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Calcium levels and nerve hyperexcitation
Why does lower blood calcium levels (or lower calcium levels in ECF) cause nervous hyperexcitaton? Why does it cause over stimulation of nerves and muscles and spasmic contractions of muscles?
This is why undersecretion of parathormone causes parathyroid tetany.
I am aware of the role of calcium in opening the synaptic vesicles for transmission of impulses and the role of calcium in muscle contraction but fail to understand how that might hep me understand the overexcitation of nerves and spasmic contraction of muscles. It actually seems that higher calcium in ECF might cause over stimulation and spasms of muscles due to sustained contraction.

I read up on the said article, and yes, it does make sense.
I however don't understand how a low ECF value of calcium would cause hyperpolarisation. Technically, for that diffusion to happen, the ECF Ca has to drop below the ICF Ca, which is extremely low.
Is there a disproptionate decrease in Ca levels, causing the ECF to drop way below the ICF level?
Also let's assume that it's not the membrane permeability to Ca that's causing the stimuli. Would a reduced ECF Ca level cause a decreased threshold level of AP in case of application of an external stimulus?
In which case, for tetanus to occur,

Welcome to Biology SE. You have written this in an area for answers, so it will be deleted by the moderators. Have a run through the tour https://biology.stackexchange.com/tour to see how the site works, as its not a forum.

This does not provide an answer to the question. Once you have sufficient reputation you will be able to comment on any post; instead, provide answers that don't require clarification from the asker. - From Review

From Uptodate on Clinical Manifestations of Hypocalcemia:

Acute hypocalcemia directly increases peripheral neuromuscular irritability [ 1 ]. As measured electromyographically, tetany consists of repetitive high-frequency discharges after a single stimulus. Hyperexcitability of peripheral neurons is probably the most important pathophysiologic effect of hypocalcemia, but hyperexcitability occurs at all levels of the nervous system, including motor end-plates, the spinal reflexes, and the central nervous system.

Guyton and Hall Textbook of Physiology:

The concentration of
  calcium ions in the extracellular fluid also has a profound
  effect on the voltage level at which the sodium
  channels become activated. When there is a deficit of
  calcium ions, the sodium channels become activated
  (opened) by very little increase of the membrane potential
  from its normal, very negative level. Therefore, the
  nerve fiber becomes highly excitable, sometimes discharging
  repetitively without provocation rather than
  remaining in the resting state. In fact, the calcium ion
  concentration needs to fall only 50 per cent below
  normal before spontaneous discharge occurs in some
  peripheral nerves, often causing muscle “tetany.”This is
  sometimes lethal because of tetanic contraction of the
  respiratory muscles.
The probable way in which calcium ions affect the
  sodium channels is as follows:These ions appear to bind
  to the exterior surfaces of the sodium channel protein
  molecule. The positive charges of these calcium ions
  in turn alter the electrical state of the channel protein
  itself, in this way altering the voltage level required to
  open the sodium gate.

It is a question of transmembrane potential. Ca++ being a cation, means that if you decrease the amount of ionized calcium in the extra cellular fluid, it conceptually is nearly equivalent to having a more positively charged intracellular fluid. This in turn means that the cell will be closer to its threshold potential for depolarization, therefore accounting for its hyper excitability.
What you should keep in mind, is that when we say something as: "this cell has a transmembrane potential of -70 mV", we always define it relatively to the extra cellular fluid.
edit: I am leaving this incorrect answer because of the interesting comments below.

Just read this answer because the question got bumped...this answer is very wrong, and exhibits a common misconception about what sets the membrane potential. Reducing extracellular calcium concentrations, if this had no influences on other channels, would have essentially no change on resting potential, because resting permeability to calcium is very low. Even if there was some permeability to calcium, reducing extracellular calcium concentrations would hyperpolarize, rather than depolarize, because calcium is low in cells.

@BryanKrause I do not understand why would hyperpolarization occur rather than depolarization. Could you please explain? I understand the membrane permeability problem, but then what is your answer to the original question about hypocalcemia?

I'd say the mechanisms are still under study, though there is good experimental evidence for a couple mechanisms: OneFace's answer suggests one of these, particularly the effects on voltage gated sodium channels. Here is one recent paper that seems to identify one mechanism, and their introduction has several other useful citations. When I have time I will write up a full answer.

As far as your answer, the Goldman equation is crucial. Permeability to calcium is effectively zero at rest, so we normally ignore calcium, but say for a moment it isn't. Opening a calcium conductance shifts the membrane reversal potential towards the calcium reversal potential, which is typically very depolarized, maybe +100mV. If we reduce extracellular calcium, the calcium reversal potential drops, though you have to reduce it a LOT to see a big effect, since the intracellular concentration is so low.

Also, no charges have to move to change the equilibrium potential: you could run the sodium/potassium pump all day long and if there is no permeability to sodium or potassium, there is no change in the membrane potential. It isn't meaningful ever to just "add positive charges" - they will always come with some other negative species, it's just that that other negative ion might not matter if there is no permeability.

You can also play around with this GHK calculator - although only Na+, K+, and Cl- ions are available, changes in external sodium concentration will give you at least the same direction of effect as changes in external calcium concentration, because both are positive ions.


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Are progenies factually half-clones of the parents?
Given that a "clone" (if anything, in the context of human cloning) is taken to be, as far as I have understood, a specimen possessing the same genome as his "father/mother", aren't all "non-cloned" organisms born out of inter-individual, heterosexual reproduction (i.e. "standard" sons and daughters), effectively "half-clones", under that same definition?*
Are "normal" sons and daughters "half-clones", as a matter of fact?

A progeny is not a half clone of its parents.

Each cell expresses both maternal and paternal genes. There are no parts of the body or even a cell for that matter that is identical to one of the parents.
When haploid gametes form, chromosomes are randomly segregated. So the gamete receives either paternal and maternal chromosomes (grandparents of the progeny) randomly. This technically means that the gamete is not an exact half of the parent's genome.
During gameteogenesis (production of sperm/ovum), genetic recombination happens between nonsister chromatids of homologous chromosomes (meiotic crossover). This mechanism creates a small shuffle in the haploid genome that the gamete is carrying.

I see now that my question was pretty unimaginative in the first place. If sons and daughters were half-clones, then there'd be no differentiation between female and male offspring and siblings would all be the same. Thank you

@Giuliano Yes. Now you know what is the mechanism behind that difference.

@AMR thanks for the correction. I nonchalantly wrote sister chromatids instead of homologous chromosome.

source: Stack Exchange

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sort: votes


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What if there are no bacteria such as Streptococcus mutans
If someone removed all bacteria such Streptococcus mutans in her mouth by starving long time, or by some chemical method, would she never have such bacteria?
In my thought, because S.mutans only spread out through human teeth, and if there are some in the air, white blood cell might kill all from the air completely because they are very little.
Is this foolish hypothesis of mine possible?
Thanks for your answer in advance.

no kissing.  no licking.  no eating food touched by other people's mouths. (sharing an apple for instance.) seems unlikely...  also total removal is hard but that's another matter.

As shigeta touched on, there's no practical way to avoid cross-contamination from other humans. Assuming by magic you delete all your mouth bacteria, there are so many paths to re-inoculation you couldn't avoid it without living in extreme isolation.
A non-exhaustive list of all the ways you could get re-inoculated:

kissing
licking
aerosolized saliva from coughing/sneezing
eating food exposed to same
Touching something contaminated then brushing your teeth
Essentially putting anything another human has touched in your mouth

Other humans get saliva on things they touch and things they breathe on. You can't breathe or eat those things without cooking them. No fresh vegetables.
Your white blood cells or your immune system in general won't help, because S. mutans is already adapted to live in your saliva and there's not (to my knowledge) any adaptive immune system components active in your saliva.

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Is there a significant difference in sedentary calorie-burn between a thinker and non-thinker?
I've read that, on average, a sedentary female burns between 1,600 - 2,000 calories and a sedentary male burns between 2,000 and 2,500 calories. I've also read that the brain itself burns quite a few of these.
Let's say two people are exactly the same, and have the exact same (sedentary) lifestyle—except one of them often does intense mathematics. Is there a significant difference in calorie burn?
If so, how much is it?

Is there a significant difference in calorie burn?

No.
The brain, while only making up 2% of our body weight, accounts for ~20% of our energy use at rest. That's because the brain, being critical for survival, is a very high-maintenance organ. At rest, the membrane potentials of all neurons - firing or at "rest" - need to be controlled/maintained.
Of all the energy used by the brain, about 25% of it is needed for signal-independent function (protein synthesis, phospholipid turnover, etc.) Furthermore, there are two types of cells in the brain: neurons and glial cells. The glial cells (about 30%) use from 17 to 40% of the energy depending on whose estimates you use. The rest is needed (by neurons) for signal-related processes - maintaining/restoring cell membrane potential, etc. - only a fraction of which is used for thinking.
The brain never rests - it is highly active even in sleep, with both excitatory and inhibitory activities needing energy. Higher mental functions (e.g. doing math problems) only shifts the areas of highest activity a little bit compared to all the activity that occurs without our awareness of it.
Finally, if we could measure glucose consumption of the entire brain while daydreaming vs. doing math, we might be able to answer that question, but the truth is, brain activity doesn't occur in isolation. Someone doing challenging math problems is using more energy in other areas of the body as well; respiration rate, heart rate, muscle tension, etc. varies with the stress of the challenge, so glucose levels alone can't be relied upon (in fact, stress would increase our body's production of glucose) to indicate energy expenditure.
The end result is that in isolation, rigorous mental activity (which can be maintained only for a relatively short duration without fatigue, so it occurs in bursts) expends very little of the total energy the brain uses.

A common view equates concentrated mental effort with mental work, and it is fashionable to attribute a high demand for mental effort to the process of problem solving in mathematics. Nevertheless, there appears to be no increased energy utilization by the brain during such processes. From resting levels, total cerebral blood flow and oxygen consumption remain unchanged during the exertion of the mental effort required to solve complex arithmetical problems.

