and Mrs B as well. Thus it seems to me like the test could suggest Mr A is the father of the child.

Or would there definetly be some "red flags" that suggest something wrong happened ?
Like, for example, if the child is a girl, that would mean both of her X chromosomes originally came from Mrs A (since John's X chromosome comes from his mother, as for all males), possibly even the same chromosome twice.

Let's consider that only Mr. A is tested, and not John. Would the child be considered genetically close enough to Mr. A that a test could attest that he is probably the child's father, granting there is no other test showing someone else as a much more likely candidate ?

Let's approach some different methods of distinguishing parents:

1: The Y chromosome. These are passed down from father to son. Therefore, if the baby is male, its Y chromosome will be the same as John's and his father's - it will be indistinguishable who it's from.

2: The X chromosome. A male baby always has one of the mother's X chromosomes. A female baby always has its father's X and one of the mother's X. A male baby of John and Mrs B would always end up with one of Mrs B's X chromosomes, meaning that this can't distinguish the father. A female baby would have two X chromosomes from Mrs B (because John's own X came from her), proving that it is the product of incest.

3: Mitochondrial DNA. mtDNA is passed on from mothers to their children, never from the father. Therefore regardless of whether John or Mr A is the father, the baby would have Mrs B's mtDNA - not useful.

4: DNA fingerprint. This is primarily based on stretches of the human genome that contain repeats of short DNA sequences (so-called STR/short tandem repeats, or VNTR/variable number tandem repeats). In both cases, the sequence is the same in individuals, but the number of repeats is extremely variable and each human therefore has a (possibly) unique combination across the different repeat locations in the genome. Because children inherit 50% of their DNA sequences from the father and 50% from the mother, John himself will have his mother's characteristic lengths in 50% of repeat locations and his father's in the remaining 50% of locations (roughly). A child of John and Mrs B would have MrA's repeat lengths in 25% of locations and Mrs B's in 75%. The fractions "100% Mr A" vs. "50% Mr A" vs. "25% Mr A" can be distinguished by this method.

No, Mr. A would not be flagged the father.
This is becasue when a parental test is done they look to what genes have the mother, the father and the baby. First they look at what genes has the mother and the baby. The one missing should be from the father.

In this case it could be possible that for example:
Mr. A: 1 gene Red hair, gene Blond hair.
Mrs. B: gene Brown hair, gene Black hair.
John: gene Brown hair (from his mother), gene Blond hair (from his father).
If the baby has: gene Black hair (from mother) and gene Brown hair (from John. Then that would prove the hair color is not from mr. A. He doesn't have those genes.  So he isn't the father.


Red neurons - Acute neuronal injury “Red neurons” are evident by about 12 to 24 hours after an irreversible hypoxic/ ischemic insult. The morphologic features consist of shrinkage of the cell body, pyknosis of the nucleus, disappearance of the nucleolus, and loss of Nissl substance, with intense eosinophilia of the cytoplasm.  -Robbins textbook of pathology

Taken from Robbins pathologic basis of disease, 9e, pg.no1265, fig: 28-13B

Why in case of neurons there is shrinkage instead of swelling as in other cells?

There is not some simple dichotomy of "neurons shrink and other cells swell" in response to hypoxia/ischemia.

Neuronal death can be necrotic or apoptotic or both, and at different stages different morphology is observed: generally swelling earlier, shrinkage later, though both are observed together early as well. Eosinophilia/"red neurons" tends to occur later as mentioned in this passage (after 6 hours, consistent with 12-24 hours) so that's probably why the author is referring mostly to shrinkage. Cells can also have swelling of some organelles, like mitochondria, despite shrinking overall.

Without further context of the passage you provided it's hard to say much more.

Garcia, J. H., Yoshida, Y., Chen, H., Li, Y., Zhang, Z. G., Lian, J. I. N. Y. I. N. G., ... & Chopp, M. (1993). Progression from ischemic injury to infarct following middle cerebral artery occlusion in the rat. The American journal of pathology, 142(2), 623.

Jenkins, L. W., Povlishock, J. T., Lewelt, W., Miller, J. D., & Becker, D. P. (1981). The role of postischemic recirculation in the development of ischemic neuronal injury following complete cerebral ischemia. Acta neuropathologica, 55(3), 205-220.

Portera‐Cailliau, C., Price, D. L., & Martin, L. J. (1997). Excitotoxic neuronal death in the immature brain is an apoptosis‐necrosis morphological continuum. Journal of Comparative Neurology, 378(1), 10-87.

Search for Exicitotoxic programed cell death. Acute Neuronal injury occur by this pathway. This is like Necroptosis. Cell shrinkage is seen due to Glutamate.  I have added some screenshots of my search,, rest you can search yourself.

Read more at
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398818/


Which of the following lacks DNA? a) An Enucleated ovum
b) Mature RBC
c) A mature spermatozoan
d) Hair root

According to me, there can be 2 answers, a and b because an ovum whose nucleus has been removed lacks DNA. And also, initially RBC has a nucleus but as it matures it's nucleus disappears. So, mature RBC should also lack DNA. Then which one will be a more appropriate answer ?

There are two answers if the question refers to genomic DNA (neither enucleated ova nor mature RBCs have genomic DNA).  However, since the question doesn't specify genomic DNA, we can exclude enucleated ova, which would still have mitochondria and therefore mitochondrial genomic DNA.  Mature RBCS (at least in most mammals) do not have mitochondria, so the safest answer is probably b) Mature RBC.

the answer will be mature DNA.
We know that except for nucleus other organelle such as mitochondria also have ability to replicate an as mentioned in the question the enucleated ovum (ovum lacking its nucleus) do have the other cell organelles, whereas for the mature erythrocytes, they lack nucleus as well as other cell organelles such as mitochondria and golgi bodies; and hence RBC can't divide on its.
hope it helps!


Are there any organisms that perform photosynthesis-like processes with thermal energy alone? The closest I can find are thermophiles, but it seems they use the chemicals present in the hot environment for energy, not the heat itself.

Thermophiles are organisms that are capable of surviving high temperatures. It doesn't mean they use or harvest the thermal energy in any way. Normally proteins start to unfold and degrade at temperatures above about 41 °C and all other organisms have a hard time coping with the effects.
Usually biology uses chemical energy. Photosynthesis is the one exception of a biological system converting the energy of photons directly into chemical energy stored in complex biomolecules for all others to use as nutrition.
Organisms that do not rely on those complex biomolecules but can support themselves are called autotroph. So photosynthetic organisms are  photoautotroph and micro organisms that use chemical energy from inorganic compounds are chemoautotroph. The inorganic compounds used can be as simple as decomposed water by radioactive decay.


Homeopathy is placebo, but isn't placebo good? I never considered homeopathy as a serious and scientific medicine, and now we have plenty of evidence supporting this (http://www.theguardian.com/commentisfree/2015/mar/12/no-scientific-case-homeopathy-remedies-pharmacists-placebos).

