text:
Do men and women have the same number of genes?
As far as I know, humans have 23 pairs of chromosomes, each one which contains a particular amount of genes. But in the "last" pair, men have a XY pair chromosome, and women have a XX pair chromosome. Does the missing "leg" of the XY pair make men to have fewer genes than women, and if so, how many genes do each sex have?

No a larger size human will have more genes:)

It is true that the Y chromosome is shorter than the X chromosome and that there are more genes on the X chromosome.

Do men have fewer genes?

One could (mis)understand three things in the expression "number of genes".

Number of gene copies (see Copy Number Variation)
Number of genes
Number of alleles

Thanks to @GerardoFurtado for correcting my semantic in the comments.
1. Number of gene copies
From the statement that there are fewer genes on the Y chromosome, one can conclude that men have fewer genes copies than woman.
This is the intuition the OP seemed to have.
2. Number of genes
Men also have an X chromosome. So men have the standard genes present on the X chromosome (but they only have a single copy of it while women have two copies; btw you might be interested in dosage compensation).
Because women do not have a Y chromosome and because there are a number of genes on the Y chromosome that are not present on the X chromosome, men have genes that female don't have at all. Therefore women have fewer genes than men.
3. Number of alleles
There is not much reason to expect that one gender would be more heterozygote than the other at autosomes (=non sexual chromosomes). Some may hypothesize that women may have more heterozygosity than men if there is stronger selection among sperm than among ovules or things like that but let's not get down this complicated path.
One one hand women have more gene copies and therefore might experience more heterozygosity, one the other hand, men have more genes and would therefore eventually carry more alleles. I don't know which side wins!
Did you mean number of genes per cell or per individual?
So far I assumed you were interested about the number of genes (or gene copies) per cells but if you want to compare whole individuals than it is a different story!
Men are on average taller and therefore have more cells. Therefore if you compare the body-wide number of gene copies, women will have fewer gene copy on average (Thanks to @JM97 comment).

For what I've read online, it isnt very clear how many genes the human have? According to this , counting the case of a human with XY chromosome, a human would have 31185 genes. But is it reliable or an aproximation? And how many it would be for a human with XX? https://es.wikipedia.org/wiki/Genoma_humano

This is an entirely different question. You might want to post it on a separate post. But I can give you some hints here. I don't know a whole lot about the details of the human genome project but a big issue in counting the number of genes has to do with agreeing on what we call a gene. Estimates of protein-coding genes I am used to tend to be around 20k genes rather than 30k (See for example Church et al 2009 or Clamp et al. 2007).

Your wikipedia article does not cite any reference so I can't tell much about the meaning and validity of these results. The number they cite by the way is 32185 (not 31185). As a side note, I find the english wikipedia often more complete and more proof read than wikipedia in other languages (but I don't speak spanish and never go on the spanish wikipedia).

yes, it's true, english wikipedia is more reliable, but I just found that article there.

@Pablo I don't see where you got that number. The page you quoted mentions estimates of ~20500. It then shows 32185 as the sum in the table, so I suppose that's what you meant. However, there's no citation for that and it's considerably more than the currently accepted estimates so I wouldn't rely on it.

@yes, I was talking about the 32185 genes sum . And my question was meant for an individual cell, but it's interesting the data about men having more cells and therefore having more genes in the total count of copies of the body. Anyway, I'm still wondering how the number of genes in an individual cell compare if you take any definition of gene for the comparision. I suppose that data might be known and might be online somewhere

As @GerardoFurtado noted in his comment, males have more genes since there are genes unique to the Y chromosome, like SRY. Of course, the fact that males only have a single X chromosome means that males will only have a single allele of each gene encoded by the X chromosome, while females have two alleles for each gene they have.

Note : the number of genes evolves.
For who is interested and can understand french, heres a link speaking, in a short way, about that, and about the eventual disappearence of the y chromosom in human genom:
http://planet-vie.ens.fr/content/chromosome-y-humain
And a link about the inactivation of one of the X chromosom in women genom (corpuscle of Barr) :  http://www.snv.jussieu.fr/vie/dossiers/kx/kx.htm

@blacksun Shall we use the edit function and add this text to your other answer? I also requested the merge of both accounts into one - so you will can edit your own answer as well as having all your reputation in one account.

To Chris : in a certain way, this answer "number of genes evolves", is self sufficient, I think. But of course, the links I posted may disappear, and they are in french, sorry for that. If I find time for, I'll try to find english references, and sum up those references

To Tyto alba :I'm in fact the author of both answers ... I didn t participate for a while, because I lost the link to this subject, which I fall on working on very different things - and answering at first like on the very generalist forum I came from, thinking it was of same kind..

It might take a few hours until this happens, depending on when the community manager team has time for that.

To Chris - ok, thank you one more time ,no problem

If you are trying to call someone writing @username will ping them. Otherwise the person isn't notified.

@Tyto alba Thanks Tyto alba, I'll try to remember that in the future ^^

Note - this is a very simple way to present things, and don't have the ambition to be a biology thesis.
Men do not have fewer genes than women, but fewer allels (variations of a gene); the allels on the x-y chromosome pair are not necessarily the same on the x and on the y (for men) or second x (for women), but they are for a part of same kind - same gene. It's like if, for a part, the y chromosome was broken, missing a bar to be an x.
One example of this is daltonism, linked to the xy chromosome pair.
Let's say that the daltonism allel is a corrupted existing allel (a variation of a gene).
To be a daltonist, a woman must have the daltonism allel on both of his x chromosomes - the daltonism allel is not a dominant allel, and if there is one corrupted allel on one x chromosome, but a normal one on the other x, the woman won't be a daltonist.
But a man is a daltonist only if his X chromosome do have the "corrupted" allel, because of the missing part of the y chromosome (compared to an x one).
If a woman has both allels, one "good" and one "corrupted", she will transmit it or not to his child, depending on which X chromosome she will give to this child.
If the father is a daltonist, he won't transmit it to his child if this child is a boy (he gives him his y chromosome genes and allels, not the x ones, and the boy takes an x from the mother, so he is xy).
But if his child is a girl, the father will transmit it to her (the girl take an x from the two of his mother and the only x from the father, so she is xx)
So, a child, to be a daltonist, must have at least a daltonist allel from his mother, no matter if the woman was daltonist or not (one x allel only corrupted or both).
Then, if this child is a girl, and is daltonist, it implies his father was daltonist too.
If it's a boy, no matter if the father is daltonist or not, he will be a daltonist as soon as his mother transmitted him a corrupted allel.
If the father is a daltonist, and if the mother has no daltonism allel at all, he will although transmit the allel to his daughters, who, while not being daltonists, will be able to transmit it to their own child.
 In the same case (father daltonist, mother with no daltonism allel at all), if the child is a boy, he won't be a daltonist and won't be able to transmit it to his own child, etc, etc.
Remember, this is a simple way to present things, and do not pretend to be at the top of today's science vision, and even more not  the truth - above the fact I'm not a biology specialist, every scientific that deserves this name won't ever be claimed to say the truth, something reserved for religions - and that's why science and knowledge,  in general as well as for each people in the same spirit state, progresses ...
Last word, concerning the numbers of genes, according to Wikipedia - but you know that Wikipedia is not always the best source ;) - a human male has an estimated amount of 21 000 genes, and a woman, something between 0 and 50 fewer genes (800 genes on the x chromosome, 50 on the y one, but some of these are commons to both. How many, I don't know ...).
Sorry for the multiple edits, I try to give my 2 cents on this question after 2 days and a night without sleeping

can you add some references to your answer?

I'm a french guy, the references I took to check my knwoledge are in french ... Maybe, you can take a look at wikipedia with the words "color blindness", 'genetics' passage, and with the word "chromosome", 'human chromosome' passage, for a first approach

Note - I edited my answer, first speaking about eyes color, to explain the principles, bu t eyes colors genes are not on the 23rd pair of chromosome. I took so the daltonism, color blindness, but this exemple is still not perfect, just a simplifaction, as it seems that daltonism may comes from a gene mutation too, and his not only inherited ...
But the principle for the inherited part is the good one, and illustrate enough, I think, the  xy and number of genes discussion. Even if in fact, there is more complexity ...

As @GerardoFurtado noted in his comment, dominance applies to alleles, not genes. There's no such thing as "daltonism gene".

