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Can anybody identify this kind of plant?
Location: Low Tatras, Slovakia, elevation: 1800 m. Can anybody identify this plant from Slovakia mountains?

Does it look like a young conifer?

I think this is some kind of Hypericum.  In Costa Rica and the Andes there is a high altitude ecosystem called the paramo in which shrubby Hypericum are characteristic species.  The area in your photo looks to be covered with shrubby species, and you are at decent altittude.  Looking at your picture (at full size) the leaves look approximately decussate which is typical of the genus, and also, the stems are ridged which is also pretty characteristic.
There is a good paper here on Hypericum of the Mediterranean region.  It mentions some groups that are shrubby or dwarf but thus far I have not been able to find a species that looks just like your picture.
Update: Possibly it is Hypericum aegypticum which looks about right relative to your picture, esp, the leaf color and size.  Also known to grow at that altitude. Decent picture here plus the one at Wikipedia both look similar to yours.
Update 2: On fresh look, the bases of the leaves for Hypericum aegypticum don't compare well to your picture, but I still think it is a Hypericum.


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What kind of house plant is this?

This is a house plant I have that I love but I don’t know what it’s called. I’d love to research it and even buy more but it’s name is a mystery. Picture taken in Ontario, Canada.

IMO, this question would be a better fit on gardening.SE.

It looks to be a Clivia; The English common names are Natal lily or bush lily.
It's a plant that comes originally from Africa but it now commonly sold as house plants.
The Wikipedia article give a good information about that plant.
Example:

Picture taken from this site.
You have also to notice this is a toxic plant and to keep away from small children or pets.

For downvoter(s), please explain why my answer is not good and how it can be improved? If you think it's wrong, please just tell what the good answer (and post it as well).

not sure about the down votes, but maybe you could add a good description or image to show the similarities between the Clivia and the plant in question.

I added some more details as requested. If someone have a better answer I would delete mine without problem.

source: Stack Exchange

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

sort: votes


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What is the gene for height?
Height doesn't seem to be linked to sex, which is surprising. I have seen ways to predict children's height and it involves taking the average of both parents height. Upon my search, I did not find the actual gene for height.

No single gene determines the height (a polygenic trait) of an individual. In fact, height is coded for by over 700 genes. Also, I'm caught quite off guard by your suggestion that height isn't linked to sex, which is obviously not true. One gene that is associated with a shorter height (to put it simply), ITM2A, is expressed more strongly in women and so helps explain a small (though not inconsequential) fraction of the height difference between men and women.

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


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Why did they expect Astronaut Scott Kelley's telomere shortening to accelerate? (they got longer!)
The NPR News article and podcast Scientists Share Results From NASA's Twins Study says:

SCOTT KELLY (NASA Astronaut): You know, the symptomatic stuff is fine. I don't have any long-term negative feelings, physically, from being in space. Now, there's the things you can't feel. And hopefully, I will never learn that those are a problem.
GREENE (Host): Those things you can't feel - well, it turns out they are as small as the protective structures at the ends of his chromosomes.
MARTIN (Host): Yeah. These are called telomeres, and normally, they get shorter with age. But what about in space?
SUSAN BAILEY (Principle Investigator): What we wanted to do was evaluate telomere length in both of the twins before and after so that we could see, you know, where they started and then where they ended.
MARTIN: Susan Bailey was one of the scientists who answered this question. She expected the stresses of space to shorten telomeres quicker.
BAILEY: And, in fact, we saw exactly the opposite thing - that during spaceflight, he had many more long telomeres than he did before he went up. So that really couldn't have been more of a surprise to us.

See also Radiation Biologist Dr. Susan Bailey Studies the Cellular Clocks of Astronaut Twins
Question: Why did investigators initially believe that Scott Kelley's year in space would accelerate the rate of telomere loss, relative to his baseline rate and the rate of his identical twin brother on the ground? What would be the postulated mechanisms?

I've added the radiation tag since it is a known difference between spending a year in space versus on the ground, but I don't know if that will be part of the answer  or not.

Dr. Bailey wrote a short piece that hints at the reasons behind why she expected what she expected:

Telomeres are the ends of chromosomes that protect them from damage and from “fraying” – much like the end of a shoestring. Telomeres are critical for maintaining chromosome and genome stability. However, telomeres naturally shorten as our cells divide, and so also as we age. The rate at which telomeres shorten over time is influenced by many factors, including oxidative stress and inflammation, nutrition, physical activity, psychological stresses and environmental exposures like air pollution, UV rays and ionizing radiation. Thus, telomere length reflects an individual’s genetics, experiences and exposures, and so are informative indicators of general health and aging...
Our study proposed that the unique stresses and out-of-this-world exposures the astronauts experience during spaceflight – things like isolation, microgravity, high carbon dioxide levels and galactic cosmic rays – would accelerate telomere shortening and aging. To test this, we evaluated telomere length in blood samples received from both twins before, during and after the one year mission.


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Tiny bug in Amman-Jordan

I saw this bug many times in my room this spring. Can any one help identifying it?!

This is likely a duplicate of Small mottled beetle identification; the species involved is a widely distributed pest.

Is it dangerous? How can I get rid of it?

Not so much dangerous as a nuisance; the question I've linked to has an answer that eventually links to web pages that discuss control measures.


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Do cats produce DMT?
Edit: If somebody (anybody) wants to add an answer so the bounty won't go to waste, please do so! The comments have already introduced me to the Kegg metabolism database, some interesting papers, and an amazing chapter on the biochemistry of cats. Thus, this question has been useful to me (and hopefully, to the community as well).

There is a question on Skeptics.SE that asks if "cats have a chemical in their brains that resembles LSD." I haven't found any similar claim online, but started wondering:

 1. Do cats produce (natural) compounds that structurally resemble LSD?
 2. Do cats produce (natural) compounds that functionally resemble LSD?

