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Are we evolving as fast as the oxygen is depleting?
How much oxygen saturation have we lost in the last 100 years? As oxygen levels dwindle and industry, deforestation,  and population increases, at what year and saturation will the low levels of oxygen become a problem in human development? Would living or sleeping with higher levels of oxygen increase cognitive or physical ability?

Athletes in aerobic sports, e.g., cycling, sometimes live and sleep at lower (rather than higher) levels of oxygen in order to increase their oxygen carrying capacity and improve their physical performance. Particularly high levels of oxygen are actually toxic over moderate time periods.  I'm not sure either of these things are what you're getting at, though.

Good estimates from ice core samples put the decrease in oxygen concentration at 0.7% over the last 800,000 years. At sea level, currently, inspired $P_{O2}$ is (760 mm Hg - 47) * 0.21, approximately 150mm Hg. Human physiology easily adapts to lower $P_{O2}$ levels, with approximately 140 million people living at elevations over 2500 m, with inspired $P_{O2}$ at 108mm Hg, and many permanent human settlements higher than 5000 m, with inspired $P_{O2}$ approximately half what it is at sea level (see West Respiratory Physiology, Ch. 9). A 0.7% decline over 800,000 years isn't going to be much of a challenge.

That is before we had chain saws. I'm looking for more recent numbers and the effects on the human body.+1 for the info though.

@Muze the impact of industry is an increase in certain gases, not a significant decrease in oxygen. The gases that have increased substantially since the industrial revolution, e.g., $CO_2$, $O_3$, $CH_4$ are low percentage gases, but have a significant effect on the temperature of the earth through their interaction with radiant energy. There isn't a significant $O_2$ depleting impact.

So there is a decrease although insignificant. It takes 10 trees to provide enough oxygen for 1 person and if those trees are cut exponentially oxygen supply will also continue to fall. yes?

@Muze Deforestation causes a $CO_2$ problem, not an $O_2$ problem. As you can see from my answer, we have a large excess of $O_2$. $CO_2$, however, is a greenhouse gas, and small absolute increases (which are large relative increases) have significant effects on the biosphere.

@Muze Claims like It takes 10 trees to provide enough oxygen for 1 person would really need a reference. You will note that, if I am not mistaken, while forests are good carbon store, many forest ecosystems do no capture more CO$_2$ than they produce as they've reached their community climax and hence not carbon sink. I would think that such statistics (10 trees to provide enough oxygen for 1 person) hide a much more complex reality and can only be misleading.

@Remi.b reference:  https://space.stackexchange.com/a/26823/18879

@Muze Your reference is a post of yours who itself refers to two posts of yours (one being downvoted and closed)! None of the link support the claim anyway and if they try to do so, they fail to consider the fact that, in an ecosystem, tree die and release the carbon they have accumulated during their lifetime.

@Remi.b some trees can live 100s to 1000s of years old and the carbon is not released in the atmosphere. Not arguing but I did get 200 bonus rep for that link.

Sure but, IMHO, whether they live 1000 years or 2 years, does not change anything that in ecosystems where trees die and others grow up is a carbon storage but not a carbon sink. Anyway... let's no chat further. I have opened the post Does an old growth forest ecosystem produce more oxygen than it consumes? to tackle the question.

@Muze a SE link is not a reliable source to back up a claim on a SE site, no matter how many votes or what bonus rep it has. The original references should be both independent and authoritative or else you run into citogenesis problems :)

Re "10 trees", you're forgetting about the oceans.


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Exactly what biochemical factors control the intensity of an allergic reaction?
I think have a functional understanding of how an allergic reaction (Type I Hyper Sensitivity) occurs: basically the allergen causes production of antibodies that attach to mast cells and basophils. Later, if the same allergen binds to those antibodies, the cells release histamine and other unpleasant chemicals.
However, it's clear that the degree of allergic reaction varies a lot from person to person. For example, if my wife goes outside all day during peek grass pollen season, she'll end up with a sinus reaction, and not much else. If I go outside for a few minutes, I'll develop that, and if I stay longer, I'll get hives, weepy eyes, and so on.
Clearly I'm more sensitive to grass than my wife, but what exactly causes this? I can imagine a lot of possible factors!

Maybe I have many more antibodies (but why?)
Maybe I absorb more of the allergen per unit time (but why?)
Maybe my mast cells require less allergen to react (but why?)
Maybe my mast cells contain more histamine per cell (but why?)
...

So I guess my question is: What drives the variation in allergic hyper sensitivity responses?

Network of possible factors that contribute to the variability of the immune reaction between individuals is still not well investigated.
Type I hypersensitivity is mediated by IgE antibodies, which means that lymphocytes B after initial contact with antigen undergo oligoclonal selection. Only these with the highest affinity towards the antigen will survive. During this process (see: germinal centre reaction) genomic regions responsible for antigen binding change their sequence in non-deterministic manner. So, each individual has slightly different set of antibodies targeting the same antigen.
Moreover, within the same antigen (allergen), different regions (epitopes) can trigger the immune reaction in different individuals.
Other, more general factors also contribute to the symptoms associated with hypersensitivity reaction. For example: hormones, infections, medications, microflora condition, genetics (eg. major histocompatibility complex) or even psychological status.
Also see:
Article 1
Article 2
Article 3

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/

sort: votes


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Taxonomy problems on algae: Is Cryptophyta a Phylum or a Class rank?
I  am currently interested in algae taxonomy (I am not an expert in the field).
I retrieved the taxonomy of my sequences with their NCBI access number via the taxonkit software (https://bioinf.shenwei.me/taxonkit/usage/).
I noticed that I get Cryptophyta at the Class rank level.
For me -phyta actually corresponds more to the phylum rank.
I checked on NCBI site and is actually tidy in Class rank ( https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=3027&lvl=3&lin=f&keep=1&srchmode=1&unlock) but for example on the algaebase database (http://www.algaebase.org/browse/taxonomy/detail/?taxonid=Xafa8c1d30aa53593), Cryptophyta is classified as Phylum.
Can you tell me why Cryptophyta is rank at the Class level on NCBI and not to the Phylum level ?
Conversely, I retrieve taxonomy with, for example, Phaeophyceae ranked at Phylum level (https://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&id=2870&lvl=3&lin=f&keep=1&srchmode= 1 & unlock) while it is normally a Class on algaebase (http://www.algaebase.org/browse/taxonomy/detail/?taxonid=L8055ac0a94735f3e).
Do you have ideas being considered? I am very interested !
Thank you very much in advance for your answers.
Best regards

It is not possible to tell which one is "correct" and which one is "incorrect";
Actually "ranking" itself is a bigger problem with entire classification system.
After the "sexual species concept" we have somewhat a grasp that many (but not all) species fall on "same rank"; but for supra-specific ranks it is theoretically impossible to tell whether the  grass  (said to be "family" rank) and a  compositae (said to be "family" rank) fall exactly on same "rank" or not; similarly it is theoretically impossible to tell whether the animal (said to be kingdom rank) and plants (said to be kingdom rank) are exactly on same rank.
Practically; we forcefully assign the taxa from different lineages into similar ranks somewhat based on apparent perception, and in some cases we develop fine divisions of ranks and develop some criteria, that is also based on perception of 1 or a team op people; but that is not absolute.
What we can theoretically confirm, the taxon "Plant" is certainly higher than  (superset of) the taxon "grass" (a subset). I.e. hierarchies (superset-subset relationship) exist along a lineage. But the concept of "rank"; i.e. assigning 2 taxa from different lineage into "ranks" is a highly subjective and controversial.
(Personally I confess I don't know whether the ranking system have any real advantage other than arranging information)
A routine change of rank usually does not make anything correct or incorrect. (if within the single lineage you assigned a phylum into order and simultaneously an order into phylum; then it would be a clear false, or jumble-up the subset-superset relation). But when you just change a vague and confusing sort of
 "weightage" with respect to taxa on other lineages; keeping all subset-superset relations unaltered; nothing actually changes!
N.B. Additionally, if a taxon (set) is broken into adjacent or more taxa, or 2 adjacent taxa (set) is fused, (without cutting a taxon from one lineage to another) that is also a minor change in "refinement" or "resolution", not a change in correct-or-incorrect-ness.

Thank you very much for your detailed answer but would you have some thoughts on Cryptophyta?

Thanks for letting me know a question. I'll update the answer as soon I'll be free to write.

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/4.0/


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How long does it take for a blocked dopamine receptor to be broken down by the body?
Do the blocked dopamine receptors get broken down by the body and if so how often ?
In other words how long does it take for the dopamine receptors blocked by irreversible dopamine antagonists to degrade ?

If you could depersonalize this question to make it about the pharmacology of haldol, we may be able to give you an answer, though it may not be very satisfying. As it is, you're asking a personal medical question (how long do you have to wait for recovery of normal function after stopping haldol), which is off topic for any SE site.

Thank you for rewording. I've retracted my close vote. This is a complicated question that will require some time to carefully answer.

Partial Answer and Suggestions
As @De_Novo says, this is a complicated, albeit very interesting, question. There are various reasons for this, such as the fact that the receptors aren't just internalised but also recycled and the fact that there may be antagonist and dose-dependent changes in receptor internalisation. There's the added complexity that receptors can have their expression changed in the short term (by internalisation) but also in the long term (by varying synthesis). You should then note that there's not a set lifespan of the receptors - there's a statistical distribution for how long they'll last at the membrane.
But I'd quite like to stimulate discussion about it so I'm proposing some smaller questions:

Do irreversible dopamine antagonists change the rates of receptor internalisation, degradation or recycling? This is likely to be the case as internalisation of receptors is often activity-dependent. Also, the shape of the irreversible antagonist could change how the receptor fits into a clathrin-coated pit.
Do the irreversible antagonists change the rate of receptor synthesis?
What mathematical models can describe the dynamics of internalisation? This might be a bit tricky since there are feedback mechanisms here (e.g. recycling --> internalisation --> degradation --> less recycling).
How does the proportion of blocked receptors affect these factors?