To Chris : I will edit it
To Dimitry: right, that's what i called "kind of gene" and "genes" to simplify, the "kind" being in fact a gene, and the "gene" being an allel .
I did proceed this way because number of people make the confusion.
And I dont want to make here a biology thesis - and I m not able to ;)
I dont want to make a biology thesis, and am not able to. But I can modify my comment i

As Remi.b said, there are different definitions of what a gene is. I found some more sources, if I understand correctly, according to the table in this wikipedia article with Data source of Ensembl genome browser release 87 https://en.wikipedia.org/wiki/Human_genome, a male human would have 14600 "pseudogenes" and a female human would have 14800 "pseudogenes" in each cell, and according this another table https://en.wikipedia.org/wiki/Chromosome#cite_note-26 , a male human would have 21000 genes and a female woman would have 21750 genes in each cell

Pablo, in fact there is no contradiction, first link speaks about 20 000 genes.
But in those genes, there are some which are not activated, called pseudogenes...

I would add your comment to my post, but since I'm not very familiar with all of this, I might slightly or moderately missunderstand you, so may be you want to add this comment to your post, and make a reference to mine stating that there isnt a contradiction in both lists. If some of them are pseudogenes because they arent activated, why in the table they only have an entry for "pseudogenes" (and not for those which are activated and which would be called simply genes?)


text:
Can you tell if a corpse was male or female by only examining its skull?
There are articles that says women have more rounded corner faces than men, than women noses are usually shorter, etc.
But are those (and other features) tendencies or deterministic features that makes you really able to tell if a corpse was male or female, by only examining its skull?

According to textbook of forensic medicine and toxicology by Ks Narayan reddy:
Qualitative differences are:

Male mandible has everted ramus, but female have inverted ramus.
Males have chin U shaped, but it's rounded in females

Quantitative differences:

Suparaorbital ridges are prominent in males but often absent in females.
Mastoid process is wider, longer and blunt in males but is narrow and pointed in females.

And there are many more differences, see the pics below:

Gautam Biswas says you can be 92% sure only via skull.

Please give a reference for this table ("Gautam Biswas" is not sufficient)

source: Stack Exchange

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text:
Are there species which is debatable if they should be classified as animals or plants?
I'm watching a sci fi series and a character who is a biologist claims "even on Earth there are species which is debatable if they should be classified as animals or plants". I looked for examples of this and I couldnt find any. Is this true? Are there species which is debatable if they should be classified as animals or plants?

No, there are no such debates. Plants and animals diverged over a billion years ago. Animals are defined by the unique molecules that are secreted by the cells, and fill the intercellular matrix, like collagen. Plants have unique cell walls, chlorophylls a and b, and plastids. The unique characteristics of plants are given here: http://www.bio.miami.edu/dana/160/160S10_10.html
Although there may be animals like sponges that don't seem to move around a lot, or corals that have symbiotic relationships with algae, simply "behaving like a plant" does not make them plants. Similarly, there are plants that move and trap insects. But taxonomists would never confuse them with animals.

According to this, the Orobanche fasciculata belongs to the Plantae kingdom but it doesnt have  chlorophyll https://en.wikipedia.org/wiki/Orobanche_fasciculata. So what we have left is cell walls and plastids for all plants, right?

Its a plant. Snakes don't have legs, but are still considered "Tetrapods". Loss of characters, such as chlorophyll in derived lineages simply means that their ancestors had chlorophyll, and then lost it. Loss characters can confuse taxonomists, but do not change taxonomy.

"(Lost) characters can confuse taxonomists, but do not change taxonomy" - this is an excellent quote.

To add, modern taxonomy relies on genetics and not morphological/phenotypic characteristics. There are unicellular organisms like euglena that can photosynthesize but they are not plants (they are not animals either).

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text:
Is there a measure of human genetic variation, where human genetic variation can differ more than 1%?
According to this
Neardenthal genetics

The proportion of Neanderthal-inherited genetic material is about 1 to
  4 percent[12] [later refined to 1.5 to 2.1 percent[11]] and is found
  in all non-African populations

And according to this
Interbreeding between archaic and modern humans

Neanderthal-derived ancestry is absent from most modern populations in
  sub-Saharan Africa

Now, human genetic variation is usually said to be between 0,1% to 0,5%
Genetics

While the genetic difference between individual humans today is
  minuscule – about 0.1%, on average

Why are the genomes of humans 99,5% the same

Human's DNA sequence is said to be roughly 99.5% equal

But here,
Human genetic variation
There are at least 6 different ways to measure human genetic variation and

human-to-human genetic variation is estimated to be at least 0.5%

Does this last affirmation and the first two articles tell us that the difference in human genetic variation, according to some measures of variation, it's actually more than 1% ? (larger than some ways to measure our genetical differences with other animals like chimps for example that are usually mentioned to highlight our similatiries) Or are there things missinterpreted in all this?

The question makes it clear that the poster is aware of the different ways of estimating human genetic variation, and he is also no doubt aware of the fact that Wikipedia is written by “people like you” who may not be experts in the field or have updated an old entry based on limited data. Let me address what appears to be the cause of confusion in this question — certainly in other questions on this topic.
For simplicity let us take a suitable round number for the Human/Neanderthal relatedness. Then the poster’s first quotation can be simplified as:

The proportion of Neanderthal-inherited genetic material in modern Europeans is 2%.

and his second quotation simplified as:

Neanderthal-inherited genetic material is absent from modern Africans.

A common conclusion drawn from this is:

The genetic variation between modern Europeans and Africans must therefore
  exceed 2%, rather than being only ca. 0.5%.

Why is this wrong?
This conclusion is wrong because the 2% and 0.5% are measures of different things.
For simplicity, a value of human genetic variation of 0.5% can be regarded as the extent by which the DNA of the coding regions of the genes of two humans differ because of single nucleotide polymorphisms (SNPs) — single base changes in the same gene (that may or may not affect the gene function). This assumes all humans have the same 20,000 or so genes.
Now let us make an overall comparison of the genes of humans and Neanderthals. Since they diverged from a common ancestor their genomes underwent changes due to point mutations, but, as far as I am aware, they maintained the same set of genes. Even if I am wrong on this latter point, the vast majority of genes — and the ones that we are concerned with are common: they both have/had a gene for myosin, for hexokinase 1, for chymotrypsin etc.
Examination of the majority of such homologous genes reveals single base differences, which must have arisen since the divergence. A combination of such Neanderthal variants in one gene — never seen as human SNPs — and the converse situation allow one to designate a chymotrypsin gene, for example, as human or Neanderthal, even though the overall DNA sequence of the chymotrypsin gene may be 95% identical (to conjure a figure out of the air).
Now consider the European/Neanderthal comparison. It turns out that a small number of genes show no (or almost no) variation between the two, but that most of these show the standard ca. 95% difference between Africans and Neanderthals (and hence between Africans and Europeans). These, then, are the 2% of genes that arose from interbreeding of Europeans and Neanderthals, after the exodus from Africa.
But 2% of genes of different origin which still retain 95% sequence identity would only add 0.1% to the modern human variation, cited at ca. 0.5%.
Disclaimer
I do not know the actual extent of variation between most human and Neanderthal genes or the details of the non-African genes of Neanderthal origin. I will be happy to edit this answer if anyone has that detail. I apologize for the geographical generalizations not present in the question, but my concern was to convey the argument without burdening it with continued qualifications.


text:
How can there not be purpose movement in the fetus until week 18, when a fetus can open its mouth and suck its fingers at week 11?
According to Fetal Movement

According to an overview produced by the Royal College of Physicians
  of Edinburgh, purposive movement begins at about 18 weeks, gradually
  replacing reflex movements

but in the same article says

At week 11, the fetus can open its mouth and suck its fingers; at week
  12, it begins to swallow amniotic fluid.

I highly doubt that open a mouth and suck its fingers can be classified as "reflex movements", then how it is asserted that there is not purpose movement in the fetus until week 18 when a fetus can open its mouth and suck its fingers at week 11?

Why do you doubt that finger-sucking is a reflex?

Did you ever put a finger in an infant's mouth :) It's about as reflexive as it can be. +1 for a well researched question though

Swallowing (Nishino, 2013) and sucking (rooting reflex) are reflexes. The fingers may just happen to be in the vicinity of its oral region (they often are; Fig. 1.), and oh boy are babies keen to grab a nipple when it's close! Mouth openings can henceforth be also reflexive, being part of the rooting reflex.

Fig. 1. Fetal hands in facial area. sourceL: ABC News
Reference
- Nishino, Front Physiol (2012); 3: 4892013


text:
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

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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text:
What are limitations of giving birth to a baby from a frozen embryo?
Recently the story of a woman giving birth to baby girl from an embryo frozen 24 years ago hit the news. After an in vitro fertilization the embryo was frozen on 14 October 1992(
Article in the Guardian)
So I wonder about the limitations concerning freezing embryos. Especially the following questions came to my mind:

How much time after the embryo has been fertilized has passed before
he was frozen?
How much more time after fertilization could pass before the embryo
has to be frozen?

