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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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Does the mesoderm evolve from the ectoderm or the endoderm?
I know the embryos of most animals develop into 3 germ layers. However primitive animals, such as Cnidarians, only have 2 germ layers - they lack a mesoderm. Therefore the 3rd germ layer must have evolved from cells which originally differentiate to one of the two more basal germ layers.
So my question is - does the mesoderm evolve from the ectoderm or the endoderm? Meaning, during embryogenesis, which cell type is the first to differentiate from the other two - the ectoderm or the endoderm?

In human,the mesoderm doesnot develop from the endoderm or the ectoderm.It develops from epiblast of the bilaminar germ disc stage.
During the week 3 of development, the epiblast of the disc invaginate and divide rapidly to form the cells of the endoderm.The division is rapid enough to replace the hypoblast layer.
Even after the endodermal layer has formed, the epiblast continues to divide at the region of the invagination.The divided cells migrate between the epiblast(soon to be the future ectoderm) and the newly formed endoderm to form the mesoderm.
REFERENCES:

Langman's Medical Embryology (13th edition) T.W. Sadler
website

Okay. So is it correct to say that just after the endoderm develops, there are cells in the epiblast which can develop to either mesoderm cells or ectoderm cells, depending on their environment?

@Alon Navon No.Nothing is environment dependent here...its all gene regulated... either mesoderm cells or ectoderm cells  No, its genetically programmed to form both.

All the cells have the same genes. Their differentiation is dependent on various chemical signals.

There is some kind of 'family tree' between cell types. Some cells can only develop to bone or cartilage, but not nuerons. Based on this, some pair of {ectoderm, mesoderm, endoderm} is closer developmentally than the third one.

yes.true.you must have followed that the endoderm and mesoderm are formed from the cells that migrate from the epiblast...the epiblast itself forms the ectoderm...

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Physiological Effect of Mannitol
Which Starling Force is affected by Mannitol?
I am either thinking hydrostatic pressure of interstitial fluid (because it increases interstitial fluid volume) or hydrostatic pressure of capillary (because it is also increased plasma volume). I read that it deals with osmotic pressure but was unsure as it is a crystalloid and not a colloid.

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Chloroplasts in an animal cell
What would happen if we inject a chloroplast organelle into an animal cell?
Will the animal cell destroy it? Or is it possible that the chloroplast will somehow survive, and even replicate? Could there be photosynthesis in such a cell, or will some of the necessary mechanisms be missing?

Not specifically related, but something you might want to know: http://blogs.biomedcentral.com/on-biology/2010/04/14/sloth-fur-has-symbiotic-relationship-with-green-algae/

To answer your bigger question:
Yes, most of this is possible - under some conditions -, and animals and animal cells can acquire chloroplasts, and use them.
E.g.: see Elysia chlorotica whose cells actively take up chloroplasts and use them, and keep them alive (though not replicating). - Though some genes of algae are also contained in the Elysia chlorotica genome - which may be considered as partial replication.
Also there are salamanders that have replicating algae within them (since embryogenesis) - even algae (with chloroplasts) within animal cells - though here the algae might be rather understood as symbionts or "cell types", and the animal cells don't have the chloroplasts by themselves.

de Vries et al. (2014) Trends Plant Sci 19: 347-350. "Some marine slugs sequester plastids from their algae food, which can remain photosynthetically functional in the animal's digestive gland cells in the absence of algal nuclei. The sequestered plastids (kleptoplasts) appear to maintain functional photosystems through a greater autonomy than land plant plastids." https://www.ncbi.nlm.nih.gov/pubmed/24767983


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Evolutionary explanation for hypoxia causing euphoria?
Why would something potentially very dangerous, such as hypoxia induce something pleasurable like euphoria? Are there any evolutionary hypotheses for this link? I'm thinking that something like the "choking game" would actually select against it, but that's probably too new.

The short answer is because evolution is more than natural selection. Many questions based on the contrary false belief are being closed a duplicate to Why do some bad traits evolve, and good ones don't? Let us know if you think the other post does not address your question and why

Your question is in essence very similar to Why can fish survive out of water?. There is an easy physiological  explanation. It evolves this way, not because it was selected for but simply as a side-effect of some other set of traits.

@Remi.b: yes, but do fish feel good out of water?

No, they don't. Feeling good is the trait of interest to you. Surviving for a few minutes was the trait of interest to this other post. Something might give us a pleasant feeling without the need for us to be selected for this feeling to be pleasant. I would recommend you to 1) follow an intro course to evolutionary biology to understand that evolution is way more than just natural selection 2) understand the physiological reason for this euphoria in hypoxia (which you can ask on a separate post) and you would then maybe more easily accept that it is just a side-effect of how the brains works.


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Why can't nucleotides when mixed together form an RNA on their own?
Why nucleotides when mixed together in the absence of a template
RNA molecule do not readily link up into a chain? We know that the bond between nucleotides side by side is stronger than the hydrogen bond between the two RNA strands, a negative and a positive one. Shouldn't then the nucleotides form chains of RNA more readily by just attaching to each other than making a dimeric RNA through a lock and key type latching?
The book that caused this question is "What Is Life?" by A. Pross (p.68), who unfortunately doesn't provide an answer.

Before asking questions about the chemistry of biological reactions you should learn some basic chemistry. This online resource may help. The role of enzymes in relation to the thermodynamics of reactions is also key.

RNA nucleotides will form chains spontaneously, having a catalyst however makes it happen faster.

The dNTPs don't just come together. They require a polymerase to break off 2 phosphates and bond the hydroxyl group to the remaining phosphate. To take a nucleotide triphosphate and add it to a growing chain of nucleic acid, the polymerase checks the fidelity of the hydrogen bonds that precede the new bond. dNTPs provide the energy for this reaction, but the enzymes require a double stranded molecule to copy. In other words, they can copy double stranded nucleic acid, but not form it from scratch.

Thanks for your answer! I only would like to clarify if the same laws apply to the self-replicating RNA (autocatalytic), with no enzymes, since the book is talking about prebiotic time.

@Karl: DNA polymerase theta is capable of template-independent DNA synthesis. Kent et al. (2016) Elife 5: e13740. https://www.ncbi.nlm.nih.gov/pubmed/27311885


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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 does a distraction cause a longer reaction time?
Does it have something to do do with the fact that the individual isn't concentrating on reacting to the stimulus, so it takes longer for it to be processed? How can this be out in terms of neurones and neurological pathways? what is happening for there to be a delayed reaction time?

Do you know anything about working memory? If you want an overall explanation, the article should be sufficient (I use "working memory" in the sense of processing time, not solely incorporation of short- into long-term memory.) You're going to find it difficult to get a "what's happening on the level of individual neurons" explanation difficult.

When one processor is running two processes, A and B, it is not running them simultaneously: it is switching between them. The switching between A and B takes time---hence the delay.

I am not sure which sort of answer is expected. The minimal answer to that would be that the more distracted you are the longer it needs to sample the stimulus space of interest as you are sampling another distracting stimulus simultaneously with your limited sensory capabilities.
Cognitive tasks get just more complex with distraction as the brain cannot know which features (of the full stimulus space from all the sensory modalities) to take into account and therefore needs to sample more data to find out which of the inputs matter for the specific task.  In most of natural situations the inputs match together in terms of experienced stimulus combinations (visual field and sound while walking for example) except for surprising situations that require to alter ones attention (a sound that does not match to the visual scenery is unexpected and might be important to check for danger). To decide whether the system can ignore such parts of the input requires computation and computation takes time. I don't think it is useful to tackle the question in terms of delayed signaling along specific neurons or pathways. The signaling itself is more or less of constant speed and not directly altered by distraction. Of course on a very basic level an increased adrenaline level or similar due to distraction might affect the "weights" of certain basic pathways as one is pushed into another state. In such cases therefore it requires the system to compensate those changes with respect to the actual task of interest as it might be biased to different reaction scheme that is not useful for the specific task.
Actually our brains are very good in focusing on specific parts of the inputs that are important for a task (i.e. cocktail party problem) but still it needs more time to correct the erroneous parts in the presence of distraction. In terms of a simple Hopfield network that does pattern completion distraction would be like an increase of the noise level which leads to a higher number of iterations required for convergence while the speed of signal transmission from neuron to neuron was not altered.


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How to surpass cell death?
Is it possible to surpass/decay cell death.  For example to disable the process muscles cells death, by tweaking the transduction pathways:

If it's not possible in our age Medicine, what it would take to do such thing in theory. The idea is to tweak the cell dying mechanisms for example to preserve neural and muscle cells for longer time. I am also curious how to disable a pathway or part of it.

Or maybe we could block cell death to increase cell death?!

Yes; It is possible to inhibit cell death.
There are several possibilities, of which many - as correctly recognized by you - involve changes in the activity of the cell death pathway (or related ones);
For a long (but still incomplete) list of commercially available drugs that inhibit cell death, please see: https://www.sigmaaldrich.com/life-science/cell-biology/cell-biology-products.html?TablePage=9559839
P.S.: Note that selectively inhibiting a pathway (note: not only cell-death) in only one cell type (or tissue - as you hinted at) usually requires a lot of tests and experimentation and isn't trivial.

How does the process of disabling a pathway work?

the processes will be highly drug and target specific


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Genetics... Translocation
Can a Translocation of chromosomal parts occur between an autosome and an allosome?
If it occurs in between allosomes,what could be the effect of Robertsonian Translocation between an X and a Y chromosome considering the fact that the small product of a Robertsonian Translocation is mostly lost!??!

