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Flora of Ice Age Europe
I'm trying to get a very in-depth idea of the ecosystem of Pleistocene Europe, somewhere around 40,000 years ago, and I can't seem to find what types of foliage (other than the obvious grasses and lichens) grew in that place and time. I'm particularly interested in the species of tree that were present; can anyone help?

40,000 is not very long ago! it would be similar to today. tundra and deciduous similar species. check this from 50,000,000 years in america, it's still similar: http://geology.com/articles/green-river-fossils/plant-fossils.shtml

It strongly depends on how far North in Europe you mean. Scandinavia would be very different from France, which would be very different from Spain or Italy. But trees would not be very abundant North of the Alps I think.


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Testosterone level in body with activites
Does ejaculation lower level of testosterone in body, Conflicting reports on internet, a firm answer would help a lot?

There are two studies that shows that level of testosterone is higher during abstinence.
A research on the relationship between ejaculation and serum testosterone level in men:

The authors found that the fluctuations of testosterone levels from the 2nd to 5th day of abstinence were minimal. On the 7th day of abstinence, however, a clear peak of serum testosterone appeared, reaching 145.7% of the baseline ( P < 0.01). No regular fluctuation was observed following continuous abstinence after the peak.
...
The results showed that ejaculation-caused variations were characterized by a peak on the 7th day of abstinence; and that the effective time of an ejaculation is 7 days minimum.

Endocrine response to masturbation-induced orgasm in healthy men following a 3-week sexual abstinence:

These effects were observed both before and after sexual abstinence. In contrast, although plasma testosterone was unaltered by orgasm, higher testosterone concentrations were observed following the period of abstinence. These data demonstrate that acute abstinence does not change the neuroendocrine response to orgasm but does produce elevated levels of testosterone in males.

source: Stack Exchange

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

sort: votes


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Protein content in sprouted beans
I have checked on Wikipedia which says that sprouted mung beans has way less protein than normal one, while on web you will find articles saying sprouted beans are best, which is true, how do I eat unbaked mung bean anyway without any processing they are so hard. Does soaking moon beans overnight really reduce protein content drastically ?

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


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Strongest bone in body
AS internet  tells is it is thigh bone which is strongest, but why, it carry only upper part of body, does not heel or any foot bones should be strongest in body as they carry full body weight ?

No, foot bones don't carry full body weight, the weight is distributed half between two lower limbs, then again half at foot between calcaneus and big toe , small toe heads. So, foot bones may not be carrying as much weight as femur.

@JM97 as a student of physics I must say all weight on  standing at least must fall on Talus bone of heel, as F=mg works toward center of earth

Again, I would say neck of femur is stronger since it's not breaking eventhough it's not in line with the direction of weight. Neck of femur is withstanding more force( due to the torque).


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Virus immunity from animal to humans
There are number of virus which have animal as reservior and jump to human to cause disease. Why dont we use antibodies of animal to cure humans?
Like rabies in bats.

I think you're asking why don't we take antibodies from previously-infected host animals and treat humans with them. In principle, that could work, but it's impractical as you describe it. You give the example of "rabies in bats". Imagine trying to get enough blood from a 25-gram bat to treat a single person. Farming bats is hardly practical, and if you're bleeding wild bats, you're probably collecting both known and unknown viruses that you're then injecting into your patient. So this is completely impractical with wild animals, which are the donors of most of the diseases in question.
However, there's nothing magical about the antibodies from the original wild animal. (This seems to be widely misunderstood, probably from movies that make medically idiotic and impossible claims.) Any antibody can be potentially valuable for treatment, whether it comes from the original host or not, and whether it comes from the live pathogen or from a vaccine made from the pathogen.
So a more practical approach is to infect a large, easily-handled domestic animal with the pathogen in question; or better yet, with a vaccine made from killed pathogens, so there's no risk of the animal getting sick or or infecting your patient. This used to be done with rabies, in fact, using equine hyper-immune serum to treat rabies patients (Production of hyperimmune antirabies serum in horses).
However, there are major problems even with this approach. It's difficult, it means keeping large numbers of large and potentially uncooperative animals around for long period, etc. Here is a WHO document reviewing some of the problems with this approach.
A third approach is to make monoclonal antibodies. This is the most popular approach now; it lets you make sterile, safe antibodies with completely defined characteristics, with minimal risk of contamination, under controlled conditions.
There are many monoclonal antibodies out there that are used in modern medicine, including some that are used to treat pathogens. However, it's worth pointing out that antibodies are not magical panaceas; they're often much less effective than conventional antibiotic or antivirals and are often more expensive and less practical to use.


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Protein food eating tendency
As I understand human love fatty food as they taste good because it has more energy which was good when we were primitive and food was scarce and unreliable,
Is there same urge for protein food too? it doesn't give much energy.

Proteins are actually pretty calorific but indeed much less than fat. From wiki > food Energy

However, we crave for proteins for other reasons. We digest proteins to get their building blocks, the amino acids. With these amino acids we can rebuilt our own proteins. Proteins are at the very center of our metabolic activity. From wikipedia > protein

Proteins perform a vast array of functions within organisms, including catalysing metabolic reactions, DNA replication, responding to stimuli, and transporting molecules from one location to another.

Many of our DNA sequence are called protein-coding-sequence (often just called gene although definition of what a gene is vary quite a bit). Those sequences are transcribed into mRNA and then translated into protein in order to have some effect on our body. A protein could be an enzyme for example.
For more information on the role of proteins in living organisms, have a look at an intro course to Biology such as for example those of Khan Academy. Khan Academy > macromolecules > protein and Khan Academy > Central Dogma.


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Muscle involved in carrying load on head
I have seen people carrying heavy load on their head especially in 3rd world countries, does carrying on head any benefit or harm, which muscle get strengthen in doing it?

Not really an answer, but an interesting related article: http://www.slate.com/articles/news_and_politics/explainer/2010/08/head_case.html


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Exhaustion of skeletal muscle and ligaments
I read somewhere that while doing lifting back should be straight(means normal curve), so that erectors muscle in back do the work but it gets tired easily. Hence we form curve on our back like when we sit on chair our back curves and this curve put stress on ligaments of spine which is harmful.
 Since ligaments dont get tired we feel curved back as easier. Does ligament have any mechanism ti get tired like lactic acid in muscles?

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


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Safety in Liposomal Amphotericin B
From reading about Amphotericin B antifungal, I understand it is quite a toxic medicine for kidney, but I am not able to find any details as to how Liposomal version of same medication is so safe, in end are not we eating same chemical, how doe s liposomal version become less toxic?

This is an interesting question.  Initially, the mechanism for the reduced toxicity (1992) was unknown, as stated in the abstract of a well-cited paper.  A paper from Oxford Radcliffe hospital in 1998 said that 15.5% of all their spending on antimicrobial agents was on these new, expensive drugs, available in many formulations, and argued the evidence supporting their use was scanty with a key study available only as an abstract.  A review in 2013 seems more favorable, but I haven't looked at the full text - by that time, one of the products with reactions at the injection site had been withdrawn, and the costs were coming down.  At the level of the individual, these stories are poignant.
The paper from Oxford Radcliffe wrote of one formulation "It has been suggested that the large particle size of ABLC (1.6–11 μm) leads to its rapid clearance by reticuloendothelial cells, resulting in lower plasma levels."  This idea has been pursued in numerous other papers (example), but I lack the expertise to evaluate it against other potential explanations.

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


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Genetic mutations in plants
I am trying to plant some trees which are usually native to colder climates into Subtropical climate, is there any possibility that if i plant these 20 trees saplings in winters they will grow to be a tree, due to some random genetic mutation, given all nutrients all provided to it?
Tree in Question is Deodar

Mutations occur more-or-less at random and are only rarely beneficial, but the trivial answer to "any chance" is yes. ———  To improve your question I suggest you think about what you really want to know. If you are interested in whether you can get that species to grow where you live ask that on [Gardening.SE]. If you want to know about genetic adaptation in trees, then you could try to reformulate your question for this site. However, I think you would benefit from reading some introductory material on evolution first.

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

I think that the potential survival of your seedlings could more likely be credited to your care and management than random genetic mutations. While, of course, DNA mutations happen during cell replication, evolution at the whole-plant scale primarily occurs over the course of generations, not the lifespan of a single plant. You may well be able to get these trees to thrive in your environment with some care and love, although they may not grow as vigorously. Here is a link to a gardening website with tips on growing ceaders in a home garden, although I agree with the commenter that you'll get much better help at the Gardening and Landscaping Exchange!
Best of luck with your horticultural endeavors!


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Excess protein consumption effect on kidney
How does excess protein consumption through food as well as through supplements affect body especially kidneys?
Why it is advice to consume low protein diet during summer ?

Have you done any research? A quick search on google scholar for "protein intake kidney" gives several articles describing possible connections to increased phosphate and urea levels on high protein diets, which could affect kidney function.

