text:
Looking for a recommendation: Anatomical diagrams of animals commonly used in laboratory testing (potential surgical procedure emphasized)
I'm interested in either a book or a place to find well-drawn diagrams of animal anatomy. The emphasis if possible would be on anything which includes material related to the nervous system of neurosurgical procedure. I'm interested in diagrams or figures for animals commonly used in testing, that is mice, rats, or others. This would be similar to the diagrams shown in medical school. I'm interested in these from the perspective of someone doing surgical procedure on a testing specimen. Any recommendations (book or otherwise) would be greatly appreciated.
Also, if there is a better stack exchange site that you would recommend me asking this on, feel free to recommend and I can move my question there. I'm outside of either field (engineer), so apologies if I'm, not familiar with which subforum to ask this on, and let me know where to move the question.

You'll probably get a better answer if you are more specific about the procedure of interest.

Neurosurgery was given as area of interest. Procedure of interest would involve operations on the central nervous system (CNS) and peripheral nervous system, particularly that of the spinal cord. Interpretation of spectral frequencies/brain waves of specimen is also of interest. I'm in the early phase of planning so anything even tangential to this would still be valued.

Neurosurgery is very broad though; you could be looking for brain atlases or neurovasculature or peripheral nerves. And now you bring up spectral analyses? You really need to have more focus before asking a question here, it's like if you asked for a book on engineering and said you're interested in electrical and mechanical and industrial, while architecture and geology are also of interest as is anything tangential.


text:
Is there a word to describe a sample of DNA that can be sequenced?
This is a question about terminology. I want to know if there is a word that is used to describe a sample as "able to be sequenced".
My rough guess would be "sequencable". But that does not seem to be a word. "Viable" would be my second guess. But seems to imply a lot more than that it can be sequenced.
What is used in practice?

As always with adopting general English words to scientific use, the exact context is crucial. What do you mean by the opposite “unable to be sequenced”? Do you mean the DNA is too degraded or has been converted chemically through age, do you mean it is contaminated with DNA from bacteria etc, or do you mean it is one of many repeats?

But if you change your spelling to "sequencEable" you'll find that it was entered by someone in Wiktionary in 2019 (https://en.wiktionary.org/wiki/https://en.wiktionary.org/wiki/sequenceable). Apparently it has been used in a mathematical sense for many years (https://books.google.co.uk/books?id=UywypI5sjvgC&pg=PA253&lpg=PA253&dq=sequenceable&source=bl&ots=uOkYs-DZ1j&sig=ACfU3U271_SuaKnQ6PqdoSHYRFdHjTq_YQ&hl=en&sa=X&ved=2ahUKEwjezLGx06n9AhWFSMAKHZhkBy8Q6AF6BAgiEAM#v=onepage&q=sequenceable&f=false). A Google search for "sequenceable DNA" finds it in Scientific American.

@David is correct; sequenceable is definitely a word; it has been used in the biological sciences for quite some time now. I can find published papers using the word dating back to 1996, so probably earlier than that even.

I think you should request migration of this question to the English language Stack. It's off topic here I think, but definitely on-topic there.

I'd just delete the question, given the trivial nature of the answer. As a regular user of SE English Language and Usage, I don't imagine they would think much of it.

source: Stack Exchange

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

sort: votes


text:
Why is DNA Shuffling more efficient than Point Mutation?
In a related post on Biology-SE the following insightful comment was made:

The advantage of DNA shuffling over introducing single mutations is
  that you have to screen fewer mutants and the activity/stability of
  the protein could be improved several hundred fold more.

Is there a mathematical argument as to why DNA Shuffling should be more efficient than introducing point mutations?
Even supposing each DNA Shuffling / Point Mutation step is equally "expensive"  (and in reality DNA shuffling seems much more work) they are both generating one variant per-step, right? So why is the variant in one case grossly better than the other?
Related Post: Directed evolution: Point mutation vs Insertion-Deletion vs Shuffling

You should read this paper. Here is the gist of what you are interested in:

Because most point mutations are deleterious or neutral, the random point mutation rate must be low and the accumulation of beneficial mutations and the evolution of a desired function is relatively slow in such experiments. For example, the evolution of a fucosidase from a galactosidase required five rounds of shuffling and screening before a >10-fold improvement in activity was detected4. Naturally occurring homologous sequences are pre-enriched for 'functional diversity' because deleterious variants have been selected against over billions of years of evolution...
Although shuffling of a single gene creates a library of genes that differ by only a few point mutations1, 2, 3, 4, 5, 6, the block-exchange nature of family shuffling creates chimaeras that differ in many positions. For example, in previous work a single beta-lactamase gene was shuffled for three cycles, yielding only four amino-acid mutations3, whereas a single cycle of family shuffling of the four cephalosporinases resulted in a mutant enzyme which differs by 102 amino acids from the Citrobacter enzyme, by 142 amino acids from the Enterobacter enzyme, by 181 amino acid from the Klebsiella enzyme and by 196 amino acids from the Yersinia enzyme. The increased sequence diversity of the library members obtained by family shuffling results in a 'sparse sampling' of a much greater portion of sequence space15, the theoretical collection of all possible sequences of equal length, ordered by similarity (Fig. 4). Selection from 'sparse libraries' allows rapid identification of the most promising areas within an extended sequence landscape (a multidimensional graph of sequence space versus function)

DNA shuffling would be more efficient if you already have a big repertoire of variants (which have a lot of point differences among them; see Cohen, 2001). When you do not have that, then introducing point mutations using error prone PCR would be better.
A detailed mathematical framework to compare these two methods, is not available. However there are many mutation models and there is at least one model for DNA shuffling too (Sun F., 1999).
Basically, for a point mutation experiment the number of mutants will depend on the error rate of polymerase. In a DNA shuffling experiment you are just creating random combination from existing variants. So, which one is more efficient depends on these (and many more) parameters. Moreover, the "efficiency" also depends on what experiment you are trying.

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Biopython - Big Discrepancy Calculating RNA melting Temperature over Literature
I experience big discrepancies when calculating melting temperature of RNA 7-mers with Biopython over values generated by a popular algorithm.
I tried the nearest neighbour algorithm with RNA and salt concentrations as described in a respective paper (thermodynamic table used as in paper below from: Freier et al 1986). Yet, the values largely differ (execute code below to see).
I tried all seven salt correction methods provided by Biopython, still I never get close to the values generated by siRNA design algorithm for the same 7-mers.
Can someone tell me how accurate Biopython's melting temperature nearest neighbour algorithm is? Especially for short oligomers like my 7-mers? Is there maybe something I am implementing wrong? Any suggestions?
Values derived from executing sample input:
http://sidirect2.rnai.jp/
Tm is given for the seed duplex of the guide strand: bases 2-7
Literature:
"Thermodynamic  stability  and  Watson–Crick
base  pairing  in  the  seed  duplex  are  major
determinants  of  the  efficiency  of  the
siRNA-based  off-target  effect"
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2602766/pdf/gkn902.pdf
from Bio.Seq import Seq
from Bio.SeqUtils import MeltingTemp

test_list = [
('GGAUUUG', 21.5),
('CUCAUUG', 18.1),
('CAUAUUC', 8.7),
('UUUGAGU', 19.2),
('UUUUGAG', 12.2),
('GUUUCAA', 14.9),
('AGUUUCG', 19.7),
('GAAGUUU', 13.3)
]

for t in test_list:
    myseq = Seq(t[0])
    tm = MeltingTemp.Tm_NN(myseq, dnac1=100, Na=100,   nn_table=MeltingTemp.RNA_NN1, saltcorr=7)  # NN1 = Freier et al (1986)
    tm = round(tm, 1)  # round to one decimal
    print 'BioPython Tm: ' + str(tm) + '  siDirect Tm: ' + str(t[1])

# Output:
>>> BioPython Tm: 10.1  siDirect Tm: 21.5  # GGAUUUG
>>> BioPython Tm: 8.2  siDirect Tm: 18.1   # CUCAUUG
>>> BioPython Tm: -2.0  siDirect Tm: 8.7   # CAUAUUC
>>> BioPython Tm: 8.2  siDirect Tm: 19.2   # UUUGAGU
>>> BioPython Tm: 1.3  siDirect Tm: 12.2   # UUUUGAG
>>> BioPython Tm: 4.4  siDirect Tm: 14.9   # GUUUCAA
>>> BioPython Tm: 9.0  siDirect Tm: 19.7   # AGUUUCG
>>> BioPython Tm: 2.1  siDirect Tm: 13.3   # GAAGUUU

Question first asked at stack-exchange: https://stackoverflow.com/questions/30037939/biopython-big-discrepancy-calculating-rna-melting-temperature-over-literature

Also asked at Biostars: https://www.biostars.org/p/140873/

What version is your Bio?

The source code for that function is available on Github, there are also some comments in there explaining what methods Biopython uses. The issue might also be that you're comparing apples and oranges, and that your siRNA Tm are not for 7mer parts of an siRNA but something else.

@ dustin: My Biopython is up to date V 1.65. @ WYSIWYG: added outputs for saltcorrection method 7. @ Mad Scientist: Thanks for suggesting the doc, yet I feel drawing conclusions from the included algorithms on my issue is beyond me. I need to think about whether I maybe misunderstood something fundamental, but this I deem quite unlikely.

I was forwarded a PERL script by the researchers behind siDIRECT 2.0. I still do not know why the big discrepancy as both the physical chemistry as well as PERL is beyond me at this point. But at least I was able to integrate that script into the larger frame of my Python program doing melting point calculations. For this concludes the topic without providing an actual answer. Thanks for your contributions.

I still want to see this question answered.

Is the issue open on github?

