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How does the body make sure that Vasoactive Intestinal Protein reaches only the target tissue?
Vasoactive Intestinal Protein (VIP) is a 28 amino acid neuropeptide that has several effects in several systems. These include the cardiovascular system, respiratory systerm, urinary system, immune system, etc. Furthermore, some of the effects appear to clash with each other. For example, studies have shown that VIP can have an antidipsogenic effect, while some have shown that it induces the secretion of vasopressin. Vasopressin is usually secreted when there is not enough water in the body. Thus, it seems contradictory that the hormone would induce cessation of thirst and secretion of vasopressin.
The hormone is  a paracrine mediator. This makes sense since limiting the distance that VIP travels allows for the hormone to only reach the intended tissues. However, it is also a neurohormone. Which means that it travels through blood and I would assume that it causes a myriad of effects. My question is, how does the body make sure that VIP does what is intended to do?

Do you mean vasoactive intestinal peptide?

@BryanKrause Yes. Sorry. I will edit the question

Vasoactive intestinal peptide (VIP) acts in the intestine, brain, kidneys, lungs, heart, blood vessels, etc. (Cardiovasc Res) and its effects all lead to the same goal: to improve the delivery of blood, glucose and oxygen to the tissues, so it's not a problem if it acts on different tissues simultaneously. Specifically, VIP stimulates thirst, water retention and blood flow through the coronary and pulmonary arteries, dilates bronchi and breaks down glycogen to glucose, among other.
VIP can act via the nerves as a neurotransmitter or via the blood as a hormone:

In research animals and in humans, VIP, administered into the coronary
  artery or intravenously, increases the epicardial coronary artery
  cross-sectional area, decreases coronary vascular resistance, and
  significantly increases coronary artery blood flow. High frequency
  parasympathetic (vagal) nerve stimulation also releases endogenous VIP
  in the coronary vessels and heart and significantly increases coronary
  artery blood flow. (Cardiovasc Res)

In humans, VIP stimulates water retention and thirst:
1) VIP stimulates the secretion of renin:

VIP has now been shown to produce an increase in renin release in a
  number of species, including humans. (Ann N Y Acad Sci)

The activation of renin-angiotensin-aldosteron system results in water retention.
2) VIP stimulates the secretion of vasopressin (Cardiovascular
Research). Vasopressin stimulates water retention. Since vasopressin (arginin-vasopressin or AVP) is dipsogenic (stimulating thirst):

given the established dipsogenic effect of AVP in the nonpregnant
  state... (JCI Insight)

and since VIP stimulates the secretion of vasopressin, VIP is also dipsogenic.
Now, there seems to be some conflict in the studies about VIP being dipsogenic or anti-dipsogenic in rats:

VIP was found to have no effect on drinking when injected centrally
  and peripherally in the eel, although it is dipsogenic in the rat
  after central injection. (ResearchGate)
Intracerebroventricular administration of vasoactive intestinal
  peptide strongly inhibited drinking in rats deprived of water...
  (Neuropharmacology)

Not to go in the details, but there may be different circumstances, for example, the level of dehydration, in which VIP can act differently...


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Protein rafts over the Phospholipidic bi-layer
Does any of you know the specific name of the protein rafts that allow proteins to float over a double layer of phospholipids, (cell membrane)?
I just feel there should be another name rather than simply "protein raft".

These conglomerations of proteins, glycolipids, and cholesterol are usually called lipid rafts.  (Google Scholar shows 84,000 hits for that term, vs. 400 hits for "protein raft".)   Here is a diagram of a lipid raft:

(Key: A: Intracellular space or cytosol, B: Extracellular space or vesicle/Golgi apparatus lumen. 1: Non-raft membrane. 2: Lipid raft. 3: Lipid raft associated transmembrane protein. 4: Non-raft membrane protein. 5: Glycosylation modifications (on glycoproteins and glycolipids). 6: GPI-anchored protein. 7: Cholesterol. 8: Glycolipid)  [from Wikimedia Commons]

As this illustrates, lipid rafts float within the membrane lipid bilayer, not "over" or "above" it. The raft is a part of the membrane, not something outside it or on just one side of it.  The raft is free to move in the surrounding two dimensions of the membrane.
One could argue that "protein raft" might be a better name than "lipid raft" since we would call a common raft a "wood raft" or "papyrus raft", but usually not a "water raft".  Whatever the worth of such an argument, "lipid raft" is the term in use.

I was under impression defferent lipid composition (i.e. more cholesterol and shingolipids than in surrounding membrane) is the defining property of lipid raft. Therefore, I find your argument for "protein raft" being a better name misleading.

I agree with @BagiM. Since the lipid composition is altered and that causes the change in rigidity, I think "lipid raft" is a nice name. The raft in your water analogy is made out of a water solution? Perhaps it is a stretched metahpore at that point... Purely semantic though. This is a good answer that clears up the confusion.

There aren't protein rafts that "float" over a bilayer. There are proteins that insert domains into bilayers, or pass through them, or bind to lipid headgroups. There are also other proteins that bind to these proteins.

source: Stack Exchange

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

sort: votes


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How can Haemophilus influenzae survive and grow alone in the human body?
Haemophilus influenzae gets its name from the fact, that it requires nutrients from blood in order to grow. More specifically, I see it mentioned that in vitro they often exhibit the pheomenon that they don't really grow in plates with blood alone. They do, however, grow when other bacteria are added that causes haemolysis (like Staphylococcus aureus).
H. influenzae is known to cause otitis media, meningitis and pneumonia. How does it get its nutrients in these places? Is there a coinfection with other bacteria that do haemolysis?

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


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Do animals exist (for example ostriches, chimps, etc.) that develop the need to mate with humans if they are soley raised and socialized by humans?
I just watched a German talk show "Nachtstudio" with the title "Die Graugans und der Mensch" (Gosling and People) about the legacy of the famous ethologist and Nobel Prize winner Konrad Lorenz (https://youtu.be/hLkWhGieZvQ). All the participating guests were former students of Lorenz. One statement in the show made by Bernd Lötsch amused me.
At the point where the conversation was about the famous experiment of Lorenz with geese,  Lötsch said that Lorenz was lucky that he had selected goslings for his experiment. He continued by saying that if he had chosen ostriches, it would be likely that the ostrich would have tried to mate with him once it had reached maturity (Lötsch 1988).
Amused by his statement and without any deeper understanding of biological theories (I'm a physicist by training), I would like to ask for critical reflections on Lötsch's statement. I would also appreciate hearing about any studies which examine hypotheses such as this.

Dogs some to mind. But the real issue is proving it, A lot of animals aren't terribly picky about mates.

Content warning: frisky kākāpō ahead https://youtu.be/9T1vfsHYiKY


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Can epigenetics have positive impact on the genes are development?
I know that epigenetics have capacity to affect and degrade the genes thereby inducing problems/illness/degradation in body functions.
Can they also make better genes or have positive impact on genes or body? If yes, can someone give some examples?

First, let me qualify the idea of "problematic" epigenetic modifications by saying that the impact of a modification on an organism is often dependent on the environment.  That is to say that outcome is dependent on the interaction of genetics (or epigenetics) and the environment in which the associated genes are expressed; e.g. a mutation or modification that confers an advantage in a nutrient-limiting environment may be detrimental when nutrients are plentiful.
Second, it is helpful to think of epigenetic modifications as reversible switches rather than entities that "degrade the genes".  In fact, the etymology of "epigenetic" implies that such changes work at a level above that of the gene sequence, i.e. gene expression.  Canonically, DNA methylation and histone modifications (acetylation and methylation) modify the expression of a gene by regulating the ability of RNA polymerase to access that gene, either by directly influencing transcription factor binding or modulating the associations of nucleosomes and DNA. Read up on facultative heterochromatin.
As for examples, I point you to a set of papers that show associations between human starvation, epigenetics, and disease / mortality outcomes across generations.
DNA methylation as a mediator of the association between prenatal adversity and risk factors for metabolic disease in adulthood

[DNA methylation] at six CpGs, including at previously [serum triglyceride]-associated CpGs at TXNIP and ABCG1, mediated the association between famine exposure and [serum triglyceride]. [DNA methylation] at these CpGs was likewise associated with the expression of genes implicated in cell growth and energy metabolism.

Note that the authors present caveats to their analyses in the discussion. The New York Times also covered this publication.
Paternal grandfather’s access to food predicts all-cause and cancer mortality in grandsons
This publication is essentially a replication of the published works concerning transgenerational epigenetics in the Överkalix cohort.  They give a concise summary of how epigenetic changes caused by environmental stress may be heritable:

An intriguing aspect of these studies is the conjecture that an epigenetic pathway, carrying information across generations, may open up just before puberty, during the so-called slow growth period (SGP). Pre-puberty may be one of several “windows” for germline reprogramming in response to nutritional signals. A number of mechanisms for transmission across generations have been suggested, usually involving DNA methylation, chromatin formation or small noncoding RNAs. After fertilization, in the preimplantation embryo, epigenetic modifications acquired early in life are then usually erased, but not fully. Imprinting on specific loci may resist the post fertilization wave of reprogramming, eventually causing changes in offspring phenotype that are not driven by changes of the DNA sequence.

If you're looking for more examples, research genomic imprinting.


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In a sugar such as a disaccharide are both ends of the sugar known as reducing ends?
For example, in maltose (a disaccharide of glucose monomers) are both of the ends either side able to be opened to form an aldehyde group?

No, in dissacharides the reducing end is situated only on one monosaccharide which is having free anomeric carbon. This carbon does not take part in glycosidic bond formation and can form open chain.

Check out:
https://chem.libretexts.org/Courses/Sacramento_City_College/SCC%3A_Chem_309_-_General%2C_Organic_and_Biochemistry_(Bennett)/Text/14%3A_Carbohydrates/14.6%3A_Disaccharides

Your answer would be better if it indicated the reducing position in the monosaccharides and the disaccheride and did not contain material largely  irrelevant to the question. Perhaps you could consider drawing a diagram of your own.

okay..will do that


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Help with gene linkage and mapping!
Here's an interesting question I've been trying to figure out:

My annotations are in red. So far, I've figured out:

We know 630 colonies survived when plated with ACD antibiotics...meaning they picked up the a/c/d resistance alleles, but remain wild-type for the b allele. The genotype would be "a b+ c d". Because SO MANY (630!) colonies seemed to inherit a/c/d together, and b completely separate from them, I would say b is the gene quite distant from the 3 other genes.