@Roland I have and while some say that it affects kidney negatively while other says it has no effect. moreover why not consume protein rich food in summer. aren't our kidney made to this work to excrete urea and phosphate, i drink more water and kidney remove poison, shouldnt kidney adapt to new levels

Great question... I have heard several nephrologists mention that there is very little hard evidence that would suggest that protein consumption should be decreased in renal failure (sounds like mostly animal studies with exceedingly high protein diets - nothing that would be done clinically). I hope this question get some attention... it would be interesting to see the state of this question.

Short answer
The ammonia resultant from the protein metabolism is toxic to the body and specially kidney. (William V. et al.)
Long answer
Protein is a poly-peptide composed by amino acids. Each amino acid has an amine group (-NH2) in its composition. In the metabolism of the amino acids, this amine group is taken, and if it isn't needed is released the to blood vessels to be transported to the liver and be turned to urea.
Needless to say since the kidney filters the blood when there is excess of ammonia in the blood vessels the kidney is the first to suffer.
I've found some papers about the effect of ammonia in the kidney but none of them where about humans. (I may try to fetch some of them later.)
Why summer?
During summer water is lost through perspiration so there's less available for the excretion of urea.
I hope it helps.
References.
1.William V. McDermott, Jr., M.D. ,Metabolism and Toxicity of Ammonia

In the why summer part, may be u intended to write perspiration instead of transpiration. I think now u will be eligible to vote, just need to reach 150

@Mesentery Thanks for the correction! English isn't my main language and sometimes I make some strange mistakes! And I'll be very happy to be able to participate and vote =D

so if one drinks plenty of water, kidney will do its job just fine, and rest of body will heal quickly with more protein?

I would assume so if the consume of protein isn't extremely excessive. I don't know where you live but  there has been deaths for protein only diets. Of course that includes eating only proteins day in and day out. If your interested i would suggest this link. https://en.wikipedia.org/wiki/Protein_poisoning


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growth limit on muscle
Is there any biological limit on muscle growth in human body, one can keep pushing body and keep growing more and more muscle but somewhere it must become diffcult for body to sustain those cells right?

Funfact: Actually there is no increase in number of muscle cells, they only get hypertrophied when the muscles become big.

@JM97 but sure larger cell need large energy reserve to stay alive , so it can go to infinity?

@AlwaysConfused thats exactly my question, just for fun ,"CAN I TURN INTO HULK if keep wprking out :P

Natural athletes have to deal with MSTN gene.

The MSTN gene provides instructions for making a protein called myostatin.
This protein normally restrains muscle growth, ensuring that muscles do not grow too large.

Just look at the top natural athletes. There are a lot of them who train for 20+ years and still can't be as large as those athletes who take steroids. Here are some examples of professional natural athletes(Bobby Pandour, Georg Hackenschmidt)

With steroids you can exceed all natural limits up until your body meets its boundaries, often accompanied by serious health issues.


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Evolutionary elimination of recessive gene
As recessive gene is suppressed, why over millions of year of evolution have not wiped them away completely, why don't they just go extinct, as people with those genes go extinct?

Possible duplicate of http://biology.stackexchange.com/q/35532/3340

Simply put, there may not be enough selective pressure to force those alleles out of the population. For example, take a hypothetical gene for eye color. The dominant allele gives brown eyes, the recessive blue, due to the lack of expression of a certain pigment-processing enzyme. So, two heterozygous (brown-eyed) organisms are crossed:
   |  A |  a |
--------------
 A | AA | Aa |
--------------
 a | Aa | aa |
--------------

which results in 75% brown-eyed offspring, and 25% blue-eyed offspring. Unless there is some very strong factor in the environment that has a negative selective pressure on blue eyes, the recessive allele will remain in the population.
OK, that's for an allele with no negative pressure acting on it. What about a disease allele, for example one that has a point or other mutation inactivating an essential enzyme, such as iduronate-2-sulfatase (I2S), a key enzyme involved in the breakdown of waste in the lysosome. It is part of a group of diseases known as lysosomal storage disorders, and is the causative agent of Hunter Syndrome.
People who have the so-called "wild-type" allele(s) of I2S have normal function, even if they are heterozygous. However, if two heterozygotes produce offspring (or if a heterozygote produces offspring with a homozygous recessive individual), then there is a chance of a child with two recessive or defective forms of the enzyme, and they are much more likely to develop Hunter Syndrome (almost no genetic disease is 100% penetrant). If untreated, this disease can have many quite horrible effects (especially given that it usually appears in childhood). The disease is also progressive (it gets worse the older you get), and while it in itself does not typically cause death, patients have (sometimes severely) limited lifetimes.
So why haven't the mutant, disease-causing forms of I2S been "weeded out" by natural selection? In a single word: heterozygosity. Studies (I don't have a reference, unfortunately) have shown that supplying a Hunter patient with as little as 10% of the typical amount of active enzyme in an unaffected person is enough to resolve the acute symptoms of the disease, and begin reversing many of the long-term effects. All things being equal, one would expect that a heterozygote carrying one functioning allele of I2S and one mutant allele would express about 50% of the amount of enzyme that a completely unaffected individual does, and this is more than enough to prevent the onset of disease. There are likely other molecular mechanisms involved to express the functional version even more, so their levels may be even higher than 50%.
So, while there is certainly a strong negative selection pressure on people carrying two copies of a mutated allele (or two different mutations, there are actually many of them) that prevent most or all expression of active protein, that same selection pressure does not apply to heterozygotes, and so the mutant alleles remain present in the population.
I strongly recommend reading through the fairly short but definitely thorough course Understanding Evolution from the University of California, Berkeley. It may explain some of the concepts I've mentioned more clearly.
Note: I once worked for Shire, which, among other things, specializes in rare diseases including lysosomal storage disorders. I specifically worked with their Hunter Syndrome therapeutic, known as Elaprase. Other companies are also working on various therapeutics.
This is in no way an endorsement of the company or its products, it's just where I learned all of this stuff.


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Health effect of worm in Guava
I ate a ripe guava, rife enough to be broken with hand, i later saw that it has white worms with one black end crawling inside it, are these worm harmful, i had unripe guava of same batch though most of them had small black spot inside, but no worm crawling, what are these crawling worms, were they present in guava from unripe stage or infected only after ripening ?

Without photos it's going to be hard to even get close to an identification.

in  biology, human parasites never lay their eggs on fruit. a fruit and a human digestive system are not the same environment. the only other possible danger is chemicals in fruit dwelling animals. flies aren't very dangerous. but there are parastic flies like tsetse and the bot fly.

re fly biology: it would be interesting to see if the fruit is attracting the fly on purpose.  I am sure that the presence of the fly larva (meat!) increases the protein value of the fruit.  Maybe having larvae in it makes the fruit a tastier treat for an animal which can eat it and spread the seeds.

It is a safe bet that a "worm" as you describe in a ripe guava or any other ripe sweet fruit is a fruit fly.

from http://www.greenharvest.com.au/PestControlOrganic/Information/FruitFlyControl.html
Fruit flies are attracted to any ripe sweet fruit.  They are also attracted to vinegar and alcohol - both produced by yeast in and on the fruit, which is the high protein food that the fruit flies are really after in the fruit.
from
http://homeguides.sfgate.com/treat-fruit-flies-guavas-30550.html

When ripe, guavas emit a pungent, musky odor that attracts fruit
  flies. Fruit flies lay their eggs beneath the fruit's skin, and the
  maggots feed on the flesh. The damage causes guavas to rot. Fruit fly
  infestations often spread quickly, but prompt treatment can get
  populations under control.

The fly large actually speed the rotting of the fruit by moving yeast around on their bodies.


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Allergy vs. Immunity
What is the difference between these two phenomena in our organism: allergy and immunity? Both cause producing of antibodies which struggle against antigens. Is it true, that allergy always leads to destruction of tissues and organs? If yes, why does destruction take place in case of allergy but not within immunity?

First line of wikipedia > Immune system

The immune system is a host defense system comprising many biological structures and processes within an organism that protects against disease

First line of wikipedia > Allergy

Allergies, also known as allergic diseases, are a number of conditions caused by hypersensitivity of the immune system to typically harmless substances in the environment.

In other words, the immune system is here to defend the organism against diseases. However, sometimes this immune system misinterprets a harmless substance and start triggering an immune response against it. Such immune response against harmless substance is called an allergy. An allergy is hence a defect of the immune system. There are other defects of the immune system though, such as autoimmune diseases.


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What happens to the ATP after it stores energy?
The title says it all. After the procceses of cellular respiration happen,  the energy is used in different activities that use it, but which are them, more specifically?