Cerebral Metabolic Rate in Various Physiological States
Does Thinking Really Hard Burn More Calories?

+1, but to be nitpicky on the energy consumption - it's 20% when in rest. During physical exercise the percentage drops

@AliceD - good point!

@anongoodnurse Excellent, excellent answer. Thank you.

Re the block quote, it's worth noting that locally, functional activity and metabolism are closely related, this is how fMRIs work (measuring blood flow as a proxy for activity).  Also, from the linked paper: "Regardless of the cause of the disorder, graded reductions in cerebral oxygen consumption are accompanied by parallel graded reductions in the degree of mental alertness, all the way to profound coma".

@augurar - I did not both those things as I was reading. My point is, or that which I was trying to get across, there is very little difference in energy expenditure overall between an awake and thinking brain and one that is furiously doing math problems. Of course a different region of the brain "lights up" on fMRI's depending on the activity (say, vocabulary tests vs. math tests), but the point remains: the question was do we burn more calories by strenuous mental activity? The answer is still "no".

@anongoodnurse Agreed, I wasn't disputing your answer, just remarking on it.

If anxiety is considered thinking then I guess there is a difference :P

@WYSIWYG - that's a good point.


text:
why dead mouse doesn't bleed when we cut their skin?
When we are pricked by a needle, we bleed nevertheless it's so small wound.
But when we do mouse anatomy, it doesn't bleed even if we cut their whole abdominal skin.
Other student asked about that, professor didn't know exactly but just guessed that mouse skin has no blood vessel. But I think it's wrong. that makes no sense.
As my guessing it's because mouse is dead when we do anatomy so there is no enough blood pressure.
Mouse have to bleed like ourselve. is this wrong?

You are talking about dead mice?

'because mouse is dead when we do anatomy '. Yes he is.

By the way, Blood-pressure can be negative (smaller that atmospheric) dependent on where you measure it (due to Bernoulli principle).

So, you should rather emphasize on blood flow, not blood-pressure.

the fact the mouse is dead is important dead humans don't bleed either. blood starts to coagulate after only a few hours.

@John: There are two stages to this.  Live animals, whether mice or men, bleed because the blood is under pressure.  (Considerable pressure, if you've ever had to deal with an arterial wound.)  After death, there can be some blood drainage from wounds, under the influence of gravity &c.  That stops when the blood coagulates.  See e.g. "livor mortis".

From personal experience, extracting organs/tissues of over 1000 mice I can give some hints:
Mice blood coagulates quite fast after death. If you need to extract blood, you are under time-pressure and many scientists extract the blood directly after death from the heart using a syringe. If you are not fast, you miss the chance of drawing blood as this can't be done after coagulation. Others cut up the thorax (post mortem) and then directly draw blood with a syringe. I personally never tried this technique but I spectated that mice bleed a bit, directly after death, when opening the thorax, however it's not much.
After drawing all blood from the heart, mice don't bleed, no matter where you cut, potentially because of low blood content remaining. (Un-?) Fortunately, I never had to cut mice that were alive.. so I cannot tell you what would happen if they were alive.
Edit: Also, in theory, the smaller an animal is, the higher becomes the diffusion/volume ratio and surface-tension/volume ratio. This means smaller animals need less active blood circulation and and their blood vessels might have a small diameter, so that most blood would be kept inside by surface tension if these vessels were cut.
Edit due to comment:
The extractable blood from mice is around 1.5 ml, and I have seen opening of the thorax within seconds post mortem with minor bleeding. Afterwards, the majority of blood (1.5 ml) was extracted directly from heart with a syringe. As this was post motrem, I cannot exclude the possibility that coagulation of blood in small peripheral vesicles already affected the observation or how heart beating would affect it. I cannot say what would happen in live mice and I am happy that I don't have this knowledge.

Live mice certainly do bleed, though their total blood volume is only on the order of 2mL.

I know it's around 1.5 ml, and I have seen opening of the thorax within seconds post mortem with minor bleeding. Afterwards, the majority of blood (1.5 ml) was extracted directly from heart with a syringe.

thank you! this did help!

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Where do the bones of dead animals go?
I've spent quite a bit of time in the wild, but I've seen little to no bones lying on the ground.
Large bones such as skulls, spines, horns, hooves are not eaten by any other animals, and even microorganisms. thanks to which they can persist for decades on the ground surface. Especially in hot and dry climates, steppe and desert regions, as well as in the arctic.
Therefore, it should be expected that a large number of bones will be found on the surface of the soil, also underground in the topsoil.
But nothing like this actually happens.
Where do the bones of dead animals go?

Can't speak for all bones everywhere, but bones get eaten quite often. When I lived in the woods, I could see a carcass disappear bit by bit in a matter of days - far too quickly for disintegration - leaving only the hardest bones bare on the ground.

Same here, weeks later the remains would be visible only as glints of ivory through the overgrowth of ivy. After an autumn's leaf-fall, nothing the next year. Still there if you dig. I found a pig's lower jawbone, teeth and all thrown out of a rabit's burrow - decades old, not seen until the rabit found it in the way of its home-building efforts.

Does this answer your question? Why don't we find animal corpses and skeletons all throughout the woods?

Even a superficial Google search will tell you by the title of the hits you get that bones are eaten, e.g. my top hit.
Osteophagy simply means bone eating. I'm not sure why it applies to herbivores in particular; maybe because it seems to be strange behavior in an herbivore, whereas it's expected in a carnivore.
Phosphate is crucial to life, but isn't abundant in 'edible nature' (plants, etc.). It is abundant in bone, however, and because it is crucial to growth and energy production, animals eat bones however they can. Some animals, e.g. those without teeth, will swallow small bones whole. Carnivores and capable omnivores will crush susceptible bones by chewing on them; herbivores will just grind away at them and consume the bits they can generate.
From Wikipedia, a cow chewing on a bone.

How about a squirrel?

Or a deer eating human bones:

This answer could be longer, but why go on? The answer is obvious.
Osteophagia: How Wild Animals Use Supplements

The O.hypothesis has the right to be, but I do not think that it is able to explain everything completely.
Let's start with O. is noted in a limited number of animal species, not in all.
It also follows from the context of the article that this is more a deviation variant due to adverse conditions than the norm.
An example would be  domestic animals that get along just fine without eating bones, because the food usually contains sufficient amounts of phosphate.
( more detail in  the next comment)

Another example, rabbits can eat the corpses of relatives.
But this happens only in conditions of critical hunger. Under normal circumstances, they never behave like this.
The situation is the same among people.
Herbivores cannot eat fresh bones, their digestive system is adapted for this.
We are clearly talking about heavily decomposed bones that have already lain for several years.
There are a few more interesting facts about this but I'm going to describe them in the following questions on the site.

@VladimirOrlov - It's not aberrant behavior, and it's not limited. True, if a diet is adequate in phosphorus, osteophagy decreases. But in nature, diets are not adequate in phosphorus. Carnivores prefer fresh bone, herbivores dried bone. Both want to eat bone. Mice and rats eat bone. One buzzard's diet is 70-90% bone. Mammal bite marks have been found on dinosaur bones. Something is not true because one prefers it to the truth. The "truth" is what is supported by the evidence. There is an adult rabbit corpse on my lawn. I love to observe nature, so have not removed it. ...

...I found it because a buzzard was on my lawn. Three days ago, it was freshly dead and didn't smell so good. Today it has been reduced to fur and a few vertebral bones and a mandible. That is evidence to me that the bones do not just get covered up. I have only seen the buzzard at it, but am not watching it 24 hours/day. I suspect creatures have been eating it bit by bit.

the rabbit is a fairly small animal, so it is not so surprising that it was eaten.
But there are much bigger animals and their bones.
in Tibet there are customs of sky burial, when the corpses are fed to the vultures.
but there the bones are specially crushed and even after that some of them remain lying on the ground.

@VladimirOrlov - Your point being?

this only happens to a small minority of bone. The first thing google kicks back is rarely the whole story.

@anongoodnurse I haven't any acceptable hypothesis. There's no reasonable explanation for this facts.

What about arm and leg bones, hips and skull, which only a hyena can chew on? And regions with high calcium content, like clay and limestone soils? Only about 50% of regions have calcium depleted water, soil and vegetation,  https://www.researchgate.net/figure/A-Map-of-calcium-hardness-as-calcium-carbonate-for-North-America-Note-that-calcium_fig2_236942539

@bandybabboon - Calcium isn't the problem; phosphorus is. Long bones get eaten (what bone do you think that bovine is eating?) The hardest bones break down eventually or not. The majority get eaten. And it's not only hyenas that are great at breaking bones.

@anongoodnurse, where i live there are just foxes and pigs, and only pigs can eat big bones, a horse femur is giant.

@bandybabboon - Which is it? First you said only hyenas could eat long bones, now you include pigs. What is the bull above eating, a dinosaur digit? Why don't you provide sources for your answer, instead of arguing with mine?

@anongoodnurse you're answer is great, The question specifically refers to large bones such as skulls, spines, horns, so I'm being logical. Skulls are huge bones and don't just fit in the leverage part of the jaw towards the molars, and horse femurs are pretty big too. I find a lot of skulls compared to other types of bones in the forests, so I think that osteophagy concerns stick-like bones. https://www.google.com/search?q=equus+femur&tbm=isch

@bandybabboon - Fair enough; I may have overread the question. I agree that the cranium is the most likely bone one will find in areas where animals live and die. Some vertebrae, but many get broken and eaten. I disagree with long bones; once in a while I'll  find a femoral head with the cartilage chewed off. For many years I had 28 acres, mostly wooded, with all kinds of carnivores and an abundance of deer. Yet on my walks through the woods, I never found long bones, vertebral bodies or antlers. I often found fur and feathers.

they rot, get eaten, or get weathered away. Under extremely rare circumstances they fossilize.
What you are talking about is called bone taphonomy.