However, I've unsure about how to proceed and determine the probably order of the 3 others genes: a, c, and d.
Here's my hunch: B--------------------C-D-A.
I'll explain:

Well, I looked and saw 942 (many!!!) picked up A/D together. So A/D are probably adjacent.
Then, 786 (many, but fewer) picked up C/D together. So C is further from D than A is far from D. The question becomes: is it "C---A-D" or is it "A-D---C"?
The insight comes in with 640 (still fewer) picked up A/C together. That means A is actually quite FAR from C, because more distance = more recombination events that could split them up. So between the "C---A-D" or "A-D---C" listed above, it's more likely "A-D---C".
Okay! We know B is far from the other ones, BUT is it like "B-------ADC", or is it like "ADC-------B"? Well, let's look: picked up B/C together is 51, but picked up A/B together is only 46. That means A is a little FURTHER from B than C is further from B, since 46 < 51.

This led me to my proposed answer: that the order is "ADC---------B", or if you just flip it around, its equivalent: "B---------CDA".

How's my reasoning? This stuff can be pretty confusing; am I approaching it from the right angles? Thanks so much; really appreciate it!

You were never told that all the genes were on a single plasmid. I think you should treat all those counts < 50 as essentially zero; cells pretty much never get both the ACD and the B plasmid; they get one or the other.

I think your reasoning is sound and your ordering very likely, but I wouldn't feel comfortable with deciding the side B is on. Actually, it's more than that: I think that by using basically the same number (~40) for everything that includes B, they want you to come to another conclusion.
Unlike eukaryotic cells undergoing meiosis, there is no crossing over in bacteria taking up DNA from the surroundings. Therefore, it shouldn't be possible for the cell to inherit A, B and C but not D, which is in the middle. Simply, from my understanding of the "experimental" setup, they added antibiotics A, B and C, so they have to assume the bacteria are wild type for D. However, it's basically for sure that those ABC-resistant colonies are also D-resistant.
Still, your reasoning is correct: comparing BC and AB should give you the side B is on, since the break could have been inside of the 3-gene cluster. However, the numbers are very close, and the "AB" and "BC" phenotypes are probably ABCD anyway, making the small difference even less meaningful (the true AB and BC are lost because they are mixed with the many ABCD).


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Why is there such a long interval between ages of sexual maturity and of reproduction in female chimpanzees?
There seems to be some disagreement on the ages at which female chimpanzees typically reach sexual maturity and when they typically first give birth, but regardless, different sources seem to agree that a number of years elapse between these two milestones.
For example, this 2018 paper from Jane Goodall and colleagues found

… an average age of 11.5 years (range 8.5–13.9) at sexual maturity and 14.9 years (range 11.1–22.1) at first birth. These values exceed previously published averages for wild chimpanzees by one or more years. Even in this larger sample, age at first birth is likely underestimated due to the disproportionate number of non-dispersing females, which, on average, give birth two years earlier than dispersing females.

In humans, there is also a substantial lag between these two events, but we understand this as a very common cultural dividing point, which places the first firmly in childhood, and the second (generally/ideally) in adulthood. The maintenance of this interval is controlled by a variety of social and societal practices and institutions, across cultures.
Do we know what maintains the lag between the biological capability for reproduction and the actual first birth in chimpanzees? Presumably there is also some sort of set of social practices among chimpanzee society that maintains this. Do we know to what extent it is controlled by mature matriarchs or patriarchs, or by actions taken by the young females themselves, or some other set of behaviours?


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Does animal blood, esp. human, really have similar salinity as ocean water, and does that prove anything about evolution?
It is an often-repeated claim that human, and in fact all animal blood is salty because we evolved from aquatic organisms, and that blood has a similar concentration of salts as ocean water, or at least as primordial ocean water.
Is any of that true? Does science know what the salinity of the oceans was billions of years ago, and was it indeed similar to the blood of today's organisms? Does that knowledge prove anything about evolution and the origin of life?
I am wondering, because I tried to Google for the answers, and unfortunately all I could find were creationists referencing each other how it couldn't possibly be true because evolution is a lie in the first place etc., and they claim that there is no empirical research that would compare salinity levels of organims' cells and ocean water.

Related: https://biology.stackexchange.com/q/74748/3340

'blood is salty because oceans are salty, and life began in oceans' is a weird way of putting it. Can you cite non-creationist sources that put it this way?

Do you have any citation for this claim being "often-repeated"? I've spent quite a bit of time studying literature on both sides of the evolution and creationism debate, and I can't remember ever seeing this argument having been made. I'm quite curious where you ran across it and who is promoting it. It is quite absurd, so I'm especially curious if it's some kind of disinformation propaganda by anti-evolution activists.

I agree that it's most likely a creationist talking point, since several creationist websites showed up on a google search, which are mostly quoting other creationists. But there are also more reputable sources making the claim. AliceD provided one, though I can't verify it because paywall. Here is another.

Also note that freshwater fish actively retain salt, and ocean fish actively try to excrete salt. This means that animals are quite able to maintain a desirable salinity even if that's different from our surroundings. This basically means that even if the levels had been the same, it'd have proven nothing at all.

@Hackworth That's a very weird link. There's a claim that ocean salinity is similar to blood salinity, but a few paragraphs later he says the (modern) ocean salinity is four times larger. The follows the claim that early oceans were this "quarter the salinity of modern oceans", but without any reference. Indeed, there's no references in the article at all, which should already be suspicious, and I couldn't find any references to a related paper or much about the author either. And as already noted, I never saw anyone claiming this is a proof life came from oceans, except from creationists.

@Hackworth Don't forget that just because a claim was (maybe) made by a scientist isn't enough to have it be worthwhile. Scientists don't receive truths from a god of science - we've designed processes that help us separate truth from falsehoods. If the process isn't followed, you really shouldn't trust the results at all. As the article stands, it's just a bunch of unsubstantiated claims, that also happen to conflict with many things we expect about the early Earth's environment. It's may be just a retelling of the actual subject of study - e.g. how saltwater fish adapt to fresh water etc.

@Gloweye And saltwater crocodiles excrete salt on their tongue, and bull sharks can switch between salt and brackish water, regulating osmosis I think via urea.

After you maybe confusing blood with cytoplasm? Like others, Iʼve never heard this claim being made about blood, but a similar claim regarding the salinity of cytoplasm is somewhat common, and makes a lot more sense biologically.

FWIW, I recall hearing the same claim in my high school health class nearly 20 years ago (in a classroom video that seemed old back then). Not that necessarily qualifies as "often-repeated", but anecdotal evidence of the claim dating back a while. (Though I'm not sure how that fits into the creationist/evolution "debate", I'd think evidence that life began in oceans would run counter to the standard creationist viewpoint, no?)

Short answer
Early sea water had a very different osmolality than blood plasma.
Background
The reference range of serum osmolality is 275–295 mosm/kg (mmol/kg) (MedScape). The osmolarity of sea water is about 1000 mOsm/l (Wikipedia), but it can vary substantially between different seas, namely between 642 and 1,480 mOsm/kg (Ninawe & Banik, 1998). Nonetheless, the range of osmolalities are substantially higher than that of serum. That's why we cannot consume sea water, without losing more water than gaining it (NOAA). According to Astro Biology Magazine, the salinity of early oceans 3.5 billion years ago, when life first developed, was even higher. So popular accounts that they are the same and that this has important evolutionary consequences are likely far-fetched.
Reference
- Ninawe & Banik, J. Mar. Biol. Ass. India (1998); 53(2): 230-36

Do you have any idea why the oceans were MORE salty in the past? I thought they are salty because water brings salt to them from surface and then evaporates, so I naturally expected them to be less salty in the past. This really surprised me.

I'd think that the salinity or osmolality of the oceans when tetrapods' ancestors first started venturing on to land (around 400 million years ago) would be a lot more important to the argument than what it was when life first developed.

I think the two pieces this answer is missing are a) Some reference to the first animals, which were likely osmoconformers (since modern sponges and cnidarians are), and b) Relative ion concentrations and the consistency of high extracellular sodium/high intracellular potassium, which user1136's answer touches on: this is the way that blood and ocean are "similar" even if total osmolarity is not.

Just a caution for anyone who is tempted to directly compare the numbers provided, you will have to first change units. The blood concentration is given in mOsm/kg, and the ocean concentration in mOsm/L. Since these are salty solutions more concentrated than pure water, it would not be appropriate to use the density of water and say 1 L = 1 kg. The density of the actual solution would have to be used. However, the orders of magnitude of these concentrations are probably still appropriate for direct comparison and lead to the same conclusion.

@electronpusher - good point. I should've converted those numbers. Can attempt to correct them in the future.

It is said that nearly all terrestrial reproduction and sperm/egg fertilization takes place in fluids just like it does for ocean fish. Mammals, insects, spiders, all have sperm and eggs that are designed like their ocean cousins. It's a stronger evidence for evolution than blood chemistry, all terrestrial animals have kept a sea-like environment in their reproductive regions.

The argument that blood plasma resembles sea-water, in essence, relies on the notable similarity in concentration of two ions in plasma and sea-water, compared with their intracellular concentration: sodium and potassium.