Quickly glancing at the structure of LSD, it contains an indole ring. Hovering over the various indoles here found one substance that occurred in animals and was consumed as a psychedelic drug.

There is a paper that writes:

N,N-Dimethyltryptamine (DMT) is an indole alkaloid widely found in plants and animals. It is best known for producing brief and intense psychedelic effects when ingested. Increasing evidence suggests that endogenous DMT plays important roles for a number of processes in the periphery and central nervous system, and may act as a neurotransmitter.

The paper also proposed the role of DMT as a neurotransmitter. However, I haven't been able to confirm DMT is naturally produced by cats.
Do cats produce DMT? If so, what is the purpose of DMT in the cat?

I suggest you try to answer this yourself using the Kegg metabolism datatbase. I couldn't find anything for Dimethyltryptamine, but searching for tryptamine gave eight pathways. I suggest you inspect each to see if there are any related compounds. If you find them, then check which organism the pathway is present in. Even if your search is negative, you'll benefit from the experience. Good luck!

@David I don't quite understand the Kegg database. It's something like all the signaling/metabolic/synthetic pathways involving tryptamine? I was able to find N-methyltryptamine here. How would you check for the organisms with the depicted pathway? Thanks for the help!

Select Felix catus from the drop-down menu "Reference Genome". I did this and the link is here. Enzymes present are highlighted in light green.

@David Is there a way to specifically find references for N-Methyltryptamine in Felix catus? The website doesn't seem to point to any.

Just the usual search tools. I tried Pub Med from within my Papers bibliographic app, but only got results for N-methyltryptamine alone, and then only about 40 going back to 1987. All seemed either synthesis in plants or exotic animals like sea sponges, or effects on animals. Sorry I can't help further.

@user1136 Are you suggesting that cats don't have N,N-dimethyltryptamine because they do not develop tolerance when given small doses?

Why are relevant parts of the question hidden as "spoiler"?

@user1136 The article is really interesting! Thanks for sharing! "This review comes to the conclusion, that “synthesis of DMT in man has yet to be demonstrated” and that the evidence for the role of DMT in schizophrenia is “currently in-complete”. This pessimistic view, however, is not shared by everybody in the field and further re-search needed to clarify this issue." I'll look for articles that cited this one.

@Arsak They aren't part of the question I am asking here. I didn't want to cluster it or make it unobvious. But, I didn't want to delete it either.

Why are cats so important here?

@AliceD Would it be better to make the question broader? (e.g. Which organisms produce DMT?)

@AlexAl oh dear, no. That's way too broad. I'm just wondering what the specific relevance is of DMT in felines

@AliceD I guess I can only say, "I'm curious about cats." And that's the truth, and a bad explanation.

@user1136 Thanks for the reference! I do find it interesting.

Yes! Many mammals, including cats and humans, produce DMT in small amounts.
DMT has been detected in blood and urine and is produced by the enzyme indolethylamine N‐methyltransferase (INMT). These do bind to serotonin receptors. Serotonin receptors are actually expressed in multiple tissues outside of the brain. However, DMT does cross the blood-brain barrier (ref), so it's possible that endogenous DMT has some neuroactive effect (I really don't know). Good question.
This 2016 paper states (referring to a 2012 review) that it was identified in urine, blood, and CSF:

A review by Barker in 2012 assessed 69 studies that reported endogenous DMT detection and quantities reported in urine (29 studies), blood (11 studies), and cerebrospinal fluid (4 studies) from 1955 – 2010 primarily comparing detection levels within healthy controls and schizophrenic patients. DMT in urine was examined in 861 individuals (635 patients), 276 patients and 145 controls were positive for DMT.

I think that's the most direct answer to you question I could find.
I didn't find anything on cats specifically, but that's likely to be similar.
This earlier 2004 paper states that it was only found in urine, but the previous study refers to studies before 2004, so I don't know why these two seem to contradict:

In mammals, endogenous bufotenine and DMT have been identified only in human urine. The DMIAs bind effectively to 5HT receptors and their administration causes a variety of autonomic effects, which may reflect their actual physiological function. Endogenous levels of bufotenine and DMT in blood and a number of animal and human tissues were determined using highly sensitive and specific quantitative mass spectrometric techniques.

Here's the entry for INMT on Kegg, and the Human Protein Atlas lists where INMT is expressed. Weirdly, that enzyme is highly expressed in the human lung.

As a neuropharmacologist who's specifically studied DMT (doi:10.1021/acs.jmedchem.9b01404), I consider it somewhat unlikely that it's a neurotransmitter, or at least one of any significance.


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Is this Indian snake venomous?
I found this snake near a small garden.
Location: India (Hyderabad, south India)
Temperature: 38 oC
Humidity: 28%
Time: 2 hours past noon (2PM).
Similar snake was found in drainage of our locality.


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What's the percentage of zoom needed to see protozoa in an optical microscope?
I was searching for a microscope and I saw some with prices of over 10.000$. However I need to buy one that can actually show me the cells of a culture I am growing at home, and I really need to know how much "zoom" I need to see them.

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

specifically, a quick Google search can show you approximate organism sizes, approximate protozoan sizes, and how magnification and size relate. Please perform your own google searches and report back what you find and what you are still confused about. Demonstrating additional effort will certainly result in your question receiving a more positive response from most of our community. Thanks, Caju!

Not an answer since I'm a long, long way from being an expert, but 10,000 dollars is far too much to pay for a hobbyist-level microscope.  300 dollars is a reasonable ballpark, and IMHO magnifications above 400X or so aren't much use.  I found this site to be helpful: https://www.microscope.com/how-to-buy/

You can see a few like paramecium with good bare eyes. A 10 magnification loup will reveal more. For general amateur use a stand held binocular ( not distance type binoculars) is very versatile, and common, traditionally 7 X to 40 x magnification. Any more magnification will require special lights ,sample preparation , etc.

When I was much younger ( and eyes were sharper) .I watched paramecium and rotifers in my aquarium. I used various microscopes all my adult life but never published , as most metallurgists could say the same.