Welcome to SE Biology. Please take the Tour and read how to ask a question here. You are expected to demonstrate you have done your own research before asking a question.Yours is a basic question that is covered in many biochemistry and biology texts, such as Berg et al. on-line. If you have any specific questions after doing that, then it is OK to post them here, explaining what you do not understand. But check previous questions first.

this is one of those questions that could be answered by a quick visit to wikipedia. https://en.wikipedia.org/wiki/Adenosine_triphosphate

Well first of all, how is ATP used in metabolic processes? The build up of molecules require energy. And the best molecule in biological livijg systems is ATP.
One of the processes that require ATP is the very process that makes it: glycolysis. The body will reconfigure the shape of glycolysis, transforming it into a precursor of pyruvate. This first phase (a.k.a investment phase requires two ATPs, dephosphorylating it into two ADPs. And to recap the payoff phase, once the main molecule is split, the molecule will breakdown into pyruvate through another set of various steps. At the same time, two ADPs will be phosphorylated into two ATPS. This phosphorylation occurs for each of the two pyruvates.
So the one of the main purposes for ATP is for the build up of molecules. The energy of ATP is released when it is convenient for into ADP + P, and is transferred to the new, bigger molecule.
Another process that ATP is involved in is activation. In neuron cells, the sodium potassium pump is constantly trying to set a concentration gradient between sodium in the cytoplasm and potassium in the extracellular fluid. And because it is working non-stop, it needs ATP to continue working. However, in the scenario where an individual is deprived of oxygen through an extended period of time, brain damage may occur due to the the absence of ATP production. The sodium potassium gradient will never be restored, and the neuron will be unusable.


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Unknown plant, can anybody identify this plant?
Location: Western Germany
Can anybody identify this plant from Germany ?

This is Phytolacca esculenta, Asian pokeweed. Because the flower stalks (berry) are standing upright, and not hanging. The berries are also closer together compared to P. americana.
Despite the name 'esculenta', this plant is also poisonous.

https://m.wikidata.org/wiki/Q17244662

Ah yes right, oversaw this fact. Thank you very much RHA!!!

@nkell13s if you think this answer is better, consider accepting this answer (the check sign).

And just FTR, it becomes a pest quite easily. Seeds are dispersed by birds and other animals. It has tubers which can grow quite large, and regrowth can occur even from parts of the tuber from my experience.

Looks like Phytolacca americana
Better known as pokeweed, Phytopacca americana is native to the western US but naturalized in Germany and other European countries. The “berries” are quite distinct.

And it is quite poisonous!  The unique color to the berry pigment is due to a class of compounds called betalains, specifically betacyanins.

You are totally right, thank you very much ! Pretty interesting plant though

I think you are right this is Phytopacca, but it is another species. See my answer below.

@RHA oooh, good call - you should get the check


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HLA typing between siblings to identify a genetic disorder
If a patient  suffering from a complex array of signs and symptoms for a disease and is having an 8/8 loci match with his sister who suffers no such symptoms can you conclude that the disease is an X-linked recessive disorder? Can u rule out autosomal dominant disorders and autosomal recessive disorders from the diagnosis?

No, you can't conclude that.
First of all, two siblings being HLA identical tells you very little about the rest of their genome. HLA genes are closely linked, and each haplotype is transmitted in mendelian fashion as a single gene.  For non-linked genes (on other chromosomes, or further away on chromosome 6), they are as or nearly as likely to have the same genes as non-HLA identical siblings.
Further, the disease of interest may (is highly likely to) be multigenic and have incomplete penetrance. The heritability of common disorders generally varies from 20-80% (Cecil Medicine Chapter 41, the Inherited Basis of Common disorders).

Technically, there is a small chance of recombination within the HLA (MHC) region, so haplotypes are transmitted in a mostly-medelian fashion.


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Butterfly/Moth identification: Puppa is half green, half brown, and 1,5cm long, found in Upper Austria
Question: What butterfly is going to evolve out of the puppa illustrated in the attached picture?
Characteristics: Puppa is half green, half brown, and 1,5cm long
Further details: I don't know if this is relevant we found it on our mint plant, presumably it has eaten its leaves along with the lice on it.

Did you pull it out of the silk in the photo to take the picture?  If so, it is probably a moth species. You will probably need to wait for it to emerge to identify it.

@user22542 No i did not pull it out of the silk, no person did. However we had severe rain once in a while in the last 1 and a half weeks and I was not present at the spot where the plant stands, hence I cannot tell if it had an impact


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Grape ivy tendrils
I have a peculiar question. I keep a grape ivy, Cissus alata as a houseplant and I cannot but wonder what exactly makes it decide to grow tendrils? most offshoots have none, only one leaf growing from a node, no matter how many nodes there are and it seems the direction of the growth - vertical, horizontal - is also of no significance. Yet, from time to time, it is like the plant randomly chooses an offshoot that starts to grow quite quickly and grow tendrils. Do you know what processes in the plant cause that?


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Introgression vs admixture
What is the difference between genetic introgression and genetic admixture ?
Are these terms interchangeable ?
Do they apply to different population scopes or something ?
The usage seems kind of vague to me.
Looking for some clarification.

The difference is referring to the directionality of gene flow.
We talk about genetic introgression when there is some gene flow from one population (say, population A) to the other (say, population B). We would say that population A introgresses into population B. If gene flow goes both ways, then the two populations A and B are admixing.
From Wikipedia > introgression

Introgression, also known as introgressive hybridization, in genetics is the movement of a gene (gene flow) from one species into the gene pool of another by the repeated backcrossing of an interspecific hybrid with one of its parent species.

From Wikipedia > Admixture

Genetic admixture occurs when two or more previously isolated and genetically differentiated populations begin interbreeding.


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Why are there sporadic lightly pigmented hairs in facial hair?
My body and scalp hair are entirely black. Until recently, I thought this was the case with my facial hair also, until I noticed a small handful of hairs that were anywhere from light brown to copper-orange to burgundy-red. There are hairs that are entirely pigmented like this and there are mixed along their length between different pigmentation colors (for example there are copper hairs that have black tips).
Can anyone explain why this is?
My own thoughts are that it is caused by some variation between individual hair follicles (different type/number of receptors on the melanocytes that color hair that cause them to respond differently to various amounts of hormones? But then what is causing the hormone shift in the first place? I am pretty sure that until recently all the hairs were black and only recently have these lightly pigmented hairs sprouted)

nascent gray hairs? this may be batter suited to the health and medical stack.


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What can I research for thesis on DNA data storage from math?
I'm a math researcher, I just finished a Master on Error Correcting Codes. I recently saw a presentation on DNA-based data storage that I loved.
I wish to continue my studies on (applied mathematics) in this subject.
I received a PhD offer and when I mentioned the subject, the possible director was receptive, but he is not well informed on the subject either, so he proposed that I come up with a research path ...
What do you think is an interesting research topic (and worthy of the community) about storing DNA data from the perspective of error-correcting codes?
Thanks for the help!

First, I think this question is off topic on a list about biology, as you will see if you take the tour and read the Help on questions. Any answer would be a subjective opinion of what might be interesting. You could try Stack Exchange Bioinformatics instead — you might get more informed opinions there. However I would be very wary of embarking on a PhD on the basis of opinions of unknown people on Q&A list. I can also warn you that a danger of someone in your position is doing a PhD on something that is of absolutely no interest to biologists. You need to find a live senior biologist first.

This is also duplicate of a question that you have posted on the Bioinformatics Stack Exchange website. https://bioinformatics.stackexchange.com/questions/4857/what-can-i-research-for-thesis-on-dna-data-storage-from-math

It is more based in computer science and bioinformatics as data structures and storage of information is using GATC instead of 1 and 0s. Of course, you can probably find some math application since there is math anywhere, but you need to investigate the topic throughly and find an area which could use work.... like any thesis.


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What do bones need to grow outside the body?
In what environment outside of a living organism can bones grow?
If I were to put an arbitrary human bone in a room and attach a bunch of tubes to it, or dunk it in some kind of solution, where would I have to connect the tubes and what stuff would have to be in the tubes/solution to make the bone grow as if it were inside a living organism?

Are you counting being sheathed in velvet like an antler as "inside" the body?

@swbarnes2 Yeah, I forgot to think about antlers, but since they're attached to a body I'm counting them as "inside" the body. I mean I want these bones to grow independent from an animal.


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

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

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

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

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

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

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

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

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

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

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

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

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

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

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


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

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

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

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

so why can't normal y chromosome recombine?

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


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This looks like a mushroom is it eatable?
This looks like mushroom it's white and there are insects feeding on it....it seems to be growing on a cascabela thevetia

Could you please add the location and season, where this fungus grew?


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Why do humans lose subcutaneous fat tissue with age?
Why exactly do humans lose subcutaneous fat tissue with age?
It appears that we either lose fat cell volume or we might actually be losing the number of fat cells with age.
One hypothesis is that as the vascular system weakens with age, the fat cells on the perimeter of the body shrink and die because they don't have enough blood flow to sustain them.  The problem with this hypothesis is that subcutaneous fat loss is very gradual and starts during young adulthood and continues. It also happens in very fit individuals too.
Another hypothesis I read before was that subcutaneous fat is loss because of a drop in estrogen levels after menopause.  This hypothesis doesn't explain why men lose subcutaneous fat with age.  Also, women start to lose fat on their hands and upper cheeks long before menopause starts.

Another thing to mention is that not all mammals have this issue. Whales retain their subcutaneous fat well into old age.