The concentration of sodium-ion in sea-water is about 450 mM, whereas the concentration of potassium-ion is only about 10 mM (ref)
The plasma concentration of sodium-ion is about 140 mM and the concentration of potassium-ion is about 3-5 mM (ref, but many clinical biochemistry sources will confirm)

That is, both plasma and sea-water are 'high-sodium, low-potassium' and the concentrations are remarkably similar.  If we contrast this with the intracellular concentration of these ions:

The intracellular concentration of potassium-ion is about 150 mM, whereas the concentration of sodium-ion is about 10-20 mM (ref)

That is, the 'intracellular milieu' is 'high-potassium, low-sodium'. Blood plasma, of course, is considered an extracellular fluid.
We can generalize further and say (Skou, Nobel lecture):

The intracellular concentration of potassium-ion is about 150 mM whereas extracellular concentration is about 4 mM.
The intracellular sodium-ion concentration is 10-20 mM whereas the extracellular concentration about 140 mM

Thus sea-water, in terms of sodium-ion and potassium-ion concentrations, resembles the extracellular milieu, leading to the somewhat hyperbolic view that "blood can also be thought of as a private ocean...".
But the similarities are striking.
At one time it was thought that this concentration difference was due to cells being impermeable to sodium-ion, a hypothesis first put forward by E.J. Conway.
It is it now known, of course, that concentration imbalance is maintained by the sodium-potassium pump, which is present in animal cells but not in plant cells (W.D. Stein). The presence of this pump allows animal cells to be in osmotic equilibrium (no change in osmotic pressure) with their surroundings. (Plant cells, in contrast, have developed a cell wall that allows high internal osmotic pressures and which may (to again quote Stein) "have condemned [them] to a largely sessile life")
The history of its discovery (and much more) is given in The Identification of the Sodium Potassium Pump, the Nobel lecture by J.C. Skou
Addendum 1: Historical Origins
According to a review by Mulkidjanian and colleagues, it was Macallum in 1926 that first drew attention to the similarities in inorganic composition of sea-water and plasma and its significance as evidence that the first animals emerged from the sea.
I think R.L. Berg (see Addendum 3), at a famous conference in 1957, also drew attention to this, but I do not have access to the reference.
But just because animals emerged from the sea does not necessarily mean that life began in the sea. Mulkidjanian and colleagues point to the fact that "inorganic composition of the cell cytosol dramatically differs from that of modern sea water" (which was also first pointed out by Macallum in 1926) may indicate that life began in a high-potassium, low-sodium environment and that life in the sea only became possible after the evolution of the sodium-potassium pump allowed organisms to maintain their 'fundamental biochemical architecture' (the chemical conservation principle).
These authors suggest condensed geothermal vapours as a likely environment for life's origin but not everone agrees.
I notice from the comments that the similarity and blood plasma and sea-water is considered somewhat heretical and perhaps not sufficiently backed up by evidence. This viewpoint has a long history in 'mainstream' science.
Pearse in The migrations of animals from sea to land (1936), for example, has this to say:

The general similarity of the bloods of animals to seawater has been interpreted as indicating that all animals originated in the sea.
...
While there are many discrepancies to be explained, it is a common belief that "blood is modified seawater" (quoting Pantin,1931).

Another good source with some great references is The Oceans, Their Physics, Chemistry, and General Biology (1942) by Sverdrup, Johnson and Fleming, which is available as an e-book, especially the section in Chapter VIII on Sea Water and the Body Fluids.
Finally, there is nothing 'creationist' about the above arguments, but creationists, in the main, don't like them.  See Is the Sodium Chloride Level in the Oceans Evidence for Abiogenesis? by Bergmann, for example.
Although I do not agree with any of the views expressed in this article (especially the view that the Flood "likely carried to the earth’s surface  many  tons  of  pulverized  crustal  material containing large amount of salts and other minerals"), it contains many good references to the 'mainstream' point of view (which the author attempts to debunk).
Addendum 2: Serum and Plasma
Plasma is liquid component of blood that is clinically obtained as the supernatant (upper 'layer') generated by centrifuging blood collected in the presence of an anti-coagulant such as heparin or EDTA.
Serum is plasma without clotting factors and is clinically obtained by first letting blood clot, centrifuging, and then collecting the supernatant.
Both serum and plasma are considered extracellular fluids, in contrast to cytoplasm, which is the intracellular fluid that 'holds' the organelles and other cellular components.
There is no clinical difference in serum and plasma sodium levels, but serum concentrations of potassium are somewhat lower (about half-millmolar or thereabouts) than those of plasma (ref)
Addendum 3
It appears that the  R.L. Berg quoted above is Raisa L Berg, the eminent Russian Darwinist and geneticist who, among many other achievements, wrote In Defense of Timoféeff-Ressovsky.
As I stated above, I do not have access to the original reference but R.L Berg is quoted in Bergman's article (also quoted above) as follows:

Berg  (1959,  pp. 169–170)  notes,  “The  most important arguments in favor of the hypothesis that life originated exclusively in the ocean” are, first, “the similarity between the salt composition of the body fluids of land animals and that of the waters of the ocean.”
He [sic] then adds that the “similarity in the salt composition of the waters of the ocean and that of the body fluids of land animals could be accounted for” only by evolution (Berg 1959, p. 170).

It would be very nice to have her views recorded 'first hand' here (the OP question has generated a lot of interest).
Perhaps someone with access to the article could post a separate answer?
Addendum 4
Adrian (in a comment) has drawn attention to the following quote,
from the best-selling book The Sea Around Us by Rachel Carson, first published in 1951:

"Fish, amphibian, and reptile, warm-blooded bird and mammal - each of us carries in our veins a salty stream in which the elements sodium, potassium, and calcium are combined in almost the same proportions as in sea water."

Congratulations on an excellent answer. I am travelling at the moment, but will see if my University library has access to the article on my return, although if it is in Russian I won’t be able to translate it myself.

I am having trouble in tracking down the the paper of R.L Berg in First International Symposium of The Origin of Life on the Earth, Moscow, August 19-24, 1957. My University Library does not have a copy or online access, and they won't process my Inter-Library Loan request (The British Library will have a copy) because I don't know the title and page numbers for them to photocopy. Apologies.

I found this answer after reading a passage in The Book of Eels, by Patrik Svensson, which references a passage in Rachel Carson's The Sea Around Us (see https://www.goodreads.com/work/quotes/2423508-the-sea-around-us, "each of us carries in our veins a salty stream..."), so this idea has been mentioned in popular science books for several decades now.

@Adrian Thanks!  I have included the quote as an addendum to the answer (comments can get deleted... )

This is the link to the report by Berg in the symposium on "The Origin of Life on the Earth": https://doi.org/10.1016/B978-1-4831-9737-1.50023-0 (paywalled). Interestingly, just this chapter costs 22 Euros on Elsevier but I found the first volume of the proceedings for 14 Euros (the actual citation by the Bergman article; on this site: https://www.booklooker.de/).

Great answer, very thorough. The quality we should all strive for.

Even shorter answer: This can be easily (well, not that easily since you need to convert mols to milligrams) answered by looking at your last lab result.
Say you had Na: 135 mmol/ml on there which would be a plausible value. That's 135*22.88/1000 mg/ml or 3.1 g/l. Sea water has around 19 g/l, so that's a clear, definite "no".
It wouldn't be quite such a strikingly obvious "No!" if you had asked about osmolarity instead of salinity. Because unlike blood, oceans usally don't have significant amounts of plasma protein. The answer would still be a clear "No" (for non-fish animals, anyway), but not nearly as strikingly.


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What is meant by Physarum polycephalum having 720 sexes?
There is currently some media hype about the slime mold Physarum polycephalum, which will soon be exhibited in the Paris zoo. This was my first time hearing about slime molds, but so far so good.
What I don't understand though is this organism supposedly having 720 sexes. This seems strange to me, as to my – admittedly layman's – knowledge, single-celled organisms like this one aren't supposed to have sexes at all, reproducing instead through cell division. It looks to me like pretty much all newspapers reporting on this have no idea either and decided to just keep it because it sounds interesting. On Wikipedia, nothing is said about hundreds of sexes at the time of writing.
What does this actually mean?

It is true that many/most unicellular organisms such as e.g. bacteria or fungi have no need for sex to reproduce, and can divide by simple cell division. However, sex (defined rather broadly) is a universal feature of life. For example see this review article by Rosie Redfield, which examines exactly what we mean by "sex". The broad definition is just recombination of genetic material, which is a universal (or nearly so) feature of organisms.
It's a little hokey to say that Physarum polycephalum has 720 sexes, as "sex", the idea of a specific category of individuals with regard to reproduction, is different from the biological idea of "sex", when we say "yeast have sex".
What Physarum has, like fungi and other similar organisms, is not really sex, but mating type (see here). Mating type really has nothing to do with what kind of sex organs a fungus has, but rather what fungi have sex with. Certain mating types only have sex with certain other mating types. But this isn't really a one-to-one correspondence like male-female. It's much weirder than that.
There are both "heterothallic" (sort of "single-sexed") and "homothallic" ("hermaphrodite") mating types of the protist, and each organism has a mating type. The homothallic ones don't need other individuals to have sex and make offspring. The heterothallic ones do need other individuals. These mating types are defined not by a sex chromosome like in humans, but by a single gene. When they say 720 sexes, what they mean is that we have found 720 different DNA sequences at the mating type gene which have somewhat different mating behaviors.
I think that your evaluation is correct that the journalists are being pretty inexact here. But I think also that it's important to recognize that basically all of biology is sexual, one way or another.


text:
How do bull semen companies get the semen out of the bulls?
Prompted by this article, which discusses the low number of bulls who sire US dairy cows.
How do semen companies extract semen from bulls?
The procedure to extract semen from humans is simple enough, but I'm struggling to picture a lab operator masturbating a fully grown bull until it ejaculates to collect semen. Is there some kind of specialized equipment involved? What does the operating procedure look like?

iirc they have a big fake cow with a hole in the rear end so when the bull mounts it, the semen can be collected.

@Tom: Any odds you might know the technical term? Search results for "Bull sex doll" mostly seem to be adult websites and stories about Devin Nunes' cow.

http://www.vivo.colostate.edu/hbooks/pathphys/reprod/semeneval/bull.html this should give you some idea. This site even has the speed of the ejaculate and other information

Colorado State University has two helpful pages that explain the main procedures (h/t Tom). Semen Collection goes through the 3 ways that are used to collect semen from animals.
Semen Collection from Bulls helpfully expands on bulls specifically:

Semen is most commonly collected from bulls in bull studs using an artificial vagina, as described below. Electroejaculation is an alternative method used with bulls that cannot mount or are too fractious for easy handling (e.g. range bulls). Finally, semen can be collected by message of the seminal vesicles and ampullae per rectum.

