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Why do we use cRNA instead of initial extracted RNA in the microarray technique?
I am recapping for the exam in transcriptomics and stumbled into a question about microarray. So, our regular workflow is to

extract RNA from cells
generate cDNA from the initial RNA using reverse transcription
transcribe cRNA from cDNA
label cRNA with biotin
fragment biotin labeled cRNA
hybridize to a plate, scan and quantitate

So the question is - since we use RNA for the further quntification steps why should we perform reverse transcription+transcription to produce cRNA while we could just use the initial RNA?
Is the cRNA more stable than RNA? Or we already make labeled cRNA using labeled nucleotides?

Could you give a source or at least application for this workflow? It sounds pretty specialised, both the biotinylation and the in-vitro transcription (cRNA) are - as far as I know -  not standard procedures.

I don't know exactly the applications of this method, the scheme was shown, for example, in this lecture http://www.binf.gmu.edu/jafri/binf636/GMU-higgs.pdf in the section about Oligonucleotide Arrays.

I can't find any mention of biotinylation or in-vitro transcription/cRNA in the slides you linked, they don't seem to have anything to do with the workflow in your question.

It's slide #16 and you have a picture in dark blue.

Ah, only checked the text of the slides, not the figures as well. I tried to answer - but the figure looks like an example that isn't very well explained (the text next to it doesn't clearly correspond to it)

by @WYSIWYG
my guess is that the final cDNA after doing RT-PCR (not the first strand) which is double stranded is transcribed to make a ssRNA which can then be used as a probe. ssDNA would also work but the cDNA synthesis followed by PCR would not produce ssDNA. You can simply use the first strand after RT but the concentration would be less. With a cDNA library, you can produce a lot of RNA using IVT.

After clarification via the comments of the OPs question:
1) The procedure you describe is not for standard RNA microarray experiments, it for olgionucleotide microarray. This type of chip is special because it has multiple probes for each gene to allow detection of special features (i.e. mutations, alternative splicing, ...).
2) The reason for the generation of cDNA with subsequent reverse transcription and biotinylation is not explicitly stated in the source of the OP, but there are some possible advantages:

Amplification of material: cDNA can easily be amplified, which would make it easier to analyse samples whit low RNA yield, genes with low expression levels or to analyse the same sample on multiple chips.
Sensivity: oligonucleotide arrays may use very short (10-25 bases) probes, for which fluorescence readout may not be sensitive enough. Biotinylation of a given RNA base (by the use of pre-biotinylated NTPs during reverse transcription) can give multiple 'marks' on each fragment, which can be read with out streptavidin coupled signals. Additionally this would allow the signal strength to change in respond to certain SNPs/mutations.

Good intro to oligonucleotide microarray but still not clear why we would convert cDNA back to cRNA after biotinylation.

@PolinaNovikova my guess is that the final cDNA after doing RT-PCR (not the first strand) which is double stranded is transcribed to make a ssRNA which can then be used as a probe. ssDNA would also work but the cDNA synthesis followed by PCR would not produce ssDNA. You can simply use the first strand after RT but the concentration would be less. With a cDNA library, you can produce a lot of RNA using IVT.


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Is it Theoretically Possible to Create a Male clone from the donor Cell of a Female?
I understand that Dolly the Sheep was created without the presence of a sperm cell. Instead, nucleus DNA from somatic cells of adult sheep were used. Since Dolly was female, i am assuming that the nucleus DNA used came from a female sheep. So, i want to know if the sex of the resulting clone is determined by the sex of the donor animal. Also, in light of the science behind sex determination in clones, would it be theoretically possible to create a male clone where a single woman contributes both the egg and somatic cells used in the cloning process?

AFAIK, mammals use sex chromosomes to determine male vs female, with males carrying a copy of the Y chromosome. It is possible to have a male with 1 Y and 2 chromosomes. So, i would guess that if you took a female embryo and microinjected a Y chromosome into the embryo at the single-cell stage, it MIGHT develop into a male.

is there any research that has been done on this topic?

I guess not specifically on creating male clones from females, but there have been IVF embyros created using 3 "parents", where one person provided healthy mitochondria to replace the mother's faulty mitochondria.

Maybe some of you could see this and I don't have to ask the question (something stressful to do in StackExchange): would it be possible to clone a female mammal from a male one, the female having two copies of the X chromossome from its male donor? If so, barring mutations, wouldn't the offspring of these be, "in a sense", like "clones" of their parents? I wonder what would happen if this pattern of mating would continue through generations. Assuming an eugenic mammal was the original male donor, I think this could help discover any "bugs" in the eugenics process by exacerbating them?

So, i want to know if the sex of the resulting clone is determined by
  the sex of the donor animal.

Generally yes for mammals and birds. In animals where the sex is determined by sex chromosomes, the sex of the clone will be dependent by the sex of the donor.
In animals (ie turtles and crocodiles) where the sex is determined by external factors (ie temperature), then the sex of clones will not be dependent on its donor.

would it be theoretically possible to create a male clone where a
  single woman contributes both the egg and somatic cells used in the
  cloning process?

Short answer is No.
Sex in mammals and thus humans is dependent on presence or absence of the Y chromosome. If the Y Chromosome is present, the mammal is male. If absent the mammal is female.  So a woman does not have the Y chromosome. Hence it is not possible to create a male from her genetic material.
Longer answer... anything is possible. A woman does not have a Y chromosome, so if you added a Y chromosome to one of her ES cells and then used those cells to form the inner cell mass of a blastocyst, then yes you can get a male.

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Is the missing "life-ingredient" in today's Earth's existence the reason why we cannot recreate life?
As far as I know, there was no report of "life" popping up in a lab or in nature so far.
Everything that we know is only some copy with similarity to previous life-forms.
We certainly can mix some amino acids and stuff, and even some of the chemicals can retain some structure for a certain time and even form some proto-RNA-like structure (not sure how they called it in one document I have seen), but it's very very far from a living organism.
Does it mean that life cannot be "sparked" in today's Earth like conditions or, was it not even sparked here to begin with? I have read, as many others have done, this article: New research supports an idea that the Red Planet was a better place to kick-start biology billions of years ago than the early Earth was. They argue that you need molybdenum to create life-like structures and that it's not common in the right form on Earth.
What do you as biologists think about the statement that life cannot evolve on Earth because the conditions in the beginning of the Earth were not good for life to develop.

keep in mind todays earth is very different than the early earth, for instance life has drastically changed the atmosphere of the earth.

I have voted to have this question removed as off-topic. Please consult the help to see what questions are unsuitable. A suitable question asks for factual answer to a specific biological problem. "What do you think about the statement..." is not such a question. However interesting it may be it is an attempt to initiate a discussion to which any contributions (answers) are likely to be subjective. That is why it is off-topic.

There is a difderence between "conditions in the beginng of the Earth were not good for life to develop" and "Red Planet was a better place to kick-start biology billions of years ago than the early Earth was". If A is better than B, it doesn't mean (at all) that B is not good enough. Thats also the point people often forget while talking about evolution.

Three important concepts about abiogenesis
Let's start with three important concepts
Definition of life
You'll need to give a good definition of life, because biologists actually don't have one (it is a matter of philosophy to define life, not biology).
Time it took for life to emerge
Life as we know it emerged only after a huge period of time (hundreds of millions of years), which we obviously cannot reproduce in a lab.
Current competition
Even if some kind of protolife would appear at some point, it would still have to face the competition with its veteran partners. Hypothetical protocells would be eaten by some microbe with no doubt.
Panspermia
The idea of panspermia (the hypothesis that the life may have appeard in outer space or in another planets, and then "contaminate" the Earth) has been on the scene in many forms for quite a long time. Regularly we hear of some study which proposes that life, or at least some key biomolecule, may have formed in asteroids, comets, in Mars or somewhere else. They're quite interesting, mainly because they suggest more than one way that life may have appeared.
Molybdenum
While molybdenum is rare in the Earth, it still exists and so the study doesn't deny the posibility that life may have formed in the Earth. Nowadays, molybdenum is used by many organisms as part of the core of some key enzymes, such as nitrogenase (the enzyme complex that catalyzes the conversion of molecular nitrogen into nitrate). Molybdenum has very interesting catalytic qualities and may have been a key factor for the origin of life.
Phosphorus on Mars
However, those studies say that Mars has higher concentration of phosphorus, which is one of the main components of life, and that was pretty rare in the early Earth. The hypothesis is interesting but, without experimental data, it is only that. The authors suggest that nowadays those phenomena may happen in Mars, so the hypothesis may be confirmed in a few years as the exploration of the Red Planet continues.

I modified the format of your answer (I mainly just added names to sections). Please feel free to roll back or re-edit if you don't like my edit.

Note that in addition to "hundreds of millions of years", there's also the fact that primordial life-creating "experiments" where likely taking place over a large part of Earth's surface, not just in a few test tubes in a lab.  So there's extreme parallelism.

This is really quite a question. And many leading biologists have tried (very hard) to answer it.
In my opinion, most of our incapacity to study which conditions can favor some form of "life" is due to a lack of understanding of what is "emergence". And moreover, about or focus on matter over processes, and the reductionist paradigm of modern science.
Life is an emergent, system-level, property of any living system. It is not the material basis of life what is important (for instance, just mixing all the biomolecule precursors in a soup has proven to be a poor attempt to recreate life-like behaviors). What is important is the way this matter is organized. But, again, what we don't understand is what "organization" even means. My intuition says that the answer will come from studying "organization" and not "matter". There is no reason to think that other life-like forms will have the same molecules (CHONPS, and water-based metabolic transformations), out of the astronomically huge universe of possible molecules that can exist by combining the finite number of stable atoms in the universe.
Then, let's understand organization. Let's understand emergence. Better, let's understand "radical emergence". Here I leave a link to some brief thoughts from one of the leading scientists of all of biology, Stu Kauffman.
Here is a more chemically-oriented opinion, by another leading scientist in the field (who recently passed away).