By answering these questions (or even by finding an experiment that measures the half life of the receptors with blocking), you could come up with an answer for the half-life of the blocked receptors.


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Pangenesis and Lamarck's theory of inheritance of acquired characteristics
I've read that Darwin had split ways with Lamarck's evolutionary ideas. Yet his theory of pangenesis seems to support Lamarck's theory of inheritance of acquired characteristics. What am I missing?

Pangenesis and Darwin's Gemmules theory suggests a mechanism so that the body's information can travel to and be transmitted by the gametes. Today we know that the information is present in every cell.
Stephen Gould estimates that Lamarck was the first to develop a truly coherent evolutionary theory.
Lamarck's biological and metaphysical theories comprised entirely correct premonitions, 70 years before Darwin. His book was "Philosophie Zoologique" and Lamarck was not illustrious in his lifetime. His lack of evidence made him an impious, profane author, of the pre-enlightenment style of Voltaire, Rousseau, and prior to Emile Zola and Jules Verne.
Scientists have recently attacked Lamarck with great energy, in favor of Darwin:
http://www.textbookleague.org/54marck.htm
Basically Darwin emulated Lamarck's skeletal theory, perhaps independently, and fleshed it out in a modern writing style. He also discovered the foundations of an entire scientific field of his own which tied into Lamarck's, and he fought the church and the science institutions with it.
The evidence of Darwin was copious and meticulous, completing the work of Lamarck (with lesser or greater brilliance, for you to judge).
Lamarck's speciation theories were correct, and his trait-inheritance theory was metaphysical.
First law
Life by it's own force, tends to increase the volume of all organs which possess the force of life, and the force of life extends the dimensions of those parts up to a extent that those parts bring to themselves;
Second law
The production of a new organ in an animal body, results from a new requirement arising. and which continutes to make itself felt, and a new movement which that requirement gives birth to, and it's upkeep/maintenance;
Third Law
The development of the organs, and their ability, are constantly a result of the use of those organs.
Fourth Law
All that has been acquired, traced, or changed, in the physiology of individuals, during their life, is conserved through the genesis, reproduction, and transmitted to new individuals who are related to those who have undergone those changes.
Darwin convinced many scientists and wrote about it continuously from his 30's till his 70's non-stop, sent letters to everyone, and used evidence to define a scientific and mechanical reality to the theory of adaptive radiation. Darwin also coined catchy phrases:
The English and French view of Lamarckism differ.
The English view slights his status, due to lack of evidence and some alchemical bases for the selection process, even though Lamarck is the father of adaptive radiation theory, in the age of the printed book.
The French view gives him more influence, firstly because he may have inspired Darwin as an eloquent writer on the topic of adaptive radiation, the father of the adaptive radiation theory, and secondly because a glimmer of Lamarckism can be found in the new discoveries of Epigenetics, non genetic inheritence.


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Identify this excreta!
A picture is worth a thousand words!
It's about 1.3cm (1/2") long. We rented a basement and I found this on a machine that was moved in a bit earlier.
I would like to know if there are any mice, rats, etc that could have come in.
We are on the island of Malta, in the Mediterranean sea.
The basement is below a shop that used to sell AC units and the basement was used as a storage. The walls have gaping holes where cables and pipes go in and out, etc. Clearly industrial and not made for the customer to see.

Where are you located? Are you in the city, the country, ...?

I added more details in the post.

I don't think it is possible to identify a species based solely on the length and appearance of its feces

Definitely too big for mice (max 7mm). Could be a rat or a bat (hopefully for you the latter). What was the width? And did you see any clear renmants in the poop? Like beetle shields, hair or plant fibers?

There was nothing around, just that poop and a clean surface around, but this is in a basement we just got. The climate is hot and humid. The only insects we've seen are large cockroaches.

Bat is the other basement creature that comes to mind. It looks like a match as explained in this and several other videos - https://www.youtube.com/watch?v=897Fb9ndids

I just looked at photos of bat poop and they look more bulky, while this one is thin and long.


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Is every neurotransmitter receptor an ion channel?
This is a rudimentary question--perhaps the answer is well known to biologists, but is every neurotransmitter receptor also an ion channel?
For example, NMDAR is a glutamate receptor and cation channel and GABA_A receptors are gated ion channels.  Is this true generally?  If not, is there a classification of neurotransmitter receptors according to abstract function (e.g. all gated ion channels would form one class, then perhaps there are others)?
Thank you in advance!  I am a mathematician just getting interested in some biology problems and trying to organize the basic knowledge in this area.  I appreciate any insights here!

is every neurotransmitter receptor also an ion channel?

No.
There are two general types of receptors for neurotransmitters, ligand gated ion channels and receptors that activate second messenger systems, for example, G protein coupled receptors. They are sometimes referred to as ionotropic and metabotropic receptors. This figure from Principles of Neural Science, Ch. 10 illustrates the difference nicely:

Very clear!  It's interesting that although not every neurotransmitter receptor is an ion-channel, every receptor does control an ion channel.  Perhaps this is too broad a question for a comment, but do metabotropic receptors have any other effects on neuronal signaling apart from affecting the post-synaptic cell's membrane potential through control of ion channels?  In other words, is the control of ion channels all that really matters for neuronal signaling via neurotransmitters?

@user334137 good question. It turns out, sgnaling at the synapse is as complex and varied as signaling in any cell. Both types of receptors can result in many downstream effects beyond immediate changes in permeability to specific ions. The main difference is in the control of the time course of the response.


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Discrepancy in time for genetic differences between human and chimpanzee to accumulate
Genetic differences between human and chimpanzee include ~50,000 amino acid changes, ~30,000,000 point mutations in non-coding sequences, and millions of insertions, deletions, inversions, genomic rearrangements, and transposable element movements [1]. The vast majority of these genetic changes are neutral [2] [3]. For neutral mutations, the expected number of generations required to reach fixation in the population is the reciprocal of the mutation rate per site per generation [4]. This holds irrespective of selection at other linked loci, changes in population size, or almost any other conceivable complication [4]. The human mutation rate, μ, is ~10-8 per site per generation [5]. Although μ can be orders of magnitude greater at certain sites, the fact that, as cited above, millions of neutral mutations occurred in the human line since its divergence from the chimpanzee line indicates that at least thousands of mutations occurred at the average rate of 10-8 per site per generation. Since the expected number of generations required for any one of these mutations to reach fixation in the population is the reciprocal of μ, this number equals ~108 generations. Since a generation is ~20 years for humans [5], the time required for any one of these thousands of neutral mutations to reach fixation is ~109 years.
According to the currently-known fossil record, the human line diverged from the chimpanzee line between 6 and 8 million years ago [7].
How is this major discrepancy between population genetics and the fossil record to be reconciled?
References
[1] Chimpanzee Sequencing and Analysis Consortium. Initial sequence of the chimpanzee genome and comparison with the human genome. Nature 437, 69–87 (2005)
[2] Harris, E. E. Non-adaptive processes in primate and human evolution. Am. J. Phys. Anthropol. 143 (Suppl. 51), 13–45 (2010)
[3] Vallender, E. J., Mekel-Bobrov, N. & Lahn, B. T. Genetic basis of human brain evolution. Trends Neurosci. 31, 637–644 (2008)
[4] Lanfear et al, Population size and the rate of evolution.  Trends in Ecology & Evolution, January 2014, Vol. 29, No. 1, Pages 33-42
[5] Kong, A. et al. Rate of de novo mutations and the importance of father’s age to disease risk. Nature 488, 471–475 (2012)
[6] Walker, R. et al. Growth rates and life histories in twenty-two small-scale societies. Am. J. Hum. Biol. 18, 295–311 (2006)
[7] Levin, N. Annual Review of Earth and Planetary Sciences, 43: 405-429 (2015)

I mean 10 raised to the 8th power.

Oh ok.... you can replace 108 by $10^8$ and 10-8 by $10^{-8}$ for a much better formatting (don't forget the dollar signs). Just use the edit button to edit that.

HTML markup is much easier to remember — 108 for 10 to the power 8 (won't show in a comment). Use  for subscripts. And that's what is being rendered by your browser.

Good literature work here and good question +1! In short, your main mistake was that you based your calculations on a single site and not on the whole genome. More info below.
Genome-wide vs sites specific mutation rate
The statistic of $10^8$ generations that you computed is the average rate of fixation of new neutral mutations per site. As considered the genome-wide statistic between humans and chimpanzee, you have to scale your predictions up to the entire genome. There are about $3 \cdot 10^{9}$ nucleotides in either the human of the chimp genome. That would result in a genome-wide mutation rate of $U ≈ 2 * 10^9 \cdot 10^{-8} = 20$  (the two is because mammals are diploids). Hence, the rate of fixation of 0.05 generation.
So, the expected time it would take for $30 \cdot 10^6$ new mutations to fix would be $30 \cdot 10^6 \cdot 0.05 = 15 \cdot 10^5$ generations. Because, such mutation can happen in either lineage (humans or chimps), we have to divide this number of 2 leading to $7.5 \cdot 10^5$. With a generation time of 20 years, that would take $1.5 \cdot 10^7$ years or 15 million years.
15 million years? Why not 6-8 million years as expected from fossil records?
Most of the discrepancy is probably due to vague approximation made in the computation. For example, you assumed a mutation rate of $10^{-8}$ while in reality, the average mutation rate is rather twice as large (Nachman et al., 2000, Kong et al., 2012, Wang et al., 2012, Rahbari et al. 2016).
Doubling this mutation rate would divide by 2 our expectation of 15 million years leading to an expectation of 7.5 million years that perfectly match the fossil records!
There is however another source that may cause an overestimation of the time needed... You assumed the absence of incomplete lineage sorting or in similar words, you assumed that the standing genetic variance in the ancestral population negligibly affected divergence among the two lineages. However, these discussions are for another time!

And you are assuming that the mutation rates stay stable over that many generations, which they probably don't.