You don't really need special lights (other that the normal below-stage light), or sample prep beyond putting a drop of liquid on a slide and a cover glass over it, to see a good many microorganisms.

Thanks for all the help, seemingly, the microscope I'm willing to buy is more than enough for what I wanna do!


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How many palindromic sequences in human genome?
I'm writing an article on palindromes (the words) and I wanted to mention the existence of palindromic gene sequences. Roughly how many palindromes exist in the human genome? I understand the number will vary from person to person. All I want to know is the order of magnitude. Is it 10^2, 10^3, 10^6?

Note that a DNA palindromic sequence does not really match the usual meaning of palindrome. .For instance, GAATTC is a palindromic sequence, but does not match its reverse, CTTAAG.  Instead it matches the reverse of its complement, which is a useful biological property. ('C' is the complement of 'G', 'T' of 'A', etc.)

@mgkrebbs. Thanks for the detail. I understand it is not exactly the same, but the principle is analogous, which is fine for my purpose.

The human genome contains approximately 1.25*10^7 palindromes longer than 6 bp (that is 8 bp or longer). Some interesting facts are also known about their distribution.

We found that 24 palindrome-abundant intervals are mostly located on G-bands, which condense early, replicate late, and are relatively A+T rich. In general, palindromes are overrepresented in introns but underrepresented in exons. Upstream region has enriched palindrome distribution, where palindromes can serve as transcription factor binding sites. We created a Human DNA Palindrome Database (HPALDB) which is accessible at http://vhp.ntu.edu.sg/hpaldb . It contains 12,556,994 entries covering all palindromes in the human genome longer than 6 bp.

And no, the number of shorter ones (shorter than 8 bp) isn't mentioned in the paper because they are considered unimportant, biologically.


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Is there other unknown-compound in Blood?
Blood is made of red blood cells, platelets, plasma etc. Let's say, then, there are these $x$ known compounds in blood.
But how can one be sure that there is no other compound other than those $x$ compounds? Does present technology ensure that there is no other unknown compound in blood that can't be detected?

@user1136  so, there is a probability that we don't know all the elements of blood, yet, right?

It all comes down to our ability to detect materials in blood. It would be impossible to rule out the existence of substances below the limit of detection, but would these materials have any significant effect at such low concentrations?

You might be interested in reading about proteomics and metabolomics. Both approaches are  capable of untargeted detection and identification of proteins or small molecules, respectively.


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Are there only a few alleles or groups of many alleles impacting protein structure and function?
I'm in the first year of Medicine and I'm studying Genetics and Evolution. I have this doubt in the back of my mind and I'm not being able to move forward without someone explaining me what's wrong with my thinking.
So I've learned an allele is a variant form of a gene, all alleles of the same gene are slightly different from each other and code the same characteristic in different forms. We know proteins can have from 20 to 34350 amino acids. Let's take a protein with 4 thousand amino acids. The RNA that formed it had 4 thousand codons, which are 12 thousand nucleotides. I didn't study mutation yet but I assume a mutation can occur in a single nucleotide in the DNA that can or cannot code for a different protein (as some amino acids are coded by more than one codon).
Ok, so let's say a super energetic UV photon reaches one of my germinative cells and mutates a single nucleotide of my DNA that changes the provious amino acid. The protein has 4 thousand amino acids. Will a single one change its function or shape? I would say it is more likely not to change, and I don't know why this reasoning can be wrong. One amino acid in 4 thousand probably will have no effect in the overall shape and function and will form a slightly different/ almost identical protein with almost identical functions. If that is right, we should have an enormous number of alleles for the same gene (e.g. if we say less than 5 amino acids won't change the structure, that are 3,2 million different alleles), instead of 2, or 3, or 4, or some small number as I was taught.
I can think in 2 explanations: The first is that if, contrary to what I think, a small change in an unique amino acid could change the protein enough to make the individual die for example. Which I doubt. The second is if we in fact had millions of alleles, but all this alleles had similar or almost identical shapes, and we could segregate them in a small number of groups (2 for example) where the functions of the coded proteins are different from the other group but identical in the same group.
Am I going too far? Could anyone explain me why this is not possible?

Hi and welcome to Bio.SE! I tried to update your title to be more relevant. Please adjust if you don't think it captures your question appropriately. speaking of which, your post is a bit rambly and the actual question is not clear -- please update to clarify to avoid receiving negative response.

The protein has 4 thousand amino acids. Will a single one change its
  function or shape?

It very well might.  High schoolers learn about the existance of sickle cell anemia, Tay-Sacks, cystic fibrosis, phenylketonuria...you must know about them too.

If that is right, we should have an enormous number of alleles for the
  same gene (e.g. if we say less than 5 amino acids won't change the
  structure, that are 3,2 million different alleles), instead of 2, or
  3, or 4, or some small number as I was taught

The is the dbSNP entry for human transferrin receptor.  As you can see there are a whole lot of recorded variants.
https://www.ncbi.nlm.nih.gov/projects/SNP/snp_ref.cgi?geneId=7037
But that doesn't mean that all of them are clinically relevant.

Firstable, a point mutation in your DNA could change definitively the fate of your hypothetical coding RNA (later a protein product). The reason relies on the nature of the mutations: Missense mutation, Nonsense mutation or Frameshift mutation. In the nonsense one, definitely will make your protein non-functional because of the insertion of a STOP signal inside your chain of nucleotides.
Talking about the susceptibility of some regions to be mutated, in general terms the most conserved regions on a protein are really well conserved because of their functional importance, that has been evolutionarily selected and prevents that the mutation rate will have a high probability.
And also, when you said: "I assume a mutation can occur in a single nucleotide in the DNA that can or cannot code for a different protein (as some amino acids are coded by more than one codon)."
Your assumption ignores the half part of history. Mutations are not restricted to small-punctual changes, but they could include big regions that alter the chromosome organization, as translocations, duplications, inversions or even loss of alleles by loss of heterozygosity.
I would suggest this resource, to get the principal concepts and ideas about this topic, but for sure this is just a general description.

