text:
Popliteal artery for a heart bypass
My father undergone surgery 10 years ago to get 3 bypasses close to the heart. Surgeons did a very long cut on his leg to get the material to make the bypasses they would later put on his chest.
What I understood at that time, is that they took three sections of the popliteal artery to obtain the material to make those bypasses, and that they fixed the cuts again to restore such artery. The reason why that artery was chosen is because it is very elastic and surgeons can extract a section and stick it together again.
My father is convinced they removed the whole popliteal artery from that leg and chopped it down to make the material they would use for the bypasses.
I am trying to find information about this procedure to find out who is wrong. The problem is that we both are completely illiterate in medical stuff, so we are lost in the mist. What I found is that the popliteal artery is important and blockage could be problematic.

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I'm not a physician, but I suspect the popliteal artery may not have been the vessel used.  The popliteal artery has a very important role in supplying the leg with blood, and maintaining the blood supply from it to the lower (distal) leg is sometimes reason for harvesting other vessels.
You described a very long cut, which sounds like what you would see for harvesting the great saphenous vein.  The great saphenous vein is the longest vein in the body, and dominates recent scientific publications in response to a query of ''coronary bypass harvesting''.  (There are publications in that batch evaluating newer endoscopic techniques in which the long cut can be avoided)  Wikipedia reviews the use of this vein reasonably well.

This is the correct answer.

I believe you are right, it must have been the saphenous vein. What I am not clear yet, if it is removed completely or just removed a section and the cut ends joint again.

@val It isn't stitched back together if that's what you ask. The reason a superficial vein is used is because collateral circulation is sufficient. The saphenous vein is not necessary.

See, generally for coronary bypass surgery to relieve ischaemia of heart, a segment of 'Great Saphenous Vein' is removed and used for aorto-coronary grafting to bypass an arterial obstruction. Due to the opposite direction of venous valves (Veins in lower limb allow blood to move upward), it should be reversed in direction before ligating.
Now you are telling that popliteal artery was used for the bypass, but I doubt it.
Although there is an arterial anastomosis around knee joint that allows slightly compensated blood flow even after Popliteal artery obstruction. So, if the great saphenous vein was not in a condition to be used for a bypass, the surgeons might have used popliteal artery.

I think the doctor will definitely clarify everything to you & he/she won't do any harm to your dad.


text:
When is it better for a gene to cause a biased sex ratio?
Because genes are selfish and want to maximise their transmission from generation to generation, if they can distort a population's sex ratio, isn't it always in their interest to cause a biased sex ratio? Or are there cases when distorting the sex ratio isn't in their interest because they decrease the overall fitness at the higher level, i.e., incur too much damage in the individual/population? Their main priority is still to subsist in a population before spreading, right?
Thanks in advance :)

I'm afraid that I'm a bit confused about what "subsist before spreading" is supposed to mean. Can you please clarify?

I’m voting to close this question because the anthropomorphic formulation of this question deprives it of all scientific meaning.

Well first if a gene is not on a a sex chromosome there is little advantage in changing the sex ratio. This is why most of the ultra-selfish genes we know about are on sex chromosomes. A gene is not helping itself spread if makes more Male offspring unless one of two things is true, it is on the Y chromosome or there is already a bias making male offspring more successful. the latter actually helps keep populations rex ratios stable since if there are more of one sex generally having offspring of the other sex is an advantage.
The most impactful sex ratio altering genes we know about result in selfish sweeps where populations can collapse as they take over and eventually prevent mating entirely. but up until that final generations with no mates the gene in question has an advantage, evolution does not care about the survival of the species or population, if a gene can improve its own ability to spread at the cost of the population then so be it. fitness at higher levels is basically irrelevant. A gene is perfectly capable of spreading by favoring itself and driving the species/population extinct. In many ways run away sexual selection is this in a nut shell, detrimental to the individual and population but beneficial to the gene.

Thank you! This is a very useful answer.

First of all, we have to define what is meant by distorting the sex-ratio.
1) Changes to the sex-ratio as defined by the principles of the underlying Sex-determination system, can be seen as extremely unlikely:
In most species, sex is determined by inheritance of sex chromosomes, which based on meiosis results in a 50:50 sex-ratio. In this system, sex is determined by the presence or exact count of the sex-chromosomes (dependent on the species). Once this sex-system is established, I would personally see it as "frozen" and very unlikely to ever change. Other sex-determination systems are based on temperature and other environmental factors, and you can safely assume that evolution of their sex-ratios is based on advantages in the spread of the responsible genes. (Either through higher transmission rates within each population, or through a higher survival of the populations as a whole.)
2) Distortion of the perceived sex-ratio within the XY sex-determination system via TRD:
Transmission ratio distortion (TRD) occurs when one of the two alleles from either parent is preferentially transmitted to the offspring. This leads to a statistical departure from the Mendelian law of inheritance, which states that each of the two parental alleles is transmitted to offspring with a probability of 0.5. A number of mechanisms are thought to induce TRD such as meiotic drive, embryo lethality, and gametic competition. Importantly, such mechanisms only affect the sex-ratio, if the corresponding selfish gene sits on a sex-chromosome.
In this context, it is important to distinguish between true meiotic drives and killer meiotic drivers, as can be read in this review-paper. Killer meiotic drives often use complex [poison|antidote] systems, in which a tightly joined pair of a killer and an antidote gene together cause lethality in (haploid) gametes lacking the antidote containing chromosome after meiosis, while the poison is still present.
In general, drive alleles are predicted to be transient and evolutionarily labile. The transmission advantage enjoyed by drivers can allow them to become fixed in a population. After fixation, all individuals will be homozygous for the driver and exhibit no drive phenotype. However, if it affects a sex-chromosome, it could cause a bizarre state: On the x-chromosome, the mechanism would create a disadvantage in propagation due to the lack of male off-springs. On the y-chromosome, it might theoretically eradicate the whole population. By the way, such systems are considered for mosquito control.
Importantly, I would also like to address the gene R2D2 is an example of the true meiotic (see original publication), which is a “selfish” genetic element that exploits asymmetric female meiotic cell division to promote its preferential inclusion in ova (while the other female haploid cells die). However, against the suggestion of a commenter, this gene is NOT able to cause a distortion of sex ratio in mice, as females are homologous in X chromosomes; the ova always contains an x-chromosome.
So I will answer your question regarding selfish-genes, if it "isn't  always in their interest to cause a biased sex ratio" with a clear NO! Distortion of the sex-ratio is an extremely rare event that can result in strong disadvantages for the responsible gene, causing its own distinction.

real life sex linked genes like R2D2 in mice disprove your statements.

The op asked in bold letters of genes always try to change the sex ratio.

R2D2 is an example of the meiotic drive through asymmetric cell-division (female). The cell always contains the x-chromosome.

This means that R2D2 is entirely off-topic.

it is a selfish genetic element which changes sex ratios to change its own spreads in the population, thus disproves your middle three paragraphs. thus the bulk of your answer. other examples include selfish X chromosomes in Drosophila obscura, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1200995/

I will edit my text in the weekend to clarify my points.

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sort: votes


text:
Non-radioactive nucleotide labeling compatible with reverse transcriptase?
Are there any methods for nucleotide labeling which are compatible with use for reverse-transcription, besides radiolabeling, and for which the regulatory framework in the EU / USA are permissive ? Regulatory obligations around radionucleides being too strict.

Biotin-labeled nucleotides can be incorporated into cDNA by reverse transcriptase.  Jena Bioscience, a provider of biotin-labeled nucleotides, has a table showing which nucleotide chemistries have been successfully used with reverse transcriptase, though you'll have to delve into the data sheets of specific products to get the references.
One reference provided on the product page for biotin-11-dCTP:
APOBEC3G Inhibits Elongation of HIV-1 Reverse Transcripts
This study looks at natural endogenous reverse transcription (nERT) in HIV.  From the methods:

For this assay, a nERT reaction was performed essentially as above, with the exception of the dNTP addition: pelletted virions were resuspended in PBS, 2.5 mM MgCl2, 15 µg/ml melittin and 0.5mM biotin-11-dCTP (Jena Bioscience), and incubated at 37°C.

Yes, Biotin is non radioactive option used for labeling of nucleotides. Various enzymes used for incorporating this biotin labelled nucleotide are:  Taq Polymerase for Ploymerase Chain Reaction, DNA Polymerase for Nick Translation, Moloney Murine Leukemia Virus Reverse Transcriptase for Reverse Transcription, Klenow Exonuclease for Primer Extension and Terminal deoxynucleotidyl Transferase for 3'-end labeling.
The detection of these Biotin labeled probes is done using streptavidin conjugated with a horseradish peroxidase, alkaline phosphatase,  or agarose/magnetic beads.
(Via: https://www.jenabioscience.com/probes-epigenetics/dna-cdna-labeling/hapten-labeling-of-dna-cdna/biotinylated-nucleotides
https://www.promocell.com/f/product-information/manual/PK-CA-BIO-DUTP-1000P.pdf)

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text:
Can I use fluorophore conjugated antibody as neutralizing antibody?
I need to order a neutralizing antibody to block a protein of interest.
The pure grade functioning antibody (no conjugates) is substantially more expensive than the fluorophore conjugatated ones.
Can I achieve the same by using let's say Ab conjugated with APC/PE as a neutralizing antibody compared to the pure functioning grade ones?
Any insight would be great.

In short, yes, most likely.  When an antibody binds to the antigen at a region (epitope) that is needed for the antigen's activity then the activity is reduced ("neutralized").  The (proper) labeling of an antibody will usually not affect which epitopes it binds to, and so it will work OK (but it may have lower titer than the unlabeled antibody).  As always, there may be some exceptions to this.


text:
How large a part of the corona-virus is coding?
If you find an example of a sequenced string of coronavirus it is about 30.000 long. Looking for example here https://nextstrain.org/ncov/europe you'll see that by far the largest part of this is actually coding. But is that because that is the entire strain or is it because they are only showing the ORF-part? If the latter is the case how large is the non-coding part then compared to the coding part?