But placebo effect is also a thing that works, strange as it may be. The placebo effect deals with the importance of the brain's role and perception in physical health. So, in my understanding, placebo is better than nothing.

But now I can't treat myself with homeopathy, because I don't believe on it. Other people believe, and are happy with it (benefiting from the placebo effect).

So, my question is, wouldn't be benefitial to illude someone (or yourself) in order to achieve the placebo effect?

The point of a double-blind trial is that treatments are compared to placebo effect. Therefore, conventional treatments that "pass" double-blind trials are better than placebo.  If homeopathy is equal to placebo, that means that homeopathy is worse than conventional treatment.  Therefore, people who treat with homeopathy are giving worse than standard care.

But placebo effect is also a thing that works, strange as it may be.
  The placebo effect deals with the importance of the brain's role and
  perception in physical health. So, in my understanding, placebo is
  better than nothing.

If you think, say, that your lung function is improving, but it's actually not, that's not a good thing.  It would be better for you accurately know that you are not healthy, then to wrongly believe you are better.


Are there venomous plants? There certainly are poisonous plants, but I was wondering, whether there are venomous specimen, too?

First, I thought the stinging nettle could be one such. After all, it's common knowledge it "applies a toxin upon touch". However, reading about the mechanics it seems that the injection is actually a much more passive procedure, which would render the plant poisonous, wouldn't it?

So what are some venomous plants?

By definition, the word "venomous" can only technically be applied to animals.  The most "poisonous" plant would be the gympie gympie tree, but if you want something "venomous", you might be able to find something similar within some species of carnivorous plants.

Yes, venom typically uses some form of injection, and doesn't need to be eaten to harm or kill you.  The gympie gympie tree uses silica tipped hairs to put a toxin into your flesh, much like how jellyfish do.  This tree is naturally found in Australia, because of course it is.  But it isn't only australia.  Stinging netals, definitely, and poison oak debatably are also venomous, since you don't have to eat them to take some form of chemical harm.


Can someone identify these fungi? Found them in Gujarat, India.
Found growing among potted plants

This may be Clitocyte odora commonly known as aniseed toadstool.

They can be found growing in small groups along the side of tree roots.

it is widespread in the temperate zones, occurring in Asia, Europe, and North America

Young specimens have a light blue texture on the cap which fades to grey in age. The gills and stem are white with no ring.

Reference

If there is a white skirt it is probably a verdigris argaric:
https://en.wikipedia.org/wiki/Stropharia_aeruginosa


Does GABA enhance or inhibit negative effects of glutamate? A study on NCBI studied the correlation between a depressive mood and chronic pain. I researched this because today I noticed unusual emotional volatility as a result of 2 days of acute back pain combined with acute muscle soreness (DOMS).
I am certain that the pain and difficulty sleeping (although I slept in on both days), and challenges with finding a sleeping position without pain, and continuous pain on most moving, standing, and sitting, that this has caused some emotional volatility on a physiological level. (Psychological effects as a direct result of temporary chemical changes in the body/brain due to acute pain; not due to neural pathways causing depression, of which I do not have, and I am a joyful person normally).
This question is not about alleviating pain, as it will go away on its own soon. The back is getting near healed by end of week and the sore muscles which have DOMS due to intense workout will also resolve on its own in a few days to a week.
Rather, my question is specifically concerning a particular phrase which I am unclear about:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

I am unclear if this is stating that GABA reduces the effects of glutamate or if it enhances the effects.
There is no clear answer to my full [temporary] issue, since the study itself states that neither the corresponding pathophysiological mechanisms of chronic pain and depression nor their mutual correlation has been identified, so there is no pathophysiological scientific answer to the chemical workings, so I can only speculate.
The end result is I wanted to discover whether increasing or lowering GABA could have any effect on my mood as a result of my pain in the short term, which is easily experimented rather safely by either taking GABA or taking a supplement that inhibits GABA. It could have no beneficial effect - no problem. It's worth a try though. I've taken GABA before BTW.
To reiterate the particular question: With regards to the statement:

Glutamatergic activity can be promoted through the breakdown of efficient inhibition of the actions of glutamate by GABA

Does this imply that GABA enhances or reduces glutamatergic activity?
Note:
I think it's saying that GABA creates glutamatergic activity which inhibits the neuroexcitatory effects of glutamate. That is, taking GABA would decrease effects of glutamate. Let me know if this is correct or not.

Glutamate causes an EPSP (Excitatory Post Synaptic Potential,) thereby making the neuron less negative depolarize) and closer to voltage required to cause an Action Potential (AP)  and thus fire.  GABA causes an IPSP (Inhibitory Post Synaptic Potential) making the neuron more negative (hyperpolarize) and further away from the voltage required to fire and cause an AP.  GABA & Glutamate receptors  are generally on different neurons that synapse with other interneurons & oppose each other, although neither one is generally the end neurotransmitter of the locus,  nor the only neurotransmitter of the neuron, so basically act as neuromodulators on the post-synaptic neuron. Glutamatergic receptors generally affect Sodium Channels &  GABA-ergic neurons generally  affect Chloride Channels. In theory, inhibiting an inhibitory neuron would be the equivalent of exciting an excitatory neuron, but since they primarily affect  post-synaptic neurons, the effect is cumulative, so the post-synaptic interneuron is basically adding up all the EPSPs & IPSPs to get a RMP (Resting Membrane Potential) & some additional stimulus must occur to get the neuron to fire (AP)


What are senescent cells doing in our bodies? I'm reading a paper that mentioned the elimination of senescent cells delays aging. I'd like to receive more information about it.

The Baker study published in Nature demonstrates that targeted elimination of senescent cells in mice results in remarkable protection from several age-related pathologies, cancer, and makes cancer cells resistant to chemotherapy. I know that senescent cells drive aging, and induce cancer. Can we grow them in cell culture as a kind of stem cells ? How might they contribute to the aging process ?

Senescent cells are cells that go into permanent cell cycle arrest. Although they may be metabolically active, they are not actively dividing. This may occur when cells in our bodies undergo damage from an extraneous or endogenous source. I understand that its role in cancer and aging is a great topic of study.


Why does an increased heart rate mean increased blood pressure? Say a person starts exercising. If their cardiac volume remains the same but their heart rate increases so that the overall result is an increase in cardiac output, will their blood pressure increase during the exercise ? If it does, why ?

In good approximation, the arterial blood pressure PA depends with

PA = PV + R x dv/dt,

on central venous pressure PV, total peripheral resistance R (also referred to as TPR or PVR) and cardiac output dv/dt (aka CO) – the usually cited equation MAP = CO * PVR is an over-simplification. Since cardiac output is defined with

dv/dt = RH * VS

as a result of heart rate (RH) and stroke volume (VS) the blood pressure should increase if heart rate increases.