@Nicolai I am not sure how fast the mutation rate evolves but to the level of approximation used here and given that we're dealing with genome-wide averages only, my intuition is that such an assumption is rather negligible.

You  have to half your estimated time because chimps have been evolving for that same amount of time not just humans. You are measuring two separate descendant lineages ,not comparing humans to their ancestor. Generations are also shorter for chimps, and presumably our distant ancestors.

@John I already did. Check out the sentence Because, such mutation can happen in either lineage, we have to divide this number of 2 leading to [..] I have now clarified what I meant by "either lineage".

@Remi.b, I see, I assumed you were referring to the incorrect mutation rate, Thanks for the clarification.

The correction for the OP's biased estimate of the mutation rate is in the last section (15 million years? Why not 6-8 million years as expected from fossil records?)

@lenantak Did the answer answered your question? Please let us know if not. If you think it did, you can click on the checkmark next to the answer.

20 years seems rather too long a generation time for both humans and chimps.

@jamesqf From OECD.org, In most OECD countries, the average age at which women give birth now stands at 30 or above [..]. I don't mean to claim that OECD countries are representative of all countries, and certainly not representative of our ancestors. Chimps only mature at about 15 years of age and then have only one child every 5 or 6 years. So, using 20 years felt like not too an awful choice but please, if you can come up with some references, I'd happily change this 20 to someone more accurate.


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Isolating a specific gene (specifically TRAV* series of genes) for sequencing
I'm trying to figure out (for pedagogical purposes) the right way to isolate and PCR the regions coding the T-Cell receptor.
My understanding is that I would need to use restriction enzymes that target regions near the start and end of the gene. I was looking at a bunch of different restriction enzymes on this site: https://www.addgene.org/mol-bio-reference/restriction-enzymes/
What I'm not sure about is: how do you pick the combination that will specifically cut out that gene and not any of the other ones? It seems like the restriction enzymes only consist of a few base pairs, and I would guess they can slice at many many sites.
Furthermore once it is cut, how do I isolate just the DNA for the gene I want to sequence as opposed to the rest of the junk DNA?

Restriction enzymes are usually only used when you do molecular cloning using plasmids or other forms of shorter DNA moleclues, since - like you said - using them on genomic DNA would cut it into much more than thousands of pieces.
Instead what you can do is perform your PCR directly on the genomic DNA (or potentially cDNA, if you want to get rid of introns).
Doing PCR on genomic DNA is often a bit tricky (i.e. you'll likely have to try different conditions to get a product), but generally possible. If you want to analyse the whole coding region it might be better to extract mRNA instead of DNA and reverse transcribe it, so that can amplify the coding region as one block, that doesn't contain Introns - PCR on cDNA is also easier than on genomic DNA.
Another thing you need to look out for is that T-Cell-Receptors (similar to antibodies) are different in every T-Cell. This means that you can't use Sanger sequencing, which will only give you a proper result if you input has the exact same sequence. To get the sequences of a mix of T-cells you would need to use next-gen sequencing.


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Why do I have super vision in purely red light?
I installed some RGBW led strips in my apartment recently.. by some I mean everything is now lit by led strips and there isn't a single light bulb left.
One thing I've noticed over the last few days is that my eyesight is significantly sharper in pure red light. Historically I've had pretty good sight but reaching 30's I've developed some nearsightedness. I don't wear glasses since I can still see things up to ~2m from me as clear as ever but reading street signs now requires me to get closer and stuff like that.
Things that require me to squint and really try hard in daylight (or white light emitted by the led's) are really easy to look at in red light. My vision is worse in blue light and worst in green light. Is there any kind of common explanation for this?


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Can you convert smells to variables?
Is there a way to map smells to numerical values of different variables?
I.e. With RGB colours, each colour is made up of numerical values from 0-255. For example, red is (255,0,0), and yellow is (255,255,0). Is there a way to do this with smells. I.e, the smell of Candy is (140,70,255), and the smell of grass is (255,34,27)? How many different sets of numbers (like red, green and blue) would you need, and what would they represent?

Given that the human genome has genes for about 700-800 different smell receptors (very ballpark from the top of my head), you'd probably need around that many numbers to encode smells into numbers


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How did craniates evolve?
Looking at most chordate phylogenetic trees, it seems that we usually have something like this:
  ,================= Lancelets
 =| ,=============== Tunicates
  \_|
    \_______________ Craniates

So, my question is, what do we think the common ancestor of tunicates and craniates looked like? Did both clades evolve from a lancelet-like ancestor, with the tunicates becoming sessile after the divergence, or are craniates descended from a tunicate-like ancestor?


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Want reference for a convention
This answer to another question satisfactorily answer one of my major confusion.

The convention is that in indicating any sequence feature† in a protein-coding gene on double-stranded DNA, a single strand‡ is represented — the one from which the amino sequence could be read using the genetic code (conceptually, with T substituted for U). Like any other nucleic acid sequence§, it is always written in the 5ʹ to 3ʹ direction in the same manner as the mRNA transcribed from it, without this being explicitly stated.

But I have another related (and overlapping question): (I'm still looking for); is whether there is a standard and universal documentation for this particular convention (IUPAC/ IUBMB/ ICBN/ ICZN/ anything such); because "conventions" are human-made rules, and particularly in field of science (where nucleic acid research is a comparatively new and institution-based (not-folk or not-colloquial) study; without "declared, universally followed, and accessible" documentation; the conventions does not make a sense. It rather feels like a rumor or viral phenomenon. I visited the IUPAC and IUBMB website home pages but I could not locate the documentation from there. Also google keyword search did not found the helpful.
So I specify my question that I want to get the standard/ official source of this convention. I would be highly grateful if anyone kindly mention the source hyperlink.
N.B. This question is follow-up of a closed duplicate question,

Actually the word convention can also mean "A way in which something is usually done" and can exist without authority or formal agreement. While this is less common in science than in, say, language, I suspect that it is the case here. I'll be interested to see if you get what you are looking for.

Surely; if I get a document from any other source I'll post it here. Btw, unwritten conventions in science and maths are those from prehistoric to medieval past. But nucleic acid research is comparatively newer and institutional (not of a "folk" like). So I felt it weird when a source for such a complicated yet important convention is obscure.


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Does an old growth forest ecosystem produce more oxygen than it consumes?
I would like to consider an old growth forest ecosystem such as a large part of the Amazonian forest. It is common to refer to such beautiful forests as a source of oxygen for the world. For example, the expression Amazon: Lungs of the planet is very common (e.g. this BBC article). I would like to question such an expression.
Questions
My questions are:

Does an old growth forest ecosystem produce more oxygen than it consumes?
Does an old growth forest ecosystem fix more CO$_2$ than it produces?

My Intuition
I understand that such a forest can be an important carbon storage and that if we were to cut the forest down, burn the wood and pour concrete on the soil (to prevent regrowth), then we would definitely release a fair amount of carbon in the atmosphere.
That being said, I am wondering whether, as of today, these forests act as carbon sink or not. It feels to me that while trees accumulate carbon and produce oxygen while growing, this carbon is released when they die and in an old growth forest a tree must die for a new tree to grow. If carbon is being fixed, then it has to go somewhere and I think it is almost by the definition of an old growth forest that there is no more room for more carbon accumulation (competition among trees prevent it). So I would tend to think that calling the Amazonian forest the "lungs of Earth" is very misleading.
Some random WWF article
This WWF article seem to suggest that, contrary to my intuition, the answer to these two questions should be "yes".

great question......

I was referring to your question whether a forest is a carbon sink, I could not see how it was related to the metaphor of forests as lungs. But I’m afraid my comment was not well-thought or funny, I’ll remove it

Does an old growth forest ecosystem fix more CO2 than it produces?

The intergovernmental panel on climate change summarizes some of the data on carbon flux here. For the amazon similar tropical rain forests, it says:

Measurements in pristine, seasonal tropical rain forests in Amazonia indicate NEP of approximately 1.0 t C ha-1 yr-1 (Grace et al., 1995a,b) and approximately 2.0 and 5.9 t C ha-1 yr-1 for dense, moist rain forest (Fan et al., 1990; Malhi et al., 1998, 1999).

NEP is net ecosystem production, which, as I understand it, is essentially the total amount of carbon fixed by the ecosystem.
It seems the tropics, and the Amazon, in particular, are important global carbon sinks. This is also discussed in this more recent article in Nature.
This isn't my field, but as far as I understand it, forests are not closed or steady state systems. They do play a role as a sink in the global carbon cycle. I would assume net carbon fixation must come with increased biomass, so I may have just avoided a key part of your question. All the same, I think the point is that, again, even the amazon rain forest is not at steady state.
As far as oxygen is concerned, the report and article don't address it. I suspect this is because there is no documented problem with global oxygen depletion.

Thanks +1! For oxygen, I would assume that if 1 mol of carbon dioxide is getting fixed, then 1 mol of oxygen is getting freed as per the stochiometry of the photoynthesis and respiration equations. As one mol of carbon dioxide is about 22 times heavier than a mol of oxygen, 1 ton of carbon fixed should lead to the production of 22 tons of molecular oxygen. But I am not sure it is that easy.

@Remi.b I think it probably is that easy, but plants and forests aren't my field. I can pretty confidently say, though, that neither the change in $CO_2$ or $O_2$ are relevant in terms of a direct effect on human respiration on this planet. It's the greenhouse effect of the increase in $CO_2$ that makes this an important issue.


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Examples of points in evolution where two species stopped being interfertile?
Apologies in advance for not using the right terminology here; I'm not a biologist. This isn't for homework or anything; just curiosity.
I'm wondering: at what point do two divergent species stop being able to breed with one another, and what factors typically come into play to cause that change toward reproductive incompatibility?
I think the question above is maybe too broad, so instead I figured I'd ask for some examples of specific places in the evolutionary tree of life where this divergence occurred. I'm hoping this will give me some direction about where to start researching to find our how this typically happens in nature.
So:
Could you guys give me some examples of specific points in evolutionary history where a species was born which was suddenly unable to interbreed with its cousin species/grandparent species/etc?
Bonus points for answers with the following characteristics:

The incompatible species are very near one another in the evolutionary tree.
The species and its near-relative exist in common knowledge.
The reproductive differences between this species and its relative are significant and easy to understand.