Can a Translocation of chromosomal parts occur between an autosome and an allosome?

In short, yes. A quick scan of a few abstracts gives both clinical and model organism examples.

[I]f it occurs in between allosomes,what could be the effect of Robertsonian Translocation between an X and a Y...

It seems Robertsonian translocations are not ubiquitous amongst the chromosomes and only involve 13, 14, 15, 21 and 22.
HTH.


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identify this plant
location: trabzon (turkey) can seen in rural areas, in woods and in some gardens.

In the American South will call that Poke Salad.

Looks like pokeweed (Phytolacca americana):

Source: https://nature.mdc.mo.gov/discover-nature/field-guide/pokeweed

Source: http://ribbonsandlines.blogspot.com/2012/09/september-at-cape-may-point-nj.html
Per wikipedia:

Pokeweed is native to eastern North America, the Midwest, and the Gulf
  Coast, with more scattered populations in the far West. It is also
  naturalized in parts of Europe and Asia.


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are dead ants returned to colony?
Do foraging ants carry dead ants back to colony for disposal or leave them where they died?  I would think they would leave them behind just based on the energy expended that would be needed to transport them.  If they brought the dead back to the nest that might indicate 'feeling' or 'emotion' which everybody seems to say is impossible.

Who's "everybody"? Neither I nor cognitive ethologists... Anyway, interesting question.

Possible duplicate of Do ants really dispose of their own dead, and how/why?

Social insects can respond in different ways to nest mates corpses. They can bury them (sometimes "entombing" is used in the literature, especially in honeybees because they can seal cells or use propolis to build tombs), eat them ("cannibalism"), but most often a specialized group of workers takes care of carrying them outside of the nest, far from the colony. Usually the older workers specialize in undertaking behaviors, it has been hypothesized that this allows to reduce the risks of contamination because older workers are already more likely to die or have fewer social interactions than younger members of the colony.

Sun, Q., & Zhou, X. (2013). Corpse management in social insects. International journal of biological sciences, 9(3), 313.

What social insects do with the corpses wouldn't be a good indicator of emotions, simply because they may bring them back to eat them, or take them away to avoid contamination. Whether insects do experience emotions is a complex topic, the most advanced piece of work on the subject has been done on bumble bees:

Perry, C. J., Baciadonna, L., & Chittka, L. (2016). Unexpected rewards
  induce dopamine-dependent positive emotion–like state changes in
  bumblebees. Science, 353(6307), 1529-1531.

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Is it correct to classify technolgy as a kingdom?
I recently read some article about a possible 7th kingdom of classification . They considered technology as a kingdom and named it Technium. Actually I was not sure whether it could be called a kingdom as of course we do not consider machines to be living. Thus my doubt was whether there is any biological significance to this claim or is it simply a term that represent technology? https://www.google.co.in/url?sa=t&source=web&rct=j&url=https://www.edge.org/conversation/kevin_kelly-the-technium-and-the-7th-kingdom-of-life&ved=0ahUKEwi1i7vgyd7XAhVCpI8KHfiTCagQFggkMAA&usg=AOvVaw0vYZQy60vYGU0WkN0cBrBi

Kevin Kelly writes some interesting books, but I don't think this is a very useful idea from him. Of course, you can classify entities (frogs, busses, rocks) in all sorts of ways but biological classification into kingdoms surely only works for biological entities. Since technology is not biological, it doesn't make sense to classify it within a biological hierarchy. I might as well classify rocks as another kingdom - Rockium.

I'm voting to close this question as off-topic because it has nothing to do with biology in the terms of this list.

The classification of organisms on Earth is a highly regulated science. It may be interesting to talk about non-living things as a "Kingdom", just to provoke discussion. But under the rules set out by the International codes of zoological/botanical Nomenclature, all higher classifications are the descendants of a common ancestor. Only living things are classified under this code. So, no, technology is not a kingdom. And the term "Kingdom" has undergone so many changes under the rules of cladistic nomenclature, that it is not nearly as relevant as it was when I was a kid (with only 3 kingdoms), since most of the familiar kingdoms are not monophyletic. https://en.wikipedia.org/wiki/Kingdom_(biology)


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Are male and female brains physically different from birth?
Male and female brains are wired differently according to this article:

Maps of neural circuitry showed that on average women's brains were highly connected across the left and right hemispheres, in contrast to men's brains, where the connections were typically stronger between the front and back regions.

But since learning in the brain is associated with changes of connection
strengths between neurons, this could be or not the result of learning.
What about physical differences from birth? Are there differences in size, regions, chemical composition, etc. from birth?

Answering this question meaningfully requires distinguishing whether you're asking if the statistical properties of brain characteristics differ by gender of the population you're looking at, or whether there are fixed relationships between gender and specific brain characteristics. Considering how complex gender itself is, the latter seems like an extraordinary claim and highly unlikely

This is just for a laugh : https://m.youtube.com/watch?v=0BxckAMaTDc

As an FYI, when discussing issue like this, it's useful to remember that in a lot of instances, intra-subpopulation variance can and often is far larger than inter-subpopulation. In other words, even if/when the brains (or other characteristics) may differ "on average" by X; but within both males and females, they differ from one another by far more than that average X difference.

@DVK: That's closely related to what I was trying to get at.

Short answer
Yes, men and women's brains are different before birth.
Background
First off, learning effects versus genetic differences is the familiar nature versus nurture issue. Several genes on the Y-chromosome, unique to males, are expressed in the pre-natal brain. In fact, about a third of the genes on the Y-chromosome are expressed in the male prenatal brain (Reinius & Jazin, 2009). Hence, there are substantial genetic differences between male and female brains.
Importantly, the male testes start producing testosterone in the developing fetus. The female hormones have opposing effects on the brain as testosterone. In neural regions with appropriate receptors, testosterone influences patterns of cell death and survival, neural connectivity and neurochemical composition. In turn, while recognizing post-natal behavior is subject to parenting influences and others, prenatal testosterone may affect play behaviors between males and females, whereas influences on sexual orientation appear to be less dramatic (Hines, 2006).
The question is quite broad and I would start with the cited review articles below, or if need be, the wikipedia page on the Neuroscience of sex differences.
References
- Hines, Eur J Endocrinol (2006); 155: S115-21
- Reinius & Jazin, Molecular Psychiatry (2009); 14: 988–9

I wonder how the information was gathered in your second paper, and whether extrapolation is acceptable. It appears to have come from dissections of fetal brains. Since no longitudinal follow-up is possible, one can state fact (there was more x here), but extrapolation has to be very, very carefully employed.

Read the Hines abstract (don't have access to full article.) Play behavior does not equal toy preference; play behavior might be grabbing a toy out of someone's hand and hitting them with it vs. sharing vs. other. I suspect this is more in line with what they meant by play behavior than toy preference, unless you have access to the whole article and it addresses toy preference? I'm genuinely curious.

The quoted Wikipedia page, whilst true, does not mention gender bias from adults on how children are treated.  Motor skills and language skills are skills which are developed through practise, and especially through practise with an adult.  Studies have found profound bias in every aspect of how both men and women play with babies, depending on whether they are told the baby is a boy or a girl - not just in toy choice, but in actively preventing perceived inappropriate toy choice.  Most adults in these studies were unaware that they were even exhibiting bias.

Dear commenters; the behavioral part is explicitly preceded by a may - it's not a real part of the question and an add-on to the answer; I am deliberately cautious here, because it is indeed difficult to establish causality post-natally. @anongoodnurse I have made the behavioral example more general now - thanks for the watchful eye. Regarding your first comment: the question, the first part of the answer and the paper are all on pre-natal gene expression, so there is no extrapolation necessary?

@AliceD - Yes, (I'm not sure I understand your comment) it is about gene expression. Tracing it back to the source, it's about gene expression in fetal brains. (No longitudinal studies possible.) I do not - absolutely do not - disagree that there are differences between male and female brains prenatally. But what that means is something different. (I UVed your answer before any comments btw.)

@Graham - When my first was born (a boy), I was still a semi-militant feminist, and dressed him in neutral colors for precisely the reason you state: I didn't want strangers/people to act in a particular manner around my son based on sex. I would evade the question. What happened is that people just wouldn't speak to my baby. So after a while, I stopped the experiment, which made strangers much more comfortable.

@Azor-Ahai A few links: A study on perceived crawling ability https://www.ncbi.nlm.nih.gov/pubmed/11063631, a study on perceived crying http://www.psypost.org/2016/06/gender-stereotypes-influence-adults-perceive-babys-cries-study-finds-43541, and a neuroscientist's viewpoint https://jezebel.com/5352031/do-parents-create-gender-differences

@Azor-Ahai And most recently, this brilliant BBC documentary. http://www.bbc.co.uk/news/av/magazine-40936719/gender-specific-toys-do-you-stereotype-children

What about physical differences from birth? Are there differences in size, regions, chemical composition, etc. from birth?

One significant, inherent difference between male and female human brains [from birth & throughout the rest of life] is that male brains are 10-20% larger than female brains.

According to a study performed by the United Medical & Dental College in Karachi, Pakistan:

In this article it is reviewed that how does the brain of a male look and function differently from a female's brain, and what accounts for these differences?

..

Male brains are about 10% larger than female brains and weigh 11-12% more than that of a woman. Men's heads are also about 2% bigger than women's. This is due to the larger physical stature of men. Male's larger muscle mass and larger body size requires more neurons to control them. The brain weight is related to the body weight partly because it increases with increasing height.