In a nutshell an Artificial Vagina (AV) uses thermal and mechanical stimulation to stimulate ejaculation. In the image below, the top item is an AV for use with rabbits and the bottom one is an AV for use with bulls. (The middle item is a director cone, which is used to collect semen from dogs.)

The procedure revolves around using a steer as a teaser to arouse and mount the bull, and then having an operator divert the penis the AV:

As one of the pages helpfully explains:

Prerequisites to use of an AV are that the male be conscious, not significantly frightened of people, and more interested in ejaculating than in killing humans.

The main alternative for less docile bulls appears to be electroejaculation, which involves applying a series of short, low-voltage pulses of current to the pelvic nerves which are involved in the ejaculatory response. You then collect semen using a director cone much like the one in the image further up.

Good self-answer I could not have done it better. Judging by the pictures it is not a job for me though.

@Tom: Same here. Though to be honest, I'm not sure which of diverting a bull's penis into an AV or masturbating a dog with your bare hands and capturing the resulting ejaculate -- which is what the director cone depicted in the answer is for -- is most agreeable.


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What are the standard bio-safety protocols for preparing plant pathology herbarium specimina?
What are the standard bio-safety protocols for preparing plant pathology herbarium specimina?
I searched google but I did not found anything relevant, nor in my textbooks. I want to know about what bio-safety precautions must be taken before preparing plant pathology herbarium specimena.
PS. It seems many teachers and students routinely prepare herbarium specimens of wild and agricultural specimens including notoriously contagious fungal plant pathogens, but they are basically pressing and drying the sample in classroom notebooks and pasting it on herbarium sheets just like ordinary herbarium specimen. Sometimes old and neglected herbarium specimens go into ordinary garbage or stray official papers.
But whenever I ask a question about it, nobody could yet mention references or protocols (I put apart the authoritative issue), sometimes they give vague reasons with buzzwords like the pathogenicity will reduce with time, or the "disease triangle" (optimal conditions) are unlikely to occur, etc.
I kindly request to provide me protocols and references about safe way for preparing plant pathology herbarium specimens


text:
Can the word phalanx also be used to describe the finger bone plus the soft parts around the bone?
I was talking in an SE chatroom about fingers, and not being a native English speaker, I had to look up the word used for the part of a finger from the tip to the closest knuckle. I came across the word "phalanges", but the Wikipedia article specifically refered to this as phalanx bones, i.e. just the bone and not everything around it. Can this term also be used to describe the bone plus all of the softer parts around it like the muscles, blood vessels, skin and nail? If not, is there a more commonly accepted biological term for the bone plus the soft tissue around it?

It's a great question, and in my humble opinion, the answer is:
Phalanx (plural: phalanges), (also Cambridge and MedicineNet) is the term for one of the bones (only) in the fingers or toes and not for all the "meat" around it. The Google images search for phalanges is quite convincing.
Someone on https://english.stackexchange.com/ might know a word for the whole bone + "meat" part of the finger.

Hmm, are you implying that asking for terminology is off-topic on this stack?

@Nzall,  No, I'm trying to explain anatomy terms. All fine, if you ask me. I was thinking, if you are asking for a term that describes the whole part of the finger asociated with a phalanx, some person on English could serve you better.


text:
What is this small black insect with an orange stripe?

Sorry for the poor quality of the second image, but a slightly different perspective may be useful.
This was taken in South Africa, Western Cape during the day.
They're fairly small, maybe around 5mm in length.
They were huddled together on an ivy leaf. I found another group of about five also huddled close together on another plant.

Some kind of Hemiptera nymph.

I guess they were grouped together because they had just hatched, and the eggs are laid in clusters.

Yes that does seem pretty similar thanks.

I checked again, and there are only three now of the other five I saw, but they're still huddled together in roughly the same spot.


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What do the the different arrowheads mean in a cell signalling diagram?
What do the different arrowheads mean in the figure below? Are there arrows upstream or downstream signalling?

Hi and welcome to Bio.SE! This is pretty standard notation. The arrowhead is a promotion, and flathead is an inhibition.

Hi James! Thanks for the answer! Do you happen to know any resources in general for these notion? and other types of pathway like dotted lines and etc?

i dont know the usage of dotted lines @Tom

There is an interesting proposal paper by Hiroaki Kitano. However  all books should provide a table of all molecular biology notations and conventions but unfortunately these are not yet available.

Arrowhead interpretation
As I said in my comment and to add to @AlwaysConfused's answer, the arrowhead is a promotion, and flathead is an inhibition.
Typically, any other notation such as dotted lines would be explained in the figure legend of the illustration.
The below definitions are generally accepted and widely used.
But don't take these definitions for granted; there are no strict usage policies for these diagrams.
Different groups may use different nomenclature and symbols.

These definitions were taken from a legend in cellsignal.com.
Upstream and downstream
The arrowheads are not necessarily linked to up and downstream signalling.
Generally, the direction of the arrow indicates upstream/downstream.
However, at a glance, this has even less standardisation than the arrowheads.
Sometimes, like in the example in the question, upstream is generally at the top, and downstream is at the bottom.
Other times it is from left to right, or right to left.
There are many examples of cyclical events which the only way to tell is by following each arrow "path" for a particular signal.

Thank you this answer will help me greatly.

The blunt head arrow means inhibition i.e. suppression.
i. e.
A -----------|  B
means A suppressing B. the factor at the arrowhead is being supressed. The factor at arrowtail is an suppresor for the other factor.
The pointed head arrow means activation or increasing activity.
A -------------> B
means A is increasing activity of B. Factor at arrowhead is being activated. Factor at arrowtail is an activator for the other factor

The "normal" (green here) arrowheads stand for a positive effect of the upstream factor or protein on the process or protein it points to. For instance, it means amino acids activate TORC1. Instead, arrows that end with a line (red here) stand for inhibition. For instance, rapamycin inhibits TORC1.

Oxygen, amino acids , energy level and growth factors are activating TORC1 gene (growth factors also cause TORC2 activation).
Then further TORC1 gene  promotes translation, cell cycle and metabolism, but inhibits autophagy. Whereas TORC2 promotes cellular metabolism and cytoskeleton.
Rapamycin and Stress inhibits TORC1.
Green arrow is used to show stimulatory effect and Red flathead  is used for showing inhibiting effect.
These arrows have nothing to do with upstream and downstream signalling.
Read further about this https://www.khanacademy.org/science/biology/cell-signaling/mechanisms-of-cell-signaling/a/intracellular-signal-transduction


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What is the relationship between cell size and metabolism?
What effect does a bigger cell have on its metabolic activity? I understand that bigger cells need more energy, but surely smaller cells may have high metabolic rates too due to their efficiency?


text:
Is this a Tabebuia impetiginosa – Pink Trumpet Tree Flower?
Is this a Tabebuia impetiginosa – Pink Trumpet Tree Flower? From Panama.

For tree identification questions please also include: 1) Pictures of the bark and leaves with an estimate of the size, 2) information about the environment within which you found the tree, and 3) an estimate of the size of the tree. All of these can be essential clues for identification. ——— If possible a picture of this plant in its environment could also be helpful. Thanks!

All I have is this photo.

Unfortunate — please edit your post to add whatever information you do have (e.g. ecological/environmental factors) and with luck someone will be able to help ...


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Is chromosomal DNA more likely to interfere with restriction mapping or PCR analysis in E. coli?
We are characterizing YADH-1 in my biochemistry lab course. Over the course of the first weeks, we harvested E. coli cells, and isolated plasmid DNA via alkaline cell lysis. A previous exam for the course asked the following question concerning plasmid DNA and analysis:
"Is chromosomal DNA more likely to interfere with restriction mapping, with PCR analysis, or equally likely to interfere with both methods?"
Since we're using EcoRI and BamHI, my thought process is that while we can predict the cuts on a circular plasmid, we wouldn't be able to predict all of the cuts on high-molecular weight chromosomal DNA, and the resulting restriction map would be useless. However, PCR can work in a complex mixture of molecules, so even in chromosomal DNA, the primers should be able to find the target sequence. Is the answer therefore that chromosomal DNA is more likely to interfere with restriction mapping?

Welcome to Biology.SE!
I think you've come to a reasonable conclusion, but not for exactly the right reasons.
The genomes of several strains of Escherichia coli have been sequenced (e.g. https://www.ncbi.nlm.nih.gov/nuccore/U00096) so you could predict the sizes of the fragments you would expect from your digest.
The genome size of E. coli is about 4.6 million base pairs and six-cutters like EcoRI and BamHI cut on average about once every 4096 bp (you should be able to figure out how to come up with that number). From that what would you expect to see if you did a restriction digest on this bacteria's genomic DNA?
Does that help you improve your answer?
(If you have access to the appropriate software, I encourage you to download that sequence and check your conclusions.)
((Also note that the specificity of PCR is dependent on primer selection, so your answer is assuming that the primers were well designed!))

Ah, it does. That means I'd get about 1100 different cuts on a map for genomic DNA, and wouldn't be able to conclude if I'd isolated the gene of interest.

Yes and each of those fragments will be a different size!  I found a relevant picture here: https://www.semanticscholar.org/paper/DNA-Probe-for-Lactobacillus-delbrueckii.-Delley-Mollet/27223427d914f7ccca92c43937d83eadbddc1963/figure/0


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Can fructose take multiple forms ? Which of these structures of fructose is correct?
When I look up the structure of fructose I get various different structures
Which of them is correct ?
Are these all just isomers of fructose ?