I am not sure I understand. Can someone just name two random species (like pelican and oak tree) and it would count as a good example. Or two more closely related species (like tiger and lions) for it to be of greatest interest to you. Or maybe species that have partial reproductive isolation (such as many great tit species among them if I am not mistaken). Or maybe event of polyploidization leading to direct reproductive isolation? What exactly are you looking for?

@Remi.b Two random species technically works, but I'm specifically looking for the point of divergence; the first of two species with a common ancestor which cannot interbreed.

Are you looking for species that are currently undergoing increase in reproductive isolation?

Loosely related: Have we ever observed two drosophila lineages that evolved reproductive isolation in labs?. Also you might be interested in a discussion on the concept of species in the post How could humans have interbred with Neanderthals if we're a different species?.

@Remi.b Not only looking for current examples; both current and historical/theoretical are accepted. Thanks for the links, too! I'll check them out.

You might be interested in classical examples of adaptive radiation, incl. Darwin finches, cichlids and anoles.

I think one problem here is with defining a specific point.  E.g. horses and donkeys (and some other equines) can interbreed and produce offspring - mules - but the offspring aren't fertile.

@Remi.b Thanks for the link! I'll spend some time reading up on this.

Two obvious answers are genome doubling in plants, and Wolbachia-mediated infertility in insects. Both can cause one-generation speciation as measured by lack of interfertility.

Polyploidy, which arises through complex genetic and ecological processes, is an important mode of plant speciation. This review provides an overview of recent advances in understanding why plant polyploid species are so ubiquitous and diverse. We consider how the modern framework for understanding genetic mechanisms of speciation could be used to study allopolyploid speciation that occurs through hybrid genome doubling, that is, whole genome doubling of interspecific F1 hybrids by the union of male and female unreduced gametes.

--Genetic Mechanisms of Allopolyploid Speciation Through Hybrid Genome Doubling: Novel Insights from Wheat (Triticum and Aegilops) Studies

Bacteria of the genus Wolbachia are reproductive parasites of arthropods. They are cytoplasmically inherited (i.e. from mothers to daughters, like mitochondria) and their phenotypic effects on their hosts range from induction of parthenogenesis in certain hymenopteran groups, to feminization of genetic males in isopod crustaceans and to induction of cytoplasmic incompatibility in many insects  ... Three ways have been suggested4. The first suggestion is induction of parthenogenesis (assuming that the infection becomes fixed in the species). This process appears to occur in the hymenopteran Encarsia formosa7; males in this species can be obtained when mothers are treated with antibiotics, however, they are incapable of mating. The second way is offered by bidirectional incompatibility (Box 1). If a population is infected with two different strains of Wolbachia that are incompatible with each other, then bidirectional incompatibility will act as a post-zygotic reproductive barrier. A promising candidate is the species complex of the wasp genus Nasonia2, 3. The third way is offered by unidirectional incompatibility (Box 1). In this case, Wolbachia is acting as just one of the reproductive barriers enhancing speciation between two taxa.

--Wolbachia as a speciation agent
In general, though, the question seems to reflect a misunderstanding. Evolutionary theory doesn't suggest, let alone require, a sudden loss of interfertility during speciation. In many cases the lack of interfertility is incidental, and isn't selected; even in cases where it is selected, you expect to see the common gradual changes rather than abrupt transitions.


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When in Ampicillin degraded (gone) in liquid TB-media? Concerns about selectivity
Question: Specifically regarding Ampicillin; When growing cells in TB (terrific broth) for protein expression - when should I expect the ampicillin to be gone due to degradation by b-lactamases? (and how much Ampicillin do people add in addition to standard 100 ug/ml)
Background: I have heard rumours that all Ampicillin (100 ug/mL) is degraded within few hours (2-3) due to the enormous amount of b-lactamases secreted by the bacteria.I have also heard that some are not concerned about this, because 2-3 hours is anyway enough for the culture to outcompete anything else that will grow after the ampicillin is gone. On the other hand, some people are also writing that they add more ampicillin every 2-3 hours to maintain selectivity; however, I dont really see the point in maintaining selectivity as long as I have plenty of protein I will anyway lyse the cells and not use them for anything else.
My growth conditions: Grow at 37 degrees till OD600=1 (takes around 3h), then induce with IPTG and grow at 25 degrees for 18h, 200 rpm the entire time.
End comment: I know you can generally change to the more expensive carbenicillin which is degraded slower, but i'm more interested in knowing "how bad" Ampicillin really is for my general knowledge (and I will anyway keep on using it). Also: Any general thoughts or references to literature on this topic, specifically for Ampicillin is appreciated.

rather interesting question. Selection pressure is very important for any type of work. And it is true, amplicilin will degrade in media due to the secretion of beta-lactumase. This is a limitation that we must face, though there are ways of getting around this.
For example, when cloning, on a plate sometime you will notice "smaller" colonies growing around a central large one. This is due to beta-lactumases. They are not a problem if you are going to take the central colony and place it into fresh media with new amplicilin. They will simply die out. No harm done.
In liquid culture it is good to not "oversaturate the culture". Usually, do not let it get over OD600 = 1. In addition, do not use old stocks, as this causes problems with selection and use higher concentrations of ampicillin if you are still having troubles selecting!
Generally speaking, 100ug/ml is standard for most selection with cloning, and should be sufficient for what you are doing. It seems that your protocol should work fine for protein isolation.
Last remarks -- it is a problem that most microbiologist do not think of. Ampicillin has its limits!
https://www.addgene.org/mol-bio-reference/antibiotics/
https://bitesizebio.com/10188/whats-the-problem-with-ampicillin-selection/

Thanks, although this is all true - is there still an answers to how bad ampicillin is? Is it really gone from the media within 2-3 hours? Also: when using TB you really should not expressed before the OD600 reaches over 1, because IPTG will not be taken into the cell before the glycerol is used up (TB can theoretically support growth up to OD600=16)

Also, are you saying that the Ampicillin is likely gone after OD600=1?


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How do PrP mutations lead to prion disease?
My understanding is:
The PrP gene in human cells is expressed as both PrP-c (normal protein) and  PrP-sc (prion disease protein). This happens post transcriptionally, that is, the normal and the diseased protein are not distinguished based on genetic mutations, rather they are synthesized based on the same gene, but differ in their tertiary structures, which makes their functions also different.
If the amino acid sequence of both proteins is the same (same gene), then what determines whether the synthesized protein will take the disease-causing tertiary structure or the normal one? Is it due to post-translational modifications?
And finally (I apologize for advance for multiple questions): how do prions, which are void of nucleic acids (being proteins), integrate into the genome of a newly infected host by reverse translation, and become a familial disease?

If the amino acid sequence of both proteins is the same,
  what determines whether the synthesized protein will take the
  disease-causing tertiary structure or the normal one?

PrP-C and PrP-Sc do indeed have the same primary structure. However, they differ in secondary and tertiary structure. The protein can take more than one shape (conformation), where the likely conformation spaces taken by the protein are due to chemical and physical interactions. Many proteins can change their shape, often this is not well understood in detail. However, we know that the conformational space of some proteins allows for several, stable conformations of a single protein; the factors which stabilize it in a conformation or cause it to switch are difficult to understand in vivo.
PrP-Sc tends to accumulate in compact, protease-resistant aggregates. Circular dichroism shows that normal PrPC had 43% alpha helical and 3% beta sheet content, whereas PrPSc was only 30% alpha helix and 43% beta sheet. Although the exact 3D structure of PrPSc is not known, it has a higher proportion of β-sheet structure in place of the normal α-helix structure. The end of each fiber acts as a template onto which free protein molecules may attach, allowing the fiber to grow.
Prion proteins therefore propagate accumulation of more and more prion proteins.

Is it due to post-translational modifications?

No.

How do prions, which are void of nucleic acids,
  integrate into the genome of a newly infected host by reverse
  translation, and become a familial disease?

They do not enter the genome through reverse translation. The DNA sequence itself is mutated and the mutation drifts across generations for as long as it is being passed on through the germline.

In the first paragraph of your response, you said that “PrP-C and PrP-Sc do indeed have the same primary structure”, so how is it that you later say “the DNA sequence itself is mutated”? If they both result from the same gene, then shouldn’t something other than the “DNA sequence itself” be causing infection persistence through the gene line?

This paper here suggests that PrP-sc is physically passed on through cytoplasmic division of cells into daughter cells, so that the phenotype rather than the genotype is passed on, and if the phenotype is advantageous for survival, a mutation might incorporate it into the genome. https://www.omicsonline.org/open-access/revisiting-cricks-dogma-and-the-impossibility-of-reverse-translation-jtco.1000110.pdf

The protein is the infectious agent. The protein spreads through to new cells, causing the refolding of PrP-C. This does not occur in a DNA-dependent fashion. You are misusing the words phenotype and genotype, they do not refer to a protein/DNA dichotomy. Different protein isoforms can be made with a single gene. Mutations are not incorporated into genomes, they occur WITHIN genomes. Genomes are, colloquially speaking, records of mutations. Prion disease is a protein environment disease, it is not innately that prion proteins cause the disease (hence PrP-C, the healthy variant).


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Why don't macaws get selenium poisoning from brazil nuts
Google research has indicated macaws love or eat a lot of Brazil nut. These are highly toxic to humans in somewhat small quantities due to their selenium content.
Given the mass difference between a human and macaw, lets say 80kg and 2kg, if toxicity for humans 'starts' around 900micrograms or ~9 nuts, maths would indicate toxicity for a macaw might be around 20% of a nut?
These figures are all based on google and the margin of error I expect is quite large, nonetheless it seems quite disparate if a macaw could consume even a single nut a day on average, without consequence?

I know that macaws congregate around mud banks and eat mud (maybe clay?) I wonder if this might have something to do with it.