Short answer
We do not loose fat (cells) as we age; on the contrary - we tend to gain fat by about 1 or 2% per decade. The place where it gets stored does change; instead of going into subcutaneous regions, it gets stored around the abdomen. A sex hormone imbalance might be the cause of this gain in visceral fat.
Background
What a coincidence! I just finished an article in the Sci Am May issue of this year (2018) on exactly this topic, literally just minutes ago.
In young folks, fat tends to accumulate under the skin, while in older folks this tends to shift to accumulation of fat around the abdominal viscera (the internal organs). Bottom line: we don't loose fat overall, we just store it elsewhere. What's more, as we age we store more fat as our base metabolic rates drop.
Why this happens is no known, but there are some interesting findings:

Sex hormones are involved; women in menopause (estrogen levels drop) gain more visceral and belly fat and loose it around the hips (they go from pear to apple);
However, a drop in estrogen is not the cause, as certain ailments lead to belly fat in young women with plenty of estrogen;
Androgen-using females (transgenders) gain more visceral fat.

These findings together have lead to the idea that a sex hormone imbalance might be the cause. However, some findings counter this idea:

Afro-Americans have less visceral fat, while Asians have more;
Blocking FSH results in less visceral fat, which may have other mechanisms of actions than estrogen.

Reference
- Wallis, Sci Am May issue 2018

Children have low estrogen and very little central abdominal fat (usually).

The question I'd ask, though, is whether the accumulation of fat is actually due to age, or whether it's a side effect of sedentary, inactive lifestyles increasing with age.  E.g. this guy doesn't seem to have a lot of subcutaneous or visceral fat: https://www.adn.com/sports/2018/07/23/73-year-old-sets-new-standard-for-old-runners-at-western-states-ultramarathon/

How sad, you didn't get a response. You got a person saying that people don't lose total body fat with age (which you never claimed, or ask about), and a person saying that visceral fat gain isn't inevitable with aging. Neither of these answers deals with your question. I think it's a common psychological flaw in humans that, when they can't answer a question, they produce a random unasked-for question from the same semantic field. Unfortunately, I also can't provide a thorough response, but I will try to at least narrow it down:
To my knowledge, the reason is not vascularization; decrepitude of peripheral vascularization was suspected for a time, but we have seen that the predilection sites of fat loss readily take fat grafts, and those fat grafts that survive the initial post-transfer phase are "permanent". Since both transferred fat and "original" fat would depend upon vascularization, the difference can't be blood supply, but must be something about the local fat itself. As has correctly been pointed out, loss of subcutaneous fat "begins" long before menopause in women. Indeed, it does not "begin" at all (to my knowledge), but rather, the loss is an ongoing process from birth, although interrupted by localized plateauing at times. Another notable feature in facial fat loss is that its predilection sites are also predilection sites for bone volume loss: maxillary and zygomatic regions. To our knowledge, the cellular processes of fat atrophy and bone remodelling are distinct; osteoclasts do not dissolve fat cells. To me, this indicates that it would be a sensible hypothesis that the process of the body removing facial volume is not a predictable side effect from cellular senescence, but rather that it is, like baldness, a programmed event which might be triggered by the epigenetic clock of aging - a programmed event that simply takes aging as its trigger, but isn't itself necessitated by senescence.
On a less fundamental, cellular level, loss of replacement of subdermal fat is realized by loss of function of fibroblasts: https://www.sciencedaily.com/releases/2018/12/181226132847.htm
But of course, this does not explain why the fat cells already in situ are removed. That explanation is still outstanding, I believe.

This fits with my understanding of the subject nicely. Welcome to the site Dr. K. Please take our [tour] and refer to the [help] for guidance, enjoy the site.

Welcome. There are a lot of unsubstantiated claims in your answer. Can you add more references, most notably in the 2nd paragraph of your answer.

Thank you. In fact, success of fat graft procedure is a common knowledge which does not not require sources, I think. It is easily found in any popular or scientific source on facial rejuvenation surgery. But I edit a source for predilection sites of bone and fat loss.


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Why exactly does the immune system weaken with age?
Why does the immune system become weaker with age in humans and in some other mammals?  Let's try to be more specific than just "everything degrades with age."

We don't know.
More precisely, we know of many, many different reasons why the immune system deteriorates with age, but we don't really know which are different measures of the same thing, which are independent factors, which factors actually cause problems and which are harmless and incidental, and so on.
There are too many age-related phenomena to try to list. There's a nice recent review Aging and the immune system: An overview which spends time on

Aging and the immune cell repertoire
Cell Intrinsic defects in lymphocytes
"Inflammaging" ("an overall decrease in the ability to cope with different stressors, accompanied by a progressive increase in the organism's pro-inflammatory status")

Each of these broad topics can be broken down into dozens of sub-topics, and the molecular and evolutionary mechanisms underlying each are rarely well understood.
It's a huge area of research, and it's not possible to give a single concise answer.

Here is one known factor. A key component of the immune system is the skin and the protection provided by insensible perspiration, and the antimicrobial peptides in perspiration. However as humans perform less exercise with age, the proper habituation of the eccrine sweat ducts fails. The ducts normally balance the passing electrolytes, in particular conserving sodium chloride. The antimicrobials are only effective with the correct balance of electrolytes. If the balance is not correct, normal skin bacteria are able to enter the ducts and block them. With the ducts blocked the eccrine glands force sweat under pressure into the surrounding skin, destroying capillaries, and depriving the skin of oxygen. The protective live barrier is compromised and the skin becomes wrinkly. Extreme examples of the effect can be seen, particularly on the lower legs, in aged persons where the skin has a parchment type appearance.

Hi and welcome to the site. Please add a source to support your answer (it is much appreciated by people who want to do more reading about it.)


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Why do humans lose subcutaneous fat from the extremities with age?
Why does fat tissue die and shrink on the hands, knees, and lower legs of most people as they age, even when they are overweight?
In most people, their bone definition becomes much more visible around their extremities.
I'm aware I asked a similar question before, but the previous question wasn't specific enough.
Why do humans lose subcutaneous fat tissue with age?
With age, humans store more visceral fat because of multiple factors that include physical inactivity, higher FSH levels, androgens, a drop in estrogen in women, and other factors.

what makes you think they do?

Bones of the extremities become much more visible with age. The bones of the upper face also become much more visible. Its very apparent on the back of the hands, the feet,and outter sides of the knees.

Are you sure that is not just due to  a loss of skin tone.

It doesn't happen to everyone.  Skin by itself is very thin without any subcutaneous fat underneath it. People do lose fat in these areas with age.


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What causes headaches (biologically)? What does it mean directly?
Even though your brain can't feel pain, thingies in your head are installed to compensate for that.
Once I thought your head starts to hurt when your brain is tired. I can't believe this any more. Several times I happened to skip sleep completely - while intellectually working (not just watching TV or something like that). The next day I didn't go to sleep to prevent breaking the day/night biorhythm. Yet I don't remember any headaches from not sleeping enough - and working instead.
However, when I was worrying about something deeply I often got a headache to the top. Also, you get headache when you're ill. You get them after drinking too much alcohol (or getting poisoned by some other things too as I've heard).
As non-biologist I believe that pain receptors are triggered when whatever they're guarding is damaged. Also I thought that they're installed so that you can do something about the cause of the pain - that doesn't seem possible in case of headaches.
But I do hope that headache doesn't mean that my brain is sustaining damage.
So what's triggering pain sensors? Is it a chemical/hormone that is released when the organism feels endangered (by illness or something else)?


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Why does ant queen keep the eggs out of her hive?
I have captured an ant queen and now I'm trying to create an artificial ant nest.
I have noticed that though she has dug a hole to hide in, she keeps the eggs out of it unless she feels that they are in danger.

I have two theories explaining why she does that:

Ants naturally put eggs in sunlight to keep them warm. In her situation, they are not gonna be any warmer of course - the jar is whole about the same temperature.
She is digging a nest and she needs some space. If this is true, where is all the dirt?

Theory number 3 suggests, that she is proud of them and she knows how curious am I to see them...

Can you post a complete picture of the ant (Please don't pull her out)?

She is very shy, and ever since she dug the hole, I can usually just see them for a moment (much like the alien in the first Alien movie). But I have one photo of the queen.

Theory number 4 could be it is maybe too warm in your jar and she is trying to keep them from heating up in the warm dark earth.

Is this the same queen as in the question, "Can I identify this black ant queen?" There is a picture on that question @skymninge.

According to various websites and literature I found,
Starting a new colony
During the mating season, Queen Ant grows wings and mate with male (flying) ant. In most of the species the queen will fly away to a new place where, she will loose her wings and dig a tunnel. She may lay eggs inside or outside because of the humidity and temperature, mostly they wait till spring, so that the humidity is high as well as warm temperature.
For laying eggs she will dig a tunnel inside and close the gates. She won't eat or move and completely avoid light, if the eggs are unhatched or some other problem occurs she will eats her own eggs. After around 8-10 weeks eggs will pop and you will get new worker ant babies. They will form the hive and feed the queen ant.

More info: http://antnest.co.uk/colony.html

My queen already ate lot of sugar. Are you really sure? I have noticed you post tons of content on this board without putting much effort in all the posts (I've been watching you). Remember that all this is not just about earning reputation.