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is it possible to use electroshock to temporary stop gross motor functions directly on the neural pathway?
Is it possible to modify that procedure and use it to send a small electroshock on the specific neural pathway and temporarily stop that gross motor function?

When the microphone detects unwanted noise—such as a humming airplane engine—it sends a sound wave into the headphone speakers that is 180 degrees out of phase with the bothersome sound. Consequently, the two waves cancel each other out, resulting in silence._

i would like to know if that procedure can be modified with electric currents in the human nervous system, so body movement is stopped, without stopping organs and damaging the body by sending the current directly in the nerve, canceling out the signal.

You can usually just say "cease all motor functions"

But seriously, this is an interesting question I may answer in detail later. A major challenge would be distinguishing between motor outflow to the diaphragm and to other skeletal muscle. Paralytic drugs require manual or mechanical ventilation. Paralytic electromagnetic stimulation would have the same challenge. That's if you could isolate motor outflow to skeletal muscle in the first place


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How does DNA codon (5`-3`) convert to mRNA?
There is a problem I stumbled upon when doing a lesson on molecular genetics (Grade 12 level).
The lesson contains many tables in this format:
I don't understand how it got to the mRNA codon considering how RNA polymerase creates mRNA. From what I know already RNA polymerase reads the anti-sense/template strand (3`-5`strand) and synthesizes mRNA in a 5`-3` direction.
For example, using the first column with the DNA codon 5`-TAC-3`, I would automatically convert it to 3`-5` complementary anti-sense strand because of the nature of the enzyme. It would be 3`-ATG-5`. Now using that anti-sense strand I would find the complementary base pairs and the mRNA strand would be 5'-UAC-3'. This is not consistent with the example given by the lesson. I can understand how to get to the answer (just find the complimentary base pairs of the DNA codon given) but it goes against what I know.
Now if the table said (3`-5`) instead of (5`-3`) it would make sense. Am I misunderstanding a fundamental concept?

In addition, I did some research and found this table. https://en.wikipedia.org/wiki/DNA_codon_table
With the example I mentioned, Tyrosine would be the amino acid if I was going directly from the DNA codon not methionine.

The table you reproduced shows the DNA sequence on the bottom or antisense strand of the gene, but the 5’->3’ notation refers to the coordinates on the top or sense strand.

Your reasoning is correct and the table is wrong. The mRNA will have the same base sequence as the sense DNA strand (with T replaced by U).

I have upvoted this answer, but would add that — although it is not the poor poster's fault — the term ‘DNA codon’ is non-standard and I can see little point at all in a table of this sort. Perhaps for mRNA codon v. tRNA anticodon, but not for this.


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What physiological processes give rise to a linear cell survival curve?
If we plot the number of surviving cells in a structure over time (assuming no replacement), the shape of that curve should imply something about the underlying process responsible for cell death. For example, if surrounding conditions mean that each cell has a constant probability of dying within a given interval, then an exponential decay curve should be seen. If the cell has a characteristic lifetime (with say a gaussian distribution about that mean lifetime), then (I guess) we might expect something like a logistic S-shaped curve.
In Parkinson's disease, the onset of motor symptoms is related to the number of dopaminergic neurons in the substantia nigra pars compacta, a small structure of just several hundred thousand neurons. The decline in cell numbers due to the disease process is indeed usually modelled as something like an exponential decay.
But there is also a normal age-related decline in substantia nigra neuron numbers. This decline is usually modelled as a linear decrease from birth through to old age, at something like 0.5% to 1% per year (Rudow et. al., 2008. Morphometry of the human substantia nigra in ageing and Parkinson’s disease. Acta Neuropathologica, 115(4), 461-470 http://dacemirror.sci-hub.tw/journal-article/fc4e7854ee0cef0146d60756536b2a88/rudow2008.pdf )
Note that this percentage decline per year is not a percentage of the surviving number (which would yield an exponential curve), but of the original total. In effect, it is perhaps best to think of it as a decline by a constant absolute number of neurons per year, yielding a straight line survival curve.
Exponential decline is memoryless (conditions simply conspire such that the probability of any cell's death is constant in a given interval, uninfluenced by the history of that cell or any other). The death of a cell with a characteristic lifespan, meanwhile, does have memory, as the probability of a given cell dying increases as that cell ages and deteriorates. But the death of a constant number of cells in a given interval somehow implies a sort of memory across cells, such that the number dying in a given interval is related to the initial number, and not to the current surviving population level.
My question is what general physiological processes are consistent with such a linear decline? i.e. is a linear decline a common pattern for neurons or any other sort of cell death, and in general, what sort of process governs it?

Note that linear functions are good approximations to many underlying nonlinear processes. Simply because a process is described with a linear function does not mean the process itself is linear.

Yes that’s certainly true and is perhaps what I’m getting at. i.e. could a linear model here actually be consistent with some underlying physiological process, or is it simply an approximate statistical fit to noisy data from some other more physiologically viable underlying non-linear process?

Progressive cell death along a spatial dimension would be consistent with this. For example, imagine a cylinder of tissue in which cells at one face die, inducing adjacent cells to die. This would yield linear decay in viability to 0.

Yes, a spatial process would be viable: nice approach (not for this particular situation I suspect, but it would work as a general concept).

I suspect that the comment by @BryanKrause is more likely to be correct but I've awarded the bounty to this answer, as it does provide a general and feasible physiological mechanism as requested, although it is likely not viable for the particular case I have in mind.


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what snake is that in northern italy

About 75 cm long. Thin tail. Camping site near Grado, Italy, northern Adriatic sea.
It climbed a tree in the rough bark and i followed it to take these photos.

It might be a better idea to embed the images in your question instead of just putting their links.

Excellent quality photos and good views of important parts for identification.

It looks like a whip snake, either a Balkan whip snake or a green whip snake. They are both present in the very north of Italy, close to Slovenia. They both vary in color, but the coloration of this one seems to be more similar to the Balkan whip snake.

See also this discussion.

Thanks. I first compared it with natrix natrix, but the pattern didn't really match. There are also many small lizards on the camping ground, a common prey of whip snakes. My snake made jerky movements with its head when it was in the low bushes on the ground, I didn't see that in the videos. I'll accept your answer, but I'm open for other suggestions (or confirmations).


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Identification of red, plum-like fruit (probably from Southern Russia)
My parents are currently on a holiday in St. Petersburg (Russia). They sent me this photo of plum-like fruits they bought on a market there (toilet paper for scale, I guess).

The fruits are 20-30mm long, have a big stone, taste sourly like red currant (based on my fathers opinion) and are supposed to come from Southern Russia (don't know where this information is coming from).
Can you please help to identify them?

Can't be certain from the picture, but they look a lot like Cornelian Cherry (Cornus mas: https://en.wikipedia.org/wiki/Cornus_mas ).  However, the ones in my garden (western US) don't ripen until late September/October.
Perhaps they could return to the market, and ask for the Russian name?

I think that's it. The pear shape, the red color, the acidic taste, the origin... everything fits. Of course this can't be verified, but I consider this question answered. Thanks!

I don't notice an acid taste with mine, more of an astringent, mouth-puckering taste until they're fully ripe, when they turn deep red, start to wrinkle a bit, and almost fall off the bush by themselves.  That said, I don't think they're at all good eaten fresh. but they make really great jam and fruit leather.  Search the web for recipes :-)


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Why more than one chromosome in an organism?
Why not one chromosome to house genome in organisms but multiple?
Is it for epigenomic purposes?

Are you asking about ploidy number or chromosome number? Do you have any reason for expecting every organism ro only have a single chromosome? Why did you suggest epigenetics? What are your thoughts?

I am asking about the chromosome number. I ask this because the chromosome numbers are not the same across different organism and I feel there could be a reason for this. I suggest epigenetics because of the need for histones to interact with genomic sequence for modulation of genes.

The problem here is in attributing purpose to evolution, when it's a series of accidents, some of which survived.  There are a number of things that can cause chromosomes to be duplicated. (Colchicine is commonly used in modern plant breeding.)  If an organsm has its single chromosome accidentally duplicated, and the offspring survive, that change gets propagated to ensuing generations...

@jamesqf Then why do we have different genes on different chromosomes and not duplicates?

@Atajera If a chromosome were duplicated, for it to stay a duplicate and not diverge, every change would have to happen at the same time to every chromosome. That's not really feasible.

@BryanKrause That explains the duplicity, how about the change to different but essential genes. Why not essential genes only on the parent chromosome if the theory is true?

@Atajera What mechanism do you propose that would cause genes to only change on one chromosome once there is more than one?

I seem to remember a related question in relation to maximum chromosome size. Those interested might do worse than look for it.

@Atajera: Understand that I am only guessing/making logical deductions here, but once you have two chromosomes, each will undergo random mutations, some of which will prove beneficial.  Carry that process on long enough, and the organism now has two different chromosomes, potentially carrying twice as much information.  (It also seems as though copying one long chromosome would be less efficient and more error-prone than  several short ones.)

@jamesqf: I agree with your theory

@BryanKrause: None but what I meant was that the change occurs in both but results in two different essential gene but not two variants of the same gene.


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Are there flies that can spray their eggs while flying?
While I was reading a few articles about parasitic infections caused by flies, to be specific Myiasis, I read something saying that some flies can spray their eggs when they are flying around their target instead of having to stay on it and lay the eggs there.
Is this true? What's the name of these kind of flies?
PS1: I include part of the source translated to English:

Dr. A. Khazani ,entomologist &  an expert in charge of the vector control program of Isfahan province, emphasized that environment hygiene is particularly important in preventing people from contracting myiasis, added: Some flies spray their eggs while flying, which may get inside the ears, nose, and eyes. and... penetrate and cause disease

Source: IMNA, A Metropoitan News Agency, June 8th, 2019
Names of the species were not mentioned in the source article.