You can do a simple experiment yourself, put hooves or bones partially buried in dirt in your yard and check on them from time to time, depending on where oyu live what happens will vary quite a lot. Paleontologist and forensic scientists have studied this a lot to understand fossil and human remains respectively.
What happens to them

Normal erosion processes and soft tissue decomposition break the bone in to smaller pieces. The same thing that breaks down rocks breakdown bone just faster. Physical and chemical weather all work on bone. Bone is soft and permeable as rock goes so it weathers very quickly.

Bacteria, insects, fungi, plant roots, or other organisms break them down and eat them. You can prevent this by drying the bone out and keeping it away from soil, (soils keeps the bone moist and makes it easy for those things to reach the bone) Bone like any organic material rots, oxygen and water make it happen faster and bigger organisms can eat them faster.

You can see the same thing with any organic material which is why we dry meat and fruit to preserve them. Also why we cover organic materials like leather or wood in oils to keep them dry. or cover them in poisonous chemicals just like you can do with bone, it slows down their decomposition. in really dry places or conditions with no oxygen bone can take very long to decay. A cow skull defleshed and nailed to a barn in the desert will take a very long time to decay centuries or longer, a bone left on the jungle floor wet and covered in dirt and leaf litter will be gone in months, assuming you can keep things from eating it, (bone is a high demand resource in forests where phosphorous is in high demand).
Different materials decompose at different rates. Under absolutely perfect conditions the bone does not decay completely, creating a fossil. I personally have pulled unfossilized mammoth bones out of clay rich desert soil in Wyoming, the bone had all the structural strength of dry rotted wood, any handling caused bone to flake off, but it was still a complete mammoth leg bone, its decay had been severely slowed by dry, cold, anoxic conditions. We do find lots of buried bone in the right environments.
Soils is not static
If you put bone on top of soil it will not stay on top of the soil. soils turns over due to thermal, erosional, and biological forces. things get buried, see frost heaving and soil creep as examples. Soil is not static it is always on the move. Deserts in particular tend to be highly erosional, which is why we look for fossil in deserts,  new rock is constantly being exposed and destroyed.
Now deserts and cold regions do have much slower rates of decay which is why you can find remains that are decades or even centuries old in such places. Bones are found in bogs and permafrost for instance.  things like sunlight, temperature, abrasion, weather and such can all breakdown bone. Also you vastly overestimate how many animals there are in such places, even if all their bones did not decay they still would not make up a noticeable portion of the topsoil. in places where the animal remains are that common they do make up a significant portion of the soil we call those coral sand beaches, where mechanically broken up animal shells make up the majority of the soil.
Sources about bone decomposition and diagenesis
https://pubmed.ncbi.nlm.nih.gov/20646883/#:~:text=Abstract,or%20as%20long%20as%2030.
https://www.scientificamerican.com/article/dust-to-dust/
https://digitalcommons.unl.edu/cgi/viewcontent.cgi?article=1061&context=nebanthro
https://www.jstor.org/stable/2400259
https://www.sciencedirect.com/science/article/abs/pii/S003101821630164X
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8224596/
Sources about soil and erosion turnover
https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/soil-movement
https://www.sciencedirect.com/science/article/abs/pii/B9780123864734000014
Bonus
Great simplified of review of decomposition.

Your first link is about buried bones: "The burial of remains below the surface has been found to effectively shut out many of the most destructive decaying agents, such as the natural elements and insect and animal activity. the other links are irrelevant, the third being only about soil, and do not support your answer (or the comment you left under my post.) I actually did the experiment you suggested inadvertently by leaving a dead rabbit where it was found. Three days later, almost all of the bones were gone. Supervoracious topsoil, maybe?

@anongoodnurse I added a few other sources for all manner of bone decomposition and diagenesis. I also ogranized them a bit more. I have done the experiment thousands of times to study early stages of fossilization. I never said osteophagy does not occur just that it is only one small part of a large variety of things that break down bone.

Let's look at the decomposition of a corpse as a whole.

Fresh
Bloat
Active decay
Advanced decay
Dry state

You can skip to the dry state, which answers your question specifically.

A prerequisite to studying decomposition is knowing that decomposers break down organic material by secreting enzymes turning it into dark liquid form that's possible for them to absorb. Foul gases are produced in the process.
Also, it's best to think about decomposition as a bunch of processes caused by several agents happening and progressing at the same time.

When you hear fresh state, think of anything that ends with mortis:

Algor mortis (decrease of body temperature to ambient temperature)
Rigor mortis (temporary stiffness of muscles due to decreased ATP which is required to relax muscles until decay starts)
Livor mortis (pooling of blood at the site closest to the ground)

Bloat happens because gut flora starts breaking through the wall of the gut. The wall is normally protected by the epithelial cell layer which has a high rate of shedding and regeneration. Since regeneration stops, flora can now bypass into the underlying tissue and start feeding on the body from the inside which results in the formation of

Gas (has foul smell)
Liquid (dark purge fluid that leaks through orifices because of increased pressure from gases in the intestine)

Autolysis also starts where lysosomes containing lysozymes break up and release the hydrolytic enzymes which break down tissue so skin slippage may occur.

Liquifaction by decomposers continues causing darkening and loosening of the exterior.
Blowflies are attracted to the foul smells (even the smell of excrement) and thus, approach the corpse early and lay their eggs which hatch releasing maggots that feed on the corpse.
Several species of insects also start feeding on the corpse but that starts later.
Adipocere (corpse wax) may also form from decomposition of fat preventing further decomposition.

In advanced decay, most tissue has liquified and loosened.

What remains from the corpse is the dry or skeletonised state. Dry here indicates that all the liquid produced from the action of decomposers has been taken up and what remains is the hard tissue, bone or the skeleton.

If the skeleton becomes covered in soil, scavengers (animals) do not eat it and it breaks down in acidic soil over a long time period.
If the soil is neutral, it takes much longer time for this to take place.
If the soil is

dry, anoxic or slightly alkaline (unsuitable for decomposer activity)
salty (has minerals which can form long-lasting hard structures)

the bones may fossilize.

When you study archaeology, you dig and find everything becomes buried very fast through burrowing and overgrowth subsidence. You can find a lot of bones when you walk a minute away from the beaten track, and very rarely on paths, often gray and beige. Humans very often move nice skulls as trophies.
Skulls provide a microclimate for moss, ants, beetles, plants, low-wind zones and snags to collect leaves. Humans like to pick them up and move them, rodents gnaw them, the jaw tumbles away, bug and bird droppings, acids and humidity dissolve them, frost cracks the pores.
Plants compete for space and grow around bones and hide them. Bugs dig networks of burrows and make the soil cave in a bit, worms place middens on the sides, A hoof or a femur will be covered by wild grass in 3-5 years, a horse skull in 10-20 years.
In the arctic there aren't horses, cows, deer, only seashore megafauna. Bones get snowed over. Else they are subject to freeze-thaw weathering, water stays in the pores of the bones, freezes and expands every day, and erodes them.
In the forest, leaf fall and sticks accumulate 1-5cm every year, trees fall over, the soil is alive with fungus mycelia and bugs, It's also quite an acid environment. Bones would be expected to stay uncovered for less than 15-20 years.
In the desert, there aren't lots of big animals, and the bones can last a very long time there, we can find awesome cadavers in regions of low biological, geological and glacial activity.
Human transportation near paths
Scavenging
Animals hide away when they are ill
Gnawing
Moss
Freeze thaw
Geological activity
Subsidence
Glacial activity
Sand dunes
Trampling by other animals

I'm not sure what's going on with the last paragraph. Also, -1 for not mentioning osteophagy. If this answer were all there was to the fate of bones, we'd be buried in bones, which is clearly not the case.

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text:
What prevents neurones from touching at chemical synapses?
The synaptic clefts are really small, but the neurones which they are between do not touch even against forces like gravity.
What really prevents them from coming into direct contact at the synapse, and also what would happen if they did come into contact?

In which type of synapse? In electrical synapses they are in direct contact, in chemical synapses the basal lamina anchors them.

Thanks! I was referring to chemical synapses. I will try to find out more about the basal lamina.

I think there is nothing preventing neurons from touching each other but there is nothing also binding them together. Usually, cells have tight junctions that bind them tight to each other, the lack of which would assume a synapse-like cleft. Beware, the rest of the neuron is scaffolded by glia and the like. No references, just intuition and discussion - hence just a comment


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Can translation ever occur without transcription?
This question is aimed mainly towards viruses with ssRNA, is transcription required, for the +ve strand RNA? If so, why?

I thought I had commented on this, but apparently not. Please clarify what you mean by "is transcription required, for them?" What is "them"? The word "them" would seem to refer to viruses, but this alone makes no sense. Your title suggests you mean "the translation of their +ve-strand RNA". Please ammend, and I would suggest you delete the second part of your question because its premise would appear to be incorrect. "If so why?" would do.

I am assuming that the question is whether, in single-standed +ve RNA viruses, translation of plus-strand RNA can occur before transcription.
First, there are many different families of viruses, and there are bound to be counter-examples to whatever I say here. However, with that rider:

We generally refer to replication of RNA viruses by RNA-dependent RNA polymerase, rather than transcription. I am not aware of any RNA virus that has an RNA polymerase recognizing promotors and transcribing specific genes. These viruses tend to replicate in the cytoplasm and therefore do not have access to host RNA polymerase.
There has to be replication, and this tends to be conservative, rather than semi-conservative. By this I mean that when minus-strands are generated they act as templates for many plus-strands, which are needed for the virus particles.
In the case of picornaviruses, such as polio, translation can occur before replication. As is common with small RNA viruses, there is a single initiation site for translation — in the case of polio, a polyprotein is produced, which is subsequently cleaved into individual polypeptides. The diagram below is from the Wikipedia entry for poliovirus and is reproduced here under the Creative Commons license.