However, in reality, the conditions are more complex. In exercise body temperature increases, which leads (via the thermoregulatory system) to vasodilation, so that the total peripheral resistance R decreases, which is able to reduce the blood pressure again.

Decreasing PV in exercise should occur on a very slow time-scale and only be relevant in long-time endurance training.

Concentrations of some hormones change in exercise. Levels of some stress hormones (catecholamines) rise and therefore increase cardiac output, but their action on peripheral resistance is heterogeneous. It goes up, if alpha receptors are stimulated, but decreases after stimulation of beta receptors. Similar to (and partly mediated by) beta adrenergic action classic thyroid hormones (e.g. T4, T3 and 3,5-T2) increase heart rate but decrease total peripheral resistance. It depends on the type of exercise if thyroid hormones rise or drop. They are increased in short-term or endurance exercise (representing type 2 allostasis) but decrease in exhausting exercise (leading to type 1 allostasis).

In summary, it depends on many factors, if blood pressure increases during exercise. In ergometry the blood pressure usually slightly rises.

References

1: GREENE BA. Cardiac output and total peripheral resistance in anesthesiology;
clinical applications. J Am Med Assoc. 1958 Mar 1;166(9):1003-10. PMID
13502096. https://www.ncbi.nlm.nih.gov/pubmed/13502096 https://doi.org/10.1001/jama.1958.02990090011003

2: Mayet J, Hughes A. Cardiac and vascular pathophysiology in hypertension.
Heart. 2003 Sep;89(9):1104-9. PMID 12923045. https://www.ncbi.nlm.nih.gov/pubmed/12923045/ https://doi.org/10.1136/heart.89.9.1104

3: Silva AS, Zanesco A. Physical exercise, β-adrenergic receptors, and vascular response. Jornal Vascular Brasileiro. 2010 9(2). https://doi.org/10.1590/S1677-54492010000200007

4: Chatzitomaris A, Hoermann R, Midgley JE, Hering S, Urban A, Dietrich B, Abood
A, Klein HH, Dietrich JW. Thyroid Allostasis-Adaptive Responses of Thyrotropic
Feedback Control to Conditions of Strain, Stress, and Developmental Programming.
Front Endocrinol (Lausanne). 2017 Jul 20;8:163. doi: 10.3389/fendo.2017.00163.. PMID 28775711. https://www.ncbi.nlm.nih.gov/pubmed/28775711 https://doi.org/10.3389/fendo.2017.00163

By cardiac volume I assume your talking about Stroke Volume, that is, the volume of blood pumped from the left ventricle per beat.

Blood pressure will probably increase.

Stroke Volume depends on contractility, duration of contraction, preload (end-diastolic volume) and afterload.

Exercise usually increases the preload (due to an increased venous return caused by muscle contractions) and contractility (due to sympathetic effects).

So, to maintain a constant Stroke Volume, and cancel out the preload and contractility increments, you need to either:

reduce the duration of contraction (by raising the heart rate beyond 120bpm/ 140bpm, for instance) or
increase the Afterload (by increasing the Total Peripheral Resistance, for instance).

Since blood pressure is positively affected by both cardiac output and Total Peripheral Resistance, unless the Heart Rate gets really high, blood pressure should increase.


Is it biologically possible for an adult's eye color to change? Can it be that the adult eye can change color? Specifically my question is about a unilateral color change, such that the color of one eye remains constant, while the other changes color over time. Can this happen? Or can it be related to light-scattering, or an illusion of some sort?

Short answer: The genes that encode eye color do not change, but the pigments in the eye can change due to external factors like diseases of medication.

Long answer: Yes, it is possible that the eye color of adults can change, and it can also only happen to one eye. It is then called Heterochromia. There are two possibilities for different colored eyes, either congenitial (genetic) or acquired. Since you ask only for eye color changes in adults, we can skip here the genetic reasons, as these show up in kids already. If you are interested in them, have a look into the Wikipedia article on Heterochromia.

The basis for our eye color is genetically determined, changes can later occur due to diseases (so if one experiences a change in eye color, it is always a good idea to consult a doctor) and also due to medications.

The eye undergoing a change in pigmentation can either lighten up or darken.

Fuchs’ Heterochromic iridocyclitis: (also known as Fuchs’ Heterochromic uveitis) The change is caused by an eye infection with different microorganisms like Toxoplasma gondii, Herpes simplex virus or Rubella (an probably others) but it can also have an autoimmune pathology. See reference 1 and 2 for more details.

Horner's Syndrome: This is a syndrome which mostly occurs in kids after damages to some nerves. This can lead to insufficient signals towards the pigment production and heterochromia. Rarely this can occur also in adults, where this is called acquired Horner's syndrome, see reference 3 for details.

Pigmentary Glaucoma: In this disease (also known as Pigment dispersion syndrome) pigment cells from the back of the iris float are seperated from the original place and float through the aqueous humor of the eye where they can produce pigment which over time changes the appearance of the eye. See reference 4 for more details.

Medications: Some of the medications against glaucoma (the prostaglandins latanoprost and bimatoprost) can cause a deeper pigmentation which will not always diminish after the end of the treatment. See reference 5 for more details.

Cancers: Some cancers as melanoma can also cause heterochromia, either when they are darker pigmented that the eye or when they are not pigmented. In both cases they influence the eye color. See reference 6 for more details.

References:

Fuchs' heterochromic cyclitis: review of the literature on the
pathogenetic mechanisms.
Associations of Fuchs heterochromic iridocyclitis in a South Indian
patient population
Acquired Heterochromia with Horner's Syndrome in Two Adults
Pigment dispersion syndrome and pigmentary glaucoma – a major review
Incidence of iris colour change in latanoprost treated eyes
Diffuse iris melanoma: Report of a case with review of the
literature

To add what the previous answer did not: not only medicines and disease change the color of your eyes. Aging does that too in most (if not all!) people. Pigmentation is usually lightest in utero and right after birth. Melanin accumulates over time and makes the hair and eyes darker.

This is why many people are born blond (or green/blue-eyed) and become brunette (or brown-eyed) over a period in their lives. It can take days - usually as a baby - or decades, depending on the individual. The rate is determined genetically, i.e. it does not, for instance, depend on how much exposure to the sun you get. Melanin in the skin can do that.


How does natural selection explain sexual display? As I understand it, animals sometimes grow more vibrant colors, bigger feathers, elaborate dances, build shiny nests, all to impress the other sex. However, these are all superfluous to survival -- any nutrition or energy spent developing these attributes or conducting these rituals are no longer usable for hunting or child rearing, for example. Given the same animal who does one of these wasteful practices versus the same animal who doesn't, in theory the latter should have the advantage in its chances of passing its genes down.

Why is it then, that sexual preference grows towards these wasteful growths and habits, rather than ignoring these sexual displays for sheer survival efficiency?