Follow the link... http://antnest.co.uk/colony.html

I can see the link. The fact that something is written there doesn't necessarily mean it's 100% right. You've also said various websites. But in fact, it's according to Myrm's ant Nest website.
But most importantly you didn't answer my question. Neither you answered my comment.

@TomášZato No need to be rude. Devashish is a great user, and has started an unanswered questions event, to take care of some of the unanswered questions. Note that he's put more info into your question than anyone else has. Again, you were wrong to be rude, don't do it again.


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How does the "giant mosquito", Psorophora ciliata manifest it's "aggresive and vicious" behavior?
On Psorophora ciliata Wikipedia states:

Not only are these mosquitoes vicious and aggressive towards humans
and other animals as adults but, P. ciliata larvae are known for
preying on other mosquito species' larvae and even tadpoles. [2]

Emphasis mine.
Now every mosquito is kinda aggressive by drinking your blood and being generally annoying. So what makes Psorophora ciliata especially aggressive? Does it scream expletives or what does it do?

The key is "toward humans". There are so many species of mosquito, and many of them prefer other animals to feed upon. I also suspect that the Wikipedia article may have been a bit hyperbolic. My guess is that it just has a strong preference for humans. I'd put this in the answer box, but I am really just guessing.

@KarlKjer Yeah, I was also suspicious about the statement on wikipedia. But that's why I asked. Those mosquitoes have attracted some media attention, so I'm hoping some real research was done. If the statement on wikipedia is proven inflated by some scientific research we can edit it.


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Test question regarding botany
I'm having a hard time understanding what exactly those letters and numbers in the task in the photo below represent, also the task says "Is the blossom formula written correctly?" translated from Lithuanian to English. I would appreciate some guidance.

These are floral formulas, a way to succinctly describe how many petals/sepals/pistils/... the flower contains, and their relations (free, fused, ...). The wikipedia page describe the meaning of each symbol.
For example, for the first one :

Up arrow : symmetry along the vertical axis
K(6) : 6 sepals (K), which are joined (parenthesis)
C(2.3) : Two large petals, three smaller, joined. (not sure on the exact signification of 2.3)
A2 : Two stamen, not joined
[C(2.3) A2] : the petals and stamen are fused
G(2) : two fused carpels

Continuing with that example, it seems to me the first formula is not correct given the schematics below : there are 4 carpels. Though I'm no botanist.


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Can anyone identify these flowers?

I'm mostly interested in the maroon and white ones in the center, or the purple and white ones in the front left corner.  They were in bloom in a garden in July at the Buffalo Harbor.  Any help would be appreciated!!

Welcome to SE Biology. Given that these are garden plants it might be worth searching on SE Gardening. If you can't find an answer there you could pose the question there. Also, you need to provide more information about the location.

They look like petunias to me, but this is far from my area of expertise

The sign agrees. They are petunias. The specific variety of the red ones is raspberry swirl. I don't know the specific variety of the purple ones.

Yea I saw the sign after I'd posted, but couldn't see an option to delete the post

@BeckieMaryland no worries! It was a little hard to spot. I didn't post it to shame you or anything, just to provide evidence for my answer :)

@BeckieMaryland take a look at the help for someone answers. If you feel like this answers your question, you can accept it by clicking the gray checkmark next to it.

The violet ones are called Violet Star Charm Petunias and the maroon ones are maybe Madness Burgundy or Easy Wave Burgundy.


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How can the same transcription factor be both an activator and suppressor of the same gene?
For example, hunchback in moderate concentrations is an activator of kruppel, but a suppressor of kruppel in large concentrations.
From what I've seen in literature, that's because the kruppel's enhancer has several binding sites for hunchback: some responsible for activation, while others for suppression. But why would hunchback in moderate concentrations bind only to activation sites, and why would higher concentration "change its preferences"? What chemical mechanism is responsible for this preference?
P.S. I provide hunchback and kruppel as an example, but this is a general question: how could the same transcription factor be both an activator and suppressor of the same gene?

It could be due to higher affinity for the activation sequence than the repression sequence and/or higher avidity for activation sequences mediated by cooperative binding. Consider that the weaker something the binds, the more of it you need to ensure that a significant portion is binding. This paper looks promising in addressing your specific example, though I haven’t read it. You may also be interested in this answer.


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How does isometric contraction work?

What exactly happens to myosin during isometric contraction? I suspect that either myosin heads just "freeze" in the middle of crossbridge cycle, or go through full crossbridge cycles repeatedly at the perfect rate so that the rate of extension becomes equal the rate of contraction (basically, a muscle isn't still, but repeatedly extends by like <1mm, and then myosin immediately contracts to compensate for this extension to keep muscle at static length - and so back'n'forth it goes).
Why isometric contractions spend energy, when physics make it clear that energy is spent only when we change velocity of something? If my second hypothesis is true and the muscle isn't in fact still, then energy is obviously being spent. But if myosin heads freeze in the middle of the cycle glued to actin, there's no reason why energy should be spent.
Say, a person is trying to lift a 10-ton rock with all the strength they got.  It's also an isometric contraction, but in this case, the second hypothesis shouldn't work, because if myosin could finish a crossbridge cycle under such resistance, it would mean that the muscle is strong enough to lift the rock. So in this case, it must get stuck mid-cycle, with the mass of the rock not letting it to finish its conformation change. If so, then why do muscles spend energy then? Myosin is literally stuck in place, and until it finishes a cycle, it won't bind another ATP.

regarding point 3 have a look at this: https://biology.stackexchange.com/questions/44019/doesnt-the-sarcomere-contract-during-isometric-contraction?rq=1 even though if myosin could finish the cycle, it doesn't necessary mean it could lift(the weight) in isometric conditions.


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(secondary) human/primate advantages over other animals?
I am trying to understand the advantages that humans have over other species, besides what you could call 'sentience-critical'.
What I mean by this is, the first set of answers you'll get is "more capable brains (in general), opposable thumbs, tools, comunication". But all that is core to sentience and civilization, not primates. I am more interested in the second set of answers, such as 'better temperature management'.
I suppose the question is, what advantages do primates have over other animals? Or, what traits are likely to be missing, compared to humans, from a hypothetical non-primate sentient creature?

Primates in general, or humans in particular?  I think the temperature management (which isn't necessarily better, just different to allow extended exercise in hot climates) is unique to humans among primates.  Otherwise the only things I can think of are trichromatic vision, and a forelimb structure that allows throwing.

Both work, and I'm actually interested in humand in particular, but since the line between what we can do as species and as sentiences is not too clear, I figured comparing our cultureless relatives to other animals could help. But those two examples are wonderful!

Pure speculation on my part but walking upright seems important as it frees up our hands for not only using tools or carry things, but it helps us stay clean because we can reach more of our body to remove unwanted pests.

@Cell that is interesting! I guess walking upright IS a primate trait! By my criteria, it'd be a trait I shouldn't demand from a civilised species... Well, that's surprising!


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How to take precise/low number of cells from cell lysate?
I would like to know that how can we take low or precise number of cells from a cell lysate? (without using any protein quantification assay).
Let say,
If I have a cell line having cell density 5x10^5 cells/mL (and its avg amount of protein concentration is 0.1ng/cell)
If I lyse these cells at the concentration of 5x10^5 cell/mL with buffer (eg., 0.1% rapigest + 10mM DTT). After achieving cell lysate, how can I take precise cell numbers from this lysate for further sample processing (e.g, alkylation, digestion etc)?
For eg., if I want to have 100cells/5ul or 1000cells/50ul , then how can I take it from cell lysate?
I know I'll have to dilute my lysate, but I'm bit confused how to achieve that based on cell concentration? how much lysis buffer and dilution would be appropriate?
Note: In my case I can't use any protein quantification assay for measuring protein concentration.
I would highly appreciate if anyone can help please.
Looking forward to hear soon.
Sincerely,

As @Price mentioned, it doesn't make sense to talk about number of cells in a lysate. Lysis breaks the cell membranes, so there are no cells after lysis. Are you trying to determine how much volume of lysate represents the contents of N cells?


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How can skull size difference alone explain behavioral differences using evolutionary theory?
I just started Robert Sapolsky lectures series on Youtube on Human behavior biology, and on the second lecture, at this point, he is explaining how evolutionary biology can be used to predict lots of animal behaviors just through the differences on the skull size of adult males and females.
He considers two groups of primates, one in which the skull of the adult male is quite bigger than the female and the other where they are about the same size. He then asks the student: "which group would display higher male aggression?" I am lost at this point. How can the size difference alone be used to answer that question? The students answer the question: "the first group (in which the males are bigger)", and the reason provided is that their body is built for it. Why and how?
Following up, the next question is: which of the species has more variability among males in reproductive success? The answer provided: "obviously, it is the first one because the males are aggressive for a reason, and that is they are competing for reproductive access." Couldn't it be that the second group had a biological variation in sperm productivity, that greatly outmatched the fight for reproductive access of the first group? I mean, how can it be this easy to conclude such a complicated process? Shouldn't you carefully consider millions of other things before concluding that one group will have higher reproductive variation simply because of differences in the size of the skulls?
Thanks!

it's an "all others things being equal" kind of statement. If I were writing an exam question based on this idea, I would certainly phrase it as "which group would we expect  to display higher male aggression"?