..

This difference is also present at birth. A boy's brain is between 12-20% larger than that of a girl. The head circumference of boys is also larger (2%) than that of girls. However, when the size of the brain is compared to body weight at this age, there is almost no difference between boys and girls. So, a girl baby and a boy baby who weigh the same will have similar brain sizes.

To offer more "tangible" figures/values..

In 2000, using MRI imaging, Nopoulos, Flaum, O’Leary, and Andreasen measured an average brain volume of 1254 cm³ for men, and 1130 cm³ for women; this is roughly a 10% difference. source
In 2004, the University of Pennsylvania Medical Center measured average male brain volume to be 1272 cm³, and for women, 1156 cm³; this is also ~10% difference. source
In 2007, the Department of Neurology at the University of California reported an average brain volume of 1363 cm³ for men, and 1188 cm³ for women; again, this is roughly a 14% difference. source

And then, regarding the differences between body size..

According to the Center for Diseases Control & Prevention, the average U.S. man weighs 195.7 pounds, while the average woman weighs 168.5 pounds. This is a difference of 27.2 pounds, or, a difference of ~14%. source

Ultimately, the reason for differences in brain size between males & females is still being heavily researched. As mentioned before, one major theory is that differences in brain size can be attributed to differences in body size. Another theory claims the reason is due to how the brain changes size with age, with male brains shrinking more dramatically than females. Regardless of the reason, the fact still remains: male brains are roughly 10-20% larger than female brains.

Additional texts to consider that explore other differences:

Sex differences in the structural connectome of the
human brain - M.I.T., PNAS journal, 2013.
A meta-analysis of sex differences in human brain structure - University of Cambridge, Elsevier Publishing Company, 2013.

Surely the trouble with taking a purely scientific approach to intelligence is that it's a pretty poorly-defined concept with no reliable way of accurately measuring?  If you want to be rigorous about it, you need to talk about more concrete concepts.

I'm not sure there is any consistent measure of intelligence. I'm also not really sure we need one, I don't think it would help this world.

After seeing the reaction that's originated from me including the note about intelligence, I now feel inclined to removed it from my answer, as it's not relevant to the OP, and is a separate topic altogether. This redaction can still be found in a previous version of my response, and in the linked article.

Remember, elephant brains are larger and heavier than humans, but it's neuron density that determines intelligence. Males have large standard deviations in intelligence, and females have small standard deviations. Overall, on average, it all equals out.

@vaxquis I agree that any strong position is unfounded. That's why the most reasonable conclusion is that there are no overall differences, hence why it's unreasonable to claim that the point has been proved (which btw can never happen in science). Lynn is not racist because of his results but because of what he makes of them and what he seems to believe that is not based on research. Read the wiki about him. Furthermore, when his science is motivated by pre-conceived moral judgements, the results have to be questioned. It is no accident that some of his studies contain methodological flaws.

@vkehayas any study by any scientist can contain metological flaws. In all honesty, as a PhD student, I seldom see articles without them. I'm not willing to discard a study just because it's biased; all studies are biased, because all scientists are human, and all humans are biased one way or the other. OTOH, I'm willing to question it; still, if a see a field with a lot of debatable research going on, I'm willing to say it's probably a debatable matter. Every person who lived with a woman saw those differences; they are better at some things, they are worse at some. (cont)

@vkehayas what interests me here, is what the difference is, why it happens, and can we do something about if, and should we? FWIW, I've removed all my comments, because, as Charles already noticed, they are obsolete after his edit. I reckon this got off-topic enough already.

I intend on leaving my comments here, because there is an implicit assumption in the question that brain size matters for something (c.f. with how interesting the question "Do males have bigger livers than females?" would be and if more than 15,000 people would want to know the answer). This answer was the only one hinting that brain size doesn't matter for much overall, despite the fact that @Charles, perhaps reasonably, took that part out later.

This is ontologically weird. You are quoting statements that say that per body weight, boys and girls have the same amount of brain; but in your own preface, you write that boys have 20% larger brains. Does not compute. ;) Also, the sentence Male's larger muscle mass and larger body size requires more neurons to control them. seems weird to me, maybe I am missing context. Just because a muscle is larger or a bone is longer does not logically mean that there need to be more nerves. Longer nerves, yes, but without being an expert, that would per se not necessarily change anything in the brain?

@AnoE "You are quoting statements that say that per body weight, boys and girls have the same amount of brain;" -- I think you may have misread the quote.. it says that, specifically at the time of birth, if a male and female baby have the same body weight, they will have negligibly different brain sizes. I don't see there being anything wrong with this statement..

@AnoE As a male and female humans age, they grow in height; there is a known link between height and brain weight (another common measurement for determining brain size). "Among parameters, the brain weight correlates best with the body surface area, followed by the body height and body weight. The brain weight is related to the body weight partly because it increases with increasing height." See here.

@AnoE And yes, generally speaking, the larger an organism is, the more neurons it needs to control its body; see this publication for more information. "..in order to explain the correlation between brain size and body size, we must fully investigate the web of associations among various biological features in groups of mammals and other animals." .. "therefore that fat and muscle might both scale closely with brain size if metabolic resources are critical." ..Also, see here.

@AnoE Also, see here. "However, large animals need more neurons to represent their own bodies and control specific muscles; thus, relative rather than absolute brain size makes for a ranking of animals that better coincides with the observed complexity of animal behaviour." .. I hope this clears up your concern(s).

@Charles, thank you for the additional information. I was not intending to downplay your answer, just to voice my confusion with the shorter version of it, at that time. I am not the only one, seemingly; the paper you linked has the statement Exactly why this would be the case remains a fundamental question in the study of brain evolution.. I'd suggest that you flesh out the answer a bit and give these kinds of contexts, or else it is mostly useful for people who already knew it or are prepared to follow all the links to study it up on their own. Still, at this moment, your answer...

... boils down to "males have +14% brain size and +14% body size". In the context of a question about "are male/female brains different from birth" this leads to a wrong conclusion on superficial reading (the conclusion could mistakenly be "yes, males have 14% more brain", while the correct conclusion should be "brain size is directly coupled to body size with neglibly relationship to sex (and by the way, males tend to be 14% larger overall)" - at least considering the references you have given.)

And finally, your links mostly reference comparison of different animals (of different size) like mouse vs. elephant etc.; the question is specifically about  humans, i.e., staying within a single species.

@AnoE IMO, the reason(s) behind differences in brain size [between male & female] is a separate question altogether, and, if it were attempted to be addressed as well in this response, perhaps I would get off-topic fairly quickly, since I would then have to talk about muscle mass, metabolic rates, height growth rates, aging w.r.t. neuronal degradation, etc..

@AnoE Only one of those links addresses animals in general, and I provided that to illustrate a relationship between the body size/muscle mass of the organism and brain size/the necessity for more neurons. Which is to say that, this behavior/correlation is not necessarily unique to humans, but is a general principle that can be applied to most all living creatures with a brain. ... it appears that I accidently provided the same link twice in two different comments, and may be why you think there are multiple links that talk about animals, and not necessarily just humans.

One point of view you rarely see is the perspective of sex differences from an evolutionary standpoint. Never mind that this is the reason why the differences exist in the first place if they do at all.
But the short answer is that Human Male and Female brains are unquestionably selected to be different (whether this means they are actually different requires a modern side by side comparison). But to build on this point, think of male and females in terms of evolution. Male and females inherently fill different roles in history and prehistory (If you want to argue that men and women didn't or don't have different roles then show me the man who can give birth to a baby). Given that there were different biological pressures behind the evolution and success of each sex, the brain has been selected (as have other parts of human physiology) to better accommodate the demands of its respective sex as it pertains to one's own reproduction and survival. This much is beyond any reasonable dispute.
Unfortunately this fact cant be used as definitive evidence of sex differences, because even though we can prove that for all of human existence the sexes have done different things what we really need is a side by side comparison of how they are today to come to any conclusion. And given that the current political climate is ridiculously politically correct, it is unlikely any study will be brave enough to publish anything anti PC or else lose funding.
Ref: (Just random references)
https://pdfs.semanticscholar.org/4510/e98234d30ea146f523039ba353520a04be3a.pdf
http://www.annualreviews.org/doi/abs/10.1146/annurev.an.15.100186.000325?journalCode=anthro
https://www.eurekalert.org/pub_releases/2015-10/nuos-wam100715.php
https://stanmed.stanford.edu/2017spring/how-mens-and-womens-brains-are-different.html
Edit:
This extension to address '@Elise van Looij' comment that this is a circular argument.
This is history. I have often heard the 'circular argument' position used to try and defend against evolution, aka which came first the chicken or the egg, but it is a logical fallacy. So for the sake of flushing out the position a bit better lets go through the points.

This appears to be a circular argument. Males and females have inherited different roles and therefor they have evolved differently
  to fill those different roles. How come they 'inherently' have
  different roles? Because they have evolved that way.