There are a lot of questions here. Can you narrow things down some?

As suggested by @kmm I deleted two questions.


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Are all emerging viral diseases of the past 100 years zoonoses?
From my basic understanding: The viruses causing Ebola, Sars and Covid-19 are all the result of a zoonosis, meanings that the viruses have passed from animals to humans.
So my question is: Are all recently (let's say 100 years) emerged viral diseases, with potential for a global epidemic, the result of a zoonosis?

At least a lot of them. I don't like linking to Wikipedia for such matters, but they have a nice list of sybtypes of Influenza A that should give you an example of how many variations you can have on the same base. From H1N1 to H5N1 and beyond, some of those variations were endemic, some caused pandemics. Some of those that stayed endemic had the potential to become pandemic.

In general, viruses don't profit much from their host dying or becoming too ill to infect others. Viruses that "rely" on humans to procreate are often not lethal - the lethal variants of the virus have a lower propensity to spread, so the less lethal ones are "fitter". Zoonoses have not been culled to be less lethal to humans, and are often much worse for us. We are "dead-end hosts" to them, We are best killed off so the viruses can spread to the preferred host, in laymans terms. Fortunately, we have murdered most mammals larger than us, so we are safer now than before.

@StianYttervik, this is a somewhat naive/narrow view of virulence evolution. Smallpox circulated in the human population for many thousands of years with a case fatality rate of 30% ...

@BenBolker There are certainly exeptions, I am making a general case. And, afaik (and googled right now) smallpox was a zoonoses, and thus is not a contrary observation. It's lethality was supported because it had an alternate (preferred host).

Basically everything is a zoonosis at some point. I'm not aware that smallpox had a reservoir host: what was it? https://biology.stackexchange.com/questions/90636/is-covid-19-claimed-to-get-less-deadly-over-time-if-so-why/90672#90672 gives starting points for the modern literature on evolution of virulence ...

@StianYttervik: How would killing off humans help a virus spread back to (e.g.) bats? (And, given that evolution isn't intelligent/directed, how would the virus "know" this?)

@ruakh That was a bit of hyperbole, the virus certainly does not know this, neither does a mass of single cell pathogens have any desire or capability of making strategy. The point is that evolution tends to favor the pathogens that multiply, and being too deadly is not a favorable trait. Zoonoses on the other hand have other hosts (bats and rodents for instance) and strain as such is not limited much by being absolutely lethal to humans.

@BenBolker Rodents, I read. But I and a googled result might of course be in the wrong - I am merely an interested chemist - not a virologist.

@StianYttervik: Re: "The point is": Well, no, you made two points: (1) that human pathogens are better off being less deadly, and (2) that zoonoses are better off being more deadly. I'm only objecting to #2. It sounds like you're now retracting your second point (or at least, not interested in supporting it)? If so, then we no longer have any disagreement.

@Ruakh if (2) is how you interpret it, then yes. It's lethality is higher, but only because that lethality is no longer an important evolutionary stress.

To my knowledge, yes. A partial list of recently emerged/emerging viral diseases (I certainly could have missed some), with probable reservoir hosts:

Chikungunya* (birds, rodents)
coronaviruses/sarbecoviruses (SARS [bats], MERS [camels], COVID-19 [?? bats ?? pangolins ??])
Ebola and other filoviruses (Marburg): (bats?)
Hantavirus (rodents)
Hendra, Nipah (bats)
Ross river virus* (various mammals)
HIV (primates)
influenza (H1N1, avian) (birds/pigs)
Lassa fever (rats)
Mpox (formerly monkeypox: monkeys, rodents)
West Nile virus* (birds)
Zika* (? "a wide range of animals in West Africa")

Starred examples are vector-borne (so perhaps of slightly lower concern - might not fit your criterion of "capable of causing a global pandemic").
Omitted:

older zoonotic viruses (rabies, dengue, hepatitis, ...)
non-viral zoonoses (malaria, plague, anthrax, tularemia)

A list of zoonoses; another from US CDC
More generally, the only other place an emerging virus could come from would be from mutation or recombination of existing human viruses. I'm not aware of such an example.

Corrections and additions welcome (I could make this community-wiki)

there are human viruses, it is just a virus that evolves with humans is not going to be that destructive, killing your host is always a bad idea and viruses evolve away from it. https://www.ncbi.nlm.nih.gov/pubmed/14666532

@John evolving away from destructiveness includes cases where a virus evolved into something destructive anyway, but died out along with the population segment that was affected by it. So while destructiveness doesn't persist, there's always the possibility of a short-lived outbreak.

Should the hepatitis family be added to the list?

In the case of monkeypox, there was a 2003 outbreak traced to pet prairie dogs, who were themselves infected by African rodents (two African giant pouched rats, nine dormice, and three rope squirrels were found to be infected), suggesting rodents are a likely reservoir.

@Mast: are there recently emerged strains of hepatitis? A very quick search suggested that at least hepB https://elifesciences.org/articles/36709 and hepC https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0153761 are pretty old.  Pointers to papers on emergence in the last century?

In theory could a virus cross over from plants?

to the would-be editor: mosquitos are the vector of Zika, not its reservoir/original animal host

Tularemia is bacterial, not viral.

thank you .....

Hepatitis D emerged in the past 100 years, without being a zoonosis
Hepatitis D is a virus which is able to replicate only in the presence of a hepatitis B co-infection.  It causes the same symptoms as the hepatitis B virus, but with greater severity and lethality.  In developed countries, it is rare except among intravenous drug users.
It was discovered in 1977, although epidemics of Lábrea fever in the 1950s were later determined to be caused by the virus.  Comparisons of known strains and the mutation rate suggest a common ancestor around the year 1930.
Hepatitis D is the smallest known animal virus (less than 1700 nucleotides), and is the only species in the Deltavirus genus.  There is no known animal reservoir.  The most similar known animal virus shares only 32% of the nucleotides of hepatitis D.
According to its Wikipedia page,

It has been proposed that HDV may have originated from a class of plant pathogens called viroids, which are much smaller than viruses.

Even if indeed this virus originated in plants, is it really true that humans were the initial animal target? That seems exceedingly unlikely, and there are other similar viruses that infect other animals as well.


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Could an exposure to a small amount of viruses result in an easier course of the disease?
According to Gunther Hartmann (Professor of Clinical Chemistry and Pharmacology at the University of Bonn) cited in this article (Süddeutsche Zeitung, in German)

Die Zahl der Erreger hat bei Erstinfektionen Einfluss auf den Schweregrad der Erkrankung.

My translation:

The number of pathogens during the initial infection affects the severity of the disease.

Leaving ethics aside I was wondering about the following:

Might it be an option to get infected by only a tiny amount, suffer only light symptoms and reach immunity (similar to a vaccination but probably more risky)?
Does the transmission path also affect the severity of the disease(inhaled vs. infected vs...)?

Edit: As Chris pointed out in his comment there is not enough research for Covid-19 yet so I would be also interested in findings from other viral infections.

Simple answer: We don't know yet as this disease is too new and we haven't done enough research on it.

@Chris Thanks for the comment, I edited the question.

SE Biology is a question and answer site — not a discussion site — about the mechanisms of biological processes. Questions are generally answered by people with biological rather than those with medical or epidemiological expertise, who are more likely to be on SE Medical Sciences. Your question asks for subjective views on factors affecting the disease. Such questions are off-topic here. I draw your attention to a list of reputable sources for information about the pandemic on Meta.

@Chris In mice the severity is always dose-dependent (for short acting viruses), thus... Also I would mention Rotaredom answer is about the viral load found 1 week after the infection, it is related but not directly. And the viral load in the lungs is of course correlated with the (lack of) pneumonia and its severity https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30113-4/fulltext#fig1 https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30232-2/fulltext https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(20)30196-1/fulltext#figures

I think the answer to your question is actually found in the paragraph surrounding the quoted statement:

Auch Gunther Hartmann, Professor für Klinische Chemie und Pharmakologie an der Universität Bonn, berichtete, nach ersten vorsichtigen Einschätzungen sei davon auszugehen, dass der Schweregrad der Erkrankung über Hygienemaßnahmen reduziert werden könnte. "Die Zahl der Erreger hat bei Erstinfektionen Einfluss auf den Schweregrad der Erkrankung."