Having a large difference between the sizes of the skulls between males and females is strong sign of sexual dimorphism, particularly of males that are larger in general.  Knowing which form of sexual dimorphism there is allows you to predict several other features. In particular large males is seen almost exclusively in animals in which the males fight each other for control of a harem AKA contest competition. This means high male aggression, since they are driving away other males. Since they drive away other males they have little to no sperm competition so they also don't need competitive sperm. These species also show drastic difference in male reproductive success, males with a harem produce many offspring males without one produce few to none.
https://www.intechopen.com/books/sexual-dimorphism/the-evolution-of-sexual-dimorphism-understanding-mechanisms-of-sexual-shape-differences

Thank you for the answer.
So, the reason we can say that the species with the larger male skull will show greater male aggression is because "large males is seen almost exclusively in animals in which the males fight each other for control of a harem". Or basically, "It is so, because it is what we see in nature." I thought, there would be some evolutionary explanation? I mean, equal size males could also, in theory, be aggressive and dangerous.
I come from engineering, and I might be missing some fundamentals here, so, please bear with me.

absolutely equal sized males could be, the question  is asking "given X we can extrapolate Y" not "What all conditions can cause Y". This actually is an evolutionary explanations, sexual dimorphism needs a reason to evolve, and for large males that situation is basically only direct male to male competition favoring large males who more reliable win said competitions. There are no other reliable reasons, evolutionarily speaking, to have males larger than females.  Given X we can extrapolate Y, it is not a guarantee but it is a fairly robust assumption.

I see. But it could also be that the bigger male could be a sexual selection (that females are just attracted to big males)? I guess, it could be, in theory, but that is not what we see in nature? So, looks like, like you said, X doesn't imply Y, but it is what we regularly see in nature. If it is so, I find it quite 'wrong' for Dr. Sapolsky  to expect new-coming student to be able to extrapolate Y from X (because there is no definite logical route from X to Y; only one of the many plausible route); that gave me the impression that X implied Y.

Since I don't know what support material or prerequisites the videos have I can't say how fair it is. But it would not be out of place if there is an expectation of competence in evolutionary concepts or primate in general. Contest competition is a pretty standard concept used when discussing sexual dimorphism and reproductive strategies. It is actually well studied in primates, and correlates with things like tesitical size, sperm production, and reproductive strategies.

I suspect the answer by @John is exactly the answer Dr. Sapolsky would be looking for. However, without supporting data from behavioral observation and actual genetics to rule out say, sexual selection, I'd remain skeptical.
The scenario posited by Dr. Sapolsky strikes me as the sort of ad hoc story telling that shows up so often in evolutionary psychology. It might be a good starting point for investigation, but the story by itself is not dispositive. We all "knew" for over a century that the longs necks of giraffes were an adaptation to grazing the upper levels of trees. It's an obvious and plausible story, but apparently the genetic evidence is more complicated and it may be an example of sexual selection (female giraffes acquired a fairly random preference for long necks), or the trend started as an adaptation for grazing higher vegetation, but was then hijacked as a tool for sexual competition (male giraffes fight by whacking each other with their necks).

This is really well studied in primates, it is not ad hoc.

@John it may be, and I'd trust those studies a lot more. I've got no problem with field studies and actual genetics. What I object to is Sapolsky encouraging a popular audience to believe that  it can be derived from hand-wavy principles of evolutionary biology. It's a plausible story, but a story is not dispositive.


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Why doesn't peritoneal dialysate leak through the fallopian tubes?
It is my understanding that the female peritoneum does not form a closed (potential) space due to its puncture by the uterine tubes. If that is indeed the case, why is peritoneal dialysis in women not typically complicated by vaginal leakage of dialysate? Similarly, why do we not expect surgical insufflation (e.g. in laparoscopy) to suffer from CO2 leakage via the same route? Does this have to do with muscle tone in the fallopian tubes, or a duckbill valve effect where intraperitoneal pressure effectively seals them off? There seem to be only a handful of case reports of PD dialysate leakage, but more suggesting flow in the other direction where sexual activity, for example, resulted in unintended pneumoperitoneum.


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Is the lac operon repressed in the presence of both glucose and lactose?
In the presence of both sugars (glucose and lactose) will there be repression of the lac operon completely?
I know that more glucose means less cAMP --> less CAP --> less positive regulation, and thus less lac operon, but does that mean there will be repression of the lac operon?

There is never a complete absence of glucose in a living being; the issue is with the amount available and amount required difference. This difference determines the rate of expression of the Lac genes after the lac repressor has been inactivated due to the presence of lactose.

According to Molecular biology of the gene by James Watson, in presence of both glucose and lactose, the lac operon has a basal level of transcription. However, when only lactose is present, the operon has an activated level of transcription, due to the CAP mechanism.


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Why pellet and resuspend E. coli for plasmid prep
For maxipreps, cant you just add all the stuff that would be in P1 (RNase A, EDTA) then just add P2? Because if we pellet cells then resuspend theres got to be a reason, right? Is it slats and other stuff in the media that mess with lysis?

The reason this centrifugation/resuspension step is done has a simple reason: It concentrates the bacteria in a much smaller volume which is much easier to handle afterwards.
For a maxiprep you typically have a culture volume between 250 and 500ml, depending on the copy number of the plasmid. After centrifugation the pellet is resuspended in 10ml of Buffer P1, for lysis another 10ml of buffer P2 are added, for neutralization 10ml of P3.
Imagine doing this with 500ml culture volume - adding 500ml of each P2 and P3. This might work for a miniprep, but definitely not for larger volumes. Additionally, the centrifugation steps are carried out at high g numbers - typically something around 15.000xg. Doing this with this really high volumes is complicated and needs big centrifuges, which a lot of people are not trained anymore to operate or have available.

I want to add that there are some kits that allow direct addition of the "lysis buffer" to the cell suspension in the medium. Of course, as you said, yield would be low.


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Is withdrawal Euphoria possible?
It is known that when the human organism is supplied with certain hormones and/or drugs that serve a certain function for a sufficiently long amount of time, he reduces, and may eventually entirely stop, production of those hormones. It is one of the reasons stopping drug abuse by going cold turkey is so hard, because the happiness hormones produced normally in the brain before, are now produced at a reduced quantity now and their neural receptors are atrophied too, so that their effect is even further decreased.
My question then is this: Could we reverse this? Create drugs with catecholamines or some other such hormone so we bombard a patient negative emotions so incredibly potent for an amount of time that after we stop injecting him with the drug, he's chronically euphoric? Maybe a way to kickstart the life of a suicidal person with depression, have them live at least a year or two in that blissful state of withdrawal symptoms to have them want to keep living, knowing it is at the very least possible to feel that way

Welcome!  It's an interesting question and I look forward to seeing the answers.  The obvious issue is that you have to keep a patient on medication for quite a while before the withdrawal will have an affect, and during that time, the patient will be far worse.  Therefore, far from preventing suicidal depression, you are rather pushing the patient that much closer to suicide for weeks or even months of time. Furthermore, I'm guessing the result would be relatively transient as compared with the treatment time.


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Definition of "genomic adaptation"
I have encountered the term genomic adaptation in some literature (for example Sikkink et al. 2017). I am struggling to parse the term, and I have not been able to find a definition for it.
Is genomic/genome adaptation the changes accrued by the genome as a result of evolution?
Or does it refer to some sort of active response by the genome to a particular environment upon introduction (of the organism) to said environment?

From glancing at the introduction it seems like a pretentious way of saying genetic. They are talking about mutations in genes. Genes are in genomes. Hence, make it sound complicated and different to disguise the fact that it is not. But the genome is in the organism and the organism is in the ecosystem, so why stop there. (But please don't.)

@David seems like you're right. So much for rigor and precise terminology.


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Which genes/proteins constitute the core components of the circadian clock?
What the title says.
For instance in Drosophila melanogaster and Mus musculus (see Patke et al. 2020) the CLOCK, CYCLE/BMAL, CRYPTOCHROME, PERIOD setup seems to be conserved. But other components also appear to be orthologs, and can be considered conserved (e.g., VRILLE from D. melanogaster and NFIL3 from M. musculus).
So in this case, what constitutes the "core" clock?

What do you mean by "the core clock"? Perhaps researching non-genetic evidence for circadian clocks might help.

Most eukaryotic circadian clocks--as far as I know--consist of interlocking transcriptional-translational feedback loops (TTFLs) and some adjacent machinery. All of this taken together would typically comprise of a number of genes and gene products. Some of these genes are conserved across eukaryota (as an example) and some aren't. My question basically resolves to which of the conserved genes (and which non-conserved genes, if any) would constitute the "beating heart" of the circadian clock in that this would represent the bare minimum necessary to be called a circadian clock.

Apologies for this being long-winded, @Armand.