[Nidia H De Jesus (image and caption) - De Jesus NH (2007). "Epidemics to eradication: the modern history of poliomyelitis". Virol. J. 4: 70. DOI:10.1186/1743-422X-4-70. PMID 17623069.
The cellular life cycle of poliovirus. It is initiated by binding of a poliovirion to the cell surface macromolecule CD155, which functions as the receptor (1). Uncoating of the viral RNA is mediated by receptor-dependent destabilization of the virus capsid (2). Cleavage of the viral protein VPg is performed by a cellular phosphodiesterase, and translation of the viral RNA occurs by a cap-independent (IRES-mediated) mechanism (3). Proteolytic processing of the viral polyprotein yields mature structural and non-structural proteins (4). The positive-sense RNA serves as template for complementary negative-strand synthesis, thereby producing a double-stranded RNA (replicative form, RF) (5). Initiation of many positive strands from a single negative strand produces the partially single-stranded replicative intermediate (RI) (6). The newly synthesized positive-sense RNA molecules can serve as templates for translation (7) or associate with capsid precursors to undergo encapsidation and induce the maturation cleavage of VP0 (8), which ultimately generates progeny virions. Lysis of the infected cell results in release of infectious progeny virions (9).]


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Can species be paraphyletic?
I thought that according to cladistics, only monophyletic groups were valid as species or any other taxa. But extinct species, like say H Erectus must be paraphyletic, as the common ancestor of H Erectus is also the common ancestor of modern man. So if species are frequently paraphyletic, how can cladistics be tenable?
Edit. Also, I'm new to this forum. The people responding here, I'm assuming are actually biologists with a specific knowledge of cladistics, right? I'm a post-grad (philosophy of biology rather than biology per se) so I'm not really looking for links which explain what cladistics is, and certainly not wikipedia. I can access most journals if there is a paper on this subject. I can't find anyone in our dept who can give me a steer on this. I realise thhis is a slightly unorthodox research method, but I'm at a bit of a dead end here!

Right, thanks. But I don't see that the species concept is the issue here. I'm really questioning whether cladistics is coherent, given that it prioritises clades (which are by definition monophyletic) as being the only valid taxa. Now, as far as I understand, it doesn't really matter which species concept we use. Cladistics doesn't seem to rely on any once species concept (Hennig's Tokogenetic concept aside)but does absolutely insist on monophyly. The vast majority of species, though, over evolutionary history, are paraphyletic, right? Just want to check I'm not making some stupid error here.

For your example; I don't think it is obvious that H. erectus is paraphyletic. The question is if H. erectus is the direct ancestor of modern man (if so H. erectus would be paraphyletic), or if H. erectus and H. sapiens share a common ancestor (which would make them related, but none of them would have to be paraphyletic). Extinct species don't have to be paraphyletic, as you seem to claim. I'm not an expert in this specific case though (human systematics), and this is merely a conceptual point.

You say that "only monophyletic groups are valid as species"... That is according to a certain interpretation of evolution that is not necessarily mainstream, (you wouldn't be taught that definition of species in Oxford or Yale) and which idealizes cladistics into simple trees, which don't reflect reality of hybridizing species like orchids and hominids, where simple tree like branching has been proven to not exist. Inflexible definitions of phylogeny should be taken with a pinch of salt, because pollen and other reproductive systems cause many species to be flexible. It's unwise to state that definition of species without being well aware of the mainstream one: Ernst Mayr definition.
Strict interpretations of species lead to problems, because
Darwin wrote:
No one definition of species has satisfied all naturalists; yet every naturalist knows vaguely what he means when he speaks of a species. Generally the term includes the unknown element of a distinct act of creation.
If you check the Wiki page on species, they state 11 contrasted definitions of species which are not necessarily cross compatible.   https://en.wikipedia.org/wiki/Species#Standard_definition:_Mayr.27s_Biological_Species_Concept
The definition of species that i was taught had nothing to do with the parental mechanisms that shaped the species differentiation from other species, and that it is a practical concensus to effectively group animals methodically, which doesnt actually reflect natures unmethodical reality.
Seeing as humans interbred with neanderthal and denisovan species, and orchids interbreed very commonly, the following image refers to an idealized phylogenetic model which is not applicable to all reproductive systems, and it isn't applicable to humans.

I think it's pretty mainstream to say that species have to be monophyletic, but not all monophyletic groups have to be species. In fact, I would even argue that Mayr's species concept is pretty close to that notion as 'reproductively isolated groups' and a monophyletic species (taxon) are not that different (of course without hybridisation across cladistic barriers). Additionally, you should avoid using terms like 'creation', especially when assuming that most natural scientists include this as an 'unknown element' to their idea about species. -1

Thanks. But it seems, then, like the vast majority  of species are actually paraphyletic? Extamt species are monophyletic, and extinct species which are 'dead ends' as it were. But all other species are parphyletic. The species concept isn't the issue here.My qusetio

Sorry. Can't delete the previous comment which I posted by mistake....Yes. That's what I thought. It's just orthodoxy that species must be clades. And that higher taxa must also be clades. I'm pretty sure they would teach me that at Oxford.

Indeed, a research professor who has been very busily involved in naming new species (i.e. nematodes) and phylogeny would rave on and on about all the amazing funny facts about species diversity, like one researcher getting revenge on another researcher by calling a species "johnsonus sillius" and the russian classification system which has 8 times more species than us, and they go through all the reproductive intricacies that mean that clades, i.e. bear species, sometimes intertwine, whereas some species have very specialized reproductive organs with barbs and where clades are better defined.

In short i suggest that the rigorous phylogeny terminology that you quote is useful for genetic measurements and in depth phylogeny study. It's recommended to first learn at least 3-4 alternate definitions of species, and first do case studies of dozens of different speciation routes, physiologies, read about actual animals and surprises and conflicts in research based on certain evolution theories, to make it more of a fun topic that logic of branching terminology. By actually reading topical zoology and botany case studies, i think that someone gains a lot of useful background knowledge.

You have to understand that a fossil "species" is very different than the common usage. A species is not really a real thing. Paleontology (and other fields) accepts the vague nature of the classification of species. All life that has ever existed on earth is really one huge messy ring species on the long scale once time is included. phylogeny is a way of imposing a classification system that helps us understand life, any such classification will have arbitrary cut off points becasue WE use them to help understand relationships on the large scale. Species is one such arbitrary distinction, it is convenient and works on the large scale with living organisms just fine, but breaks down on the finer scale or once deep time is included.
For fossils you group by noticeable/measurable differences, while trying to make allowances for differences that should occur within a population (like sexual dimorphism). Paleontologists accept that a "species" is just an approximation, which is why the finer the scale of the cladistic analysis, you rely on individual specimens and not grouping them into a species. Ideally all cladistics would be done this way but it is completely impractical, in extant life becasue of huge population numbers in fossils becasue of incomplete specimens causing missing variables. On an analysis using any group as taxa, including species, it's fine if they are paraphyletic becasue they are only approximations.
You can find a more in depth exploration of  cladistics here enter link description here
And a general review of cladistics here enter link description here

Right. Which is why I'm asking, really. Hennig (and many others since,  such as Wiley and Lieberman, Baum and Smith, Ridley, Tudge, Ghiselen etc etc)  explicitly claim that Claude based species are the natural (as opposed to merely nominal) kinds of biology. So,  as a philosopher, it is of interest to me that this isn't really coherent,  and as a philosopher  of science it is of interest that this has occurred. It seems to me that it could work if we defined monophyletism synchronically, and allow groups which were at one point monophyletic, but as far as I know,  no one does this.

Ah I see a bit more of what your asking. You might want to change your question to reflect this. Part of the difference is how a clade is defined, in Paleontology the most common usage is: X plus Y and there most recent common ancestor and all of its descendants , becasue the assumption is you will never find a direct ancestor, or at least if you do you will never be able to demonstrate it.  species and clade are not interchangeable. and by their own definition all defined clade are monophyletic.

Species which are defined as a clade have to be monophyletic but  that way of defining a species are not commonly used. Mostly because while very accurate is is also largely useless in practice.

The boring but probably most correct answer is: it depends on the species concept that you accept.
Basic evolutionary theory predicts that paraphyletic species (as defined by a variety of concepts) should be generated under a wide range of processes.
The vast majority of species is described from gross morphological states ("morphospecies"). They can be wholly paraphyletic, as can species under nearly all concepts, except those that insist on monophyly (e.g. phylogenetic species concept of Cracraft 1989, deQueiroz and Donoghue 1990).
A problem to consider is one of the source of data. For example, a species can be monophyletic at a particular gene, but not at great many others. Broadly speaking, this is known as the "gene tree vs. species tree" problem.  A particular set of relationships can be recovered from analyses of a single genetic region, drawn from a wide statistical distribution of (for example) genealogies. Ideally we would have the genetic sequence within region(s) that cause(s) populations and species to be differentiated.
Depending on population size, after some amount of time (potentially very large), all genes are expected to be monophyletic in each descendant species, a condition that is then called "reciprocal monophyly."
Separately, you can take a look at https://en.wikipedia.org/wiki/Paraspecies for a straightforward treatment. As for your specific example, here is a great treatment of the subject: http://evolution.berkeley.edu/evolibrary/news/100501_xwoman

Can species be paraphyletic?

Yes, as you have explained in your post.

So if species are frequently paraphyletic, how can cladistics be tenable?

The grouping of lineages into species is necessarily somehow arbitrary. However, the relationship between lineage is free from any subjectivity. The reconciliation you need to go through is to accept that the concept of species, despite being so much used, is of no use to phylogenetic (or only to facilitate naming).
Cladistic and phylogentics is tenable because it does not depend on the concept of species which itself is arbitrary. You can learn more about the semantic of the concept of species in How could humans have interbred with Neanderthals if we're a different species?