Short answer
Survival does not get your genes into the gene pool, reproduction does.
thus reproduction based selective pressures can be stronger than survival based ones. there are plenty of organisms that die during or right after mating because of this.
Consider an example In species A finding a mate is fairly rare, it may only happen a few times in an organisms life. if individual X is guaranteed to mate and reproduce when they find a mate but will die after mating, and individual Y will not die after mating but only has a low chance to mate then the genes from X will spread much faster than the genes for Y, because mating is already a rare event, but X genes spread every time while Y genes will also only spread once or often not at all, and will also take much longer.
Or to put it another way, a chicken is just an eggs way of making another egg, the survival of the chicken is only useful as much as it facilitates reproduction.
Any mutation  that happens to make you better at attracting a mate will spread, how it does so is basically irrelevant as long as it works, loud noises, bright colors, eye spots anything that draws the females attention works. studies on several bird species have shown even the colored bands used to identify birds for study effect their mating chance is they are right colors. Animals often already have a variety of biases for their attention hijacking them is an easy way to improve your chances of mating.  Of course once a way evolves that reliably improves mating chances preference for that becomes favorable as well which can lead to a run away selection feedback loops AKA Fisherian runaway
https://link.springer.com/article/10.1007/BF00172135

The point is that it's not only wasteful, but counter-productive to survival.

If you're a red bug in the lush green of the amazon you are painting a target on yourself. This has the effect of increasing your selective pressure. If you survive with a target on your back, and wasting energy on pigments, then you must be very good all of the other things necessary for survival.

So, with natural selection, the higher selective pressure on an organism with a target on its back will be a more selective filter, only allowing the most performant little red bugs to survive and mate with each other, "quickly" giving them an edge over their less colorful brethren, and resulting in a biodiversity that flaunts its ability to survive today with extravagant colors and nests.

The mating dances might be a different story, I'll let someone else tackle that.


Can someone identify this odd looking spider? I found this spider crawling on my tile floor. We live in rural central Virginia.  I’ve found spider species with similar looks but nothing exactly like this. Its size was less than 1 inch. Can anyone identify it?

I agree with JulPal's comment from August.  It looks very much like a male Thiodina (now renamed Colonus) sylvanus.  As with many Salticids, the females look rather different, and it turns out that there is apparently a similar species of Colonus in the area, which can be distinguished in the field by the fact that the white mark on the carapace is not a block so much as a thick longitudinal line.
I attach an image from Tree of Life, with the link below:

http://www.tolweb.org/Thiodina_sylvana/5911

It is Tarantula which comprise a group of large and often hairy arachnids belonging to the Theraphosidae family of spiders


Why are eyes more sensitive to flicker in periphery — contradictory answers In terms of the perception of flickering by CRT monitors, This answer suggests that peripheral vision has faster response and is thus more sensitive to flicker due to being provided by rod cells.

But in another answer it's said that rods are saturated at daylight and even at twilight. These two answers are in contradiction, since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.

So, how to reconcile these two answers?

I think the most likely explanation is that ambient lighting conditions in the room where OP was sitting, as described in the original question, might not have been bright enough to saturate the rods. Under mesopic conditions, both rods and cones are active. Hence your statement that

  ...since the light from CRT mentioned in the question pointed to by the first link above is quite above the photopic threshold.

may not hold. Since rods indeed have quicker responses, the periphery may be more sensitive to the flickering of a CRT or light bulb.

Note, however, that cones have flicker fusion frequencies of up to 90 Hz (reviewed by Perz, 2010), and CRT screens and light bulbs flicker at frequencies following the mains (50 or 60 Hz). Hence, cones may still be able to pick up the flickering. Since OP reports on an anecdote, experimental conditions may have been suboptimal and their report might have been unreliable. So we cannot exclude OP was using photopic vision, regardless their report.

Reference
- Perz, Master's thesis, Eindhoven University


How does your body know when it is infected so it can invoke a fever? How does your body know when it is infected with a virus or bacteria so it can invoke a fever or ramp up the immune system?

During infection certain macromolecules present in the pathogens (pathogen associated molecular patterns) such as lipopolysaccharide launch the innate immune response, through toll like receptors. This leads to production of pro-inflammatory cytokines and also other inflammatory mediators like prostaglandins, thereby causing inflammation and fever.

An opinion by non-technical observer.

If you know the function of a hive, you know that bees communicate with each other, touching and rubbing chemical information. In a few minutes the information reaches the center of the hive and returns to individuals which are caring of it. It is widely accepted that a hive is a unique individual, composed of thousands of insects each with its own function.

I believe that we can make the observation reverse.
The man (and animals) are agglomerations of cells that pass chemically information to each other. Information reaches the central system, which responds by activating the necessary functions.

In case of infection, viral or bacterial, blood flow to the affected place very quickly, scrolling faster and thus raising the temperature. Similarly in the blood activates the necessary antibodies, which communicate with each other chemically referring where necessary. Pile up in the affected areas, resulting in swelling.

Other functions, such as sweating, vomiting or pus, are ways to excrete toxins (such should not be blocked). If we imagine the human body as a great hive where each cell is a member that transmits information and responds to stimulation of central system, acting in cooperation, the operation according to me is very clear.

How do the bees know that they are dying, if not passing to collecting companions honey too thick?
Sorry for non-technical opinion, if not useful delete it.


What tools can help me determine if a plant homologous protein interacts with an ncRNA in the same way? First post here, so bare with me if I violate any etiquette or formatting rules.

Let's say I've got a protein in humans. When it interacts with an ncRNA found in humans, it does something that I'm very interested in.  I see a highly homologous (~85% AA identity) protein in plants, and it's widely conserved.  I'm interested in eliciting the same activity of this protein in plants.  Only problem is that there's no native plant-produced ncRNA to interact with my protein of interest in the same way.  So I had an idea:

What if I introduce a transcript to plants that addresses this problem?  If the plant version of this protein interacts with this (introduced) RNA in the same way it will be really cool.  I'd like to test this hypothesis with some synthesized constructs.  But before I plunk down thousands of dollars on a few constructs, I'd like to explore any predictive or analytical tools to strengthen the case.  I'm aware the odds are against me.

Thanks!

The ncRNA sequence from human may bind to the plant protein in the plant cells, but so what? You may be able to say the plant protein works as RNA binding protein, but no more than that.
Another concern is that the plant protein may not recognize the same RNA sequence to the human protein.

There are several ways to find RNA partners of RNA binding proteins.

SELEX

This method is used to find consensus sequences that your protein recognizes in vitro. Once you find consensus sequences, you can search ncRNAs from the plant.

CLIP

This is similar to Chip assay. You could find real targets of your RNA binding proteins


what is the effect of soda water on digestion? what is the effect of soda water on the process of digestion? As it has been seen that after drinking soda the process is increased...I just want to know that what is the chemistry behind this?

Soda, anything carbonated causes bloating, which stretches the stomach. Mechanoreceptors in stomach detect the stretching resulting in parasympathetic innervation to GI smooth muscle. This causes an increase in GI motility.