Welcome Merlot. "Almost"? Personally I can almost afford a new car. I'm not sure if such a creature exists, but if you were to add the results of your investigations to the body of the question (even if inconclusive) that would definitely improve the question. I find that Google Translate is handy for translating quoted, why not give it a try.

@JiminyCricket. I translated that part of the source & put it in here.


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How do the chemicals in our skin react with stainless steel?
What acid/chemical in human skin can react with stainless steel to leave a black mark on the skin? Why is it secreted/produced in larger quantities by some people and not by others?


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Humans best at long distance running: purely physiological or is it a function also of ability to pace?
I have read that although certainly other land animals are much faster over short distances, a human can run down any other animal over time, so that if a human is hunting like a gazelle, etc. eventually the human will catch up. I am wondering if this is purely a physical thing or if humans, knowing how to pace themselves, avoid exhaustion while the gazelle just runs as fast as it can and then collapses -- is it possibly because humans are smarter that they are better long-distance runners? (Now, some birds are able to fly for thousands of miles and I guess also in water we can't compete.)
EDIT: I understand that humans have some physical attributes that contribute to their long-distance abilities but is the ability to understand pacing also part of it?

there are studies of human biology which will list all the different physiology and ability-to-pace-iology (that's morphology?) specializations that make humans run long distances. I donno if you researched this at all, cos previous research is already good reading when you find it.

i will change question, because i have seen nothing about the mental aspects.

Humans are efficient runners, but just as a reference, I think there are some interesting answers here that call into question whether humans are really the best at long distance running. https://skeptics.stackexchange.com/questions/6114/can-trained-humans-run-faster-than-all-other-animals-on-a-marathon-distance

While humans are certainly in the upper ranks, they are not the absolute best.  Sled dogs almost certainly take first place, at least in decently cool weather.  Horses are a bit better (as measured by endurance races over the same course, e.g Tevis Cup vs Western States 100), but it's close enough that some humans are better than some horses. But the real factor here is something you haven't mentioned: intention.  AFAIK humans are the only mammals (migrating birds are something else entirely) that deliberately set out to run long distances.


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Why largest cats so much larger than canids?
It is striking to me that there is no dog-like creature larger than a wolf while there are at least two species, tigers and lions, many (at least twice and probably 3 or 4) times the size of the largest wolves. I would guess it has something to do with hunting style, packs vs individual hunters although lions do sometimes attack in groups. I am not saying I would like one to exist, but why is there nothing like a 400-500 pound wolf?


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Is there an example of a species wherein the female lays eggs in the male?
There are of course many species which lay eggs in the bodies of another species and also many species where either the male is eaten after mating or the male dies soon thereafter. So it seems possible that a species might exist where the female lays fertilized eggs in the body of the male with whom she mated or even a different male. I could see however the problem being that there is a significant time gap between mating and the eggs being ready to be laid, so perhaps there are no cases of the former but perhaps there are cases of the latter?
Note: Looking for a form of egg-laying that is destructive to the "host" -- where the developing larvae eat the host, like in the cross-species case.

Is there an example of a species wherein the female lays eggs in the male?

Yes.
Pipefish & Seahorses to name two.
Both widely mentioned in many wildlife programs as being an example of what you've asked.

Watch a video of flatworms penis fencing.
Nature never disappoints, it created a real kicker. Some species of flat worms are hermaphrodites, they have penises but also produce and carry eggs. No flatworm wants to be the mom as it uses a lot of energy and food, so the flat worms fight to inseminate each other.
They fight with their penises. the loser gets their eggs fertilized and is the designated mother of the relationship.
all information I used was drawn from Matt Simon's "the wasp that brain washed the caterpillar". If you are interested in weird abilities of strange creatures, I would really recommend checking it out.

They're hermaphrodites, so both, not really what the question was asking for then.

I did see that, my answer was more of a comment to share this cool flat worm story. they clearly have an interest in freaky animals. But I was unsure if it would fit. Hope this helps either way


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Extract mutations from fasta sequences
I have a large amount of protein sequences in the .fasta format and I would like to extract only the amino acid mutations from these sequences, so that, in the end, I want to have a list that looks something like this:
I456L, W675T, etc
Is there a program or way to do this?
Thankful

Are all of your sequences of the same protein, are they all the same length, do you know which one is the WT / baseline?

Yes, the proteins are of the same, in the same length and I have a reference genome to compare

I'd blastp, and parse the alignment you get back.

I would suggest posting this question on https://bioinformatics.stackexchange.com/questions.


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What are the minimum conditions required for "open-ended evolution"?
According to a paper about artificial life systems, the following four conditions have to be fulfilled for "open-ended evolution":

Condition 1: A rule should be enforced that individuals must meet some minimal criterion (MC) before they can reproduce, and that
  criterion must be nontrivial
Condition 2: The evolution of new individuals should create novel opportunities for satisfying the MC
Condition 3: Decisions about how and where individuals interact with the world should be made by the individuals themselves
Condition 4: The potential size and complexity of the individuals’ phenotypes should be (in principle) unbounded

My question
Must these conditions be met for open-ended evolution to occur? If so, do we have evidence that all of these conditions fulfilled in nature? If not, could you give examples where one or more conditions are violated?

Could you clarify point 2 for me please, individuals don't evolve. Do you mean that mutations/immigrants is allowed to affect variation in fitness?

Also on point 1, in principle open ended evolution can occur without a minimal criterion. If all individuals within a population contributed the same number of offspring to the next generation then there would be no minimal criterion (no variance in reproductive output through i.e. no drit or selection) but evolution could still occur by mutation.

@rg255: I don't want to unnecessarily inflate this post but you can find a clarification in the linked paper on page 3 where condition 2 is explained in a short paragraph on the left hand side. The example given therein is about giraffes.

@rg255: I would ask you to give your answer below and not in the comments - Thank you.

Even reading that paper I can't figure out what they mean with condition 3. Do they mean the individual is completely free to interact with all of its environment?

@Downvoter: Please explain the downvote as is good practice. How can I improve the question?

@vonjd Please read Why is voting important?, especially the last paragraph. Additionally, mouse over the vote buttons on both questions and answers and read the tooltips that pop up. Voters are under absolutely no obligation whatsoever to explain their votes if they don't want to, instead relying on the tooltips to do the explaining for them. They may also comment and/or edit with improvements, if such a thing is possible and they have the volition. Demanding explanations for every downvote is not a generally-accepted practice.

In principle open-ended evolution can occur with condition one violated. Because evolution is simply a change from one generation to the next (see answers here, here, and here), the is no requisite for a "non-trivial minimal criterion". Such a minimal criterion (e.g. survival to sexual maturuity) would imply that evolution is occurring by drift or selection, because being non-trivial implies that some members of the evolving population will fail to reproduce. However, evolution also occurs by mutation (and migration).
For example, we can have a population at generation $1$, and each individual within that population produces one offspring, present in the next generation. This means no variation in reproduction exists. If generation $2$, the offspring of generation $1$, carry new mutations then the characteristics of generation $1$ and $2$ can differ, and the descendant generation has evolved from the ancestral state. This can be seen in mutation accumulation lines as an example:

"In a typical mutation accumulation experiment a single inbred and
  highly homozygous line is replicated.  Each of the replicated lines is
  maintained at a very small population size (usually brother sister
  mating, or in plants, selfing).  These lines are maintained for many
  generations.  During that time mutations accumulate, and the lines
  generally decline in fitness, and the variance among lines increases." - UVM Blog

So the answer to your question, these conditions are not necessarily met in nature. However, that doesn't mean evolution can't be open ended - the conditions outlined in the paper are flawed when trying to compare to nature. Evolution can occur when the "minimal criterion" is trivial (when all individuals are capable of meeting the criteria). The existence of a non-trivial MC only implies drift (e.g. some don't reach survival to sexual maturity by bad luck) or selection (e.g. some don't reach sexual maturity because they carry a genetic disease which kills them first). A trivial MC says that there is no drift or selection, but says nothing of mutation. I have since spoken with one of the authors who describes a non-trivial MC as the same thing:

"Regarding nontriviality, it should at least be possible that some
  individuals do not meet the MC"

Note: I have only focussed on condition 1, because this condition is not necessarily met in nature, thus your question is answered (are all conditions satisfied in nature)

I am now in touch with the authors of the paper. A big problem seems to be that there are different definitions and approaches in the biology and the Alife community. So I guess from a biological point of view (so to speak) your answer makes absolute sense and therefore I undownvoted it and upvoted/accepted it. The authors gave me another paper which might also be interesting for you to understand their point of view a little better: http://eplex.cs.ucf.edu/papers/lehman_alife14.pdf

@vonjd I also reached out to the authors for clarification of their non-trivial MC - see edits


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What don't we know about cancer?
I was wondering, after decades of research what we do not know about Cancer yet as in what unanswered questions are still puzzling biologists about cancer?
I have read that cancer research, in its modern form, is a quest for biological immortality. Does this hold any truth?

I think this thread will become a jungle very fast and very soon, so I suggest you to have a look at the cancer research reviews of the last 2 years to get a grasp. Have a look at cancer hallmarks and at other important key concepts, you will most certainly answer your question yourself :) I am not a cancer researcher so I cannot comment on the topic in a detailed fashion (I work on plants), but that's what's going to happen.
In general, I'd say that what we don't know about cancer is a "common ancestor" of all types of it that will enable us to tailor a one-sized cure.


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Fluoroquinolone mitochondrial and genomic DNA adduct
What could be possible consequences of covalent bond mitochondrial and genomic DNA adduct by Fluoroquinolones, our study was done by Fluoroquinolone Toxicity Study NFP. All 50+ participates who took Ciprofloxacin and Levofloxacin were positive. In vitro study showed DNA adduct after 3.61 min. We are FQAD victims not scientists. We would like to know what may be consequences of DNA adduct.