30Kb is the total length of the genome, including non-coding regions.

And I think the reason why it's not easy to find a % of non-coding region(s) stated for almost any virus is that it's not very certain how much is actually non-coding given all the "tricks" (non-canonical translation) viruses use https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.0.042499-0

Viral genomes are, in general, mostly coding - often in multiple ORFs.

It is about 92% of the RNA that is protein-coding. ORF10 is not coding according to newer results, see e.g. Jungreis, Sealfon, and Kellis (2021). The article is about identifying protein-coding ORFs and distinguishing them from non-coding ones.


text:
Exact definition of homoplasy?
I am a poor mathematician looking into the Sars-Cov-2 genome. Is there a proper definition of the word homoplasy? Is it just mutations that happened independently or does there have to be indications that the mutations give an improvement in fitness?

Homoplasy just refers to the fact that the mutation happened independently. While several sources only discuss homoplasy as a phenotypic characteristic, and in contrast to homology (and thus suggest an adaptive implication), in general,  there is no assumption that the mutation gave increase in fitness (see this paper).

According to Wikipedia (obviously not the final authority on scientific questions, but often reliable), homoplasy occurs

when a trait has been gained or lost independently in separate lineages over the course of evolution

There's nothing in this definition about the fitness implications of the trait (beneficial, deleterious or neutral).
"Trait" is a more problematic/nebulously defined term, because you have to carefully define what the trait means in different lineages, but in this case it's probably relative to aligned sequences, e.g. "a G at position 575 of the aligned sequence", or "a deletion from positions 575-580".


text:
ABO allele frequencies: Why use the EM algorithm?
In textbooks and lecture notes and slides posted online, determining allele frequencies using blood type information (ABO), under the assumption of Hardy-Weinberg equilibrium, is accomplished using the EM algorithm. It seems to me, though, that this problem can be solved using basic algebra: If $a$, $b$, $o$ are the frequencies of the $A$, $B$, and $O$ alleles, respectively, and $p_A$, $p_B$, and $p_O$ are the proportions of the population in question displaying blood types $A$, $B$, and $O$, then
$$
p_A = a^2 + 2ao,\quad p_B = b^2 + 2bo,\quad\text{and}\quad p_O = o^2.
$$
Inverting the third equation gives $o$ in terms of $p_O$:
$$
o = \sqrt{p_O}.
$$
Plugging that into the first equation and rearranging, we get the quadratic equation.
$$
a^2 + 2\sqrt{p_O}a - p_A = 0
$$
Solving using the quadratic formula and throwing away the negative solution, we get
$$
a = \sqrt{p_O + p_A} - \sqrt{p_O}.
$$
Symmetrically,
$$
b = \sqrt{p_O + p_B} - \sqrt{p_O}.
$$
Thus, we've solved for the allele frequencies $a$, $b$, and $o$ with only basic algebra.
In the standard textbook case in which $p_A = fa = 186/521$, $p_B = 38/521$, and $p_O = 284/521$, this gives
$$
a \approx 0.21,\quad  b\approx0.05, \quad\text{and}\quad o\approx0.74,
$$
which is close to what you get after a few iterations of the EM algorithm.
Question (finally): If the above calculation is correct (if not, please let me know!), what is a "simplest" non-synthetic (real data, from the literature) example of an allele frequency computation from phenotype data that actually requires a sophisticated technique like the EM algorithm?


text:
Inward rectifying potassium channels during undershoot of action potential
My professor said that inward rectifying channels help move the membrane potential back to the resting potential during the undershoot phase of the action potential. The membrane potential would have to be lower than the equilibrium potential of potassium for this to occur (inward potassium driving force), but the membrane potential never goes below the equilibrium potential of potassium during the action potential. So, when are potassium rectifying channels actively passing ions?

I hope I can maybe shed some light on this concept for you.  Rather than complicate anything more than necessary, let's start small and build. To directly answer your question, these channels can function as leak channels (so ions are always flowing through them at some rate) or can be open at select voltages (ions will only flow upon voltage-selective opening of the channel).
Here's a little more detail.  These channels are involved in a number of physiological processes (not only in neurons, but smooth muscle and cardiac cells as well).  One such process is, as your professor pointed out, to drive the membrane potential back to rest after you hyperpolarize the cell following an action potential.  I completely understand your confusion with this concept because in order to properly answer your question, I've gone through a number of resources to make sure I give the most complete answer possible.  Here goes:
Maybe the most important part!!!  These inward rectifiers were originally called “anomalous” rectifiers because, let's face it, they're goofy.  They don't do what you expect them to do (as you have pointed out).  Part of the reason is that there are molecular mechanisms that cause these channels to be blocked and preferentially permit an inward conductance, despite what you'd expect.  There's a decent review article on these channels that might help your understanding (the introduction is the most important part).  You can find it here http://physrev.physiology.org/content/90/1/291#ref-233.
Now I'll try to get into a different explanation that kind of oversimplifies things, but I believe might help.
Remember that the gradient is not solely electrical in nature, it is an electrochemical gradient.  Now you're probably thinking to yourself "I know that, dude, don't patronize me!"  I only bring this up because it appears your biggest concern is how the electrical properties of the gradient regulate K+ flow across the membrane (heavily considering the electrical driving force by focusing on membrane potential minus the Nernst potential for K+).  However, flip that thinking for a second.  Specifically, think about what happens during an action potential solely in terms of concentration.  Your rising phase is sodium influx to the cell (you go from lots of sodium outside the cell to lots of sodium inside the cell).  On your falling phase, sodium channels close and potassium channels open.  Thanks to the good ol' Na+/K+ pump, you have a gradient of little K+ outside the cell and a ton inside.  So what happens?  All that K+ rushes out of the cell (as you would also predict from the electrical component of your gradient now!).  That means you had a lot of K+ inside and a little outside, but you now have a lot outside and a little inside.  This goes on too long and you get an undershoot/hyperpolarization, but you have to get back to your resting membrane potential.  Enter the inward rectifiers.  These K+ channels open and (again, thinking solely about concentration) the K+ is going to flow down the gradient back into the cell.  If you throw in the electrical component, remember this:  Neurons exist in a multi-ion system which complicates things like reversal potential for a single ion.  This is a complicated subject that I won't get into, but it boils down to reversal potential being a different property from equilibrium potential, which becomes important in a multi-ion system.

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text:
How does cholesterol affect the fluidity of a plasma membrane?
I was previously taught that cholesterol affects the fluidity of a plasma membrane. At high temperatures, cholesterol decreases fluidity and at low temperatures cholesterol increases fluidity. The Khan academy and Wikipedia pages below say the same thing.
https://www.khanacademy.org/video/cell-membrane-fluidity
https://www.wikiwand.com/en/Membrane_fluidity
Yet, in a current college course, the textbook ("Molecular Biology of the Cell 6th" by Bruce Alberts et al.) says that cholesterol reduces the mobility of the first few CH2 groups of a phospholipid's two fatty acid chains. In this way, the cholesterol makes the lipid bilayer more rigid and decreases the lipid bilayer's permeability to small, water-soluble molecules. However, it says that cholestrol does not actually make the membrane less fluid.
Is the textbook from my current course just a more nuanced explanation, or have I misunderstood something else?

Actually, cholesterol has different effects on the fluidity at different temperatures. When it is cold, cholesterol increases fluidity, preventing the membrane from freezing. When it is warmer, cholesterol decreases fluidity.

Lehninger say the same thing. Sterols decrease fluidity

At normal temperatures, cholesterol makes the lipid bi-layer stronger but less fluid because of the way that it forms hydrogen bonds with neighbouring phospholipid and glycolipid heads and fills the space between the bent fatty acid tails. Unfortunately I am still confused about how increasing and decreasing temperature impacts the fluidity.

I've posted a brief answer, but I don't have a link to the Bruce Alberts text to address the specific claim of the CH2 groups.

Cholesterol certainly affects plasma membrane fluidity. In 1978 Cooper found that increasing the ratio of cholesterol to phospholipids decreased the membrane fluidity. This also reduces membrane permeability and reduces the survival of the cells (red blood cells in that case). I imagine this is where the textbooks draw their conclusions.
More recently Rog et al., 2008 demonstrated the importance of the hydroxyl group in the cholesterol by replacing it with a ketone. This affected fluidity and flip flop rate.

In High temperatures, cholesterol stabilises the plasma membrane through raising the melting point, meaning the degree of fluidity is kept the same.
In Low temperatures, cholesterol intercalates between the phospholipid bi-layer and therefore prevents clustering. Clustering is the stiffening of phospholipids (which can be caused by low temperatures) This controls fluidity.
Cholesterol can also decrease the permeability of the cell membrane towards hydrophilic molecules and ions such as Sodium and Hydrogen.

While this is correct, sourcing your information is important.

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text:
What regulates production of first transcription factors during development?
In my biochemistry class, we learned that transcription factors regulate the transcription of genes. However, transcription factors are also coded by genes, so what activates the transcription of genes that code for the first transcription factors during development?

The first transcription factors for the first transcription after fertilization are already present in the ovum (egg) before it is fertilized.
Generally, all the machinery needed for transcription, translation, and the rest of the many necessary cellular functions are already present in a cell before it divides and develops.  This chain of dependency goes back eons of time to the origin of cells and the very origin of life.


text:
histones in the Hershey / Chase experiment
When DNA is injected into the cell why aren't histones(protein) also injected and why wouldn't the radioactive sulfur therefore also be present in the infected cell

Bacteria do not have histones - the DNA is just naked in the cytoplasm. Therefore no protein was transferred.