Due to presence of hydrogen ion in soda water ,H+ ion Concentration in stomach is increasing (common ion effect) it helps in digestion.


What causes the yellow and brown spots on our sour cherry tree? So at the end of spring (maybe at the beginning of summer) our sour cherry tree started producing these yellowish/brownish spots on its leaves. Can you help me identify the couse of this? What can we do against it? I cannot see any bugs on it, my best guess would be some kind of a fungus, but I am way far from being an expert. Thank you in forward for the answers!
Edit: I am located in Hungary. The brown spots are not bigger than my nails, but the yellow area can cover even the whole leaves. Also, the capillaries visible on the leaves can turn red, as you can see on the pictures. Unfortunately, the exact species of the cherry is unknown to me.

The tree is most likely sick. Plant diseases take years to develop versus diseases in animals caused by either bacteria, viruses, or parasites. This is because the tree has thick cell walls that can be a huge barrier hindering viral infection. Another thing is that trees lack a circulatory system and rely on partial water pressure from the air to draw water from the roots up to the leaves.
Your tree might have a virus that is slowly killing it. Which insects are endemic to your region? We can deduce the virus if we know the main types of bugs living in your area.


what kind of lizard is this Found on ground by house in residential neighborhood in Fort Pierce FL. looks mature maybe 17".

Nice find. It's a common basilisk or jesus christ lizard, distributed throughout central america, they grow to 27 inches and can run on water, the male is bigger than the female:

https://travel.mongabay.com/colombia/images/colombia_1513.html


What is the difference between vegetable and fruit? Is there any exact definition of vegetable and fruit? How can new plant be classified?

A true fruit is a ripened ovary that usually starts ripening when it is fertilized. And vegetable is any vegetative part of the plant which is edible and contains stored food probably in the form of starch.
These definitions are not exact as there are a lot of fruits which are fruits but do not strictly follow the given definition. See Syconus, Composite fruits, Sorosis.etc

Classification is based on several different criteria, for example the mode of reproduction, arrangement and design of flowering parts and flowers and also on the basis of habitat and habit.

From a culinary point of view, the difference between a vegetable and fruit is are they sweet or not.

Hence eggplant, tomatoes and bell peppers which are biologically fruits are considered vegetables.

Potatoes which are tubes, are considered vegetable. Kale which are leaves are considered vegetable. And cauliflower which are flowers are considered vegetables.

The question of fruit and vegetable would be might be tested if somebody made a very sweet and soft carrot, at which point I am not sure what the master chefs of the world might say. Could a soft and sugary sweet carrot be able to graduate into the word of fruits and leave the world of vegetables behind?


Can plants live forever? I know that some plants die for old age like a
lettuce. But there are trees like Baobabs or larger Ficus in the tropics of whom we don't know their age. And trees like spruce reaching 9950 years old, which die for environmental factors and not by age.

However, E.g. when we multiply vegetatively an olive or cacao tree, we use a fragment or clone from a unique individual passing the same genetic information, again and again.

Then, can these plants live forever?

The answers to these questions often boil down to "what do you mean by live forever?".

You've included vegetative cloning, so I infer that counts as one living organism for your purposes. In that case, the answer is absolutely.

Pando is at least 10 thousand years old and only getting larger. The Cavendish banana is about 150 years old, but produces at least 70 million tons of bananas yearly.

See here for other giant clones. Of particular interest is King's Lomatia, represented as a species by a single, sterile, individual. Fossilized triploid leaves are too old for carbon dating(at least 45 thousand years old), so it's essentially unknown how old it is.

I would be comfortable declaring Pando immortal, since it's way too big to be eaten, too resilient to burn down, and has already survived the middle and end(at least!) of an ice age. That just leaves (ha) disease and basically nothing else as possible threats.

Forever no. For thousands of years yes. And not only plants, other organisms have what is called biological immortality. Look here for some examples https://en.m.wikipedia.org/wiki/List_of_long-living_organisms


Do Angiotensin II Receptor Blockers (ARBs) or other factors control the level of ACE2 expression? [coronavirus receptor] Because ACE2 is used by SARS-NCoV-2 to enter the cell, I am curious what factors determine its expression.  Interestingly, myocardial infarction increases ACE2 expression in the heart in an animal model ( https://www.ncbi.nlm.nih.gov/pubmed/15671045 ).  The paper found no significant effect from ramipril, an ACE inhibitor, but I don't think I can assume ARBs would work the same way.  (I am suspicious they might increase it based on the increase in the product Ang(1-7) level - https://www.nature.com/articles/hr200974 )  Note that soluble sACE2 can bind cells that did not produce it, by an RGD independent association with integrin beta 1.

Anything that influences the amount of ACE2 on cell surfaces is a useful answer.

I should follow up with some things I've found.  As a starting point, the normal expression pattern is available at https://onlinelibrary.wiley.com/doi/pdf/10.1002/path.1570 - note the staining of simple squamous epithelium in the alveoli and the endothelia of blood vessels.  Another paper details a sharp decrease in expression with age in rats, but I don't know if that extends to humans.

For regulation of expression, I was surprised to see that Google Scholar actually provides a very good assortment of search results, easier to work with than PubMed, which were topped by the MI regulation I described in the question.  Additionally https://onlinelibrary.wiley.com/doi/abs/10.1002/path.1670 (yes, that IS a different link) describes ACE2 expression in renal disease but not in normal kidney.  ACE2 expression correlated with proteinuria, but negatively with GFR. https://link.springer.com/article/10.1007/s00125-008-0988-x  There are discordant notes in some other situations: for example, subtotal nephrectomy decreased ACE2 expression in a way that was partially prevented by ramipril. https://portlandpress.com/clinsci/article/118/4/269/68827/Reduction-in-renal-ACE2-expression-in-subtotal

The mRNA and protein are both described in atherosclerotic lesions: https://onlinelibrary.wiley.com/doi/abs/10.1002/path.2357

In the lungs https://jvi.asm.org/content/79/23/14614.short describes a positive correlation with differentiation state in airway epithelium.  The regulation by HIF-1 alpha in hypoxia seems of special importance: https://journals.physiology.org/doi/full/10.1152/ajplung.90415.2008 but it is complicated (both positive and negative).

ACE2 is also expressed at high levels in placenta during pregnancy - at least in rats. https://journals.physiology.org/doi/full/10.1152/ajpregu.90592.2008

Last but not least, pharmacologic data is reviewed at https://link.springer.com/content/pdf/10.1007/s11906-008-0076-0.pdf which describes up-regulation of ACE2 by angiotensin II receptor blockers, ACE blockers, and mineralocorticoid receptor blockers.  This includes the common drugs lisinopril and losartan.  (see also https://onlinelibrary.wiley.com/doi/full/10.1111/jcmm.12573 ) Unfortunately the paper did not report substances inhibiting ACE2 expression.  But https://journals.physiology.org/doi/full/10.1152/ajpheart.00239.2008 reported that high glucose (!) or PKC inhibitors could reduce ACE2 expression.  (but the high glucose was causing kidney injury, which as described above could mean more ACE2...)  The anti-diabetes drug liraglutide increased ACE2: https://academic.oup.com/endo/article/156/10/3559/2422879  To top it all off?  SARS itself decreases ACE2 expression, and this might be part of the process injuring the lungs: https://www.nature.com/articles/nm1267

This is by no means a complete survey, and there is much I don't understand.  The relationship between ACE2 biology and the emerging COVID-19 risk groups seems apparent - as is the urgent need for research to determine which manipulations to ACE2 expression have positive versus negative effects on the prognosis of that disease.