@KarlKjer Not according to this, though I don’t know how trustworthy it is.

this is good article but about amazona parrrots. The clay is really good call. But it detoxicate only quinidine by 60%.

Interesting question. You should consider, though, that the excretory system in birds is quite different from mammals. For example, they have two different types of nephrons. You've assumed the toxic dose is proportional to mass. It's not. You have to account for differences in kidney function, even in humans.

One explaination is that macaws (Ara sp.) eat clay and other food item which absorb the toxins. Here is the full answer from Wikipedia:

Like all macaws and most parrots seeds and fruit are the major part of the diet of the genus Ara. The particular species and range of diet varies from species to species. Unlike many birds macaws are seed predators not seed dispersers, and use their immensely strong beaks to open even the hardest shells. Their diet overlaps with that of some monkey species; in one study of green-winged macaws in Venezuela they shared many of the same trees as bearded sakis, although in some cases they ate the seeds at an earlier stage of ripeness than the sakis, when they contained more poison. Macaws, like other parrots, may consume clay to absorb toxic compounds produced by some poison...but with further research we now at last know it is just to eat life saving sodium that is missing. As well, the toxic compounds of some foods may be neutralized by compounds, such as tannins, found in other foods consumed at the same time...but we have found that it is untrue and really just to gain access to sodium missing otherwise in their diet because of the area they live in.

Source: Wikipedia - Ara (genus)

Your premise Is bad. Selen Is not ONLY toxin And  your answer actually doesnt answer thé question. However with that clay Is actually quite good call but i didnt find any information on selen but other chemicals such as quinidine.


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Are there chromosomes that we inherit that are not recombinated?
We do have chromosomes that recombinated ,but aren't there pure chromosomes that are not recombinated that people would have?

As you say people, I will assume you are talking about humans only.
Except for the small pseudo-autosomal regions (PAR1, PAR2), the Y-chromosome and the X-chromosome do not recombine together. This means that if you are a girl, then you have inherited a X chromosome from your father who did not recombine in your father (but might have recombined in your father's mother if that's where this chromosome come from). If you are a boy, then you have inherited a Y chromosome from your father who never recombines.
There is also mitochondrial DNA (mtDNA) that does not recombine but mtDNA is not organized into chromosome.

what can cause a y chromosome and x chromosome to recombine?

Y and X chromosome recombine at the pseudoautosomal regions. It seems that those regions exist to allow segregation of the two chromosomes during meiosis.

so why can't normal y chromosome recombine?

Do you mean "why can't the non PAR part of the Y recombine?"?


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What kind of owl does this moth look like?
I found this moth and I noticed that it looked like an owl to me and remembered something about how some moths camouflages look like predictors?  What kind of moth this is and what owl does this moth resemble? Would this moth be a newer species than other moths because it came after the owl? The wing span is 5.5 inches across. The eyes of the wing are transparent allowing light to pass through like reflecting eyes.

North American Great Horned Owl

First of all what a nice foto!
I think this is Antheraea polyphemus. According to Wikipedia, the moth has an average of 15 cm (6 in).

The purplish eyespots on hind wings give its name - from the Greek myth of the Cyclops Polyphemus.

And about the defence strategy it's quite interesting. As a green caterpillar, it is camouflaged by its color. However, if it's noticed then it starts to do pose like Sfinx to look less like a caterpillar, if it's still attacked by threat then it is started to make a clicking noise with its mandibles - sometimes as a prelude to or accompanied by defensive regurgitation of distasteful fluids.

When threatened, adult Polyphemus flip the front wings forward and also often flap the wings exposing the large hind wing eyespots - possibly to startle potential predators. The eyespots are possibly to protect an adult from Blue Jay.

The pattern on the hind wings of the polyphemus moth resembles that on the head of the great horned owl (Bubo virginianus).

I hope it is enough. I add that owl too.

I like it.....+`1


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Is there a correlation between B12 deficiency and cardiovascular disease?
I've read in several health sites that state that high blood homocysteine, as well as low B12 intake, is not only correlated, but actually causes cardiovascular diseases. In order to verify those claims, I've looked for related studies and found controversial results. This one, for example, observed no positive effects from B12 supplementation:

In this randomized double-blind trial, high-dose vitamin therapy had no effect on the outcome measures of stroke, CHD events, or death.

The author speculates several possibilities for the negative results, including that high homocysteine levels could be merely correlated, but not actually causing the problem.
I wonder if there have been advancements on that matter. Is it known whether low B12 causes cardiovascular diseases, or is merely correlated? If it is just a correlation, then what is causing both low B12, high homocysteine and increased cardiovascular disease? In particular, have any study observed if a diet rich in red meat, for example, has the positive effects that pure supplementation failed to show?

Low B12 intake cannot possibly be a fundamental cause of cardiovascular disease given what we can  read here and here. At most, one might postulate that B12 intake could influence the development of cardiovascular problems due to an unhealthy lifestyle.

Can you edit your post to include a link to the health sites that state low B12 intake causes cardiovascular disease? B12 deficiency causes hematologic and neurologic problems, not cardiac or vascular. Perhaps you're thinking of B1 (thiamine)?

Is it known whether low B12 causes cardiovascular diseases?

Yes, it is known. B12 deficiency does not directly cause cardiovascular disease, and I would be suspicious of any health site that says it does. B12 deficiency causes hematologic and neurologic problems.

Why is low B12 correlated with high homocysteine:

Low B12 is correlated with high homocysteine because it is a cofactor for the conversion of homocysteine to methionine by homocysteine methyl transferase. Low folate will do the same thing (cause an elevation in homocysteine).

These cofactors and metabolites are involved in methyl donor reactions that are particularly important in the production of blood cells and myelin. Strict nutritional B12 deficiency (reduced intake) often occurs along with other nutritional deficiencies.
The primary hematologic problem is anemia, with associated changes in the morphology of certain white blood cells. The anemia, if severe and prolonged can contribute to cardiac problems of other causes. You also see paresthesias (often symmetric), a shuffling gait, and other odd neurological problems including depression and psychosis.  B12 supplementation does not always reverse the neurological problems.
You can read about B12 deficiencies in Cecil medicine Chapter 225 and 167, Harrison's Chapter 74, and in this review.


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What is the big plant with white flowers on the photo?
What is the 3m tall plant with white flower? It is from Central Europe and there is a creek near to it. I have a guess, but I want to know for sure...

Is the small one the same species?

More high res photos here:

https://ibb.co/cAaUMU
https://ibb.co/ih4Zo9
https://ibb.co/eJSyFp
https://ibb.co/gstS89
https://ibb.co/kQ2OWU

Probably Angelica sylvestris. (No time to look more closely now)

The small one looks like Ground Elder (Aegopodium podagraria)... Were the leaves serrated?

@JulPal I think so. But they looked like the big plant, which was 2.5m tall...

The photos are high res, but out of focus and motion blurred so it is really hard to identify accurately.

They both look like poison hemlock (Conium maculatum).  It can grow up to 3m tall and grows in moist areas including along creekbeds. One of it's common names is European Hemlock.  It is toxic to some domestic animals and humans.

Source: United States Department of Agriculture

Source: http://natureid.blogspot.com/2011/11/poison-hemlock-111211-elkhorn-slough.html

According to wiki it can grow only 2m tall. I checked other photos, the flowers are smaller and not that dense. I thought first it is https://en.wikipedia.org/wiki/Heracleum_mantegazzianum but the leaves are different. It is in the https://en.wikipedia.org/wiki/Apiaceae family and I suspect I had phototoxicity from it on my leg, but I am not sure. It might be unrelated.

The closest I could find based on the leaves is Angelica atropurpurea . No idea what it does in Europe though, it should be in America. :D

I concur, not Conium maculatum the overall habit is completely different.  Also, if you just took these photos and are not at particularly high altitude C. maculatum should have finished blooming (it has finished at least a few weeks ago in the Central US).  C. maculatum has a distinct mousey smell which is hard to miss, and it very toxic to the point it should not be handled with bare hands.

@inf3rno if you had touched H. mantegazzianum, you would have known, trust me. I slightly touched it with the rear of my knees and after a couple of hours I couldn't bend them without almost screaming in pain. It is not a pain you cannot be sure of.

@inf3rno: Huh, according to the USDA it can grow to 3m tall - maybe that's just in the US.  I'm glad it wasn't Giant Hogweed (H. mantegazzianum).  I've never touched it as LinuxBlanket has but we were given a flyer at work earlier this year warning us about it

@LinuxBlanket Well then I was lucky with my plant. I had only rash and now 1 week after it some small red blisters. I used sunscreen on it, I am not sure whether it was phototoxicity or my skin was red because of other kind of toxicity. I am not even sure what I touched, I started to look for toxic plants only after I had the rash and I found this. I am pretty sure it is some kind of Angelica, but there are so many species... :-)

@Linuxblanket Reaction to H. mantaggazianum varies greatly between people and depends strongly on exposure to the sun.


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Animals as organ donors and organ's life expectancy
Recent attempts to find reliable organ donors was using genetically-engineered (GE) pigs as heart donors.
The pig's DNA is altered so that its tissues will appear identical to the patient's tissue and will not be attacked by the patient's immune system and rejected. A pig's heart is anatomically close enough to a human heart to fit to the task. All it takes is to make a GE and raise it until it is of the right age.
The issue is as follows: a human's life expectancy is much higher than that of a pig. If the patient is young enough, and the transplant succeeds, then the human will live far longer than the average pig. Will the heart hold-up throughout the lifetime of the human, or will the human need a new heart in say a decade or two?
EDIT: I have realized that actual attempts were so far limited to valves, and not entire hearts or other organs. Looking for an analogy in a human-to-human transplant, or animal-to-animal experiment, what would happen if the organ receiver is much younger than the donor itself? will the transplanted organ live the lifespan of the donor (its "original" lifespan), or will the transplant extend the life of the organ to that of the receiver?