Comparing Biopython MetlingTemp to other calculators.
I have written the recent version of MeltingTemp in Biopython's SeqUtils.  I have extensively tested the Tm calculations against other programs like MELTING and Primer3Plus and other online Tm calculators with consistent results, thus I'm pretty confident that there is no gross error in the module. The simple answer in this case is: the calculation of siDirect is wrong.
Sources of discrepancy.
One minor thing: Many programs calculate k as k = total Oligo/4. MeltingTemp uses k = Oligo1 - (Oligo2/2). Thus to mimic this behaviour, you have to use
dnac1=50, dnac2=50

instead of
dnac1=100

And now the major thing: Oligo concentration is usually given in nanomolar. However, if you look at the calculation in the Perl script, siDirect seems to use micromolar!
my \$tm = ( 1000 * $dH / ( -10.8 + $dS + 1.987 * log(0.0001/4) ) - 273.15 + 16.6 * log(0.1)/log(10) )

The critical part here is:
log(0.0001/4)

which should be:
log(0.0000001/4)

Thus, you have to pass 1000-fold higher oligo concentrations to Biopython's MeltingTemp to get the same result as siDirect:
>>> from Bio.SeqUtils import MeltingTemp as mt
>>> print mt.Tm_NN('GGAUUUG', dnac1=50000, dnac2=50000, Na=100,
                  nn_table=mt.RNA_NN1, saltcorr=1)
20.1472140567
>>> print mt.Tm_NN('CUCAUUG', dnac1=50000, dnac2=50000, Na=100,
                   nn_table=mt.RNA_NN1, saltcorr=1)
18.1074422939

This is of course wrong if your primer concentration is 100 nM, but that's the result you get from siDirect.

A very insightful and thorough answer, thanks. I can't help but wonder why siDirect went for micro molar.

Thank You for your in-depth answer Markus. Indeed striking that siDirect - one of the most used oligo tool on the web could be so fundamentally wrong. This saves SeqUtils's honour!

I just received a PERL code snippet by the researcher behind  sidirect2 which allows to calculate the Tm. I still do not know the source of the calculation discrepancy as the thermodynamics is beyond me.
I post the code to conclude the question here. The can below can be saved into a .pl file and run from shell with the respective RNA sequence as a string argument.
Code:
#!/usr/bin/perl

# ====================
sub tm_RNA {

# Calculating Tm for RNA-RNA hybrid using nearest neighbour method
#
# usage: $tm = tm_RNA('GGCUGCCAAGAACCUGCAGG') ;

my $seq = lc ($_[0] // '') ;
$seq =~ /^[augc]+$/ or return '' ;

my $dH  = deltaH_RNA($seq) or return '' ;
my $dS  = deltaS_RNA($seq) or return '' ;

my $tm = ( 1000 * $dH / ( -10.8 + $dS + 1.987 * log(0.0001/4) ) - 273.15 + 16.6 * log(0.1)/log(10) ) ;

return sprintf("%.2f", $tm) ;
} ;
    # ====================
    sub deltaH_RNA {  # delta H parameters
    my $seq = lc ($_[0] // '') ;
    $seq =~ /^[augc]+$/ or return '' ;

my %rna_dH = (
    'aa' =>  -6.6,
    'uu' =>  -6.6,
    'au' =>  -5.7,
    'ua' =>  -8.1,
    'ca' => -10.5,
    'ug' => -10.5,
    'cu' =>  -7.6,
    'ag' =>  -7.6,
    'ga' => -13.3,
    'uc' => -13.3,
    'gu' => -10.2,
    'ac' => -10.2,
    'cg' =>  -8.0,
    'gc' => -14.2,
    'gg' => -12.2,
    'cc' => -12.2
) ;

my $sum_dH = 0 ;
    foreach (0..length($seq) - 2){
    my $dinucleotide = substr($seq, $_, 2) ;
     $sum_dH += $rna_dH{$dinucleotide} ;
}

return $sum_dH ;
    } ;
    # ====================
    sub deltaS_RNA {  # delta S parameters
    my $seq = lc ($_[0] // '') ;
    $seq =~ /^[augc]+$/ or return '' ;

my %rna_dS = (
    'aa' => -18.4,
    'uu' => -18.4,
    'au' => -15.5,
    'ua' => -22.6,
    'ca' => -27.8,
    'ug' => -27.8,
    'cu' => -19.2,
    'ag' => -19.2,
    'ga' => -35.5,
    'uc' => -35.5,
    'gu' => -26.2,
    'ac' => -26.2,
    'cg' => -19.4,
    'gc' => -34.9,
    'gg' => -29.7,
    'cc' => -29.7
) ;

my $sum_dS = 0 ;
    foreach (0..length($seq) - 2){
    my $dinucleotide = substr($seq, $_, 2) ;
     $sum_dS += $rna_dS{$dinucleotide} ;
}

return $sum_dS ;
} ;
# ====================
# Calling main method:

my $seq = shift;
    $tm = tm_RNA($seq) ;
    print $tm  # returns value to stdout

all_licenses: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/


text:
Identify this ladybug-like insect, with yellow eyes and cream spots
I have spotted this cream spotted ladybird like insect on my terrace. I live in Hyderabad, India and it's rare to see such an insect here. I have tried using image searches but haven't found any good matches. The underbelly is brown with some spots of yellow at the side. It is approximately 1-1.25cm in length. It's very hot around here generally but today is a cool day (30 deg C) and lightly sunny.

Excellent photo. That's a basil plant, no? Can you [edit] to add your approximate location in the world to aid in identification.

Thanks. That's a mint plant, commonly called pudina here. Location is Hyderabad, India.

Could it be Clinteria? https://indiabiodiversity.org/group/beetles_of_india/observation/show/17244829

I think (without any expertise in this area, so take with a grain of salt), that this is a beetle in the genus Clinteria. This is a genus of beetles found in Asia and are relatively common.
Specifically I think this is Clinteria klugi, which has large pale yellow to red spots on the elytra and broad similarly coloured bands of the edge of the pronatum.
Lots of good photos can be found on INaturalist.
Incidentally, I think you might be confusing the bands on the pronatum for its eyes. The pronatum is kind of like a shield for the thorax, and in the case of this beetle, the head too. The eyes will be dark (as is needed to absorb visible light) and on the head, which is tucked under the pronatum.

Solved. The pictures match exactly what I had seen. Also check https://sar.fld.czu.cz/cache/article-data/SaR/Published_volumes/2020-1/115-132_jakl_2.pdf for more details about the beetle.

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


text:
Is the answer: enough time?
Are there probability calculations about when a given gene mutation turns out to be an advantage rather than a disadvantage for the respective individual and then proves to be an evolutionary advantage over generations?

Probability hurdle: It takes ? x generations for a mutation to actually turn out to be an individual reproductive advantage. How much higher is the chance that the embryo is already stunted?

Probability hurdle: At the same time, numerous other individuals in the respective ecological niche also mutate, which may bring them other, but even better advantages. They win the reproductive competition, the first mutation perishes even though it was good.

Probability hurdle: even if the mutation is an advantage (e.g. light-sensitive cells, feathers, lactose tolerance), a mistake can wipe out the respective individual. Or the habitat changes too quickly. Or invasive species conquer the previously successfully occupied niche in the system. Or other parallel mutations are counterproductive. The mutation dies even though it was good.

Is the anser: there was enough time?
Are there algorithms that can capture all of this? Or AI-based simulation models?

Welcome semco543. We can't know what the answer may be unless you ask an actual question. Please take our [tour] and refer to the [ask] section of the [help], then [edit] to clarify what you're asking. Remember, one clearly focused question per post. (Though, what you've stated in your 3 postulates is quite right broadly)

You are treating mutations like they are all the same. Look at Covid for e.g., you can change some parts of the spike gene more or less with impunity and get more or less fit, but some other parts are impossible to change and produce viable virus. You would need probability calcs for each individual possible mutation...

As a new user of this site, please do us the courtesy of finishing the [Tour] (we know you haven’t.) And pay us the respect of providing a title that reflects your question so that users can judge whether it is of interest to them, indexing will be useful.

I think the keyword you are looking for further reading might be "fixation": https://en.wikipedia.org/wiki/Fixation_(population_genetics) which is the process of one allele becoming the only allele in a population. It is possible to study fixation both of neutral variations and non-neutral variations that have some influence of selection.
Do not expect some simple equation or "AI model", though, especially in the variable circumstances you describe where fitness is a function of frequency.


text:
What is the difference between "microproteome" and "peptidome"?
I know that "peptide" is sometimes used to refer to both microproteins and short peptides derived from longer proteins (post-translational), but I do not know whether this extends to "peptidome" versus "microproteome"?


text:
What are common culture temperatures?
In literature, authors sometimes refer to 37°C as a common culturing temperature. As I understand it, those are temperatures that are conventionally used for incubators in laboratories. For mesophilic bacteria, I found that common culturing temperatures are 28, 30 and 37°C. However, I was wondering whether that can be translated to Archaea, Fungi and/or algae research. What are the temperatures that people typically use in the laboratory to investigate mesophiles from these taxa?


text:
Weird Insect on Window, SW London
Insect is avout 5 cm long, antenna to tail, was on a windows. Tried to transfer to white paper, but it moved to a wall[

The overall appearance and shape points to a mayfly (in Ephemeroptera). However, I don’t know what species it is.


text:
Is there such a science in which the knowledge of biological processes (e.g., evolution) would be mathematically axiomatized and inferred (deduced)?
There is the following Mathematical Challenge Twenty-three
Mathematical Challenge Twenty-three: What are the Fundamental Laws of Biology?
* This question will remain front and center for the next 100 years. DARPA places this challenge last as finding these laws will undoubtedly require the mathematics developed in answering several of the questions listed above.
And I'm just wondering if there's such a mathematical field in which we can formalize and prove biological theorems.

Given that evolution selects for anything that works, I'm not sure what kind of non-trivial Fundamental Laws of Biology might exist or what "biological theorems" might be.

@Armand I agree with your "evolution selects for anything that works" which in turns implies that biological events are fundamentally contingent and any possible mathematical formal theories must necessarily be of the nature of incompleteness.

However, I'm still holding out some hope that knowledge of biological processes could still be had by examining the proof life-cycle of a suspected biological theorem-statement B throughout an ordered sequence of formal theories:

Inception: When B is undecidable.
Conception: When B is provable (thus decidable)
Extinction: When ~B is provable (both B and ~B are decidable).

However, all this is purely just a thought (a hope).