Your answer focuses on extreme cases when mutations are more than a single amino acid, but I think the question was most concerned with the effect of a single amino acid substitution.

Right, but in the case that you codon, for example, codifies for Tyr (UAU) have the possibility to have U->A and results into the STOP codon (UAA) and it definitively modifies the fate of your potential protein. This is a related example, isn´t it?


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Has an ectopic pregnancy's blastocyst ever been made to implant?
Has an ectopic pregnancy's blastocyst ever been successfully extracted from the Fallopian tube and made to implant in the uterus?

Yes, this has been done by

Wallace, C. J. (1917) Transplantation of ectopic pregnancy from fallopian tube in cavity of uterus. Surg Gynecol Obstet 24, 578-579
Shettles, L. B. (1990) Tubal embryo successfully transferred in utero. Am J Obstet Gynecol 163, 2026-2027

Shettles has a questionable reputation at best, and I don't know what to say about the 1917 report. I would also note Shettles 1990 case report was of a case 10 years prior.

Not in an independently confirmed case.
A paper was once published claiming this was performed successfully:

Pearce JM, Manyonda IT, Chamberlain GV. Term delivery after intrauterine relocation of an ectopic pregancy. Br J Obs Gynaecol. 1994; 101:716–7.

This article and several others by the same author Malcolm Pearce were found to be fraudulent and were retracted:

Lock S. Lessons from the Pearce affair: handling scientific fraud. BMJ. 1995; 310(6994):1547-8.

What do you mean by "independently confirmed case"? Reproducible?

@Geremia The one I referred to was an obvious case of fraud once investigated. The ones you refer to in your answer were 1) a case report 10 years after the fact by an also troubled researcher, and 2) a case report from 1917. Both from single authors claiming to have done something thought to be quite difficult, and neither with any follow-up. Though it's possible they are real, they each have little more support than a Bigfoot sighting.

I'd also add that none of these articles are cited afterwards by anything but papers discussing ethics, suggesting that they have had no impact on clinical practice.

What is that? IVF successfully implants embryos (albeit at a low rate, <37.1%, depending on female age). Are in vitro conditions better than those in the Fallopian tube?

@Geremia There's a huge difference between implanting an IVF embryo de novo into the uterus, where it belongs, versus taking one that's been growing in a fallopian tube, where it does not belong, extracting it, and then reimplanting it in the uterus long after the time it would have normally implanted. There are good reasons this is not the typical course for dealing with ectopic pregnancy.

Extracting it intact is the hardest part?

Let us continue this discussion in chat.


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Neuroscience and learning of a single neuron
Can you teach an alphabet to a neuron?
If yes, how?
How does a neuron 'learn' new information, do all individuals learns similarly ?

No, you cannot teach a single neuron an alphabet.
In general, the way the brain learns and stores information is by adjusting the strength of connections between neurons. Therefore, there is not really any information in a given neuron, but in the pattern of how it's connected to other neurons.
For the example of the alphabet, there are a lot of different pieces of information to tie together: there will be different neurons that respond to the visual shape of a letter, the word that names the letter, the sounds that the letter represents in spoken language, the words that contain the letter, etc.
A general neuroscience textbook like Purves is a good place to start learning about how brains work. You might also learn about how artificial neural networks learn. They are definitely different from biological nervous systems, and the learning mechanisms vary, but they share some characteristics such as the information being represented in the strength of connections between units, usually called weights in an artificial network.

Hmm, does that mean that if someone were to record a group of individuals recalling the same information, it is somewhat possible to predict the neuronal firing patterns that will lead to the recall of said information.      Following which, if the same electrical activity was replicated in a nascent set of neurons that has yet to learn the information, that individual is able to 'learn' that information.                                               Thanks for the book recommendations, I'll definitely check it out


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Where do the protons in the mitochondrial intermembrane space originally come from?
I'm currently reviewing this concept in cellular respiration. The book which I'm using is Reece, Minorsky, Campbell's Biology and while it does a good job at explaining the process involved in the electron chain transport. I think it lacks of clearing out my doubts concerning initial protons.
Let me explain, the part where I'm stuck at is, where do originally the protons in the mitochondrial intermembrane space come from?. I understand that there is a proton gradient and the translocation of this protons in the proton pump is key during the electron shuttle process but, how did those initial protons come?. In other words, during the formation of the mitochondria in the cell, have they always been there? or are they part of some bigger molecule and that those protons are detached from them so that there is an initial gradient that triggers the process for the first time?. In other words, how does that initial spark or kick off begins?.
In most animations I've found, the explanations take for granted that the protons are freely moving in the intermembrane space such as here and also here but what do those videos lack is the explanation of how (as mentioned above) do those protons got there in the first place.
I'd like somebody could help me to clear out this doubt. I feel that as an addition to the answer, I'd like to know how does the mitochondria forms in the cell?. Since I believe there might be steps involved, I'd appreciate that the answer could explain those steps so I could easily understand, because as mentioned. I'm still confused on that part as well.

Well, proton gradient is set up by using protons of NADH2 and FADH2.Their proton is transported to the intermembrane space leaving behind NAD+ of FAD in matrix. Did I get your question correctly. You have asked about the source of protons I.e. which energy molecules provides them, haven't you?Also, the protons transported from NADH2 and FADH2 are more than what is coming out of F0-F1 particle so there is an excess of proton in intermembrane space.

@Abner Alfred Thompson Let me explain, I can understand that there might be protons due to water content in the cytosol from which during the formation of the organelles happens I believe in mitosis. But how does exactly there is an excess of protons so that a gradient is initially established in the intermembrane space?. I had believed that it was due to any terminal hydrogen from a peptide, aminoacid of protein contained in the intermembrane space and that when this gradient is held initially the process of electron chain can commence and go on in a cycle.