As a new user you are welcome to SE Biology, however you should be aware that there are a couple problems with your question that might have been avoided if you had taken the tour and read the help on answering questions. The first is to express yourself clearly — 'mt' and 'n' should be written in full in the title for clarity and to help indexing. The second is that questions here should be self-contained. Nobody should have to go to another site or download material to understand your question.

Sorry David, I did remove the link. Thank you.


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Why are the pulmonary vein and artery not like the rest of circulatory system?
I'm learning anatomy. What I learnt is that we have arteries that have oxygenated blood which appears red in color, and branch blood to arterioles to deliver blood to cells via capillaries from where de-oxygeneated blood is collected via venules into veins to go back for oxygenation. So:

artery = oxygenated
vein = de-oxygenated

However, in defining the pulmonary vein and pulmonary artery, I see the reverse of these definitions.
The pulmonary artery is for de-oxygenated blood.
Why is it so?

Ask youself, what function is served by pulmonary circulation? What function is served by systemic circulation? What part of the anatomy connects the two?

It is true that nearly all arteries carry oxygenated blood and nearly all veins carry de-oxygenated blood, but that is not what defines them. Arteries are blood vessels that carry blood away from the heart, and veins carry blood towards the heart. If you look at the situation in that light, the naming makes sense: the pulmonary artery is carrying de-oxygenated blood away from the heart to the lungs, and the pulmonary vein is carrying the re-oxygenated blood back to the heart, to be pumped through the rest of the body.

Although these complicate classification.


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Can two different species in the same genus generally succeed in the same habitat?
This plant-care website writes

In the context of plant care, usually most plants within the same genus need the same environmental conditions suitable for plant growth. If the genus of a plant is known, the information can be used to apply the appropriate levels of plant care.

I'm wondering if this is true in general. A more general question would be, if I know that two species are in the same genus, what phenotypical similarities will they have?
So far I've only found that genus classification is based on genetic similarity, but that doesn't say anything about what phenotypical similarities there may be between different species in the same genus.

It is not correct to say that genera are based on genetic similarity. Different lineages diverge genetically at highly variable rates, and there is no set cut-off for what defines a genus. Instead, genera are based on publications, which could be over 100 years old. Genera are not a biologically real category the way species are, so one genus may hold hundreds of species, while another, only one. Most of these genera were defined before molecular data was possible. There are no set phenotypic criteria for the definition of a genus, except that a well-described genus should have at least one fixed character that defines it. So in answer to your question, yes, two species in the same genus (congeners) will often exist in the same habitat. There would be selective pressures to separate them in terms of the niche that they occupy. The publication you referred to is simply a best guess: if you don't have information on the habitat requirements of a species, it would most likely share many similarities with its close relatives. Phylogeny is predictive, but different species in the same genus need not be identical in terms of their ecological requirements.

I don't think you can generalize either way.  For an example, take penstemons: https://en.wikipedia.org/wiki/Penstemon  Hereabouts I can find 3 or 4 species growing in the same conditions, within a radius of 3-4 m.  I can also find other species growing in close proximity but very different conditions, e.g. wet meadow vs dry, rocky slope.


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Why do (some) cats chase their own tail?
Is this just playful behaviour or are they unaware that it's their own body part ?

The question is too generic. I have had cats who had no interest in their own tail. The answer would probably have to do with animal psychology. It might even be a bit philosophical.

@takintoolong re: "I have had cats who had no interest in their own tail." thank you. although this is kind of obvious, I will edit the question to reflect your comment, just in case

I will try to answer this. First of all we have to make a claim. This behavior can be found in many animals behaviors but it is much more common in dogs.

In cats there is a few reason for that:
Born hunter
Feline predators have a genetic desire to chase anything what is moving. So the chasing tail behavior can be just game for practising hunting skills.
OCD
But if this behavior doesn't stop after the cat grew up it might be a serious problem.  Just like any compulsion behavior in general it might indicate that your lovely cat has obsessive compulsive disorder. If this is the case, your pet can become much more aggressive, hyperactive.

Source
Perfect Paws: Predatory Behavior of Cats
Psychology Today: It's Alive! Why Cats Love Laser Pointers
Pet Place: Feline Hyperesthesia (FHS)


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Why does pyruvate from lactate and pyruvate from other sources follow different pathways in gluconeogenesis?

My teacher taught me in a lecture that PEP forms from Pyruvate by two ways, based on their sources, that is -
1. If the Pyruvate was from lactate (by lactate dehydrogenase action), it gets shuttled into mitochondria and is successively converted to OAA and PEP, by enzymes PC and PEPCK(mitochondrial) respectively. This PEP is then shuttled to cytosol for rest of gluconeogenic steps to take place.
2. Whereas, if the Pyruvate was from any other source, it is shuttled to the mitochondria, where it is converted to OAA by PC. It is then shuttled to cytosol by malate shuttle and then converted to PEP by PEPCK (cytosolic).
Why the difference in mechanism?
Please correct me if any of these steps are wrong.

Thanks for the corrections. But my main doubt was that why does the Pyruvate from lactate follow a different way to become PEP rather than the other way (when Pyruvate is produced from other sources), or vice versa. The question could also be framed this way - 'why does two mechanisms exist for conversion of Pyruvate to PEP?' Thanks.

What is the basis of the right portion of your diagram which is new to me? The vast majority of the PEP used for gluconeogenesis is generally thought to occur in the cytoplasm from oxaloacetate made in the mitochondrion and shuttled out via malate as indicated in the left of your diagram. Even though there is evidence for a mitochondrial PEPCK, this has no known role in gluconeogenesis. Even if it did, how could it distinguish pyruvate from different sources?

In any case, please rewrite your question so that  your diagram is only an illustration of the text. The question should not rely on text on an image as it is not possible to index it and it discriminates against people with sight problems. You can do this by carefully describing the key steps in words. Please quote the source for your diagram or explain if it is from notes taken at a lecture.

Sorry mate. Did not think of that while posting the diagram. The diagram and source of the content was from a biochemistry lecture. But, I found other sources (like this one: https://www.ncbi.nlm.nih.gov/m/pubmed/24497630/) where mitochondrial PEPCK was linked to lactate (Here, silencing of mit. PEPCK in rats was seen to increase lactate and lower plasma glucose). Thanks.

According to this research paper (http://m.jbc.org/content/284/40/27025), the presence of two different PEPCK's may have to do with the 'cytosolic redox state' because both pathways result in production of one NADH + H+ in cytosol. Although I didn't get the clear picture, I got a superficial idea why this stuff is like this. Wow, the human body is truly wonderful.

That's interesting. If you like I'll set that out clearly in an answer when I have a moment. It's worth putting on file.


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Quantify Protein Denaturation with Change in Solubility
I plan to run a lab which compares the impacts of ethanol and methanol, in varying concentrations, on the denaturation of whey protein.
Change in water solubility is a good indicator of the degree of denaturation in a protein, but online research doesn't seem to be showing any exceedingly simple method of quantifying a change in solubility. Can protein precipitation be used to measure solubility? If so, I have access to a centrifuge, ammonium sulfate and just about any other chemical compound. Are there any better methods, altogether?
Is change in solubility the only factor which may reflect denaturation?
Thank you

How do you plan to actually measure the protein?

By mass scale. I need a way to find the solubility of the protein solution, as in solution of saturation.

How pure is your sample?

I’m varying the samples by solution of ethanol or methanol (Ex 1:1 ethanol/water ratio).

Mass of protein is kept as a constant, as well as volume of solution

To answer your question though, the whey protein I’m using is 95% pure.

There are many ways to assess protein denaturation. Keep in mind that denaturation and precipitation are not necessarily coupled. For instance, detergents can denature proteins and yet make them quite soluble. It seems that you are asking two separate questions here. If you decide that protein solubility is what you want to measure, we can suggest some simple protocols.

I have decided to simply separate the formed precipitate from the solution with a centrifuge, filter the precipitate with filter paper, determine the mass of the precipitate, and find a ratio between that mass and the full mass of the utilized protein sample. Is that a good way to assess the degree to which the protein was denatured? It seems to me like my best option...


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What are the potential dangers (if any) facing the twin girls recently born in China with their CCR5 gene modified?
According to this Nature news article, a Chinese researcher claims to have made the world's first genome-edited baby using the popular CRISPR–Cas9 genome-editing tool. A gene called CCR5 was modified before the embryo was implanted into the mother. The CCR5 gene is known to produce a protein that is utilized by the HIV to enter human immune cells, and the genome editing performed is expected to make the babies HIV-resistant despite their father being HIV positive.
As a Chinese, I am deeply concerned with the ethical consequences and scientific impacts of this highly controversial experiment. However, to form an opinion for myself, I believe that I first need to know the potential dangers, either expected or speculated, that the twin babies might face in their life. Unfortunately I am not familiar enough with molecular biology to be able to know and judge these myself, and the reports in the media seem very vague on this issue.
So please let me ask: What are the potential dangers (if any) facing the twin girls, and how sure are we now about these dangers, their consequences, and possible countermeasures?

None of the research has been published, so nobody can say anything on this specific case, if it is even true.

@canadianer, but the question is pretty general. There has been lot of debate about the dangers of genetically modifying embryos (off-target modifications/unexpected effects of targeted modifications).

@Michael_A Did I say otherwise?

@canadianer I thought your comment could be read as pointing out a problem with the question. My comment was to highlight that there was no need to alter the question. Anyway, this is a secondary discussion. I'm out.