I think the question is too open to give a definitive answer, but several directiosn can be pointed out right away.
Laws of biology are not rigorous
Due to the inherent complexity of biological systems, the laws of biology are less susceptible to mathematical analysis than those in physics or chemistry. Firstly, this is because many of these laws are statistical in nature. Secondly, because there are too many parameters influencing a biological system to study the influence of each of them in a controlled way.
As an example one could give the Central dogma of molecular biology, which holds true for many organisms and serves as an important guiding principle, but doe snot obey in 100% of cases - e.g., it is violated by RNA viruses.
On the other hand, Mendel laws could be formulated in very rigorous mathematical terms, but quickly get obscured when we are dealing simultaneously with many genes and traits, and have to resort to statistical reasoning, see quantitative genetics.
Population genetics
Population genetics puts evolutionary study on a rigorous mathematical basis, and much of the developments are based on simple but powerful mathematical models. Here it si worth looking at Crow&Kimura's An Introduction to Population Genetics Theory,a nd also on the texts on the coalescent theory Gene Genealogies, Variation And Evolution: A Primer in Coalescent Theory and Coalescent theory: an introduction.
Physics of biological systems
Biophysics is a well-developed field, although it studies only specific aspects of biological systems. Good mathematically solid reference here is
Keener and Sneyd, Mathematical Physiology: I Cellular physiology. See also this post for more discussion.
Finally, a more fundamental, but also more obscure view on the evolution and function of biological systems is from the point of view of spontaneous symmetry breaking and non-equilibrium thermodynamics, associated with the names of Phil Anderson, Ilya Prigogine and Erwin Schrödinger - you may find the list of references in this post.

Thanks for the answer and helpful information within.

Prelude

Fwiw, I think the situation for the thread question and for the Mathematical Challenge Twenty-three is very bleak, hopeless: It's not possible even in theory (no pun intended) to formally theorize life processes in general — natural biological life on any planets, or ALIFE (Artificial Life, e.g. John Conway's Game of Life).
First of all, there's uncertainty of physical facts. For natural biological life, that's manifested by Heisenberg's Uncertainty Principle which would govern not only sub-atomic particle reactions but also macro biological life's evolution.
Take a particular asteroid for example. Its birth, formation, interstellar trajectory are all but a Karma-Fourier summation/superimposition (so to speak) of physical uncertainties — from the uneven distribution of energy and matter after the Big Bang, to the random matter expansion after the super nova of the first generation star, to the chaotic swirling birth of the second generation star system, all the way to "What did the dinosaurs see before the chicxulub impact ?".
Secondly, although mathematics doesn't have Heisenberg's Uncertainty Principle, it has the counterpart: Axiom of Choice. If two choice functions f1 and f2 exist in which Choice is necessary, it logically entails an uncertainty, non-determinateness on whether or not f1=f2, and truth non-determinateness is also alluded to in the following passage:
"We prove that the satisfaction relation of first-order logic is not absolute between models of set theory having the structure  and the formulas  all in common. Two models of set theory can have the same natural numbers, for example, and the same standard model of arithmetic, yet disagree on their theories of arithmetic truth".

The answer

So then, it's submitted in this answer, in so far as mathematics is the language of sciences, biology included, mathematical fundamental laws of biology and corresponding proofs are a tall order to accomplish.
However, it's also submitted here, there is a way forward.
As long as we're not naïve thinking that we're entitled know all biological laws – in full details – the way the Creator (Mother Nature?) does, we're endowed to be able to meta-mathematically formalize some kind of a categorization — a tree — of various FOL biological formal theories, and explore subsequent available pathways (branches) toward understanding a variety of different possible life forms, evolutions.
The meta-mathematical formalization of this categorization will still make use of the canonical definitions of FOL formal systems, theorems, provability thereof, but it also includes meta-proofs of syntactical undecidability as occasions arise.
In some details, the meta-mathematical formalization centers around:

Relieving Plato/Tarski/Gödel semantical truths, interpretations of the duty of being valid in making mathematical inferences: There are no longer meaningful semantical truths — only facts of syntactical provability. Iow, the only truth of a formula (interpreted as "sentence" or not) is the fact of it being provable or not, syntactically decidable or not.
A syntactical proof should be investigated in a context of a collection of relevant sets of axioms — not just one single axiom-set. Iow, a proof is only one instance in the set of proof-varieties (or formal-system varieties).

General Definitions

It's not feasible to detail all relevant definitions and proofs in one post so this answer might be a live post. But we can start with some definitions in the following sections.
Def-1 - Formal theories
A formal theory T (of an axiomatic formal system F) is the set of syntactical theorems of F closed under deduction via FOL rules of inference.
Notes:

The language of T is denoted by L(T) which is L(F).
(T ⊢ f) ⇔ (F ⊢ f) [f being a formula written in L(T)].
In (T ⊢ f), if T is well-known or understood we can omit T and write (⊢ f).
proof(f) ⇔ (T ⊢ f), where T is understood.

It's trivial that given f is a formula, given any two T1, T2, and given the following set definitions

S1 = {f | (T1 ⊢ f) and (T2 ⊢ f)}
S2 = { f | undecide(T1 ⊢ f) and undecide(T2 ⊢ f) }

S1 and S2 exist, S1 is non-empty, while whether or not S2 is empty is contingent on the nature of both T1, T2.
Def-2a - Provability inheritance
If (For all proofs of B: proof(B) ⇒ proof(A)) then:

theorem A is an ancestor of theorem B: ancestor(A,B)
theorem B is a progeny of theorem A: progeny(A,B)
theorem B is genetically inherited from theorem A: inherit(A,B).

Def-2b - Provability base-pairing & nucleotides
Let _C1, _C2 be axioms in the following manner

_C1 ↔ C11 ⋁ C12 ... ⋁ C1m
_C2 ↔ C21 ⋁ C22 ... ⋁ C2n

where only one of C11, ..., C1m is provable, and only one of C21, ..., C2n is provable.
Without loss of generality, each of C11 and C1i is then undecidable, and so is each of C21 and C2j.
Consequently, the formula
(C1i ⋀ C2j)
is also undecidable, which we can use as a new axiom and in which case in turn the theorem (C1i ⋀ C2j) is called a provability base-paring where each of C1i, C2j is called complementary nucleotide of the other.
Def-3a - Formal theory addition — f.(T1 + T2)
Let T1, T2 be general, f be a particular formula.
f.(T1 + T2) = S1 union {f} — up to deductive closure, and f ∈ S2.
Def-3b - Formal theory multiplication — f.(T1 * T2)
Let T1, T2 be general, f be a particular formula.
f.(T1 * T2) = S1 union {f} — up to deductive closure, and where (undecide(T1 ⊢ f) xor undecide(T2 ⊢ f)).
Def-4 - Grothendieck-Multiverse (gM)
A Grothendieck-Multiverse, denoted by gM, is a non-empty collection of theories in each of which the provability of a formula f is evaluated:
gM = { x | (x is a theory) and ((x ⊢ f) xor neg(x ⊢ f)) }.
A gM is also called an underlying provability realm (field) of all formulas written in a language L.
Def-5 - Contingency
The formula f is defined to be contingent when the followings are all satisfied:

f is not a logical theorem
neg({f} ⊢ ~(x=x)).

Proof-to-Truth homology/shadowing
Def-6 - Mathematical truth & falsehood
A mathematical truth is a quadruple (S,T,f,gM) defined per the followings:

S and NEG(S) are meta statements — written in natural language — with NEG(S) being the negation of S
T stands for TRUE
f is a FOL formula of which the provability S asserts
Exists(x):

TRUE(x ∈ gM)
TRUE(neg(x ⊢ ~(n=n))) [i.e., x is syntactically consistent]
TRUE(x ⊢ f).

A mathematical falsehood is similarly defined as (NEG(S),T,~f,gM), where (S,T,f,gM) is a mathematical truth.
Note:

If S is a meta-statement and TRUE(S), then where convenient,

S ⇔TRUE(S).

Similarly, if S is a meta-statement and TRUE(S) is false,

FALSE(S) ⇔ NEG(S) ⇔ NEG(TRUE(S)).

Provability-varieties — Proof lifecycle & extinction
Let f be an underlying formula, gW a Grothendieck multiverse that can be partitioned into the following three equivalence classes C1(f,gW), C2(f,gW), C3(f,gW):

C1(f,gW) = { x | (x ∈ gW) and undecide(x ⊢ f) }
C2(f,gW) = { x | (x ∈ gW) and decide(x ⊢ f) and neg(x ⊢ ~f)}
C3(f,gW) = { x | (x ∈ gW) and decide(x ⊢ f) and neg(x ⊢ f)}.

Def-7a
The set
{C1(f,gW), C2(f,gW), C3(f,gW)}
is called a proof (provability) life cycle relation R of f in gW, and is denoted by f(R(gW)), or f.R.gW or fRgW when convenient.
Def-7b
A triple
(Ci(f,gW),Cj(f,gW),Ck(f,gW))
is called a life cycle of f in gW — i, j, k being pairwise distinct.
Def-7c
The triple
(C1(f,gW),C2(f,gW),C3(f,gW))
is called the natural life cycle of f in gW.
In this case,

C1(f,gW) is called the inception (of the proof of f) in the cycle
C2(f,gW) is called the conception (of the proof of f) in the cycle
C3(f,gW) is called the exception/extinction (of the proof of f) in the cycle
R is defined to be the underlying natural life cycle relation.

Def-7d
Given a natural life cycle relation fRgW that is unique in a gW, C3(f,gW) is defined to be a Chicxulub extinction, on (the provability of) f, and denoted by Chicxulub(C3(f,gW)), per the following:
Chicxulub(C3(f,gW)) ⇔ (Exists(C3(f,gW)) ⇒ (Choice is necessary)).

I think the problem is trying to reduce all of the biology to a simple set of axioms. Even in physics one does not do this. Moreover, in physics one often formulates the laws in axiomatic form, but describing real situations requires combining several laws, taking account for specific geometry, characteristic scales, etc. - none of which is axiomatic or predictable from the first principles.

I agree. Such problem of placing importance on the semantics of the individuals in the domain of discourse, imho, also occurs in FOL mathematics and the the remedies seem to be based on two techniques: axiom-schemas (e.g. PA's induction-schema axiom), and going to 2OL, HOL.
My suggested answer is based on extending these two techniques a bit further: by going to meta level and inspecting possible homology (in functions, and relations) among related formal theories.

This, I think, would be in line with Grothendieck's universe (https://en.wikipedia.org/wiki/Grothendieck_universe) which is in essence a meta universe comprising of many FOL smaller universes (domains of discourse).


text:
Heterozygous traits with advantages over homozygous traits
I used to believe that there are "good" alleles and "bad" alleles and having two "good" alleles could never be worse than having one "good" and one "bad" allele.
However with sickle sell anemia having one "good" and one "bad" allele confers stronger immunity against malaria (though it can also cause hematuria and other generally undesirable outcomes).
Are there any other examples of this?

https://en.wikipedia.org/wiki/Heterozygote_advantage

Welcome to Biology.SE. The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site as are "homework" questions unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Under researched questions may be subject to down-voting and closure. Please take the [tour] and consult the [help] starting with [ask] for details.