Right. So if species are frequently paraphyletic, why is it regarded as unacceptable for higher taxa (which are usually seen as more arbitrary) to be paraphyletic? As in the idea that reptilia are not a legitimate grouping.  How can the fact that even species are not by nature monophyletic be reconciled with cladistics claim that only monophyletic groups are legitimate? Many thanks, by the way.

Probably because as you go to the detail, it becomes harder (impossible?) to really name monophyletic groups only. This is even more problematic as we would ought to rename groups at every small discovery about the ancestry of a lineage.


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Do allergens have structural similarities to pathogens?
The conventional popular explanation of allergies is that the immune system confuses allergens with pathogens and reacts to them as such.  Is there any merit to this explanation?  If so, I would expect it to be possible to predict which proteins would be allergens by their structural similarity to pathogens.  Is it?  If not, how else could we explain which proteins are allergens and which aren't?

Have you done any basic research?The wikipedia article is a good read to start with. I think you should go through this to finf out What should you do before you ask the question?.

Allergens are antigens. Please do some research on what each term refers to. Wikipedia is an excellent resource.

@MattDMo Sorry, I think I meant "pathogen" instead of "antigen".  I will change my question.

@SanjuktaGhosh You seem to have linked to the page on homework questions.  This is not a homework question.  Is this the page that you meant to link to?  And I have done research to try to answer this question myself.

Low effort questions are closed under the tag 'homework question' and I meant to link it to the 'What should I do before I ask the question? ' paragraph. You have to share your research (mentioned in a paragraph below it).

@SanjuktaGhosh no, not all low-effort questions are to be closed as homework. See the recent discussions on meta. Homework is for homework, low-effort can be closed as too broad, unclear, or using a custom close reason.


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What bacteria do unborn babies contain?
This Scientific American article states that "[human] infestation [by bacteria] begins at birth". This would suggest that unborn babies are free from any bacteria. However, if the mother catches a bacterial infection, her unborn baby risks catching it, too. This would seem to contradict the Scientific American article.
Presumably, when a human egg is fertilized by a sperm, the resulting cell may be free of any bacteria. At some point, bacteria begin to colonize the growing human body. Which bacteria are the earliest to colonize, and at what point in the development cycle does this occur?
In particular: does the health of the foetus depend on the presence of certain bacteria?

"However, if the mother catches a bacterial infection, her unborn baby risks catching it, too." Sorry, I just caught this; I thought you meant perinatal infections. In general, this applies to viruses and a few bacteria/protozoa: Listeria, spirochetes, toxoplasma, etc. However, these are the exception. Your statement makes it sound commonplace. It's not.

related:http://biology.stackexchange.com/questions/44457/do-the-bacteria-from-unborn-babies-have-benifits-on-health?noredirect=1#comment77482_44457

Babies are bacteria-free at birth. The meconium (the first stool) contains no bacteria if secured early enough.

Meconium is a sterile mucilaginous material that accumulates in the fetal intestine and is expelled soon after birth. It contains secretions of intestinal glands, gut constituents (proteins, bile acids, fatty acids, and steroids), and components of amniotic fluid and vernix caseosa.

Bacterial colonization of infants begins at birth - literally. They pick up bacteria from the mother's vaginal canal in passing, which they swallow. This is not seen in infants delivered by C-section. The importance of colonization picked up through normal birth is such, that some hospitals are swabbing the vagina of mothers delivering by CS and colonizing the oropharynx that way.  Breast-milk also contains lactobacilli and bifidobacteria that probably contribute to the initial establishment of the gut flora of newborns.
And, yes, an infection the mother has while delivering must be taken into account. Herpes and Group B strep are both dangerous for a neonate.

The first microbes to colonize the intestines of newborn babies are the aerobic bacteria Escherichia coli and Streptococci. Later, the gut is colonized with anaerobic bacteria, e.g. Bacteroides, Bifidobacteria, and Clostridia. In 1–2 y, the gastrointestinal tract of infants has developed a natural microflora, which resembles the microflora of adults.

The infant continues to pick up bacteria from all people they come into regular contact with, including nurses.

The effect of the maternal flora on the initial gut colonization may be less than expected as the fecal flora of infants started to resemble both the fecal flora of the mother as well as that of the first nurse.
  Breast milk may contain bacteria which colonizes the gut as well

Infants aren't overwhelmed by infection due to the presence of  antimicrobial peptides found on their skin, GI tract, and immunity is conferred via breast milk.

Several AMP have been characterized in vernix and skin of the newborn, indicating a well-developed innate immune system, which may play a pivotal role at the time of postnatal colonization.

Antimicrobial Components of the Neonatal Gut Affected Upon Colonization
Dynamics of gut colonization and source of intestinal flora in healthy newborn infants
Protection of the Neonate by the Innate Immune System of Developing Gut and of Human Milk
Establishment and development of lactic acid bacteria and bifidobacteria microbiota in breast-milk and the infant gut

I have found these articles which contradict what you write: https://www.sciencenews.org/blog/growth-curve/baby%E2%80%99s-first-bacteria-arrive-sooner-we-thought http://symbionticism.blogspot.ca/2013/08/got-moms-bacteria-breaking-silence-on.html http://directorsblog.nih.gov/2014/05/28/not-sterile-after-all-the-placentas-microbiome/

@JamesNewton - I've seen contradictory studies (few) as well. Frankly, I don't think they're enough yet. I read the umbilical cord blood study (not a report of it). I also could cite animal studies. If mammals were born with some bacteria, germ-free mammal lines would be impossible. While I agree that the uterus is not necessarily germ free (and therefor the placenta is also at risk), right now this is a bit new, like Helicobacter pylori as causative of ulcers was. Time (and more research) will tell.

@JamesNewton - Also, I have a lot of contradictory seeming-evidence: The two people born aseptically who survived SCID in an aseptic environment (they had sterile feces), germ-free animal models (as mentioned earlier), and the results of many studies linking bacterial colonization of the uterus with infertility, miscarriages, etc., as well as the results of studies of anmiotic fluid and PROM (premature rupture of membranes) in neonates. Maybe coincidental, but not ready to throw the baby out with the bathwater yet.

@JamesNewton - Finally, there are some who feel the science in that study was poor, and that this aspect was underreported.

In medicine, there's a saying: Be neither first nor last. I've taken that to heart for 30+ years. I don't jump on bandwagons, but am not the last one to try something new. The health of my patients - not my ego - are my primary concern. My favorite role models in medicine (I have a bunch) are Barry Marshall and Robin Warren. That should say something. (P.S. If you have a better answer, please post it.)

Just a note: I have read that baby earthworms inherit the gut microflora (Verminephrobacter sp.) from the mother before they are born.

@WYSIWYG - I cannot speak to earthworm placental function at all. Lots of crazy stuff happens in other kinds of mammals, let alone invertebrates.


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What is the simplest autotrophic cell?
Very simple cells, such as Nanoarchaeum equitans, require a host to provide certain essential ingredients for life. Complex life-forms (like humans) require a whole ecosystem of other life-forms to survive (either externally, to provide food, or internally, in a symbiotic relationship).
What is the simplest cell that has been discovered so far that can live in an environment where there are no other life-forms, not even in a decomposed state? Does such an organism exist, or is all life inextricably dependent on other life?

I guess one of the chemoautotrophs.

What kind of environment with 'no other life-forms' are you thinking about? Amino acids are found in comets, and the oxygen in the air is biological in origin.

I'm imagining an artificial laboratory environment. I doubt that such an environment would exist naturally so long after the first proliferation of life.

@WYSIWYG  I'm not sure that the word "autotrophic" is entirely accurate here. I can imagine that there are simple organisms that create their own energy but which require molecules created (and perhaps discarded) by other organisms, so they are still dependent on the other life forms. Does the word "autotroph" explicitly exclude such interdependence?

@JamesNewton yes

@WYSIWYG In that case, my question can become: what candidates for the status of pure autotroph exist?

If by "simplest" you mean smallest genome, then according to Brock's Biology of Microrganisms (13th ed, p 319) the smallest autotroph is Aquifex aeolicus, a chemolithotroph bacterium. It's genome is 1.5M bases, about 1/3 of that of E.Coli, and was sequenced in 1998 (https://www.ncbi.nlm.nih.gov/pubmed/9537320).
The genome is densely packed though and still carries some 1,500 open reading frames. The authors of the genome sequencing paper states that "metabolic flexibility seems to be reduced as a result of the limited genome size", which I guess is some evidence of "simplicity".

I'm not sure if this is exactly what you are looking for, but since I was looking for an answer to a similar question to you (what's the simplest living organism), I just found about this,

"The Simplest Living Organism Ever Has 437 Genes and Was Made in a
  Laboratory"
"a self-replicating bacterium invented by Venter and his team that
  contains just 437 genes, a "genome smaller than that of any
  autonomously replicating cell found in nature,"

Now I dont know if artificial organisms count in your question, and if it complies with the other requirements you were asking
https://motherboard.vice.com/en_us/article/craig-venter-created-the-simplest-living-organism-possible-in-a-laboratory


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Why are there different species of bacteria?
The usual (high school or intro to bio) explanation for diversification of species comes from multicellular, usually sexually reproducing organisms, and seems to be closely tied to the biological species concept.  It is that once organisms are different enough, they will be unable to exchange genes and therefore gradually become more distantly related.
This is not really applicable to species of bacteria which can exchange genes through horizontal gene transfer (obviously not all can, but many can).  It seems to me that if HGT rates are low relative to mutation rates, the same process of diversification could take place.  However if they are high (and random), it seems like either species would not exist as discrete entities or would exist only because the environment was only favorable to specific collections of genes.
Is there a commonly accepted reason why species should exist among species which have horizontal gene transfers (ie is there a reason to expect that HGT rates will usually be very low), rather than bacteria existing as a continuous gradient?