Update: a NEJM podcast today described this biology as 'complicated' link.  It is clearly of interest, but still under investigation.  For example, losartan is presently the subject of two clinical studies news, presumably these ClinicalTrials

Over-expression of ACE2 in case of ACE inhibition has been found: Carlos M Ferrario et al.,  Effect of angiotensin-converting enzyme inhibition and angiotensin II receptor blockers on cardiac angiotensin-converting enzyme 2, https://pubmed.ncbi.nlm.nih.gov/15897343/
These findings seem to be confirmed by findings that vice versa,  in the opposite situation  of high levels of AngiotensinII  downregulation of ACE2 occurs:
Deshotels MR, Xia H, Sriramula S, Lazartigues E, Filipeanu CM: Angiotensin-II mediates angiotensin converting enzyme type 2 internalization and degradation through an Angiotensin-II type I receptor-dependent mechanism. Hypertension 2014; 64: 1368–75 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4231883/
Two studies, however,  apparently did not find any down- or upregulation, which is in line with the reference you cited:

Ramchand J, Patel SK,  et al., Elevated plasma angiotensin converting enzyme 2 activity is an independent predictor of major adverse cardiac events in patients with obstructive coronary artery disease. Plos One 2018; 13: e0198144
Walters TE, Kalman JM, et al., Angiotensin converting enzyme 2 activity and human atrial fibrillation (...) Europace 2017; 19 (8): 1280–7

As your question seems to be unsettled here is my individual opinion:
The feedback circle you suggest makes sense as a mechanism of  upregulation (more product leads to more production). Why not have more input if output can be made and has been generated in larger and larger amounts? However, there also is "demand or no demand" down the cascade. A large amount of product that accumulates  thus may signal a lack of its being needed - I'd cast my vote for down-regulation of the expression of input receptors, as I'd vote for "we have enough". So contrary to your answering your question I'd suggest a high amount of product Angotensin (1-7) might cause a down-, not upregulation of ACE2.
Over-expression of receptors, to my knowledge, explains drug addiction and getting used to medication.
If in surplus of ligand hormone (in that case Angiotensin II) all receptors are "filled", it makes sense to  broaden the basis and up regulate expression of ACE2. Thus,   a block of ACE (not ACE2!) by ace-inhibitors would not lead to overexpression which seems coherent with the results of  the study on blood pressure medication you cited.
Interestingly, there is an alternative pathway of ligand transformation, and an alternative product of ACE2, it's Angiotensin (1-9). It think it is a possibility that those ACE2 cells do  over-express that are engaged in the modification of AT 1-9, not AT II, as ACE-inhibitors ("beta blockers" in German) do not address or inhibit renin production which should remain elevated. Renin becomes Angiotensin I, the alternative ligand of ACE2. However, downward that alternativ pathway, it's ACE again that transforms, and its being inhibited dampens "demand".


Lifespan of helper T cell CD4+ cells or helper T cells are produced in Thymus. How long these cells live? For example, RBC live for 3-4 months.

I will respond with a "story-like" approach. You may already know some info but I want to be sure I can help you fully understand!

Unlike RBC, you are born with all the CD4+ (or Th, as I refer to them) you will ever need in your lifetime in the primary organs of the immune system -- they are already specialized and ready to be used, and this has taken place in the thymus. On the other hand, RBC get renewed through erythropoiesis every ~120 days.

In utero, the thymus and bone marrow (primary organs) now supply secondary organs (lymph nodes, the spleen, the MALT) with the various cells they’ve made (B&T). However, only 5% leave the thymus, as 95% are recognized as "anti-self" and are killed. So this would be the first "killing" of Th cells. B cells live in the peripheral layer, while T cells live in the deep lymphoid tissue and the lymphoid dullet.

The dendritic cell will "wander" into the lymph node, carrying the fragment of antigen presentation on the MHC class 2 molecule-Dendritic cell resides between the B cell area and the T cell area. Now, the first specific thing occurs in the immune response, when the T cell receptor attaches to the antigen and tells cell says to make antibodies.

Now -- as of here, we have a lot of Th (and B) cells doing nothing while the antibody is being produced. Some of the Th will be killed, while some will serve as "memory Th cells" so that the next time such an antigen is present in your body, the response will be quicker. At this point, it's hard to distinguish which Th cells are dividing, and which are dying. The average lifespan has been reported to be >17 years.
 Source: https://www.ncbi.nlm.nih.gov/pubmed/24492253

I hope I have been able to help.


NADP and NADPH in in vitro metabolisme test I did an in vitro metabolism test using chicken liver S9 as the source of the enzyme. I did two different of method experiment. one was using NADP and second was using NADPH as the co-factor. my compound was fipronil, and I expect it to be metabolised become Fipronil sulfone (through oxidation reaction). The results, when I use NADP, fipronil sulfone formed was very low concentration, but in contrast, when using NADPH, I got high amount of fipronil sulfone.
what is the different using NADP and NADPH in this experiment?
Thank you for sharing the informatio.
Kind regards

Alex

Are you sure your question is accurate?

NADP in solution does not exist... it can either be NADPH which is the reduced form (has gained an electron in the form of a H atom and now has the potential to give that electron to another molecule in the solution) or NADP+ which is the oxidised form (has lost an electron in the form of H atom and now has the potential to gain an electron from the solution).

In your experiment, Fiprinol to Fiprinol Sulfone is an oxidation reaction, so the enzyme catalyses the removal of an electron from Fipronol, and it does that with the help of NADP+, which is missing an electron itself and therefore takes it from Fiprinol (oxidises it) to give a high Fiprinol Sulfone yield.


Venom Denaturing with Heat My friend got stung by a stingray yesterday and the lifeguard quickly stuck her foot into hot water (she said the water burned slightly on contact) and remarkably, she was walking without pain in a hour. I have heard that rattlesnake's bites can be helped by applying heat to denature the proteins. I am assuming this is what happened here, please correct if wrong. Because I am often in areas where immediate help in cases of animal bites/stings is not available, this is important to me as a first response as I get the person to help.

What kinds of venom are susceptible to denaturing by heat? How do I know which the previous categories a given venom falls into?
Is there a rough temperature I should aim for to denature the venom?
How likely is it that I would end up doing more harm by applying heat out of ignorance than doing nothing till I get to help (could be a day or more depending on the location)?