(1) Males and females have inherited different roles? I don't think this is true. Males and females have inherited different potential roles (and maybe an inclination for, or biology best suited for those roles). However no one personally has to fulfill any role. And the roles evolution selects for (namely what is best suited for reproduction) changes over time and between environments. However it is true that those that excel at certain roles best suited for reproduction and survival, will possess traits that will propagate to the larger population by virtue of exponential growth of those genes in the population.
(2) We have evolved differently [solely] because of these roles? No. We have evolved only to reproduce effectively. And this statement isn't limited to just things that reproduce sexually. Biological "roles" are a consequence of the environment. Right now we are still the product of ancient environments because not enough time has passed between then and now for that biological legacy to have been erased. And this is why I put forth the position that the pressures human populations faced for millions(?) of years which unquestionably shaped our biology, can be used in the modern day to make educated hypothesis about our modern (still relatively ancient) physiology.
(3) How come they 'inherently' have different roles? Because in each generation the creatures that did those 'roles' made more babies than the ones that didn't. This is simple math now. 2 A and 2B. 2A reproduce and make 4A. 2B make 1 baby B. Old generation dies, new generation is now 4A 1B. Repeat until B = 0.  Now if you want to go all the way back to when there were no roles, you can do that. Go back in history until we reproduced asexually, were hermaphrodites, or no life existed, or some other condition was met. There is no circular-ness in my opinion because you can follow the path back until all starting conditions are different (and thus the circle ends).
But to reiterate the important point because it might be buried in the rest of the text. We have evolved to be a certain way. This way may change in the future and is probably changing right now. But as we exist right now, we are the product of time in the distance past. That passed has shaped us to be a certain way. And we haven't evolved to be radically different from that way yet because not enough time has passed since then for our fundamental makeup to have changed. Think about it; when did the social roles of Male and Female change? 50 years ago? 100 years ago? 1000 years ago? 10,000 years ago? We took millions of years to evolve into this variant of ape that we are. Our ancestral legacy is still strong with us.
But this turned into a discussion of evolution. Instead of what we can learn from evolution. Which was the real purpose of this post.

Are studies being done, then, and just not being publishing because the results are non-PC?

In some cases yes, studies are rejected from journals on the basis of not being politically correct. Really this has been a big issue for sometime as it relates to research: 1) https://www.acsh.org/news/2016/08/11/political-correctness-prevents-advancement-of-science 2) https://www.nas.org/articles/Political_Correctness_in_the_Science_Classroom 3) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1299305/ 5) https://scimedskeptic.wordpress.com/2017/03/06/political-correctness-in-science/ 6) https://www.realclearpolitics.com/articles/2014/03/10/science_and_reason_vs_political_correctness_121866.html

This appears to be a circular argument. Males and females have inherited different roles and therefor they have evolved differently to fill those different roles. How come they 'inherently' have different roles? Because they have evolved that way.

See my edit addressing your points.


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Typical firing patterns of (some) motor neurons
Since it is not so easy to imagine and visualize the behaviour of the muscles in the fingers, hand, and arm of a violinist performing a fast and accentuated trill vs. a slow and soft vibrato, I try to imagine and visualize how corresponding motor neurons do fire.
I assume there are some motor neurons that are immediately responsible for the speed and amplitude of the movement of a finger performing a fast trill, and — partly the same, partly others — that are immediately responsible for the speed and amplitude of the movement of the same finger performing a slow vibrato.
The behaviour of these motor neurons — during the trill or the vibrato — can be recorded as corresponding sequences/trains/bursts/chats of spikes.
I wonder:

How may these spiking and/or bursting patterns look like?

Maybe like this?

fast and accentuated (= large amplitude) TRILL, each group corresponding to one movement (up-down) of the finger

slow and soft (= small amplitude) VIBRATO, each group corresponding to one movement (to-fro) of the finger

I can't answer the whole question, but what I do know:
An actionpotential can't have a small amplitude, the amplitude is always the same. If a neuron gets excited enough there will be an action potential, otherwise there won't.
"When the depolarization reaches about -55 mV a neuron will fire an action potential. This is the threshold. If the neuron does not reach this critical threshold level, then no action potential will fire. Also, when the threshold level is reached, an action potential of a fixed sized will always fire...for any given neuron, the size of the action potential is always the same. "
quoted from https://faculty.washington.edu/chudler/ap.html
Neurons have a maximum firing rate, a point where they cannot fire faster. (http://blog.eyewire.org/why-do-neurons-fire-at-a-maximum-of-about-200-hz/)
So to move faster your body can't fire faster. But it can fire more: more neurons fire if you want to move faster, and less neurons fire if you want to move slower: https://blogs.scientificamerican.com/scicurious-brain/when-you-run-fast-your-brain-runs-faster/
I do think your first row of spikes is kinda correct. Neurons fire as long as you move your hand/finger(s) in a certain direction, and as soon as these neurons stop firing and their complementairy neurons start firing you move your hand to the opposite direction.

"An actionpotential can't have a small amplitude, the amplitude is always the same" - this is not true in a series of action potentials. Many cells show amplitude reductions in their action potentials when firing several spikes in close proximity. Though I'm not sure why you brought this up since it has little to do with the question.

@BryanKrause do you think that there is going to be a somewhat continuous but erratic like graph at each spike points in the picture OP mentioned? something like seismograph?

@gfdsal Not sure what you are referring to or asking.


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Are there nerve endings on or inside the corpus cavernosum/spongiosum?
The penile skin has many nerve endings, but what about the inner structure of the penis?
There are two dorsal nerves on either cavernosum. But it is unknown whether these nerves provide sensitivity to the corpus cavernosum/spongiosum externally or internal.

Asking a question that no one has answered again doesn't improve your chances of it being answered. Did you do any research on this? If you have, can you please edit to add to your question?

Cannot find information on this topic.


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Is osteoid an uncalcified substance?
I recently learned about Osteoid (the substance secreted by osteoblasts during intramembranous ossification), and I read that it was an "unmineralized organic component of bone."
Now, does this mean that Osteoid is un-calcified?? I don't know if I can equate unmineralized with uncalcified but I just wanted to make sure.


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Difference between feral and domesticated honey?
Is there any significant differences in composition (and/or taste) between the honey of wild ("feral") honeybees versus that of domesticated ones used in beekeeping?

I think your question is on-topic but just for info cooking.SE might also have been a possible place where to ask this question.

Domesticated bees are often used to fertilize crops, so their honey consists mainly of nectar from a single type of flower: e.g. clover, orange, alfalfa, blackberry, and more.  Feral honey (or honey from garden hives) presumably comes from a mix of whatever flowers happen to be growing around the hive.

@Remi.b Not so sure, since when it comes to cooking, wild honey can be pretty hard to come by!!! :-D


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How can ionized amino acid form be important for the catalytic activity?
I can imagine that protonated amino acid form, particularly at the active site, is important for the catalytic activity so hydrogen bonds can be created between the substrate and the enzyme. However, I cannot imagine how the ionized form can be important for the activity?
Both forms are important for the activity as stated in this study:
https://www.ncbi.nlm.nih.gov/pubmed/7306491

The pH dependence of log V/K for dihydrofolate showed that a group with a pK value of 4.7 must be ionized and that a group with a pK value of 6.6 must be protonated for activity

I cannot understand how the ionized form is important for the activity, could some one help me to understand that?

Without seeing a crystal structure it's hard to tell. But the abstract suggests 2 carboxyl groups, on a glutamate and aspartate. The abstract also mentions a lysine is necessary to maintain active conformation. Could the negative carboxyl group form an ionic bond with a postively charged lysine?

@user137, I am not sure, but isn't the ionic bond too strong for enzyme-substrate complex?

Enzymatic reactions are chemical reactions. Chemical reactions involve charge ("electron") transfer. Charge transfer occurs more readily if there is a large gradient in charge density between the attacking active site group and the attacked atom of the substrate. Many enzymes (yes, it is really quite common) use ionic forms of aspartate or glutamate as a catalytic amino acid residue.
For example, some enzymes belonging to the alpha/beta-hydrolase fold family (e.g., haloalkane dehalogenases, epoxide hydrolases) use a deprotonated aspartate as the nucleophile (which attacks an electrophilic atom of the substrate); the specific position of the nucleophile within the enzyme and its interaction with other groups in the enzyme enhance the nucleophilic nature of the aspartate, a phenomenon called "oxyanion hole."

Ollis et al. (1992) Protein Eng 5: 197-211.
https://www.ncbi.nlm.nih.gov/pubmed/1409539

Although the answer provided by @MartinKlvana is correct, I would like to clarify the question of the strengths of non-covalent interactions in proteins, as this seems to be the basis of the poster’s problem. As I would put it:

Life is dynamic. So the chemistry of life depends on weak interactions that can be made and broken.

Ionic interactions are similar in energy to other non-covalent interactions
According to Berg et al. and the Wikipedia article typical ranges for non-covalent interactions are:

Ionic interaction: 1.4 kcal/mol (3Å in water — depends on distance and dielectric constant)
Hydrogen bond: 1–3 kcal/mol (depends on distance and angle)
Van der Walls interaction: 0.5–1.0 kcal/mol (depends on distance)

This is in contrast to, say the covalent C–C bond with an energy of about 100 kcal/mol according to this site. Thus, the ionic bond is clearly a relatively weak bond.
The charged state of a residue involved in enzyme mechanisms is often partial and dynamic
As the reader will know, the percentage ionization of a residue depends on its pKa and that of the medium. In neutral solution a histidine side chain (pKa 6.0) would be only 10% protonated. At the active site of a protein things may be different however. In a hydrophobic environment the acidic side chains of aspartic or glutamic acid may have far less tendency to ionize, and thus have an effective pKa much higher than that in water (4.1). The proximity of other residues may also influence the ionization or protonation by accepting or donating a hydrogen ion.

The point of this is that the residues involved in catalysis are often effectively less charged than a fully charged residue in solution, and
  this allows the ionization or protonation to be reversed at the end of
  the reaction, returning the enzyme catalyst to its original state.