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

This is an example of a rather common phenomenon called overdominance or heterozygote advantage. It can be due to many reasons: the two alleles affecting the same phenotypic trait via different paths, the phenotypic train being due to interaction of many linked alleles, the alleles having multiplicative effect, etc.

The heterozygotes may exhibit increased disease resistence. In case of sickle cell disease, the phenotype is related to the infectivity of plasmodium. In the heterozygotes, the infectious agent is less likely to propogate within red blood cells.
Interestingly, researchers have speculated that other alleles in human may confer disease resistence in the heterozygous condition but are detrimental in the homozygous state.
These include PKU(Phenylketonuria) an inborn error of metabolism, in which the heterozygous fetus may be resistent to miscarriage caused by a fungal toxin(Ochratoxin A), and Tay-Sachs disease, in which the heterozygotes may be resistant to Tuberculosis.
You may refer to given link for more details;
https://www.pbs.org/wgbh/evolution/educators/course/session7/explain_b_pop1.html


text:
Could a tree grow in a low pressure environment?
Could a tree grow in a low pressure environment? If you had a pressure say, 10% of that of Sea level could a tree grow if it was in the proper soil and watered regularly?

related https://biology.stackexchange.com/questions/1242/what-is-the-lowest-pressure-at-which-plants-can-survive

Does this answer your question? What is the lowest pressure at which plants can survive?


text:
Thistle-ish plant in Texas
I found the plant below in Fort Worth, TX at the end of March this year, and can't identify it.  It looks a bit like a basketflower, or some other thistle-like plant.  It was the only one growing where I found it, and, in several years of frequently walking the area, I have never seen another that I recognised as being the same.  I apologise for the washed-out quality of the top of the plant in the first picture; I couldn't get a clearer shot with a cell-phone camera in very bright sun.
The plant was probably about 2 feet tall, and the main part that looks like it will eventually flower was about the width of, and half again the height of, my clenched fist.

I deleted my previous answer (which was correct but didn't ID the growth on the top) And am going to attempt to clear up all the issues related to this question and the image of the plant you provided
The plant in the image you gave is in the genus Salsifies (Tragopogon):

Western salsify has linear, grass-like leaves that clasp the stem at the base. Prior to bolting and flowering, the leaves can be readily mistaken for grass. However, they have a smoother and more rubbery-like feel than grass leaves, have hairs in the axils, and exude a milky juice when broken. Source: https://www.montana.edu/extension/invasiveplants/documents/publications/extension_publications/Western%20Salsify_revised%202017.pdf

There are multiple salsify species that fit the plant in the image, but only one of which is in the Texas range. (Source: Tragopogon-dubius range map, Tragopogon range map)
The plant can be narrowed down to the species Yellow Salsify (Tragopogon dubius)

Tragopogon dubius (yellow salsify, western salsify, western goat's-beard, wild oysterplant, yellow goat's beard, goat's beard, goatsbeard, common salsify, salsify) is a species of salsify native to southern and central Europe and western Asia and found as far north and west as northern France. Although it has been reported from Kashmir and India, recent evidence[citation needed] suggests that specimens from these areas may be a different species. Western salsify has been introduced into North America where it has become widespread, being reported from all the continental United States except for a few in the far south-east, and all provinces of Canada except Newfoundland and the northern territories. Source: https://en.wikipedia.org/wiki/Tragopogon_dubius

The plant has a strange structure on the top, the cause of which was being debated. After some research it appears to be a case of Witch's Broom Disease also known as Phytoplasmas And according to this Wikipedia article:

Witch's broom or witches' broom is a deformity in a woody plant, typically a tree, where the natural structure of the plant is changed. A dense mass of shoots grows from a single point, with the resulting structure resembling a broom or a bird's nest. It is sometimes caused by pathogens.

Until recently this disease was thought to be only found on trees. But recent discoveries show that this disease is found on a range of plants. Interestingly enough in Novemeber 7, 2015 this disease was first reported to be on Tragopogon dubius (reported in Iran) and was confirmed after DNA tests.

In a survey conducted for phytoplasma diseases in 2014, T. dubius witches' broom disease was observed in vineyards and green areas of Bajgah and Zarghan localities. The characteristic symptoms of T. dubius witches' broom were flower virescence and phyllody, crown proliferation and witches' broom. Since the symptoms were suggestive of phytoplasma infection, plants were assayed for presence of phytoplasma by PCR amplification. Total DNA was extracted from 0.3 g of midrib tissue of four witches' broom affected and two symptomless T. dubius plants (two plants per location), using the procedure of Zhang et al. Total DNA samples were tested by both direct and nested PCR assays using phytoplasma universal 16S rDNA primer pairs P1/P7 and R16F2n/R16R2. That amplify fragments of 1800 bp and 1250 bp, respectively. Expected fragments were amplified following direct and nested PCR from all symptom-bearing but not from symptomless plants.
Source: https://bsppjournals.onlinelibrary.wiley.com/doi/epdf/10.5197/j.2044-0588.2015.032.017

According to Wikipedia this disease is caused by phytoplasmas or basidiomycetes but can also be caused by fungi and herbicides:

Diseases with symptoms of witches' broom, caused by phytoplasmas or basidiomycetes, are economically important in a number of crop plants, including the cocoa tree Theobroma cacao, jujube (Ziziphus jujuba) and the timber tree Melia azedarach. Source: https://en.wikipedia.org/wiki/Witch%27s_broom

The most known cause of this disease is the fungi Moniliophthora perniciosa (Stahel) Aime. Other causes are more likely, such as herbicides.
This wikipedia paragraph informs us of how this disease is spread:

Phytoplasmas are pathogens of agriculturally important plants, including coconut, sugarcane, sandalwood, and cannabis, as well as horticultural crops like sweet cherry, peaches, and nectarines. They cause a wide variety of symptoms ranging from mild yellowing, small fruit, and reduced sugar content to death. Phytoplasmas are most prevalent in tropical and subtropical regions. They are transmitted from plant to plant by vectors (normally sap-sucking insects such as leafhoppers) in which they both survive and replicate.

The exact type of phytoplasma is fairly hard to figure out, so I encourage you to post this on https://naturalist.org for scientific attention
There are many types of phytoplasma, here are some examples of Aster Yellows Phytoplasma (Phytoplasma asteris):

https://www.inaturalist.org/photos/88865514, Photo 88865514, (c) Chris Kreussling (Flatbush Gardener), some rights reserved (CC BY-NC), uploaded by Chris Kreussling (Flatbush Gardener)
https://www.inaturalist.org/photos/30163460, Photo 30163460, (c) Colin Purrington, all rights reserved, uploaded by Colin Purrington
Here is a picture of the flowering plant Yellow Salsify (Tragopogon dubius), of which the plant in the picture has been identified as:

https://www.inaturalist.org/photos/289034746, Photo 289034746, (c) Hans, some rights reserved (CC BY-NC), uploaded by Hans

you state "features such as range and plant structure.. " I generally recommend that all species ID posts (especially those making definitive claims) include explicit and cited evidence explaining why the answer is correct. It's an improvement that you've started adding some citation for your post's quotes/images (and this post adds much improved detail/support for the disease), but your posts would be improved if your quotes/links/references actually provided more direct support for your ID (vs just miscellaneous info about the species).

Keep the miscellaneous info, but please provide direct evidence supporting for species identification. (in this case, what specifically about the features and location are you using to ID this plant?). Thank you

@theforestecologist I am trying my best, please don't get too hard on me. Will add citations

I am not intending to be"hard". We have an expectation here that species ID posts (and really any post) provide explicit and elevant references supporting claims made. The internet is full of misinformation, often times stated definitively, which adds to reader's confusion. We don't want to "add to the noise". Even experts need to provide evidence as a paper trail. In the end, this site is not about getting the right answer, but about sharing accurate/useful info with peer review. Your ID expertise and improved post format are appreciated, but please keep improving with explicit support

@theforestecologist Sorry about that, improved post, added range map citation. Did I do everything right?

yes, that is improved. Thank you!

@theforestecologist No problem! Appreciate your support :)

Let us continue this discussion in chat.

Thank you!  I was uncomfortable with the initial identification not mentioning the disease, since this didn't match the examples of the species with which I was unfamiliar, but this revised answer makes me much more confident in the ID, and the additional information is very helpful.  I would also like to credit @SirThinksalot, who first mentioned phytoplasma in the comments on the original answer.

@LSpice Sounds good! Thank you for your acceptance of my answer :) I simply googled infection of Tragopogon dubius and Witches Broom came up. Google is your best friend when researching diseases.

I can’t make minor edits here, but I would suggest fixing the various misspellings for disease scattered throughout this answer. More importantly, when you quote from Wikipedia, you should really link to the actual article you’re quoting from, not just to the Wikipedia base domain, just like you do with the other sources you cite. As it’s currently written, it’s very difficult to find the source on Wikipedia to verify or read more.

@JanusBahsJacquet Thanks, fixed, and fixed, please let me know if I missed anything :)

Much better – just the first Wikipedia link missed (presumably to the Yellow Salsify article itself)!

Yes, this is yellow salsify but it seems to have contracted a phytoplasma infection that has retarded its normal flower development - and somewhat altered its overall growth habit, causing the blooms to end up halfway between petals and leaves.

Thank you!  An original identification as yellow salsify left me unsure, given that ti didn't match numerous other examples with which I was familiar, but this additional information made me more confident.  I wound up accepting the other answer, which gives more details about phytoplasma, but I would like to say explicitly that you were the first one to identify the disease, in comments on a now-deleted answer.


text:
What interaction among wasps is this?
I found the following collection of, I think, wasps on a sidewalk in Fort Worth, TX in mid-December.  It looks to me like the aftermath of some battle, and it's not surprising to me that wasps had some sort of battle, but I can't understand what would have made them die in this frozen tableau.  (I mean frozen in the sense of "not moving," not cold; the temperature was probably high teens or low twenties Celsius.)  What might have happened here?

Most likely that they envenomated (stung) each other at roughly the same time.
You have two species of wasp here, possibly a common wasp (Vespula vulgaris), the German wasp (Vespula germanica) or one of the many USA-based yellowjackets (Vespula or Dolichovesupula species) as the smaller, yellow one, and a larger hornet species, possibly the European Hornet (Vespa crabro). Because they are different species, they are competing for resources, so they might well attack each-other.

Good answer. It looked like a duel to me as well. I wonder which wasp won? They both look scary to me.