We can't really answer such speculative questions here, please see the help. It's also encouraged to cite any supporting information when asking questions, though I don't think that will change the issue I pointed out.

http://time.com/5159889/why-pig-organs-could-be-the-future-of-transplants/  I have provided the supporting information in the link. I hoped the researchers did refer to that issue but find no reference to it. That was an attempt to understand whether all organs in the body age at the same rate or is aging related to some key factors which do not affect all organs equally.

@BryanKrause I have edited my question so that it relies on actually observed cases.

@BryanKrause there is a good deal of work on this subject. An answer can be made based on real data.

@DeNovo I think your answer is fine and will be helpful for the OP, but it doesn't directly answer the question asked which was about the life expectancy of a pig vs. human and how that impacts the lifespan of a xenotransplant, and about hearts, not valves. Allotransplants and mechanical valves also have limited lifespans.

@BryanKrause that's my point. Graft survival seems to be independent of the expected lifespan of a donor. It's about other issues.

@DeNovo For a valve. I think it's pretty unclear what the survival of a heart will be without speculation.

tl;dr
Graft survival, even with allotransplantation (human donor to a human host), is not equal to an average human lifespan. It's much shorter (11-16 years on average). Porcine grafts (which often last over 15 years) do not seem to be limited by the average pig lifespan (which, google tells me is 6-10 years). In both allo and xenotransplantation, graft failure and host survival are issues of the immune response to the graft, not of the expected lifespan of the donor.
Full answer:

Will the heart hold-up throughout the lifetime of the human, or will the human need a new heart in say a decade or two?

Lets answer this, first, for a heart transplanted from a human donor, an allograft. Even from a human donor, the heart is unlikely to hold up for a normal human lifetime. Heart transplant survival has improved greatly over the last five decades, but median survival in an adult is now 11 years. In pediatric patients, it's 16 years. The main problems are cardiac graft vasculopathy, malignancy, infection, and immune rejection. Transplant is a treatment, not a cure, and a major challenge of transplant as therapy is managing the immune response. Rejection and graft vasculopathy are (generally) related to immune injury of the transplanted organ. Malignancy and infection are related to immune suppression of the host.
Xenotransplant (transplantation from a non-human donor) adds an additional complication to the challenge of managing the immune response. Here, the range of non-self antigens is even greater, and the graft will be attacked by complement and other aspects of the innate immune system, as well as the adaptive immune system. This leads to graft destruction, often in the first hour after transplant. There have been advancements using transgenic pigs that solve some of these problems, with improvement in survival in pig to primate trials. Personally, I'm skeptical that CRISPR techniques will easily solve all of the problems of transplant immunology, but transgenic animals have moved things forward substantially over the last 15 or so years (see this review)
As far as porcine valves are concerned, they are treated to reduce their antigenicity (a protocol that hasn't worked for cardiac xenotransplants). Paradoxically, graft survival in older patients is quite good, with most valves lasting beyond 15 years. This may have something to do with age related decrease in immune function, but regardless, porcine tissue (at least from a valve), seems to hold up quite well.
There is good access to data on cardiac allotransplant survival (both adult and pediatric) directly from the international society for heart and lung transplant. There is a good review of pediatric transplants here. You can read more about cardiac graft vasculopathy here
As far as xenotransplantation is concerned, there was an excellent issue of the international journal of surgery, november 2015, that has a number of articles reviewing xenotransplant. Many are available without a paywall, and it's a good place to read up on this. This article from that issue discusses immunological challenges in xenotransplantation from pig to primate. You can read more about this here, but it's beyond a paywall. A good discussion of the overall history of xenotransplantation was reprinted in that issue, here


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can self-fertilization in flowers be called asexual reproduction?
Suppose a flower having both male and female reproductive parts is self-fertilized then can this be called asexual reproduction...?I'm quite confused cause in this case the fusion of male and female gametes do take place but again the gametes are from the same parent....please help.

I'd be interested in your reasoning why some common and known definition that seems to fit still doesn't. What makes you think "sexual" reproduction needs two, not one?

"... from the same parent"... that must stay the same and may not change, may not exchange genes while alife or staying the same... The fact that "mitosis" is not confined to diploid people I find confusing.   It is no trivial thing (to me) to "learn" that it just does not seem to make sense to duplicate some "haplo" in order to exchange genetic information that has got to be identical. Related answer pointing at proof reading as an underlying motif.  What's the sense of exchange if there is some identical copy that 's  being exchanged with.

According to this article from Berkeley, asexual reproduction is:

Any reproductive process that does not involve meiosis or syngamy

Using this definition of asexual reproduction and knowing self-fertilization involves meiosis and syngamy, it is not asexual.

Is there a strict definition of meiosis? If there were no crossing over or mingling  of genes that would still be meiosis? - So only diploids can have sex?


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Can you gain valid toxicological data about a detergent in cell cultures?
I just looked at a paper that in one assay tested a variety of chemicals and chemical mixtures against human cell cultures. They exposed HEK 293 cell cultures for 24 hours to the various chemicals.
One aspect I find dubious is that the chemical found to be the most toxic is a detergent. I only have negligible experience with cell culture experiments, but my assumption here would be that any kind of detergent would obviously disrupt the cell membrane and kill cells. And this kind of mechanism is not really transferable to actual humans, something that only disrupts cell membranes wouldn't be very effective against the entire organism.
How valid are toxicological experiments made in cell cultures with substances that are detergents or have similar effects? Does this make it impossible to draw any conclusions about toxicity as I suspect? Or can you still gain valid toxicological data about this kind of chemical from cell culture experiments?

I'm intentionally not linking to the specific paper as I want to focus on the general question, and I suspect this would side-track the discussion.


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Learning tensors for evolutionary or developmental biology
I'm looking for book recommendations on tensor algebra for use in biology.
Tensors are being used increasingly in evolutionary biology and developmental biology, it seems.  For example, here is an example of an empirical study that makes use of tensors in its analysis of data: http://rspb.royalsocietypublishing.org/content/282/1819/20151119
There are lots of books on the mathematics of tensors, and many introductions online.  So far, what I have found is that either (a) the presentation is heavily oriented toward physics applications, or (b) the presentation begins from an abstract algebra (or category theory?) point of view.
I'm willing to work through physics-style or abstract algebra presentations of tensor concepts and methods, but I am wondering whether there are any textbooks or other introductions that someone would recommend for biological applications.
(I have read the brief appendix on tensors in Sean Rice's book Evolutionary Theory.  Although I've found his other mathematical appendices and most of the mathematics in the book accessible, the tensor material in the book is too brief for me--I need more.)

The field of tensor decompositons has been discovered in many fields simultaneously, each with their own notation. Many modern notation in fields like CS or STAT have originated from the work of Tamara Kolda
http://www.kolda.net/publication/koba09/
However, this is restricted to the CP and Tucker decomposition, and we have many others now. See
https://arxiv.org/pdf/1609.00893.pdf
and
https://arxiv.org/abs/1708.09165


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Is the number of protons in the mitochondrion sufficient for ATP synthesis?
If the proton concentration in the mitochondrial matrix (based on its pH) is multiplied by its volume, the total number of protons in somewhere in between 2 and 8.

My question is whether this is sufficient for ATP synthesis, if 2–3
  hydrogen ions are required for each molecule of ATP synthesized.

My calculation is as follows:
pH = –log[H+]
The pH of the mitochondrial matrix is ca. 8. Thus, [H+] = 10-8 M (moles per litre).
If the mitochondrial volume is 0.2 μm3 this is equivalent to 2x10-10 μl = 2x10-16 litre
Using Avagadro’s number as 6x1023 it follows that:
Total number of protons in the matrix of a mitochondrion = 10-8 x 2x10-16 x 6x1023
= 1.2 (although other figures may give a value as high as 8).
If a pH of 6.8 is considered for the inter-membrane space along with a 0.1 fl volume, the number is 6.7 protons.
I found a paper where the question is adressed. First, the definition of pH at very low volumes is challenged, along with its measuring techniques. Second, it proposes novel mechanisms for proton availability in such situations.
(http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0045832)

Can you please explain how you got to the numbers 2 and 8? For the moment, the question is unclear as we have no idea what calculation you've made and what you misunderstanding is. Also, the number of protons in a piece of matter is not the same thing as the number of free protons.

The calculation is as follows: pH=-log [H+], in mitochondrial matrix around 8. Thus,  [H+] =10(-8) M. If a mitochondrial volume of 0.2 um3 is considered (as it has been reported), Then: 10(-8) M2.1x10(-16)L6.022x10(23), gives a total of 1.26 H+, for example. Similar numbers can be obtained when other reported mitochondrial matrix volumes are used in the calculation.

You should edit your post to include that calculation. While you're at it, try rewording it so that it's a clear question, instead of just a statement. It's an interesting point, though

This is a chemistry question. Not really a biology question. I think Chemistry.SE would be a better fit for your question.

@Remi.b I'm guessing the chemists would say it's a biology question, since it's about mitochondria. But, again, it needs to be a question before we can say for sure what it's about :)

I don´t know how to edit the post. The question would be: how is it possible that  the stoichiometry for ATP synthesis is 2-3 H+:ATP, when there are around 2-8 total H+ in the mitochondrial matrix?

There is an edit link at the bottom of the post. If you edit it with that info, I think it will be a good, answerable question. If nobody else answers it by the time I get home, I'll answer it.

@Mithoron, If you refer to the conversion between um3 and L, I believe that 1 um3 is 1x10(-15) L (dm3), 1x10(-12) ml (cm3), and 1x10(-9) ul (mm3)

OK, then it's at least not a matter of miscalculation, but still it's just about water and pH, so still general chemistry. More to the point, you could easily pick a small enough part of any highly diluted solution, where there would be no H3O+ at all, but statistically there would be probability of finding of H3O+ in a different moment directly related to pH. As far as your synthesis goes, there are a lot of more or less acidic protons in there, just waiting to be used.

I find "a lot" hard to calculate or discuss. Could you help me? Have you got any idea of how can I calculate such probability? I´m sorry if the question didn´t match the forum spectations. Still, I think that mitochondrial function IS a biological question, even though in this case involves some chemestry bases.