The two structures on the left are correct; the one on the upper left is the alpha-D-fructofuranose form, while the one on the lower left is the beta-D-fructofuranose form.
Fructose is a ketohexose (a six-carbon sugar with its carbonyl group present as a ketone group in the molecule's open-chain form); the carbonyl carbon (the 2-carbon, to be precise) is optically inactive in open-chain fructose, as the oxygen and two carbons bonded to it adopt a flat trigonal planar geometry, but, when the carbonyl group is attacked by the 5-carbon's hydroxyl group to form the cyclic fructofuranose (fructose in a five-membered ring) configuration, the 2-carbon changes from being part of a (trigonal planar) carbonyl to being part of a (tetrahedral) hemiketal, introducing an additional stereogenic center that wasn't present in the linear form.  The arrangement of the substituents around this new stereogenic center is essentially a random crapshoot, with half of the new fructofuranoses having the hydroxyl pointing in direction 1 and the hydroxymethyl pointing in direction 2 (the alpha form), and the other half having the hydroxymethyl pointing in direction 1 and the hydroxyl pointing in direction 2 (the beta form).
There are, by the way, eight other configurations that fructose can take; three of them (plus the two you've already drawn) are for D-fructose (the naturally-occurring-in-the-vast-majority-of-naturally-occurring-fructoses form), while the remaining five are for L-fructose (which occurs only very rarely in nature and is essentially useless for most living organisms), which has the hydroxyls on the 3-, 4-, and 5-carbons pointing in the opposite direction.1

The alpha-D-fructopyranose and beta-D-fructopyranose forms have a six-membered pyranose ring, rather than the five-membered furanose ring; these are formed when the hydroxyl group attacking the carbonyl is that attached to the 6-carbon, rather than the 5-carbon, and are actually energetically much more favourable than the fructofuranose forms, making up essentially 100% of crystalline fructose and 70% of fructose in aqueous solution.
The open-chain D-fructose form is acyclic, with the 2-carbon actually being part of a carbonyl group rather than a hemiketal.  It is present in only minuscule concentrations in aqueous solution, but serves as the intermediate between all of the various cyclic forms of D-fructose.
L-fructose can adopt the alpha-L-fructofuranose, beta-L-fructofuranose, alpha-L-fructopyranose, beta-L-fructopyranose, or open-chain L-fructose forms, which are essentially equivalent to their D-fructose equivalents apart from their opposite chirality.

1: In the L-fructofuranose configurations, this takes the form of the hydroxymethyl group hanging off the 5-carbon pointing down rather than up.


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Are highly-polyploid organisms more resistant to ionising-radiation-induced DNA damage?
Homologous recombination, although most famous for its use to mix together maternal and paternal alleles during meiosis, is most commonly used as a DNA-repair mechanism, allowing cells to repair double-strand breaks (lesions where both strands of the DNA double helix are severed at the same, or nearly the same, level), such as those produced by (and responsible for the main lethal effects of) overexposure to ionising radiation.  In this process, the broken ends are cut back asymmetrically, producing single-stranded flaps at the ends; at least one of the flaps engages and base-pairs with a strand at the same level on a sister chromatid (if available) or a homologous chromosome (if we’re still in G1 and no sister chromatids are yet available), producing either one or two Holliday junctions; new DNA is synthesised to fill the remaining single-stranded gaps; and ligases and (sometimes) endonucleases complete the repair and separate the two pairs of strands.1
Although eukaryotic cells have two other methods of repairing double-strand breaks (non-homologous end joining [NHEJ] and microhomology-mediated end joining [MMEJ]), homologous recombination is, when possible, the highest-fidelity repair method:

NHEJ consists of a DNA ligase grabbing the loose ends (taking advantage of the fact that the two strands usually aren't broken at exactly the same level, leaving short complementary single-stranded flaps on each side of the break) and gluing them together; if the cell’s DNA contains multiple double-strand breaks, there is no guarantee that the ligase will join the ends with their correct partners (especially if the strands didn't break cleanly, and a few nucleotides or bases were damaged or snapped off), and, if the wrong loose ends are joined together, various severe chromosomal aberrations can occur (such as fusion of chromosomes, translocations of material between non-homologous chromosomes, deletion of segments of chromosomes, production of ring chromosomes, etc.).  In contrast, since homologous recombination relies on the cut-back broken ends recognising their counterparts in the same location on a sister chromatid or homologous chromosome, it is impossible for the wrong ends to be joined together; the worst that can happen is that material is exchanged symmetrically between homologous chromosomes, an essentially-completely-benign occurrence.
MMEJ relies on the presence, sprinkled liberally throughout the genome, of numerous repeated short identical DNA sequences; when a double-strand break occurs, each of the broken ends is cut back to the nearest one of these repeats, one strand is cut away from the repeat on each end, leaving a pair of complementary single-stranded flaps, one on each broken end, and these flaps are then stuck together and the whole thing stitched up by a ligase.  This process, by its very nature, always results in the loss of the segments of DNA immediately adjacent to the break; if the break occurs between two repeat sequences, one of the two repeats will be lost, as will the entire unique segment between them, while, if the break cuts through a repeat, the bisected repeat will be lost, as will both of the unique segments flanking it, as will one of the pair of nearest undamaged repeats upstream and downstream of the original break.  Homologous recombination, in contrast, results in no loss of genetic material.

The main drawback of homologous recombination is that it requires an identical, or near-identical, template; if - say - double-strand breaks occur at near the same level on both examples of a particular chromosome in a diploid cell in G1, or if any double-strand breaks occur in a haploid cell in G1, the damage cannot be repaired by homologous recombination, and repair (if possible at all) must be carried out via one of the two aforementioned lower-fidelity methods.
One would, thus, intuitively expect (at least so far as concerns double-strand breaks and the repair thereof) that in DNA repair, as in data recovery, the more homologous copies (even if damaged) that are available, the better the chance of successfully rebuilding a working genome or boot drive; i.e., the greater the organism’s ploidy (its number of homologous copies of each chromosome), the greater its ability to repair DNA damage involving numerous double-strand breaks, such as that produced by ionising radiation; e.g., a diploid organism would be less able to repair radiation-damaged DNA than a tetraploid organism, which would itself be more vulnerable to radiation-induced damage than an octaploid organism, which would still be less resilient than a hexadecaploid organism, which would, in turn, have a harder time piecing its genome back together than a dotriacontaploid organism.2
Is this actually the case in practice?

1: There are two variants of this pathway.  In the double-strand-break repair (DSBR) pathway, both single-stranded flaps engage with the homologous chromatid/chromosome, producing two Holliday junctions; all DNA synthesis, and the first pair of ligations, occur prior to the junctions being cleaved; and the portions of the chrom(atids/osomes) distal to the junctions are sometimes exchanged between the two, depending on how, exactly, the Holliday junctions are cleaved.  In the synthesis-dependent strand annealing (SDSA) pathway, only one flap engages, producing but a single Holliday junction; the homologous DNA serves purely as a template, with the intruding strand disengaging once it has acquired enough additional length to bridge the gap; and the balance of the new DNA is synthesised after the two ends have already stuck back together.  (Alternatively, see Wikipedia.)
2: This assumes an autopolyploid organism (one where all however-many chromosome sets are from the same source and equivalent to each other), such as any of the extant sturgeons (all of which are either autotetraploid, autooctaploid, or autododecaploid); for an allopolyploid organism (one produced by putting the entireties of two [or more] genomes from two [or more] related organisms into a single cell and letting that develop into an organism), such as bread wheat (allohexaploid), the chromosomes from (say) genome A refuse to hang out with those from (say) genome C, and the organism is functionally merely diploid (albeit with a greatly-increased monoploid number).


text:
Why do tails of some lizards break so easily?
When I was younger once I have tried to catch a ground lizard by its tail but,
unfortunately the tail got broken and the lizard ran away.
Why did the lizard's tail get broken so easily while other animals have stronger tails?

It's a self-defense mechanism, the tail falls off during threatening situations, to which the reptile responds by excessively contracting the tail muscles. This process is known as "Autotomy", or "Self-Amputation". Other animals have got "stronger tails" simply because such self-defense mechanism hasn't been developed.
https://science.sciencemag.org/content/20/500/149.2
Check this link for more in depth information!


text:
Do some genes follow Rock-Paper-Scissors model of dominance?
Assuming there are at least 3 alleles of the gene $G$ in total - $G_R$, $G_S$ and $G_P$ - is there any gene for which the following is true?

$G_R$ is more dominant than $G_S$.
$G_S$ is more dominant than $G_P$.
$G_P$ is more dominant than $G_R$.

Note that the "rock-paper-scissors pattern" is more formally known as a "non-transitive relation". You may be familiar with a transitive relation, where if A>B and B>C, then A>C. If instead A>B and B>C, but A<C (C>A), then it's known as a non-transitive relation, like the one you describe here.

A quick search gives this same question in this Reddit post.
Apparently, there is not yet an existing example of such dominance of three alleles on one another.
That said, if you're interested in rock-paper-scissor patterns in nature, then you will be interested in the side-blotched lizard. It has three genetically encoded male "sexes", that also determines their behaviour. At a population level, the three sexes follow a rock-paper-scissor pattern of successful sexual competition, in that orange-throated individuals can outcompete yellow-throated ones, which can outcompete blue-throated ones, which can outcome orange-throated ones. A simulation has been carried out to model the underlying genetics, but that model doesn't involve a rock-paper-scissors pattern of genetic dominance.

@ruakh You mean "outcompete", not "outcome".

@CJDennis: Yeah, I noticed that typo a few days after proposing the edit. (I also should have written something like "[...] but to be clear, that model [...]" instead of just "but that model".) But given that the edit took almost two weeks to get approved, it doesn't seem worth proposing a new edit just to fix such minor issues. :-/

@ruakh Too late now, but you can edit your edit before its approved.

@CJDennis: Oh! Oops. Good to know. :-P


text:
Are there any ways to force DNA-origami to create a geometric shape from non-nucleotides (not from DNA)?
I mean, can we create with the help of DNA-origami figures that would not consist of DNA, but, for example, carbon? Is it even possible?

Can you explain your question in more detail, and link to the relevant study you mention? Carbon can be made into a geometric arrangement called fullerene, for instance, but that may be different than what you're asking. https://en.m.wikipedia.org/wiki/Fullerene

Using DNA-origami, we can get various nano-objects of the desired shape. Such objects consist of DNA. I ask, can we in theory with the help of DNA-origami get nano-objects that will not consist of DNA, but some other specific atoms, gold, carbon, etc?