@Abner Alfred Thompson As I mentioned every explanation takes for granted that initially there is a surplus of protons taking this intermembrane space as a pool of protons. But as I mentioned before, where do they come from?. Is it due water, any peptide, protein, aminoacid initially present in the intermembrane space?. You mentioned that the transported protons from NADH2 and FADH2 are more than what comes out from F0-F1 particle, but again this is when the cycle is happening. But what it was that initial surplus source?. This is my question?. Can you help me to clear out this doubt?.

You can understand this if you consider the entire events of oxidative phosphorylation and electron transport chain.The amount of H+ from NADH2 and FADH2 going in is way more than what's coming out.This is what's the cause of proton gradient.You can see this video on YouTube to get your doubts clarified : https://youtu.be/wX7J2JtxM08 .Also,there is a minor error in this which is pinned in the comments section but it won't affect your understanding.Hope this helps

@Abner Alfred Thompson I understood the part that the amount of protons going in to be more than what is coming out but my question was more aimed at the ab-initio aspect. something more like Big Bang thing. I hope this makes clear my question. Probably this part isn't necessarily critical to understanding the process. But I felt that it is my general doubt. Come to think of it, if you put a sugar in a solution, you know there will be more oxigen due to its presence in the molecule, plus what it was in the water and probably from the air in the surroundings dissolved in that water.

@Abner Alfred Thompson In other words, is it possible to pin point when the process exactly begins?, i mean when the cycle isn't possible?. Maybe the precise moment when the first APT synthaze in the intermembrane space is created?.


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Why do children not have the Acid Mantle?
Post puberty humans begin to secrete a substance called Sebum which changes the neutral PH of our skin from ~7 to 4.5-5.5. This has that advantage of serving as a protective line against pathogens and discourages larger organism like lice. My question is given these benefits, why are children not born with these advantages?

Kids don't have many dermal infections, mostly flu, respiratory and digestive infections. the acid mantle didn't prevent the black death fleas and the flu epidemics.

This question is wrong. Sebum isn't a "protective line", in fact excess sebum production (an exceedingly common problem) invites pathogenic bacteria to feed, causing acne and pimples. I don't see any evidence of sebum protecting against lice. See my question at https://medicalsciences.stackexchange.com/questions/13862/why-isnt-there-a-larger-effort-to-reverse-and-block-the-effects-of-androgens-on for an explanation of how damaging puberty is for skin.

@user1258361 The Acid Mantle is a very well accepted phenomenon subject to a great deal of peer-reviewed research (see here: https://www.ncbi.nlm.nih.gov/pubmed/30125885). The prominence of Lice on children is acceptably attributed to the lack of the acid layer, but if you have a source that suggests otherwise, please provide. And your linked question is somewhat irrelevant, excess of anything is negative, that doesn't negate the positive effects that proper distribution has.

You -do- realize that secretion of cetylpyridinium chloride would be a far superior barrier against pathogens, right?

I'm fairly certain that constant contact with cetylpyridinium chloride would result in quite a few negative side-effects, and I'm certain that the human body doesn't have the mechanism needed to synthesize cetylpyridinium chloride.


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How does anaerobic burst-flight performance scale with mass?
Quails employ anaerobic burst flight to escape predators and the Quetzalcoatlus northropi have most likely used it during launch and climb out, then transition to soaring.
Now, I have read these papers, from Marden, Witton and  C.J. Pennycuick
I won't play pretend I really don't know that much about bird flight mechanics, so I easily got confused reading them.
How does anaerobic flight performance scale with mass?


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Sensory-motor pathway from visceral organs
Does anyone know is which nerves carries the transmission of sensory-motor impulses from the visceral organs? Is it splanchnic nerves?
There is conflicting evidence in the literature. On the one hand, many sources told that splanchnic nerves belong to the sympathetic nervous system. On the other hand, there is information that sensory-motor impulses from the visceral organs travel along the splanchnic nerves. And there is a slight contradiction, because sensory-motor impulses usually go not in to to the sympathetic trunk, but to the dorsal ganglia. But the splanchic nerves connect just with the sympathetic trunk, and not with the dorsal ganglia.
For example, in this study:
https://www.ncbi.nlm.nih.gov/pubmed/22209656
sensory transmission pathways have been found to go to the spinal cord through the dorsal ganglia, which, to my knowledge, are not associated with splanchic nerves.


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What's the smallest flier that migrates?
Painted ladies and monarchs migrate hundreds of miles (~1.61 hundreds of kms).
Are there long distance fliers that are significantly smaller?
Dual question: Are fliers' migration distances strictly a function of size? Or are there any fly-sized 1000-mile migrators?

The marmalade hoverfly (Episyrphus balteatus) flies to Southern Europe and back every year.

It's difficult to track and find them compared to birds and butterflies, here is a study witch citations: https://onlinelibrary.wiley.com/doi/epdf/10.1111/j.1570-7458.2007.00568.x?purchase_referrer=scholar.google.fr&tracking_action=preview_click&r3_referer=wol&show_checkout=1
it is now known that large numbers of E. balteatus migrate South during the autumn period. Therefore, it has been sug-gested that a comparable migration to the North helps tore-establish E. balteatus populations in northern Europe during the spring. There are many records to show that some hoverfly adults are active so early in the spring that they could not possibly be long-distance migrants. Nevertheless, although some adults remain active late into the autumn, few authors have managed to find females in overwintering sites
studies have suggested that E. balteatus migrates in large numbers during late summer and autumn to the Mediterranean area and only return to central and northern Europe during the following year(Aubert et al., 1976; Gatter & Schmid, 1990; Kehlmaier & Martínez de Murguía, 2004; Hondelmann et al., 2005).
https://www.sciencenews.org/article/flying-insects-tell-tales-long-distance-migrations

That's pretty small! How long do they live? Vanessa's take 6-ish generations to make the Africa-Europe-Africa trip each year.