@MattDMo The DNA injected onto the bacteria was T2 bacteriophage DNA.

It's true that eukaryotic chromosomes have histones associated with them. But the DNA in the Hershey-Chase experiment was viral, no histones.


text:
How is the recipient's probability of survival calculated in Hamilton's Rule?
This is Question 99 from the 2012 USABO Semifinals Exam:

Assuming that "snonting" is an altruistic behavior that is maintained due to kin
selection, consider the following situation:

A reproductive male, X, lives with his mate near his parents. His other
siblings are all females and no longer live nearby. Based on your observations,
you know that X is likely to produce 12 MORE offspring during his life. His
parents, however, are older and will only produce 3 more offspring during
their lives. One day, a situation arises where X’s parents have a 50% chance of
death. However, if X snonts, his parents will survive with 100% probability.
Given this information, use Hamilton's rule to predict the maximum probability
of death that X can incur in this situation in order for snonting to be favored.

I calculated the answer based on Hamilton's Rule (r⋅B>C), where r = 0.5, B = (1-0.5)⋅3, and C = x⋅12. Solving for x, I arrived at an answer of 6.25% probability of death for individual X. However, the answer listed on the test is 12.5%, which I assume is arrived at by giving the recipient a probability of survival of 1, instead of an increased probability of survival of 0.5. I am wondering which interpretation of Hamilton's rule is more accurate, or if I have misinterpreted the question.
Thanks!


text:
Can the mutation rate vary for individuals of the same species, growing in similar environments?
Suppose we consider several populations who originally inherited their genome from the same ancestor, and that we put for a few thousands generations in similar environments.
Could the mutation rate vary between the different populations or within the same population, but between different time points?

Yes.

between individuals: https://academic.oup.com/mbe/article/34/2/419/2528250
between individuals: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4617969/
hypermutation (transient): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1087688/


text:
GO term for orthologous gene IDs
I have a list of orthologous gene IDs from the first supplementary file in here.
The gene IDs are of the following type:
EOG6STSR2
EOG60ZRJB
EOG6SBFJ2
EOG6P5KX3
EOG6B5PRW

I want to do the GO term analysis for these IDs. I tried mapping them to FlyBase IDs from OrthoDB and then using DAVID. But many of the orthologous IDs are not getting mapped to the FlyBase ones so I'm not getting proper results.
Is it possible to get the GO term analysis done directly for the orthologous gene IDs without mapping them to the FlyBase IDs?

You mean the .bed files in the study?

Yes. I got the orthologous gene IDs from the fourth column of the bed file.

I have a solution for accurate ID conversion but it makes use of a small script (that you'll have to write). The idea is quite simple and the implementation is easy. Would that be fine or you just want an existing reliable ID converter?

I'm comfortable with writing a script. I had written one initially which took the file from OrthoDB, extracted the lines with DMEL as Organism ad then mapped the IDs in the given file.


text:
Map gene IDs to Ensembl gene ID
Forgive me if this question is too trivial.
I have the gene IDs of the following type
EOG6STSR2
EOG60ZRJB
EOG6SBFJ2
EOG6P5KX3
EOG6B5PRW

from the first supplementary file in Comparative validation of the D. melanogaster modENCODE transcriptome annotation .
I'm not sure as to the type of the IDs. I learned that IDs beginning with EOG are Eukaryotic Orthologous Group IDs but I couldn't find these particular ones in any of the databases.
Is it possible to map them to Ensembl IDs or any of the other commonly used ones?

These are not gene ids, but groups of orthologous genes -- try to search for the ids on Google, I can find this page http://cegg.unige.ch/orthodb6/fasta.fasta?ogs=EOG6STSR2&swaptree= and thus you should be able to download the sequences and ids from OrthoDB.
Note that, strictly speaking, the are no Ensembl ids for Drosophila, only FlyBase ids that are also used by Ensembl.


text:
Reason behind colour of hibiscus and sunflower
What is the reason for the red colour of hibiscus and the yellow colour of sunflower?

Welcome to Bio.SE! What attempts to answer this question have you already taken? We ask that all question posters here attempt to search for an answer to their own question and explicitly indicate what research they've already done, what they learned, and what is still confusing or unknown to them. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail, and it will likely be received more positively by our community. Thanks!

Flower color is result of reflection of light due to various color pigments. Evolutionary such pigments were selected due to various reasons like to attract pollinators (Dyer et al 2012). There are two major types of flowers pigments

Carotenoids (produces yellow, orange and red colors)
Flavonoids (produces red, purple, magenta and blue colors)

However, flower color is affected by various other factors (e.g. other pigments, metal ions and its chemistry etc.) along with above pigments.
Hibiscus' dark red color is outcome of Anthocyanins which is water soluble flavonid (Grajeda-Iglesias C et al 2016). However, this pigment is highly unstable and depending on pH of the surrounding it can be red, purple, blue or black. (More details in this book). Hibiscus contains majorly delphinidin-3-O-sambubioside (Dp-samb) and cyanidin-3-O-sambubioside (Cy-samb) as the major anthocyanins (DU and Francis 1973). Chemical reaction responsible for generation and utilisation of these pigment is shown below (borrowed from Grajeda-Iglesias C et al 2016)

In above image, at low pH values $AH^+$ produces red color while  and $(A)$ produces purple/blue, which is thermodynamically unstable. In addition to that co-pigments like Hydroxylatedbenzoic and cinnamic acids, hydroxyflavones (which all are colorless) are also responsible for not only stabilizing these chemical products but enhances the color (Grajeda-Iglesias C et al 2016).


text:
Does this article call into question the theory of evolution?
https://www.quantamagazine.org/neutral-theory-of-evolution-challenged-by-evidence-for-dna-selection-20181108/
The article above challenges how mutations work in evolution. Does this disprove the theory of evolution?

That article is discussing the fine points of how to interpret mutations and says nothing that seems even remotely related to the validity of evolutionary theory?  If there is something in that article that makes you think it might conflict with evolutionary theory please add it to your question and make sure it is clear that you have taken the time to understand this theory.  Otherwise your question is likely to be perceived as creationist trolling and will probably be removed.  A useful introduction to evolutionary theory: https://evolution.berkeley.edu/evolibrary/article/evo_01

Would you please quote the relevant parts instead of just posting a link? Posts should be self-contained, to make sure they are still valid in a future when the link isn't working anymore.

Questions on this site must be intelligible in their own right. The site is intended as a self-contained Q&A site, and in any case it is impolite to expect users to go to some other site to read something. It may also be dangerous as an external site may be booby-trapped. I need to understand your question by itself. That is why I have voted it off-topic as unclear. If you are able to present the argument yourself in a manner that conforms to allowable questions for SE Biology — for which you should take the Tour (you haven't) and read how to ask a good question — I shall reconsider.

First, please note that the article you link is not a peer reviewed article. It is a popular, easy-to-read article.

Does this article call into question the theory of evolution?

No, it does not. What makes you think it does?
The article talks about a very old (and somewhat still ongoing) debate about the relative importance of genetic drift vs selection in evolution. I suppose that you may have portrayed selection as being the only evolutionary process and I suppose that reading about genetic drift as being another evolutionary process may have make you feel like "we were wrong all along" while in truth we have always known a bout it. Note that even Darwin with his very limited understanding of evolutionary processes (compared to what we know today) knew that there are other evolutionary processes than selection.
You might want to read about genetic drift. As a start you could read the following:

Evo101 > Genetic drift
Biology.SE > Why is the strength of genetic drift inversely proportional to the population size?
Wikipedia > Genetic drift

Don’t feel the trolls.

@David — How do we know the OP is a troll as opposed to someone who is starting to explore the limits of their indoctrination?

You will know from experience that there is a body of people who are generally not biologists but do not believe in the theory of evolution on religious, rather than scientific grounds. Such people — possibly from motives they consider morally justified — seek to take every opportunity to publicize their views and frequently abuse this site. One post-hoc means of identifying them is that they never accept an answer. How many of yours have been accepted? (cont.)

…This is a question and answer site so I think one should attempt to discourage such trolls by rigorously applying the site's criteria for on-topic questions, especially when, as in the current case, one is dealing with a new user (no evidence of a previous interest in biology) who hasn't taken taken the trouble to take the tour even (evidence of no interest in the site). A biological question asks for a biological answer. A question of the type "doesn't this prove the theory of evolution" is an attempt to start a discussion (off-topic), at best, or to use the platform to make a statement…

…In this case the question is not self-contained so — as you should be aware — does not fit into our model. We do not exist to discuss articles published elsewhere, nor do we have a mission to convert the indoctrinated. If you feel you must respond, use the comment box to explain why the question is off topic but provide your links to point out where counter arguments can be found.

@David — Thank you for your detailed and thoughtful response!  I know you're correct about fundie trolls, but I also know of individuals who have managed to escape their programming.  Unless you can prove this individual is only here to troll I see no harm in pointing them at places they could begin educating themselves or in Remi.b giving a brief answer and additional links.  While it looks to me like my original comment was in line with your suggested response, I'm happy to hear how it could be improved!

@tyersome — whether or not the poster is a troll, the pertinent question is whether the question is on-topic. You may not realize that users with sufficient points ('reputation') who wish to vote to close a question are presented with several defined categories, as well as a free-form onet. Remi.b will be familiar with this. The question indsputably falls in the "unclear" category as it is not comprehensible by itself. This is a self-contained Q&A site not a missionary. I have no idea what the argument is. If the poster wishes an answer, he must first ask a question that conforms to the site.