Approximate translation:

Gunther Hartmann, Professor of Clinical Chemistry and Pharmacology at the University of Bonn, also reported that, after initial careful assessments, it could be assumed that the severity of the disease could be reduced via hygiene measures. "The number of pathogens influences the severity of the disease in initial infections."

Notice that the language is not absolute but rather asumptive: "initial careful assessments," "It could be assumed," "could be reduced."  It's tentative language and suggests that research is ongoing.  Furthermore, if you search for that quote, you'll find that this is not published in peer-reviewed journals; it's simply a preliminary observation to encourage the public to limit intake of pathogens.
We already know that in some other cases the viral load affects the severity of symptoms. But we don't actually know that that's the case with COVID-19.  In fact, initial reports from Italy suggest that there is no statistical difference between viral loads between symptomatic and assymptomatic cases of COVID-19. So Chris's short answer is absolutely right; we don't know.  For all practical purposes, it's just as well to assume that it's the case, as it will lead to more hygeinic practices, but further research will be required to demonstrate that it is actually the case.


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Fossil record of previously thought extinct animals
I was watching this video from the Youtubers SciShow titled "7 Animals We Used to Think Were Extinct (But Aren't!)." Some of the extinct animals, were suspected to have gone extinct close to half a billion years ago, which leads me to believe that their fossils were obviously found in layers corresponding to those time periods and not in newer layers; however, since these animals are known to be still present today, I was wondering how it is possible that they do not have fossils in newer layers of the earth. Similarly, What caused the sudden stoppage of fossils?
I know very little about evolution, biology, and fossil records except from what is taught in high-school, and haven't taken a biology course in a few years, so if it is possible to get a simple answer that a biology ignorant person could understand I would greatly appreciate it! Thank you!
https://www.youtube.com/watch?v=e_TjrqWTV5s&t=187s

The formation of fossils is exceedingly rare. A number of unlikely events must all line up for us to find one. So there would be no reason to expect that we would find a fossil of anything but the most common and easily fossilized organisms. The probability of NOT finding a fossil is much greater than finding one.


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Insect Identification (badly damaged corpse)

The photo is of the insect in question in a strainer. The body of the insect is just over half an inch long. I see a separated wing cover and leg in the photo as well.
My location is New Hampshire, USA. Given that it is February (middle of winter), I don't think it was sourced locally.
I believe that this came from a packaged item that would have been sealed in San Diego, CA or possibly in Asheville, NC. The packaging likely occurred no earlier than June or July of last year. The packaging would have occurred indoors in a manufacturing-type setting.
After coming out of the packaging, this individual was submerged in liquid on a stir plate for 36 hours, so it took quite a beating.

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What determines the spiral direction of plants?
Some plants and vines spiral clockwise as they go along (right direction) and some spiral anticlockwise (left direction). What determines which direction they spiral along? At first, I believed it to be determined by which hemisphere you are in (influenced by the Coriolis Effect), and this result could be tested by finding spirals in both northern and southern hemispheres and comparing their directions. However, the very first spiral I found seemed to cripple that idea.

The spiral I found spirals first in the right direction, then suddenly decides to spiral in the left direction, and then further along in the right direction again. Since the Earth does not arbitrarily change its rotational direction, this phenomenon must be explained by some other explanation. The change in rotational direction seems to be abrupt, almost like a catastrophic event. A few that I thought of:
1: Arbitrary. The spiral seeks merely to latch onto something, and will try both directions to see if either work out.
2: The spiral is somehow influenced by the night day cycles. Since the spiral switches from right to left back to right having been subjected to two sudden changes, the only large changes I can think of is the day night cycle.
I live in Australia, by the way.

Relevant article: http://www.nasa.gov/vision/earth/livingthings/16jul_firemoss.html (moss grow in a spiral in microgravity conditions).

Is the rare change in direction of spiral possibly due to the weather conditions of a particular day? Such as a cloudy morning in spring with a sunny late afternoon? Or any weather conditions counter to the seasonal daily normal weather?
Just an un- researched, unstudied thought while trimming my Wisteria!

First of all, you assumption seems to be incorrect. Plants in same part of the world can twine in opposite directions.
Little seems to be known exactly. Gravity has nothing to do with plant's chirality (or "handedness") or spiraling:

How plants do this is still unknown. Darwin proposed that it was "autonomously induced." This came to be known as the internal oscillator theory. In the 1960's the gravitropic overshoot theory explained mathematically how circumnutation could spontaneously occur as a result of forces related to gravity and growth. Recent experiments on the Space Shuttle have demonstrated that gravity is not necessary for circumnutation.

Here is another link to a blog, but it does contain reference to original paper on observation of chirality. Main conclusion, taken from the abstract, is:

The predominance of right-handed helical growth in climbing plants cannot be explained by hypotheses attempting to link plant growth behaviour and global location. One alternative hypothesis for our findings is that the widespread phenomenon of anticlockwise twining arises as a function of microtubule orientation operating at a subcellular level.

To elaborate a little on that, remember that actin filaments as well as microtubules are all chiral polymers. That is, they form spiral structures with defined orientation. Even more, microtubules all start roughly from the nucleus away to membrane, so this might suggest cellular mechanism for preference toward twining chirality. However, this does not address your observation that given plant changes direction of growth twice.

This answer is outdated; The mechanism has been identified recently, and published in Science. See below for an answer from user42885 that provides the explanation.

Having had a self-sown pumpkin grow in my back yard I can tell you what happened with the tendril in your picture.
The tendril started growing straight, with a couple of branches. When one of the tendril branches touched something (looks like the middle one in your picture), the tip began to curl as it grew, in order to latch onto it. Shortly after, the previously straight section of tendril began to contract, and in the process, to curl.
Curling helps the contraction process hugely. For each rotation in one direction, another part of the tendril has to curl the other way, since both ends are now firmly attached to something (the ground and whatever the end touched). Note that going from the bottom, the tendril curls three times one way (labelled right), five times the other way (labelled left) then twice the first way again (labelled right). There are a total of five rotations in both directions.
It would be interesting to see if every tendril starts curling the same direction as every other one, so maybe you can check a few different ones to see if this is the case.
The entire process is touch sensitive. The tips of the tendril will grow in the direction of what they are touching, so I would guess that the chirality would be random, depending on the particulars of how the tendril was touching the other object. I have, however, seen the tips grow back on themselves, causing one layer in one direction and another layer on top in the other direction, so it seems environmental, not predetermined.
Here is a link to a time lapse film showing the process in motion.

The math seems to add up. Interesting explanation!

Very interesting observation. Would be interesting, whether it is consistent with the recent Science publication, referred to in the answer of user42885, that provided a mechanistic explanation for the century old problem.

tendril coiling occurs via asymmetric contraction of an internal fiber ribbon of specialized cells. Under tension, both extracted fiber ribbons and old tendrils exhibit twistless overwinding rather than unwinding, with an initially soft response followed by strong strain-stiffening at large extensions.

Source: Gerbode et al. 2012, Science, How the Cucumber Tendril Coils and Overwinds (link to scientific article) (link to press article)
PS: I was searching for an explanation to the twisting, and came across the above article before this one. What a wonderful world that we all observed this phenomenon, and that our curiosity was excited by the observation. Thank you for the article.

The best reading for the topic is "a comparison of chirality patterns of climbing plants in Peru and Brazil" from "assymetry in plants" which sais that:
The mechanical or physiological basis for dextral versus sinistral orientation of circumnutation among apically twining plants has not been determined, despite several papers on the topic in recent years ((Thitamadee et al. 2002, Kitazawa et al. 2005, Goriely and Neukirch 2006, Edwards et al. 2007, Mugnai et al. 2007, Edwards and Moles 2009, Isnard and Silk 2009, Stolarz 2009 Bastien and Meroz 2016, Smyth 2016). The majority of the data supporting a general hypothesis that twining is caused by microfibril orientation and their overlying microtubules is based on research on the roots and seedlings of mutant forms of Arabidopsis thaliana ...
Chapter 12 states that 80% of plants in brazil from 20 species have the same winding chirality.

So, this discussion began several years ago now. I recently decided to grow up, more than out, to conserve space. So, I've tried climbers more. When I had several different plants growing, I noticed they all climbed clockwise.
If the original author still lives in Australia,  I propose an experiment.
I live in the Northern Hemisphere,  just outside Vancouver, Canada. Australia and Canada have differing growing seasons. If we were to exchange seeds and observe the same seeds, from the same packages, and document their growth, it would rule out hemispheric affects.