Hi @user38715! According to the Science News article in com.prehensible's great answer, they only live for about a month! They accomplish a tremendous amount in a short period of time, and they're gorgeous too!


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What kind of lichen is it (no. 2)?
I think i found very interesting lichen. I discoved it at 1.15 PM CET in Prague nature conservation area called Divoka Sarka.

I took this picture on the place of my discovery.
One piece of this specious had cca. 6 cm. And it look like a shrub.

And this is micro photograf with magnification about 200X.

This is a fruiticose lichen, meaning one with a bushy growth habit. They are common in my native state of Texas (USA), where they hang off of oak trees. Your photos look much like them. I have seen other examples in the rainforests of the Pacific Northwest, in both Oregon and Washington. I can't name the species.
In the upper left of your first photo, I see a thick, stem-like structure. This looks to me like the holdfast, the place the lichen attaches to the tree or other support.

i know it is hard to try find with this information something more then your answer mister. Of course i know that my discoveri can be put into fruiticose lichen, but i hope for much more accurate answer here. But u know the fruiticose lichen is more often on trees. This one was on the ground and thats fascinated me ! Even more fruiticose lichen is usually pollutation intolerant and i found it in the capital city of Czechia. And u know maybe it not even lichen, but dead moss, shrub. But still thank you :)


text:
Could something akin to Cyanobacteria evolve on earth today or are all available niches taken for different kind of life to come to be?
The most basic form of my question would have to be: could new life form from molecules as happened with the first life on earth, here on earth? If not why not?

Are you asking about abiogenesis? There are many similar questions here, check the 'related' list or the tag [tag:abiogenesis]

It seems that this Question answers my question.


text:
Why can AB people receive blood from A, B or O?
AB people don't have agglutinins anti A or anti B so it might seem they can receive any type of blood. But if the donator is A for example, it's own blood will have agglutinins anti B that will agglutinate the AB blood. So why can AB people receive blood from non AB people?


text:
Why does dissociation of carbonic acid cause a decrease in pH?
When a molecule of carbonic acid (H2CO3) dissociates, the two products are a bicarbonate ion (HCO3-) and a hydrogen ion/proton (H+). Because of the addition of a hydrogen ion, this process causes a decrease in the pH of the blood, and if someone breathes too slowly and doesn't quickly remove CO2 from their body, respiratory acidosis will take place.
However, why is it the case that the addition of this hydrogen ion lowers pH? While this might sound like a stupid question, it's also the case that the dissociation of carbonic acid produces a bicarbonate ion, which is a weak base. Therefore, the dissociation produces both an acid and a base in a 1:1 ratio. Therefore, the concentration of hydrogen ions relative to bicarbonate ions doesn't actually change. Given this fact, wouldn't there be no change in pH at all?
I read a paper on carbon dioxide transport which addressed some of my other questions but didn't touch on this precise point.

I've voted to close (migrate to chemistry). They may close it as well if they have a similar homework policy

@DeNovo This question doesn't concern any homework I have (my class only briefly mentioned the buffering system). Everything I ask (at least to this point) on the Bio Stackexchange concerns my personal understanding of these topics.

@Korvexius sorry, I know it's confusing, but here we consider "homework" to be the work, in the general sense, that you should do before asking a question. It's not specific to school assignments.

Any acid that releases a proton when it dissociates in water will also produce a conjugate base. We can conceptualize this as $\ce{HA <=> H+ + A-} $. In this particular example, $\ce{HCO3-}$ is $\ce{A-}$.  The strength of the acid is determined by the extent to which the acid, $\ce{HA}$, dissociates. This can be expressed using the equilibrium constant for this reaction, which has a particular name, $\ce{K_a = \frac{[H^+][A^-]}{[HA]}}$, (where $\ce{[X]}$ is the concentration of $\ce{X}$ at equilibrium). The larger $\ce{K_a}$ is, the further the reaction moves to the right (or, as it is often expressed, the smaller the $\ce{pK_a}$, which is $\mathrm{-log_{10}}$ $\ce{K_a}$).
Here, the addition of any $\ce{HA}$ will produce $\ce{H^+}$ and $\ce{A^-}$ in an aqueous solution (the blood), and decrease the $\ce{pH}$. $\ce{A^-}$ is only a base insomuch as it can form $\ce{HA}$ by combining with $\ce{H^+}$. This can occur if you add (or, as occurs in the kidney, reabsorb) $\ce{A^-}$ with some counter ion other than a proton. Then you can drive the equilibrium to to the left, towards $\ce{HA}$, decreasing $\ce{[H^+]}$. Otherwise, $\ce{A^-}$ derived from $\ce{HA}$ will not drive the equilibrium one way or the other. $\ce{H^+}$ will still dissociate as determined by the $\ce{K_a}$.

Bicarbonate will make the mudium basic ONLY WHEN it is bonded with some cathium that came from a strong base.
E.g. NaHCO3 is a basic salt because NaOH is a stronger base than H2CO3 is an acid. That way Na+ will stay completely dissociated while HCO3- and water will become H2CO3 and OH-.
H2CO3 is considered an acid because it ionizes in H+ and HCO3-. Some of the HCO3- will bond with water and form OH- and H2CO3 again. This is an equilibrium. But If we have only one HCO3- that didn't yet bonded to water and formed H2CO3 again, we will have more H+ in the medium, and it will be acid. In fact, there is a constant called Ka that measures how much HCO3- and H2CO3 are in a solution in a given time.


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Meaning of "f.a." in the species name
What does "f.a." stand for in the name of the "Wickerhamomyces menglaensis f.a." yeast species mentioned in this article https://ijs.microbiologyresearch.org/content/journal/ijsem/10.1099/ijsem.0.003350 ?

The link to the journal seems to be broken. Can you check the doi and include it instead?

it's also nice if you include a complete citation :).

