text:
Hormonal terms Somatotrophin or somatotropin?
Are Somatotropin and Somatotrophin hormones the same? It's confusing because when you type in Somatotrophin in google, it says, "a growth hormone secreted by the anterior pituitary gland.", but there's no Wikipedia about it. But when you type in Somatotropin, there's whole Wikipedia for this stating that it's a growth hormone. I am 100 % sure that there is a difference between these two terms: tropin and trophin because Wikipedia itself says not to be confused with these terms and has articles separately for these two terms. So, Can anyone help me be clear about these two terms?

Yes
They are the same thing, and both are old-fashioned terms for what is now termed specifically growth hormone (i.e. not generically as in "a growth hormone"). It is clear from the Wikipedia entry for growth hormone that this is equivalent to somatotropin.
I could not find a specific scientific reference that states that the two are the same, but I present a line of reasoning based on a search for mention of the terms in books using the Google ngram.

The initial similarity in the curves in the left-hand frame reflects, I think the competing use of the terms when the hormone activity was first discovered. Eventually somatotropin won, although the use of growth hormone is much more common now (right-hand frame).
If you look at the books cited by the ngram in which somatotrophin is used, you will find that many are in the field of animal science, especially dairy science in relation to the lactogenic effect of the hormone. Years ago I worked in this area, and remember that growth hormone had such lactogenic effects.  Presumably somatotrophin stuck in this area, whereas somatotropin was more generally used, especially in human endocrinology.
General Dictionaries and possible reasons for variation
I am hesitant to quote non-scientific dictionaries on scientific topics, but in this case it is probably justified, and it also addresses the difference in meaning of ‘tropin’ and ‘trophin’, referred to in the question.
The Merriam-Webster online definition of somatotrophin redirects to:

somatotropin
  variants: or less commonly somatotrophin

Chambers on-line only has somatotrophin, But my own 1994 printed edition has:

somatotropin or somatotrophin a polypeptide growth hormone

My Chambers Dictionary iPhone app also has both.
And Saunders Comprehensive Veterinary Dictionary, 3rd ed. (2007), according to a citation in the Free Medical Dictionary, has:

somatotropin, somatotrophin
  growth hormone

If you check the meanings of the two suffixes in Merriam-Webster:

-trophic
  of, relating to, or characterized by (such) nutrition

Whereas

-tropic
  1 : turning, changing, or tending to turn or change in a (specified) manner or in response to a (specified) stimulus
  2 : attracted to or acting upon (something specified)

It seems probable, therefore, that the original form was somatotrophin, but, either by confusion with the second definition of -tropic or a North American chemical aversion to ‘ph’ (as in sulphur/sulfur), somatotropin became dominant, except in the field of animal science. Perhaps that is why the Oxford Dictionary, both online and in my printed edition of 1991, ignores somatotropin completely. However you would have difficulty ordering somatotrophin from the chemical supplier, Sigma-Aldrich/Merck, whereas somatotropin is available.


text:
B -Cell activation by helper T cell
When Dendritic cell travels to nearby lymph node with antigen presented on MHC II molecule, the helper T-cell residing there gets activated. But what happens to B- cell residing there? Does it get activated too when helper T-cell is activated and start producing antibodies for that specific antigen?

Naive T cells hang out in the lymph node waiting for antigen presenting cells (APCs) like DCs to present processed antigens on their MHC molecules. Naive B cells similarly hang out in the B cell zone and are capable of interacting with other T cells and follicular dendritic cells (FDCs). Antigen that ends up in the lymph ends up traveling to the lymph node, where B cells internalize, process and display them on MHC molecules. This is because B cells are also APCs.
Activated (and differentiated) T cells that were previously activated by DCs can identify some of these B cells clones through the TCR-MHC interaction. The B cells process the antigens like DCs, so the resulting heterogeneity of the processed peptides means a fair chance a T cell will recognize it. The result is that B cells receive an activating signal through the BCR and costimulatory receptors.
Differentiated T cells also secrete different profiles of cytokines. For example, Th1 cells secrete IL-12 and IFN-y whereas Th2 cells secrete IL-4, IL-5 and IL-13. Not exclusively, just predominantly or in greater amounts.
The receptor signaling in conjunction with certain cytokines can induce class switching to the resulting antibody production. This swaps the constant or Fc region of the antibody to a different isoform. So Naive B cells are IgM/IgD, and if the cells is receiving Th2 cytokine stimulation, class swtiching results in IgE antibodies, for example.
For elementary immunology I like to reference Cellular and Molecular Immunology, 8th ED. by Abbas et al., but 9th ED is out so keep that in mind. The field somewhat rapidly evolves.

There are a couple ways the adaptive immune system can be activated: Naive T cells require a co-stimulatory signal from professional antigen-presenting cells (Dendritic Cell); naive B cells require accessory signals that can come either from an armed helper T cell or, in some cases, directly from microbial antigens(NCBI, B-cell activation by armed helper T cells). So, within your question the helper T cell would activate naïve B cells through T cell-dependent activation. Though T cell-independent activation is possible (Wikipedia, B cell).
The activated B-cell would then begin producing antibodies while also undergoing clonal expansion to produce a foci of B cells that are specific for the antigen. Most of these clones differentiate into the plasma cells, also called effector B cells which produce a first wave of protective antibodies and help clear the infection, but a fraction persist as dormant memory cells that survive in the body on a long-term basis after having gone through a highly mutative and selective germinal center reaction (NCBI, Human memory B cells; Wikipedia, memory B cells).
Great visuals if you look at Google images "t dependent b cell activation".

So , Can the B-cell be activated to proliferate without phagocytosis of antigen and that antigen being presented on MHC II molecule on the surface of B-cell?

@ShawnDypx At this time I have to say no, antigen presentation is the only way that we know of that activate B-cells and they present the antigen on MHC II molecule on their surface to activate T-cells. Though we do know that interferon's can play a role with activation but they aren't what actually activate the B-cell (Keifer et. al, 2012).

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sort: votes


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How are Antibody and T-cell receptor different?
Since the helper T-cell bonds with specific antigen presented by dendritic cell and that same helper T-cell also activates B-cell by bonding with antigen presented by B-cell, it made me think that the antigens presented by both of them should be same.
If that specificity is true, then what's the difference between an antibody and T-cell receptor? Because both T-cell receptor and Antibody are specific to an antigen.

I'm not sure if this is a homework question, but either way it would help if you state why you need help answering these questions and what you have found so far.

Hi Shawn. You should try narrowing your question. You're asking about antigen presentation and about antibodies vs. T-cell receptors. These are both broad questions in and of themselves. I'm not sure how one would write a good answer to your question as it is currently phrased.

B cell receptors (BCR) work on a similar paradigm, but a different mechanism than the TCR completely, structure aside. When a B cell encounters an antigen that binds to it's BCR, the receptor-antigen complex is internalized where it's processed onto class-II MHC.

Source: UP Manila Lecture, Marilen Parungao (link)
The peptides have to be processed to ~22-residue fragments to load on MHC-II, and the whole antigen is thus fragmented on the extrinsic processing pathway. To be specific, one antigen becomes many different peptides on many different MHC-II on the same B cell. You can imagine this produces some diversity among peptides suitable that at least one Th cell with similar specificity might bind. Class switching and somatic hypermutation that the B cells undergo help them attain greater utility and specificity, and the membrane-bound BCR is alternatively processed so that the c-terminus domain traffics antibodies to be secreted (2).
On the other hand, the TCR is specific with a little wiggle room to a particular MHC-I or II loaded peptide, with the exception of yδ T cells which have been shown to be largely MHC-independent (3). The same situation follows, however, that your antigen presenting cell or APC has many different peptides of the same antigen loaded on MHC, just as cells expressing MHC-I might, which means that the T cells are also not recognizing the same exact peptide sequence. Since they originate from the same antigen, however, your cytotoxic and helper T cells can be specific for the same "target."

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"Blood circulation". Why blood bleeds in atmosphere ?
If our body's blood pressure is 120 mm-Hg then why blood goes out of our body in 760 mm -Hg pressure if we have cuts?

In your example the blood pressure is  actually 120 + 760 = 880 mm Hg. So , higher than atmospheric pressure.

That's actually the gauge pressure that we measure. Gauge pressure is the amount by which the pressure measured in a fluid exceeds that of the atmosphere. So, when we say that our blood pressure is 180mmhg, it's wrong. In reality, the blood pressure is (180+760)mmHg inside the blood vessel, and our blood pressure exceeds atmospheric pressure by 180mmhg.


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Do Noroviruses include many families?
Wikipedia says Caliciviridae Family.
My notes say that Norovirus includes the following
Noroviruses

Norwalk-like viruses
Caliciviruses
Astroviruses and some small gastroenteroviruses

which is a larger definition including at least two families than the Wikipedia definition.
I think

Caliciviruses $\subset$ Caliciviridae
Astroviruses and some small gastroenteroviruses $\subset$ astroviridae

so the note is taking subsets among different families and classifying them into abstract class called Noroviruses.
Extension based by Chris' excellent answer.
Criteria of Noroviruses

(+)sense ssRNA viruses
Structure and replication:

1) only (+)sense ssRNA,
2) simple nucleocapsid viruses,
3) only viruses transmitted by fecal-oral route,
4) size about 30 nm in diameter.

and then final classification of Noroviruses by these criteria
Noroviruses

Noroviruses $\subset$ Norwalk-like viruses ($\subset$ F. Caliciviruses)
Some Astroviruses ($\subset$ F. astroviridae) and some small gastroenteroviruses (what?)

which, however, does not make sense since Caliciviridae $\not\subset$ Astroviridae.
I do not understand what is the point of referring to the viruses by the sentence

Astroviruses and some other round/small gastroenteris viruses

which are not part of Astroviridae.
Which viruses of Caliciviridae are similar to Astroviruses that are apparently round and small gastroenteritis viruses?