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Do new neurons divide propotionally?
Do new neurons divide propotionally?

if i try to improve my reasoning skills,are the new neurons only made for that specific region of the brain that controls reasoning skill?
i have heard that one side of the brain controls the other side of the body, if i try to use my non-dominant hand(left hand in my case),are new neurons only made for right side of the brain,does it improve only some of the brain regions?

There is no evidence of new neurons except in the hippocampus and the olfatory bulb, and the evidence in humans is still controversial.
Skills are not acquired by the addition of new neurons, but by the formation of new pathways between existing neurons. These pathways are highly specific, while your examples are rather vague, like the sort we read in pop magazines: "brush your teeth with your non-dominant hand to become smarter" - it would be great if it were that easy, unfortunately this is just pseudoscience.

Thank you, I always thought that it was real.

So If you take too many IQ tests you won't get smarter in other areas(things) other than the IQ test , you only get smarter at IQ tests, right?

Similarly some brain games, tests claim that they can boost your brain, however they only form new pathways between existing neurons in your brain, therefore you only get better in that specific pattern of the game, test, if this is true most brain games are pseudoscience, am i right?

Yes, most likely the claims of common "brain games" are essentially pseudoscience

It seem's you are assuming that your / the adult human brain produces new neurons over time- this is (largely) incorrect: neurons are non-dividing cells and are all formed throughout embryogenesis and very early childhood / infancy (see also this question).
Only very exceptions to this are known as adult neurogenesis (generation of new neurons), the most likely or active region in humans would be the hippocampus, however the extent or importance of the process in humans is still not really known. Additionally the hippocampus is an area of the brain that mostly holds memories and is not really related to reasoning skills or body / motor control.

If i use my non-dominant hand, does it improve some regions of the brain while having no effect on the other regions of the brain?

"Regions" is to broad: it will have no effect even in the same "region" as a whole.. Anything learned will make new pathways between existing neurons. But these are highly specific, and you wouldn't expect any improvement except in the very skill you have practiced, regardless of the brain regions used in that skill.

@Gabriel are the "new pathways between existing neurons" in the same regions of the brain that was used in that skill?

Not an answer, but a clarification. By "hippothalamus" (a probable typo) above it is probably meant "hippocampus", as is mentioned in wiki link. It is hippocampus which is known "to hold memories", but it is a part of a larger "memory" circuit and is a bit similar to temporary memory responsible for holding only recent memories and integrating recent memories into long-term memory.
This overview of neurogenesis can also be useful.

Yep, that was an error in my answer, thanks for pointing it out - I fixed it now (normally this should probably have been a comment to my answer, but you probably don't have enough reputation for comments yet)


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Surface perception
I'm looking for research studying:

How small and compressed together do particles of a surface need to be to be perceived as solid surface to human touch? E.g. sand still feels grainy. Has there been research on how much it varies between different areas of the body?
Same question, but for where the line of pain lies - walking on gravel can be painful, while walking on sand isn't.

Any pointers to relevant material much appreciated!

Both sensations are dependent on pressure (i.e. area over which a force is distributed). Remember that stepping on one nail is incredibly painful but lying on a bed of nails may not be.

1) Discerning between solid and granular
It is the distribution of the touch receptors in your skin that enables the distinction between solid and granular objects.

The ability to recognize two separate points applied simultaneously to
  the skin from a single point is called two point discrimination.
  Two point discrimination varies with location on body surface. It is
  about 2 mm on the finger tip and increases to over 40 mm on the back.
  (vcu.edu)

Image source: Annals of Neurology, CC licence
2) Touch vs pain
The sense of touch is enabled by touch receptors and pain by pain receptors (nociceptors). In general, pain receptors are activated by greater pressure than touch receptors. Walking on gravel (sharp-edged stones) likely applies greater force on a certain area of your skin than walking on rounded pieces of sand, so it will more likely cause pain.

Mechanoreceptive nociceptors have a high threshold for activation—they
  respond to mechanical stimulation that is so intense it might damage
  the tissue. (nobaproject.com)

More info:

Whole-Body Mapping of Spatial Acuity for Pain and Touch (Annals of Neurology, 2014)
Pain sensitivity and tactile spatial acuity are altered in healthy musicians as in chronic pain patients (Frontiers in Human Science, 2015)

This is exactly what I was looking for - thank you for the summary and references!


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Origins of the body mechanics theory
In physical therapy and occasionally in sports coaching, there's often a precise description of the mechanics of what happens during the movement (which muscles are engaged, which joint moves where etc). I couldn't find any information on where that knowledge comes from - observation and "probing" for engagement alone would not be enough as some muscles are tiny and/or hidden under bigger ones. So, how was the theory developed?
Example: how do we know these are the muscled that perform external rotation (at the shoulder, for instance) ? https://en.m.wikipedia.org/wiki/List_of_external_rotators_of_the_human_body What tells us every single one is necessary? What tells us another one isn't involved?
(please let me know if this is better suited for a different StackExchange)

Its funny that one of the first uses of electricity was to test muscles from donor corpses.


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How do crocodiles stay fit?
My 8 year old son asked me a question I could not answer (and Google, at least in so far as we tried, was no help either).
We were watching a documentary about Salt Water Crocodiles in Northern Australia.
The crocodiles seem very energy efficient: they barely move if they don't absolutely need to (and when they do, it is mostly to eat). Particularly, they hardly ever run, but when they do they are very fast and powerful.
So the question he asked me was: how can crocodiles remain so fit if they don't do any exercise?
If humans just sat around and moved only to eat, ran only when they absolutely had to, our muscles would atrophy. Other mammals seem to be in a similar boat to us humans.
Why not crocs? What distinguishes animals that need to exercise to be strong from animals that don't?
This is the closest question I could find here, but I don't think it assists in answering this question: Do insects' muscles become stronger with exercise?

Imagine their strength and speed if they would exercise.  In other words: what make you think they are currently at their maximum potential?

It is a good point and the proposed answer below seems to suggest there is some truth to that. But still mammals seem to have a lot more built-in 'inefficiencies' (presumably for training) than do crocs. By inefficiencies I mean tendency to exercise without the direct outcome being food: whether play and hunting against long odds (or in the case of humans straight up exercise). And we seem to need those 'inefficiencies' to survive. Why do some species rely on external stimulation to reach fitness while others (apparently) much less so?

Let us start with difference between humans and crocodiles. There are lot of differences but the one which matters in current discussion is thermophysiology.
Unlike humans, crocodiles are cold blooded animals (more specifically ectotherms). These animals needs to get heat from environmental sources to maintain their body temperature. As contrast to humans who can get heat from internal metabolism. That is the precise reason crocodiles are seen always not moving and basking in sun light when it is cold (while go to shade or water if it is hot). Read this for more elaborate strategies they use. If you want scientific reference, you can check this, this or this.
On your exercise point, there are few reports which suggest exercise can enhances aerobic capacity in young crocodiles. In this study they actually put crocodiles on treadmill and checked affect on their respiration. This report suggest  crocodile uses 3 different kinds of muscle mechanisms for lung ventilation. These three act differently in different conditions (means one acts during rest while other during high metabolism). However I couldn't find any information regarding atrophy.

how can crocodiles remain so fit if they don't do any exercise? What distinguishes animals that need to exercise to be strong from animals that don't?

Short answer: Their body metabolism.
Their body metabolism is different from human's. Although doing exercise  might help in their aerobic capacity as mentioned in reference above.

Great answer. Thank you. Though I don't quite understand it as it pertains to strength and adaptation. Humans and mammals seem to need to stimulate muscles in order to develop them to their potential. Superficially, it appears that crocodiles do not. I understand that the distinction you draw (which makes more sense) is between cold/warm blooded (as opposed to crocodiles/mammals), but what I am missing is (a) whether the lay observation that they don't need exercise as much as mammals is true and (b) if true, why?

@rafraf Not the case for all mammals I think, for example the bears that hibernate do not lose nearly as much muscle mass as humans would during the same period of not doing any physical activity

rafraf : your questions are right. Unfortunately, I couldn't find any good studies related to muscle atrophy in crocodiles. On other hand @Zavior is also correct.


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How would substances that have anti bacterial characteristics interact with yeast?
This question has its origins at home brewers where the question was asked how would substances with anti bacterial qualities interact with yeast a fungus?
No one at home brewers was really sure so I thought I would ask here.
LINK

Welcome to Bio. That would depend on the type or class of substance. Can you narrow the question down?

Substances that exhibit antimicrobial activity do so because the microbe itself is susceptible to the mechanism of action. For example, some bacteria crosslink their peptidoglycan cell wall with a transpeptidase (aka penicillin-binding proteins), and penicillin antibiotics block this step. Other bacteria don't do this, and so if you use penicillin there will be no effect.
Likewise, some antimicrobial methods have very broad efficacy against everything, like drugs that inhibit ribosomes, or at the extreme end, bleach. Being said, ginger as in the homebrew link is shown to have a broad action on microbes as denoted in the following article. The question now is does ginger affect yeast?
Google search "gingerol antifungal" (gingerol is apparently one of the potent effector molecules in ginger) and you get a host of results detailing it's efficacy on C. albicans. This doesn't necessarily mean it has the same efficacy on S. cerevisiae, but it does mean that, and this is just a number out of the literature, but a 10% ginger solution may have deleterious effect on fungal growth.
Outside that, I can't really find anything on the actual antimicrobial mechanism of action for ginger, either, so it's difficult to say other than for some reason, they inhibit microbes. They did show that 6-gingerol induces ROS production in tumor cells, which results in DNA damage, but I'll continue to look for an explanation.
What remains, now, is too broad. The ways that antimicrobials interact with different microorganisms is a lot to consider and I can only be about as broad as I've written above without going into a novel worth of text. Hopefully this was helpful!
You can check out this Sigma page on antibacterial modes of action to get an idea of the ways different antibiotics are made to affect microbes.