Some examples
Although the functional role of Asp-27 (the presumed pKa 4.7 group) in tetrahydrofolate reductase would appear to be to donate a proton to the substrate, the details of this reaction are not completely clear. So it is easier to illustrate this point with two classic enzymes.
Serine Proteases (Trypsin etc)
More details of this can be found on the web and in any biochemical text, but the following illustration taken from Berg et al. illustrates the key point I wish to make.

This is that during the reaction the histidine is able to alternate between being protonated and unprotonated, receiving a proton from the adjacent serine.
Lysozyme
Here the mechanism of action involves two acidic groups, one charged (Asp-52) and one (Glu-35) uncharged. This difference is because the latter is in a hydrophobic environment. During the course of the reaction however it is able to ionize, but returns to its protonated form when the reaction is complete. This is shown in the illustration below, taken from a Nature Structural Biology review article by A.J. Kirby.


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Why are sugars like mannose expressed on the outside of eukaryotic cell membranes?
Bacteria are able to adhere to sugars (e.g. mannose) on the exterior of eukaryotic cells, leading to infection and disease. Why have eukaryotes not evolved so as to dispense with sugars on their cell surfaces? I assume there must be a positive aspect to having these sugars. What is it?

I have modified your question, in particular making it clear that you are referring to eukaryotic cells (as implied by ‘infection’) and removing all references to cell walls, which animal cells do not possess. Although this is late in the day, I would point out that you are expected to show evidence of your own research before posting here. My own answer is partially based on internet searches for the function of cell-surface sugars.

The “positive aspect” or reasons why the surfaces of eukaryotic cells contain sugars are various. Major ones appear to be cell adhesion and cell–cell interaction.
In fact, the variation of the sugars in certain cell-surface antigens (blood group antigens and histocompatibility antigens may represent the kind of evolutionary response to infectious agents mentioned in the question. The situation with the major histocompatibility antigen is complex, but variation in blood group antigens is thought to be a response to the malaria parasite — reviewed by Cooling.

This is a simple referenced answer to the question by someone who is not an expert on cell-surface sugars, posted to help resolve it. If you have more recent or comprehensive information or references please either edit the answer or post a comment.

I'd look on it from the other side. Thoose structures have certain purposes, such as stability or signaling purposes. Due to their short doubling time compared to most cells of more complex organisms, bacteria is able to adjust to changed condition rapidly and therefore adapts to it's environment. (Just think of mechanisms of resitance to antibiotics: plasmids for example with the information for β-lactamase ere exchanged even between differnet kinds of bacteria) It would therefore not make a lot sense for the slower cells to adjust their usefull structures in order to avoid bacteria, which change way faster.


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Career advice for a bachelor of biology with russian STEM diploma
I'm from Russia. I majored in biology(genetics), wrote a bachelor's diploma in the field of psychogenetics, and graduated with mean grade of roughly 4 out of 5. Back then some circumstances arose that prevented me from an academic career (including lack of biotech companies in my area), so I had to make do with an entry-level job. Biotech companies in Russia can afford to be picky and hire only experienced staff even for an entry-level position such as lab technicians. With a lot of people in the field looking for a job, and a few biotech companies, I don't have a lot of chances there.
I've heard that Russian diplomas in STEM fields are valued abroad, probably more than they are in Russia; that brings me here. What are my chances of finding positions as a junior lab member, lab technician, etc. in a biology-related field overseas with my higher education diploma and practical experience (achieved during two years of lab work in the university)? What skills/qualifications do I need to get to improve my chances? What direction would you suggest to start my research on possible employers? Could you give me any further tips on career track?

Are you interested in graduate school? I know America has a lot of biology BS lab techs. A Ph.D. program might be an easier way to getting your foot in the door overseas, if you're willing to put up with an extra 4 - 6 years of schooling, and your job opportunities with a Ph.D. might be better. If you speak English as well as you seem to write it, your language skills are probably fine. I don't anything about the job situation in Europe though.

You might be interested in reading Paula Stephan’s book: how economics shape science ( talk: https://www.healthra.org/download-resource/?resource-url=/wp-content/uploads/2013/08/Stephan_9_2012.pdf ). In short, the general problems with biology unfortunately are global; p.s.: Switzerland or Germany are quite strong in biotechnology, and not even overseas

You may be able to get a position as a lab technician in Europe, but otherwise in most places you'd need to do a Master's as well. There are plenty of pharmaceutical companies in Switzerland but I am not sure on the qualifications required for an entry-level position. I'd suggest that you build your skill-set around the position you want. You haven't said anything about what you would like to do.

In my opinion this is a general problem throughout the life science industry all across the globe. Personally I work in the UK and although I am now in a slightly better position, the beginnings were tough - very tough (despite having a MSc). The money still isn't great but not as bad as what it was during my first two years.
I do have quite a few friends in Germany who tried to establish themselves as scientists there, very few did. Most ended up pursuing careers in Life Science Sales are something else all together. I am not saying you can't make a living in the life sciences but it's hard

There are quite some positions offered in bioinformatics, but I think they often require at least a master diploma. That being said, you can learn a lot by yourself using online resources. So if you have time, you might try to follow some online course (for instance on coursera or edX) to see if this is a kind of career that could suit you.

I'm voting to close this question as off-topic because it is not about the science of biology.

maybe try Academia.stackexchange?

You have so many questions, and it seems like you have no idea what to do next. So you better ask Russian guys who are really into this as

Good FAQ with a lot of cases from real life:
https://vk.com/career_in_biology
More like Career in Biology 101:
https://vk.com/science_career (also they have a chat in Telegram)
Career adviсe and pretty decent list of positions: https://blastim.ru/
Winter biotech school (in my opinion you have good chances to get there as they do it for people just like you): https://vk.com/futurebiotech
Completeish list of biological summer schools where you can get hands-on experience: https://vk.com/coolresearch


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Would chimpanzees and humans normally be in the same genus if we weren't so sensitive about it?
Listening to the BBC's radio program The Why Factor particularly poignant episode What Can Chimps Teach us About Politics? hosted by Professor James Tilley, I heard Professor Frans de Waal of Emory University's Yerkes Primate Research Center, and author of Chimpanzee Politics say:

The differences are so small; normally we would put humans and chimpanzees in the same genus, but because of sensitivities in the human species we’ve not done that.

I'm wondering if this is an opinion, or arguably correct. I understand that taxonomy is an "evolving" discipline, but are there scientific arguments or viewpoints that would suggest that chimps and humans would be in the same genus if not for public, social or individual sensitivity to the idea?

To the silent, anonymous "primarily opinion-based" close-voter; I've specifically asked for "scientific arguments or viewpoints" that chips and humans would normally be in the same genus in order to rule out individual opinions. The source of the quote is obviously someone with academic standing in primatology, I'm now asking for the scientific basis behind it, ergo, only answers that are not primarily opinion-based would be appropriate. Let's first wait for the science-based answer instead of invoking the insta-close option.

I'm not the "opinion close-voter" but it seems to me assignment to a particular taxon level, such as genus, is usually (always?) a matter of opinion, and not something with a firm scientific, factual basis.  That two species are related by common ancestry is subject to scientific assessment, but whether you designate  that relationship as being within or outside a particular an arbitrary taxon level like genus is simply an issue of opinion and judgement and not of real-world fact.

The designation might not be a simple, bright line demarkaction, but the data might exist to allow one to say "In these branches of the animal kingdom, species with the same degree of genetic difference are indeed classified as the same genus".  There might be enough examples to strongly suggest that human and chimps are treated in an exceptional manner.

@mgkrebbs If I posted the question "is assignment of an organism to a given genus purely a matter of personal opinion, or is there some well defined science behind it, albeit somewhat subjective?" would you be interested in posting an answer and seeing how it flies? Or I could ask something like "Is the advent of fast, cheap whole genome sequencing turning traditional taxonomy on its head?" I like stackexchange's question and answer format, allowing for multiple answers as well as comments and voting on those answers.

@swbarnes2: But how would a genetic criterion deal with extinct species, for which there isn't any genetic info?  Also, if humans and chimpanzees were to share a genus, why shouldn't gorillas and orangutans be included?

taxonomy-related: What’s in a Name? Taxonomy Problems Vex Biologists

I have not seen any research that synonymizes Pan and Homo, but that doesn't mean someone hasn't tried to propose it in the literature at some point.  The proposal to synonymize the two genera of course would need to be based on accepted techniques and not emotion (such as just having a particular fondness for chimps).  And such a synonymy would necessarily synonymize all the ancestors that existed since the most recent common ancestor of humans and chimps, or a new structure for the evolutionary relationships would have to be proposed.
I think it's important to note that while there is a right answer when it comes to the structure of the evolutionary history of species, there are no right answers when it comes to naming conventions.  The names exist for our convenience.  Phylogenetic trees themselves which show evolutionary relationships are utilized for other research such as understanding the evolution of traits.  So I don't know if this researcher is thinking there is some need to re-evaluate the structure of the relationships between humans and chimps for the sake of advancing science, or if he's just trying to get his opinion across and/or cause discomfort.
Related posts

How could humans have interbred with Neanderthals if we're a different species?
Does it make sense to classify all humans in a single species?
Is there a consensus on whether or not race exists on a biological level?
Do humans have enough biological differences to be grouped into races or subspecies?

Very good answer +1. I added a bunch of related posts to your answer.