Important notes:
I am not going into the ethical aspects of editing/removing CCR5 in human embryos, neither will I discuss potential effects of introducing that mutation into the human population. Both of these are very important issues, but out of the scope for this answer.
  As of now I'm not aware of any reliable sources of what was actually done in this case, so I will also keep my answer general / hypothetical without going into any specifics of these particular girls.

That out of the way lets get into the potential problems that could be caused by removing the CCR5 gene from  human embryo using the CRISPR-cas9 system. These can mainly be grouped into two classes: off-target or side effects of the procedure itself and any effects of a non-existing/functional CCR5 by itself.
One additional point I want to mention is that removal of CCR5 does not make one completely immune to HIV, because some strains of the virus (can) use the CXCR4 as a co-receptor instead.
1. CRISPR-Cas9 off-target effects
The CRISPR-Cas9 system has become very popular with scientists in the last few years, because it allows genome editing in very many organism with previously unmatched efficiency and speed. However, people only recently  - when the potential medical use of the system was being considered - started to look into the specificity of the system. What they found was, that while CRISPR-Cas9 is supposed to be very sequence specific it often also induces mutations in genes that were not supposed to be targeted.
There is a quite a lot of ongoing research to reduce these off-target effects, one good example being to use two variant copies of the system that each only cut on strand of the DNA at neighbouring sites (instead of cutting both strands at one site as is normally done).
If such mutations occur while genome editing an embryo the possible effects are very hard to predict - it could be anything from completely harmless to cancer inducing. If one wants any reliable estimate for this, it would be necessary to check for any off-target mutations by sequencing the whole genome of the edited embryo. That however requires (even with very modern techniques) removing at least a single cell from the growing embryo before the IVF procedure can take place and might therefore reduce chances of the IVF being successful.
Main source: Extensive review to CRISPR off-target effects
2. Side-effects of CCR5 removal
Normally it would be very hard (read: basically impossible) to predict what potential side effects the removal of a specific gene would have, even if there are e.g. mice where this has already been done but only studied for specific medical aspects. In this particular case however, we are in luck because there is a naturally occurring mutation called CCR5-Δ32 that also renders the protein completely dysfunctional. We can therefore pretty safely assume that the CCR5 removal by CRISPR-Cas9 will have similar effects to this mutation.
Since CCR5 is a gene expressed by immune cells, it  - unsurprisingly - has influences on various immune functions, but mostly seems to be affect infectious diseases. As this review puts it:

In summary, there are ample data to suggest that CCR5 is involved in both positive and negative regulation of immune functions that relate to the regulation of leukocyte trafficking during infectious and postinfectious diseases.

One particular risk that seems to correlate with non-functional CCR5 is both initial infection and disease progression by flaviviruses. It has been reported that the CCR5-Δ32 mutation increases the risk of being affected by both the Tickborne encephalitis (TBE) virus and West Nile Virus, both of which can affect the nervous system if the diseases progresses far.

Nice and detailed answer that raised a question for me: First, as a side note, is there today an update to add to this question? For example, it appears from my readings in 2022 that single-strand cut is a "feature" operationnal in CRISPR. Second, would there be a possibility to gene-edit a human organism AFTER it has born (and thus reducing the potential side effects during pregnancy)

2019-09-29 update: the answer below is based on a scientific paper that seems to have a major flaw, see https://www.statnews.com/2019/09/27/major-error-undermines-study-suggesting-change-introduced-in-the-crispr-babies-experiment-shortens-lives/ (mirror): the 2 authors have requested that the journal that published their study, Nature Medicine, retract the paper.

The study {1} was published earlier this month and pointed out some side effects of the CCR5-∆ 32 mutation:

Abstract: We use the genotyping and death register information of 409,693 individuals of British
  ancestry to investigate fitness effects of the CCR5-∆ 32 mutation. We estimate a 21%
  increase in the all-cause mortality rate in individuals who are homozygous for the∆ 32 allele.
  A deleterious effect of the∆ 32/∆ 32 mutation is also independently supported by a significant
  deviation from the Hardy–Weinberg equilibrium (HWE) due to a deficiency of∆ 32/∆ 32
  individuals at the time of recruitment.

The article {2} gives an interesting overview of the challenges to use CRISPR gene editing on embryos.

References:

{1} Wei, Xinzhu, and Rasmus Nielsen. "CCR5-∆ 32 is deleterious in the homozygous state in humans." Nature medicine (2019): 1. https://doi.org/10.1038/s41591-019-0459-6 ; Open access through: https://www.nature.com/articles/s41591-019-0459-6.epdf?referrer_access_token=WPFpaFyStI8YbTTEMfC_ttRgN0jAjWel9jnR3ZoTv0Oj3tn20k72VWFe-jjXtNEJHlLKXYkKaqGD9skHjnGnvJUTVNbCDm7LZzwrct9UdoYEGjuFiNmdY_PBv1mOtejfdSOBNIfiYYPHQKxPBPquqX2okvaHuqrbH-cPOgidfYQQoHehy580Z2p1e1IWOQCICnlOBtWq97g3ThPRT3rg3zh0Xu3TB1_y4uDZyqTR0sI3w-e2BhL5AOM01Ot08-PkdJ-2aNqhmxMR6DJJtSfoBfxwDFzkQT_EkudaLLr7jixVT1WokrmAXf_uU6A8hxuZ5-0c1tjYXcnq7amqV7lPTw%3D%3D&tracking_referrer=www.theatlantic.com
{2} Heidi Ledford. CRISPR babies: when will the world be ready? Nature 570, 293-296 (2019). https://doi.org/10.1038/d41586-019-01906-z (mirror)


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How much of my ancestry will match with my brother?
Recently, my brother (full sibling) got his ancestry checked from MyHeritageDNA. They have a similar service like 23 and me and I've found out that both companies are offering the basic service almost the same, with some add-ons which are different.
My question is that if I (I'm a male) send my DNA sample to either organization, how different should I expect the results to be?

Welcome to SE Biology. We expect posters to do some research of their own before posting. Have you considered the genetics and tried to work this out yourself? What do you expect? If you tell us we can tell you if your logic is correct or not.

Should match pretty well. Are you a boy or a girl?

As both you and your full sibling are males, it means that you share the exact same Y chromosome. You also share the same mtDNA as you have the same mother. All the rest is just a bit of segregation and recombination that will lead to minor differences but generally speaking, your ancestry data should be very similar. Specific disease related data might vary though.


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What spider species is this?

I saw this spider yesterday and it was the first time I saw one. It had a log slender body and an almost tail like end. It also can apparently jump. Just wanted to know what species this is. Location (Cavite, Philippines)

Please provide your location and the approximate size of the spider. It'll ensure you get an accurate answer. Thank you.

It's one of the more unusual Jumping Spiders - similar, as Charles said above, to the North American spider Marpissa pikei, the Slender Jumping Spider (see second link below).  Yours is even thinner and more stretched out, but still clearly a Jumping Spider, from the long, heavy front legs and the big eyes on the front of its head.
Your species appears to be a spider called Mantisatta logicauda (first link below)

http://www.peckhamia.com/salticidae/diagnost/mantisat/longi-ph.htm
http://bugeric.blogspot.com/2012/07/spider-sunday-pike-slender-jumper.html


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Is this a worker, or something else?
As far as I understand, this is a buff-tailed bumble bee (Bombus terrestris). It was collected (dying) inside my house in Santiago, Chile. The species was intentionally introduced not far away, for agriculture, some years ago.
Looking for descriptions, I see it is huge for its species, queens reportedly being 20-22 mm (1, 2). I also learned that workers span a wide range of sizes, depending on age (but not this large, supposedly.)
Now, for the caste/sex, I'm stuck due to lack of experience. This site suggests looking at pollen baskets in the hind legs for females (I think I see one, but can't be sure since I don't know exactly what to look at, despite browsing some example photos), but then hairy hind legs (again, I think I might see them, but I'm much less confident) and facial hair for males (I don't really have a point of comparison, but it has some short, black hair in the frons: see expanded photo). Common descriptions also suggests buff color for the tails for queens, but I have seen white-tailed queens around too.
I'd really like to acquire the experience needed.
Is this an old worker, or something else?

this is very likely a queen as they are 20-23mm long but to give a definitive answer you need to measure the lenght of the wings,if they are 38-43 mm it is a queen.the body of a male is 14-16mm the lenght of the wings are 30-33mm and the workers are 11-17mm long and the wings are 22-34 mm long.this is not an answer only some easy to find information.

@trondhansen, thank you! I also read that queens are supposed to have a shorter tongue, which doesn't seem to be the case. I was wondering if there could have been a selective pressure towards larger individuals, vaguely analogous to leg length in cane toads in Australia

I mean, introduction is still relatively recent. Wingspan is about 45 mm BTW (about twice the body length, like all three queens, workers and males)


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What species is this gray bee?
Is this a bee at all, is it just an albino Apis mellifera?
It is roughly the same size as regular honey bees, and was pollinating lavenders along with many of the latter. There was a couple of these white ones.
Here is a photo I took. Sorry for the bad quality.

The bees were seen (and the photo taken) on December 11 (late Spring), at about 1 pm in the eastern border of Santiago, Chile (South America), at the foothills of the Andes, at about 950$\,$m of altitude.
I'm aware that it is possible that the information I provide is not enough to identify the insect. If so, any advise on how to get more meaningful information will be appreciated.
Thanks in advance

Your picture is of too low quality to be sure, but based on general habitus I would say that 1. Yes, this is a bee and 2. No, it is not Apis mellifera.


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What bug is this? (England)
I have found this small bug on the wall in my bedroom, and have been trying to figure it out what it is for months.
There are more of this kind. They are tiny, I can't see how they look like with bear eyes. I can only see their proper shape by zooming in. I have seen them on my wall, in my drawer and on paper tissue.
I live in England in a very humid, dumpy flat.
I have also found bites or allergic spots on my body, but don't know if this bug causes it or something else.
Any idea what it is?