Welcome to Biology.SE! Are you asking whether the folding of DNA in "DNA origami" can be used to manipulate other nanomaterials?  Or did you mean whether DNA structures can be used as a scaffold to pattern other nanomaterials? Something else? Please edit your question to clarify and add links to relevant papers.  ——— You may also benefit from taking the [tour] and then consulting the help pages for additional advice on [Ask] questions effectively on this site and then edit your answer accordingly. Thanks!
(Also note that DNA contains carbon — did you mean graphene or something similar?)

I interpret your question to ask this:
Can DNA origami be used as scaffolds for the guided assembly of other non-DNA structures?
Yes.  From what I've read, two- and three-dimensional DNA structures can be used for nanoparticle assembly and as a nucleation factor in the crystallization of proteins and minerals.  You can find these examples and more in a lengthy review from 2017.1  Specifically, read section 6.6, Programming the Structure and Conformation of Non-DNA Materials.

Fan Hong, Fei Zhang, Yan Liu, and Hao Yan. DNA Origami: Scaffolds for Creating Higher Order Structures. Chem. Rev. 2017, 117, 20, 12584–12640.


text:
How do we know how long hermit crabs live in the wild?
This article states that hermit crabs in the wild are extremely difficult to track because they constantly change shells and even gender.  Later in the article, they say that hermit crabs can live 4 decades in the wild.  How can they know this if they can't follow a single crab for an extended period of time?

Hermit crabs increase in size over time and this is used to provide a minimum estimate for their age1.
You may also find this article interesting.

Reference:
SantAnna, Bruno Sampaio, Christofoletti, Ronaldo Adriano, Zangrande, Cilene Mariane, & Reigada, Alvaro Luis Diogo. (2008). Growth of the hermit crab Clibanarius vittatus (Bosc, 1802) (Crustacea, Anomura, Diogenidae) at São Vicente, São Paulo, Brazil. Brazilian Archives of Biology and Technology, 51(3), 547-550. https://dx.doi.org/10.1590/S1516-89132008000300014


text:
Why this fish is accompanying stingray?
During snorkelling a couple of months ago on Canary Islands I've been watching stingrays which I think are "Roughtail stingrays". Often this fish (on pic) was accompanying those stingrays. So what kind of fish is this and why it's hanging around stingrays?

Stingray:

I've seen this behaviour many times so I'm sure it's not a coincidence.

Welcome to Biology.SE! Interesting question — did you observe any interactions between the fish and the ray? For example, did you ever see the ray feeding and how did the fish react? My suspicion would be that the fish is hoping to benefit from the ray's foraging. ——— You may also want to take the time to go through the [tour] and the help pages starting with [Ask] questions effectively on this site. Thanks!

@tyersome thanks for the hint. No unfortunately I haven't seen any interactions between them. This fish is kinda just hanging around. If you come closer to the stingray the fish will flee and leave the stingray. Also I haven't seen other species of fish hanging around stingrays, it was always the same. I was thinking maybe it's looking for protection? This is completely sandy coast with no cover for fish, maybe hanging around stingray is safer, meaning if it flees the fish will know that danger is around. Maybe stingray sensing danger much better than this fish.

The fish it seems is one of weevers

Curious — the only thing I've been able to find about stingray symbiotic relationships  are mutualistic relationships with cleaner wrasses and commensal relationships with fish and coastal birds that capture small animals disturbed by foraging by the stingray.  In the absence of any observed interactions the latter still seems like the most likely explanation to me, but I guess you'll just have to go back and make more observations to be sure!

@tyersome Probably in a few years :) Though it's not easy to get close to them because they are flee fast. There's some sort of interaction can be seen on this video https://youtu.be/Gjz52RtPakA if you increase size. It seems fish just swim close to stingray and wait nearby for something.


text:
What is this very tiny (3mm) centipede-like insect?

My kid found this little guy in his bedroom. It’s about 2-3mm long. Lots of legs, and white rings around its abdomen.
Any idea what it is?
Edit: Location in San Jose, CA.

Welcome to Biology.SE! For identification questions please edit your post to include the location (e.g. country and region — the more specific the better) where you observed this creature. The location can be an essential clue for identifications. ——— If possible clear, closeup photos of the creature from multiple angles would also be helpful. ——— Please take the time to take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site. Thanks!

Related: What kind of insect can this be?..., Can anyone help confirm this tiny insect larvae?, Bug Identification: Is this small tubular, black bug...,
How to protect my mounted insects..., What is the name of the critter depicted..., What small insect is this?, What bug is this...

That is a dermestid larva. A beetle from the family Dermestidae https://en.wikipedia.org/wiki/Dermestidae, common name, skin beetle. They eat dried skin, or flesh, and are generally the last insect to feed on a carcass. They are the bane of insect collectors, because they eat dried insects right off the pin.


text:
Where can I find the data on the geographical distribution of the species of Drosophila within various areas of the world?
Let X denote an arbitrary geographic area where drosophilas occur in the wild. I will need the answers to the questions of the following type:

What is the three most occurring species of the genus Drosophila within X?

Where can I find the data on the geographical distribution of Drosophila species within various areas of the Earth?

@user1136: I don't see how TaxoDros can help to answer a "What are the three most occurring species of the genus Drosophila in this particular country?" question. I have not found any source that contains such information.

Source: pinterest.com
I have been unable to find data on a global scale, for now here's a map on the USA.

Pinterest.com is not a source. It is a (closed) shop for stolen goods. And a map of the US doesn’t answer the question.

First, I don't see how your highly subjective opinion lacking any basis can be following the Community Lines. Second, I advise reading the picture description in order to avoid wasting your time in such comments.

— My opinion is based on the many images stolen from websites I run and which were marked up with Pinterest’s own code to flag that they shouldn’t be copied to Pinterest. I had to request their removal, which Pinterest honoured. I was able to identify them by searching for reference to my website, and presumably you could have identified the source of the image you posted. Asking readers who may be partially sighted to read text rendered as graphics is discriminatory, but in this case clearly does not answer the question as posted.  My comment explained my down-vote.


text:
Human Anatomy and Physiology - The Muscoskeletal System
In the human limb skeleton can you identify a bone which is rather feeble and does not have much role in supporting body weight or maintain posture, and doctors use pieces of it to transplant to other broken bones, where necessary?

For bone grafts, they usually use parts of the bones, so their removal should not result in problems with the "body weight maintenance" or "posture."
Parts of the fibula (calf bone) can be used, for example, as a graft to repair avascular necrosis of the femoral neck or congenital pseudoarthrosis of the tibia (shinbone) (International Orthopaedics).
For spinal fusion (joining the vertebra in the spine), they typically use the bone from the iliac crest (the top part of the pelvis) (OrthoInfo).
Other bones that can be used as grafts:

Parts of the ribs and certain skull bones for reconstruction of the facial bones
Parts of the mandible for tooth implants
Upper part of the tibia for various purposes
Distal part of the ulna for correction of the wrist in rheumatoid arthritis


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In human embryology, what starts ovum cell division?
Maybe I am not using the correct search keywords in Google, but I cannot seem to find anything beyond basic information taught in schools about fertilisation of the egg by the sperm.
After the sperm has fertilised the ovum, I know that the zygote starts with one cell, then divides into two cells, then four cells and so on, but what initialises cell division, and how does the cell divide?

Actually an ovum doesn't ever start cell division because once it is fertilized by a sperm the combination of the two cells is call a zygote.  In humans, the zygote proceeds with the many steps following fertilization leading to the first division; this takes on the order of 24 to 30 hours.  At that point the set of cells may be termed an embryo or various other technical terms.  The succeeding cell divisions occur by the normal cell division mechanism, which is called mitosis.  In the context of the development of the human embryo, an early stage cell division is often called cleavage.
More details are available from the links in the above.  For greater technical depth on the initial stages of the division of the zygote, you might want to see this article.

Thanks for pointing me in the direction I need to go in order to answer my question. Although I am not yet 100% sure on all this, I am not sure I can completely accept your answer as of yet. It's the mitosis part that's causing me an issue. I may be wrong, but I am under the impression from reading that mitosis (or even cleavage) is not the complete mechanism/process of cell division. I need to get this all straight in my head before I upvote or accept this answer.


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Taq Polymerase's stability at high temperature
I was asked a question as to what is so special with Taq Polymerase that makes it quite stable at high temperatures though its functioning is the same as other DNA polymerases like that of mesophiles.
I just think it's the adaptation of that particular bacteria in that high-temperature environment. But I want to know if there is any strong reason for this stability.

Well, the evolutionary reason is the one you mentioned: the thermostability of Taq allowed its bacterium to colonize high-temperature environments. That, however, does not say anything about the molecular reasons for this difference.
I found this very good answer on Quora. The end of the post has several references for its claims.
Long story short, the stability of a proteins folded state depends on the difference of free energy $\Delta G$ between the folded and unfolded states. However, $\Delta G = \Delta H - T \Delta S$, which means the difference in free energy can either come from a bigger difference in enthalpy (for example, salt bridges, hydrogen bonds, hydrophobic interactions and such in the folded state) or a smaller difference in entropy (for example, a low number of "not-rigid" amino acids like glycin , or a high release of water from folding).
While enthalpy is often the reason for stability of folding, it seems like for Taq polymerase the difference actually lies in an unusually small difference in entropy between the two states.
Edit: here is one of the best references of the post. Open the link above to find more. https://www.ncbi.nlm.nih.gov/pubmed/24174290

Can you please cite an original source i.e. a research article/review?

@WYSIWYG As I said, the end of the post I linked had all the references. Anyway, here you go: https://www.ncbi.nlm.nih.gov/pubmed/24174290

Please edit your answer to include this reference information — comments are intended for suggestions and discussions intended to improve answers (or questions) and should not be used to post material that belongs in the answer itself.  You also might want to consult the help pages for additional advice on [Answer] effectively on this site. Thanks!