I don't understand your new question. What do you mean with understand? What is the purpose of your work?

@Chris Thank you for your comment! I included the criteria of classification for Noroviruses.

You want to know how the Norovirus was selected taxonomically?

@Chris Yes, I think so. In above definition, noroviruses include some viruses from Caliciviruses, Astroviruses and some other small gastroenteroviruses.

Which doesn't make sense. Ciliciviruses include Noroviruses, but not Astroviruses. The only belong to the same group.

@Chris Thank you for your comment! I added the criticism to the body. I think the last point is trying to refer to some viruses in Caliciviridae that have some characteristics of Astroviruses that are small/round gastroenteris viruses.

You are mixing different things here: Virus are grouped based on their genetic material (dsDNA, ssDNA ssRNA and so on) into several groups (see here for details), then grouped into families, subgrouped into a genus and then into species.
So it is: Group > Family > Genus > Species.
What you have here are are different positions in this classification.
The names you mention belong all to the same tree:
Group: IV ((+)ssRNA-Viruses) > Family (Caliciviridae) > Genus (Norovirus) > Species (Norwalk Virus).
The Astrovirus belongs into the same group, but then form an own family.
To answer your question: No, since the Norovirus forms its own genus in the caliciviridae family.

Last sentence - do you mean genus (not family)?

Thank you, Chris, for your excellent answer! I have been completely confused by different naming systems that have been used. Besides those two systems, there seems to be also some conventions. I am trying to understand what is the initial point of making a abstract entity "Noroviruses" and including some viruses from different families into it.

I take NCBI's taxonomy any day over what wikipedia says. According to NCBI Caliciviridae includes Lagovirus, Nebovirus, Norovirus, Recovirus, Sapovirus, Vesivirus, Secalivirus, etc. For example:
Viruses; ssRNA viruses; ssRNA positive-strand viruses, no DNA stage; Caliciviridae; Norovirus; Norwalk virus; Chiba virus
Anyway, due to the absence of universal phylogenetic marker genes, viral taxonomy is mostly based on capsid shape and isn't thus very accurate..

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Is Sinus node conduction necessary for heart beating?
Assume a patient with previous cardial infaction which SA node not possible to activate action potential anymore.
However, SA trying to beat unsuccessfully repeatedly waisting energy.
Therefore, I thought in this discussion about the possibility to stop Sinus node from trying to start action potential; which was deleted but the article about the SSS (sick SA) and remodelling is about its goal. The proposed treatment (laser ablation) of AF/AFL can backfire and cause SN (Sick Node) through remodeling. Assume there is no bypass of impulses through SA node.

Can the heart still beat through AV node and bundle? Yes.
Do you have any evidence that [heart] can "beat" properly on just the AVN? Yes, see article. Short-term mechanisms where electrical/metabolic remodeling. Long-term mechanisms where irregular rhythms and complete heart block can occur because of anatomical remodeling.

I want to know if these pacemakers are in series or parallel.
If they are in series, then laser operation can be dangerous to the SA node.
The series connection is however the idea which I get from many schematic drawings:

Do you have any evidence that it can "beat" properly on just the AVN? Loss of the SA node almost always leads to irregular rhythms very quickly (and with relatively bad outlook).  Can you look up some complete heart block examples and see if that covers your question?

The SA node is not necessary for contraction of the heart.
The reason that this works is exactly what you mentioned: schematics.
They are in sequence, but within that sequence, there are multiple autonomous signal generators in the heart, where spontaneous depolarization occurs to initiate contraction: the SA node, the AV node, and the purkinje fibers.
The SA node fires the most rapidly, 60-90 times per minute - which is the average normal heartrate, because in most people the signal for contraction arises from the SA.
The AV node fires at 46-60 times per minute.  If it receives the signal from the SA node then it depolarizes in sequence like the normal sequence we learn.  But if there is no SA node signal received, the AV node will depolarize on its own.
The last "generator" are the perkinje fibers.  If there is no signal from previous nodes, they will spontaneously depolarize.  However, they depolarize VERY slowly, at a rate usually under 40 bpm.  This severe bradycardia is potentially life-threatening, but allows the heart to keep some circulation going if there is a sudden complete AV node block - but prompt treatment is critical.
Regarding the lack of necessity of the SA node:
In fact, in some cases of supraventricular tachycardia (for example IST, see here) that are not responsive to conservative treatment, they will actually ablate (surgically destroy) the SA node in order to slow the heartrate down because a persistently extremely high heart rate can be dangerous.
Good question!

Extension to Doctor Whom's clear answer.
Clearer problem

It is debated whether the pathophysiology of IST and POTS results from
  abnormal autonomic regulation or abnormal sinus node function.

Radiofrequency Catheter Modification of the Sinus Node for “Inappropriate” Sinus Tachycardia
Location modification: Superior aspect of the crista terminalis.
Benefits

presyncope can resolve with sotalol
palpitation can resolve with β-adrenergic blockers
some patients (about 1/3) did not require any medication after operation

and other highlights

superior vena cava syndrome and dual-chamber pacemaker with patient with earlier A-V ablation

Postural Tachycardia Syndrome and Inappropriate Sinus Tachycardia: Role of Autonomic Modulation and Sinus Node Automaticity
Ceteris paribus condition

have IHR condition (Intravenous propranolol and atropine were given to block the sympathetic and parasympathetic limbs)

Findings

Treatment of IST and POTS should focus on sympatholysis, reserving sinus node modification for patients with continued debilitating symptoms after beta‐blockade and possibly ivabradine.

It is open research topic how the SA node should be ablated (removed) and how much.
I did not find any meta-analysis about the issue.

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Is there sufficient evidence that human cells are not intelligent?
Being structurally composed of one or more cells, which are the basic units of life.
Yet within a cell, there seems to be the same behaviors that define life:

Regulation of the internal environment to maintain a constant state;
Organization: Don't most cells have organs?
Metabolism.
Growth ~ not sure about this one.
Adaption ~ Think this is accurate, but I'm not well versed in cellular biology at all.
Response to stimuli. Cells interact with external whatnots.
Reproduction - Cells do this, at least many of them.

Most of what lead me to this question came from chapter 5 of Spontaneous Healing by Andrew Weil, M.D.. I'll type the parts relevant to the discussion below - in case he's wrong and I'm basing my thoughts on wrong information. bold sections indicate my interjection

DNA takes the same form in all organisms, from human beings to viruses - an enormous molecule with a double-helix structure made up of two chains of sugar molecules, with "rungs" linking the two chains. The rungs form between complementary pairs of nitrogen-containing subunits 'nucelotides', whose specific sequences differentiate the DNA of one organism from that of another. Only four different nucelotides occur in DNA; they are the "letters" of a genetic code spelling out "words" of information that direct the construction and operation of all forms of life. The so-called Central Dogma of modern molecular biology states that DNA replicates itself in order to pass its genetic information on from one cell to another and from one generation to the next reproduction; DNA also transcribes its information into another macromelecule, RNA, that can travel out of the cell  nucleus; RNA, in turn, transslates this information into the manufacture of specific proteins that determine the structure and function of organisms. regulation? These three processes - the replication, transcription, and translation of genetic information - are the most basic processes of life. They are also amazingly intricate and risky, because there are so many points at which things can go wrong.

Snipped for relevance.

Therefore, sophisticated mechanisms have evolved for the repair of this molecule in order to assure nearly error-free transmission of genetic information from one generation to the next, even in the simplest forms of life. organization, regulation, reproduction - evidence of response to stimuli?
All of the mechanics of replication, transcription, and translation are directed by a special class of proteins called enzymes. A great deal of the genetic code specifies the manufacture of enzyme molecules, which, in turn, oversee the chemical reactions that develop the genetic code into biological reality. evidence of intelligence?

much snipping.

In practical terms, they (enzymes) function as ingenious machines that alter the substrate molecules: cutting them apart, putting them back together, snipping particular pieces off them, adding others back, all with astonishing precision and speed.

more snippage

Therefore, polymerase I actually proofreads its own work, editing mistakes as it directs the synthesis of new copies of DNA.

He goes on to talk about plasma membranes, which seem to be how cells interact with the "outside" world..

Is there a question somewhere in here?

Is there "sufficient" evidence that human beings are intelligent?

Hi!  You need to edit your question to make it more obvious as to what you actually want answered, then please flag it for reopening :)

something you would need to clarify is your definition of intelligence

You seem to be asking if single mammalian cells are capable of intelligence. Yet, in your introduction, you mention that within a cell there are these seven characteristics that are fundamental in defining life. Then, you target more of your supporting quotations and interjections toward the definition of life. Of course cells are alive. You are alive, and so are the bacteria on your skin. Your title question is:

Is there sufficient evidence that human cells are not intelligent?

You have strayed from your question in your line of reasoning. Let's get back to answering the title question.
Is there sufficient evidence that human cells are not intelligent? The definition of "intelligence" is controversial, but let's look at Wikipedia:

Intelligence has been defined in many different ways including, but not limited to, abstract thought, understanding, self-awareness, communication, reasoning, learning, having emotional knowledge, retaining, planning, and problem solving.

Human (or any mammalian, fungal or bacterial) cells are able to communicate, and solve problems, but most likely lack abstract thought, understanding, self-awareness, reasoning,  and emotion. Retaining and planning are somewhat more difficult.  Cells are able to retain information about a state of "being" and transmit that to progeny, a recent phenomenon known as epigenetics. Does this qualify as retaining and planning? I don't know. Cells also change based on environmental pressures through stochastic processes (a process known as evolution). Does this qualify as learning? Probably not, since the changes are usually pre-existing. The human equivalent would be finding out that you can swim by falling into water and not drowning. Did the person "learn" how to swim, or did they already possess an aptitude for it?

but most likely lack abstract thought, understanding, self-awareness, reasoning, and emotion...
I'll give you abstract thought, but what are the grounds against self-awareness vs. proofreading?