This is a booklouse (order "Psocoptera"), and from the inflated hind femora likely a member of the family Liposcelidae; that family is common in domestic situations as a stored product pest, so while they may not be responsible for your skin condition, you'll still want to have them removed (look for other questions featuring domestic book- and barklice for suggestions on how to do that).


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Frog identification - two different frogs seen in New Zealand
Me and my friends saw these two frogs in man-made ponds in an area which is undergoing development for residential use. Anyone able to identify these beauties?
Also would be interested as to how these frogs got there, as the pond wouldn't have existed 2-3 years ago and there are none nearby.
Location these were found can be seen in the following link:
https://www.pic2map.com/yibrir.html

the first frog(the green one) resemble GREEN AND GOLDEN BELL FROG - Litoria Aurea

Description of the frog -

Have golden-bronze colored spots
Have a black line from the eye to the nostrils
Found in northern Island

And coming to the second frog it resembles Southern Bell Frog - Litoria Raniformis

**Description of the frog - **

Have a distinctive black line running through their back
Found almost everywhere in new Zealand
They have black-brown patches on their skin (can increase in blackness based on the surrounding environment)

Coming to your question , the golden bell frog seems to stay in small temporary water ponds even puddles
On the contrary the southern bell frog lives permanently in a pond so probably it lives somewhere nearby
That'll be it


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Can endemic diseases be acute?
Diseases can be classified as :endemic ,or pandemic,...etc.
 An endemic disease is an infectious disease which is generally or constantly found among people in a particular area.
Disease conditions are :

acute: rapid onset , severe symptoms and brief duration.
chronic:gradual onset and long duration

Can an endemic disease be acute? Or is it always chronic ??

Endemic and chronic/acute are unrelated properties of a disease. Endemic is a description of the frequency of a disease in a population or in an area. Chronic/Acute is a description of the state or course of a disease in an individual.
For example, influenza is endemic in North America: the frequency goes up and down, there's always a few people who have it, but most people don't. Periodically the influenza virus mutates, and becomes much more successful at infecting people. The frequency of the disease goes way up, and influenza becomes epidemic. However, regardless of whether the disease is endemic or epidemic, the disease processes is usually acute: it comes on suddenly, it gets worse for a few days, and then it get better (or you die).
Malaria in endemic in much of Africa and SE Asia (it's always around), but the disease can be either acute (you have fever, chills, prostration), or chronic (the parasite lives in your body, and you can be a source of the disease, you don't necessarily have obvious symptoms, but may be suffering long term damage.


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How do Neurotransmitters get into the neurons?
This may be a dumb question. I'm not a Neuroscientist. I'm just trying to learn more about the brain to improve my AI learning algorithms…
I understand that there are different kinds of neurotransmitters that either increase or decrease the possibility of firing an electrical impulse through the axon. I also understand that these Neurotransmitters do not actually pass through the whole cell (Correct me if I'm wrong…), so they only travel from the Cell's terminal to the next cell's body.
So my question is: How do these Neurotransmitters get into the cell's terminal? Blood? And the more important question: How are these Neurotransmitters distributed among the different neurons? It cannot be at random, or equally distributed, because we have different "reactions" to different Neurotransmitters. For example if Dopamine is produced it gets sent to these different cells in our brain which makes the activation of its cell more likely (if I understood correctly). Dopamine is also known to increase our feelings of lust and makes us more focussed (and more). But if Dopamine got sent to ALL of the Neurons in our brain, thus make the activation of EVERY cell more likely, it would bring total chaos to our brain. (Eg. Make our fear-part of the brain activate more easily, but this is not the case.). So how are these Neurotransmitters distributed?
Thanks in advance

The general rule (though like much of biology there are exceptions) is that each neuron releases a specific neurotransmitter: neuron types are often named by this principal neurotransmitter plus the suffix -ergic: a cholinergic neuron releases acetylcholine.
There are also similar molecules that do in fact act throughout the body, but we don't call these neurotransmitters, we call them hormones. Sometimes they are exactly the same molecule: epinephrine, also known as adrenaline, is both a neurotransmitter and a hormone; it can act as both because different receptors have different affinities, and the circulating hormone levels are typically much lower concentration than the amount that can be released in a more confined space.
Additionally, neurons have receptors for different neurotransmitters, so for example dopamine does not affect all neurons, only neurons that have dopamine receptors. Different cell types can also have different types of dopamine receptors, and those receptors can do different things to the cell. The same neurotransmitter could be excitatory to one cell and inhibitory to another.
Broad simplifications of nervous function such as:

Dopamine is also known to increase our feelings of lust

really don't say anything broadly about the function of dopamine. I could similarly say that computers control airplanes: that statement is true even though you will fine airplanes not controlled by computers and because you will find the vast majority of computers don't control airplanes. However, if I turned off all the computers in the world, a lot of airplanes would have their function impacted.
How do neurotransmitters get into neurons?
Most neurotransmitters are synthesized within neurons from other ingredients. GABA, for example, is derived from an amino acid glutamate. Glutamate itself is also a neurotransmitter. All neurons that release neurotransmitters have pumps that concentrate these neurotransmitters into vesicles. Neurons often also have transporters to pull released neurotransmitter back into the cell so it can be reused, for example a common class of psychoactive drugs are the serotonin reuptake inhibitors: these drugs inhibit the protein that pumps serotonin back into serotonin-releasing cells.
General statement
Use of knowledge from neuroscience to improve AI algorithms has moved far beyond what a novice can contribute to. If you want to utilize biology in AI algorithms, you have to be prepared to become an expert in both. I'd suggest starting with a basic neuroscience textbook if you want to learn about neuroscience, for example books by Purves' Neuroscience or Kandell's Principles of Neural Science.


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What is this species of green frog found in store-bought flowers in France?
Today I found a frog in a big flower composition bought at a french shop (living in Grenoble, south of France).
It started snowing today, and I'd like to keep it until it's warmer outside.
So could someone tell me what species it is ? (To check what it eats and if it's legal to keep it)
Thanks !

(I'll edit with more pictures if it's needed and if she moves)
Edit :

Please update your post with the size of your frog. Thanks!

I think this is a type of green frog

This looks very much like a tree frog of which there are many similar looking species. Without knowing where your flowers came from or more characteristics about the specimen, it'll be difficult to provide an accurate answer*.
One possibility may be the European tree frog (Hyla arborea).
According to Wikipedia:

Members of the H. arborea species complex are the only representatives of the widespread tree frog family (Hylidae) indigenous to mainland Europe.

which is supported by genetic work by Stöck et al. 20081

Description [source]:

Small (3.2-5 cm in length)
Slender body shape with long legs and smooth dorsal skin+
Usually green (but variable) with dark brown lateral stripe across eye caudally to groin and whitish ventral skin surface.
Gripping discs on toes

The range of this species also includes much of France:

 Image Source
+ Although the description states this species has smooth dorsal skin (possibly like the OP's specimen -- I can't tell for sure), many of the pictures I've seen seem to suggest that the dorsal skin of this species is actually rather granular. For example, see here.
*Feel free to update your post with additional info and perhaps a better response will be added.

 Citations:
 1 Stöck, M., Dubey, S., Klütsch, C., Litvinchuk, S.N., Scheidt, U. and Perrin, N., 2008. Mitochondrial and nuclear phylogeny of circum-Mediterranean tree frogs from the Hyla arborea group. Molecular Phylogenetics and Evolution, 49(3), p.1019.

I think the European tree frog is more than a possibility. This looks exactly like one.

@RHA I agree it looks like a pretty good candidate. My concern came from the skin texture. Most images I've seen seem to suggest H. arborea actually has rather granular dorsal skin, whereas the OP's specimen looks to have smooth dorsal skin (which matches the description I quoted). This lack of clarity was the only reason I shied from giving a definitive response.

I think it looks smooth when the skin is wet. I've seen the Europeam tree frog a number of times in the wild and this looks like one. Besides, there is no realistic alternative in Europe.

@RHA Ok cool -- fair enough. My only thought was that perhaps some nonnative had been transported with the flowers. I appreciate the first-hand knowledge since its quite hard to catch a glimpse of one across the Atlantic :p


text:
What is this insect I found in my kitchen?
So I found this bug crawling around near my kitchen sink. There were two others, but not any sort of swarm. I think they're some sort of insect larva, as they don't have a bunch of legs like a millipede or woodlouse, but I have no idea what kind. There also seem to be several shed shells nearby, if that helps.
As for location this is in the upper Midwest.
Here's the top of the thing, with screwdriver for scale

And here's the underside.

It looks a lot like a Dermestidae larva. But hard to tell which one based on the picture. Maybe Anthrenus (common in habitations).

That is a larva of a dermestid beetle (Family, Dermestidae). https://en.wikipedia.org/wiki/Dermestidae Dermestid beetle larvae feed on dried material, and are the last insects to clean up a carcass. They are the bane of insect collectors, as they will eat a collection right off the pins. They leave nothing but dust and their shed skins behind.

Those do look quite a lot like it. Perhaps they were after the bread crumbs near the toaster, as I found a couple more shells under it. (They certainly do shed a lot.) How concerned should I be about these?