Yes. HGTs rates are likely to be low because the restriction system digests foreign DNA. Therefore you can note that each bacteria has a unique set of restriction enzymes. Your question seems to consist of two parts 1. How correct is the common definition of a species and 2. Why does HGT not cause all bacteria to coalesce into a single "species". I think it is the second question that you are interested in; am I right?

Restriction system is not the only factor, though. I have to look up on this.

HGT is not very different from sexual reproduction when it comes to speciation - in fact, it's often considered a kind of sexual reproduction. Just as organisms with sexual reproduction (e.g. most animals or plants) form species and not a continuum, bacteria can form species too.


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Is there an RGB equivalent for smells?
Millions of colors in the visible spectrum can be generated by mixing red, green and blue - the RGB color system. Is there a basic set of smells that, when mixed, can yield all, or nearly all detectable smells ?

It would be so cool if this could be used in video games. Like if the player walks into this room, make the smell equal to $x$. But I think we have to wait a long time until this becomes possible haha.

Not an answer, but instead of and RGB style system (with 200 receptors) some of the more experimental systems mix common sents to get a new smell. There are a few "sents" that make up a large selection of artificial smells in our food an fragrances.

Actually, RGB can't reproduce the entire visible spectrum. If you're curious, read up on the color triangle. The mind-blowing thing for me is that how the primary colors were chosen is somewhat arbitrary, but they do correspond to where each type of cone (we have three types) is most responsive.

The question was whether there is a combination of basic smells that, when combined, would allow us to experience the equivalent of a 'smell rainbow'.  i don't think anyone has answered this yet

It's probably also worth mentioning that there's no consistent theory for what smell actually is - i.e. alternatives like vibration theory which describe things shape theory can't (but vice-versa is also true). Once it's known how it actually works then it can be broken down into its basic components and categorized into the resulting "human perception spectrum" like RGB does for light.

in a way, the answer to your question is 'we have no idea' - it is tempting to imagine, but our sense of smell is much more personalized than our visual system and, across individuals there is really minimal similarity in activity in the piriform cortex (for instance) where odors are interpreted after initial decoding, compared to the visual cortex.

@Kevin you make me nostalgic. Back in 2001 (I was 10 then) computer magazines were crazy over scent reproduction for movies, web perfume catalogs, web tours (click a door, wait 10 seconds to download, repeat). I remember them noting that audiovisual storytelling will elicit desired reactions (mountains evoke awe) but smells wont (rotten wood may evoke nostalgia instead of the intended disgust). Here is a link from those times: https://www.wired.com/1999/11/digiscent/

There are about 100 (Purves, 2001) to 400 (Zozulya et al., 2001) functional olfactory receptors in man. While the total tally of olfactory receptor genes exceeds 1000, more than half of them are inactive pseudogenes. The combined activity of the expressed functional receptors accounts for the number of distinct odors that can be discriminated by the human olfactory system, which is estimated to be about 10,000 (Purves, 2001).
Different receptors are sensitive to subsets of chemicals that define a “tuning curve.” Depending on the particular olfactory receptor molecules they contain, some olfactory receptor neurons exhibit marked selectivity to particular chemical stimuli, whereas others are activated by a number of different odorant molecules. In addition, olfactory receptor neurons can exhibit different thresholds for a particular odorant. How these olfactory responses encode a specific odorant is a complex issue that is unlikely to be explained at the level of the primary neurons (Purves, 2001).
So in a way, the answer to your question is yes, as there are approximately 100 to 400 olfactory receptors. Just like the photoreceptors in the visual system, each sensory neuron in the olfactory epithelium in the nose expresses only a single receptor gene (Kimball). In the visual system for color vision there are just three (red, green and blue cones - RGB) types of sensory neurons, so it's a bit more complicated in olfaction.
References
- Purves et al, Neuroscience, 2nd ed. Sunderland (MA): Sinauer Associates; 2001
- Zozulya et al., Genome Biol (2001); 2(6): research0018.1–0018.12
Sources
- Kimball's Biology Pages

It's fascinating. Are there people who can approximately evaluate the 200-parameter RGB smell counterpart? Do dogs have more than 200 or is their smell superiority caused by something else?

@LubošMotl - Dogs have higher sensitivity, i.e., more receptors in terms of sheer numbers. Their olfactory spectrum is not so different than ours afaik

Thanks! Maybe they're less pretentious, too. I think that if a man weren't feeling painful, he could smell quite some details about many things and other people, too. ;-)

Also, dogs get a lot more practice, starting from a very young age. Though it turns out humans aren't too bad at it if they really try. Read Surely you're joking Mr Feynman for details.

@LubošMotl AliceD's second paragraph alludes to the fact that the olfactory responses don't have a great correspondence to the chemical structure... There are certainly variations in odor sensitivity and discrimination between people, but it isn't at all clear that the 200 "smell motifs" have any particular meaning individually. This seems like a difference from RGB where there is a perception of the individual colors, but maybe not: for example, it seems silly from a perceptual standpoint to say that white is "more red" than black, though this is clear in RGB or physical terms.

i think the idea of a base set of odorants, like red green and blue, is flawed, although this is a nice summary of how olfaction works

@dblyons - Overmind's answer below seems supportive too

The information in Purves is significantly out of data with the fields current literature. The olfactory code has still not been worked out, though it is likely combinatorial. There is also extinguishing effects. After a certain point, ORs are taken off the surface of the OSN, and the ability to detect that volatile chemical diminishes.

@AMR - long time no see! yes of course there's adaptation; just as in the visual system. The senses are complicated.

Can those inactive pseudogenes be used to send information over smells?!? No I don't believe in government conspiracies, why do you ask?

If there are $100$ kinds of receptors there should at least $2^{100}$ distinguishable scents. How can there only be $10000$?

There are many, many more parameters than 200! As an example, look at the nomenclature system for olfactory receptors (ORnXm).

"OR" is the root name (Olfactory Receptor superfamily)
n = an integer representing a family (e.g., 1-56) whose members have greater than 40% sequence identity,
X = a single letter (A, B, C, ...) denoting a subfamily (>60% sequence identity),
m = an integer representing an individual family member (isoform)

Members belonging to the same subfamily of olfactory receptors (>60% sequence identity) are likely to recognize structurally similar odorant molecules.
So, if we have 56 families, and each family has 26 possible subfamilies that can each detect a specific range of molecules, then you have a 1456-characters "alphabet" to describe all possible smells. Now humans will have more or less of each type, some types will not be there but be present in dogs, etc... Now if you take any actual smell (complex molecules with multiple odorants), it will be represented by any number of specific receptors going on at the same time. So if we set a limit of 100 receptors activated simultaneously per whiff (imaginary, no idea what the real number is), there are 1456^100 possible combinations of receptor activations for any 100-odorants smell.
References:
Glusman G, Bahar A, Sharon D, Pilpel Y, White J, Lancet D (November 2000). "The olfactory receptor gene superfamily: data mining, classification, and nomenclature". Mammalian Genome. 11 (11): 1016–23. doi:10.1007/s003350010196. PMID 11063259.
Malnic B, Godfrey PA, Buck LB (February 2004). "The human olfactory receptor gene family". Proceedings of the National Academy of Sciences of the United States of America. 101 (8): 2584–9. Bibcode:2004PNAS..101.2584M. doi:10.1073/pnas.0307882100. PMC 356993Freely accessible. PMID 14983052.
Glusman G, Yanai I, Rubin I, Lancet D (May 2001). "The complete human olfactory subgenome". Genome Research. 11 (5): 685–702. doi:10.1101/gr.171001. PMID 11337468.

This seriously needs a reference or two.

I added three...

Having the possibility to name such a big number of genes in a family doesn't actually mean, that there are so many genes. Your first reference tells us that there are 330 human olfactory receptors (rather than 1456), so please read these references.

If you re-read the answer, it is clear that the 1456 is a maximum. I was not limiting the answer to humans either. If there are 26 possible subfamilies, the number is 1456. Even if humans only have 330 receptors, what is important is how many different families and subfamilies are they distributed into. Just as an exercise, let's say those 330 receptors are part of 330 subfamilies (1 of each). Let's say a typical smell has ~20 odorant molecules. That is 330 ^ 20 possible combinations of receptor activation.

Most of the olfactory genes are pseudogenes.

Nonetheless, I have updated my numbers in my answer. Thanks. +1

This seems to be addressing how many smells there can be, rather than how many axes. Compare: with RGB, there are three axes, but we often encode colors using a level from 0 (black) to 255 (very bright) on each axis, giving 256^3 colors. By comparison, you are saying one way to think of smell is as a 330-axis thing with only levels 0 (not present) and 1 (present), which would give 2^330 possible smells, but then constrained so that at most 20 axes are 1 at a time, which reduces the space to 330 choose 20 (not quite as big as your 330^20). But that doesn't mean there are 330 choose 20 axes!

@DanielWagner - indeed, man can discern millions of colors

Where is your evidence that there are 26 possible subfamilies - from the 26 letters in the alphabet? I'm terribly sorry, but biology doesn't work that way.

@AliceD The ability of man to discern millions of colors is a bit dependent on circumstance... The studies that report people can determine millions of colors are really talking about contrast sensitivity. The number goes way way down if you would instead present colors sequentially. Even the paint colors in a hardware store can't be reliably distinguished when they aren't held together.