Proofreading is an entirely mechanical/chemical process. When a nucleotide is inserted into a double stranded DNA molecule, it pairs with the complementary nucleotide by hydrogen bonding. Complementary nucleotides also possess a space-filling quality such that an incorrect pair produces a "bump" or "dip" in the helix. All proofreading does is look for this type of physical inconsistency. Hardly self-awareness.

Why is the nucleotide inserted? How does it look? Why does it look?

@user1432 I couldn't parse that. It's inserted to replicate DNA. Proofreading looks for this physical inconsistency in a variety of complicated mechanisms. And the "why" is simply to reduce the error rate in DNA.

Intelligence in evolution and in the field of AI is often defined as the ability to apply previous or existing abilities to successfully solve entirely novel problems that were not present or trained for in the first place. Intelligence is always adaptive. For instance, I've never ever in my life performed the addition of 10 plus 10.1234 but I'm intelligent insofar as I understand the operation well enough to be able to apply it to new numbers. I know the answer is 20.1234. A proofreading enzyme is very inflexible in its catalysis and does only one thing, regardless of context.


text:
Organism with the greatest amount of gold as percentage of body mass
I've read that the human body contains trace amounts of gold:
http://www.tellmehowmuch.net/how-much-gold-is-found-in-the-human-body.html
http://web2.airmail.net/uthman/elements_of_body.html
Are there other species that are known to have significantly higher ratios of gold to body mass?
And while there seems to be no definitive answer about the benefit of gold being in the human body, are there any species for which gold has demonstrative bodily uses or benefits?


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Insect identification: Fly with eye strip

Location details:
Country - India,
State - Tamil Nadu,
District- Chennai.
Found this fly in my backyard keen to know its exact name. Thanks for the help

The antenna seen here is not that of Scathophaga (which would have a strong bristle at the front base of the last segment); I'm thinking Tabanidae, but not knowing where the photo was taken IS a huge handicap (from the OP's handle, perhaps Indian subcontinent?).  Another photograph showing the rear end of the critter would be nice as well (but probably impossible; I'm sure the animal is no longer available).

@ArthurJFrost side view & additional pics added.

@Charles location details added.

@Ναείστεαισιόδοξοι The large space between their two eyes doesn't match up with fly you mentioned and any link can be provided will be useful to confirm this species.

Looking at the bottom photo the way the wings are held and the spines coming off the scutellum (the white plate just before the wings) now suggests to me the family Stratiomyidae (Soldier Flies); having no detailed knowledge of the Indian fauna of that family forbids me from speculating further.

Definitely Stratiomyidae, probably genus Odontomyia. Very widespread and species-rich genus.
Here is an example of Odontomyia - not the same species - https://www.flickr.com/photos/63075200@N07/sets/72157632905103705/.

Can you add a source, an image and explanation why you think this is correct? As if now it's just a comment really.


text:
What are an internal and external exons?
I read the book: Essential Genetics and Genomics It has a table summarizing the properties of the "typical" human gene:

It has a gene feature Size of internal exon, what internal means in this context?
When I searched for it I found mentions about external exons, but found no definition.
I strongly suspect they mean:
External exons are the first exon right after the 5' untranslated region and the last exon just before the 3' untranslated region and all the other exons are internal exons.
As turned out this was almost right, but had a mistake which is wonderfully pointed out in the accepted answer.

Yes, the internal exons are those that aren't at the ends, which are often referred to as terminal exons1.
However, exons are sequences of nucleotides that are incorporated into the mature mRNA — i.e. they don't have to be (entirely) protein coding.
It is probably simplest to think of exons as being the transcribed regions that are not introns — i.e. they are the sequences that don't get spliced out during transcript maturation.
In other words, the 5'UTR is typically§ part of the first exon and the 3' UTR is typically§ part of the last exon.
§Note: I say typically, because sometimes introns are found within the UTRs2,3.
Reference:
1: Bolisetty, M. T., & Beemon, K. L. (2012). Splicing of internal large exons is defined by novel cis-acting sequence elements. Nucleic acids research, 40(18), 9244-9254.
2: Eden, E., & Brunak, S. (2004). Analysis and recognition of 5′ UTR intron splice sites in human pre‐mRNA. Nucleic acids research, 32(3), 1131-1142.
3: Paolantoni, C., Ricciardi, S., De Paolis, V., Okenwa, C., Catalanotto, C., Ciotti, M. T., ... & Giorgi, C. (2018). Arc 3′ UTR splicing leads to dual and antagonistic effects in fine-tuning arc expression upon BDNF signaling. Frontiers in molecular neuroscience, 11, 145.

Thank you for the precise answer and references.

You're very welcome!


text:
Is it advised to calculate QED parameters for salts?
QED (quantitative estimation of drug-likeness) is a score which helps you to predict if a small molecule is desirable as an orally absorbed drug, described in the Quantifying the chemical beauty of drugs article.
Its calculation is based on well defined chemical properties such the number of hydrogen bond donors and acceptors, aromatic rings, rotable bonds, octanol-water partition coefficient etc...
All of this properties can be derived from the structure of the molecule. One can use for example the QED module of RDKit
I develop a compound database for drug discovery. Some compounds are salts where one ion is the organic molecule and other is common inorganic ion such as $\ce{Na+}$, $\ce{Ca2+}$, $\ce{Cl-}$, etc...
When I load the salts into the database I derive their non-salt form, just the organic molecule.
My guess is that I should only calculate the QED score and its associated parameters, or any chemical parameters for ADME  for the organic molecule, but not for the original salt compound.
My logic is, when we apply a drug as a salt orally it will dissociate into ions, so the organic bio-active molecules will be separated from the inorganic ions. Of course the inorganic ions will be present in the gastrointestinal fluid, but in such a small quantity compared to the other inorganic ions (often the same type) that they will have no significant effect.

QED is quantum electrodynamics: https://en.m.wikipedia.org/wiki/QED_(play) ;)

I found the answer when I was reading about InChi in more detail.

For example, to a bioscientist “glutamic acid” and “glutamate” are the
same thing, but to a computational chemist the loss of a proton, or
its variable site of attachment is critical.

So the guess in the question is OK in a bioscientist perspective, but not for the computational chemist perspective, and since this is biology oriented computational chemistry question both the ionic and neutralized form must be considered.
To test this I calculated the Quantitative Estimation of Druglikeness (QED) for in a simple case for , sodium acetate, acetate (just the organic anion) and acetaldehyde. Their mean QED:
sodium acetate: 0.2777
acetate: 0.3498
acetaldehyde: 0.4298
The ionic forms (sodium acetate, and just the acetate anion) are less likely drugs since ions, since ions has an extremely low chance to pass biological membranes passively. The sodium acetate has lower likelihood then acetate, because it contains 2 ions and the QED algorithm has now way to tell which should be the drug and assumes that both ions must pass the membranes which is a great penalty.
In conclusions the QED parameters should be calculated both form the neutralized and organic ionic forms. The in-vivo relevance of the two forms will heavily depend on the chemical environment, since they will be in a dynamic equilibrium, which mostly depends on the PH of the micro environment. The QED parameters should not be calculated from the salt form, since we are not interested in the QED of the inorganic ion, further many more inorganic ions will be present next to that.


text:
Why do most theories assume "only" sexual reproduction can cause genetic diversity?
The reason cited for sexual reproduction trumping over asexual reproduction broadly relies on the advantages of genetic diversity.
This completely overlooks the fact that a mutant which is able to reproduce asexually with some amount of genetic variation (editing, randomizing etc) would have more inclusive fitness?

Actually, the idea that sexual reproduction promotes genetic diversity is a more a  myth that a reality. If you actually look at papers the develop models of the evolution of sexual reproduction, they rather talk about the evolution of a modifier locus and the importance of recombination and linkage disequilibrium. In any case, "promoting genetic diversity" is not a reason for which sexual reproduction would evolve as it refers to a species wide statistics. Finally, seeing diversity as "beneficial to the species" is also a potential misunderstanding.

Your question is based upon the false belief of what models of the evolution of sexual reproduction tell. It is also based upon other misunderstandings explained above. For these reasons, I am voting to close.

I did not imply group selection. I was just stating that the books I have read (introductory) state that sexual reproduction survives mutant asexuals because of the advantages of genetic intermingling (e.g. the Red Queen hypothesis), this has the side effect of promoting genetic diversity.

Can you please clarify sexual reproduction survives mutant asexuals? Also, just after you say because of the advantages of genetic intermingling (e.g. the Red Queen hypothesis). I don't know what you mean by "genetic intermingling" but RQ hyp. refers to an evolutionary arms race and does not (directly at least)  "explain a fitness advantage".