Regarding snake venoms, they tested 28 snake venoms at 100'C: 19/28 of the venoms were still very dangerous after 5 minutes at 100'C.

"Heating all venoms led to the denaturation and loss of some proteins; however, most of the venoms retained a significant number of proteins. Seventeen venoms contained more than seven proteins after heating, whereas five venoms contained only one to three proteins. All but nine of the heated venoms had substantial hemorrhagic activity, and Agkistrodon piscivorus piscivorus venom had very high activity, almost four times that of the second most hemorrhagic venom from Crotalus viridis lutosus."

There is a good chance that land animals have higher heat tolerance spiders and snakes can experience a lot higher heat than marine organisms.

study of marine venoms and hot water says:
Sting ray venom is especially fast to denaturize in heat, and most fish spine venoms are. HWI hot wat immersion is recommended for fish spine stings by some organizations. They did tests to find that box jellyfish, sting rays and other sea creatures stings react significantly to HWI.

They tested that 122/138 marine envenomations were improved by HWI from a variety of surveys.

there are 50,000 marine stings a year from 2000 species and
about 5 million snake bites, 2mn envonomings and 20-125,000 deaths by snakes every year from 400 species out of 3000 species of snakes which are dangerous to humans.

Dangerous snake and spider bites are generally treated in hospital, and the only wise thing to do is not to not make your blood go around your body very fast by being active after a bite, stay calm and alert.

Hot water immersion is the best treatment for stings from marine fish, as the above paper says.

However, I  do not see that this paper claims the fish venoms denaturize in heat.
The above mentioned paper states that immersion of the stung part of the body in hot water alleviates the pain, swelling and other symptoms. It does not prove or offer the mechanism of this action.

That being said, venoms comprised of proteins should be more susceptible to denaturation.  The venom of Trachinus draco, dracotoxin has been characterized and it is a single polypeptide. It is also proven that it is sensitive to heat.

But, there is not much research done in fish venoms and not everything is so clear. For instance, from my own experience, I know that Trachinus Draco sting inflicts pain, that is not due to tissue damage alone, but due to some biological mechanism. It is said that this pain can grow so strong, that people far from the coast would sometimes amputate their fingers.

This pain quickly dissapears after immersion in hot water. But, all the research done on the Trachinus draco toxin so far says that this pain is not caused by the dracotoxin itself, but by some other, smaller molecule, that can be dialyzed. Paper from 1962. says it is due to  serotonin, but it remains an open question, particularly because all venom extractions so far were made by dissecting tissue around the venom glands, so it could contain parts not usually injected by the fish.


Can we change the direction of a neurological signal? My question is can we change the direction of a neurological signal? When a neurological signal is generated it goes to the brain. Along the way it passes synapses. Can we make it change it's pathway to go through another neurone instead of the neurone it was going to ?

"Neurological signal", or as I would put it, action potential, or activity propagation can be modeled as current in an electrical circuit. Trick is that such a circuit contains a bunch of highly regulated and non-linear and non-static elements. Imaging bunch of potentiometers (variable resistances) in your circuit. And all of them behave depending on something else in the system. So certainly currents will go somewhere, but level of control and complexity is phenomenal.

An example that should let you appreciate possibility of rerouting is simple Pavlovian conditioning. Neutral stimulus (bell) that has no evident connection to stomach, after conditioning elicits response there. Even though circuitry is very complicated and signal propagation is hard to investigate, this is an evidence that changing path of signals is very possible in some way. (Of course, conditioning require changes in higher-than-stomach systems, some intermediate levels).

On more practical note, we can readout neuronal activity in region A (of brain, muscle or else) and rely it via electrical stimulation somewhere in brain or muscle or gland. Both parts of this are available technology. As of drugs, some people report "seeing" sounds while intoxicated, this might be an example of such temporary effects.


Why do we have nerves in our teeth? Toothache is a useful signal to us as we can visit the dentist who can try to fix any problems with our teeth. But what is the natural biological role of toothache? Does toothache make animals take action that helps them to deal with their dental problem?

Because your teeth evolved as a sensory organ.
The material teeth are made of evolved first in placoderms, it existed to sense the electrical current in the water around it, so it has to form around a nerve. in modern animals the nerve mostly functions in sensing stress and thermal stress on the tooth.
And because mammals are weird.
Teeth did not evolve to be permanent, they evolved to be lost and replaced, that is what everything that is not a mammal does. So having a nerve was not a big disadvantage (in say, reptiles) since that nerve would eventually wither and die as the tooth was lost. toothaches were not permanent they were a temporary irritation, and served do dissuade any behavior that caused them, like trying to eat food that was too hard, it was little different than the pain of thorn telling you not to grab sharp things.
Mammals are unique in retaining their teeth throughout their life so now a system shaped by evolution to be temporarily has been dragooned into something permanent. So now what would be a temporary irritation becomes a permanent thing when the tooth is damaged in mammals. Worse permanent teeth means things like stress on the teeth is even more important since you are stuck with damaged teeth so mammals actually make the nerves bigger. The addition risk of a toothache is not an issue because mammals are stuck with that risk anyway because they retain the tooth. The earliest mammals did not have long lifespan so the risk of a debilitating toothache was minimal, however we their descendants live for decades, so a structure evolved to last a year or two now has to survive for decades and it just fails sometimes. Evolution can only change what it has it cannot throw out a problematic system and start over from scratch, so it often gets stuck with such haphard thrown together solutions (kluges) And we unfortunately have to pay the price in this case

I would guess that humans and "smarter" animals (animals with strong cognition, culture learning etc.) figured out that some kind of oral hygiene and diet helps against toothache. However, it turns out that apparently animals don't get tooth decay and don't need special oral hygiene.

In any case, nerves in teeth cause pain when a tooth breaks. This allows animals to develop an avoidance response in the future: "This kind of nut/bone/bark/root/seed/whatever may seem tasty, but chewing it last time hurt for a long time. Avoid it." It might even prevent any broken teeth in the first place if chewing starts to hurt. As @BryanKrause wrote in the comments, it serves the same purpose as pain anywhere else.