"Forma asexualis" as explained in another paper

The authors favor the use of the expression forma asexualis (f.a.) in the
  description of anamorphic species of the genus
  Cystobasidium and this decision follows the current
  practice of reclassification of asexual yeast taxa (see
  e.g. Lachance 2012; Groenewald and Smith 2013;
  Daniel et al. 2013; Selbmann et al. 2014)

Lachance MA (2012) In defense of yeast sexual life cycles: the
  forma asexualis: an informal proposal. Yeast Newslett
  61:24–25

Nice answer. So does f.a mean the asexual strains of the same species?

@WYSIWYG: yes. Before this change, the anamorph and teleomorph had to have different names, and were even in different genera... because they had different appearance.

@WYSIWYG: actually the rules are more complicated for the existing names https://en.wikipedia.org/wiki/Teleomorph,_anamorph_and_holomorph#One_fungus,_one_name i.e. they didn't force them out; that's why you mostly see "f.a." in combination with sp.nov (or more rarely comb.nov.) on a search.

So what do sp. nov. and comb.nov. mean? Could you also add your comments to the answer as it would be useful to others?


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What plant have I collected?
I have collected this plant from the soil in a park in Belgium. I thought it was a child of a plant which was growing nearby but when the leaves started to grow I realised it is a different plant.
When I was collecting it, it was at the stage of having only the seed leaves (still visible in the photo) which are elongated and about 2.5 cm long. In the park, on the ground from where I collected it, these plants were growing in large quantity close to each other. After about 1 week from bringing it home the leaves started to appear. Now about 3 weeks later the leaves are about 2-3 cm long.
Could you help me identify it?

Further clues
First of all, this plant is very abundant in the park but I can also spot it in other places, e.g. close to sidewalks within a walking distance from this park.
This is the plant in the original environment from where I collected it:

I could also find it growing in a pocket of a tree - this suggests to me that the seeds might have fell from a height, so this plant might be a tree (?)

The ground of the park is largely populated by wild garlic. Other than that, some nearby plants are a hornbeam and elderberry.
Here are some further photos of surrounding plants that might be a hint for you:

It might help if you also had the remains of the seed itself.

Unfortunately I don't have the seed. This weekend I will go to the same park and perhaps collect some further clues :)

Try to identify nearby trees also. Even if the the leaves do not match, this could be helpful information regarding the environment.

To help you start ruling out species: not Corylus avellana; not Robinia pseudoacacia (which both show up in your pictures). That cherry is of more interest, but I think your seedling is not quite representative of Prunus avium

Leaves make me think Acer is likely, and the presence of a decaying maple samara in your 3rd image is a giveaway that maples are nearby...

You definitely have a seedling with prominent cotyledons still present.
My initial guess is Acer pseudoplatanus (sycamore maple, or just called "sycamore" or "planetree maple" in parts of Europe)

 Source: Wikimedia
You can see a detailed image of an A. pseudoplatanus seedling here and a time-lapse of a seedling growing to the point of cotyledon release in Neil Bromhall's youTube video.
According to the range map available from Euforgen, A. pseudoplatanus is present (blue) throughout Belgium:

As for confirming nearby adults, you're looking for a tree that looks as follows:

 Source: Blue River Nursery
For more information regarding identifying the adult, please see Virginia Tech Dendrology

Scientific study of the cotyledons of this tree can be found from two New Phytology (76th issue) papers from the 1970s: Ampofo et. al 1976, pp 31-39 and Ampofo et al. 1976, pp 41-52

Wow, very interesting! I didn't expect it because the adult leaves are different. Thank you for solving the mystery! :)

@camillejr Sure!. But please go back and check to see if you can find a mature tree to confirm my suspicion or not.

No need to guess here, this looks very much like a seedling of A. pseudoplatanus (Gewone esdoorn in Belgium and The Netherlands). This is the most common Acer in Belgium. Other relatively common species are Acer platanoides and Acer campestre, but but their leaves differ and I've never seen these have seedlings this abundant.


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Entropy during neuronal signaling
to begin with: I have some background in cognitive neuroscience, but have not intensely studied the biochemical background of neuronal signalling, so please correct me if my basic understanding is wrong.
As studying the generation of action potentials and EPSP/IPSP at synapses, I noticed that as those processes make use of the gradients, the actual signalling process works by resolving these gradients (i.e. the molecules flow without having a constant energy supply pushing them to do so). The big part of energy consumption during neural signalling is then actually needed for restoration of these gradients, transmitter reuptakes etc.
So if the above is correct, does that mean that the information "flow" in the brain is done by increase of entropy (which I intuitively understand as a increase of "unorderedness", but im not a physicist either...)? I have been told that biological systems actually want to resist the "natural" direction of entropy in that they want to keep themselves "ordered" to survive. I would have hence found it more intuitive if signalling would be acquired by an active decrease in entropy (followed by some sort of "passive" restoration). Is there any reason why that is not so? Are there other examples of signalling where that is the other way round?
Or am I just lacking understanding and messing up definitions?
Thanks for your help

In my view, thinking of entropy as something biological life has "wants" about is a bit mistaken. In general, entropy arguments regarding biology run into a major problem in that the interesting physical laws involving entropy required closed systems, and no biological system is closed, so it's a bit moot.
It makes more sense to think about what benefits "fighting against entropy" gives a biological organism, and I also think it makes more sense to think in terms of potential energy rather than entropy (even though they are of course related).
Neuronal signaling is best when it's rapid. By pumping ions against their gradient ahead of time, neurons establish a concentration gradient (which you can view as a decrease in entropy). This is indeed the active part. This also stores energy in the gradient, in that if a 'gate' were opened, the gradient would tend to equilibrate. Because the ions involved are charged, additional sensors in the membrane can respond to this changing electrical gradient.