Yes, it certainly is. But I cannot guarantee that all have been properly determined.
For that, we would have to find the basic unique values (like the Red, Green and Blue in the case of colors).
Currently, we have 10 unique human detectable smells:
The wood-like smell, the floral/fragrant one, non-citrus, chemical, sharp(garlic-like), sweet, menthol, peanut-like, lemon and decay/dead-like (those are labeled by researchers as W1 to W10). A reference of the 10.
The your RGB-like-values for smell should be something like that.


text:
Creating BLAST database with nucleotide "place holder"
I have a set of nucleotide sequences that contain some special characters with multiple meanings:

H -> C, A or T
K -> G or T
M -> C or A
R -> G or A
S -> C or G
W -> A or T
Y -> c or T

I would like to create a BLAST database with that sequences.
The "place holders" seem to be a known vocabulary (at least for the query sequence).
It is also possible to create a database (using makeblastdb), with sequences containing the "place holder" characters. However, the characters are always recognized as mismatch.
Is there a way to tell BLAST recognizing the characters above as match if the query sequence fits?
If not, I could imagine to "expand" all combinations for each sequences by replacing the "place holder" with it's concrete nucleotide, but that may grow up the database... Or is there another solution to face that problem?

There is no such option. You would have to edit BLAST source code.

I had thought so, thanks for confirming! Modifying the sources would be an option of course, but to much effort for me. Just for interest, is there a public repository for the BLAST sources? I didn't find one (only the downloadable zip package).


text:
High frequency tone/ringing in movies/music and its effects
I was watching a horror movie and I noticed during a scene that there was a high pitched noise playing in the background. It had been playing for a while before I noticed it and when I took notice it started to irritate my ears, however this isn't my concern. I noticed that while this noise played during the scene I was in a trance-like state almost felt like I was hypnotized, so my question is can these high pitched sounds be used put the viewer/listener into a trance-like state or hypnotize them and if so are there any scientific studies that prove or debunk my theory?

Firstly, my diagnosis: "nocebo effect". Secondly, this is probably entering the psychology/social sciences(/economics?) domain... See if this video hurts too: https://www.youtube.com/watch?v=O2hO4_UEe-4

Thank you for your input i didnt think id ever get any answers

Noo don't think like that! I am not saying you will not get any answers, I am saying, that if you modify the tags, it will very much likely boost your chances of getting those answers :). We need people like you, and the correct Stack Exchange site: http://cogsci.stackexchange.com/, or the correct tags will open your question up to different experts (see: @NormalHuman, believes in your question too).

I understand what you meant. I just didnt expect to get a reply since i posted this well over a month ago

Still I dont think it was a nocebo effect as I didnt feel I was in harms way at any point. It was more like i was being forced or tricked into focusing on what was on the screen the sound drew my in and before I knew it I was as i said earlier in a trance like state I was just kinda blank if that makes sense?

Hmm, I honestly do not know, as in I think I am not the expert here? Let's grab some popcorn and see who answers it fastest :)

I find that certain music puts me in a state where I fall out of consciousness and everthing around me just doesnt exist for a time so i wanted to know if this is something that can be intentionally induced through sound

Thanks for replying atleast this is something that is very intriguing to me as I would like to utilise this if a technique exists


text:
What are the blue and white things on this Sunburst lichen?
I am a amateur photographer I found some interesting things when I got home and looked at my photos. There are some blue/white cocoon. I  like structures on top of the sunburst lichen. I live in Colorado and took these photos on January 23.

I have improved your title a bit but this is not sufficient. Please describe what you tried to capture in the photograph (name of the fungus), your geographical location and climatic conditions.

Hey thank you! and please excuse me for a minute I'm trying to figure all this out so I can be more specific in questions and examples. I'm very excited to be a part of this community thank you!

I had trouble doing this on my phone but I appreciate your time. I'll keep in eye out more of these because I can't find the good image of them on Google. So I might be able to upload some better images to the Internet.

The blue part you highlight are similar to the blue parts present more generally on other portions of the lichens, aren't they ?

There you go the top photo shows them a bit more clearly the color must be pretty close my phone automatically adjust colors a little bit. I'll be revisiting the area to find more of these I'll try to get better photos.

Lichen species looks like Xanthoria parietina

The small blue creatures coould possibly be (oribatid) mites.
I have them under my the binocular when I study lichen pretty often.
Their asociation with lichen is well documented

A mite was my thought too. I had no idea of the order or anything though


text:
Question about alternative polyadenylation
I know that alternative polyadenylation creates different transcript isoforms. My question is whether alternative polyadenylation ever results in differences in the terminal/last exon? The only case I can think where it might be is if the terminal exon is alternatively spliced?
EDIT:
I think what I was trying to ask was for a given gene, what factors could cause the transcripts to end in different locations. I drew a picture and it helped me figure it out a little
Here are 4 transcripts for a given gene, each of which end at a different location. Exon's C and D end in different locations because D is completely different exon than C that is being spliced to exon B. Exon on C and E start at the same location, but exon E is shorter, due to a UTR-Alternative polyA event. Exon B and F start at the same location, but F is shorter due to a Coding APA change. So alternative polyadenylation drives the formation of transcripts 1,3,4 while alternative splicing drives the formation of transcript 2. So I guess to rephrase my question, are there any other biological process that can affect where a transcript ends

I am finding it difficult to understand your question. Could you draw a diagram to explain what you mean please?

Are you asking if alternative polyadenylation is always associated with alternative splicing of the last exon?

@Vinay Swamy: I hope my suggested edit didn't change what you were trying to ask!

According to a 2011 review1 alterntive polyadenylation sites can be located upstream of the 3'UTR (i.e. within introns or exons).  When these sites are used it results in transcripts missing exons at the 3' end and can force alternative splicing.  This alters the final protein product.
This figure from that paper may help make this clearer.

Figure 1. Schematic Representation of CR-APA and UTR-APA
CR-APA produces mRNA isoforms with distinct C-terminal coding regions,
  resulting in distinct protein isoforms. UTR-APA produces distinct mRNA
  isoforms with different-length 3′ UTRs but encodes the same protein.
  Longer 3′ UTRs usually contain cis-regulatory elements, such as miRNA
  and/or protein binding sites, which often bring about mRNA instability
  or translational repression. CR-APA, coding region-alternative
  polyadenylation; UTR-APA, 3′ UTR-alternative polyadenylation. Light
  green boxes, untranslated regions; light blue boxes, shared coding
  regions; dark blue and yellow boxes, unshared coding regions; lines,
  introns.

Reference:
1: Di Giammartino, D. C., Nishida, K., & Manley, J. L. (2011). Mechanisms and consequences of alternative polyadenylation. Molecular cell, 43(6), 853-866.

Alternate splicing can result in the same protein. Perhaps you can add a note below the figure.

@WYSIWYG — I'm undoubtedly missing something, but I'm not sure how that relates to the OP 's question or to my answer ...

I mean that alternate splicing need not affect just the CDS, it can change the UTRs and can potentially expose cryptic polyadenylation sites, zipcodes etc. See this article, for an example.

@WYSIWYG — Sure, but my understanding is that the question is about whether alternative polyadenylation ever alters the protein produced.  You seem to be discussing how alternative splicing can affect the transcript.

Frankly I didn't understand what OP is asking. They didn't clarify.


text:
Which database has the ready made 16S rRNA Multiple Sequence Alignment File that I can download directly from?
In my case, I need the ready made 16S rRNA Multiple Sequence Alignment File for E.coli and use it to generate the phylogenetic tree file in Newick format. I've tried using the one from utexas website, but I get too many errors when using the alignment file for tree generation, either the file size is too big or the input file is not a fasta file, so I tried to read the alignment file in R using read.alignment() function and it reads fine. Still I get this error when I used it to generate the tree.
So, can someone tell me where do I get a ready made Multiple Sequence Alignment File for 16S rRNA of E.coli being the reference sequence?
Thank you.

Try to use the MEGA software. You download in this website: https://www.megasoftware.net/

What format is your alignment file in? Have you considered NCBI MSA Viewer or the Genome Workbench

It is in fasta format and the file size is 27 MB (too big for NCBI MSA viewer).

How about using Genome Workbench then? It probably does not have size limits.


text:
How to reduce the number of sequences in a Multiple Sequence Alignment?
I have a Multiple Sequence Alignment, where there are around 5000 sequences. There also exists many sequences where, there are so much of non-sequenced regions (for instance, AU----CGGGCA--NNNNNNNNNN).
So, by trial and error, I found a threshold value of 25%, so I removed the sequences which contained more than 25% of non-sequenced region (N's here), retaining around 400 sequences in the alignment, by writing a simple R script.
But, I would like to know, if there is any other standard method to do this, because I do not think, removing sequences based on finding a threshold for the percentage of non-sequenced regions, by trial and error is more efficient.If there is, can you please tell me, how to do?
Thanks in advance.

To remove sequences that contain ambiguous sequence is pretty straightforward. You can do it programmatically instead of doing manually. What do you mean by proper method? Can you please clarify what your objective is?

Sure, I removed the sequences with a simple R script. I do not think, removing sequences based on finding a threshold for the percentage of non-sequenced regions, by trial and error is more efficient. I was wondering if there is any standard way to do it.

That totally depends on your judgment. There can be sequence blocks that do not contain ambiguous bases. You can take them if you think the entire sequence is not necessary. This could be done only for local alignments. For doing global alignments, you should take a call on whether or not the number of ambiguous bases is too much. It would also matter if the ambiguous bases are present together or spread out. A stretch of Ns would be worse than the Ns being spread out. You can try MSA with and without these sequences and see if there is any significant change in the consensus.

Deciding the threshold depends on your prior knowledge about the sequence region. The software is unaware of the biology. For e.g. the N could be in non-conserved regions: it would not probably affect the MSA. If they are in the conserved regions, they could distort the analysis. Anyway, can you please [edit] your question to clarify the exact objective (as you mentioned in comments)? Comments are not searchable and can go unnoticed. Moreover, the post should be self-sufficient.

I edited my question.

As there are too many sequences, finding the consensus regions using online MSA viewer tools is not possible. I will try to find any offline tools available for this purpose. It's stretches of N's, present towards the ends of almost all the sequences in the alignment.