@anongoodnurse If they're both dead, seems like a pyrrhic draw to me.


text:
Who is this spider, and what is it carrying?
I'm in Fort Worth, and, while out on the trails yesterday, I saw a whole bunch of funnel-spider webs.  Nearby I saw a strangely textured web in the grass, and, when I leaned closer to investigate, saw something that looked a bit like a spider like a spider with some extra parts.  At first I thought that it might be two spiders (and I'm not 100% sure that it's not), but, on looking at the pictures I took, it looks more like one spider carrying something.  See the blob on the bottom right of the spider.  It doesn't obviously look to me like wrapped prey.
Assuming I'm understanding correctly that this is a spider carrying something, rather than a very large spider with an unusual body plan, I'd estimate it was about 80% the size of a wolf spider.  As an additional, very rough, guide to size, you can see some blades of grass in the background.  Although this picture was taken yesterday, it may be relevant to mention that this has been an unseasonably warm October (it was about 90 ℉).

Its the exoskeleton of a spider. The thing thats "carried" is the carapace which usually sits at top and is still attached over some skin of the abdomen.

@Lukas4235, re, cool, thanks! So this is not a living spider at all, but the result of some sort of molting, or the remains of a dead spider, or something like that? If you would like to leave this as an answer (especially if you can make out from this washed-out picture what kind of spider it is, but even if not), then I would be pleased to accept it.

yes it molts in order to grow. With that it can regenerate extremities, chelicerae. I don't know which spider, initially I would have guessed some jumping spider whre this comvex carapave and thick legs occur. but with that web thats unlikely. you can go to inaturalist website, search for spiders in the location you found that and compare.

Re, thanks!  Since this is 10 days old, I don't think that there's a rush to ID the spider, so I would be happy to accept your comments as an answer.


text:
Why do humans have sex for recreational purposes?
It never made sense to me why human beings crave sex other than for reproducing. It controls our society. It causes heartache, jealousy, anger, low self-esteem etc.  Sometimes humans will have sex over and over again even though they have no intention of producing a baby. I know it feels good but it doesn’t make sense to do something that risky unless you want a progeny. Why is this so?

I’m voting to close this question because it is posed in relation to the author’s philosophical opinions, rather than as a biological problem such as comparison with animals that only copulate when the female is “on heat”.

"I know it feels good but it doesn’t make sense to do something that risky unless you want a progeny"

This right here is where you are tripping up. It's not about what one wants. It's about the continuation of the human race and not risky at all from that perspective. In that case, anything that increases those chances is a good thing.
Just like eating. How often do you think "I better eat something so I don't die" instead of "I want to eat that thing because it tastes good" or "I want to eat to get rid of this unpleasant hungry feeling."

Yeah you make a good point…….


text:
Movement of the Ribcage during movements of the Thoracic Spine
I want to find a rough relation between the angle of rotation of the thoracic spine and the corresponding segmental movements in the skeleton of the ribcage. I have come across some research which explains in detail the anatomy and axes of rotation for costovertebral and costotransverse joints.
I have also come across literature providing the movements of ribcage in the case of inhalation/exhalation.
However, I haven't found any literature that details the overall/partial movement of the thoracic wall or ribcage bones during thoracic movements. (flexion, side bending, axial rotation etc.) There is also a previously asked unanswered question regarding this topic.
Can anyone suggest any previous work/paper/book/website that can provide me with a detailed kinematics of the thorax region?
Also, can the rotation/translation of ribcage bones be approximated if I know the angle and the axis of rotation of each thoracic vertebrae?


text:
Average surface area of the outer portion of a human skull
I tried Google. I tried Bing. People don't seem to measure the surface areas of skulls much. I was only curious before. Now I need to know. I don't really wants to know about the face of the human skull, just the top, sides, and back "flat" portion of the skull. What is the surface area of this?

Welcome to BiologyStackExchange. Sometimes you have to search through primary sources (e.g. research articles), for example using Google Scholar: Sholts, S.B. et al. Variation in the Measurement of Cranial Volume and Surface Area Using 3D Laser Scanning Technology (2010)

your gonna have to get the linear measurements and do the math yourself, the skull is such a complex shape, surface area is not a useful measure so it is not recorded much and your guidelines are too vague for a meaningful estimation. .that or find a good 3d model and extract the data.


text:
How to access Target Data for PRS analysis on GWAS Dataset
I am working on conducting a PRS analyses on a GWAS Dataset that deals with the alzheimer's disease. The data is split into cases(Participants with the disease) and controls(participants without the disease) dataset. After this, I have performed Quality Control on this dataset. To calculate PRS analysis, I would need to have a target dataset that consists of genotypes that are typically formatted as PLINK binary files. How would I access these binary files and how do I access the target dataset from UKbiobank?
Cases Dataset

Controls Dataset

I have tried to access the dataset from the following link but to no avail:
https://biobank.ndph.ox.ac.uk/showcase/label.cgi?id=263
For reference, the dataset must be in this format:
https://drive.google.com/file/d/1uhJR_3sn7RA8U5iYQbcmTp6vFdQiF4F2/view?usp=sharing

Welcome to the Biology Stack. Please take a [tour] and visit the [help] for more information on this Stack and what we do here. You would be better off putting the required format in a code snippet box. You can do this by editing your question and using the preformatted text button on the tool bar - it looks like a pair of curly braces: {}. You might also find a better answer at our sister Bioinformatics site, but you should avoid cross-posting and request migration if you want to do this.

What do you mean by target dataset?

The page you link says the following:

Researchers must use the gfetch client (available from the Downloads section, instructions for use in Resource 668) to access the actual underlying genomic data or download them from the European Genome-phenome Archive (EGA).

Have you used the gfetch client? Do you still need to obtain the data or do you just need to convert it? It seems to be similar to the formats you've linked, e.g. BED/BIM/etc.


text:
In what sense is PCR a "nuclear-derived" technique?
The International Atomic Energy Agency (IAEA) has launched an initiative, ZODIAC, to combat pandemics that originate in animals. In part, this involves the deployment of kits utilising real-time reverse transcription–polymerase chain reaction (real time RT-PCR), which is described here as a "nuclear-derived" technique.
Nothing about the description, or my understanding of it from Wikipedia makes it clear how nuclear technology, isotopic composition, decay, etc. are involved in the real time RT-PCR technique, but the involvement if the IAEA implies a connection: what is this connection?

“Nuclear” here could be referring to a biological nucleus, though it is unclear from the linked website.

Nuclear-derived? DNA in eukaryotes is derived from the cell's nucleus, maybe that's what they're talking about? Alternatively, you can use radionuclide-labeled bases to do PCR-based sequencing, although that has been almost entirely supplanted by using the much safer fluorescence-based techniques.

I’m voting to close this question because it doesn't seem like it's really a question of Biology.

From what I can tell from other press releases involving IAEA it seems that they're referring to the use of radioactive labels historically used in quantifying PCR products. These days it's principally done using fluorescence rather than radioactivity. Why this is at all relevant to IAEA seems like more of a political question rather than anything involving biology. My guess is that there is some UN policy that gives IAEA jurisdiction over "nuclear-derived techniques" and they're using this umbrella to include PCR, perhaps so they can spend IAEA money on COVID-related initiatives.

That’s very interesting and I dare say you’re right. As a moderator, I suppose you get the final say on what is and is not on topic, but have to say I’m surprised that the history of PCR isn’t.

[HSM.SE] is the appropriate venue for that type of question, but I don't think this one would fit there either. The problem that I see is that this is opinion based (and thus off-topic for this site) since it is asking about why a non-scientific claim is being made.

@user924308 I'm open to other views and expect my actions to be reviewed by others in the community, but I think the question as asked is not particularly close to being about the history of PCR. That is, I don't think a biologist would think of PCR as a "nuclear-derived technique", that designation is only really of relevance to the IAEA as a political entity. As you can see in the comments from acvill and Matt, for a biologist, "nuclear" means "related to the nucleus of a cell". Radioactive compound are "radio-" to us biologists, not nuclear.

I think "why does the IAEA consider PCR to be a 'nuclear-derived technique when modern PCR does not use radioactive materials" could be a good Politics.SE question, though.


text:
How many non-pairing bases can a PCR primer have in directed mutagenesis?
I'm not including a lot of details here, because the problem I'm working with is actually more complex.
Say you have the DNA sequence
5'-...tct gcg gtg gtt ggc att ctg ctg...-3'
Could this sequence base pair with the primer:
3'-aga cgc cac ctt gcc taa gac gac-5'
.. or would the 4 non-bonding bases be too much?
I do realize there exists a better option, which still codes for the desired amino acids:
3'-aga cgc cac cac gcg taa gac gac-5'
Which only has 2 non-bonding bases.

It depends to some extent on experimental parameters. For example, how long can your oligos be? This old publication has a functional site-directed mutagenesis primer with 9 mismatches, but the oligo is significantly longer than the comparator oligos, and it required significantly higher concentrations of $MgCl_2$ (Figure 1). The extra length will buffer the sequence overall against mismatches, as you can imagine, and the higher $MgCl_2$ will lower binding stringency (caveat emptor).
The Addgene blog has the following recommendations for site-directed mutagenesis primers:

As a rule of thumb, 11 bp of complementary sequence on either side of the desired mutation (usually 1-3 mismatched bases) is sufficient for your primers to successfully anneal to the plasmid of interest during the PCR reaction. Ideally, your primers should be free of palindromic and repetitive sequences, but if present, a minor extension can usually ensure that the 3’-base(s) do not form secondary structures. The introduction (or ablation) of a restriction site through mutagenesis vastly facilitates the subsequent process of screening for succesfully mutated clones. Forward and reverse primers are designed to be complementary, but each primer may extend beyond the complementary region as long as an overlap with a minimum 6 bp is maintained. This overlap ensures that the PCR generates a nicked circle rather than a linear product (see figure).