Unless you have a precious insect collection, I would not worry too much. They really are specialists on dried materials, and don't generally go after food in my experience.


text:
Hardy–Weinberg equilibrium for SNPs
I have a SNP stats file structure, which contains all information about genotypes and imputed SNP/INDEL imputation qualities, allele frequencies and minor allele assignment.
SNPID   RSID    chromosome  position    A_allele    B_allele    minor_allele    major_allele    AA  AB  BB  AA_calls    AB_calls    BB_calls    MAF HWE missing missing_calls   information
--- rs200405949 NA  10023   CCAA    C   C   CCAA    923.32  16.662  0.012   911 6   0   0.0088756   4.8216e-17  1.0638e-05  0.024468    0.47987
--- rs201803828 NA  10097   CCA C   C   CCA 930.29  9.711   0   924 4   0   0.0051654   -0  1.0638e-06  0.012766    0.50802
--- rs185444096 NA  10177   C   T   T   C   291.03  45.234  0.712   216 12  0   0.069231    9.6433e-17  0.64152 0.75638 0.80608
--- rs200882690 NA  10299   TA  T   T   TA  292.62  43.613  0.744   219 12  0   0.066921    4.8216e-17  0.64152 0.75426 0.79622
--- rs56377469  NA  10469   G   C   C   G   239.25  474.83  225.9   38  69  20  0.4929  0.10014 2.234e-05   0.86489 0.42593
--- rs7341907   NA  10869   C   G   G   C   239.29  474.8   225.89  38  69  20  0.49287 0.10014 2.234e-05   0.86489 0.42597
--- rs149305563 NA  14665   G   A   A   G   267.44  66.53   2.973   144 16  0   0.10755 0.10741 0.64155 0.82872 0.79468
--- rs149079262 NA  14690   C   G   G   C   207.26  115.51  14.189  56  25  1   0.2135  0.12672 0.64153 0.9117  0.79388
--- rs141156662 NA  15883   A   G   G   A   259.05  71.908  6.001   131 13  1   0.12451 0.20633 0.64154 0.84468 0.80157
--- rs202192731 NA  17614   CT  C   CT  C   7.893   142.55  789.45  1   39  581 0.084231    0.27659 0.0001117   0.33511 0.47425

I managed to assume/figure out the meaning of all columns but two - HWE and information.
HWE:
I assume HWE means Hardy–Weinberg equilibrium, and is actually a chi-square value obtained via Pearson's chi-squared test, and using only samples from the same dataset (and not compared to some general dataset, e.g. GWAS). Using HWE , we can then calculate the p-value using the degrees of freedom (one in this case) via the gamma function (e.g. via p-value calculator), and if the result is significant, this means that the specific SNP is not in HWE, hence this SNP is either in linkage disequilibrium, or needs to be rejected/ignored because of genotyping (i.e. data obtaining) errors. If so, what significance level is mostly used/best for such cases? In the Hapmap II paper, SNPs are removed if they are not in HWE with a p-value < 0.001.
information:
I have no clue what it means or how it's calculated.

Regarding "information": specifying the software used for analysis could be of help. As of now, I have no idea of what it is.
Regarding "HWE":

Not knowing the software I am not sure, but I can guess that In the column you already have the pvalue.
There is no clear agreement on the threshold, and not even if SNPs outside of HWE should be removed or not. You can give a look to this paper (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2796342/) to start understanding. The choice depends a lot on the study sample and the questions you are trying to answer.


text:
GEN file format, SNPs and alleles
I have a few questions I can't seem to get a straight answer to, regarding the .gen file format and also biology in general.
The .gen file format specifies SNPs for individuals.
Since each SNP has associated allele A and allele B, I assume that the file only contains Causative SNPs, and not Linked SNPs, since the former reside in the gene, and the later don't. Since each SNP in the file has an associated gene (actually genotype, some combination of allele A and B). Correct?
SNP indicate a single position in genome, so why can allele be identified with a sequence larger then one? Or does it indicate just a starting point, where each allele can be of different length, which can be greater than 1?
Allele should be a particular variant of a specific gene, but in other places I saw the definition "Alleles are alternative forms of a particular sequence.". The later seems more logical, if looking at the .gen file, but it's contradictory to the first statement. So, what's the correct definition?
EDIT:
After further research I came up with findings, demonstrated in an example row for .gen file:
--- rs200405949 10023   CCAA    C   0.249   0.745   0.007   0.005   0.84    0.155 ...

--- - chromosome number, which is missing because it can be inferred from the filename, belonging to each chromosome
rs200405949 - ID of the SNP - a single nucleotide which can vary between samples/people; there are usually only two possible variations, but in rare cases there is a third or even fourth - which are ignored in .gen?
10023 - allele pair (base pair) coordinate/position inside the said chromosome. Either both major and minor allele are made of a single nucleotide (in which case the SNP coordinate/position inside the said chromosome might coincide with this position), or one of the alleles will have more than one nucleotide and the other allele will be the same as the first nucleotide of the former allele - because we need only one distinct sequence, and all other combinations of same nucleotide length are automatically the other allele?
CCAA - (usually?) major allele - the most common allele (specifically in this context, a single nucleotide or a sequence of nucleotides) for a given SNP (or near it, i.e. somehow connected to it) IN the cohort in question, i.e. the cohort being all the samples/people in the experiment/.gen file (hence, the number of samples equals the number of triplet columns after the 5-th column onwards). It occurs in more than 50% of the times COMPARED to minor allele. Compared to minor allele, they both start with C - shouldn't they differ at this SNP position by definition? Also, more than one nucleotide is specified here - why? SNP always has one nucleotide...
C - (usually?) minor allele - the second most frequent allele (specifically in this context, a single nucleotide). The SNP site can be bi-allelic (mostly picked/studied), in which case the major and minor alleles are the only possible alleles, but some sites are tri- or quad-allelic - in which case we don't have the info for the third (and fourth) allele variants, but we know they are even less common then the major and minor alleles?
0.249  0.745   0.007
0.005   0.84    0.155
... - each subsequent triplet of values then indicate likelihoods of homozygote CCAA/CCAA, heterozygote CCAA/C, and homozygote C/C genotypes (allele pairs) at this SNP, respectively, for one sample/person (each allele is present on one of the two copies of the said chromosome, either maternal or paternal). If one of the three values has a value 1 and the other two have 0, I guess this actual SNP was (somehow) tested for, hence we can be 100% sure which allele pair it is, and if not, then the probabilities were somehow deduced (e.g. from other, somehow related SNPs perhaps). What if they add up to less than one? Or even what if all of the three values are 0?
Are my conclusions correct? And what about the open question?

Based on https://www.sciencedaily.com/terms/allele.htm, each gene can be represented by a set of alleles, and alleles are just alternative forms of a particular single-nucleotide sequence; and since they can posses 2 different forms for the given genome (resulting in a 3 distinctive combinations), they are called SNPs. Besides alleles, there are also other in-between single-nucleotides in the gene, but these are the same for the whole population of a given (e.g. human) genome. True?

The definition of allele depends on the context.
If you look at the DNA of a single person you have usually two copies of each autosomal chromosomes. Each copy is called an allele. If you know look at the sequence at a specific position, you can say one of the two bases are located at one allele and the other base on the other allele.
Beside this there is a definition of allele if you take a look at a many persons or a whole population. Here you call an allele "as alternative forms of a particular sequence".

But how is SNP, which indicates a single nucleotide, associated with a major and minor allele, since either one can be of length greater than on? Does it mean that starting from the specific SNP position, it can either be the start of the major or the minor allele?

From what I could find the .gen file format for SNPs was developed for the IMPUTE2 program and is generally meant to be a flexible file format for SNP data. The description of the file format is supposed to documented here (multiple pages pointing to that link), sadly that link is broken / the site is removed.
However, I found some other descriptions of the format:

In the GEN format each SNP is represented as a set of three
  probabilities which correspond to the allele pairs AA,AB,BB.

from here

The genfile contains predictor values, one row per predictor.
  --gen-skip indicates how many header rows (typically 0 or 1);
  --gen-headers indicates how many header columns (typically 0 to 5).
  --gen-probs should be 0, 1, 2, 3 or 4:
   0 - haplotypes - predictor values should be "0 0", "0 1", "1 0" or "1 1"
   1 - dosages - predictors provide the (expected) number of A alleles
   2 - two probs - providing probability of being AA or AB
   3 - three probs - providing probabilities of being AA, AB or BB
   4 - four probs - providing probabilties of being AA, AB, BB or NA, where A and B are the A1 and A2 alleles

from here
Like finswimmer already wrote in his answer, it is very important to be clear about what is considered an allele in the context of SNPs. For the .gen file format this is the identity of the base at a given (SNP) position and since humans have a diploid genome, the allele of a specific individual can be one of three versions (usually called AA, AB & BB).
Regarding your specific points:

Since each SNP has associated allele A and allele B, I assume that the file only contains Causative SNPs, and not Linked SNPs, since the former reside in the gene, and the later don't. Since each SNP in the file has an associated gene (actually genotype, some combination of allele A and B). Correct?

The alleles in the .gen file refer to the respective SNPs not genes.
There is no reason to assume that an given .gen file only contains certain SNPs; if it does this is not due to the data format.
The SNPs in a .gen file do not generally have to be linked to a gene.

I've added example, can you comment on it and answer the remaining of my questions?


text:
Why V(D)J recombination only happens in B and T cell development?
Does V(D)J recombination only happen in B and T cell development? Can it happen in other types of cells?
If V(D)J recombination only happens in B and T cell development, why other types of cells cannot have V(D)J recombination?

Edit 1:
V(D)J recombination rearranges the DNA sequences of maturing B and T cells that encode proteins for recognizing antigens, so that different B and T cells may recognize different antigens for initiating further immune response.
Recombination  activating  gene  1  (RAG1)  and  RAG2  proteins are essential for rearranging the DNA sequences in V(D)J recombination. RAG recognize specific DNA sequences, called recombination signal sequences (RSSs), that are adjacent to the variable regions of the genes that encode proteins for antigen recognization.
V(D)J recombination occasionally happens in natural killer (NK) and dendritic cells [1, 2].
So the answer to my question is that V(D)J recombination is not restricted to B and T cell development.
I would like to thank @swbarnes2 for pointing out the importance of RAG1 in V(D)J recombination. Also thank @MattDMo for introducing me to the community guidelines.
This question is not my homework. I am just curious why V(D)J recombination seems to be only discussed in the context of B and T cell development.
References:
[1] Kuo TC, Schlissel MS. Mechanisms controlling expression of the RAG locus during lymphocyte development. Curr Opin Immunol. 2009;21: 173–178.
[2] Borghesi L, Hsu L-Y, Miller JP, Anderson M, Herzenberg L, Herzenberg L, et al. B lineage-specific regulation of V(D)J recombinase activity is established in common lymphoid progenitors. J Exp Med. 2004;199: 491–502.