I have edited the question so that it is clearer. It should also make the unexpressed assumptions — addressed in my answer — more obvious. If I have changed your meaning, do say so, but try to keep things clear.

@David, thanks a lot. I added the numbers for inter-membrane calculation, and the reference to the paper I mentioned.

The question, as amended, can be summarized as:

If there are 2–8 protons in the mitochondrial matrix (as calculated
  from a pH of 8) is this sufficient for ATP synthesis, if 2–3 hydrogen
  ions are required for each molecule of ATP synthesized?

The initial deficiency in the argument was that it did not consider the inter-membrane space, and my answer was:

According to the generally accepted Mitchell Hypothesis, the generation of ATP in the
mitochondrion is due to an electrochemical gradient between the
mitochondrial matrix and the inter-membrane space.
This gradient is predominantly a pH gradient — the [H+] is
higher in the inter-membrane space than in the matrix
The flow of protons down this gradient is responsible for the
production of ATP.
The H+ gradient is maintained by protons being pumped across the inner mitochondrial membrane by the flow of electrons through the electron transport chain. (i.e. The H+ concentration is kept low in the matrix and high in the inter-membrane space, even though protons are continually flowing into the matrix.

i.e. For ATP synthesis to occur there is no requirement for a high steady-state concentration of hydrogen ions in the mitochondrial matrix — quite the opposite (as is reflected by the pH 8). A relatively high concentration of hydrogen ions is only required in the inter-membrane space — as is indeed found.
The amended question assumes a pH of 6.8 for the inter-membrane space, and calculates 8.9 protons to be in this compartment.
The poster still does not state specifically what the problem is — there is still a concentration gradient of hydrogen ions, and a vast body of experimental evidence shows that it is this gradient of hydrogen ions that drives ATP synthesis.
So the implied question does not seem specific to ATP generation, but to the concept of pH in cellular compartments of small volume. There is obviously something wrong here, and the paper quoted — which addresses this question — suggests some possible explanations:

That the pH measured is incorrect because of the methodology
That the hydrogen ions are not free but associated with negatively charged species (possibly phosphate ions) from which they may be released, as required.

The latter point had occurred to me before reading the paper. In summary:

The steady-state hydrogen ion concentration gradient is sufficient to drive ATP synthesis, with many hydrogen ions at any time passing through the membrane in one direction or another.
Many of the hydrogen ions in both compartments will be buffered in a manner that allows there release
The naive calculation is likely to be an underestimate because the pH in the inter-membrane space may be much lower.

If I were an ox-phos person I would know how many molecules of the ATP synthase complex there are per mitochondrion and the number of protons pumped into the membrane space per unit time. Such information would, presumably, bear on the problem.

Thank you for clarifying the question. Electrochemical gradient, as you mentioned it, relies on the CONCENTRATION gradient. The formula du=RTln(C1/C2)+zFdV, allows you to know if the transport is energetically favorable.and gives you a number for that energy change. The actual pumping however relies on the quantity, not on concentration. It is true that protons are pumped frome the inter-membrane space to the matrix, and that the concentration is higher there (about an order of magnitude).

My guess is that the volume of the intermembrane space will be smaller as well. But I will search the number to give you an actual quantity, to avoid subjective definitions, such as "small".

I´ve just find a paper that adresses this question, I leave it here in case anyone is interested:The Final Frontier of pH and the Undiscovered Country
Beyond
Wojciech Bal1
*, Ewa Kurowska1
, Wolfgang Maret2
1 Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Warsaw, Poland, 2 King’s College London, Diabetes and Nutritional Sciences Division, London,
United Kingdom

@RosaliaMoretta — Your enthusiasm for a numerical approach to biology is admirable, but it is perhaps expressed in a manner other than expected on this list. As a poster your first obligation is to express your problem clearly. Your question still has an (unhelpful) title that appears at odds with your question, which is still not clearly explained. I will edit it slightly, but you need to correct the focus on the matrix alone, and present information on the pH of the intermembrane space. If the paper you mention is relevant you should summarize it and provide a journal reference.

@RosaliaMoretta I enjoyed your question, and this answer is excellent. Since you're new, let me point out what you should do when someone answers. Choose the best answer by clicking the little gray checkmark next to it (which turns it green). You should also upvote any useful answer when you have the upvote privilege. This answer should get both (an upvote and a checkmark).

I'm also surprised i was the only one to upvote the question... It's useful and quite clever

In view of the amendment to the question I have amended my answer, shortening the initial answer and adding to it in the light of the reference cited. I think @DeNovo for explaining the acceptance system, but suggest the poster should not be pressed to accept an answer she may not find satisfactory. I never taught or conducted research in the oxidative phosphorylation area, and am aware that there are people better placed to answer this question. But they are not on this list and it is August.


text:
Skeletal muscle has got many many peripheral nuclei. What does "peripheral" mean here?

Cardiac muscle has got a central nucleus similar to smooth muscle, but skeletal muscle you may recall has got many many peripheral nuclei.

What does "peripheral" mean here?

Maybe you can add the source of the citation to have a clearer context

@havefun More info added

Skeletal muscle nucleui are peripheral located because they have a large muscle tone compared to the cardiac and smooth muscles.

'Peripheral' in this context refers to the position of the nuclei within the skeletal muscle cell.  They are in the periphery (outer part) of the cell body rather than central as in most cell types.  More specifically, they are "subsarcolemmal", i.e. just under the sarcolemma, the cell membrane of the muscle fiber cell (source):

(Image from Wikipedia)
The many nuclei of a skeletal muscle cell are spaced out along the length of the cell (source 1, source 2).


text:
About Frameshift Mutation
I am coding a DNA translater, based on the homosapiens genome, & i knowing that the data provided from NCBI is surely not 100% precise (there may be some base changes / removes etc...)
, & i want to prevent/bypass those mistakes to get a 'close' list of the REAL chain of proteins produced, so i was wondering how the frameshift do not change an entire species, taking into consideration that if 1 or 2 bases are removed , => then all the dna/rna translation will be modified therefore => ALL proteins will change & even the start/stop codons will change its location
(am not a biologist, am asking why the frameshift doesnt do that & create a new species from 1 or 2 base changes??)

It does change the location of start/stop codons, but they still remain the start/stop codons

Genes (here defined as protein coding sequences) are not perfectly aligned the ones after the others in the genome. In fact, in humans (like in most eukaryotes), only a small fraction (of the order of the percent) of the genome directly code for proteins.
Each gene translation unit starts with specific markers. Not even talking about what will be or won't be transcribed, a translation unit starts with the start codon (AUG). Hence, a frameshift mutation will only affect the gene in which (or even, only the exon) in which the mutation happened.
For writing a software that finds coding sequences (and translate them), you will need to learn much more about genetics. You might want to have a look at an intro course on molecular genetics / central dogma / translation, transcription such as a number of the biology classes on Khan Academy for examples.


text:
What type of wasp is this?
I've been trying to match this wasp to photos, but it seems like every species has something that doesn't quite match up. I killed it in my home in Indiana, USA. My best guess is a Northern Paper Wasp (Polistes fuscatus). Does that seem right? I read they can sometimes be dark in color like this one.

It is hard to tell from the image, but using this species key for Polistes wasps, it is reasonable to conclude that your wasp is either P. metricus or P. fuscatus.
If you look at this image of a P. metricus female, you can see the dull reddish markings on the abdomen:

On your image, you can see the same markings on the abdomen, at a different angle:

Based on these markings, your wasp is most likely Polistes metricus. You can read more about this insect here and here.
Here is a link to the image I modified.


text:
Can a plasmid cause cancer?
Can a plasmid cause cancer?
According to wikipedia, plasmids are normally present in bacteria

They (plasmids) are normally present in bacteria , and sometimes in eukaryotic organisms such as yeast [(my translation)]

Let's say we inject yeast (by digestive tract) into a H. Sapiens (we will be focused in the yeast's plasmid only). Is it possible for plasmids to get into eukaryotic cells presents in the digestive tract?

Is it possible for plasmids to get into eukaryotic cells presents in the digestive tract? is a completely different question

Canonically, bacterial plasmids will not replicate in eukaryotic systems, due to a lack of the necessary control (regulatory) elements which will lead to expression.
It is possible though to construct shuttle vectors that can propagate in prokaryotes and eukaryotic cells (e.g. yeast or mammalian cells like the immortal HeLa cervical cancer-derived cell line).
What you are specifically asking is whether horizontal (lateral) gene transfer between prokaryotes and eukaryotes occurs, and whether it has an effect on the eukaryotic cell. This 2016 paper is an excellent and recent article discussing this question.

Can a plasmid cause cancer?

It has never been demonstrated, to my knowledge.

Is it possible for plasmids to get into eukaryotic cells presents in
  the digestive tract?

Very few bacteria can penetrate a healthy intestinal lining. However, in many  disorders of the gastrointestinal system, such as in inflammatory bowel disorders, the intestinal lining is compromised, which certainly allows the passage of prokaryotes and/or DNA into human circulation. However, a functional transfer of plasmids from prokaryotes to eukaryotic cells is not demonstrated. Whether the hypothetical transfer would lead to carcinogenesis is also not demonstrated.

A wide variety of intestinal bacteria leave their compartment and cause disease at other sites. This happens all the time.  Often enough that there is at least one patient in your local hospital for exactly this reason right now :)

I want to understand what you mean, the comment is unclear in intent. Gut microbes cause disease all over the body, but can they cross a healthy intestinal lining and the gut-blood barrier? And can you give an example of a disease 'at other sites' caused specifically by gut microbe infiltration, so we are on the same page? Gastroenterology is a very rich field and it's not my strongest point and the specifics are, well, quite specific. Cheers!