This is a pretty big question so I'm going to focus on the core points.
It's not nearly so either-or, and really a range of two things: trait diversity and stability. Sheer diversity isn't sufficient to improve rate of adaptation. Stability in the sense that it's a good idea to hold on to successful traits.
In sexual reproduction, you have two sets (one set of traits from each parent) of proven survivable traits to draw from. Very roughly, it doubles the amount of positive feedback toward maximizing fitness for the environment the pair finds themselves in - of which pathogens are a major and quickly changing component.
In asexual reproduction, you have a single tested set of traits. Asexually reproducing organisms thus depend on things like horizontal gene transfer - proven traits from another organism. This has the effect of prolonging the amount of testing that takes place (one organism vs two), causing asexual organisms to be more adaptable to the circumstances they find themselves in compared to sexually reproducing organisms and vice versa.
Where I have written "proven" here, I am referring to the fact that the traits in question have survived in combination with the organism's other traits, as opposed to a totally new mutation that could have consequences before the organism has a chance to reproduce.
Related literature

Genetic variation in organisms with sexual and asexual reproduction
"With realistic environmental changes small alterations in any particular measurement or trait are usually sufficient to keep up with the changes, but fitness, since it depends on a large number of traits, will be selected with greater intensity, which may be enough to confer a distinct advantage on sexual reproduction." An advantage of sexual reproduction in a rapidly changing environment.
Bacterial adaptation to pathogens: What antimicrobial resistance has taught us about horizontal gene transfer.

Can you please backup your claims with a reference? I don't understand what you call 'trait' here. It sounds like you confound number of parents with number of traits. There are fair number of literature on the evolution of sexual reproduction but I have never seen anything sounding like your answer.

Is there any study on HGT being used particularly by asexually reproducing species? If this is an evolutionary winning card, I'd expect it to show a high prevalence for instance in rotifer Bdelloidea.

Yeah: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4632278/


text:
"Immortal Genes" common to all organisms?
Author Sean B. Carroll mentions that there are about 500 genes common to all organisms. They have to do with the essential DNA machinery and so forth.
What are these genes? Where can I read more about this fascinating concept?
When you google immortal genes you get mentions of Sean B. Carroll. What term do others use for these genes?
"When we compare the genomes of Archaea, bacteria, fungi, plants, and animals, we find about 500 genes that exist in all domains of life... The functions of immortal genes are central... processes such as decoding DNA ... and making proteins. All forms of life have depended on these genes since the origin of complex DNA-encoded life early in Earth's history." (Making of the Fittest, pg 79)

I've not heard the term. However, "Housekeeping genes" are genes that are always turned on as a basic function of being alive.

That’s the term you get when a physicist writes about biology.

Please provide a reference with a preferably a link for Carroll's statement. Otherwise your question is unclear.

Ok I added quote from his book. I would LOVE some details on what these genes are or what term others use for them.

In order to expand my answer (did you read it?) in an appropriate manner, could you indicate how much biochemistry you know. For example, can you think of 100+ genes that would be required for ribosomal protein synthesis in any organism? Do you know what replication, transcription and translation are? Have you heard of glycolysis. If your answer is generally "no" then the expansion of my answer will need to be different from if it is yes.

their called housekeeping genes

Introduction
I believe that Sean B. Caroll is confusing:
• the minimum number of genes required for a viable organism
with
• those genes that are present in all organisms — so called ‘immortal genes’
I will deal with each in turn.
The minimum number of genes required for a viable organism
I have not read the book from which the quotation is taken. From its context and my knowledge I think that the author is mistakenly interpreting ‘the minimum number of genes required for a viable organism’ as ‘the genes present in all organisms’. This is because he seems to be referring to work from the laboratory of Craig Ventner on engineering mycoplasma.
Mycoplasma are among the smallest organisms capable of independent life. They have a genome of about 500 coding sequences, but as parasitic organisms they devotes some of these genes to their parasitic mode of life, while they lack others that the host provides.
The number of 500 may actually be too high: a figure of 300 is quoted in this description, who had plans of Ventner’s plans to build an organism containing a minimal genome containing only such essential genes. There is more on this in a Wikipedia article entitled Mycoplasma laboratorium. It should be noted that the word “immortal” does not appear in either account.
‘Les Immortels’ — genes present in all organisms
The poster would like a list of those genes essential to life, but I know of no such list. How would one go about composing one?
First, one has to set the rules. Do parasites, such as mycoplasma, which are dependent on their host organism, count? Do human beings count? We require amino acids and vitamins, but obtain them from food rather than synthesizing them ourselves. So although it is necessary that a self-sufficient organism have the enzymes for synthesizing the 20 amino acids of the genetic code, these are not all present in humans. I would suggest that we have to restrict ‘les immortels’ to self-sufficient organisms.
Second, one has to decide whether one is talking about a set of genes for accomplishing a function, or individual genes with a structural relationship in all living things that suggests a common identity. For example all cellular organisms (i.e. excluding viruses) must have ribosomes to synthesize proteins, but the protein complement of those ribosomes differs among organisms. Thus, the ribosomal proteins necessary to engineer a minimal mycoplasma may differ from those present in a bacterium such as Escherichia coli, and will certainly not be common to humans. I would suggest we would have to go for the latter.
Having made this decision, one  would get a team of undergraduate students to take all the genes in the genome of E. coli (or even of a mycoplasma) and perform BLAST searches to see whether they are present in representative organisms. Unfortunately I am no longer in a position to torment undergraduate students in this way, so I will have to start a list myself and encourage others to add to (or subtract from) it.
The List — a start
The genes for DNA replication, transcription of RNA and protein synthesis constitute the low hanging fruit here. My area is (used to be) protein synthesis, so I will start there:
Protein Synthesis
Large and small subunit and 5S ribosomal RNAs (3)
Ribosomal proteins (≤32)
Protein synthesis factors — EF1, EF2, IF1 and possibly others
Aminoacyl tRNA synthetases (20?)
tRNAs? — but all that is conserved is probably the anticodon (and sometimes not even that)
Accessory enzymes for protein synthesis:
Pseudouridine synthase
rRNA methylases?
DNA synthesis
B-family DNA polymerases?
RNA synthesis
? Evolutionarily related, but complicated because of multi-subunit nature
But if DNA synthesis is a problem, the reactions leading from RNA to DNA are surely not:
Enzymes of nucleotide metabolism
Ribonucleotide reductase (two subunits)
Thymidylate synthase
Uracil DNA-glycosylase?
Tetrahydrofolate reductase?
Enzymes for interconversion of nucleotides — Adenylate kinase? Nucleoside-diphosphate kinase?
Metabolism
This requires some work. One cannot specify either aerobic or anaerobic metabolsm, but in either case one needs oxido-reducto enzymes. Enzymes of hexose metabolism — hexokinase? Enzymes to metabolize key intermediates like glutamate and glutamine, and enzymes for introducing different groups in synthetic processes. This could make an interesting crowd-sourced project, or, failing that, a game for your next Biochemistry Christmas Party.

Aren't the number of genes common to all organisms and the number required in a minimal organism different concepts? Related, sure, but different.

@JackAidley — They are indeed. However, it is Sean Carroll — to whom the poster refers — who is confusing the two and actually refering to the number in a minimal organism. I tried to make that clear in my answer. Thus, a minimum set of genes might require 50 ribosomal proteins (say) but it may be possible to identify only a half a dozen (if that) that are common to all organisms. Likewise a system for replication and transcription is required, but the divergence between eukaryotes and prokaryotes may be such as to exclude common components (not my field).

I would be happier if you included that in your answer directly.

I have now edited my answer to address the valid point made by @JackAidley. The original answer was more directed to the poster and the extent of his biochemical knowledge, but the purpose of SE Biology is to provide answers of general utility, so the current answer refers to aspects of biochemistry with which the naive reader may not be familiar. The partial list is new. I realize it is scanty, but it is better than nothing, and nothing is what was there before.

@user253751 — As I wrote, it’s pretty much a party game, although nobody else seemed to want to play. You can make lists of what you like, but if you include parasitic organisms it seems to me you are cheating unless you include the genes supplied by the host. And it seems obvious to me that whatever wording the poster used, he wanted to know what the minimum list was for self-sufficient life. Not that it matters what the poster intended, but that seems to me the more interesting question.

This statement is approximately correct.
According to the data in Zhang, 2018, as illustrated graphically by author Alex P.R. Phillips, there are 307 shared essential genes in the three domains of life.  That figure does not show shared nonessential genes - and I would question how "nonessential" a gene really is if it has been conserved in multiple groups since the last common ancestor of all life!  Additionally, that figure only covers major model organisms and there are probably a few that are present in other members of each domain.  Note that the statement you quoted was only about "500 genes that exist in all domains of life".  It doesn't say they can't be lost and replaced in some species.
The paper cited above is free, and if you have the patience I think you should be able to run down the updated list of all those genes in the supplemental data.

It seems likely that Carroll's claim is untrue, in fact there are a much smaller number of genes shared between organisms and genes that provide core functions appear to have independent evolutionary histories in many cases (source).
It is unfortunate that Carroll does not provide a reference for this claim, so I do not know where he was getting his data from but the book was written in 2006 which is the infancy of whole genome sequencing so that may be the cause for the error. But, even so, by 2003 evidence was pointing to a much smaller number, and even the earliest genome comparison papers (e.g. here) weren't finding conservation on the scale suggested by Carroll.
So, rather than "around 500" immortal genes, it appears that there is  a much smaller number of genes that both common to all life and share evolutionary history, perhaps 30 or so and, remember, these numbers can only ever go down as we sequence more species so it's entirely possible that it will turn out that there are no genes that are universal and share common evolutionary histories in all organisms.
You may wonder how this can happen when there are so many core functions that a cell must surely have to function. The answer appears to be that new genes able to perform these functions evolve, perhaps specialised to operate under particular conditions, and - for a time - the organism carries both versions of the gene until eventually losing the original gene in some lineages. You can see this pattern of evolution in organisms where an enzyme is known in two forms and some carry one or the other, while some carry both (here's detail on one such example).


text:
Examples of natural graded transcriptional responses to extracellular ligands
In this paper (1) from 2001 the authors show that the mating pathway in budding yeast yields a graded transcriptional response to increasing concentrations of pheromone, and claim that:

To our knowledge, this is the first example in eukaryotes that extracellular signals can be propagated in a simple graded fashion.