You may have a look at these papers: https://doi.org/10.1093/bioinformatics/btg109, https://doi.org/10.1093/bioinformatics/bth126 and this overview on POA. I haven't used the POA tools directly. Read the overview just to understand how PacBio generates consensus. The papers are still open in my tabs.

@User — By what method were these sequences generated?  If you do Sanger sequencing of PCR amplicons, you often get long runs of noisy sequence after the "real" sequence has been read.  It sounds to me like you might just need to trim off the junk from the ends of your sequences rather than throwing most of them away.

@User as tyersome said, these Ns would have arisen because of sequencing errors and thus do not represent the actual sequence. Moreover, we don't know what this sequence is: is it a gene, does it span the entire geneic region or ORF etc. If you don't define the boundaries of your sequence (based on the biology) your MSA cannot be used to infer biology. MSA is also used for obtaining consensus of sequencing reads; this strategy is used in PacBio and Nanopore. The objective there is different. So what is your objective?

I downloaded the alignment from a database and no information regarding the N's (uncertain nucleotide positions) is given, so my clear objective is to find the consensus or evolutionarily conserved sequence regions and use this, along with it's phylogenetic tree, in a software tool that does RNA secondary structure prediction.

It would be helpful to know your application. For some applications, having ambiguous sequences is not necessarily a problem as long as you have a mechanism to handle such non-informative positions. The information from the other positions may still be valuable.
An alternative to removing the sequences (rows of the alignment matrix) with many Ns would be to remove non-informative or poorly aligned positions (columns of the alignment matrix) from the alignment. It depends to some extent on what your goal is. Tools such as gblocks can be used in this way.
For example, if your goal is to perform clustering or phylogenetic estimation of the region, or identify highly conserved regions, then removing poorly aligned or non-informative columns would be worthwhile.
On the other hand, if your goal is somehow related to the entire sequence (e.g. protein structures or open reading frames), then removing rows/sequences may make more sense. But it is still not clear to me that you really need to remove ambiguous positions. For some discussion of this you can see this old researchgate thread or this biostars thread.

The bioconductor package "ShortRead"  might be what you are after.
It has a function "clean" to remove sequences with ambiguous bases. It also can remove duplicates if you need to.


text:
16S rRNA and 5S rRNA datasets
I need 16S rRNA and 5S rRNA (Gammaproteobacteria - E.coli) Secondary structure files in ct format.
I tried looking for them in different RNA databases, could not find one. Can someone tell me where to find such datasets?
Thanks in advance.

This site has secondary structure maps for rRNA from different organisms but they are just pictures. Not sure if it is helpful.

Thanks. But I was looking for the secondary structure files in ct format. I found it in RNA STRAND v2.0, please check the answer below.

RNA STRAND v2.0 - The RNA secondary STRucture and statistical ANalysis Database
http://www.rnasoft.ca/strand/
16S rRNA: secondary structure file in ct format
http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00111&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00111
5S rRNA: secondary structure file in ct format
http://www.rnasoft.ca/strand/show_file.php?format=CT&molecule_ID=CRW_00573&check_out_the=View+the+RNA+sequence+and+secondary+structure+for+molecule+CRW_00573


text:
Where can I obtain the sequence of the E. coli ribosomal RNA precursor?
I have found separate sequences for 16S rRNA (from the small subunit) and 23S rRNA and 5S rRNA (from the large subunit). I need the full precursor rRNA sequence, which I cannot find.
However the complete annotated sequence of the E. coil genome is available:
https://www.ncbi.nlm.nih.gov/nuccore/U00096.3?report=fasta
Does changing the T to U of this sequence give me the complete rRNA sequence?

Generally most organisms have multiple copies of the genes/regions coding for ribosomal RNA (since it's needed quite a lot). Additionally these regions can be repetitive or otherwise similar to sequence or place correctly in the genome, therefore it's generally harder to find good genomic sequences for rRNA compared to other genes.
Based on your link, it seems that you are looking for the rRNA of E.coli; the GeneBank entry corresponding to the fasta file you linked contains the annotation of the full genome and has 7 entries for sets of ribosomal RNA (named rr[slf][A-H]*).
If you take any of the sequences spanning one of these regions you should get the sequence of the full precursor. However, there are things you should be aware of:

there will likely be minor sequence differences between all 7 regions
Apparently most of the e.coli rRNA operons also have tRNA genes mixed into them (these are different for all 7 operons)
replacing the genomic T with U will make the sequence look like RNA, however ribosomal RNA is often also edited post-transcriptionally, so the sequence you get may not fully match the mature rRNA sequence.

Another website that gives a better readable overlook over the rRNA operons in e.coli is this, it also contains source links & seems to match the genbank entry from what I can see.

Example on how to find rRNA region from the geneBank entry:
This is a (shortened) part of the annotation of the GeneBank entry, which shows the 'A' ribosomal genes :
gene  4035531..4037072
  /gene="rrsA"
rRNA  4035531..4037072
  /gene="rrsA"
gene  4037141..4037217
  /gene="ileT"
tRNA  4037141..4037217
  /gene="ileT"
gene  4037260..4037335
  /gene="alaT"
tRNA  4037260..4037335
  /gene="alaT"
gene  4037519..4040423
  /gene="rrlA"
rRNA  4037519..4040423
  /gene="rrlA"
gene  4040517..4040636
  /gene="rrfA"
rRNA  4040517..4040636
  /gene="rrfA"

As you can see the genes in the region/opernoccur in order rrsA, ileT, >alaT, rrlA, rrF (the fact that this is an operon can not be inferred from the GeneBank entry) and if you take the corresponding region of the fasta sequence (nucleotides/characters 4035531 to 4040636) you'll get (most of) the primary transcript sequence.
  Since promoter & terminator Sequences are not annotated in GeneBank (or any/most other genome assemblies), you can't easily get the sequence before the first and after the last gene. One  potential source for these might be the other ressource I linked, which lists some sources for terminator sites.

* This is expressing all names as regex. i.e. for rRNA operon A there are rrlA, rrsA & rrfA; same for B,C,...

@User I added an example of what I meant with that paragraph

Thank you very much, this helps to find most of the operon sequence. @User


text:
What are the differences between carnitine forms?
I've heard of L-carnitine, acetyl L-carnitine and L-carnitine L-tartrate. What form(s) occur in meat? What form does the human body manufacture?
Is L-carnitine just a shortened name for L-carnitine L-tartrate?

L-carnitine and L-tartrate are two separate compounds - though a lot of "nutritional supplements" will package them together and seem to refer to them like they are one compound.

Carnitine tartrate is a salt between carnitine (cation) and tartrate (the conjugate base of tartaric acid, anion). So in this case, tartaric acid is not covalently bound to carnitine.
The salt formulation is a little tricky, because carnitine is itself a zwitterion at physiological pH (it has both a positive and negative charge) and so is overall uncharged in pure form. I think the tartrate salt is formed because tartaric acid is more acidic (first pKa = 2.89) than the carboxyl group of carnitine (pKa = 4.09), which leads carnitine to become protonated and therefore +1 charged in a concentrated mixture. The formulation sold by Lonza (which seems to be a major provider) appears to be a ratio of 2 cartinine (68%) to 1 tartrate (32%), which would indicate that tartrate acts as a -2 anion in this mixture (this is a bit surprising as the second pKa of tartaric acid has pKa = 4.40, but maybe I'm missing something).
You can recognize that this is a salt from the naming: the form tartrate indicate a conjugate base of an acid (as in lactate, acetate), and when used in a two-component name like carnitine tartrate (or, sodium acetate) refers to a salt. On the other hand, a carboxylic acid covalently bound to another group is given the suffix -yl, so tartryl carnitine would indicate tartaric acid bound to carnitine, as in fatty acid oxidation.

Carnitine is a molecule that allows transport of carboxylic acids (including fatty acids) across mitochondrial membranes and is involved in fatty acid metabolism. Like many biomolecules it exists as the L-enantiomer in the cells. It can be coupled to any carboxylic acid and in that case is called acyl-carnitine. L-Carnitine L-tartrate is a drug formulation and is a mixture of L-carnitine and L-tartarate (tartarate is not covalently coupled to tartaric acid).


text:
Why can we control our breath rate but not our heart rate?
Even though we cannot survive for more than few minutes if we stop breathing or if our heart stops, why is it so that our heart beat is controlled involuntarily while breathing can be voluntarily controlled to a certain extent. I just noticed that blinking of eyes also falls in this category; though we involuntarily blink and our eyelids close involuntarily in bright light, there is still voluntary modulation. What kind of evolutionary changes and natural selection could have led to these kind of voluntary modulations i.e. cortical control over these processes?

Perhaps to make tasks like eating and speaking possible. Note that you cannot voluntarily stop breathing indefinitely.

You already know why these processes cannot be voluntary. There is some level of voluntary control on breathing but it is overall involuntary. So if that is your question then you should note what @canadianer said.

evolution does not have consciousness or will. It does not make choices. Living beings are formed through mutations, natural selection,genetic drift etc.

@WYSIWYG involuntary and unconsiously doing something is different.

@DivyaPrakash they more or less mean the same. Moreover I never mentioned the word "unconscious".

Many unconsious activity like walking, writing, understanding and interpreting language are possible even though none of them are quite certainly involuntary action

@canadianer while eating and speaking breathing could also have been stopped involuntarily. There is no reason for making it voluntary to eat and speak.

@DivyaPrakash There is no debate here about subconscious control of voluntary activities. You still have to clarify your question. Plus your above comment to canadianer just sounds philisophical and not scientific.

I specifically want the answer in terms of certain evolutionary advantages if possible.

@DivyaPrakash Evolutionary advantage of what?? Little voluntary control on breathing or heart beat being involuntary. I am sure you know why that latter is advantageous.

@WYSIWYG Little voluntary control on breathing, I guess. As for the advantageousness of latter I am going to research more about what could happen if heart beat was made voluntary.

Let us continue this discussion in chat.