We call this a common garden experiment

I have been told that the direction of twist should be clockwise as long as the growth is vertical. This would mean the tendrils going out horizontal could go either way but the twisting vines should be prodominately clockwise as they grow upward. Googling pictures of American Bittersweet vines provides a good example of this.
Tendrils that have twists in both directions are better suited to holding up under tension as they tend to be able to just untwist without kinking when pulled on. You might see this occur during high winds for example. What I am suggesting is that tendrils may be a special case as they have a unique fuction and often a non-vertical orientation.

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Meaning of "Domain with function to find" (FIIND)
From NALPs: a novel protein family involved in inflammation.

FIIND - Domain with Function to Find.

What is the meaning of this name? Does it mean "Domain with an unknown function"?
I'm translating an article in which this domain is mentioned, and I found three different translations of the term into Russian: "Domain with an unknown function", "Domain with a search function", "Domain with identification function".
I think the first translation is the most logical one, but I'm asking just in case, because I'm not an expert in this field.

The NALP subfamily. Finally, a large subfamily of the CATERPILLAR proteins is composed of 14 NALPs (also called PANs36 or PYPAFs37; FIG 2.) and is characterized by the presence of an amino-terminal PYD. This modular architecture is found in NALPs 2–14 (short NALPs), whereas NALP1 contains an additional domain — which our group has designated FIIND (function to find) — and a CARD, forming a carboxy-terminal extension. With two notable exceptions (NALP1 and NALP3), the NALP genes are located in two clusters on human chromosomes 11p15 (NALPs 6, 10 and 14) and 19q13.4 (NALPs 2, 4, 5, 7, 8, 9, 11, 12 and 13) (TABLE 1). Interestingly, the 11p15.5 region is an important IMPRINTED region and has been implicated in the imprinting disorder Beckwith-Wiedemann syndrome and in various human cancers, including Wilm's tumour38.

In my opinion it is broken English, presumably contorted in this way to provide an acronym.  To find out what the culprits intend it to mean you would need to read the paper. Dictionaries will not help.

I was pretty certain @David's comment was spot on, that this was some one-use funny acronym from just this paper, but a search of Google Scholar suggests that it has indeed been propagated sufficiently to have meaning beyond this paper, while also originating, as these things do, in some clumsy one-off usage.
One of them gives a clear definition that is consistent with what you supposed:

The acronym FIIND (domain with function to find) was coined several years ago to indicate a highly conserved protein region with unknown function[4]

D'Osualdo, A., Weichenberger, C. X., Wagner, R. N., Godzik, A., Wooley, J., & Reed, J. C. (2011). CARD8 and NLRP1 undergo autoproteolytic processing through a ZU5-like domain. PloS one, 6(11).
The paper they cite (reference 4 in the previous quote) is in fact this one:
Tschopp, J., Martinon, F., & Burns, K. (2003). NALPs: a novel protein family involved in inflammation. Nature reviews Molecular cell biology, 4(2), 95-104.
...which probably looks familiar since it is in fact the paper you started from. Importantly, though, this is not a generic term for a domain with unknown function, it's a specific domain which was known to be highly conserved (and since found in several other proteins) - it's just that it's specific function was at the time unknown.
This paper is a recent review of NLRP1 that may also be useful and has some discussions of what has been found of the functions of the FIIND:
Mitchell, P. S., Sandstrom, A., & Vance, R. E. (2019). The NLRP1 inflammasome: new mechanistic insights and unresolved mysteries. Current opinion in immunology, 60, 37-45.


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Why do patients with type 2 diabetes not show the body wasting seen in type 1 diabetics?
Type 1 diabetes results from the destruction of the cells in the pancreas that produce insulin, while type 2 diabetes is characterized by so-called "insulin resistance", presumably a reduced responsiveness of the body's tissues to the effect of insulin.  More succinctly, in type 1 diabetes, insulin is not produced at all, while in type 2 diabetes, insulin is produced, but it is ineffective.
Based on this description, one would expect that type 1 and type 2 diabetes would look similar, with maybe type 2 diabetes being a milder form of the condition.  This is not the case, however.  The diseases are markedly different, at least when it comes to their effect on body weight.
Type 1 diabetes results in wasting:

The images show a type 1 diabetes patient before and after insulin treatment.
In contrast, type 2 diabetes is associated with obesity, exactly the opposite scenario.
If the body does not respond to insulin in type 2 diabetes, why don't those afflicted waste away, in the way that (untreated) type 1 diabetes patients do?

Comments are not for extended discussion; this conversation has been moved to chat.

I have changed your title to reflect the content of your question. How obesity produces type 2 diabetes is a valid question — it could well be asked separately — but is not what you are asking.

The following is based on a conversation I had with a senior biochemist in my university who conducts grant-funded research on the relationship between diabetes and heart disease. It can be criticized for the paucity of external sources from which its veracity can be checked. However, although the question is based on a misconception I thought it should be addressed. Perhaps others could help improve the answer by supplying references etc.
The following points about Type 2 diabetes mellitus are relevant.

‘Type 2 diabetes’ refers to a disease which encompasses conditions
with a spectrum of severities.
This means that the description of it being “characterized by so-called ‘insulin resistance’” — alternatively expressed as cells being refractory to insulin — in fact means that there is a variation in the degree to which the cells are refractory. In many cases, although this leads to a higher blood sugar, it does not result in the complete breakdown of fat and muscle protein found in type 1 diabetes, where insulin is completely lacking.
Type 2 diabetes does not result in an increase in fat deposition and body weight. In many — but not all — cases it is caused by overweight.
In type 2 diabetes caused by overweight there is a gradual loss of fat. It is not apparent in a ‘snapshot’ of type 2 diabetics, many of whom have such large fat reserves that it will take a long time before these are broken down.
In severe type 2 diabetes the situation eventually becomes similar to type 1 diabetes as the beta cells of the pancreas can be destroyed. In these cases insulin injection is required.
Normally type 2 diabetes is controlled with drugs that reduce the glycemia — metaformin is currently the agent for the first line of treatment — and by lifestyle changes, especially in diet. (The treatment of type 2 diabetes was reviewed by Juan José Marín-Peñalver et al. in 2016 and considers their mechanisms of action etc..)

In starvation, the breakdown of both fat and protein starts at the same time as soon as glycogen stores are depleted (source - p.385). Why would an untreated person with diabetes 2 on isocaloric diet lose weight (fat or muscles)? Two important reasons for wasted appearance in diabetes 1 are 1) loss of glucose due to glycosuria and 2) dehydration due to polyuria triggered by glycosuria.

@Jan — OK. The fat reserves are usually completely depleted before the protein, but I will take the phrase (mine not my source's) out.

It is still a parallel process. Initially, more fat than muscle will be lost, but at the time when fat stores are depleted, there will be already some loss of muscle. But the question is why would a person with diabetes type 2 lose weight at all when on isocaloric diet?

@Jan — You will notice that I waited three weeks before answering this question because of extreme pressure of a project I am working on. I felt I should try to answer as I had said I would in a comment apparently transferred to chat. I am still interested in improving my answer and finding appropriate biochemical sources, but it will be a week or two before I have time to do more than add comments. (The answer to your point would seem to lie in the hormonal control of fat turnover. I had thought that this would be through glucagon, but my colleague thinks not.)

Type1 diabetes is an autoimmune disease where insulin producing cells are killed by the immune system. Many cells need insulin to be able to transport sugar from the blood. Without insulin they won't be able to use the blood sugar and people start to urinate sugar because of the high blood sugar levels. So the insulin levels will be low and the blood sugar levels will be high in type1 diabetes.
In the case of type2 diabetes the insulin production is not affected and cells cannot transport sugar fast enough, because they don't sense insulin properly. This results high insulin and high blood sugar levels. As the disease progresses, the insulin producing cells can die off and we can end up with a similar condition as we have in type1 diabetes.
Both have connections to weight. Insulin is a hormon that facilitates fat storage and fat conversion from sugar and it inhibits fat breakdown. So when insulin is low in type1 diabetes, then people have a hard time to gain weight. On the other hand insulin resistance is associated with obesity. So typically obese people suffer from type2 diabetes and they can lose weight as the disease progresses.

If the tissues are refractory to insulin, that includes the adipose tissue, so your statement that the increased concentration of insulin prevents them losing weight doesn’t make sense, and according to my source is untrue.

@David You are right, I tried to find a reference for it, but failed. Probably it is just an urban myth. I edited my answer.

@David If it is any truth in that high insulin + IR causes weight gain, then probably it has something to do with leptin. I don't have time to investigate this.