Here's another paper (2) from 2005 showing the same thing, but with single-cell fluorescence microscopy instead of flow cytometry.
Given that these papers are around 20 years old, I assume other pathways with similar signaling dynamics have since been found, but I'm struggling with finding good examples.
Is anyone aware of other pathways where the dose-response relationship between an extracellular stimulus and a transcriptional response is graded, as opposed to bistable? The organism is irrelevant, as long as it's a eukaryote, it's a natural (i.e. not synthetic nor mutated) pathway and the results have been shown by some single-cell analysis technique.

Poritz et al. (2001) PMID: 11571757
Colman-Lerner et al. (2005) PMID: 16170311


text:
Why is the antibody light chain essential for function?
Humans and most other mammals produce antibodies consisting of two heavy chains, each linked to a light chain. Both heavy and light chain contribute to the variable region, and thus the antigen specificity of the antibody.
In contrast, cartilaginous fish and camelids have been found to produce heavy-chain-only antibodies, and thanks to their small size and ease of synthesis, camelid antibodies (nanobodies) are predicted to revolutionize antibody therapeutics.
This makes me wonder: why is this not possible with human (genetically engineered) antibodies? Apart from the fact that removing the light chain would alter antigen specificity, what hinders a heavy-chain-only human antibody from being functional? What is so fundamentally different between the camelids heavy chain (and their variable region) and the human equivalent?

It is possible with genetically engineered human antibodies. scAbs and related scFvs (single-chain fragment, variable), which are even smaller, have been around for at least a couple of decades.

This was the kind of answer I was looking for. I realize my question doesn't reflect that. Thanks!

In case someone else finds this: https://www.nature.com/articles/d41586-021-01721-5

I suspect it has to do with the fact that since the camelid scAbs are expressed in vivo, they undergo the normal recombination and affinity maturation process there as individual variable regions.  Thus, one can easily isolate high-affinity scAb mRNAs from the blood of a suitably-immunized camelid and proceed with cloning and production.
Human heavy chains undergo affinity selection while paired with light chains and so in vivo processes wouldn't work to generate heavy chains that on their own bind well to the given antigen. I suppose one might generate a display library with only heavy chain genes, but at a typical library complexity of 10^7 you wouldn't be able to cover as much of the "conformation space" as with an in vivo single chain affinity maturation process.
PS - the bit about "revolutionizing antibody therapeutics" seems like marketing hype for a 20+ year old idea.

Thanks. I guess I assumed that in vitro selection would be relatively straightforward with today's technology. But perhaps you're right about the library complexity not being large enough. And yeah, "revolutionizing" might be an exaggeration, but camelid antibody keep popping up every so often, so I really thought it was a newer discovery than 20+.


text:
Will this strategy work for verifying successful cloning of a DNA fragment into a plasmid vector?
So I am in a bit of a time constraint. Essentially, I inserted a DNA fragment via molecular cloning which contains a unique RE site. I need to confirm whether my colony has or does not have the fragment.
I need to do this in one day so would this work as a confirmation strategy:

Pick colony and perform colony PCR with primers around RE site.
Cleanup the PCR product and digest using the enzyme which was inserted.
Run on a gel. If a cut is noticed, this confirms that the colony had the inserted fragment (containing the RE site).

Would this strategy work? Are there any notable issues people can for see in this strategy?

Yes, your strategy would work, with the caveats already mentioned by @Cell.
Depending on which restriction enzyme and PCR buffer you use, you might even be able to skip step 2. NEB has a good list over their restriction enzymes and their activities in some common PCR buffers. With some reasoning that information is often applicable also to restriction enzymes of other brands.
Depending on your primer availability, another quick strategy is to simply use a primer pair such that one primer binds inside your fragment, and the other binds to the backbone. This should result in a PCR product only if your cloning was successful, and also verifies correct direction (in case you used blunt-end or single-site cloning). Two possible problems with this approach is:

If you get no bands at all you may not know if what failed was your cloning or the PCR reaction. The latter can be easily controlled for with a well-thought positive PCR control.
You may detect cases in which more than one copy of your fragment have been inserted. Although such cases are rare, it sometimes happens that inverted repeats of 3, 5, 7, ... etc copies get inserted in tandem.

One issue is if your fragment amplified is too small you may not be able to see the positive result of two bands because they run off the gel. Also the RE may not cut a small fragment efficiently.
I would recommend extracting and purifying plasmid, then do a double digest using the unique fragment cutting RE and a RE that only cuts the backbone. You should either see linearized plasmid DNA or two bands that are probably both >1 kb and easily resolvable.

I would question the cutting efficiency since often PCR amplified products have restriction ends and are easily cloned into vectors.

Maybe it depends on how far away your primers are but according to this NEB article you need to some extra DNA sequences on both sides of the cut site for efficient cleavage https://www.neb.com/tools-and-resources/usage-guidelines/cleavage-close-to-the-end-of-dna-fragments Since you didn't specify I assumed the worst case where your cut site is at the very end of the amplified product.

Yes, usually its 4 to 5 bp..... my "double check" primers would amplify 500bp from each side of the RE site. It should cleave well. In addition 1,000bp vs 500bp would be very noticable


text:
What is the evidence for cognition being mainly confined to the brain?
We believe that the processes of cognition are mainly confined to the brain.
What is the evidence for that?
I understand that the brain shows increased oxygen saturation in fMRI scans while thinking intensely. Therefore, we can conclude that brain plays a role in cognition. But how do we conclude that the rest of the body plays a negligible role in it?
In other words, how can we be certain that the brain's role in cognition is not a supportive one rather than an almost exclusive one?
I know that there is enough evidence for brain having a role in cognition, however my curiosity is mainly that why do we confine it to the brain alone? In other words, how are we certain that cognition is not spread outside the brain?

I think tetraplegics generally have no troubles with cognition, so we can rule out all four limbs. There are people living without stomach, half of lungs, without kidneys, with severly shorter intestines, smaller liver, no eyes, no tongue, non-functional ears, heart-transplants ... yet all of them (can) have normal cognition ... However, even a tiny damage to the brain can lead to significant cognitive disabilities. So ... which organ do you propose as an alternative center for cognition? :)

By studying countless insults to the brain, all aspects of cognition have been identified, even pinpointed to particular parts of the brain, not only in humans but in other animals as well. We know where memory is, where speech centers/understanding speech is located, where pleasure is perceived, etc. Dogs trained to be still in MRI machines exhibit the same patterns in the same places with certain stimuli. A heart transplant (or other) doesn't make the recipient think like the donor. Look up fMRI; that maps cognition as it happens.

@Domen Thank you for your comment. That is definitely a good piece of evidence.

@vkehayas Yes, thank you. Actually, my question arose out of similar contemplations.

@anongoodnurse Thank you for your comment. Insults, injuries, and fMRI do establish that brain has a role in cognition. What I wondered was how can we be sure that it has almost exclusive role, rather than a supportive one?

@Domen Could you please add your comment as an answer? It did help me understand the reasoning behind the idea.

I have extremely good "gut intuition"... which is found in the brain. What kind of cognition is not found in the brain? What are you imagining any other organ can do in terms of cognition? Which organ? The liver? The heart? You've been given plenty of replies.

@vkehayas I would not say a brain in a jar cannot cognate, it is just very difficult to demonstrate cognition. Brain in jars for animals when connected to circuitry can control robots. https://www.science.org/content/article/lamprey-brain-drives-robot#:~:text=Through%20trial%20and%20error%2C%20the,or%20circle%20patterns%2C%20Fleming%20says.

Also, people that go into comas and brain death have great vital signs from all of their body, although we can see from their brain activity that it is different and causing the coma. brain death: https://www.life-source.org/latest/what-is-the-difference-between-a-coma-and-brain-death/

Who said cognition was confined to the brain (I mean, before you posted the question here)? Definitions probably vary somewhat, but most seem to include experience and sensory information as inherent components of cognition, so I'm just curious where that opening statement came from. Particularly the word "confined." This question might actually be better suited for Philosophy.

The single best evidence is injury and deformity.
You can lose any other part of the body without impairing cognition but brain damage especially damage to specific parts of the brain alter or damage cognition. Losing a foot or a kidney or an eye does not suddenly make you unable to speak, but damage to the language center of the brain does. Cataloging the effects of damage to different parts of the brain has actually given a fairly decent map of what different parts of the brain do before we started scanning active brains.
https://uwmsktc.washington.edu/sites/uwmsktc/files/files/TBI_cognitive.pdf
https://www.biausa.org/brain-injury/about-brain-injury/basics/function-of-the-brain
Animal brain removed from their bodies and connected to circuitry can learn.
As for how can we be certain, we can't, that's not how science works. We can say it is extremely likely given existing evidence and there is no evidence to the contrary, to the point it can be safely assumed, but science does not deal in absolute certainty.

Thank you. The links were educative to me.

Degeneration of the muscles controlling the vocal cords will also lead to loss of speech. When you look up closely, phrenological claims such as "brain area X does Y" crumble, although certain brain areas are associated more with certain functions than others. Attaching a brain to a mechanical "body" to perform a function proves that a brain cannot affect the world and receives no sensory inputs without a body. The body is not just the hardware that runs some neural software, it determines how the brain works and provides it with its purpose. You just need both by order of evolution.

@vkehayas - "phrenological claims"? Phrenology infers characteristics from the shape of the skull, not the brain, and no normal modern person believes that. The brain would work pretty well if it had the right (and uninterrupted) conditions of nutrients, gaseous exchange, temperature, etc., but no one can come back from that to tell about it. And of course, sensory input would be gone, but that doesn't mean thinking would disappear. Insanity might ensue, but we don't know, we can't know. A quadriplegic has decreased sensory input as well, but can still think.