And what makes you assume such a common core exists? Nature, unfortunately, doesn’t always play according to our rules.

I'm not assuming there is such a "core". That was precisely my question: whether or not some subset of the transcription factors and whatnot involved in the various circadian clocks across species could be considered to constitute a "core" based on persistent involvement in the clock despite speciation and other evolutionary processes. Once again, I apologize for framing my question poorly.


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Storage of bacteria in MgCl2 at 4 degrees
I have a small question to which I am unable to find a proper answer.
Will bacteria in a MgCl2 buffer (or similar solution) at +4 degrees Celsius survive storage for 1-2 days? Or will they die?
What about at -80 degrees Celsius?
I am guessing that they can be stored at -80 degress but not at +4 degrees because they will continue to be metabolically active in the latter scenario but will die as they will have no nutrients to consume.
I would be grateful for your comments and inputs.

Highly dependent on the bacterial species and the buffer composition. Unanswerable in current form. We would need the above to give a sensible answer .

Speaking generally, a cryoprotectant is usually needed when storing bacteria at -80C. Even then, it's normal to see upwards of 90% viability loss with common protectants like glycerol, PEG, and Trehalose. Some bugs will survive for days or even weeks +4C while others will almost completely die off overnight. Some bacteria can even be stored for long periods of time at room temperature with little to no change in the viable population size.


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What part of the skin is damaged under sun exposure?
How exactly does extensive sun exposure lead to skin damage and increase cancer risk. In which part of the skin is the sun doing the most damage. Is it in the epidermis or beneath ? I would like to know if UV-protective tattoos would be possible.

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

Roy, @theforestecologist is completely correct. Long story short, though, tattoos are a kind of skin damage, and may cause cancer.

https://www.youtube.com/watch?v=GRD-xvlhGMc - https://www.youtube.com/watch?v=V9K6gjR07Po


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What does hypolithial mean
I'm writing a thesis in biology and my supervisor asked me to find literature about beetles living under rocks - specifically she wants me to find something about hypolithial diversity. However Google doesn't even recognize the word 'hypolithial' so I'm kind of stranded without any references on where to start searching.
I know that hypo lithia comes from ancient greek and means below stones, but nobody mentioned it like that in the literature.
Has anybody heard of this term or knows a similar one which I could use for my research?

Google for sublithic or hypolithic.
You'll find lots of things like (https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-11274-4_767) with further references and links

Scholar provides some useful results..


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do platelets cytoplasm contains DNA?
I'm a 12th-grade student and I have an entrance exam this year.
I have a question in biology. I would appreciate you if you help me <3
as we thoroughly know platelets are multiple pieces of a big cell which is called megacaryocyte so they do not have any nucleus. so I wanna know if they cytoplasm contains any type of DNA or not? I'm sure that without the nucleus there can't be any linear DNA but I doubt on the cycle DNA.
thank you


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Is there interphase between meiosis I and meiosis II?
Is there interphase between meiosis I and meiosis II?
After 2 haploid cells are formed in meiosis I, do the cells go through a period of interphase (G1, S, G2) or do they go directly to meiosis II?

When meiosis starts it is suppose to produce a haploid so because of this there is no need for further replication or growth.

Telophase I, is followed by an interphase, called interkinesis, similar
to the mitotic interphase.
During interkinesis the chromatin is partially uncoiled; however, there is no replication of the genetic material, because each chromosome already consists of two chromatids.
Furthermore, the sister chromatids in interkinesis are generally not genetically identical, because crossing over in prophase I has reshuffled genetic material
between the maternal and paternal chromosomes (i.e recombination).


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Are enhancers and silencers considered as epigenetic modifications?
Are enhancers and silencers considered as epigenetic modifications? I am confused as it seems like enhancers and silencers are sequences on the DNA and how they work is through binding with proteins, while epigenetic changes seem to be changes made to the bases for instance adding a methyl group.

No.
Epigenetic information is (by definition) NOT included in the nucleotide sequence, but affects genetic expression.
Enhancers/silencers are themselves nucleotide sequences, and therefore not epigenetic information.
Methylation is an example of epigenetic information, but a DNA sequence itself is genetic information, even if it affects a gene.
CgATgCCAg= Genetic
Acetylation of a histone/DNA methylation= epigenetic
Hope that helps!
Further reading: http://www.whatisepigenetics.com/fundamentals/

Welcome to Biology.SE! Thanks for the clear answer.

@James Thanks, looking forward to contributing to and learning from the community!

The biosphere chatroom is sometimes quite active if you fancy saying hi!

Even with basic answers it is good practice to add sources to allow users to background read on the topic

Strictly speaking, enhancers and silencers are not themselves epigenetic modifications. Rather, they are genetic elements that directly regulate gene expression through their interactions with various proteins.
An epigenetic modification is a chemical change to DNA bases, generally through either methylation or acetylation.
Enhancer and silencer sequences can be, and often are, epigenetically altered by the addition or removal of these chemical groups. This is not uncommon along the course of development for many genes, whose expression must be regulated differently at various stages of development. Enhancers and silencers are also epigenetically regulated in different cell types, which enables cells to use the same genes found in every cell to maintain different cell type identities.
So in short, enhancers and silencers are genetic regulatory elements, but they are very often epigenetically modified. Hope that helps.

So there are certain combinations of marks we've found that tend to mark regions of DNA that will enhancer/silence expression of reporter genes when we stick them into plasmids and do reporter gene experiments. People often define regions and call them 'enhancers' using these biochemical marks alone, but it's an approximation. There's no guarantee all such regions will be enhancers/silencers, and there's certainly no guarantee that all enhancers/silencers will have the marks.

Epigenetics is defined as heritable changes in gene activity and expression that occur without alteration in DNA sequence (not encoded in the sequence), and it is influenced by chemical modification of the DNA like in the case of methylation. Enhancers and silencers are sequences of DNA, like genes, but they do not encode for proteins, rather they have gene-regulatory effects. An enhancer/silencer can be methylated and thus be epigenetically controlled.


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Why is there complementary base pairing for DNA?
Why is there complementary base pairing for DNA? Why can't A pair with C given that they can all form hydrogen bond?

When you say that "A pair with C" can you please provide a diagram to show what you mean and how you envision they would fit together?

It's to do with the physical space the base molecules occupy. There are 2 classes of molecules in DNA bases, purines and pyramidines.  One of each always pair together as there will be a total of 3 ring moieties present.
E.g., Adenine (a purine) pairs with Thymine (a pyrimidine).

If you were to pair 2 pyrimidenes together, you would induce a kink in the DNA backbone and destabilise it.
That said, there is no chemical reason 2 purines or 2 pyrimidines can't hydrogen bond, and they do. This causes mismatches and DNA mismatch repair enzymes recognise the torsion it induces in the DNA backbone and they replace the mismatched base in the proofreading process. If the enzymes miss one mispairing, which can happen as it occurrs often (but the enzymes are very effective), then you end up with a mutation.

When you say that two purines can hydrogen bond to form an anti parallel double helix, or alternatively two pyrimidines can hydrogen bond to form an anti parallel double helix, can you draw or describe how you envision the H-bond donors and a H-bond acceptors would align with each other?

I don't have/can't find a good diagram of this from a quick look. Maybe someone else will find one. It is structurally less stable, so the bonds are likely semi-transient, switching between single, double, and triple bonds depending on molecular vibrations and so on. They all contain O, N and H groups with varying electronegativity though so the most proximal of those are likely to interact. I'm afraid I don't have a very good answer for you though.


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Muscle layers of pharynx and gi tract
Why does pharynx have an internal longitudinal muscle layer and external circular muscle layer, while oesophagus and the rest of gastrointestinal tract have inner circular and outer longitudinal muscle layer?


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Are hormone secretion variations the same for a pair of monozygotic twins?
I have recently read a paper about how stress affects morning salivary cortisol levels in an individual. I am conducting a study on monozygotic twins and was wondering if cortisol levels would fluctuate similarly in a pair of twins, or whether cortisol and other hormones are unrelated to the genetic makeup of the twins.

Bartels et al. 2003 is a review that reports an estimate of the heritability of the cortisol level of 0.62. In comparison to most traits, it is a relatively high heritability.
So, in short, the answer is "no". Cortisol level variation is lower among twins than among unrelated individuals. If the definition of heritability is a little bit unclear to you, you should have a look at this post.
The reaction norm of cortisol level (and other stress response) with varying stress level also seems to be heritable (Ilsing and Hoelsboer 2006, Volckaert et al. 2012).