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Do hedonic chemicals in humans work as anhedonic in other organisms?
We have various neurotransmitters that cause pleasure or feelings of love in humans. Do they work in this way for all other animals and organisms ?
What about reptiles, insects, crustaceans ?
I don't know how far science is assuming the state of subjective experience in other organisms, but how far can we say that other organisms would feel the effects of neurotransmitters in ways that we would recognise from our own experience ?
For instance, we could assume that another primate experiences dopamine in a similar thing to humans, but what about non-mammals, animals of other classes ?


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Is this a sentry palm?
I "inherited" a plant and was trying to identify it (to understand how to take care of it - plants usually have a hard time with me).
I belive this is a sentry palm (from photo matches gathered on Internet) but my leaves seem much more narrow than the ones on the pictures.
The plant is in France and is probably not a fancy one (in the sense that it should probably be available in Ikea or a general plant store).

Note: this question should be made to gardening.stackexchange.com

@GiacomoCatenazzi: I had no idea that such a site existed (I will have to look again at the new members of the network). Yes, that would have definitely been a better place.

I highly doubt that this is a sentry palm. It seems to be a golden cane palm, also known as areca palm or butterfly palm, Dyopsis lutescens.
Here is an image for comparison:

And here is a close up of the leaf:

This whole structure is just 1 leaf. What you called "leaves" in your question are actually just leaflets (or foliolum in Latin).


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What is this insect from Brazil

Im assuming 'cicada' with this insect but which one ? Small size- c1c-2 cm -

A better assumption would be "planthopper" (superfamily Fulgoroidea), but beyond that I admit to not having a guess.

I think you're right ....

This neotropical leafhopper belongs to the subfamily Coelidiinae. According to this publication though, there are 25 genera & over 75 different species, and so, I'm having a difficult time narrowing it down from there (my current best guess would be genus Jikradia).

If I'm not mistaken, this insect is displaying an alarming signal by spreading its wings like that.. it must have felt threatened by you when you were taking the picture (assuming that it wasn't already like that when you approached it).
For more information on this subfamily, I strongly suggest that you explore the text of the previously linked publication, as it contains great information regarding the various tribes of subfamily Coelidiinae, including distribution, origin, host plants, a bit of history, and so forth.

Brillient - it was 'alarmed' when i first noticed it ( probably more alarmed after afew bright flashes hit its eyes )


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Could I use spiders to catch unwanted insects?
I was wondering if its possible to catch spiders and place them in my greenhouse in order to kill unwanted insect that feast on my plants? I don't really mind presence of spiders since then are not dangerous in my country (Czech republic).
Common species that live outside are Araneus diadematus, we got many that live in presence of human like Tegenaria domestica, but I read that they are type that live at human build constructions and can't really survive outside.

Spiders can definitely be used for pest control along with some beneficial insects, such as ladybugs. Some care should be taken in case the introduced spiders actually cause more harm by, for example, killing ladybugs. An alternative approach is to grow plants that attract beneficial spiders and insects:
https://dengarden.com/gardening/Useful-Insects-For-Plants
https://www.organiclesson.com/beneficial-insects-garden-pest-control/
Perhaps you'll get more info over at gardening.stackexchange.com.

What you describe is called biological pest control. Lacewings and earwigs are more common, but there are ways to use spiders.
http://unossc1.undp.org/GSSDAcademy/SIE/Docs/Vol4/Rearing_spiders.pdf
http://www.annualreviews.org/doi/abs/10.1146/annurev.en.29.010184.001503?journalCode=ento


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Difference between 'fitness' and 'fitness effects'
Term 'fitness' is pretty obvious, but, often 'fitness effects' is commonly used in many research articles in the field of evolutionary biology.
I suspect that 'fitness effects' has a different meaning than just 'fitness'. I found that it's really difficult to find the distinction between the two terms just by googling.
So, if some expert in the subject is reading, please clarify.

Fitness
Fitness is some function of the probability of survival and fecundity for a given genotype. Fitness is therefore a single value per genotype.
Fitness effect
A fitness effect is a component of fitness. For example, for a given bi-allelic locus, the fitness effect of allele A is -0.05 in comparison to the allele B, meaning that the allele A is deleterious and the allele B is beneficial. There is a fitness effect for each allele, for each trait and, if you interested in  genetic interaction (epistasis) and genetic-environment interaction, then there can be a fitness effect for each gene and each trait in each genotype in each environment.
Example
It is typically common to assume a model of $n$ loci, where the fitness effects at each loci are $1$, $1-hs$ and $1-s$ for the three genotypes AA, AB and BB respectively (diploid population). $s$ is the selection coefficients and $h$ is the dominance coefficient. The fitness of the individual is often obtained by multiplying out the fitness effects at each loci. The worst possible fitness is therefore $\left(1-s\right)^n$.

Fitness effect of an allele seems to be an 'effect size' which is calculated relative to fitness of other allele.


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A simple question about amoeba (Naegleria fowleri)
I have a very simple question about Naegleria fowleri amoeba. Some experts claim that boiling the water for 15 minutes kills Naegleria. However, I have studied somewhere that Naegleria can turn into cyst forms when the environment or the atmosphere becomes harsh to protect itself. So the question is that is it possible for Naegleria to survive boiling temperature if the water is boiled for 15 minutes at 100 degree celcius by converting into cyst form and enter the nose of human and kill the human?

I have studied somewhere that Naegleria can turn into cyst forms when the environment or the atmosphere becomes harsh to protect itself.

This is true, and can happen for a multitude of reasons, including extreme temperature (hot or cold), lack of food, and overcrowding.

Is it possible for Naegleria to survive boiling temperature if the water is boiled for 15 minutes at 100 degree celcius by converting into cyst form and enter the nose of human and kill the human?

In short: no, this is not possible. According to a publication by the Environmental Research Center, & U.S. Environmental Protection Agency:

At 51, 55, 58, 63, and 65°C, Naegleria survived about 30, 10, 5, 1, and <0.5 min, respectively.

That being said, just by going off the figures from the publication, there's no chance that Naegleria would survive for 15 minutes in 100°C boiling water.


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Are pheromones capable of activating changes to the Phenotype of a complex organism?
I know that pheromones are means of communication between the same species, but are they capable of changing the phenotype of an organism, may be influencing the expression of the genes of a said organism.

Pheromones are means of communication between individual within a species, not between species.

[A]re [pheromones] capable of changing the phenotype of an organism[?]

Yes! It actually necessarily does, by definition. If a chemical produced by an individual does not affect the phenotype any individual of the same species, then it is not a pheromone! You will note that behaviour is part of an organism phenotype.
Pheromones can have drastic impact on an organism phenotype. Most notable examples are from social insects, such as caste differentiation in termites (Matsuura et al. 2010).


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Why is ethanol osmotically active if it can enter through the plasma membrane easily?
This has been bugging me for a while, and I can't seem to find an answer to it, and I am sorry if I am asking a lot with this question(s). Firstly, I keep finding sources suggesting that ethanol is osmotically active, but I also know that ethanol can enter the cell readily through passive diffusion, and some sources also say it uses transport proteins - what causes osmotically active behaviour, then?
Secondly, and this is very closely linked to the above, why do cells shrink in the presence of ethanol of high concentrations, if it is able to enter readily, unlike, say, ions? The mechanism seems to be far more complex than I have found regarding simple osmosis for ions and such.
I would like to add that my confusion may also be due to conflicting information I am getting, whether the cell shrinks or grows (or does one then the other), so it is hard for me to even picture if the solution acts as if it is hyper- or hypotonic.
SECOND EDIT: Seems that there is evidence from some sources that suggest ethanol can affect the osmolarity of the solution without itself being "effective", whatever that means. Something to do with the lipid membrane. Again, I keep editing this so people might... possibly... have something to go off when answering this.

I would also add this seems to be a similar case to urea, so answer would likely deal with that case as well.


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Are all cone cells connected directly to the brain?
Coming from a computing science background, I noticed that cameras have orders of magnitude fewer wires than pixels. For example, the Raspberry Pi Camera v2 has 8 megapixels, but only 10 wires connecting it to the board. In human-made systems, it is preferred to time-multiplex pixels over few wires or, even better, already compress or encode image information on the camera.
I was wondering if the human optical system features something similar. Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain? Or is each cone cell ("pixel") connected directly to the brain?
(In case the latter: Wow! The optical nerve must have a huge bandwidth.)

This isn’t my field so hopefully someone can give you a better answer, I just wanted to say that there is some processing in the retina. The signals from many photoreceptors are integrated by and/or into retinal ganglion cells, whose axons make up the optic nerve and number much less than the total number of photoreceptors.