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How to map the N6-dimethyladenosine by primer extension?
I am trying to map N6-dimethyladenosine on rRNA using primer extension (low dNTPs assay) method. But i am not able to detect map my position. I went through some articles they mentioned like they hydrolysed the RNA but they did not mention exactly by which hydrolysis method (enzyme, alkaline). can you please help me?
Great. I used (10 g) of Total RNA for primer extension reaction with 100,000 cpm [- 32P]ATP-labeled oligonucleotide. After annealing at 55–60 °C for 15 min and chilling on ice for 2 min, 1 unit of reverse transcriptase (Expand RT, Roche) and 1 unit of RNase inhibitor were added and an extension reaction was performed at 42 °C for 90 min. The extension products were ethanol precipitated and analyzed on 6% polyacrylamide, 7 M urea gel. (DOI 10.1074/jbc.M308997200)
This method specialized for 2’o methylation on rRNA, my interest is N6-dimethyladenosine (M26-A). In the literature M26-A blocks the RT I did not get the extension. In this publication, they have mentioned the RNA was hydrolyzed but hydrolysis has many different types (alkaline, enzyme) (https://doi.org/10.1091/mbc.E15-02-0073)

It would be helpful if you could give more details of the method and your experimental strategy, together with the reference(s) to the method. Your question is quite specialized.


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Are polyploidal organisms parasatized by selfish genes? And if not, why not?
Certain prokaryotes are polyploids. For example, Thermus thermophilus has about five copies of its genome (http://jb.asm.org/content/192/20/5499.full). One extreme polyploid, Epulopiscium fishelsoni, has tens of thousands of copies of its genome (http://www.pnas.org/content/105/18/6730.full). (Some eukaryotes are polyploid as well.)
As each copy replicates separately it would seem likely that spontaneous mutations would arise and over time, and such an organism would become a hybrid of many distinct genomes coexisting in a single cell.  This seems like an ideal place for selfish copies to arise (though perhaps no more so than any other organism - I think I've read that even prokaryotes are prone to plasmid parasites).
So, does this happen?  If not, why not? Is there some copy-checking mechanism (some extremeophiles seem to have a DNA-repair mechanism) or some mechanism that inhibits reproduction by genomes that are (somehow) determined to not be contributing to the overall metabolism of the cell?

Do you have some basis for supposing that they don't? I agree with your premise, and every genome I've ever looked at is absolutely riddled with selfish elements (and thats just haploid organisms).
You only have to look at most replicons (plasmids etc) and they usually harbor a greater than average density of these types of element. Thus me agreeing with you that polyploidy likely invites it even further!
Also, what makes you think there is no copy checking mechanism nor DNA repair mechanisms 'supervising' the process?

Is there any reason you are talking about polyploidy in bacteria only? I don't know much about bacteria polyploidy. I typically doubt they recombine unlike most eukaryote polyploids.

Joe Healy: Edited question, thanks.  Remi B: bacteria/archea have the most extreme polyploidy, but one could generalize the question

In short, being haploid or polyploid should not protect you from Selfish Genetic Elements (SGES).
Almost all eukaryotes are polyploid. Plants are the oft-cited example. Wheat, I believe, is hexaploid for example. Polyploid bacteria are the exceptions typically (if we consider ploidy to be of the whole genome). However, even in truly haploid bacteria, the genome in any given cell is usually actively being replicated, so some of the genes are actually present more than once.
Regardless, replication and repair is an enormously well controlled and regulated process: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1479556/

SGEs can take many forms depending on your definition and are ubiquitous in nature as far as we can tell. Plasmids which harbour addiction factors, insertion elements, transposons, prophages etc are all technically SGEs. See here for a review:
https://www.ncbi.nlm.nih.gov/pubmed/21227262
I can't find any literature on SGEs in polyploidy directly, but it is well documented that bacteria harbour a considerable amount of selfish DNA - it seems likely that this will be the same if not worse in polyploidy. Plasmid detection is a difficult computational and experimental process (http://bioinformatics.oxfordjournals.org/content/early/2016/11/18/bioinformatics.btw651.full) but one of the hallmarks of plasmid sequences are typically addiction factors (a gene that the host cell must maintain in order to survive - usually an anti-toxin to neutralise a toxin present on a different DNA molecule) as well as phage genes.

To address a couple of things specifically:

As each copy replicates separately it would seem likely that spontaneous mutations would arise and over time

This is somewhat true, there is always minor variation in a population (else evolution wouldnt work!). Sometimes you'll find this is also the case in a single cell - but less often. All cells we have found so far have DNA replication and repair mechanisms - https://en.wikipedia.org/wiki/DNA_repair. The frequency of mutation in the genome is not directly linked to the amount of selfish elements though, making your second point contentious:

This seems like an ideal place for selfish copies to arise

I agree with the premise of polyploidy probably inviting more SGEs (thinking specifically of IS elements and transposons here really), but not because of mutation - rather, just because there are more DNA molecules and sites present for those elements to incorporate into.


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Do young children grow in spurts
It is a commonplace of my friends and relatives to remark that a young child (younger than 3 years) has had a recent "growth spurt". The underlying assumption is that young children do not grow taller continuously and steadily,  but have periods of rapid growth between periods of slow growth. But is that assumption true? I'm sceptical; I'm inclined to believe that growth is steady, and the idea of growth spurts is a flaw of perception.
So, what research have I done so far on this question? I've seen the height-age charts for children, and they are smooth, so there are no growth spurts synchronised across all children. But that smooth averaged growth could result from the average of many non smooth growth rates. So the question is about when considering a single child. A web search about children's growth spurts shows numerous parenting web-sites that assume that growth-spurts happen, without asking whether growth spurts actually happen. I found an old press release from Emory University about some research supporting the idea, but no better information.

What research have you done to answer this yourself? The Biology.SE community has agreed that questions that show little or no prior research effort are off-topic on this site unless you have shown your attempt at an answer. Please [edit] your question and tell us where you've looked for answers, what you do know about the topic, and where exactly you still have questions. Unresearched questions may be subject to down-voting and closure.

@MattDMo The community might have so agreed, but the Help Center information about what is on topic does not say so. The Help Center does say that doing research is part of asking a good question.

@MattDMo I didn't find any Bilogy Meta posts that support your assertion that the the "community has agreed that questions that show little or not prior research effort are off topic". And in fact I did mention some research, of sorts: the content of height-charts for children. I have now amended my question with the, near useless, results of a Web search.

I have to agree with @MattDMo - there needs to be some sort of research on the question being asked or else you get (1) exceedingly vague questions that are unanswerable or (2) questions that are so basic that they are easily answered by looking at a Wikipedia page or some other basic website. If the person asking the question wants someone in the community to take time to write a thoughtful answer, I think we should expect the question asker to do the same.

@Raedwald you found right in the help center where it says you need to research your question beforehand and tell us what you know, so I don't understand why you're making such a big deal out of this. You've been part of the SO/SE system long enough that you should know that you need to try and help yourself before seeking the help of others.

Growth is neither even nor constant, It can vary quite a bit from month to month as hormone levels change, the growth curves you are seeing are a rough average.
You are having a hard time finding anything because it one of those pieces of knowledge that is so old people only rarely research it directly focusing more on deviations from it and you will likely only find good reference to it in textbooks. For a layman this means searches based on the terms you think you should use never find what you want, something as simple as adding the word "textbook" can make a huge difference. Google scholar will also help.
http://adc.bmj.com/content/51/3/170.short
https://books.google.com/books?id=YA-LdtyHJ9QC&pg=PA226&dq=evolution+of+the+growth+spurt&hl=en&sa=X&ved=0ahUKEwjkl4zCztjRAhVB74MKHRiuB7kQ6AEIHzAA#v=onepage&q&f=false


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Ligaments at the posterior superior iliac spine
In Causes of Back Dimples, it was determined that these 'Dimples of Venus' are created by

a short ligament stretching between the posterior superior iliac spine and the skin. They are thought to be genetic. (@Johnny)

The linked article in the answer to my original question says nothing more other than the fact that dimples of venus are normal dimples (not medically significant).
DrLumbago.com states:

The sacroiliac joints move together as a single unit.  From the back it is common to see a pair of dimples on the buttock near the base of the spine.  These are sometimes called the “dimples of Venus” and they are a landmark for the top portion of the sacroiliac joints.