Remember, the reason we make antibiotics is so that they will work in eukaryotic people.  So antibiotics usually target proteins or processes in bacteria that eukaryotes do not have, or where the eukaryotic version of that target is different enough that the antibiotic doesn't react.  So most yeast will be unaffected by most antibiotics.


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What are the "minimum requirements" for a single cell?
I saw a description of the "minimum requirements" for a cell at http://creation.com/origin-of-life in the section called "What are the minimum requirements for a cell to live?" and I'm wondering if this is scientifically accurate - and if not - what are the real requirements?
[note/warning - the link above is to a creationist site - I'm only quoting this source because I'm trying find the science involved and I didn't find other sources talking about all the necessary pieces. I'm not trying to promote creationism with this question so please don't attack the source or me for bringing it.  If you can find a non-creationist source which outlines these requirements, I'll be happy to update the question and remove this source.)
In summary it lists the requirements as follows:

cell membrane
way of storing information (DNA)
way of reading 2. to make components needed

RNA polymerase
gyrases to untwist DNA
ribosomes to make proteins
(a few others I omitted b/c I don't know if they're really important)

means of creating fuel (ATP synthase)
a means of copying the information for reproduction

The context of the question is similar to Can scientists create totally synthetic life? and a question I wrote What is the most complex biological organism (or precursors) that we have been able to synthesize from raw materials?.
I'm trying to understand what would be involved in making a cell from scratch. Somehow I found this source but I don't know if it's accurate.

An even more minimalistic approach would use a single molecule to do the enzymatic job while storing evolvable informations. In this case RNA alone has been proposed as substitute for proteins and DNA in a very minimal cell. In theory also DNA alone could do the same. However the minimal tasks needed to be done: maintain the self (to be compartimentalized), to grow (to have a flux of molecule not in equilibrium), to divide, to maintain the information stably enough to be useful for the next generation and at the same time prone too mutability to evolve.

So to make cells from scratch you would need: amphiphilic molecules to form a membrane, a decent mix of simple molecules (sugars, nucleic acids, peptides) that serve as reactant and building blocks for more complex things, some simple catalyzer (metals, minerals, pepetides, aptamers, etc..) to run the reactions, enough energy to maintain lots of reactions running and keep them far from the equilibrium. Of course, lots of time...

@alec_djinn - could add you comments as an answer so I could upvote them?

The website is called creation.com; how ironical :P

I don't think this question makes much sense. Just because many cells living today satisfy that list of "requirements", that doesn't mean it's the only way to arrive at self-reproducing entities. If you define life as self-reproduction, then any molecule that catalyses its own synthesis is "alive". Beyond self-replication, the requirements gets pretty arbitrary. If you for some reason list a lipid membrane as "required", then yes you need some lipids. Otherwise not.

I specifically didn't mention the minimum requirements of "life" to avoid these discussions.  I think the concept of a cell is pretty universal and fundamental aspect of all life today. The fact that some people can choose a definition of less sophisticated structures that have characteristics of life is irrelevant for this question.  If you want to make a "cell" (which I think is pretty well defined) - what's involved?

looks like from the discussion below that there are some differences in the definition of a "cell" - but it seems there is more consensus than disagreement.

"so please don't attack the source" Too late. What you will never find at any creationist website are the "minimal requirements for an intelligence/consciousness", because all such known, scientifically demonstrated minds require... you guessed it, brains, cells, DNA and other parts that ID claims require intelligence, which require cells, etc. ID is a circular fallacy and/or relies totally on faith in minds without parts humans need to be intelligent. Furthermore, ID goes backwards from science; simple to complex, and is thus doomed to fail to answer any life or universe-origins questions.

So, to make cells from scratch you would need: amphiphilic molecules to form a membrane, a decent mix of simple molecules (sugars, nucleic acids, peptides) that serve as reactant and building blocks for more complex things, some simple catalyzer (metals, minerals, pepetides, aptamers, etc..) to run the reactions, enough energy to maintain lots of reactions running and keep them far from the equilibrium. Of course, lots of time...
An even more minimalistic approach would use a single molecule to do the enzymatic job while storing evolvable informations. In this case RNA alone has been proposed as substitute for proteins and DNA in a very minimal cell. In theory also DNA alone could do the same. However the minimal tasks needed to be done: maintain the self (to be compartimentalized), to grow (to have a flux of molecule not in equilibrium), to divide, to maintain the information stably enough to be useful for the next generation and at the same time prone too mutability to evolve.
One more point. Life itself doesn't strictly require to be compartmentalized.
You can think of a network of chemical reactions that have the ability to grow, to replicate its components etc but without a cell membrane. However I think that a cell-like form of life is somewhat more likely to happen.

Why a down vote? The answer is pertinent and correct...

I downvoted because it is basically a list of what is needed in a typical cell, not a minimal cell. Hence it doesn't really address the question. Apologies for not commenting earlier. Happy to upvote after edits. Please ping me.

Well, maybe it was not clear enough but as catalysts I have listed metals, mineral and peptides instead enzymes and a have specified that a mix of simple molecules will be needed, this is what would make a cell 'minimal'.Indeed the difference between a minimal cell and a proper cell is the complexity of its building blocks. So, the minimal cell requires the same basic components of a normal cell, but you may expect to have a simpler version of them (less complex, less diverse, less optimized).

Thanks :) good edit and +1 for the RNA enzymatic activity

Cell is the structural and functional unit of life, made up of a small mass of protoplasm delimited by a semi permeable membrane and capable of self reproduction without any living medium. This is a proper definition of cell and the minimal requirements would be all these mentioned here.
You can also see cell theory by M.J. Schleiden and Theodor Schwann.
But most importantly not only genetic information and membrane are required, most required part will be Cell should be capable of self reproduction without any living medium
Like for example RBC is not called cell cause they can't reproduce themselves. But nerve cell is called cell cause though they are not divisible but in embryonic condition the cell division occurred. Also in case of virus, as they can't reproduce without a host,they can't be called cell.
Red blood corpuscles aren't cells have a good proof in this article (check blood trivia part)
red blood corpuscle

Nucleus in case of eukaryotic. But there should be genetic information in prokaryotic cell.

You do realize that the 'C' in 'RBC' stands for 'cell'?

Good to start with a working definition of a cell though, since it is relatively meaningless to answer this question without one. Are your italicized definition a quote or your own?

@fileunderwater actually no. It stands for corpuscle. Not cell. It's very big misconception and sometimes given in book too which is wrong.

@fileunderwater Originally it was called Red Blood Corpuscles.

And I Italicised the definition given in any good book of cell biology. Obviously isn't my own.

@WYSIWYG Well, in that case there seems to be some disagreements, since the American Society of Hematology at least seems to label them Red Blood Cells.

If it does then I am afraid there might be some different logic used there. As you will understand,  RBC is not cell because it can't self reproduce and greatly depend on bone marrow. Where as cell can definitely reproduce itself.

@Demietra95 Well, that's fine. It's just a good idea to add references when you quote something. "Any good book" could be just about everything, and might not be helpful when answers to the question might actually hinge on the specific definition used.

It's probably because they are derived from erythroblast (~immature RBCs), which do have a nucleus. However, the most useful point is probably that definitions of cells aren't black & white. Lots of cells are dependent on other structures to survive (not just RBCs and bone marrow), and the passage "...capable of self reproduction without any living medium" isn't without problems.

For my study I used a book by Sailesh Guha. If it was capable of self reproduction without a living medium then viruses would have been considered as cells. But they doesn't come under cells.

*they don't come under cells  (viruses) .

@fileunderwater Not disagreeing. I just said that originally they were called corpuscles but "red blood cells" is a standard term.

@Demietra95 Incapable of self-reproduction without a living medium goes for many parasites as well, especially obligate intracellular parasites (e.g. some bacteria, fungi and protozoa), but these are arguably still cells.

@fileunderwater I agree with you that there are various intracellular parasites who are incapable of self reproduction and comes under prokaryotes. But they are part of arguments too. In term of evolution they can be defined as the misg link between  molecules

*In term of evolution they are the link between living molecules and and developed cell. But like viruses they are the part of argument whether they are cell or not. Completely It can't be denied neither accepted

I will also recommend you the virology course offered by Columbia University in mooc  where it's seen how they are defined as the neither a complete living cell neither non livings.

@Demietra95 I don't fully understand your last comments. Are you saying that many unicellular (especially intracellular parasites) and maybe some multicellular parasites shouldn't be labelled cells? If so, that would be quite controversial and far outside the mainstream. Also, many intracellular parasites are eukaryotes, not prokaryotes. We should probably move this to chat though.

@fileunderwater according to the proposed cell theory it should  reproduce.  If it doesn't but it has all other living characteristics it doesn't come under a living cell. They stay in a middle portion where neither they can be called living cells neither non living beings. As when they get host, they do reproduce but without it they can't stay alive, they are as good as non living particles. Though I do agree it has many controversies related with it. Even generally in any wiki article or same ranked articles do propose other theories but till now it isn't completely excepted. :)

Here I found a good reference of my words www.redbloodcellbooks.com/rbc7.html check blood trivia part.

Though this may be an old post, there are some things that aren't quite right. First off you are mistaking Terminal Differentiation as not being a cell. Many cells in multicellular organisms are terminally differentiated and will never reproduce themselves. A part of a Red Blood Cells terminal differentiation is to lose most all of its organelles and its genome. Also you make mention of Cell theory, but no where is cell theory does it say that a cell has to be able to replicated itself, only that it arose from a preexisting cell that was living. RBCs fit that definition just fine.