Are all cone cells connected directly to the brain?
No.  Cones connect to ganglial cells.
Let's explore the numbers.  Our eyes contain about 6 million cone cells, 90 million rods, and comparative handfuls of additional photosensitive cells (ipRGC's) that don't play a role in vision.
The optic nerve is a bundle of roughly 1 million fibers (perhaps up to about 1.7 million).  So by just running the numbers, it doesn't fit.
I was wondering if the human optical system features something similar.   Does the eye compress, encode or time-multiplex the image "pixels" it captures before sending the information to the brain?
Let's focus on photopic vision (color vision, which happens when lighting conditions are sufficient).
Our perception of color starts not with the cones, but with ganglial cells in the retina.  This is different than how an RGB camera works; our brains don't process color in terms of "pure cone signals".  Instead, color is processed in three channels; a "red-green" channel that measures the difference between L cones and M cones;  a "yellow-blue" channel that adds input of L and M cones and subtracts out contributions from S, and a "brightness" channel that computes the sum of all cones.  This is referred to as opponent processes.  Maybe we can call this encoding.
In addition to this, there are ganglial cells in our retina that contribute to edge detection.  These cells work similarly to ganglial cells that perform difference measurements for opponent processes, only they connect to the same cone types.  Since ganglial cells connect locally, if there's a large difference between stimulation of two cones next to each other, it's an indication that there's an image of an edge of something projected onto that spot.  If we can't distinguish individual cones, but these things can distinguish edges which to us are the more interesting property, maybe we can call this lossy compression.
Outside of this, a huge amount of our brain is devoted to visual perception.  There are some really strange quirks about our eyes; most popular is the existence of the blind spot.  Additionally, our 90 million rods are squeezed more into peripheral vision, leading to fuzzier imaging in photopic conditions the farther away we are from the fovea.  Furthermore, chromatic aberration can be quite a pain, but L and M cone sensitivities are very close to each other.  So where absolute sharpness matters, we have less S cones around; in fact, in our foveola, there's nothing but L and M cones.  Our brain makes up for this, by stimulating us to move our eyes constantly and rapidly (saccades).  As we do so, the visual cortex goes into overdrive, filling in that blind spot, crisping up that periphery a bit, painting in an illusory blue in our center vision, etc.  Though this involves "moving the camera around", we could maybe call this a sophisticated, high level form of time multiplexing.
Much of this information is available from wikipedia articles, though you might need to know what to look for; so here's a starting guide:

Cone_cell for cone cell counts
Fovea_centralis for cone density in center in vision, with picture
Optic_nerve for count of optic nerve bundle fibers
Opponent_process for opponent process theory
Receptive_field contains discussion of edge detection

Fascinating to read your answer! We basically have a Sobel operator in our retina.


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Linkage Disequilibrium - What does it mean when D < 0?
What does it mean when you have a situation where your D<0?

Consider two bi-allelic loci, A and B with alleles A1, A2 for A and B1, B2 for B. Negative values for D means that A1 is more often associated with B2 than expected. Similarly, A2 is more often associated with B1 than expected.
More info on Wikiedpia > Linkage Disequilibrium or on any intro book to population genetics (see here for recommendations). If there is anything in particular you do not about the definition of LD, feel free to ask a question by highlighting what is unclear to you.


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Kinetic mathematical model of glycolysis?
I am looking for papers containing kinetic mathematical models of glycolysis, hopefully in mammalian cells (or as close as possible, say yeast). The papers I have found do qualitative analysis (bifurcations, stability analysis, etc.), but do not actually fit the model to data, so you cannot be sure of the accuracy of the kinetic constants involved. The work I need to do depends critically on having reasonably accurate estimates of those kinetic constants.


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What is difference between the malaria (cross) types?
When the doctor does the diagnose she says "you have malaria. 2 crosses". Now, I've heard those crosses go from 1 to 5, and historically I've had from 1 to 4, but I wonder: what is the difference between them?
Also there's this popular thing of people saying that an odd number is more dangerous than an even number. Is this scientific or something?
Cheers


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Is scratching in humans vestigal?
Scratching and biting helps furred animals dispose parasite insects from their surface. Is it a productive action for humans who have less fur, have hands that can pinch off parasites and can help each other out?
If evolution were perfect, humans would never scratch, and to resort to pinching off any actual parasites - scratching and biting could break skin and expose it to germs.

What? Humans keep scratching not as vestigial reaction but as environmental response.

These two idioms imply a very long history of scratching: scratching one's head; scratching someone's back.

Scratching is a response to itching.  Pinching an itch doesn't work nearly as well to relieve the itch.  And at least in much of the technically-advanced world, itching is not caused by parasites.  (Not limited to humans: both my dogs and horses like being scratched, despite no obvious signs of parasites.)

Humans usually scratch to stop itches. Because scratches are a more high-priority sensation than the itch, the nerves stop transmitting the itch signals to your brain for a while.


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Tryptophan Operon Working Mechanism
The Trp operon has 2 methods to check for presence of tryptophan, one indicating the absence of free Trp and the other the absence of charged Trp tRNA. If both methods showed absence of Trp there is tryptophan synthesis. However, the synthesis of tryptophan involves 5 enzymes to be synthesized, and usually we find all the amino acids in a protein such as an enzyme. Therefore, there is high probability that Trp is found in these 5 enzymes. Where does that Trp come from if there is neither free tryptophan nor charged tRNA for Trp?

You're right that if there was really a complete lack of Trp, then the cell wouldn't be able to make the enzymes. But the cell doesn't have to wait until [Trp] drops all the way to zero -- it can induce expression of the operon when the concentration gets sufficiently low (in practice there's some continous relationship between [Trp] and expression). Note that there's always going to be a little bit of Trp around as there are constantly proteins being degraded (and resynthesized).
But you're on to something -- in fact there is some bias towards lower usage of a particular amino acid in enzymes that are responsible for synthesizing that amino acid. Here's the paper: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1839009/ although the effect isn't that high for Tryptophan.


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Any good fish books out there?
I recently read "What a Fish Knows: The Inner Lives of Our Underwater Cousins" by Jonathan Balcombe. The first part was the best where the author explained how fish are very advanced creatures because they have been around a lot longer than other vetebrates.
Are there any other books out there similar to this one? There seem to be tons of bird research books. Of course, birds are relatively easier to study than fish. (Their size and ability to fly makes them difficult to track. But, at least they are not underwater and sometimes stay in one area for awhile. Fish are pretty much constantly on the move.)
I am not really looking for a text book unless you know of one that is interesting to read and not just a list of facts...unless a text book would be a good place to start.
I have read Colin Tudge's books on trees and birds. I wish he would write one on fish.

As a fisheries biologist these are what I would recommend to read.These are all science entertainment books(i.e., factual, but fun to read).The first 2 are more fish biology. The second  2 is more fisheries ecology.

Your Inner Fish: A Journey Into the 3.5-Billion-Year History of the human body.
Neil shubin
Demon Fish
Juliet Eilperin
Four Fish: The Future of the Last Wild Food
Paul Greenberg
Cod: A Biography Of The Fish That Changed The World
Mark kurlansky


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Is APB an antagonist of the mGluR6 receptor?
APB is a glutamate analogue specific to the mGluR6 receptor of ON retinal bipolar cells. It is used in research into receptive field processing by blocking the ON channel. Why is it not called an antagonist?

I have changed the title of this question to reflect its more restricted scope, corrected the spelling of glutamate — the poster should take the trouble to ensure the spelling of key molecules is correct — and changed "function" to "use in research". It is now in a suitable form for SE Biology, so that it is appropriate to vote the answer of @BryanKrause as correct.

Of interest
https://link.springer.com: "Are partial agonists antagonists? A key property of partial agonists is that they display both agonistic and antagonistic effects." With BryanKrause: "it's still an agonist". By definition,  any antagonist's intrinsic activity is zero". Agonists may be - partly - antagonistic. No other way round. Slightest effect will make it an agonist.

APB (2-Amino-4-phosphonobutyric acid) is a metabotropic glutamate receptor agonist, not an antagonist, and in many publications it is indeed referred to as an agonist, so I think your question is somewhat ill-posed. For example:
Yamashita, M., & Wassle, H. (1991). Responses of rod bipolar cells isolated from the rat retina to the glutamate agonist 2-amino-4-phosphonobutyric acid (APB). Journal of Neuroscience, 11(8), 2372-2382.
You can find many many more by searching "2-Amino-4-phosphonobutyric acid glutamate" on Google Scholar.
The reason that APB suppresses ON bipolar cells is because metabotropic glutamate receptors are often inhibitory rather than excitatory. Glutamate is typically thought of as excitatory because ionotropic glutamate receptors such as AMPA and NMDA receptors are non-specific cation channels that depolarize and therefore excite cells. Metabotropic glutamate receptors operate through g-protein second messenger cascades. In ON bipolar cells in particular, there are cation channels that are closed by mGluR6 activation, which therefore inhibits them.
Here's a review article that describes this as well as other basic information about bipolar cell function:
Euler, T., Haverkamp, S., Schubert, T., & Baden, T. (2014). Retinal bipolar cells: elementary building blocks of vision. Nature Reviews Neuroscience, 15(8), 507-519.

Thank you Bryan. As you can tell from my question I am an interested amateur! My source describes the molecule as an analog for glutamate but its function is to block the G protein coupled receptor and prevent any neurotransmitter action that would otherwise result in the closing of the sodium channels. So, in a sense, the analog is performing the role of an antagonist. This was my confused thinking anyway!

@adlibber No worries, interested amateurs are good targets for StackExchange sites. :) "My source describes the molecule as an analog for glutamate but its function is to block the G protein coupled receptor" -
Then your source is either wrong or they aren't actually using 2-Amino-4-phosphonobutyric acid but a different molecule. APB might prevent glutamate from binding the receptor if it is higher affinity than glutamate (not sure if it is but could be), but it's still activating the receptor like glutamate and is therefore an agonist, and it would cause the sodium channels to close.