Posterior superior iliac spine (PSIS) marked in red

Image made by DBCLS (Polygondata is from BodyParts3D) CC BY-SA 2.1 jp, via Wikimedia Commons
Ligaments of the PSIS
Cooperstein & Hickey (2016) has an image of ligaments connected to the PSIS, but unless I am mistaken, the image doesn't seem to have the ligament(s) involved with the dimples of venus.
It seems from the description in Kumar, et al. (2014) that the "dimples of venus ligament(s)" are connected to the skin, and seeing that ligaments are fibrous connective tissues that normally connect bones to other bones, I am intrigued to know more.  What is the name of these "dimple of venus ligaments" and what is their purpose?
References
Cooperstein, R., & Hickey, M. (2016). The reliability of palpating the posterior superior iliac spine: a systematic review. The Journal of the Canadian Chiropractic Association, 60(1), 36.PMCID: PMC4807681
Kumar, A., Kanojia, R. K., & Saili, A. (2014). Skin dimples. International journal of dermatology, 53(7), 789-797. DOI: 10.1111/ijd.12376

It seems from the description in Kumar, et al. (2014) that the "dimples of venus ligament(s)" are connected to the skin, and seeing that ligaments are fibrous connective tissues that normally connect bones to other bones, I am intrigued to know more. What is the name of these "dimple of venus ligaments" and what is their purpose?

First, re: what a ligament is, you're correct in your understanding that ligaments generally bind bones to bones (vs. tendons), but the term is used more broadly as connective tissue that binds things together, holds them in place, is a remnant of a fetal structure, or a mesenteric fold. Your wikipedia link acknowledges this. Some examples are:

Round ligament of the liver: a remnant of fetal structure
Broad ligament of the uterus: a mesenteric fold
Median arcuate ligament: this one actually binds two muscles together
Sternopericardial ligament: binds the pericardium to the sternum

The unnamed short ligaments Kumar describes (and wikipedia, quora, and stack exchange have repeated), are probably unnamed because they are difficult to isolate and study, and they are not clinically relevant. They may even be theoretical. There are no studies on them indexed in medline, and they aren't discussed in any anatomy text I've read. Dimples are generally thought to be caused by fibrous connections between the skin and muscle, bone, or other deep tissue. If you ever cut into the back of a cadaver or surgical patient, you'll see that there are a great number of unnamed fibrous connections to the skin. It's not unreasonable for Kumar to invoke them as the cause for these dimples.


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Why there is such low diversity of higher plants in sea?
I think it could be because of mycorrhiza or maybe because of the problem with flowering and seeds.
But really, I don't know.
edit:
by higher plants I meant Embryophytes

Welcome to Biology.SE. The concept of higher / more evolved lineages is undefined. You should probably just name what lineage you call "higher plants". Maybe you meant Angiosperm or Embryophytes, ...?


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How can we define complexity in the context of biology?
Can somebody provide a definition of complexity in the context of biology?
Is it something of a personal opinion on the side of the user to decide precisely what s/he means by using the word complexity or is there something all biologists can agree upon? Is there any "standard" for the use of the term complexity or is such standard simply unattainable in our current level of knowledge and/or understanding of the living world?
To the moderator-I want to know What is complexity in biology?  in GENERAL, not only in the specific example of measuring it for an individual. One can argue complexity can be used to compare and even to "cast a vote" about the superiority or inferiority of many objects of study in biology, not just individual organisms. What about the complexity of an ecosystem, of a particular organ, of the interactions of macromolecules and so on. Are they not legitimate instances when the term complexity can be used without inferring to its meaning? This is the purpose of my question, not to merely measure the complexity of an individual. This is why I don't think it's duplicate of the question you mentioned. How is my reply?

Totally subjective. Just like saying in a paper that X was very Y (Y being big, small, long, complex etc)

So, there isn't anything like some biological "standard" for complexity. Is it what you're saying?

Biology is a broad subject. You probably need to be more specific for useful answers. What subjects of biology are you interested in? In loose terms, relative complexity is often used (something is more complex than something else), but clear definitions (where there are any) are likely to be sub-field dependent.

Biology is a rabbit hole that only gets deeper. Real complexity is falling further than anyone else ever has and trying to see an end in sight. You can also construe this as insanity, but to each their own.

@RozennKeribin To me, this question seems broader, so I don't think it is a duplicate (it might be too broad though).

As I mentioned above, I think you need to narrow down the answer set. Otherwise the question is too broad/vague. Complexity is just a word, and it is used differently in different areas of biology. Therefore, there doesn't exist a single definition, and a question such as "What is complexity in biology?" is too broad to be covered in the SE-format.

I don't think this question is a duplicate, but the answer seems trivial: there isn't a single definition of complexity.

I think marking this as a duplicate is the best solution - although the question here is more broad than the question there, I think the accepted answer to that question is 100% applicable to this one, and I don't think it is possible to come up with a better answer. That answer makes clear why having a definition for complexity is important, explains how the answers you get will completely depend on that definition, and gives some examples for the OP to consider when possibly reformulating the question.

I had to once again edit the question to satisfy you. Are you going to accept it now?

Oh, come on, what would it take you to accept a good question about complexity in biology?


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Is cell-free Life possible?
I think most of the people on this site know about the famous Baltimore paper describing the ability of the poliovirus to replicate itself without the need of cells but I want to expand on the issue and ask could it be possible to have truly "cell-free" Life-e.g. life forms that do not have cells in any form according to modern biology but yet can be considered "alive" by its standards? This is the first paper in historical context describing the possibility of creating a self-replicating molecule in the laboratory. Well, it's about a viral genome and it only can self-replicate so it's not like it's alive according to what we consider "true" living organism, but nevertheless it triggers an interesting chain of assumptions in my mind. What if we could design a system where nucleic acid can evolve outside of cells? Then, what if we managed to provide an energy source t drive this evolution outside of the context of cells? Would such nucleic acid evolving on its own in a test tube depending only on the energy source we provide and on the specific conditions in the test tube be considered equal to a gene evolving in a "true" living organism? What if then we managed to add more nucleic acid's molecules to the system, just enough to have all the components involved in the replication of the evolving nucleic acid molecules synthesized by the system itself? Then can we consider this system analogous to a living organism, e.g. truly alive? What if we continued adding nucleic acid molecules to the system to the point when it was able to produce ATP from organic molecules used by what we commonly consider to be "alive", e.g. entities we prescribe the name living organisms, like glucose, for example. Then what would be the difference between this chemical reaction system and a genuine living organism? What if we continued building up this "in vitro metabolism" to the point when we have a genuine "molecule laboratory" testing the fitness of new nucleic acid molecules to itself. A true evolving, replicating and self-organizing molecular "machinery" we could "grow" in a test tube. Would we then consider such a thing a genuine living organism and if so why?
Yes, I know it's a "fringe question" and out of the scope of almost all branches of biology but nevertheless I think it's one of those questions that can "capture our mind". So, do you think there could possibly be such a thing that we could deem "alive" but have no cells at all? Something organized in such a way that we can readily call it a life form but yet not organized in the "way we think" about Life in general? If this is possible, when do you think this system of reactions could be called genuine living organism?
To the moderators-my question is different than the question "Why isn't a virus alive?" because it has a much broader perspective than it-a cell free form of Life can be anything-from a self-replicating "grey goo" to an evolving tornado. Viruses are only one small particular subset of possible answers. Plus the question you are referring to isn't about synthetic biology and the possible diversity of life forms as is mine but is only about a particular aspect of what we call a virus-its pertaining to the set of life forms or not. My question has both different direction and different set of objects it's aimed at. How can the two be identical, then?

The link is broken.

Possible duplicate of Why isn't a virus "alive"?

I fixed the link.

Oh, no this question is not about viruses! At least not only about viruses. here I ask the question can we even characterize something as alive if it has no cells at all. Could we call something alive if its organization isn't based on cells? The issue is much broader than the question: Are viruses alive?. For example, the first living organism at the origin of Life might as well have been the entire ecosystem. Then how is this connected with the question are viruses alive?

I only briefly glanced at the paper, but it sounds like they are describing viral RNAP activity in cell extracts. You could hardly say it can "replicate itself without the need of cells".

Nevertheless, it's the first paper mentioning the ability of something to be able to replicate on its own without the need of cells. My question is: How far can such molecules go? and further Can we ever consider anything replicating and evolving without the need of cells truly alive?

@YordanYordanov, although, like some of your other questions, I think this question might be closed. But I have to say, I really enjoy reading what you write. Never change =D

This web site is not for discussions like "So, do you think there could possibly...". Please provide definition of Life that you like and we can argue.

-1 because not a real question

The answer entirely depends upon your definition of what is life. Such definitions are to be discussed on Philosophy.SE, not here. Once you came up with a clear definition (probably a list of clearly defined conditions; which will be hard to do) we can discuss what forms could satisfy those conditions.