Is once per day the optimal sleep pattern for all mammals? If a typical human body clock is 8 hours sleep, 16 hours awake, interested to know if any mammals have:

a 12 hour body clock (4 hours sleep, 8 hours awake)
a 6 hour body clock (2 hours sleep, 4 hours awake)

And very interested to know if any mammals' sleep patterns are on an "as-needed" basis - i.e. simply sleeping whenever tired, without ever establishing any particular pattern over the days/weeks

So as we know that every mammal needs atleast some amount of sleep or a resting period to perform cognitive functions through out the their day, this however can vary drastically based on the mammal's habits, such as if they are herbivores or carnivores, their place in the food chain (if they are a predator or prey), their habitat, their body size etc.
Starting with humans (to set a point of reference), we ideally need 7-8 hours of sleep in a day. Getting less or more sleep than this ideal can have a lot of different consequences (ranging from feeling tired and foggy to heart conditions and even death). A study performed by a group of researchers to find out the ideal sleep duration in humans showed that just after 14 days the people getting 8 hrs of sleep showed average cognition and a healthy mind, those getting 6 hrs of sleep per day for 14 days showed a similar reaction time to a person with blood alcohol level of 0.1% (which is considered legally drunk in most places), and the group getting 4 hrs of sleep per day for 14 days were tending to fall asleep while performing basic cognitive tasks. This show exactly how important sleep actually is.
Now moving on to some other mammals.
A very commonly discussed example is that of giraffes. Giraffes generally exhibit a cycle of just 2 hrs of sleep per day, and some days they just tend to not sleep at all. A lot of factors contribute to their sleeping habits. Firstly since they are herbivores, and primarily feed on leaves, they need to eat a lot of leaves to get enough energy for their body, having a large body also contributes to this. So, they tend spend about 75% of their day just eating. Other than this since giraffes are prey and a good source of food for lions, they need to stay awake and alert at all times. Sometimes they will take little 10 min long powernaps (this is when they are the most vulnerable, so they don't do it often).
Carnivores however (like lions) sleep a lot more, due to their diets (just like us they feel sleepy after eating) and also since they are minimal risk of being attacked as they are on top of the food chain.
Next lets talk about some sea mammals, they have a hard time trying to snooze because of them being underwater.
Dolphins have very interesting sleep habits as they have to actively come to the surface to breath. Dolphins practice something called "unihemispheric slow-wave sleep", this basically means that they only rest one hemisphere(or side) of their brain at a time(so that they can be awake and asleep at the same time), this is what uni(one) hemispheric(side) means. Slow-wave sleep refers to the deepest phase of sleep, meaning when the one hemisphere is sleeping it is out like a lightbulb. This way dolphins tend to sleep a lot, they have sleep cycle of about 8 hours of sleep a day (resting each hemisphere for 2 hrs at a time). So the dolphins you saw at sea world last year could have been half asleep (literally).
Some birds also practice this uni hemispheric sleep.
I can't think of any animals that sleep "as needed" because activities like sleep and wake are rhythmic and control various hormones and metabolic reactions of the body, this is primarily why we have sleep patterns so that other activities in the body can be done in a habitual manner. This is maintained by our "biological clock", which is the term used to define the natural sleep-wake cycle in animals. The biological clock is regulated by a hormone known as  "melatonin".
So yeah, these were some examples I remembered off the top of my head. I have provided some links to why sleep is important, ideal sleep habits in humans and other mammals and some other stuff for further reading.
Hope this answer helped you understand sleep better.
Sleep: a good investment in health and safety - https://pubmed.ncbi.nlm.nih.gov/19042703/
The Transcriptional Repressor DEC2 Regulates Sleep Length in Mammals - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2884988/
How Animals Sleep - https://www.sleepfoundation.org/animals-and-sleep#:~:text=Giraffes%20need%20less%20sleep%20than,of%2030%20minutes%20per%20day.
Melatonin: what you need to know - https://www.nccih.nih.gov/health/melatonin-what-you-need-to-know
This is an animated video series explaining sleep in different animals (highly recommend watching this):
Part 1 - https://www.youtube.com/watch?v=HA1EPRbMMQU
Part 2 - https://www.youtube.com/watch?v=EJzUKsJ-uhA
Part 3 - https://www.youtube.com/watch?v=S4uX2KeEifM
Rare Genetic Mutation Lets Some People Function with Less Sleep (this might also interest you) - https://www.scientificamerican.com/article/genetic-mutation-sleep-less/

The circadian is already complex. No need to further complicate it.
Melatonin and light exposure regulate the day night cycle. Because night occurs once per day, by definition, this is how it is regulated. Humans in artifical environments may adapt a different schedule but in natural sunlight it is the simplest regulatory pattern.
There are other patterns that are the opposite of this and those are anti predator adaptations.


can magnesium bicarbonate be absorbed in the mouth? Can Magnesium Bicarbonate be absorbed in the mouth?"
  Magnesium Bicarbonate occurs naturally in some mineral waters.

Technically, the human mouth do not absorbed anything. The human mouth is just a first line of defense mechanism against external microbial (In terms of saliva). If in terms of physical aspect, it just helps you to reduce food size and shape it for consumption.

Real absorption do not happen in the stomach neither. Stomach is where acids are used to break down your food and subject to higher lethal effect to kill microbial. The absorption only begins in the small and large intestine. (This is why drug delivery is such a hot topic in research labs).

To answer your question, yes. We need magnesium to survive and so we do absorb magnesium. In fact we can't live without magnesium, we need it for certain vital functions for our body to be normal. (Only in small magnesium amount, we don't need a lot of it).

As for bicarbonate, our body do not need it. In small amount, it is not toxic to our human body but in high volume, this would be a serious issue. When we breath, on cellular level, gas exchange occurs. Oxygen is supplied into our healthy cells while carbon dioxide is removed from our cells into our blood.

This is where it gets tricky, we do not store carbon dioxide in the form of gas when removing it via breathing out. We actually store carbon dioxide in the form of Bicarbonate in the plasma of our blood (Do note that its plasma, not RBC). When it is transported to our lung, this bicarbonate will be converted to CO2 and removed as we breath out. Hence, we do not absorb bicarbonate unless it reacted with some other elements or salt to produce some byproduct that we could use.

I hope you find this useful.

Regards

Price


Can the Quarternary Extinction event be linked to the spread of mankind around the world? Evidence is presented in a variety of media by Paul S. Martin as his 'Overkill hypothesis', particularly in Twilight of the Mammoths.

The internet describes this idea as 'controversial.' Other than the works of Paul Martin, what evidence has been presented supporting this hypothesis?

Only in islands can this hypothesis be supported.  But islands are NOT continents, and that raises problems with the hypothesis.  The most inconspicuous of which is timing.

In Australia, the gap between man setting foot on Australia and the extinction of Australia's megafauna was 17,000 years. Too long.

Man left Africa and set foot in Eurasia more or less than 50,000 years ago, yet the extinction of Eurasia's megafauna happened 10,000 years ago. Too long.

The oldest discovered American, "Eve", was discovered in a cave in Mexico's Yucatan Peninsula and dated to be 13,500 years old, 500 years older than the supposed time that man crossed Beringia. This could imply that man crossed Beringia at a far earlier date, yet the dating of the extinction of America's megafauna coincided with that in Eurasia. Too long.

There's also into consideration the Younger Dryas climate chaos phenomenon, which did coincide with the extinction of the 30 genera of Pleistocene megafauna, a handful of microfauna and plants, not to mention the Clovis culture itself.

If man was the cause of the extinction event, the gap between man setting foot in new lands and the megafaunal extinction would've been a few generations, not a few millennia.