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How many cells does a single blood cell generally visit in its lifespan?
Taking the point of view of a single RBC travelling through blood vessels, approximately how many cells will it affect throughout its lifetime? As blood tends to provide O2 as a whole, I am taking "affect" as being in the general oxygen transfer vicinity of a body cell.
Assuming that:

a RBC lives about ~120 days (source)
There are 60,000 miles of vessels in the avg adult human body (source)
There are ~5 trillion non-RBC type cells in the body that presumably need O2 (source)
Avg speed of 3 mph (source)
Blood cells are uniformly distributed, so any blood cell has the chance to be at any part of the body

So 120 days at 3 mph = 8640 miles travelled by a single blood cell. This represents 14.4% of the human bodies' vessels or about ~720 million cells affected by a single RBC.
Does this back of the envelope calculation make sense?

Not sure what you're trying to achieve here. Why wouldn't you take into account the probability of following the same path twice or more - and why are you concerned about a single blood cell when they act in concert? What's the objective of the calculation except to pass time.?

I have no problem with this kind of speculation; it's fun to wonder about the importance of a single tiny red blood cell, so kudos to you! My only objection is that it seems to presume to never follow the same path twice. Did you take into account that it must pass through the lungs every go round? Also, only about 80% of those miles are capillaries, where exchange is greatest. Anyway, I like this question, but it has no precise answer because of chance/randomness.

@ARogueAnt. - What's wrong with passing time wondering about a single red blood cell? It seems a decent use of time to me (given, an elderly biologist).

TL;DR: No. It's a fun little thought exercise, but unfortunately off the mark.* Most of my statements will be given, i.e. repeated numerous times in the medical literature as factual, though I can't say with certainty how they came to be so.
Assumption(?) #1 Assumption that the 60,000 miles of vasculature in the body all comprise of capillaries where exchange might take place.
Counterargument: In reality, only 80% (50,000 miles) is comprised of capillaries, where presumed "visits" take place. The rest is comprised of the heart itself, all arteries, arterioles, venules, and veins. There are (depending on how they are counted, not including the azygous system) about 30 major veins collecting blood from capillary beds; the larger they are, the more often they will be traversed by the blood cell, until they enter the superior or inferior vena cava on every return. The cell will see the same insides of the heart every go round. I don't want to do the math (I hate math) but (if) there are about 5 liters of blood in the circulatory system, and (if) the heart beats 100,000 times per day (average adult male, of course, just because), and (if) you know exactly how much of that volume is taken up by red blood cells, you can calculate how many times that one cell will visit the same heart every day (I think.)
Assumption(?) #2: Assumption that the red cell will never travel through the same vessel twice.
Counterargument: (See above for where it will travel for sure every day.) Your assumption(?) is based on equal probabilities encountered at every bifurcation in the arterial system, in other words, that every bifurcation in the vascular system is created such that the probability of going in either direction is equal. (Was that a tautology?) That isn't quite so. The probability of a red cell entering vessel A or vessle B (in the literature, described as daughter 1/d1 or daughter 2/d2) at a particular bifurcation varies with the diameters of a and b (with the larger diameter receiving more blood) and the angles of bifurcation (less important but still matters.) (This is just the mouth of one of those rabbit holes.) Randomness is not perfect at bifurcations, especially at the arteriolar level (active muscles will get more red cell visits than inactive muscles, etc.) This doesn't even take into consideration the effect of  endothelial damage (which causes drag in blood flow, thereby affecting the probabilities of entering d1 or d2) which commonly occurs with aging but can start in utero, and which is more common in youth than one normally supposes.**
All things are never really equal, so, as I said in the beginning, No. The longer answer is, "I like this question, but the calculations are off due to the human circulatory system and the lack of randomness at particular bifurcations within it.
*But I like your curiosity and tenaciousness. That you bothered to do some research and put it together here is refreshing, and though my answer is without doubt incomplete/flawed, you deserve one. So here it is (with my apologies for its quality.) I wish an anatomist was interested in answering; the quality would be so much better!
**As an intern, I once had the very sorrowful experience of admitting an healthy appearing, exuberant 4 year old child to the pediatric surgical service. The only presenting symptom was that the child started squatting during exertion (not good), and on exam, had a murmur which was caused by aortic stenosis. This was long before imaging studies were as sophisticated as they are now. The pediatric cardiac surgeon took him to the operating room (OR) to replace the valve, but there was so much atherosclerotic aortic damage that there was no healthy tissue which could hold sutures in place. The child died in the OR. I don't know what would have been done today, but had the child stayed home, they might have had a couple more years with the parents, who hoped for an uneventful procedure.  So the exercise involved in this answer was fun, but the memory it brought back is still quite sad.

I would focus on capillaries, much like anongoodnurse's answer. I'd go about thinking about the problem a bit differently, though.
From https://www.vhlab.umn.edu/atlas/physiology-tutorial/blood-vessels.shtml there are about 10 billion capillaries in the human body: capillaries being the places where vessels narrow to where only a single red blood cell can transit. These are where the "visits" happen. You can't base it on distance traveled, because most of the distance traveled is through very large vessels, where blood is really just being transported from place to place rather than "doing" anything.
On each "loop" through the circulation, a given blood cell is only going to enter one capillary. It'll be in a very small arteriole on one side, then go through a capillary, then come out in a very small venule. Before the arteriole it would have been in progressively larger vessels; after the venule it'll be in progressively larger vessels. However, the work of "visiting" other cells is mostly during that brief sojourn through the capillary.
To know how many of the 10 billion capillaries a blood cell visits in a lifetime of 120 days (=10,368,000 seconds), all we need to know is about how long a "round trip" is.
It's hard to find any solid reputable estimate for this round trip time. This very old paper:
Tarr, L., Oppenheimer, B. S., & Sager, R. V. (1933). The circulation time in various clinical conditions determined by the use of sodium dehydrocholate. American Heart Journal, 8(6), 766-786.
estimated a transit time of an average 13 seconds specifically from an arm vein, through heart and lungs, to the mouth. Travel time is going to be a lot slower to the legs, for example. I see various estimates thrown out of averages somewhere between 20 seconds and a minute. Overall it doesn't really matter for an order-of-magnitude estimate; let's just pick 30 seconds.
That would mean a blood cell has about 10,368,000 / 30 = 345,600 trips through the circulation. That number is small enough relative to the 10 billion capillaries that we can approximately assume no "repeat visits" and say 350,000/10,000,000,000 = 0.000035 = 0.0035% of capillaries are visited by one blood cell during the lifetime of that cell.
Capillary beds can be a bit complex and we've made a bunch of assumptions along the way, but I think even if you were very generous with some of those estimates you'd still stay under 0.1%.

If capillary beds make up 80% of our circulatory system (easy to believe), why do you say, most of the distance traveled is through very large vessels? Higher velocity travel is in larger vessels (travel in the aorta is - I believe - more than three orders of magnitude greater than through capillary beds), but (and it's a big but) as I stated, I hate math. If capillaries are 50K miles of vasculature, it doesn't compute if most of the time, the RBC's are actually in capillary beds, miles and miles of them, and it's there that they spend most of their time (they crawl along......slowly.)

(I purposely didn't take physical distance in account.)

@anongoodnurse Well, think about a capillary in your leg. A blood cell may travel more than a meter through the aorta, iliac, and femoral arteries before taking a relatively short trip over a mm or less through a capillary and then heading back through progressively larger veins. A huge proportion of the circulatory system is small vessels only because there are so many of them. I'd think of it the same way as roads...traveling between cities you might spend hours on a highway, and only a minute or two on a local road, though there is way more pavement dedicated to local road than highway.

In any event, it doesn't really matter for the calculation I presented. All that matters is that on one trip, a blood cell is going to go through just one capillary (or a few; it's kind of hard to define what exactly "one capillary" is in the capillary beds, just talking orders of magnitude here). Whatever % of time it spends in any kind of vessel, that's one visit per round-trip through the heart and lungs.

I believe we're mostly on the same page, just using different frames for calculating. Agree that actual distance traveled is in larger vessels, but fewer "visits" occur there.

@anongoodnurse Yes, we're definitely on the same page there; OP's calculation was based on distance. I'm saying you can't think in terms of distance, because much of the distance traveled is through vessels where nothing is being delivered, that is, there are no "visits".

In rereading the OP's question, I think your answer is the better one. Good explanation! +1.


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Standard notation for crossings (female, male)
Is there any standard for the notation of a crossing (hybrid) which tells me which part is the mother and which is the father?
Example
StrainA: egg cell
StrainB: sperm cell
Which notation is correct?
StrainA x StrainB or
StrainB x StrainA
or isn't there a rule for this?

For plants, seed (egg cell) parent is shown first and pollen (sperm) parent second.
The rule is mentioned in wikipedia,
http://en.wikipedia.org/wiki/Hybrid_(biology)
section : in plants.
Another mention of plant example:
https://www.rhododendron.org/v50n1p36.htm

Thanks. Do you have a scientific reference for this?


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Minimum and maximum exposure to virus
Is it possible to say that there is a maximum exposure time for the virus so that even an exposure time beyond that - will leave us with the same chances of infection?
If so, is there a way to estimate the interval between the minimum exposure time for infection and the maximum exposure time for infection and what happens inside?

No, on cannot say it this way, since further expose always carries a risk of getting infected.
However, one could argue that after certain time of exposure one is nearly certainly infected, so being exposed longer doesn't really change the result. This statement could be formulated more rigorously in terms of compartamental epidemiological models. If we take the figure for the SIR model in the linked article, we see that the number of the susceptible individuals (S) quickly drops about time 0.2-0.4, after which it is almost zero, i.e., there are almost no uninfected individuals in the population.