By these parameters, I think that your suggested primer might be ok in theory, but would be more likely to work with additional homology (maybe 2-3bp) upstream and downstream.
It will likely be a finicky reaction as you are pushing beyond the rule-of-thumb limits for mutation size.


text:
How does natural selection interacts with sustained mask use?
At leasts in some European countries, the number of respiratory (non-covid) infectious diseases on children this term is higher than last year and similar to pre-pandemic years in spite of social distance and use of masks. On the other hand, we are seeing how covid variants more infectious are appearing. So my question is: is the use of masks (or social distancing) increasing (from the point of view of natural selection) the (already) higher advantage of more infectious respiratory viruses? At a first sight, it seems to me that the answer is no, but I'm not an expert, and I wonder if this has been studied. In other terms: are we sure that we are not making (with social distance measures) current respiratory viruses (such as influenza) more infectious?

can you link to the sources indicating the general increase in respiratory illnesses? For influenza in the USA at least this appears to be the opposite of the case (I know that you mentioned Europe, but it's hard to imagine that it's so decoupled): https://www.cdc.gov/flu/weekly/weeklyarchives2020-2021/week53.htm (ILINet chart comparing flu seasons). Some flu strains are thought to have effectively gone extinct due to COVID safety measures: https://www.webmd.com/lung/news/20211025/covid-pandemic-may-have-driven-a-flu-strain-into-extinction#1

It's an interesting idea. I suspect the figures for an increase might be as much to do with alert parents being liable to report trivial sniffles more than before - that being said - if you can provide a bit more info to say where you got the figure and how it was worked out (if available) then we'll be in a better position to judge.


text:
Colorful Large Wasp (?) on Milkweed Arizona USA
Observed this very colorful insect on Asclepias subulata (Desert Milkweed) in Phoenix Arizona. About 8 am, temperature about 90F, sunny, late-September.  When flying it seemed to have a narrow waist like a wasp.  About 5 cm long, appears rusty-red in flight (not surprisingly given its size).  As the pictures show, it was enjoying a bit of nectar from the flowers. Would love to know its name so I can greet it properly next time!

Possibly a tarantula hawk (because of its red wings and metallic blue body), and because they inhabit the Southwest US. It being on the flower in the picture makes sense as “...adult tarantula hawks are nectavores and feed on flowers”. They have very painful stings, but as with most insects, if nobody bothers them, they won’t bother you.
The females hunt down and paralyze tarantulas and lay their eggs in them, hence the name. Freaky, isn’t it?

Reference

Very good.  I also found this info https://www.desertmuseum.org/kids/oz/long-fact-sheets/Pepsis%20Wasp.php


text:
Insect Egg Case, and if so, What Insect?
Observed this object today (early October) in Sabino Canyon, on the north side of Tucson AZ, in a riparian area.  It's attached to a mesquite tree (Prosopis spp).  It's attached to one side of the branch, it does not wrap around the branch.  About 1.5 - 2 cm along the maximum dimension.
Looks like some kind of insect egg case and I'm curious if anyone can confirm and knows the insect.

A local graduate student relayed the answer to me.  It is an ootheca of a praying mantis.  There is some additional background on the egg life history here.  Wikipedia reports there are three mantid species.  The upper-left picture of the ootheca here is essentially what I observed, so we may be looking at the genus Stagmomantis.  There are some other great pics at that last site.

Hi Bryan, self answers are great but we like answers to have some support and a bit more information than one line. If someone gave you a tip, now you could write a good answer by using that tip to find a reputable source that describes a praying mantis ootheca that looks like yours, include a cited picture, and maybe even get a guess at a particular species based on your location, if possible.

I shall expand the answer in a few minutes.


text:
When the CD4+ gets activated and help B cells, does it have to be the same pathogen?
Does the peptide (presented by the class II HLA molecule) that activates a CD4+ T cell need to be from the same pathogen as the antigen recognized by a B cell when the CD4+ T cell promotes the activation and differentiation of that B cell?

This is just a guess, and hence a comment. I don't know of any mechanism preventing it being from a different pathogen/source of antigen, but since co-infection is typically quite rare, it would be rather unusual to find a B cell recognizing one pathogen while taking up a completely different other one and presenting it via Class II MHC. You also need to keep in mind that the antigen recognized by the BCR and internalized by the B cell is directed into the MHC II processing pathway for presentation to T cells.

Yes I guess that makes sense, small question though, does the peptide presented via class II MHC has to be from the pathogen the B cell recognizes? Can it not be something else? (if the B cell is infected by a virus, a peptide from that virus for example)

I think this mostly reduces to the question of whether the B cell presents (via class II) anything that is not recognized by its antibody, which they may.  But immunologists are cleverer than the rest of us and they always have some scheme or other to make the unexpected happen.

@MikeSerfas The key sentence in the first link being "Antigen presentation through B cells can be through [...] or antigen non-specific (BCR independent)"?

Mainly, the B cell which has been activated, needs to "summon" the CD+ T cells to "come for assistance", by handling a pathogen that was recognized earlier - and now the adaptive immune system is trying to bring resources to close the deal with the pathogens.
Generally, there will be mature CD+4 T-Cells floating, but in low amount when there is no clear call for activation.


text:
Do hair cells in the ear also vibrate at frequencies outside our hearing spectrum?
(The question has its origin because I asked myself in how far frequencies outside our perception can harm our hearing.)
First of all, the energy of a mechanical wave (in this case, the sound wave, which stimulates periodic movements of a gas) is proportional to both amplitude and frequency. Often, I read that it is written that energy depends only on amplitude, but when I have two waves with the same amplitude, and one has a higher frequency than the other, it apparently carries more energy. It has a shorter wavelength and moves the molecules much faster over the same distance. Since $E = F * s$, a wave with a higher frequency must carry a greater force (and therefore energy) to overcome the inertia of the molecules more quickly.
I'm not entirely familiar with how the ear works, but I do know that it has three sections. Waves enter through the outer ear, continue to vibrate the eardrum with their frequency, the middle ear amplifies this, and then somehow it goes into the inner ear, where there's a fluid-filled cochlea with hair cells. Certain frequencies can only reach specific spots due to the cochlea's geometric structure, allowing differentiation of pitch. Specific hair cells vibrate more strongly for certain frequencies, opening ion channels and sending signals to the brain, or something like that.
However, what I'm wondering now is whether it's really about the geometric structure or the fact that the hairs are of different lengths, thus having different natural frequencies, and frequencies that match their natural frequencies simply stimulate the right hairs through resonance? If that's the case, one can consider it similar to a forced oscillation, for example, when ultrasound reaches the hairs, we're far from the resonance case, so the hairs vibrate at ultrasound frequencies, but the displacement is extremely small, is that the reason they don't transmit signals?
How can I understand this? And if ultrasound stimulates the hairs to tiny vibrations, where does the rest of the ultrasound wave energy go? Do the hairs heat up, or do they simply reflect it (since in non resonance case the energy transfere between an exciter and oscillator isn't really good... try to excite a spring with a weight attached to it with a significantly faster frequency than its natural frequency from above, and you'll see that even when you wiggle it with high amplitude, the oscillator hardly moves from its position but only twitches faintly at your specified frequency, so same frequency but lower amplitude means the energy almost stays in the exciter itself)?
TLTR: Are vibrations in the ear stimulated at frequencies beyond our perception, and what is the reason we don't perceive them even when we increase the amplitude (decibels)? (And I'm referring to vibrations that don't originate through bone conduction, I've also read about this possibility.)

Hyperphysics has a good overview of human hearing from a physics perspective you may want to check out. It should clear up some misunderstanding you have.
First, the idea that hair cells in the cochlea are like strings that vibrate at their resonance frequencies is interesting and I understand how you would think that is what happens, but it is wrong. Each individual hair cell has 50-150 stereocilia linked together. When longest ones move, they pull on the second-to-longest ones, which pull on the third-to-longest ones, and so on until they all move. This collective movement is what triggers the nerves to fire and signal that a sound was heard. (source)
This leaves the question of what causes the longest sterocilia to move. The base of the hair cells are imbedded in the basilar membrane while the sterocilia are connected to the tectorial membrane. Both membranes are between fluid filled canals. This image shows the arrangement very well:

The basilar membrane had different physical properties along its length. For this reason, when a sound causes vibrations in the canals the basilar membrane only moves relative to the tectorial membrane at certain spots. The relative movement of these membranes causes the sterocilia to bend, which cause the hair cell to trigger the nerves.
Now that all of that is out of the way, we can finally answer the question: why does turning up the amplitude of ultrasonic sounds (i.e. sounds with frequencies above human hearing range) not trigger hair cells eventually? To quote a 47 page report on how humans detect ultrasonic sounds: "The impedance-matching function of the middle ear, necessary to transmit sounds from the outer to the inner ear, is known to be unable to handle ultrasonic frequencies (Pumphrey, 1950)." Literally all that stuff I just talked about is irrelevant. Ultrasounds are unable to be transmitted by the middle ear no matter how large the amplitude is. The only way ultrasounds could ever trigger the nerves is if they bypass the middle ear, such as by vibrating the bones of the skull.
That report's source does not elaborate on why the middle ear is unable to do this, but I found this paper that focuses on the middle ear as a physical system. From figure 3, we see that ultrasounds, which are above 20kHz, have extremely little gain from the middle ear, meaning they are barely transmitted at all:

Sidenote:
"Often, I read that it is written that energy depends only on amplitude" This is only true for electromagnetic waves. In mechanical waves, the energy is proportional to the square of the amplitude and the square of the frequency.

The "vibrating string" metaphor would apply to the basilar membrane rather than the individual hairs.


text:
How can SNPs be well-defined if chromosome lengths differ?
I don't have a background in biology, but is trying to learn more about genetics; I have watched many videos about SNPs and still feel confused about the concept of a single nucleotide polymorphism. According to wikipedia, a SNP "is a germline substitution of a single nucleotide at a specific position in the genome". What I am most puzzled by is the concept of a 'specific position in the genome', if chromosome lengths differ, how can we talk of a 'specific position'?
For example, if we have two arrays of items that are of the same length:[A,C,C,C,A,T,G] and [A,C,G,C,A,T,G] then it is straightforward to that the entries at the third position of each array are different. But with chromosomes, their lengths differ, so it might look like: [A,C,C,C,A,T,G] and [A,C,C,C,A,A,T,G], now how can we say what corresponds to what? Do we say there is a SNP at the fifth/sixth base pair?
What about something more different like [A,C,C,C,A,A,T,G] and [C,C,A,A]? How do we know what corresponds to what? What are the SNPs?
What if two individuals each has a chromosome 1 that differ by many base pairs, how do we know what corresponds to what?