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Which side of the DNA helix is used for describing SNPs?
In genetic research I often come across references to single-nucleotide polymorphisms (SNPs).  An example is rs3184504(C;T).  As far as I understand it: In this case rs3184504 refers to a specific point in the DNA genome, and (because this one occurs in a non-sex human chromosome) it indicates the nucleotides at that point in each copy of that chromosome.
But how does one determine which strand of the DNA helix it references?  Is there a convention?  Or is the strand indicated in the SNP reference (in this case rs3184504)?
If one strand is C;T then the opposing strand will be G;A ... but in the context of the gene in question I assume it matters which strand is referenced in the SNP.  E.g., if the code following this SNP on the chromosome in which rs3184504 has C is:
CTCGA...
GAGCT...

this is a different genotype from the SNP indicating a C on the other strand:
GTCGA...
CAGCT...

So the SNP description is only meaningful if it also indicates the strand, right?  If so, how does the SNP descriptor do that?

@WYSIWYG is correct, but in view of the brevity of his answer (and a second answer contradicting him) I provide chapter and verse.
The definition of RefSNP reference number is given by NCBI as:

“A reference SNP ID number, or “rs” ID, is an identification tag
  assigned by NCBI to a group (or cluster) of SNPs that map to an
  identical location.”

It is important to realize that this number bears no relationship to the numbering of the DNA sequence:

“The rs ID number, or rs tag, is assigned after submission.”

To find information about the position of an SNP from its rs number one can search the NCBI dbSNP. In the case of rs1384504 the first few lines of the first entry in the search results is:
Variant type:   SNV
Alleles:        T>A,C,G
Chromosome:     12:111446804 (GRCh38)

This indicates that the SNP is at position 111446804 on Chromosome 12, which has a T in the reference genome, and this lies in a gene designated SH2B3. (You can find this from the links on this page.)
It can be seen on this page that the orientation of this gene happens to coincide with that of the reference chromosome. However a nearby gene, PPP1CC, is in the opposite orientation and contains a SNP rs367543175 C/T. The start of the entry for this is
Variant type:   SNV
Alleles:        C>T
Chromosome:     12:110720185 (GRCh38)

…indicating that the SNP is at position 110720185 on Chromosome 12, which has a C in the reference genome, i.e. on the anti-sense strand of this gene.

And, of course, most human SNPs lie outside genes, so the concept of sense and anti-sense strand does not apply.
Conclusion
To find out whether the reference base in a designation for a SNP lying in the coding region of gene corresponds to the sense or anti-sense strand of that gene, one has to access the documentation for that SNP. This information is not embodied in the allele data appended to the reference SNP ID number.

It is described with respect to the reference sequence. See the VCF format description.

DNA has a "sense" strand and an antisense strand. The sense strand for that gene is the one you care about when discussing SNPs in that gene, because its the one being transcribed (and, as a result, the one affecting the organism). For more information about sense and antisense strands, there are some pretty good explanatory youtube videos and Wikipedia entries.

Whether or not you are interested in the sense strand of a gene (and most SNPs fall outside genes) the allele variation in an RefSNP reference number, about which the poster asks, does not necessarily relate to that strand. @WYSIWYG was correct, as I document in my own answer.


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Is evolution a means to an end?
In "The Red Queen", Matt Ridley frequently argues that evolution is a means to an end, without providing much explanation for such a big statement.
Is this a fact in biology? Do species mutate their genes so they can reach an optimum state, like the coelacanth fish that (allegedly) remained unchanged for the last 300 hundred million years?

The universe does not know neither care. It does not aim. There is no intention in evolving.

This is a good question to ponder but the answer is straightforward and is so very old and tiring to expound on. Evolution is not teleological. Case closed. This is discussed and answered everywhere on the internet. I vote to close, as duplicate of this and this and this and so many more.

Possible duplicate of Why do some bad traits evolve, and good ones don't?

It's been a decade since I read "The Red Queen" and I don't recall Ridley making any such suggestion. Could you quote some of the material that makes you think this?

@CharlesE.Grant in my 2003 copy published by Harper Perennial, at page 31: "[The coelacanth] has stayed the same - a design that persists without innovation, like a Volkswagen beetle. Evolving is not a goal but a means to solving a problem"

Good question--I think the first point to address is "a means to an end" seems to imply willful action. That is, evolution (according to Ridley) would be a conscious effort by a species to optimize the gene pool for survival of future generations; a rationalization for each species to mutate and diverge.
This is not the case, for a couple of reasons. First, evolution is largely due to environmental factors that exert much more control over the genetic drift of a species than any internal (i.e. willful) factors, such as sexual selection. Additionally, optimal performance is often sacrificed for the sake of reproduction (peacocks, now functionally flightless). All sexual selection happens in the context of the organism's environment--phentoypes can change, but if there's only one food source on your island, it's the limiting factor and will exert strong evolutionary pressure to maintain certain traits.
Second, no evolutionary trait is guaranteed to push the species towards a so-called optima. The influence of sexual selection on populations has left many species (again I lean on peacocks as an example) expending energy on developing traits that do not make them more viable or "optimized" as an organism, but instead make them more desirable mates and thus more likely to reproduce and pass on their genetic material. Peacocks could be much more resilient to predators without all that extra plumage, but they've traded off flight for mating success.
Finally, as an aside, evolution happens on such a large timescale that individual populations would barely be able to change their genetic makeup in the course of a single lifetime. This point is not as robust, but if general societal consensus was driving evolution, there would be extinct species littering the corners of the planet. Ridley seems to have missed the mark a little--nobody is doing anything to cause evolution; evolution happens to you over many years of mutations and environmental pressures.

In a comment I ask you for specific passages that give you this impression (since when I read The Red Queen I came away with the opposite impression). You provided the following quote.

in my 2003 copy published by Harper Perennial, at page 31: "[The
  coelacanth] has stayed the same - a design that persists without
  innovation, like a Volkswagen beetle. Evolving is not a goal but a
  means to solving a problem"

OK, that does make me wince a little. "means to solving a problem" does sound a little anthropomorphic to me. I think he may be trying to address the notion that evolution is some sort of metaphysical process driving towards greater complexity or sophistication. Or to put it another way he's arguing that there is no arrow of "progress" associated with evolution. Organisms that are not equipped to deal with their environment die out. Organisms that are well equipped to deal with their environment may persist with relatively little change for millions of years (at least as long as their environment doesn't change).

To quote a writer, We are trying to unravel the mighty Infinite using a language which was designed to tell one another where the fresh fruit was.

"Do species mutate their genes so they can reach an optimum state". No, for several reasons.
Species do not mutate their genes. Individuals suffer mutations.
Many species are in an environment that changes as fast as they can evolve, because of geophysical change, or other species including H.Sapiens. In these cases there is no optimal state to reach.
Evolution often means speciation, not genetic drift within one species.
Adaption often occurs by combining traits already in the gene pool, rather than by new mutations, which are rarely beneficial.


text:
Do plasma B cells express the BCR or only produce soluble antibodies?
Is the B cell receptor still expressed on a B cell once it has begun to produce soluble antibodies? Is there a gene change that prevents the membrane-bound form from being produced anymore?

B cells can secrete antibody before they are terminally differentiated into plasma cells, so there is a phase during which both membrane-bound and secretory antibodies can be produced by the same cell:

When a naïve or memory B cell is activated by antigen (with the aid of a helper T cell), it proliferates and differentiates into an antibody-secreting effector cell. Such cells make and secrete large amounts of soluble (rather than membrane-bound) antibody, which has the same unique antigen-binding site as the cell-surface antibody that served earlier as the antigen receptor (Figure 24-17). Effector B cells can begin secreting antibody while they are still small lymphocytes, but the end stage of their maturation pathway is a large plasma cell

--Molecular Biology of the Cell. 4th edition.
Plasma cells, generally speaking, have little or no surface immunoglobulin, but it's been claimed that some subsets of plasma cells do have surface Ig:

Surprisingly, although IgG PCs downregulated surface IgG expression, IgA and IgM PCs expressed their respective isotype both intracellularly and on the plasma membrane (Figure 1A, lower panel). Importantly, concordant Ig’s were also detected on the plasma membrane of IgA and IgM, but not IgG, PCs isolated from BM or colon LP indicating that this property is a characteristic of PCs present in their physiological niches

--A functional BCR in human IgA and IgM plasma cells

Once B cell starts secreting soluble antibodies, it is no longer a B cell, it is called a plasma cell hence normal B cells do not secrete soluble antibodies before becoming plasma cells. It is the BCR that is secreted. B cells can either differentiate into memory or plasma cells.  Plasma cells produce soluble antibody molecules closely modeled after the receptors of the precursor B cell. The plasma cell continuously produces soluble antibodies.
I hope this helps since I did not directly answer your questions because they were based on inaccurate information/bases. Please let me know if any other questions based on the information I provided

Welcome to Biology.SE! Your answer sounds reasonable, but it is much more likely to receive a favorable response if you include supporting references (primary literature is best). Without that support non-specialists in immunology will have difficulty in verifying your claims. ——— That you for taking the [tour], however you may also benefit from consulting the help pages for additional advice on [Answer] effectively on this site and then edit your answer accordingly. Thanks!


text:
Is reverse tonotopical organisation possible?
In human cochlea tonotopical organisation is that higher frequency sounds are detected near the entrance whereas lower frequency sounds are deep inside the cochlea. Is this tonotopical organisation (high frequencies at the entrance, low - deep inside) justified by some physical or biological constraints or it doesn't matter and we could in principle have cochlea where low frequency sounds are detected at the entrance?

There are indeed constraints: in principle, low-frequency sound waves travel better in viscous media (look here for a simple explanation). The idea behind that is that being sound a vibration in the medium, it causes its molecules to move. The faster the movement (that is, the higher the frequency) induced by the wave, the more the particles will disperse their energy by crashing into each other. This leads to more loss of energy for high-frequency waves compared to low-frequency ones when travelling in a medium.
Now, all of this leads to the detection of high frequencies being better at the beginning of the canal. However, here is the law that quantifies the loss of amplitude of the wave with distance. As you can see, the damping is higher for high frequencies, as well as high viscosities. However, plugging in some sensible numbers (20 kHz for very high-frequencies heard by humans, 1500 m/s for the speed of sound in endolymph, 1 centipoise for its dynamic viscosity, 1 kg/liter for density) gives a negligible loss of intensity (something like 0.0001. I'm sorry for the poor formatting, but I'm on my phone right now and I hope you will try to run the calculation yourself).
Now, a possible need for the accurate detection of even higher frequency sound waves in water for the fish in which the cochlea appeared is possible. However, I neither know if that is the case, nor if the difference would be a significant one.