The numbers of susceptible (S), infected (I), and recovered (R) individuals can be normalized by the total number of the individuals in the population ($N=S+I+R$), and then interpreted as the probabilities of a person being uninfected ($p_S=S/N$), infected ($p_I=I/N$) or recovered ($p_R=R/N$). These probabilities will behave in time in teh same way as shon in the figure (but with different y scale), i.e., the probability of being ininfected would first be nearly constant, and then quickly decrease to nearly zero.


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The probability meaning of Covid variants
In the CDC webpage about Covid-19's variants the next sentence appears:

This (the United Kingdom) variant spreads more easily and quickly
than other variants.

In the ECDC paper about Covid-19's variants we can see that:

Several modeling studies corroborate the postulated increased
transmissibility of VOC 202012/01 (the scientific name of the United
Kingdom variant)

In a Nature article from last week written:

Several research groups suggested that B.1.1.7, which was first identified in the United Kingdom, was spreading more quickly than previous variants...

The probabilistic meaning of these sentences is not clear to me. Does this mean that the risk to be infected by the British variant is X times greater? E.g. if I was exposed to the British variant for 10 minutes, my chance of contracting is equal to the chance of contagion the original variant for 10 * X minutes?
Is there any nuance I miss?

The studies referenced do not have any such specifics about transmission probability.
What they observe is that a variant is becoming more common. Modeling the spread gives a different R0 value for the variants vs the reference strains:

In line with previous
modelling studies, the R0 for VOC-202012/01 was estimated as 75% more transmissible than other variants [35].
Davies et al. modelled data from three English regions to estimate that VOC 202012/01 is 56% more transmissible
(95% credible interval (CrI): 50-74%) than previously identified SARS-CoV-2 variants [32]. Danish modelling
studies performed in January 2021 estimated that VOC 202012/01 was 36% more transmissible than other
variants [ECDC communication with Danish authorities].

(from your second reference)
They infer that the variant is more transmissible because the modeled number of people subsequently infected per infected person is greater. The reasons for this cannot be easily determined by the methodology they refer to, and there is no simple way to map this onto probability of infection given some exposure; they are just describing what happens in real-world conditions, on average.
What you can infer is that there are some types of contact that occur in the real world that wouldn't result in transmission with the old strain that do result in transmission of the variant. This could be because more infected people produce enough virus to spread to others, it could be because shorter contacts lead to infection, it could be because infected people have different behavior that leads to more contact with people to potentially get infected; you can't tell the difference from these data.


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What prevented invertebrates from discovering flight a second time?
Vertebrates evolved powered flight three times in history, being pterosaurs, birds, and finally, bats.
Invertebrates were the first to evolve flight on the planet... but flying insects remained the only one, with all flying insects descending from a single common ancestor to a boot. This is while insects are famous for their extreme morphological plasticity and fast speciation tendency.
So the question is - what prevented invertebrates from discovering flight more than once, especially considering that bats prove that you can still successfully try to emerge into a niche already occupied by other species (birds, who themselves coexisted with pterosaurs for tens of millions of years) and that invertebrates have more anatomical plasticity compared to vertebrates?
This question is NOT about: How evolution works

Yes, it is. That is the correct question and answer to explain this. It's not possible to give another answer.


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Micro-intradermal spasms in the legs after exercise
Heyo !
When i'm doing physical effort that involves and then rest, I feel small and suddle of what feels like contraction all over my legs (but not feet); It stops by itself after a few minutes and there's no pain at all, just a strange sensation. It's like having pin and needle when coming and ending, but it's less "noisy" and more precise in each "contraction" and can it really feel things are moving/contractiong/whatever but I can't see anything with my eyes.
The things, they are so small in "size" and strengh and too shallow to be muscle while being too deep to be skin. From the sensations, my best guess is blood vessels exploding but don't have any bruises. My other hypothesis is dermis doing some folky things but yeah, no idea...
Thus my question: What is this thing ?

Pins and needles are different from tiny spasms, which are called fasciculations. In either case, it's certainly not caused by exploding blood vessels, which would leave a mark resembling a bruise, as RBC's and the heme group from RBCs can migrate through tissue pretty easily and, more importantly, blood vessels aren't given to exploding like that. Read about fasciculations and discuss it with your doctor. Sometimes there is a medical cause.

Thanks ! Can you put your comment as an answer so I valide it ?

Sorry, I misunderstood before. No, I cannot put it as an answer because we don't provide answers to questions seeking medical advice. Note I only gave you a term to research, and reassured you that blood vessels aren't given to behaving as you wondered about.

I wasn't seeking medical advice, I just wantd to know what were these...

i was resting and looking at my leg the other day, and there were little muscular contractions in the thigh muscles, i thought they were a heartbeat at first and actually they were just random little movements inside the thigh.

Has commented by @anongoodnurse, it's called fasciculation.


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Does modern theory of evolution include modification of physical environment?
Does any branch of modern evolution theories include aspects of evolving organisms modifying the physical environment?
An example from the evolution of life could be early stage introduction of oxygen and carbon dioxide to the atmosphere from single cell bacterial growth, thereby establishing a basis for growth of more complex organisms.
See also somewhat related question: https://physics.stackexchange.com/questions/22771/does-the-universe-follow-a-general-physical-and-computational-principle-of-evolu

Yes, such processes are considered but there is still a lot of work to be done in this field.
Because the question is open-ended I will just define two concepts of interest and let you go through papers if you want to understand how such processes are modelled.
Niche Construction
Niche construction is the process in which an organism alters its own environment. Sometimes, niche construction takes a broad definition and it then refers more globally to any environment change that is induced by an organism regardless of whether the individual/lineage experiencing the environment is the same one than the one causing the modification. Under this broad definition, niche construction has the meaning as ecological engineering to my understanding.
Some obvious examples are bird nests, beaver's dam and humans's houses. The process of niche construction gets really interesting when the niche is inherited by future generations.
Ecosystem engineering
Ecosystem engineering is the process in which an organism alters the its environment and the environment of other lineages/species. Ecological facilitation is one class of examples.
Ecosystem engineering vs Niche Construction
To my understanding, the term niche construction is more often used in the evolutionary ecology literature, while the term ecosystem engineering is more often used in the ecology literature. Note again that (in my understanding) niche construction in its broad sense takes the same definition as ecosystem engineering but not in its narrow sense.
Models of niche construction in evolutionary biology
There are a number of models of niche construction in evolutionary biology. I am not expert in this field and am not able to make a good summary (would take a while even for an expert anyway). Here are a few papers (that I haven't fully read) that you may want to consider

Niche construction - Odling-Smee et al. 1996
The evolutionary consequences of niche construction: a theoretical investigation using two-locus theory - Laland et al. 1996
Evolutionary consequences of niche construction and their implications for ecology - Laland et al. 1998
Macroevolution of ecosystem engineering, niche construction and diversity - Erwin 2008

Note that depending on your level of understanding of evolutionary biology, these papers may be a bit complicated to fully understand.


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How does imatinib recognize the constitutively active Abl-BCR even though it binds to the inactive conformation?
In chronic myelogenous leukemia (CML) ABL-BCR is constitutively active (always on) and it can be inhibited by imatinib and dasatinib. A study says that imatinib binds to the inactivated state of the (Abl) enzyme while dasatinib binds to the activated state of the (Abl) enzyme (i.e. can recognize multiple states of the enzyme).
from the study I concluded that Abl is studied as a model for Abl-Bcr fusion protein but What I don't get is :
How can Abl-Bcr be constitutively active and can be recognized in multiple states (activated and inactivated)?
Thanks

Can you please add links to these studies you cite?

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3513788/

Should your question maybe be: How does imatinib recognize the constitutively active Abl-BCR even though it binds to the inactive conformation?

Briefly: According to the paper you are linking, Abl-BCR is not "recognized" by the drugs in the active or the inactive state but rather it assumes a conformation that is similar to the active or inactive state of Abl once the drug binds. Simply put: the paper does not study what conformation Abl was in before the drugs bind, they rather discuss the conformation after the binding of the drugs.
Just to provide some background: Abl is activated by fusion to BCR because the regulatory part of Abl gets damaged such that the tyrosine kinase is constituously active. This damage is in the regulatory part of Abl and not in the nucleotide binding pocket (the part where the drugs bind and the part that strongly changes conformation between the active and inactive states).
Both imatinib and dasatinib (like other kinase inhibitors) are competitive inhibitors that bind to the ATP binding pocket. This means that both drugs occupy the ATP binding site, preventing ATP from binding and the ABL protein from executing its kinase activity no matter whether it is in the active or inactive state.
The difference is that imatinib binds to (and blocks) the pocket where normally the phosphate groups of ATP bind, forcing Abl (and Abl-BCR) into a conformation that is similar to the inactive state. The drug can still bind to the active state but upon binding, Abl changes its conformation and then looks similar to the inactive state.
Dasatinib on the other hand binds to (and blocks) the part where normally the base of ATP binds. This part does not strongly change its conformation between active and inactive state and thus dasatinib should be able to bind to both active and inactive conformation. However note that the ability of dasatinib to bind to either conformation is simply a hypothesis they state in the paper and is not substantiated by data (in fact they themselves say that the data indicates that dasatinib binds stronger to the active conformation).
Note no matter which conformation the protein has (active or inactive) it cannot perform its function as soon as any of the competitive inhibitors binds because the inhibitors block the ATP binding site and without ATP, Abl cannot phosphorylate anything because ATP is the source of the phosphate group which Abl would normally transfer to its target.
Some more background on how Abl works: Abl is a tyrosine kinase which means that it transfers a phosphate group from ATP to a tyrosine residue to its target protein. Also: Abl has some regulatory parts that control whether it performs its tyrosine kinase activity. In the inactive state it will not do anything even in the presence of ATP and its target protein. In the active state, it still needs ATP and its target protein to perform its kinase activity.

but don't you see that "recognize multiple states" means it was inactive or active before binding  ?