@anongoodnurse Do you mean that you agree with my arguments or that you missed their point? Because demanding absolute localization of cognitive functions in a one-to-one correspondence with specific brain areas is high-resolution phrenology and it's not supported by evidence. As for artificially re-creating the physiological environment that the rest of the body provides for the brain to sustain its function, you must be able to see that it re-inforces my argument, right? Lastly, does a quadriplegic's condition suggest to you that the body is not necessary for cognition? If so, how?

@vkehayas so you think a computer needs the internet to run programs just because it needs the internet to download them? As a pointed out a brain in a vat of jelly connected to nothing but wires can still learn, input is needed but a body is not the only form of input.

@anongoodnurse Unfortunately I do not have the time nor do I think this is the place to have such a discussion. If you are curious though, I encourage you to read primary research or at least something recent (last 40 years or so). On the topic of the dualism you appear to espouse, read on "embodied cognition", e.g. Damasio, Varela, Lakoff etc.

@John Imagine a computer that atrophies if it stays unplugged from power or disconnected from the internet and that can only grow if those conditions exist. Now imagine a computer that can have multiple power sources and ways to connect with other computers and grows --in a similar way to biological evolution-- according to the sources available and those that it "prefers". I encourage you to read about structural and functional plasticity during development and in adults. I do not doubt that if we try we will be able to sustain a healthy brain without the rest of the body. But why?

@vkehayas none of which shows cognition is not happening in the brain, it just shows that the brain needs certain conditions to operate, which well duh.  I am curious as to what you think is being argued because you don't seem to be giving any arguments against the brain being where cognition happens, just that the brain is not the only part of the body, which nobody is arguing.

We can monitor brain waves from people in comas and brain death. Even though their organs are fine and so are their heart and limbs, their brain scan looks like this:

Thank you. However, I would beg you to consider that this is only an evidence for brain having a critical role in cognition, not an almost exclusive one. I know that there is enough evidence for brain having a critical role in cognition, however my curiosity was mainly that how can we confine it to the brain alone. In other words, how can we be certain that cognition is not spread throughout the body.

To support such a claim, you need to be able to answer questions such as: "What led to coma/brain death?", "What is the result of the loss of brain function?", without invoking the rest of the body.


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What advantage do dogs have in clearly disclosing whether they are afraid or unafraid in a conflict?
Dogs are known to clearly show whether they are afraid or unafraid with the posture of their tails during a conflict.
How and why is this beneficial?
My limited understanding makes me feel that, in any social setting, disclosing whether an actor is afraid or unafraid would almost always be unfavourable for the actor. Is this incorrect?
Isn't it better for the less confident dog to try to bark out the stronger one and if it doesn't work then simply walk away, rather than broadcast that it is afraid of the stronger dog?

It is better for animals to broadcast their qualities, and size one-another up before risking injury in conflict. As pack animals, dogs are particularly sensitive to where they are placed in a hierarchy. So it is better for them to telegraph their qualities than to engage in conflict that may hurt them.

Dear Karl, Thanks for your answer. Isn't is better for the less confident dog to try to bark out the stronger one and if it doesn't work then simply walk away, rather than broadcast that it is afraid of the stronger dog?

it may be difficult to run away after you've just found out the hard way barking doesn't work...

I think that it is wrong to think that dogs do not have any emotions, or complex social strategies. However, it is a common mistake to think that dogs are like humans, only not quite as smart. We place our feelings and strategies on them, because they are our companions. But I don't think they engage in the kind of complex mental "chess" games that we do.

@JohnDvorak I understand. What seems surprising is that, rather than running away immediately, dogs continue barking even after broadcasting their low confidence.

@RiteshSingh I would presume that there might be some unconscious tradeoff game - bark might indicate that dog would fight if it is inevitable but the posture indicates it would rather not.


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Does the 'President' have 2 Billion Leaves?
The world's second-largest known tree, the President, in Sequoia National Park is 3200 years old and is said to have 2 billion leaves (Source: https://youtu.be/vNCH6uhB_Bs?t=59).
Is this correct? And how was this number arrived at?
In other words, how is such an insanely large number possible?

The US National Park Rangers count them. But that makes it a mathematical question, not a biological one, so it should be obvious that it is off topic here.

Strictly speaking, S. giganteum is a conifer so it has needles, not leaves. So count the individual needles on one twig (they're really small), multiply by the number of twigs per branch and the number of branches on the tree.

@David That number was obviously not 'counted'. It was arrived at by an estimate based on botanical facts.

@jamesqf Thank you! That explains the huge number which was my primary curiosity. Could you please add it as an answer so that I can accept it?

If you know the answer, why ask the question?

@David I want to know what botanical facts made that estimated number so huge.

Botanical facts? I imagined they extrapolated from the empirical observations of the numbers of leaves per branch and the number if branches per metre rise in the trunk, allowing for the pattern of sub-branching. But it is hardly a question of biological principle. As I have indicated, it may be answered by some general mathematical formula, if you plug in the constants. A good scientific exercise, but not a question likely to find interest or answer here, I would imagine.

@Ritesh Singh: Because it's not an answer, just my guess at how that number might have been arrived at.  I don't know how whoever did that video got their number...

@jamesqf It is closest to an answer. My main question was how is such an insanely large number possible.

@RiteshSingh, I upvoted your question. As a physicist that's a member of a lot of Stack exchanges, I wonder if you could help us by committing to the Materials Modeling proposal? We really need help, and would very much appreciate if you could commit!

@user1271772 Done sir/madam, Thank you! :)

@user1271772 Also recruited a few friends to commit to it :)

@RiteshSingh! Thank you so much !!!!!!

One way* to come up with an estimate of how many leaves - or needles, in the case of Sequoiadendron giganteum - is simply to count the number of leaves on a twig (or a number, to get a good average), then the number of twigs on a branch, and then count the branches on the tree, after which it's just multiplication.
Now one reason that the number seems so high is the way the needles grow.  Unlike for instance pines, which have long needles arranged in sparse clusters of 2, 3, or 5, or spruce & fir, which have medium needles arranged along the branches, the sequoia has lots of tiny needles arranged on twiglets.
Link with picture of sequoia needles: https://www.monumentaltrees.com/en/trees/giantsequoia/giantsequoia/
Picture of pine vs spruce & fir: https://www.finegardening.com/article/fir-vs-spruce-vs-pine-how-to-tell-them-apart
*But I don't know whether it's the way used to get the number in the link.

Thank you for the pics. This answer completely satisfies by curiosity! :)


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What does the "Psi" in "Psi broth" stand for?
When making competent cells I've been using a medium called "Psi broth", which per liter consists of 20 g tryptone, 5 g yeast extract and 5 g MgSO4. Today I got curious about why it's called "psi". Is it an acronym like SOC and LB?

Psi is the Greek letter ψ.  Psi broth is sometimes referred to as ψ-broth.
Here's an example:

L-Broth or ψ-broth can be used instead of SOC medium, but efficiency may
  be reduced.

L-broth： 10 g Bacto tryptone, 5 g Bacto yeast extract, 5 g NaCl, pH to
  7.5 with 1 M NaOH, bring to a final volume of 1 L, and autoclave.
ψ b-broth： 5 g Bacto yeast extract, 20 g Bacto tryptone, 5 g
  MaSO4･7H2O, pH to 7.5 with 1M KOH, bring to a final
  volume of 1 L and autoclave.

This only partly answers the question. The key thing which is missing is where the "psi" came from. (e.g. why "psi" and not "zeta" or "epsilon" or even "gimel"?)


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Understanding the genotype written in terms of two genes
I have some doubt in understanding the following genotypes: HCV-Tg/AID(+/+), HCV-Tg/AID(-/-) and HCV-Tg/AID(+/-), where HCV-Tg stands for "Hepatitis C Virus (HCV) core proteins" and AID for the gene "Activation-induced cytidine deaminase". So it is about two different genes. It is clear though what is meant by for example AID(+/+) in terms of ist alleles, but in the case I am talking about these are two different genes. In the case HCV-Tg/AID(+/-) it could for example mean that one allele is mutated at each of the two genes, but it could also mean that in the first gene (HCV-Tg) one allele is WT and in the second gene (AID) one allele is mutated. And lastly it could also mean that in the first gene both alleles are WT and in the second gene both alleles are mutated.
Can somebody help me understand what is exactly meant ?
Many thanks.


text:
Can a creature fly and also walk?
These creatures, fly and walk, and have perfect eyesight and follow me everywhere I go.  They have many legs, they are about 1 inch and their color is almost translucent, but a very light shade of brown.  They smell me at all times and bit me like a mosquito.  I have used 2 pesticide companies to exterminate, but no one is able to identify the critter so I can't kill them.  They also have a very strong heartbeat. I know because they like to be under me.  They move so quickly that I haven't been able to catch a picture.  Please help me to identify these nasty things, so they can be destroyed.

Sounds like a puzzle! It is going to be impossible to ID this species without more info and probably without a picture. Where do you live? How come you know they have a strong heartbeat but did not manage to take a picture?!


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Evolution as a directed graph exploration?
First of all, I am not biologist, nor good in chemistry/physics.
Secondly, I am really eager to understand.

So I think of a "life" (of a certain whatever being) as a space of somewhat properties. Having a wings is a property. Being tall is a property. Ability to speak as humans do is a property as well.
Properties can be combined. Nearly like Lego blocks do combine: one can build both: a) quite elegant structures, b) total absurd of those blocks. Like with Lego, not necessarily each block can be composed with each block. There are some (probably extremely sophisticated!) rules, defining what can be combined with what; thus set of all properties you might get in future depends upon all the properties you already have. In other words, you present defines all the possibilities of your future.
There is at least one measuring system: it takes a set of properties as an input and maps it to a, let say, number (or something else, which obeys ordering; number feels like the most simple example) denoting how "good"/"bad" this particular combination is.
As a natural consequence of all above-mentioned, there is a directed graph, where: A) vertices represent all possible sets of all possible (respecting rules) combinations of all possible properties; B) directed edges represent the possibility to "evolve" from one concrete set of properties to another one concrete set of properties.