OK so its an agonist. Thanks for taking me through it :-)


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Did you know that the fact of evolution is as well established as the fact that evolution is impotent?
We all know that evolution is a fact. Fact is a truth known by actual experience or observation. Evolution is defined by mutations, gene migration, natural selection and genetic drift. The first two create variation while the latter two sort variation, and this is something that we know by actual experience or observation.
But, we also know by actual experience or observation, that evolution can't create new genes. The biggest observation of evolution in action is Lenski's E.coli experiment. After more than 67.000 generations, which translated into human generations is equivalent to around one million years, this experiment resulted in 0 - zero new genes. Most of the changes in this experiment involved streamlining the genome, deleting genes no longer needed, or reducing protein expression. One of the changes involved something that proponents of evolution refers to as evidence for bacteria evolving a "key innovation" But, nothing structurally new evolved. After about 31,000 generations there was a mutational transfer of one pre-existing gene(citT) from one location to another which resulted in the ability of E.coli to grow on citrate under the oxygen-rich conditions.
How can we explain this fact of impotence of evolution? Well, quite simple. The total number of mutations in the history of life is estimated at 10^43, while the average E. coli gene size is 1000 bp which gives a library of 10^602 DNA seqeunces. Meaning, even with all evolutionary mutations spent, and with a functional landscape of size 10^100, still there is a 459 orders of magnitude lack of mutational resources to explore this library and find new functional landscapes.
So evolution is indeed a fact, but the fact is also that evolution can't create anything new that is useful.

I'm voting to close this question as off-topic because this is a polemic, not a question.

@Mario: What is your definition of "new gene"? One amino-acid residue substitution can dramatically change substrate specificity of the gene-encoded enzyme . . .

Is evolution a fact?
Let's start with a little bit of semantic.
In lay terms, it is easy and pleasant to just say it is a fact but the reality is that there is no fact in science discoveries. Hence, evolution is not a fact. Evolution is a theory in the scientific sense. In other words, evolution is a set of hypotheses that are extremely strongly supported by evidence.
Have a look at Is evolution a fact? for more info about this semantic.
Do gene duplication occur?
Your question is based on the false claim that gene duplication do not occur. This is simply wrong. There are thousands of evidence of gene duplication.
Evidence of gene duplication with neofunctionalization (that is the duplicated gene take a new function) are rarer but still very common. Consider for example

Qian and Zhang (2014) review evidences of gene duplication with neofunctionalization in the the Saccharomyces (yeast) genus only.
Beisswanger and Stephan (2007) as well as Calvo-Martin et al. (2017) review evidences of gene duplication with neofunctionalization in the the Drosophila (fly) genus only.

In fact, tandem duplications also occurred in the Lenski experiments (Blount et al. 2012)
Gene creation
There is a simple logical fallacy in your argument. When you say

After about 31,000 generations there was a mutational transfer of one pre-existing gene(citT) from one location to another which resulted in the ability of E.coli to grow on citrate under the oxygen-rich conditions.

The claim refers to a tandem duplication. Therefore, this claim seems to suggest that "gene creation" and "gene duplication" are different things. In fact, we never use the term "gene creation" in evolutionary biology. We talk about gene duplication and neofunctionalization. Neofunctionalization is the process by which a gene takes a new function, different from the ancestral gene before the duplication. But it is essentially the same thing. Gene rarely (if ever) come to existence all of sudden out of nothing with a single mutation. In general, gene duplicate and then slowly diverge, one gene taking a new function. This is how the number of genes (and the number of functional genes) can increase eventually through time.


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Calcium and nitric oxide: does a numerical relationship exist?
Currently, I am trying to understand how nitric oxide and calcium are related during the production of the former (I am not a biologist nor a chemist, so my knowledge about these topics is very poor). I would like to know if there are some papers or experiments that present a model (or, at least, some numerical data) that relate the concentration of nitric oxide with the concentration of calcium.
I've read somewhere that one of the effects of nitric oxide in synaptic transmission is the reduction of calcium influx, but how does it happen quantitatively? I've started my research considering the model reported here where NMDA is assumed to be main calcium source so that the time derivative of calcium concentration is directly related to the NMDA current. Now, I think this model should be slightly modified if I would consider the effects of nitric oxide; I've found a model that describes how nitric oxide synthesis occurs, but what is missing for me is the link between calcium concentration and nitric oxide concentration.

It seems that you want to have a look at neuronal nitric oxide synthases. Not an expert on this but there seem to be some references in this paper:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3514612/pdf/fncir-06-00082.pdf

@vkehayas Thank you for your reply. I will read the paper you cited hoping to understand something more about the topic. However, at first glance the paper explains detailly all the biological aspects of nNOS but I don't see how nitric oxide is related to calcium. I will check later.


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What exactly is a centimorgan?
Centimorgan's aren't physical distances. The analogy that I could come up with is if you had an array with 10 items,
A = [a, b, c, d, e, f ,g ,h ,i ,j, k]

The distance of a in the array is closer to b than k, ie A[0] is closer to A[1] than A[10] so that the centimorgan of A[0] and A[1] is less than A[0] and A[10]?

I personally like to talk in Morgan (M), instead of centiMorgan (cM), because the Morgan has a more intuitive meaning than one-hundredth of its value.
Morgan
If two loci are at distance 1M, it means the expected number of cross-over happening between these two loci is 1. If they are at 0.1M, then the expected number of crossover is 0.1. If they are at 1.4M, then the expected number of crossover is 1.4.
centiMorgan
As the typical distance of interest is much lower than the Morgan, we typically talk in centiMorgan.
Rate of recombination
If in a given meiosis, there is 0 crossover between two loci, then the two alleles from the same haplotype will end up in the same gamete. If there is 1 crossover, then the two alleles from the same haplotype end up in different gametes. If there are 2 crossovers between two loci, then the two alleles from the same haplotype will end up in the same gamete.
In short, if the number of crossovers between two loci (which expected value is the number of Morgans) is even, then the two alleles from the same haplotype will end up in the same gamete.
At very low Morgan (say 0.000001M), the probability of having an odd number of crossovers is low and the recombination rate is therefore low. As the number of Morgans increases, this probability of having an even number of crossover approaches 0.5. The recombination rate can therefore never be greater than 0.5.
Physical distance
Note that as the recombination rate per nucleotide varies throughout the genome (and among genders and among lineages), the distance in Morgan between two loci is not a simple function of their physical distance in number of nucleotides. The two are obviously correlated though.
Human genome
In the human genome, the average per nucleotide recombination rate is of the order $5\cdot 10^{-8}$ (Wang et al. 2012). This means that 1 cM is about 1.5 millions of nucleotides.
Highly Related posts
This question has actually been answered several times already. You'll find more information, some drawings and some math at the posts

Recombination frequencies
Genetic linkage greater than 50 centimorgans

For a more introductory post, have a look at

Why do we need two markers to measure a recombination rate?

1 centimorgan is equivalent to the percent recombination frequency for 2 genes during the crossing over step of meiosis. You can calculate it with
(number of recombinant offspring)/(total number of offspring) * 100%
and the result will be in cM (centimorgans).
If you have many offspring that are recombinant for the 2 genes, you can see that you'll get a high percent recombination and therefore linkage (not physical) distance. Since there are many recombinant offspring, it can be inferred that the 2 genes have a lower likelihood of translocating together, since they are likely to be physically distant.
In the case where you have very few offspring that are recombinant, you'll get a low percent recombination and linkage distance because 2 genes that are close together have a greater likelihood of being translocated together during crossing over.

This is actually wrong. You are confusing a distance in cM with a probability of recombining. They are not quite the same (also they are good approximation for closely linked loci). Please have a look at my answer or to  the two posts I linked at the end of my answer.

Oops, my mistake. Isn't looking at recombinant offspring a "good" metric for inferring probability of recombining, though?

Yes it is but it is not the issue here. The distance in cM is not equal to the probability (in percent) of recombination. It is approximatively equal for low distance but start to get widely different for higher distances.

The Morgan is a unit of how likely two traits will be conveyed together in offspring - also known as linkage.
Centimorgan's are not physical distances because the chromosome has specific variations in how well it crosses over when it recombines.
For instance in men and women there are more crossovers and this makes the genes appear to be further apart as they don't translate together in Meiosis...

The recombination frequency of two genes on the same chromosome is expressed in centimorgans (cM).
1% recombination frequency is a distance of 1 centimorgan (cM) on the gene map.
1 centimorgan roughly corresponds to one million base pairs of DNA.
The actual distance between two genes on a chromosome may vary, but this serves as a useful approximation to estimate the distance between two genes on a chromosome, in terms of the number of base pairs.

1% recombination frequency is a distance of 1 centimorgan (cM) on the gene map is wrong. It is a good approximation but is not correct. Please have a look at my answer for more info.


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brain and fingers movement theorie
I heard somewhere that when we want to do a repetitive movement of one finger (ex the index) . Our brain (in a very crude way) sends a first message to move all the fingers, and then a second message to hold the fingers that we don't want to move.
The person who said it, was explaining about brain evolution and the fact that the old reptilian part of our brain is the one that send the first message and the higher brain sends the second message.
So is that true ?
If so, do other parts of our brain work like that too? For example more complex behaviors, like sexual mate choice?

The body indeed uses lateral inhibition / surround inhibition. When using a muscle, neighbouring muscles are sometimes activated to. So active muscles are excited while nearby muscles are (partially) inhibited (Beck and Hallet 2011)
This surround inhibition is true for fingers (Sohn and Hallet 2004).

It would be good if you could add a reference stating that indeed each finger is associated with a single 'independent' homonculus.

Thanks for the comment @Remi.b . I went on google and found new information stating that the finger theory might be true. Will update my post..

@tocka This is an entirely different question. You might want to keep it for a different post. Don't forget that you will need to provide reference for the claims on which your question will be based and to make sure to correctly define the behaviours of interest.