I adapted my answer to try to be more clear as to why it is completely irrelevant for the function of the drugs whether Abl was in the active or the inactive conformation before the drug binds.

I'm convinced with your explanation, concluding that: ATP binding site can occur in the active and inactive conformation while the enzyme is still activated by means of absence of it's regulatory part which has different binding site from that of ATP.

My score prevent me from upvoting :D

You're welcome, thank you for your valuable information.


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Why does the blood not clump and result in death?
In this question's accepted answer, it is said that the blood type will slowly change to that of the donor's.
When the blood in the person is about 50% his own and 50% that of the donor's.
i.e, 50% A group blood (his own) and 50% O group (donors blood),won't the antibodies in the O group react with the A-antigens and clump?

Some people do die from graft vs host disease after bone marrow transplants involving ABO incompatibility, but not usually from blood clots.
Foreign red blood cells don't usually form significant clumps (or clots) as a result of an antibody interacting with a surface cell antigen. They can form tiny clumps, however, that are not life threatening, but simply plucked out of the bloodstream by macrophages.
The typical reaction consists of foreign red blood cell detection and destruction (broadly called hemolytic anemia.) So anemia is a problem, but normally not significant clumping/clotting.
Safety and impact of donor-type red blood cell transfusion before allogeneic peripheral blood progenitor cell transplantation with major ABO mismatch.
Blood transfusions and the immune system
Consequences of ABO incompatibility in allogeneic hematopoietic stem cell transplantation.


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Why do we use mice in labs?
Why do we use mice in labs for experiments targeting humans ? Are they near humans biologically speaking ?

Interesting question in principle, but what research have you so far done to find an answer? It's a question that is addressed pretty much in every introductory textbook. In short, mice are often not good models for humans, that is indeed a big problem. But often it is not ethical or even possible to do experiments with humans (you're not allowed to insert things into peoples' brains, for example, or kill and dissect them), so animals are the only option. And animals can be bred to have specific characteristics.

Maybe start by skimming Wikipedia's page on Model Organisms, then edit your question with any specifics that remain unanswered?  Jamesqf covered a few pragmatic reasons, but there are a lot of other ones

Quite apart from ethical issues*, there's simple practicality.  Mice are about the smallest & fastest-reproducing mammal.  Mouse generation time is about 10 weeks, vs maybe 15 years for humans, and have average litter sizes of 6-8, vs a bit over one for humans.  Life span is correspondingly shorter, so experiments can be done over the entire life, or for multiple generations.  Mice occupy a lot less space, and are a lot cheaper to feed, which is a consideration when applying for research grants.
(And in the early days of research, one could just catch wild mice, instead of having to ship in some exotic species such as monkeys.)
*Which not everyone subscribes to. We do have ample historical evidence of humans used as lab animals.

you explain why this is a good model organism, but not why it is used in research targeting humans.

@Hachiloni: I DO explain that.  Because they're cheap, obviously :-)

algae are also cheap but you can study them to understand humans. Why mice are suitable for that?

@Hachiloni: Mice are mammals, algae are plants.  The biology is considerably different :-)  It's a matter of optimizing cost vs relevance of results.  You'll find that a lot of research IS done with plants, or with fruit flies, because they're even cheaper than mice, and the biology being studied is similar enough.  Likewise other research needs to be done with different, more expensive, animals such as primates, and sometimes (as with vaccines) human testing needs to be done.

Comparing mice and macaques (as human models and practicability for labs) would be interesting.


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can you tell someone's age from a DNA sample?
So as I understand it telomeres shorten as you age. Working under that assumption..  let's say you were investigating a crime and there was some DNA evidence that had been left behind. Could you determine the age of the DNA owner by looking at the telomere length?

Not that easy. Depends on the cell type that you have. Different cell types have different telomere lengths.


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Mitosis and Colchicine
I'm preparing for an Olympiad and while I was going through some of the old papers I found a question. I googled it but a lot of people have different answers to it. Please help.
A student treats some onion root tips with colchicine that is responsible for arresting cell division at the metaphase stage (by dissolving spindle fibres) and further prepared a slide of the root tip staining with acetoorcein (stains chromatin) and observed under high power of compound microscope. He is well aware of the cell cycle given alongside.
Question: Which of the following is not true about his observation?
a) Most cells are in Interphase
b) Most cells are in the metaphase
c) No cells are in anaphase or telophase
d) Chromosomes could be observed better than a slide prepared without colchicine
treatment.
According to me the answer should be (c) because if colchicine arrests cell division at metaphase, anaphase and telephase being the subsequent processes would not happen. But a lot of people are saying it should be (a) or (d). I'm stumped, any help would be appreciated.

Single answer question, I presume ?

The question is asking which is NOT true.  You are correct that C is true - very few cells should be found in anaphase or telophase.
D is also true.  When spindle fibres are dissolved, chromosomes/chromatin would not be tightly bundled or packed in the cell and it would be easier to see them with an acetoorcein stain.
A and B are trick answers.  In a regular tissue, most cells are in interphase at any given time.  Interphase is the regular functioning period for the cell.
However, the question is referring to onion root tips which are primarily comprised of actively dividing cells (meristem tissue). The colchicine would affect most cells and most cells would be found arrested in the metaphase.  http://w3.marietta.edu/~biol/introlab/Onion%20root%20mitosis.pdf
Therefore for onion root tips treated with colchicine, most cells are not found in interphase.  A is the correct answer.


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Are evolutionary mutations spontaneous?
My question is whether mutations which lead to evolution occur by any environmental force or it occur spontaneously? I have read in genetics that x-rays, ultraviolet rays and chemical mutagens are the causes of mutation but how are they responsible for evolutionary mutations?

Why do you distinguish between "mutation" and "evolutionary mutation"? What do you think is the difference?

I think all mutations do not lead to evolution and I wrote evolutionary mutation because I wanted to know the variations that contributes in evolution.

Your comment shows that you do not understand the definition of evolution. I would recommend that you have a quick look at a short intro course to evolutionary biology such as Understanding Evolution by UC Berkeley for example.

Mutations occur spontaneously because all molecular processes are stochastic in nature: DNA replication is an imperfect process. However, certain external factors can increase the probability of a mutation to occur or even cause specific types of mutations.
Both spontaneous mutations and this kind of externally driven mutation contribute to the genetic variability that is the basis for evolution. It is sufficient that variation exist for evolution to be possible, no matter the origin of this variation. X-rays are probably not common in nature, but there is plenty UV on the surface of earth, and there probably exist chemical mutagens that are formed without human contribution.

You should also mention that mutation is a highly biologically controlled process. Many experiments have shown that mutation rates themselves can change in response to evolutionary pressures. So at least some mutations are not just the result of "imperfections" in DNA replication but are actually an evolved feature of the replication mechanism.

This answer is very related

@Nathaniel Interesting, sources for that?

Evolution is, by definition, not spontaneous.
Be wary of conflating "mutation" with "new or changed features".
Mutation is only one of many causes for feature change between generations; inheriting traits from parents is another. Changes in nutrition and education can cause population-wide changes in height and IQ, without being based on mutation. All these things can lead to new features without mutation being involved at all.
The term mutation covers a lot of things which can cause inheritable and non-inheritable visible changes in future generations.
A genetic mutation (as opposed to an in-utero developmental mutation, etc) is a change in genes. The mutation may be in a non-functional section of the genome, so may do nothing. Or it may cause cell division to fail and kill the child. Or it may do anything in between.
But it's not evolutionary. No mutation is, since mutations are one-off incidents.
Now, over time, favorable genetic mutations may be selected for, and built upon by other mechanisms of feature change, to the point where everyone has it. Again, this is not instant, and will take many generations to spread through everyone.

In a sense all mutations "lead to evolution". The genetic make up of the population has changed. Some mutations become "fixed", are persistent in the gene pool. You are thinking of evolution as progressive, it isn't; it is statistically adaptive.
Is melanin depletion (pale skin)"evolution"? In gloomy high latitude places it enhances vitamin D production. In hot low latitude places it makes melanomas more likely.


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What is solitary flower?
I am Just confused whether solitary means single flower in the whole plant or one flower on one branch of the plant?

Solitary flower means one flower at a specific position of a plant. It usually accompanies with another word either terminal or axillary.
Soliary terminal means a flower present at the apex of the main stem or its branches. e.g.  Trillium grandiflorum.

 Image taken from http://ohioplants.org/inflorescences/
Solitary axillary means a flower arising from the axil of a leaf. e.g. China
rose.

Image taken from https://commons.wikimedia.org/wiki/File:China_rose.JPG

 This is Sida rhombifolia. This picture is clearer.
No. It doesn't mean that a plant has a single flower.It speaks all about the position of the flower. Think of roses , they are solitary terminals and are in numbers in each plant, always growing at the apices of branches.
Source: My two years of learning Botany as an additional Undergraduate subject.


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What makes the hepatic portal vein unique?
What makes the hepatic portal vein unique?, is it because it begins and ends with capillaries or because it carries digested food.

Homework questions and questions that show little or no prior research effort are off-topic on Biology unless you have shown your attempt at an answer. For more information see our homework policy.


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How screeching affects the body?
Most times when I hear a screech (such as moving a sharp object on a chalkboard thereby causing such unpleasant noise), my body twitches. There are also other unpleasant sounds that causes the twitching, but whenever it sounds only my dad, my brother and I that feels it, but my two sisters and my mum says they don't feel anything. My question is:
Is there any scientific term for this feeling?
Is it hereditary?
What happens in the body or brain when the sound is produced?

This is the answer: http://www.livescience.com/16967-fingernails-chalkboard-painful.html.