Yes indeed! A comma changes everything! Thanks


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Concentrating cell concentration after subsampling
I need some help with regards to a concentration correction. I am measuring how many cells detach from a rock vs sonication time. Becuase I start from a rock, I cannot make aliquots and measure independent samples. So I put my rock in 10 mL of PBS and and sonicat for 1 min and sampled 0.8 mL. With this sample I measure cell density using flow cytometry. I then placed the rock to sonicate for another 2 min (a cumulative time of 3 min of sonication) and subsampled 0.8 mLs again. I did this for a cumulative time of 30 min, with subsampling at 1, 3, 5, 10, 15 and 30 min. This means that I was left with 5.2 mL of sample after my final subsampling (0.8 mL per subsample * 6 = 4.8 mL; 10 mL - 4.8 mL = 5.2 mL).
I measured my cell density using Flow cytometry and was given a events/uL concentration. But I think that every time I am subsampling I am effectively increasing the concentration (events/uL) because my cells are being resuspended from the rock into an ever decreasing suspension. Is this correct or will the events/uL that the FCM is showing me the final concentration independent of this diminishing volume? If not, how do I correct for this to get a comparable events/uL?
Here is an example of the conctrations over time after a cumulative 10 min of sonication (i could not figure out how to insert a table, hence in picture format)

So the solution for this can be in two ways:

calculate the total number of events (evenst/uL * total volume of sample at time X) and then devide by the initial volume.

or perform a correction factor, by calculating the volume reduction factor (subsample volume / volume before subsampling) e.g. at 60 seconds: 0.08/10.
You then calculate the reciprocal of this. and multiply by events/uL

NB: In these calculations is not included the fact that cells are being removed in each step, and as such there is still some dilution happening.


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Sequencing inaccurate at the primer site
The times I have sent a sample to sequence, both the forward and the reverse primer sites, show high inaccuracy while the rest of the gene is correctly sequenced. Because of this, the sequences of my in silico construct and the sequenced sample do not align in this section; but they do align at the rest of the gene almost 100%.
Is there a reason for this? Is this simply a sequencing artifact or is should I trust the sequenced sample and assume that the primer sites have mutated?

The beginning is always garbage, you can safely disregard. Though, the fact that you have a sequencing result at all means the 3' end of your primer matches the template.

The very extremities of sequencing reads obtained by most if not all sequencing technologies are usually of lower quality, though more often so in the 5' region. You should disregard this data, or better yet design additional primers further away to encapsulate that region too if you desperately need it.
Below is a fairly typical output from FASTQC analysis of Illumina sequencing data. You can see how the quality is at its peak in the middle of the read (base index on the x axis. You'd likely see a similar thing for Sanger sequencing which is presumably what you're using.

What would a good score mean? and what would a good score be? I imagine from the colors that anything on green is good, but just to know a bit more about sequencing.

It can vary by sequencing technology, but most techs these days use something called “Phred-33” scoring. It’s a logarithmic relationship that roughly speaking means a Phred score of 30 (on the Y axis in the pic above) means there’s only a 1 in 1000 chance that base was called incorrectly. Most people accept 30 as a reasonable quality for sequencing, also helped by the fact that you have many millions of overlapping reads (in NGS), so even if a base is miscalled in 1 read, chances are there are many other reads you can refer to that would have the correct call.


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Relation of pH and amino acids in microtitr assay
I am testing a Biolog plate (https://www.biolog.com/products/metabolic-characterization-microplates/) in which the wells test for the optimum pH at which my bacterium grows. Aside from having a range of pHs (3.5 - 10), two pHs (4.5 and 9.5) are tested with a range of amino acids (and some other compounds such as urea).
My question is why would there be any interest of testing these amino acids at two different pHs. My guess is just to test for any oligotrophys but on the other hand they could have then prepared these assays with any other set of random compounds. Is there any specific to amino acids and pH that I am missing.
Here is the picture of the different compounds tested in the micro-titter plates.


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Carbon dioxide concentration in alkaline media
I am running a batch experiment using penicillin bottles where I have bacteria growing for 21 days in a highly alkaline media (pH 10). I am measuring the CO2 and O2 content in the headspace over time, but I am specially interested in the CO2 production. Usually I can simply use the CO2 content measured with a gas-chromatographer (GC) but because of the pH of my media, the CO2 will be dissolved into my media. This I have seen in the sharp drop of pH over time as well.
I want then, to calculate the amount of CO2 that has dissolved into my media. I know I require Dalton's Law of partial pressures and Henry's constant/Law. The thing is that, I am a bit confused because as I measured the pressure inside my closed bottles, the pressure in these bottles became negative. So my calculations are returning a negative value for my concentration of gas in the solution. Furthermore, I do not know if the formulas I used (Dalton  and Henry), take into consideration the pH of my aqueous media.

What salts are present in you media? Something like calcium will precipitate with carbon dioxide and removed from your system.

It's just a TSB media adjusted with CAPS buffer. No precipitation was observed.


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Can emulsion test be used to detect phospholipids?
The emulsion test- causes a white cloudy colour when lipid is dissolved in ethanol and then water added.
Can this be used for phospholipids? I am aware that they are polar so may arrange in a circular formation in water but would the test still work?
Thanks

Yes, the test will still work. And you are correct about the phospholipid's process of forming 'circles' in water. The reason the test still works is because alcohol increases the permeability of the edge of these circles by making them less structurally stable. This then allows the ethanol to enter.
The hydrophilic phosphate head is not soluble in alcohol as it is not a lipid, but after the alcohol can bypass these heads, they can interact with the inner hydrophobic 'tails', which are soluble. The white emulsion/layer will then form.
This can be seen in the experiment of using alcohols to test the permeability of cell membranes. -See this investigation carried out by Westminster College.


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How do nerve impulses travel so quickly?
Nerve impulses must travel incredibly fast to achieve the functions they do. However, I have been taught that sodium ions move down the axons by diffusion (thus causing depolarisation of the next part of the membrane etc, and this is the action potential).
However, I was under the impression that diffusion is a very slow process? How can this be the case?

There is a large gradient created by selective permeability of Na channels and as you're probably aware the speed of diffusion is proportional to the electrochemical gradient.
Very small numbers of ions actually cross the membrane during depolarisation and subsequent AP events.


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Why are some neurones unmyelinated?
As far as I am aware, most of the central nervous system consists of myelinated axons and most of the peripheral consists of unmyelinated.
What is the reason for this?
Would it not be more efficient to have them all myelinated?

It's a pretty long story: http://www.ashdin.com/journals/JEM/235996/

In this answer I'm building off of @Fizz's pointer to the nice paper by Laurence Knowles, "The Evolution of Myelin: Theories and Application to Human Disease" [1].
First -- I just want to point out that your question is adaptationist, which means that it assumes that myelin is on some axons and not on others for a reason. Whereas maybe evolution just hasn't gotten around to it yet, even though myelinating all axons would actually be beneficial.
That said, here are two of the main downsides of myelination:

It might cost energy. This one is a bit controversial, but at least one study has found [2] that while myelin decreases the energetic cost of firing an individual action potential, the whole apparatus involved in myelin (e.g., in the CNS, the oligodendrocyte, its processes, and the sheath itself) actually costs more energy than it would cost to just open all of those ion channels without saltatory conduction.
Myelin and its associated oligodendrocytes/Schwann cells take up space. This is likely to be especially important in areas of the nervous system where there are a lot of neurons packed into a small area.

So from the adaptationist perspective, the question is whether the benefits of myelinating an axon, such as increased conduction velocity, increased conduction fidelity, axon protection, and supplying the axon with nutrients, are worth the downsides of taking up space and possibly increasing net energy use.

http://www.ashdin.com/journals/JEM/235996
http://www.jneurosci.org/content/32/1/356

Not to mention, when neurons are tightly packed, there is little need for increasing the transmission speed. It's not like an alpha motor neuron where you need to send a signal a long distance.

Would it not be more efficient to have them all myelinated?

If the transmission of weak signals would be highly efficient, this could be painful - and distracting (e.g.: also see  https://en.wikipedia.org/wiki/Allodynia). However, it is nice to be able to sense weak signals that persist ("itching").
Schmelz et al. 1997, J. Neurosc. show that inefficient unmetylated neurons transmit the signal that we perceive as "itching", if the weak signal persists.
Note that - as indicated in above publication - neurons that sense an immediate environmental threat to which we should respond immediately (e.g.: if an object that we grab is extremely hot or extremely cold) are more efficient.Their activity will generate a strong sensation of immediate "pain" - and consequently call us to take an immediate behavioral response and to avoid this threat.

Myelinated neurons are neurons whose axons are surrounded by myelin; the myelin has has an insulating effect and allows the axons to conduct neural impulses faster - but at some metabolic cost, so neurons are not myelinated unless there is a significant advantage to they're being able to conduct faster.


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Question regarding circulatory system of the body
Does the highlighted part in the picture mean that if you take a single blood cell, it traverses through all the veins in the circulatory system ? (Including all the organs)

No.  An individual blood cell will complete the whole loop but can take any route through the circulatory system to do this.  For example, a blood cell leaving the left ventricle may immediately pass throughout the coronary arteries to supply the musculature of the heart or alternatively could carry on down the aorta.  Another cell could be swept down the subclavian artery to the arms and back through the corresponding veins, whilst another could follow a route through the external iliac arteries to the legs and back through those veins.
That being said, all blood cells will pass through the central elements of the pump every cycle.  These are the right atrium, right ventricle, pulmonary trunk (common part of the pulmonary artery), the left atrium and the left ventricle.
Other than these locations, the movement of blood cells will be random.

I agree.                          :-P :-)