Based on those assumptions, I am going to define what "evolution" is:
Evolution becomes nothing but a finding a shortest path in that unbelievably huge directed graph. I assume most of the readers don't understand algorithms, so brief remark: "shortest-path" problem is one of the hardest even known; roughly saying, it takes "infinite" time and hence is impractical for humans; however, this perfectly explains why evolution takes billions of years - indeed, it's not that hard to define graph, which can't be solved faster than that.
But in order to find shortest path, which is known well from algorithmic theory, you have to be as broad as possible. You try to explore as many vertices, as possible, which means you're creating creatures with all those properties (see #2) and measure their "goodness" with help of your metrics (see #3). The problem here is that you have to track/memorize all the paths you have tried already; especially those, which are proved to be deadends: otherwise your graph exploration will never terminate: you will cycle over the routes you've seen already, but forgotten.
The other thing of great importance, is how expensive your computation is. It runs billions of years and thus you have to guarantee that it's defended properly, can't be lost because of stupid mistake or unexpected circumstances; and the best known way to do this is to copy information about entire process (since very beginning) to each and every Life-being you ever create. The more copies you got, the more reliable entire system: even if you loose all of them momentarily and exactly single creature will survive, it will be sufficient to continue your computation (to continue evolution) relying on the information it accumulates.
Taking into consideration the dimension of the graph we're talking about, that "backtracking" requires enormous amounts of memory. Hence, you need perfect compressing technique to pack your data in the most compact way. And it seems to me that DNA is exactly for this reason (probably not only for this, but this one is definitely important).

What I'd like to hear, is how logical entire thinking I've demonstrated, ignoring numerous details (which I even not aware of)? Could it work like a dramatically simplified representation of evolution? Did I define the DNA's role correctly then? Can you extend this "graph analogy" with fresh details? Am I missing something really big and fundamentally important?

UPDATE:
1) @IMil:

Evolution becomes nothing but a finding a shortest path in that unbelievably huge directed graph.

What makes you think that evolution followed the shortest path?

Evolution does not. In order to find one, you have to try all of them (i.e. all possible paths starting from all existing vertices), measuring "shortness" according to a particular metric system you've accepted. Thus, "try them all" becomes an iteration over all possible properties in all possible ways (see #1 on the top of OP). Some of them clearly better than the other one (already known, seen in past and memorized somehow); but that does not discover the "best" path yet: there are, generally saying, unknown number of vertices you haven't visited yet, haven't measured yet, haven't tested out yet.. So, imagine you do not memorize what you have seen; what's than? What will happen if your metric system will get changed one day? - You'll have to start from the beginning rather than re-measure known subgraph (which is much more faster).
2) @Cort Ammon:

"There is at least one measuring system ... denoting how good/bad a combination is." This may be true telelogically, but we have no clear indication as to whether such a measure exists in a physical sense. Personally, I find it's more effective to think of there being at least trillions of measuring systems, each doing its own thing, which may or may not even be associated with evolution directly, such that the gestalt of all of those systems gives the behavior we see. While we can think of systems as "striving for good," we can also think of them as "just doing their own thing." Both approaches model nature quite well, with their own quirks.

I can't agree with you here. Having any positive number of metrics does not contradicts to the statement "there is at least one"; as well as having a "superposition" of any positive number of metrics does not.

So what we end up finding is that your definition is akin to saying "A written language is nothing more than a construct which admits finite sequences of letters".

Exactly. What I am saying, is that there exists an enormously huge graph of all possible combinations of all the letters. If you allow you letter sequences to be infinite, than graph itself becomes infinite as well; however, since it takes place in Nature those must be physically limited like everything else. Some of those letters indeed unite into words, which do make sense; the other sequences are just nonsense (with respect to the given metric system: hence, there might be cases, when one metric system disagrees with another one, it's OK). Then evolution becomes a process of searching for the greatest novel ever written (once again, according to the preferable metric system - even if it itself is some kind of "summary" of millions/billions/trillions of factors we're not aware of).

As a programmer, you probably have already heard of evolutionary algorithms and esp. genetic algorithms used for optimization problems.

One thing you are leaving out is that evolution takes place in an environment, and the environment is always changing, sometimes drastically. Retaining information about previously helpful adaptations wouldn't necessarily be helpful in the long run, since changes in the environment may have negated their utility.

a) Finding the shortest path in a graph is not a particularly hard problem - Floyd-Warshall is O(V^3). b) Modelling evolution as a path in configuration space is theoretically neat, but leaves out almost all the details.

I am afraid this is not a question about biology is defined by SE Biology, which is a question and answer site, but an attempt to initiate a discusion. Any supposed "answers" will only be matters of opinion, which is why I am voting this off-topic.

You may want to look into something called fitness landscape which sounds like the basis of your model and one thing we know about it is evolution is crap at finding the shortest path, it often locks itself out of the best path even, it is all about finding the local high. https://en.wikipedia.org/wiki/Fitness_landscape

@John actually I might post an answer along those lines if the question was "what is a good conceptual model for evolution using examples from computer science or statistics" - if you equate a fitness landscape with a likelihood surface, then a particle filter arguably does something suspiciously evolution-like.

But in order to find shortest path, which is known well from algorithmic theory, you have to be as broad as possible. You try to explore as many vertices, as possible, which means you're creating creatures with all those properties (see #2) and measure their "goodness" with help of your metrics (see #3). The problem here is that you have to track/memorize all the paths you have tried already; especially those, which are proved to be deadends: otherwise your graph exploration will never terminate: you will cycle over the routes you've seen already, but forgotten.

Evolution is an optimizing algorithm, but it isn't necessarily the best optimizing algorithm of its type. For example, genetic algorithms used by humans often have certain features that biological evolution doesn't, like carrying over the best solution from generation to generation. Biological evolution doesn't do that: if by chance you're fitter than any of your kids, tough you'll die anyway.
In that spirit, biological evolution doesn't go out of its way to explore as many vertices as possible, or to avoid "cycling over routes you've seen already" (impossible in practice because not many evolved traits can be reversed exactly. But when such reversals are possible we do see them happen. Many lineages have seen gains and losses of limbs, of flight, or moving in and out of aquatic life like ping-pong balls...). And in fact evolution has no memory of the past. We can make inferences about the past when looking at current organisms, but the only thing evolution acts on is the organism that currently exists.

It runs billions of years and thus you have to guarantee that it's defended properly, can't be lost because of stupid mistake or unexpected circumstances

You mean, like the Permian extinction? Those guys were pretty much lost I'm afraid. Same with all other extinctions.

Hence, you need perfect compressing technique to pack your data in the most compact way. And it seems to me that DNA is exactly for this reason (probably not only for this, but this one is definitely important).

What evidence do you have for DNA being the most compact form data could possibly take?

What I'd like to hear, is how logical entire thinking I've demonstrated, ignoring numerous details (which I even not aware of)? Could it work like a dramatically simplified representation of evolution?

Your basic idea, that mathematics, computer science and the field of optimization algorithms in particular can inform our understanding of evolution is sound. But finding the shortest path along a directed graph doesn't strike me as the best metaphor. Think more of finding the fitness peaks in a traits landscape, such that finding them is an NP-complete problem. Here are different algorithms that are used in this kind of problem:
https://optimization.mccormick.northwestern.edu/index.php/Heuristic_algorithms
Note that your requirement to remember past solutions is akin to the Tabu Search, but that's only one possible algorithm. Most heuristic algorithms don't do that.

Did I define the DNA's role correctly then?

No, you didn't. DNA enables the hereditary transfer of certain traits, which allows biological evolution to run as, um, well, an evolutionary algorithm. That is its role in the optimization process that is evolution. It does not copy the entire history of the evolutionary process; it just copies the molecule at hand, and the fact that it contains traces of what happened to previous copies is an epiphenomenon. And in fact it does not allow Evolution to re-create previous iterations of itself.

Can you extend this "graph analogy" with fresh details? Am I missing something really big and fundamentally important?

It seems to me you are treating evolution teleologically, imagining how you would design an ideal optimizing process to generate life and seeing if evolution matches. As this and other answers have found, it doesn't match (as an aside, I'm not sure the ideal optimizing process you envision would even be better than evolution. Tabu search isn't the best of all the heuristic algorithms). But more fundamentally, the assumption that evolution must be the best possible process for doing... what you think evolution is supposed to do, is unfounded. It might be true, it might not. It is generally more productive when looking at evolution to focus on what it does, and not on what we think it intends.
This is not to say teleological thinking has no place at all in evolution, insofar as one can argue that if something is optimized in some way, because it was created through an optimizing process that was optimizing for some specific characteristic(s), then it isn't absurd to use teleological language like "wings are for flying". They are, not in the sense that somebody wanted birds to fly and so made them wings, but in the sense that every characteristic of wings is what it is because it makes them good for flying. Because bird ancestors reproduced or not partly on the strength of their flying abilities.
In other words, if something was fine-tuned by evolution, then we can talk about it being "for" something. It's very possible that DNA is one such thing; maybe some traits of DNA are there to make evolution work better in some way or another(ETA: note even there the primary purpose wouldn't be "to make evolution work better", it would be to promote the reproduction of the organisms carrying that DNA. But if "evolution working better" in some way promoted that, then sure). But evolution itself isn't such a thing. At least I don't think there is evidence that it is.