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Brain evolution in the age of the caesarian
I have just been reading an account of the evolution of human intelligence in Matthew Syed’s recent book on diversity, called “Rebel Minds”.
He is not the originator of this idea, but he suggests that the limiting factor in the growth of the human brain beyond it’s already prodigious size is the size of the female birth canal, so that, above a certain size it had killed the mother and itself at birth.
I am not a biologist.  But I wondered whether there is any evidence of increase in brain size in the past (say) 50 years as more gravidae give birth by C-section?  Is such a change possible or probable as this procedure becomes more common?  Or are there other limiting factors, such as the weight that can be carried by the spine?

50 years - maybe two human generations - is hardly long enough for evolution to have a measurable effect.  Also, head size is not high among the reasons why C-sections are done.  Nor AFAIK is there any fundamental reason why human brains(or other species) could not continue growing after birth.  (E.g. marsupials.)

@jamesqf Thank you.  Yes it is obvious, now you mention it, that 50 years was a ridiculously short suggestion.


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Genetics and Heredogram - Proving the teacher is wrong
I want serious help here. I'm in first year of medical school and I jut had my second test in Genetics. One question of the test gave us a heredogram and asked us what was the most probable type of genetic disease the family had. There were 2 types of disease that would fit the heredogram. Recessive autosomal and Dominant X-linked. I put both and explained why both them fit. But a lot of my colleagues put only one of them. He said after that he wanted X-linked, because the heredogram had more trends of X-linked diseases. I just don't bite that. This is not the way we calculate probability. For example a autosomal disease can happen in 44 out of the 46 chromosomes while the X-linked only in the X chromossome (1.5 in average). Also, what if recessive diseases are more common than dominant. What if most of the people with X-linked diseases are infertile or if most of them dies. All of these reduces the chance of a given heredogram being Dominant X-linked. We can't say something one based on the trends.
The heredogram is the below.

Do you agree with me? I really need some opinions of other people so we can contest the teacher. Otherwise half of the classroom will get a zero.

This site does not exist to give opinions so people can contest their teachers. It exists to provide objective answers to problems of biology which are of general importance and interest. The title shows a particular petty arrogance which is more likely to antagonise people than gain their sympathy.

I think you are making this too complicated. You don't have enough data from this diagram to make any sort of rigorous statistical judgement. You are just looking for clues.
Note that in the first generation offspring of the affected male founder, all the female offspring are affected and none of the male offspring are affected. This is exactly the pattern you would expect for a dominant X-linked trait.
For an autosomal recessive trait, you'd expect roughly equal numbers of male and female offspring to be affected in the first generation where once parent is affected and the other is a carrier. This is true regardless of all the red herrings you raise about the number of autosomes, fertility, and lethality. So this is a little odd looking for an autosomal recessive trait. It's a tiny sample size, so not impossible, not definitively ruled out, just a little unlikely.
Diagrams like this don't usually give you a definitive result, but they can indicate where to start looking.

In my opinion, we cannot say autosomal recessive is more unlikely. Consider the first and second generation only for example. An affected father, a non-affected mother, 3 affected daughters and a non affected son. Given the disease is Dominant X-linked the chance of the parents have that children is (1/2)^4=1/16. While if the disease was autosomal recessive (1/4)^4 = 1/256, that is 16 times less. But consider an Dominant X-linked disease is 23 times less common than an autosomal (what could be completely true given the number of chromosomes). Than now autosomal is MORE LIKELY than X-linked.

@JoãoMaldonado No, you are miscalculating the likelihoods. The likelihood of the data given the Dominant X-Linked model is exactly 1. For the first generation of offspring for an affected father and unaffected mother, the female children are necessarily affected, and the male offspring are necessarily unaffected. No other pattern is possible.

For the autosomal recessive model, the father must be carrying two copies of the recessive mutation and the mother must be a carrier, with one copy of the recessive mutation. The status of each of their offspring is essentially a coin flip depending on which copy they inherit from the mother, so the likelihood of the observed 1st generation is (1/2)^4=0.0625. You may have a point that somatic chromosomes outnumber sex chromosomes, so that might boost the likelihood a little (this is called a prior), but it isn't going to be as simple as multiplying the likelihood by 23.

I’m not saying it is that simple. Just that it is not correct to say that X linked is more likely for sure. Also, you misunderstood the probability I calculated. The question is: what is the probability that an affected father and a non-affected mother have 4 children, 3 females affected and one male not affected.

If the disease is Dominant X-linked there is a likelihood of 50% of a random children be a female affected and 50% of the children be a male not affected. So the probability of that couple have 4 children with the pattern said above is 1/16. If the disease is recessive autosomal there is 25% of a ta from children be female affected, 25% female not affected, 25% male affected, 25% male not affected. The probability of the couple have tha 4 children as I said is 1/256

Also. If we have the statistic # people in that community (or the world considering the distribution is uniform) with autosomal recessive diseases divided by # of people with X linked dominant diseases and we consider and we consider both types of diseases live the same, have the same probability of finding a couple or having a fertile child etc. Then it would be as simple as multiplying this number to the 1/16 we calculated. Of course it is not like this. People with X linked diseases could be more or less fertile or find more or less couples or having more or less fertile children and etc.

My point is that no one can say that one disease is more likely than the other or ask that in a test. Inferring the mode of disease is something extremely complicated and by what I searched is only done with algorithms and computers, that calculate an error of the estimate, because neither them can say for sure what it is. So asking that in a test is very questionable, what he could have asked is to say what types of diseases would fit that heredogram or ask for only one of them, considering that more than one are possible to answer.

"The question is: what is the probability that an affected father and a non-affected mother have 4 children, 3 females affected and one male not affected" No, you're calculating the wrong thing. All we're interested in here is the probability of observing the disease or not given the inheritance model. The genders of the offspring are treated as a given for the purposes of this estimation.  I'd suggest that you review this material with your professor, because you're working from some fundamental misunderstandings.

I really doubt I’m misunderstanding statistics, I can be misunderstanding genetics. I’m already graduated in bot Mechanical Engineering and Math. The point for me using the sex into consideration was t standardize the ratio. I’m not concerned in the probability of that heredogram being autosomal recessive, but the ratio of the probability of it being autosomal recessive divides by the probability of it being Dominant X linked, i.e. how many times it is more likely that the given disease is autosomal recessive considering to the other option, based only on that heredogram

And as we HAVE to use the sex when we thread X linked diseases, we also have to use with the autosomal to calculate that ratio. If the sex weren’t important they would just vanish when the ratio is calculated. I’m not concerned with the 1/16 or the 1/256. But with the ratio (1/256)/(1/16) = 1/16 (by coincidence). You calculated the same ratio as I.

If you really want to understand why I calculated that way consider just a couple with an affected male having only one child, female and affected. Let’s make the question: What is the chance of this heredogram be referring to a Dominant X linked disease. Answer: Probability of the disease in the male population multiplied by the probability of males with that type of disease find a couple, multiplied by the probability of couples with an affected male with that disease have a living child, multiplied by the chance of that child be female, multiplied by the chance of that child be affected.

Then you divide trust  by the Probability of all genetic diseases in the male population multiplied by the probability of males with an type of genetic disease find a couple, multiplied by the probability of couples with an affected male with any genetic disease have a living child, multiplied by the chance of that child be female, multiplied by the chance of that child be affected with the same disease

Sorry but you are misunderstanding statistics at least as involved in interpreting the diagram. In formal terms we're using the diagram to do a maximum likelihood test to choose between two models. You assume one model, calculate the probability of the observed pattern of disease given model, then assume the other model and calculate the probability of the observed pattern of disease. The probability of the observed pattern of disease given a model is called the likelihood. You choose the model with the greater likelihood. No need to take ratios.

You are introducing a host of complications that are unneeded for this question. Given two models we're simply asking which model "better" explains the data right in front of us.  Check out any text on statistical genetics and really, please talk to your professor.

You can do that, you can calculate the probability only based on the disease model or pattern. But as I said, there are more things involved. A more complete estimation is the one I presented above, where we have to know many other things beside the disease pattern . If you calculated 2 likelihoods and both of them are 50% the you would say they are equally likely? No.  What you can say is: Considering both diseases are equally frequent in the population and all affected have the same life standard and life expectation and all other important things, then now they are equally likely

But if the frequency of one disease in the population in greater than the other than the chance of that heredogram being refereeing to this disease is greater as well.

You are introducing a host of complications that are unneeded for this question. Given two models we're simply asking which model "better" explains the data right in front of us.  Check out any text on statistical genetics and really, please talk to your professor. I hate to engage in credentialism, but you started it: Me: MS Applied Math and 15 years working as a bioinformatics programmer, and of course your professor is presumably a trained geneticist, so they "outrank" us both. Of course, I could be wrong, but so far it's two against one. Seriously, consider that you may be wrong.

I think neither one of us are wrong, we are just calculating different things. You calculated which model fit better. You did that 100% right. But the question was not which model fits better but whic disease type is more likely. These are different things. Let’s finish this topic with me presenting you a different question. Suppose we discover another type of genetic disease model that affects only 7 people in the role world. All the affected are female and they have only female daughters. All the daughters are blond, blind, have septum deviation and die before 30 years ild

On a pragmatic basis, statistics is the art of making decisions in the face of uncertainty. Many of the complicating factors you added are simply unknown, or even unknowable. Faced with a patient in the clinic you have to do the best you can with the limited facts you have: the pattern of inheritance in the family tree. As I said, it's not a definitive test, but it gives you a place to start looking.

Then you as a geneticist see a random heredogram. There is an affected mother, a non affected father, and 4 female daughters that are bold, blind, have septum deviation and died at 20 years old. By what you said I would say the new X disease model is the one that fits the best right? But is it more likely?