The reason we can compare SNPs between different people is because sequencing reads are aligned to a reference genome with a fixed set of coordinates for each chromosome (local alignment), rather than aligning the entire chromosomes of two different people (global alignment). For instance, 10:3424234 refers to the 3424234th base-pair on chromosome 10 on the reference genome.
Say we wish to compare this particular SNP between two different people; we can sequence both individuals and reads covering the 3424234th base-pair on chromosome 10 will be produced and aligned to the same part of the reference genome; we are certain that the reads originate from the same part of the genome in both individuals. Then, it's trivial to look at this position and see whether it differs between the two individuals. It therefore doesn't matter if one individual has chromosome 10 twice the length of the other (although this would never be the case in reality), as long as the read originates from the same part of the genome in both individuals, they can be compared.

I have accepted this answer although I don't fully understand it. Could you please tell me where I can find out more how "reads covering the 3424234th base-pair on chromosome 10 will be produced and aligned to the same part of the reference genome"? Any textbooks recommendations?

In the image, say that we are interested in base pair 114. Read2 is aligned to that position and tells us the genotype at this position. If we do this for two people, then we can compare the sequences on the reads to see if they are the same or different. Does that help?

Please allow me to ask 2 different questions: How do we know that Read1 is correctly aligned? There are 2 discrepancies. How do we know that Read3 is correctly aligned? Is this all done by statistical/computational methods?

Yes, the reads are about 25 base-pairs long, and there are sophisticated algorithms to make sure they are aligned correctly, e.g. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2705234/

Read3 has two extra C's in the middle, does this imply this person inherited a mutation (or two mutations), specifically, 2 C insertions? It looks like this procedure works because human genomes are largely the same.

Yes - exactly right on both counts.

It may be easier to understand this with an analogy. Think of the genome as a book, and the chromosome as a chapter in the book.
If someone were copying the book by hand (as was common before the invention of the printing press), they'll make some mistakes. The vast majority will be copied correctly, but here and there they'll misspell something, and might even occasionally leave out of duplicate a word.
These mistakes are analogous to mutations during genome replication. As long as they're rare, you can easily recognize all the common parts of the original and copy, and the places with the errors stand out as SNPs.
E.g. if you go from

The quick brown fox jumped over the lazy dog

to

The quicck brown fox jumped over a lazy dog

you can see that an extra "c" was added in the second word, and the second "the" was replaced with "a". But for the most part the two sentences are the same. And just as we're able to make sense of the sentence with these errors, the genome has enough redundancy (as well as "junk" that has little effect) that the genome still works with a few errors and might even be beneficial (but some can cause diseases, or be catastrophic enough to prevent the organism from developing at all).
SNPs aren't the only kinds of mutations, they're just some of the easiest to analyze because they stand out so well. For instance, humans have 46 chromosomes, while great apes have 48. Scientists have determined that human chromosome 2 resulted from the fusion of two chromosomes from the common ancestor of humans and apes. The analogy would be an editor deciding to combine chapters of the book when releasing a new edition (although in evolution there's no editor making conscious decisions, it just happened accidentally, as if the chapter heading was left out when copying). It took some genetic sleuthing to determine whether this was originally two chromosomes that merged in humans, or one chromosome that split in apes; you can read about it here.

Agreed this is a good analogy. Some other aspects that the analogy helps with is showing why you need context; if you just had the word "quick" it would probably be hard to ID the typo as just a "SNP", just like in OP's 4-7 base examples (maybe the original was "duck" and both the q and i are inserted). But, once you have the whole sentence, it's clear where exactly the difference lies. It also doesn't matter if you only started copying from Chapter 3, or have extra introductory pages; it's still clear where the exact change is from the local context, regardless of the total length.

Good analogy, thank you.

But as more and more mutations occur (like in 500 million years), the genomes will become less and less comparable, right?

@NoppaweeApichonpongpan Yes, although there are still meaningful similarities. There are some genes that control some basic biological processes that are common to very disparate species. It's kind of like the way most fairy tales begin with "Once upon a time".

Or the way each chapter of a book begins with "Chapter ##".

so it might look like: [A,C,C,C,A,T,G] and [A,C,C,C,A,A,T,G], now how
can we say what corresponds to what? Do we say there is a SNP at the
fifth/sixth base pair?

We say the second one has an insertion at 5.
Have you read the vcf format?  It describes how all kinds of variants are documented.
https://samtools.github.io/hts-specs/VCFv4.2.pdf

What about something more different like [A,C,C,C,A,A,T,G] and
[C,C,A,A]? How do we know what corresponds to what? What are the SNPs?

Absent any context, why would you want to compare two completely different sequences like that?
If you really wanted to compare them, surely single nucleotide polymorphisms isn't the right way to think about the differences.

I don't yet have a clear picture of what an organism's genome is 'supposed' to look like. Thank you for your answer.


text:
What is the size of different mouse brain cells?
I am trying to isolate microglia from the adult mouse brain. I wondered if I would get pure microglia culture if, after homogenization, I filtered cell suspension through a 70um filter. But I could not find information about the sizes of different brain cell sizes.

Welcome to Biology.SE. This is not simply an answer site, but instead a site that promotes self-learning with some expert help. Consequently, questions that show little or no prior research effort are off-topic on this site. Please [edit] your question and tell us where you've looked for answers (with citations), what you do know about the topic, and where exactly you still have questions. Please take the [tour] and consult the [help] starting with [ask] for details.

In situ, cortical neurons have soma commonly in the range of 10-20 um (see for example https://en.m.wikipedia.org/wiki/Pyramidal_cell); it doesn't much matter if you talk of mice or any other mammal.
I'd recommend reading methods sections in papers that try to do something similar to what you want, rather than trying to invent a method from the bottom up.

Thank you for your answer. The problem is I got a protocol for microglia isolation in my lab, and they told me that it works fine. However, it doesn't work for me so well, so I'm trying to make slight changes to adapt this protocol to work better.

@Monika1223 It can be really frustrating when people ask about just part of their problem pertaining to their narrow solution without context. StackOverflow has called it the XY problem: https://meta.stackexchange.com/q/66377/401068


text:
What is the cause for these patterns on my kiwi fruit?

Have a look at the top right side of the fruit. There are these grid like vellular patterns over it. The fruit seemed tender at time of taking the photo.
Unsure if the pattern developed over ripening or not. Never paid attention except when I took it out of the bag.

It looks like a giraffe pattern: https://www.google.com/search?q=voronoi+in+nature&sxsrf=AJOqlzUHKjvL203Q28o9-8-PQ5bHU_sXVA:1679211970845&source=lnms&tbm=isch&sa=X&ved=2ahUKEwjW-5iIwOf9AhXqVqQEHZcnAf4Q_AUoAXoECAEQAw&biw=1707&bih=863&dpr=1.5

These are blemishes from rubbing of the fruit while on the vine (against other fruit or a branch) or possibly from damage from water sitting on the skin or from a mite or similar parasite.
There should be no or very minor damage below the skin on the part of the fruit that you eat.

That pattern is called a voronoi it corresponds to cellular shrinkage boundaries, like mud-cracks, giraffe patterns, puff balls, jackfruit skin, cell mushoom pores, fly wing veins, leaf cells, bubble cross sections, skin cells, and it can be found on interactive graphics like https://www.google.com/search?q=shadertoy+voronoi&sxsrf=AJOqlzVOpCKLmiwgEsDk2lcZzMhurWRgAw:1679212442864&source=lnms&tbm=isch&sa=X&ved=2ahUKEwiq5aLpwef9AhW6T6QEHVx5C7oQ_AUoAXoECAEQAw&biw=1707&bih=863&dpr=1.5

@bandybabboon you should write your own answer, perhaps citing this one, but giving some more background on Voronoi patterns in nature - how and why they form.


text:
How is mRNA made in a lab
I'm not a biologist, but I think I have a sound layman's understanding of how mRNA vaccines are made. At least this is how it was explained to me:

create some mRNA
get it into a cell (with the lipid nanoparticles)
the cell uses the mRNA, sort of like a blueprint, to create a protein (like spike protein from COVID-19)
the body sees these proteins, attacks them and learns for the next time

So far so good. But what I can not find anywhere, is a (layman, sorry) explanation of that first step: how we can create mRNA in a lab.
In a podcast (Stuff You Should Know) it was explained that it's fairly simple and they just enter the required sequence in a computer.
That's all well and good, but I'm interested in how we can actually create a specific mRNA sequence in a lab from scratch.

In the case of the COVID-19 mRNA vaccines, the mRNA is synthesized by in vitro transcription. The gene of interest (e.g. the SARS-CoV-2 Spike protein) is cloned into a plasmid and transcribed by RNA polymerase. The mRNA is then purified and packaged in a lipid bilayer. NHGRI has a nice infographic explaining the full process.
RNA can also be made by solid-phase synthesis, though this tends to be expensive and low-throughput.


text:
Bimodal melting point of animal fats?
This could fit into Chemistry, Seasoned Advice or other SE forums. The largest number of "close" questions seems to be here; apologies if I'm in the wrong place.
I've noticed when cooking some meats - most notably real mutton, from older sheep - that quite a bit of fat renders out long before the meat is cooked, while some remains even after high-temperature grilling or sautéeing. When working with ground meat (patties/burgers, sausages, patés), the effect seems more dramatic, with a distinct separation in fat release between two rendering-temperature ranges.
Assuming that the phenomenon is real, and not an experimental or observational artifact, can someone here explain the cause? Some possibilities:

Distinct populations of fat types, whether by glyceride number, aliphatic chain length, cis/trans isomers, mixed within each fat-body?

Anatomically distinct (perhaps microscopic) fat bodies with different functions, hence compositions?

Other anatomic factors, like encapsulation of fats with varying degrees of containment by membranes or other structures?

As a cook, one often wishes to maintain high fat content. Expensive Wagyu ("Kobe") beef must be cooked very lightly to retain all the marbling. And there are many distinct ways to cook hamburgers to retain fat while adequately cooking the meat for safety and organoleptic properties. So insight into this kind of melting/rendering behaviour might be useful in recipe design and execution, in the same way that making puff pastry requires careful temperature control when mixing fat into détrempe and beurrage, as well as paste temperature during folding/rolling.
Thanks for any thoughts.

Not going to answer formally because I don't have the ambition to research this. My guess is that it's a combination of factors, including anatomic factors (encapsulation of fats with varying degrees of containment by connective tissue) and physiologic, i.e. we make a number of fats, some that melt at lower temperatures and higher temperatures and everything in between, and maybe you're noticing two of the more common triglycerides melting. I used to make soap (a lot for a long time) and rendered fat from everything from deer/goats to bears ( lots of hunters around here)...