Everyone should probably note that the cited paper only depicts poliovirus polymerase replicating viral RNA, not the virus itself. This is merely polymerase doing its job; similar to what happens in a PCR reaction, but with RNA. PCR reactions do not constitute living organisms. Additionally, the replication of RNA and the replication of a full virus are massively different things; it still needs the cell to do that.

This question is basically asking, "what would a thing that we currently don't know exists be like, with as few constraints on it as I can come up with?". I don't know whether to flag is as too broad, opinion-based or unclear. I disagree that this requires a definition of "life" to be answered, but it does (at the very least) need more constraints on what kinds of features would be required for something to be "considered alive" by the standards of modern biology. Or is that what the question is asking for? Again, unclear, too broad, whichever.

I edited my question. Now, can you accept it isn't a duplicate of "Why isn't a virus "alive"?" or you still have issues here?

You've added constraints and specified the question, that's for sure. Now the problem is it betrays a deep lack of understanding of how cells work, apparently thinking it starts with nucleic acids that self-replicate and things like energy, every other molecule in the cell, ATP (!!!!!) are optional bells and whistles that can be added later. It is too long to be addressed in comments and an answer isn't appropriate to ask further questions; if you want a discussion on this I would be willing to chat though.

I agree to continue our discussion in the chat rooms but I would prefer to stay in the same room we opened yesterday- http://chat.stackexchange.com/rooms/55362/discussion-between-yordan-yordanov-and-rozenn-keribin .It's on another question but I think it's better to stay there and not create a new one specially for this question.

Oh, come on people, how do I have to modify my questions so they can be able to stay on this site?

The references I site in this answer may interest you: http://biology.stackexchange.com/a/19737/6307

Thanks for the reference canadianer, however, as far as I can see they haven't got as far in "artificial evolution" as I describe in my hypothetical example here, so I put the question in a broader context.

Your updated question, as I said in a comment is much more precise but also describes a biologically and thermodynamically absurd scenario that betrays deep misconceptions about how cells work and what they need to work. Having said that I've realized it has an answer, so I'll give it:

Would we then consider such a thing a genuine living organism and if so why?

As in every case in science where previously-sharp categories become fuzzier through the discovery or creation of entities that fall in previously-empty intermediate zones, "we" would debate ardently about whether those things should be considered "genuine living organisms" or not. There would be several possible outcomes to these debates:
1) All of the new intermediate entities demonstrate that in the space of characteristics things can have, the old category as previously defined no longer forms a sharp cluster, but a sharp cluster still does exist that is pretty close to that old category; in that case the old category gets a new definition, and as a result some entities might change their classifications, or not. Real-world example of this kind of definition change (though not necessarily caused by the appearance of intermediate steps): how stars and planets went from their antique definitions of "stays put in the sky vs moves around" to their current very-different definitions.
2) The new entities demonstrate that what was thought to be a sharp cluster in the space of characteristics is just... not. A clear, universal, unambiguous definition is thus impossible. One possibility is that the cluster dissolves entirely; the category as a whole is thus abandoned (many abandoned taxonomic terms can be seen as examples of this).
3) The old sharp boundaries no longer exist, but there is still a definite cluster in the space of characteristics that can be pointed to, it just has fuzzy borders. Like colors, which blend into each other but we still know there is "red" and "blue" and they're not the same. In that case, like with colors we might abandon the edge and focus instead on doing like we do with colors; defining the entity by looking at what "a good representative of this category is" and "what an ambiguous representative of this category is", thus giving a reliable idea of where the cluster is, where it isn't, and where the boundary is, even if it's fuzzy.
4) Sometimes you do need sharp definitions though, especially in science. In that case there are two possibilities:
4a) Use different definitions in different contexts, depending on which characteristics of the cluster interest us at any given point. "Species" is an excellent example of this; a paleontologist, a vertebrate biologist, a plant biologist, and a bacteriologist will use the same word to talk about similar concepts (a grouping of organisms with specific ecological and evolutionary significance), and they will use different criteria to determine what a species is in each case, meaning they have different definitions.
4b) Settle on an arbitrary boundary based on certain criteria that cuts through the fuzziness, with the understanding that it is arbitrary, other criteria would have yielded a slightly different boundary and different classifications for given entities that exist in the fuzzy zone, but it is useful for whatever purpose to have that boundary and thus a boundary will be chosen. Debate might continue a long time over where the boundary is, and potentially involve different people using different boundaries as in 4a, or not. Classic recent example is the definition of planet, and the process that led Pluto to no longer be considered one. This can also involve the creation of new categories, like "dwarf planet" in the case of the redefinition of "planet".
So to answer your question "would this be considered genuine life?", the answer will be "yes", "no", "it depends" or "neither" depending on which of those outcomes the debate ends up settling on. And we cannot know which outcome it will be, because the choice that will be made will entirely depend on what the space of characteristics will be like that makes a currently-sharp boundary fuzzy... And obviously we do not already know what the space of characteristics is like because those discoveries or inventions that will prompt us to revisit what we think of as "life" hasn't happened yet ! (well, not the ones you posit. Obviously the definition of "life" itself has already undergone the processes I describe many many times as it got better understood !).
(note I'm not even getting into the vernacular, and whether it will follow scientific usage or not and at what rate if so. It's interesting to note it still in many ways hasn't caught up with (or is just unrelated to) today's biological definition of "life" !)
(I will also add that I cannot posit an outcome even based on the specific scenario you describe, for two reasons: first, the decision would be a communal one made by professionals in the field, and I am a single person and not a professional biologist. Second, the specific scenario you describe already goes against everything we currently know about life, so, yeah.)

This is actually a big part of my question @tomd . How to determine the precise moment when something becomes a form of life but at the same time go out of the "specifics" of any one's particular field? However, it's part of my question this answer doesn't answer so I will wait the author's response here in the comments section.

@YordanYordanov "How to determine the precise moment when something becomes a form of life but at the same time go out of the "specifics" of any one's particular field?" You keep assuming that such a precise moment exists. It might, and it might not. If it exists then the answer to your question is trivial, but currently unknown: a clear discontinuity will be observed and be the basis to decide if something is life or not, but you're talking about observations that haven't yet been made so we can't say what the discontinuity would be. If it doesn't exist then your question is a non-sequitur.


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What are those brown scars in the eyes?
I have recently realised that one of my friends had brown scars or marks inside his eyes. He says that he doesn't know what they are and has been there since young. What could this possibly be ? Are those parasites ?

Do you mean the lines in the white part of the eye ? Because that are blood vessels

Yeah, but why are they brown

The photo quality is bad but they are actually not how one would expect blood vessels to look like. Or it it just natural?

The photo is not of sufficient quality to allow for even an educated guess. Sorry. It's interesting, though. I'm a doc and I've never seen anything quite like it. If you could get a really good picture, I'll do some research.

@JM97 - That's the iris! You can't even see the pupil in that photograph. Are you sure you don't want to update your profile?

humans do make mistake.

one can see two lines from iris rim into sclera.

The image is not clear, but it is possible to have essentially "freckles" on the sclera. Just like on the skin, these can be harmless or not, but judging here gets into personal medical questions which we do not allow.

@BryanKrause - Those aren't typical pigment deposition. I'm very interested in what they might be.

@anongoodnurse  I have found a clearer picture.


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quantification of glucose utilization in different metabolic processes
Glucose is commonly associated with ATP production. However, only a small fraction of glucose is utilized this way.
The intermediates of glycolysis, TCA cycle, etc. are precursors to various anabolic pathways and are ultimately involved in amino acid synthesis, nucleotide synthesis, fatty acid synthesis, etc.
Has glucose utilization in different pathways been quantified? What approximate percentage of glucose is used in different pathways?
Certainly, the numbers could vary between organisms, different cell types, cell microenvironment, etc. It helps to have an intuition of how much glucose is used where.

A general answer to this question is not possible because of the difference in organisms and cell types mentioned. However there are some more basic problems with the question. 1. Where is the glucose coming from? Assuming even a single organism such as man, there are a variety of possible diets. 2. The extent of synthesis depends on the nutritional state of the animal and whether cells are dividing. 3. In the paragraph "Has glucose utilization…", the second sentence is incomplete and meaning of the first sentence is unclear.

My question originated while reading a paper which claimed that only a small fraction of glucose eventually ends up undergoing oxidative phosphorylation. Most of the intermediates of the glycolysis and TCA cycle are precursors for biosynthesis of amino acids, nucleotides, etc. I naturally wondered how much of glucose is used where to garner an intuition.

Well give us the reference. Then we can see what the system is.