Your theory is based on many false assumptions.

Evolution becomes nothing but a finding a shortest path in that
  unbelievably huge directed graph.

What makes you think that evolution followed the shortest path?

The best known way to do this is to copy information about entire
  process (since very beginning) to each and every Life-being you ever create

DNA doesn't intentionally store information about the evolutionary process. Some genes get lost completely, and mutations are, in general case, irreversible. That should be obvious in case of viral DNA/RNA, where there is simply no space for historical data. Many species, and groups of species, become extinct, and since the fitness of any species is determined by how well it fits in the ecosystem, extinction of dinosaurs makes "backtracking" of mammals impossible.

Can you add sources to your answer?

you really should expand on the shortest path comment as well, as it stands it is not informative.

As for the shortest path: I'd say the burden of proof lies on the author. Evolution is driven by random mutations, and if you draw imaginary paths from, say, last common ancestor of chimps and humans to us (or chimps), there is no reason to believe that the actual path was the shortest one.

Thanks for your answer. Please, see UPDATES at the bottom of the OP.

You can prove your model trivially if you start from the assumption that all evolution consists of altering DNA.  I think the general consensus is that that's a good place to start, but there may be more as we discover.
Now the issue is that, from this model, we can show that your graph approach is trivial.

A node in the graph is associated with one sequence of DNA
Edges between them represent changes that may occur in DNA.

Thus I simply redefined "Property" to be "the presence of a particular sequence of nucleotide."
Generally speaking, we recognize that there is some conversion function from this sequence of nucleotide into "properties" we care about.  This means the graph I described above is isomorphic with the graph you were looking for.  Of course, as you noted, that function is extraordinarily complicated.
"There is at least one measuring system ... denoting how good/bad a combination is."  This may be true telelogically, but we have no clear indication as to whether such a measure exists in a physical sense.  Personally, I find it's more effective to think of there being at least trillions of measuring systems, each doing its own thing, which may or may not even be associated with evolution directly, such that the gestalt of all of those systems gives the behavior we see.  While we can think of systems as "striving for good," we can also think of them as "just doing their own thing."  Both approaches model nature quite well, with their own quirks.
So what we end up finding is that your definition is akin to saying "A written language is nothing more than a construct which admits finite sequences of letters." (That's the definition of a "formal language," by the way).  While technically true, it misses out on basically all of the nuance of language.
And there's also the concept of epigenetics which studies ways gene expression changes which don't involve changing DNA.  This is an open field.  We still do not fully understand what is going on there.  But it certainly does appear to play an role, and it does not immediately fit into the simple mapping from DNA to properties.

It is a great answer, many thanks! I update OP, please checkout the very bottom, there is your name. BTW, do you realize how close your statement to the Godel's theorems? I omitted this question in the OP, but still... question seems to be extremely important. If one show how this idea isomorphic to somewhat formal language... ;)

@SerejaBogolubov I love Godel's incompleteness theorems, and Tarski's undefinability theorem, but few people appreciate their implications.  And, of course, when it comes to systems that are really operating in the world of real numbers rather than integers, they don't imply quite as much as we might like.

@SerejaBogolubov As for your edit, I agree that "trillions of metrics" is "1 or more."  My point of that was to show just how inordinately difficult it is to use that "1 or more" phrasing, except in brutally abstract settings (such as with Godel's incompleteness theorems).  Those metrics also most definitely do not superpose in a meaningful way.  Biological systems are notoriously nonlinear.  At some point, I think those issues start to add up, and the fact that modeling life as just an abstract representation of DNA starts to fall through long before you get the opportunity...

... to raise enumeration issues.  I could see drawing an analogy to coin flips.  You might have some theory like Gambler's Ruin which says that after some countable number of coin flips, the gambler must lose, but failed to model the probability that the real coin lands on its edge instead of heads or tails (1:6000 for a US nickel), and how that influences the game.  (I "won" a DnD game by rolling a die so that it landed on an edge instead of a face.  The DM was a big fan of a comic in which the only way to win that game was to roll a die on edge)


text:
Why can't we directly use the DNA instead of the RNA in a DNA microarray analysis?
When proceeding to a DNA microarray analysis, I saw that the molecule that's taken from the cell is the RNA, which is afterwards converted to DNA by a reverse polymerase. But why not taking directly the DNA out of the cell?
EDIT : still about the DNA microarray method, I'd have another question: how can one be sure the DNA strands of the matrix are going to hybridize with the sample that one want to test?

Your second question has little to do with the first one. Please consider opening another dedicated post for this second question.

Before posting a question like this, please stop and think. If you had asked yourself what you are analysing by microarray you would know the answer. I am voting to close this question as it does not show sufficient prior effort.

The context I've heard of that method was exclusively DNA sequencing.I didn't know it finds applications in analysis of RNA - because I'm no professional, you know, which is why I post a question here. Your comment is even more useless than my question.

You guys are so stupid... You're so posh with your little conventions, you think science is a game with precise rules, and the one who's not rigorous enough has lost. Please consider the mortal people like me and their right to access to the sciences.

In each diploid cell, there are exactly 2 copies of every single gene.  No matter what the cell type, no matter what you do to the cell.  (Barring exceptions like some blood cells and cancer)
But RNA expression is what differs between cell types and conditions.  Some cells make some RNA, some make others.  Under some circumstances, a cell might make more of one RNA than at another time.  Changes in RNA are what is worth measuring.  DNA doesn't change.
RNA is converted to DNA because DNA, being double-stranded is more stable, less likely to degrade.

RNA is extracted an analyzed because one possible application of a microarray is to quantify mRNA levels. As with other methods (for example RT-PCR), RNA is first reverse transcribed into DNA to make it compatible with the downstream protocol. Most procedures are indeed optimized for working with DNA, so it is easier to reverse transcribe RNA as the first step than to tweak everything else to make it work with RNA.
You can also start a microarray protocol with genomic DNA, but then you are looking at something completely different than gene expression. A possible application of a microarray in this case is genotyping.
Wikipedia has a lot of information about microarrays.


text:
How does fungi network transfer substances between plants?
How does fungi network transfer substances between plants?
I recently read a short article about fungi network. And I am wondering  about how fungi network works (Mechanism).

Plants have fungi network. And a plant which lost it gets prone to insects.

Wikipedia link


text:
Is there any mechanism that prevents DNA of an eaten entity's cell from affecting that of own?
When we eat food I heard that our digestive enzymes disassemble the DNA of the eaten cells so that the DNA cannot affect us. Then, is there any mechanism (that prevents the eaten cell's DNA from affecting us genetically) in cell-scale level? Or is it only in organ-system level(e.g. digestive system)? It seems that germs and viruses don't have the mechanism, as we manipulate them as genetic transferor. But I want to know if nucleate cells have the mechanism.

Possible duplicate of Do we consume dna, proteins of other organisms?

@kmm You may be right and your link has nice answers, but my question's key point is about cell-scale level, so I think it a bit diffrerent. But if nuclease and cell membranes are only mechanisms then my question can be duplicate either..

While not required for your main question: Viruses (and bacterial viruses) can have a stringent coupling of particle size and amount of DNA, which can prevent the inclusion of large pieces of foreign DNA (a practical problem for the early days of genetic engineering / cloning).

@tsttst I didn't know that! So your comment can be one way that primitive creatures like viruses use to prevent foreign DNA from interfering with its oen.

Cells have cell membranes and sometimes cell walls that keep random molecules from entering the cell. Only small, uncharged molecules can pass freely through the membrane. Complex structures of proteins embedded in the cell membrane regulate the passage of charged or large molecules. Pathogens like viruses or bacteria have had developed equally complex structures of proteins that can fool the proteins in the cell membrane to gain access to the interior of the cell. In other words, the cell membrane is almost always going to keep naked DNA from entering the cell, but viruses can get around this, by packaging their DNA in protein capsules that can compromise the cell membrane.
To create GMO, viruses are often used to transport the foreign DNA into the cell. Alternatively, the cell membrane can be attacked with chemicals, high voltages, or even mechanically punched holes, that allow DNA to pass through the membrane.
Bacterial cells will sometimes allow the passage of naked DNA, but this is very rare in plant and animal cells.

So you mean that it happens at digestive organ system level with nuclease?

I have no idea what you mean by that. All cells have cell membranes, it part of what makes them cells.

A ha, then outside of the cell the DNA is broken into smaller structures so that the cannot activate, and even unbroken DNA is blocked by cell membranes. Then can DNA injected by means you mentioned activate inside the cell's membrane?

@KYHSGeekCode Yes, it should. In fact that is how transfection works. Link - https://en.wikipedia.org/wiki/Transfection

@RoniSaiba I did well to adopt yours. Thanks!


text:
Why don't fish get hurt with so many sharp fish bones?
Why don't fish get hurt with so many sharp fish bones? And why don't fish feel pain when they swim? Don't those sharp fish bones stick into the flesh while swimming?

...Why don't we get hurt with so much sharp  roots of our tooth? And why doesn't  those sharp roots stick into the flesh while we eat?  Something like that...

https://en.m.wikipedia.org/wiki/Connective_tissue

Connective tissues prevent fish from being hurt by its bones. They surround the sharp bones so that the bones do not hurt its organs/flesh.
However Of course the bones can hurt the fish, but the situation is quite imaginable.
If a fish is smashed or gets too much force, its connective tissues cannot protect its organs much(like our clothes cannot protect us from bullets, or our broken bones penetrating our organs when we encounter a serious car accident despite our connective tissues covering the bones - the bones just damage our connective tissues and organs, and so on...) and its organs get hurt.
Your worry can happen in human case too (but much weaker version), we can think of our hip bones sometimes pressing our flesh between the bones and the chair we are on.