...and there was definitely a range of fats in any one animal fat, and definitely some encapsulation such that pulverizing was necessary to get it. Interestingly (or maybe not), the same is true of plant fat production: it's not just one kind of fat. Sometimes there is a very wide mixture that includes fats that are liquids at room temperature right to fats that you need a chisel and hammer to break up at room temperature (these would be long, very highly saturated fats. Pure coconut oil can be fractionated into several groups with different melting points, one a liquid, another a goop, etc.)

One last comment. Adult sheep have seen more extremes in temperatures than lambs. Animals produce different fats in cold temperatures than in warm. Maybe you're seeing this phenomenon as well. If there were an Organic Chemistry site, this would be a good fit there, I think.


text:
Are nastic responses growth responses?
I know they are non directional movement responses, but like tropic responses, does their movement involve growth?


text:
Why electrical synapses are more common in invertebrates?
I suppose it's because they live in an environment where there's a constant vulnerability to predators and they need to respond quickly. But it's not really the case for many invertebrates and besides many vertebrates too live in such environment.

I think this falls under this Q&A: https://biology.stackexchange.com/questions/35532/why-do-some-bad-traits-evolve-and-good-ones-dont There's not really going to be an answer besides "that's how they evolved".


text:
How do organs grow to the exact shape and size?
We all know that organs begin to grow in a foetus around three weeks after fertilization. But how does the body know exactly which shape and size the various organs need to grow to?

I think this is too broad; you're talking about a whole field of biology ("development") that would be taught across multiple university courses, and the answer won't be quite the same for each organ and can be answered at multiple levels of analysis (e.g., at a systems/overview level, down to individual regulatory genes and products).

"Organogenesis" might help you in your research. It appears "signalling" is key, but not the only factor.

other search terms that may help are "developmental biology" Hox genes" "intrinsic regulatory mechanism" and "feedback mechanism" here is an article to start with. https://www.frontiersin.org/articles/10.3389/fcell.2021.820391/full

The other answers are good. The other part of this answer is that we don't exactly know how it happens in all cases, but we have a lot of knowledge of what influences it.

Thank you @BigMistake!

Thank you @BryanKrause!

Thank you @DKNguyen!

Thank you @John!


text:
Understanding certain limited biochemical impacts of egg yolk
I am researching the use of isolated egg yolk lecithin (EYL) in food preparation. I am interested in its ability to act as an emulsifier without having ancillary negative impacts. I am aware that some people have negative dietary reactions - intolerance (as a separate issue from allergic reaction) to egg yolks. So my question is whether the components in isolated EYL are the same ones that typically result in dietary intolerance or are there other, different components in "natural" egg yolks that might be a cause, where EYL might typically be clear of them.
In attempting to research this on the Internet I have found few details on the chemicals/compounds in egg yolks, let alone which are prone to dietary intolerance. Most of the material I find deals with egg allergies (frequently lumped together as related to "whole eggs, egg yolks, or egg whites"). There are some articles specific to egg whites because of their use in vaccines. That, however, is not helpful for my question, both because of their focus on egg albumin and the allergy issue rather than intolerance from ingestion.
As I had a previous question "closed" for being "off-topic" because appearing to seek answers to medical questions, I want to clarify that I am only after greater granularity concerning egg yolk composition and digestibility so I can do further research.

You'll need to identify research indicating that a phenomenon of egg yolk intolerance that is not an allergy 1) exists, and 2) is sufficiently well-defined to attempt to find a mechanism. Otherwise there is no biological question to answer.

Thank you @Bryan Krause. I now understand how to reformat the question.

I would also consider moving your post to SE Biomedical Sciences where I imagine people are more familiar with the medical conditions you mention.

Thank you for the suggestion @David


text:
Is it possible to consider chlorophyll a as an accessory pigment?
I understand that chlorophyll a is the primary light-capturing pigment. However, in last week's exam, one of the questions asked whether chlorophyll a can function as an accessory pigment.


text:
Can saltwater bacteria grow in petri-dish using the same agar nutrient media?
I am planning on growing bacteria from a seawater sample to do a research project on the relationship between pH (lowered using sulfuric acid) and the bacterial concentration of the water sample (colony forming units per $cm^3$ ). I am planning on using the following procedure:

Would I be able to use the same procedure, or would I need to make modifications to the agar nutrient media because the bacteria I am using would be used to a higher salinity? I am using standard plate agar.

Normal media are at approx "physiological saline" concentration which is usually about 0.9%. I would have thought that seawater bacteria would need saline to be about what they are used to.

Bacteria all have unique ranges of environmental conditions that will support their growth. If we assume they are growing in the saltwater and not just existing, Marine bacteria would at least need to be halotolerant, since they're growing in 3.3-3.7% saline. Some of them will be halophiles, meaning they require at least 1.7% salt (~2x physiological saline). Another point of interest is that media specifically made to culture marine bacteria don't just have higher salinity, they use several other salts (besides NaCl) to reach this salinity level. Some of these may just be buffering agents, but they also provided different dissolved ions (magnesium, calcium, potassium, borate, bromine, strontium, etc) that can be found in seawater a varying concentrations, and could be growth promotion factors for some marine life.
The halophiles will not grow on agar media made for non-halophilic bacteria. The halo-tolerant organisms might grow, as long as their other growth requirements are met. But if the salinity is outside of their optimal growth range, they will likely be more sensitive to other environmental variables, like changes in pH.
If you're only interested in testing pH as a variable, you should use a growth medium with salinity similar to that of their natural environment. If you are interested in their overall environmental growth requirements, you could start with a salt tolerance test at a pH close to neutral, and then do the pH testing at various salt concentrations to see how those factors interact.


text:
Need help to find a dendrology question
Hi I have over 200 people around the world who are willing to collect pictures and/or measurements from trees. The question is, what is the one question we can answer with that information? what is the ONE question in dendrology this information could give an answer to?

Welcome to the Biology Stack Exchange. Please take the [tour] and visit the [help] for more information on this site and how it works. This site looks for questions that are able to be answered with factual references and as such are single questions. This question is likely to be answered with opinions rather than facts as per the don't ask page

I don't think this is a good fit for this site, but you might try searching the key words "citizen science" plus your interests to find projects open to contributors.

I'm not sure that I understand. What question do you want to answer? What do you find interesting? Climate change response? Why not turn to your volunteers for suggestions?


text:
Neuronal reflex circuit
I am having trouble understanding an exam question.
I am given a diagram which looks like this:

I am having a lot of trouble understanding this diagram since it looks unlike the diagrams usually depicted in biology books.
There are two questions to be answered regarding this diagram:

The patellar tendon is tapped just below the knee to trigger the muscle reflex. As a response, the
lower leg is briefly extended.
Which of the numbered neurons in the diagram in the figure above release a transmitter
substance during this reflex?
Stimulation of which neuron or neurons could have caused this signal in neuron 7? (There is an image of the neuron where one can see that the level of the signal goes down).
Since this is a practice exam, I have the solutions, apparently for question 1 the solution is neurons 1,5,7 and 9 and for question two the solution is neurons 6 and 9.

As far as I understand, the solution for question two is due to the fact that only neurons 6 and 9 can send a negative signal, symbolised by the negative sign. For question one, I understand that there is a reflex happening in the extensor muscle, which is why the signal is transported to the spinal cord and back without going on to the brain. However, I am left with a few questions:

What is the cross from neuron 5 to 8 and neuron 6 to 7 supposed to signify?
Generally, why is 1,5,7 and 9 the correct solution for question 1?
In question one: Why is the flexor muscle not at all involved, since as I understand the flexor and extensor muscles are antagonists, so if one contracts the other would have to expand?
in question two, is it even theoretically possible to get a signal from neuron 6? In which case would that be?

Thank you in advance for your help!


text:
Why is there no Ligase in Ligation Independent Cloning?
Ligation Independent Cloning literally says no need Ligation, but it still needs ligase to anneal the fragment to vector. And the Protocol used T4 DNA Ligase for anneal process. What does this mean "Ligation Independent"?
SLIC Protocol

Please provide a proper scientific reference for the method — your link is not to such, and in any case is dead.  You write that ligase is needed in the annealing step, but this is not true. What makes you think that?

@David Ligase works for annealing the Cohesion end.

Annealing means hybridization by complementary base-pairing.  It involves non-covalent hydrogen-bonding. Ligation is a separate process in which the hybridized species might be covalently joined. In LIC the long overhangs keep the recombined together without ligation being needed in vitro. This happens in and by the transformed bacteria.


text:
Can nerves in the human body be spliced with a form of electric wire?
This may be a ridiculous question, and is hypothetical, but I'd like a well-supported answer.
Is it possible to splice copper wire (for example) into the human nervous system? Would the charge carried along the nerves then travel into the wire?
Say for example that I wanted my reflexes to be improved (because I know electrical current travels significantly faster through copper wire than our nerves), and wanted to replace a section of my nerves with copper wire. Would it work?

No, it wouldn't work.

Actually 'current' (in biological context impulse) moves faster with nerves (https://hypertextbook.com/facts/2002/DavidParizh.shtml) than copper wire (http://hyperphysics.phy-astr.gsu.edu/hbase/electric/miccur.html#c1).

Bryan - I appreciate your answer, but do you have a source to back up your claim?


text:
Non fluorescent DNA stain to visualize Drosophila polytene chromosomes
I am working on designing a lab for an undergrad genetics course which involves dissecting and visualising polytene chromosomes from Drosophila salivary glands. I need a non-fluorescent non-antibased staining for the DNA to visualize the chromosomes, as we won't have access to antibodies or an episcope (only compound microscopes). Does anyone know of a DNA dye that could work?

Giemsa stain should work. It is traditionally used in karyotyping staining. It results in G-banding.


text:
Database for commercially available restriction enzymes?
I need a database that contains a complete list of commercial restriction enzymes: name of the enzyme & recognition site.

You are probably talking about type II endonucleases, there are a few databases available from the companies which sell these enzymes like NEB or Thermo Fisher. Additionally tools like NEBcutter, where you can paste a sequence and get all recognition sites for restriction endonucleases in this sequence are useful.
I linked them below in the references.
Edit: Thanks to @Michael_A I have added the lonk to the Rebase Database. It is a database which tries to be a complete ressource on restriction enzymes.
References:

NEB Enzyme Finder
Anza Restriction Enzyme Finder Tool
NEBCutter
Rebase

I think you should add rebase to this list, it is is an overt attempt at a 'complete' and includes information about commercial availability.

@Michael_A Thanks for the tip, I added the info.