Edit 2:
Added some highlights to my edit 1.

Why would other cells need to undergo somatic recombination like B and T cells do?

you are the one posing the question, therefore you need to support its validity. Hypothetical "what if...?" questions are off-topic here.

Your question already has 3 downvotes and 3 close votes because 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. Please see our homework policy for more information. Your 2 questions can be easily answered with a Google search or by looking at a textbook.

"Homework" is interpreted to mean any academic or other assignment, test preparation, or task given in relation to a class, educational setting, or self-learning. Our goal is not to simply be an answer site, but rather a site that promotes self-learning with some expert help along the way.

The genes that do recombination likely aren't expressed in any other tissues.  A quick look at expression of RAG1 shows expression in immune cells, and not really anywhere else.

It's not just "likely" they're not expressed in other cell types, they just aren't period. Otherwise DNA rearrangements could run amok and cause a lot of damage. They're very tightly controlled in developing T and B cells, along with mature B cells undergoing hypermutation.

I think genes like RAG1 are already tightly bound to work only on receptor genes and nowhere else; there's just no point in rearranging receptor genes in cells which will never express them.


text:
Does cataract condition cause red film when sun is shining?
Since two years ago I have a red film in my field of vision when the sunlight (or a white spot) is at the border (or even lightly behind) of the vision field, the red color is especially obvious at the shadows or dark places (it seems logical that the film color is more visible where there is less light).
My eye doctor recently diagnosed a little bit opalescence of my eyes, that is, a beginning cataract.
So my question is simple : does cataract condition cause a red film when sun is shining at the vision field border ?
I have an explanation for this : at the eye border the white sun light goes trough the skin and is colored red by the blood, then because of opalescence the red light propagates into the whole vision field, thus creating a red film. So if this explanation is correct then any people with a cataract condition should see a red film in such situation, that is what I want to check. Should be quite simple.
(Without strong spots there is still a mild gray film, making black appearing grayish and making shades differences less obvious to see than before this condition. Vision tests on green or red background doesn't make any differences)

"Should be quite simple." What research have you done to try to answer this question? Have you read about cataracts and 'redness of vision"? FWIW, most early cataracts are completely asymptomatic. Almost everyone gets them as they age.

@anongoodnurse I find no info about relation of vision redness with sun and cataract, so it seems that it has nothing to do with cataract, but I want to be sure of this. And this "should be quite simple" to check as I have a very early cataract, so anyone with a cataract, even with very early one, should be in the same situation as me.

Exactly! You have answered your own question. Millions of people have early (and asymptomatic) cataracts (myself included) and this is not a reported resultant effect.


text:
Which moth is this?
City name - Mohali (Chandigarh)
Season - winter(after rain of western disturbance)
Location - IISER Mohali hostel near tube light of mess
Time - 21:49, 22 February 2019
Size - 1.5cm

2:

I'll swear it's a hawk moth, which hawk moth is another matter though.

Providing geographical location is good but it need not go into details which nobody else would be aware of. For example, you should indicate in which part of the world (and country) your location is and what is the general weather/vegetation conditions in that region. Any average person (even an Indian) may not know where Mohali is. You have mentioned about the weather but you should clarify what "western disturbance" is. Now, the specific details about your institute hostel and mess are not relevant unless you have a unique ecosystem. In that case you should explain the local conditions.

It does look like a gray hawk moth "species" with hind wings folded underneath. The body shape seems right, but the size estimation seems too small.

It resembles a Laothoe species, indeed member of the hawk moth familie. However, all Laothoe sp described on Wikipedia have a wing span over 7cm and none of them occurs in India.

It's bombyx mori moth


text:
protein size range for ultrafiltration or nanofiltration
I am hoping to concentrate mixed proteins in homogenized leafy vegetables such as kale, spinach etc (after removing pulp and fibers) as a first step in further investigations (second step using size exclusion to isolate frations), but am unsure what pore size is appropriate for ultrafiltration membrane as I do not know the dalton range of the mixture.
Is there a typical range of protein molecular sizes in Daltons found in plant matter?
Would appreciate any pointers.

Why not do SDS-PAGE and determine the size range?

Mind that protein isolation goes beyond size exclusion.

apologies for the abbreviated terms, edited question. I am a chem eng and fairly ignorant about biochemistry laboratory techniques. So, is it sensible to perform electrophoresis on the raw extract to determine the MW range? Can I do that without concentrating and "cleaning up" the raw extract? I was going do that as a later step.


text:
Is the chemical composition of urine detrimental or beneficial for a tree?
Seeing as a lot of people around the world urinate against trees it came to mind that I never thought about how the tree responds to this.
Is it detrimental for a tree if people urinate against them?
When looking on the internet, I found this explanation about urine:

Human urine consists primarily of water (91% to 96%), with organic
  solutes including urea, creatinine, uric acid, and trace amounts of
  enzymes, carbohydrates, hormones, fatty acids, pigments, and mucins,
  and inorganic ions such as sodium (Na+), potassium (K+), chloride
  (Cl-), magnesium (Mg2+), calcium (Ca2+), ammonium (NH4+), sulfates
  (SO42-), and phosphates (e.g., PO43-). What Is the Chemical Composition of Urine?

Of course, it is possible that the small amounts present in urine are negligible in contrast to the amounts a tree absorbs on a daily basis.
What I am wondering: is the chemical composition of urine detrimental or beneficial for a tree?

Tom, this is a wonderful improvement from your previous [now deleted] post, and I'm glad you took the time to do some of your own research and include it here. Really great to see the newly added effort! Thanks! +1

related. Also, my +1 to this question and @theforestecologist comment was not enough to express how much the improvement in this question is appreciated. I wish I could upvote again...

In most instances, plants benefit from animal litter, which is why it is sprayed in fields, and used to get bigger crops. Everything in moderation obviously, there is an optimum influx of animal litter which increases plant growth, which in the case of humans weeing, is much lower proportion than cows. other human activities are a lot more detrimental to trees, i wouldn't worry about weeing on them. a big tree can probably benefit from about 1 cubic meter of wee before it got detrimental. ideally you have to keep the pH at about 6.4

a large tree can probably benefit from about 1 cubic meter of wee for a year before it gets detrimental, but not in the same place at the same time.

@com.prehensible the old saying, everything in moderation seems applicable?

Indeed. for cow urine here is a study: http://www.scielo.br/img/revistas/hb/v27n4/06t01.gif

Here is a book about dry-matter production of urine treated plants. If we consider that trees are large plants, it's fair to apply the study to trees too:
The findings of the study suggested that urine and urine products are equally as effective as mineral fertilizer especially in sandy soil and that splitting the application is a useful strategy to manage urine and urine products for optimum dry matter production.
Some plants do live in harsh environments with chalky pH and other specifics, and they may weakened by it. It's safe to say most trees are unaffected or improved by some urine, although the biggest trees are because of rain and steady underground streams (groundwater).

but just like anything in biology amounts matter, if enough people urinate against a tree it can cause salinity issues. But you need a ridiculous number of people to cause that. Note dog urine is far more concentrated so it can reach the problem levels much faster, trees visited by dozens of dogs in a day suffer for it.

@com.prehensible I am sorry, I completely forgot this question (multiple SE's sometimes clutter my mind). If I understand correctly (correct me if I am wrong), it depends on the kind, size and (in the case of dogs) the concentration of the urine and its amount are all important factors.

And the rainfall too. Sorry am in car can't answer.

Speaking specifically about blueberry bushes as a perhaps extreme example, they thrive in acidic soil and nitrogen-laden soil. However, dog urine is bad for blueberries, as the high nitrogen content overwhelms the plant and damages fruit production. Dog urine is only slightly acidic (pH 6-6.5) and can often be alkaline, which also changes the soil acidity in the direction that is not good for blueberries. The acidity and nitrogen content of dog urine can depend on diet.
If there's a plentiful supply of rainwater and the soil has the right nutrient balance and acidity for the plants and trees living in it, then urine will disturb that balance, strictly speaking, however marginally. More urine could damage plants if it changes the soil constitution outside the comfort zone of what is growing in that soil.


text:
What is the name of this spider I found in The Netherlands?
This spider is smaller than 1 mm and fast.
The spider has tiny hairs on orange coloured legs. The backside of the spider is dark-brownish and has a small red stripe in the middle. I have taken pictures magnifying 25x using a lens of some watchmaker glasses. As a reference the lens of the lamp shining on the spider is 6mm.
Found inside my house on the second floor on the attic.
The location is North-Brabant, The Netherlands, location on maps.
I have searched all over the internet but I keep coming back to mites which this specimen doesn't resemble.
Unfortunately the camera isn't as good as my eyes, although a little zooming is possible.

The spider skittered around again today and I managed to take a picture, unfortunately not a zoomed one but maybe some characteristics will be recognized.

I think it is indeed a mite - have a look at genus Anystis or Tetranychus.

@JimN Yes that is it! I never thought to search for spider mites. Would you like to write an answer so I can accept it?

I believe you are looking at a spider mite of the genus Anystis or Tetranychus. Both of these have The Netherlands in their range.
Here is an info page on the two genuses, includes a map of observations and a gallery of photos that you can even filter to only view images from a certain range. You can also filter the gallery to group photos into species categories.
Anystis: https://inaturalist.ca/taxa/249515-Anystis
Tetranychus: https://inaturalist.ca/taxa/203334-Tetranychus