The intent of the comment is to correct an error in your answer. Pathogenic enterobacteriaceae often penetrate the intestinal lining. This is a common cause of sepsis, endocarditis, meningitis, and a rare cause of pneumonia (pneumonia that cultures positive for enterobacteriaceae is more often due to aspiration). Certain types of gastroenteritis are caused by invasive infection as well. Your gut is a good barrier most of the time, but gut and mouth bugs often get through. Sometimes the result is transient bacteremia. Sometimes it is disease.

I stand by the statement that very few bacteria penetrate healthy intestinal lining. Perhaps I should have mentioned it is known that even in healthy individuals, there exist small amounts of viable bacteria in the urine and in healthy blood, even though, in medical circles, both are typically referred to as sterile environments. And, as you say, if any lining is compromised, bacteria and other microbes will certainly access circulation.

the statement you're standing by is unsourced and disagrees with my medical and infectious disease specialist training, my clinical experience, and basic textbooks on medical microbiology, internal medicine, and infectious disease.

Look, you wrote an otherwise good answer with an error in it. I'm trying to help you make it a better answer. :)

Clearly we are talking about different things. Help me understand: you're talking about special, medical cases in which bacteria pass from the lumen into the body. I don't doubt that. And I'm talking about the general case, where a healthy intestinal epithelium is, albeit a rich bacterial niche, an entry barrier for organisms even as small as bacteria. From Medical Microbiology, ch. 95: Microbiology of the Gastrointestinal Tract: Once the mucosal barrier is breached, bacteria penetrate through the intestinal wall into the normally sterile peritoneal cavity and its surrounding structures."

Happy to help :) You are correct. A healthy intestinal epithelium is an entry barrier for pathogens. The thing to remember, though, is that, while normal physiology (barrier holds) is normal, pathological processes are common. That barrier is violated in every living human. Sterile compartments are sterile, not just because of barriers, but because of active clearance mechanisms within the sterile compartment. Consider, for example, the neutropenic patient. One of the most common complications in these patients is gram negative bacteremia of enteric origin.

Bacteria get through. When they do, if we have enough WBCs, they clear them (among other mechanisms), which involves bacteria getting into eukaroytic cells. Your answer is good. Horizontal transfer of a plasmid from a prokaryote to a human would be an unexpected and exciting finding. The final point you try to make supporting that argument is just a little off because of a common misunderstanding (held by many very smart and accomplished people), which I expect you hold because you just haven't had the very specific education that would help you understand how often pathologic processes occur.

these are not special medical cases, they are common, everyday medical cases that have occurred in every living human :)

Very good! Upon review, my last sentence could be misinterpreted, or worse, could be misleading - I've adjusted it to clarify that it's not an in principle case but an in practice case of prokaryotes passing into human circulation. I hope it will be clear to anyone reading that prokaryotes are found in what is referred to as 'sterile' bodily fluids, and they become especially prominent and potentially problematic if barriers and/or clearance mechanisms are compromised. Glad we rounded it up and added a few supplementary points as an addendum for others to peruse. Cheers!

good edit. I'm still not going to upvote, though, because you still seem to misunderstand that this statement: Very few bacteria can penetrate a healthy intestinal lining is incorrect. A wide variety of bacteria can penetrate a healthy intestinal lining, and they do so in the absence of prior gastrointestinal disease. The blood compartment, for example, stays sterile because WBCs clear those bacteria. The physical barrier is only part of the mechanism. A sterile compartment stays sterile because of active clearance mechanisms.

Your rudimentary statements are correct. However, what you now (finally clearly) stated is absolutely far from being correct and has never been demonstrated. Provide sources if you make strong claims like A wide variety of bacteria can penetrate a healthy intestinal lining, and they do so in the absence of prior gastrointestinal disease. Some reasons below:

(i) only a very small fraction of total bacteria cross the lining even when the entire barrier is disrupted to an extreme extent. (ii) only a very small fraction of bacteria functionally equip hemolysins or other known toxins to lyse enterocytes or disrupt tight junctions, or affect their shape in order to penetrate the lining. (iii) even affected enterocytes purge their contents into the lumen (Chassaing et al. 2017) (iv) even inflamed gut linings, like in colitis, are permeable only to small molecules, and permit no access to bacteria.

(v) in the vast, vast majority of gastrointestinal issues (i.e. abnormal conditions) what is known and demonstrated to occur is the expulsion of water and other small molecules, activation of the nervous and endocrinological system but not the entry of bacteria. (vii) bacterial encroachment has not been observed nor documented in any person who is not disposed or immunocompromised. in fact, it is only observed in diseased people, and only in very limited parts of the digestive tract. My two cents: Very small fractions of very few types of bacteria rarely cross a normal gut lining.

I've been saying the same thing ever since my first comment. Many species of bacteria leave the GI compartment. I see this all the time in clinical practice. Certainly the dose is small, but it happens often. The gut is not a perfect barrier. Active clearance mechanisms are also needed in order to maintain sterile compartments. If you would like me to answer more thoroughly than I have in this long back and forth comment section, feel free to ask a question.

I see this all the time in clinical practice reveals bias, no? Unlike anecdotal medical practice, I'm sure you understand very well that biology, and also epidemiology, rely on experiment and statistics, and the very central concept of random sampling. This determines the healthy norm. By way of example: pulmonary embolisms are not the norm, they are extreme events, and no internist making the case that they happen to everyone if they live long enough should convince us that thrombogenesis is a frequently-occurring, healthy, normal occurrence in lung vasculature. Let's agree to disagree.

I seem to be failing to communicate the issue here, because you keep misunderstanding. For your analogy, sepsis would be the pulmonary embolism, bacteria escaping from the GI compartment and being cleared by the immune system would be clot formation. Clot formation happens often. Bacteria are often stopped by the immune system rather than the epithelial barrier. We know a barrier is not sufficient to prevent enteric bacteria from disseminating to other sites. I'm well aware of the importance of appropriate statistical methods. I teach those methods to residents and other physicians.

Your statement was in the context of an argument about bacteria somehow not being near eukaryotic cells on a population level. The relevant frequencies here are not the average or most common state of the GI tract. This is a pathophysiology question. Does this happen with a frequency that could cause disease? That's the question.

I agree with your conclusion (I don't believe plasmid transfer between prokaryotes and humans occurs), but your barrier argument doesn't make sense in this context exactly because this is already a well established mechanism for pathogenesis in infectious disease. Here, the identification of enteric pathogens in many body compartments in clinical practice is exactly the kind of data that counters the argument "bacteria can't do this because they don't cross the barrier". You do not need to establish, e.g., the prevalence of positive blood cultures in a healthy population.

In addition to understanding the importance and role of random sampling, if you want to progress in your field and do good work, you need to understand which class of data allows you to draw which conclusions and what kind of evidence supports, suggests, or opposes what kind of hypothesis.

Let us continue this discussion in chat.


text:
I am interested in Sociobiology. Which academic field should I study?
I like to study Sociobiology and evolutionary psychology. Which academic fields concentrate on these sciences in bachelor and master degrees?

I'm voting to close this question as off-topic because it is about career advice, not biology.

So to continue with what Remi B says, of course it is going to require quite a bit of chemistry for it all. Chemistry in sociobiology distinguished areas among each other, where even nuclear reading make a distinction for it all.

This could be reworded to be more oriented toward field of study/self education advice rather than career advice, It may be more acceptable then.

What fields are sociobiology and evolutionary psychology?
Sociobiology (aka. social evolution) is a subfield of evolutionary biology.
Evolutionary psychology is a subfield of both evolutionary biology and psychology. Evolutionary psychology is, for the moment, very theoretical without much (if any) empirical testing. For this reason, not only natural scientists
 and social scientists work on the subject but some philosophers have also contributed (such as Daniel Dennett for example).
How to become a researcher in one of these fields?
Biology.SE is not BiologyCareerAdvice.SE. We have way too few information about you to give reliable career advice anyway. Also, I am not trained in any way to give you carrer advice.
That being said, a priori, start with a Bachelor in Biology and follow up with a master in Evolutionary Biology. Because evolutionary psychology is very inter disciplinary, I would personally advice to go with whatever broad field of study attracts you most. If you are more into psychology than biology, please go with psychology. If you are more into philosophy than biology, then go into philosophy.
Short intro to evolutionary biology
For a very short intro course to evolutionary biology, you can have a look at evo101 by UC Berkeley.

Remi. Please discourage people looking for career advice on here.

@TheLastWord Yes, I think you're right. I added Biology.SE is not BiologyCareerAdvice.SE. We have way too few information about you to give any reliable career advice. Also, I am not trained in any way to give you carrer advice.


text:
I'm not sure, are there 46 or 92 DNA strands in each somatic cell. Whatever, how many, then these strands join together to make a 6 or 7 ft long DNA?
When a cell is not divided it has DNA in chromatin form. Usually it is written in books that DNA is 6 ft long. In each cell there are 46 chromosomes, so there are 46 or 92 DNA strands. When a cell is not divided, do all these strands join together to make a 6 ft long DNA strand?

no its total length, each chromosome is a separate strand

This is a science website. Please, keep it clean, keep it metric! 6.5 feet ≈ 200 cm.
The exact length is subject to quite a bit of variation from estimates to estimates, at least according to hypertext.com (non-peer reviewed). All estimates are in between 1.5 meters and 3 meters. Hypertext.com cite "Cell." The World Book Encyclopedia. Chicago: Field Enterprises, 1996

On the average, a single human chromosome consists of DNA molecule that is about 2 inches [(~5 cm)] long.

They deduce from it a total length of 230 cm which mean that they computed 5 * 23 * 2 = 230 cm.
This total length is hence computed from the diploid genome but counting only a single chromatid per chromosome. For a haploid genome, the length would be closer to 115 cm and for a diploid genome when counting the sister chromatids, the length would be about 460 cm.

I've have this doubt for the longest time about a chromosome being a monad or diad and when. DNA is always in the form of loose chromatin fibres at all times except during metaphase- when it is condensed onto chromosomes. If you were to condense these chromatic fibres into chromosomes, it would form monads with one sister chromatid only. While during metaphase they form dad's with 2 sister chromatids, twice the dose and thus twice the length of total DNA