I would have hence found it more intuitive if signalling would be acquired by an active decrease in entropy (followed by some sort of "passive" restoration)

I think you might be mixing up the "action" verbs here. Think about pushing a rock up a cliff or lighting a firework. If you want that rock to be a signal, it's going to be a much more dramatic signal falling down the cliff than it was pushing it up the cliff. It's going to be much more dramatic lighting off the firework rather than extracting the needed ingredients from various places and assembling them. Processes that release stored energy tend to be a lot more dramatic and "active" despite being "passive" in terms of needing to add energy (besides activation).


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What concentration of hydrogen peroxide kills mold?
There are numerous articles online which claim that household 3% hydrogen peroxide can kill mold growing on household surfaces, yet I haven't managed to find scientific studies that show that. My question is what concentration of hydrogen peroxide is sufficient  for killing household mold (defined usually as a reduction of 99% or some other number)?
I have tried searching online for studies regarding the efficacy of hydrogen peroxide in killing mold, and for the minimum concentration of hydrogen peroxide for killing mold, but I didn't manage to really find information on that, though I am not that skilled in finding such information and also don't have much access to scientific literature.

The CDC Guideline for Disinfection and Sterilization in Healthcare Facilities provides a good overview of various disinfectants and their effectiveness against different kinds of pathogens, along with citations if you're interested in more detail.
This document doesn't evaluate the effectiveness of Hydrogen Peroxide against Stachybotrys (black mold) specifically (the CDC specifically recommends Chlorine Bleach for this purpose), but it does describe it's effectiveness as a fungicide. Note that the level of disinfection needed to control pathogenic fungus in a healthcare setting is likely much higher than needed to control black mold in a house, but it can give you a sense of how effective Hydrogen Peroxide is overall:

A 0.5% accelerated hydrogen peroxide demonstrated bactericidal and
virucidal activity in 1 minute and mycobactericidal and fungicidal
activity in 5 minutes [656]
...
A 7% stabilized hydrogen peroxide proved to be sporicidal (6 hours of
exposure), mycobactericidal (20 minutes), fungicidal (5 minutes) at
full strength ... [655]
...
The 7% solution of hydrogen peroxide, tested after 14 days of stress
(in the form of germ-loaded carriers and respiratory therapy
equipment), was ... fungicidal (>5 log10 reduction in 20
minutes),[663]
...
A new, rapid-acting 13.4% hydrogen peroxide formulation (that is not
yet FDA-cleared) has demonstrated sporicidal, mycobactericidal,
fungicidal, and virucidal efficacy. Manufacturer data demonstrate that
this solution sterilizes in 30 minutes and provides high-level
...
Commercially available 3% hydrogen peroxide is a stable and effective disinfectant when used on inanimate surfaces
disinfection in 5 minutes [669]

From this, it seems like you'd want to use accelerated Hydrogen Peroxide, or 7% stabilize Hydrogen Peroxide to ensure fungicidal disinfection. 3% Hydrogen Peroxide is effective against bacteria, but the studies cited didn't test it against fungi.


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How does Liebig's law affect the growth of specific characteristics on a plant
I am familiar with the law of minimum, that is that the growth of the plant is dependent on the least available nutrient/resource.
I visited a farm in which they purposefully shaded tabaco plants to guide the growth of the plant (e.g. to make the plant grow taller and wider leaves with better concentrations of nicotine). I am wondering if this applies to other nutrients/plants. Example: Does deficiency in nutrient X guide the growth of spinach with Y% more iron?


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Do flies avoid infrared light?
If flies avoid IR light, many places can be kept free from flies using IR light. We see insect repellers in many restaurants, but they don't seem to work well. Can IR be a safe & effective alternative?

Hi and welcome to Bio@SE. What have you done to answer your question? you should edit your question to add this information, it will help you get more specific answers

What kind of "flies"?

I doubt very much that sunlight, what they like to bask in, is an issue for them. UV and Blue light you mean? is use in fly traps?!?! flies are made to spend all day in light, and IR by it's nature is the most beneficial light as it's in between a mug warmth and an LED. anything warm is likely to emit IR.


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Is this model of understanding of what's natural selection and what's not, correct?
Here in this account I just want to make sure, that I've grasped the concept of natural selection as is usually spoken by evolutionary biologists, truly the wording here are non standard and in some sense sloppy, yet I want to make sure that I've got this concept right.
My account on what constitutes natural selection and what's not:
We say that there is a causal relationship from [A] to [B], to mean that there is a process in which A is a part of, that results in changes in B.
Also we can paraphrase the above by saying that there is a causal relationship that [A] has on [B]; or by saying that [B] is the consequence of a causal relationship from [A].
Now Natural selection seems to require those as prerequisites:

There is a causal relationship from some [hereditary material g] to the [survival and reproductive status of individuals harboring g].

More precisely and incorporating some standard terminology this is:
There is a causal relationship from a [genotype g] to [absolute fitness of g].
We call such hereditary material as fitness related hereditary material.

A variation exists between some fitness related hereditary material as regards their final causal effect on the degree of their fitness in a common environment $E$. Mathematically speaking, this is:

$\exists E, g_1, g_2( E \text { is an environment } \wedge g_1,g_2 \text { are fitness related hereditary material } \wedge g_1 \neq g_2 \wedge fit_E(g_1) \neq fit_E(g_2))$
In English: There exists an environment $E$ and $g_1, g_2$ where both are fitness related hereditary material such that $g_1$ is different from $g_2$ and fitness of $g_1$ in enviornment $E$ is different from fitness of $g_2$ in environment $E$.
Two fitness related hereditary material that have the same final effect on the degree of their fitness (even if through different causal mechanisms) in a common environment $E$, are said to be isofit$_E$, while those that differ are said to be anisofit$_E$. Formally:
$g_1 \ isofit_E \ g_2 \iff fit_E(g_1)=fit_E(g_2)$
$g_1 \ anisofit_E \ g_2 \iff fit_E(g_1) \neq fit_E(g_2)$
Of course anisofit fitness related hereditary material might even have a difference in the direction of their effect on fitness, so a positive direction means that "the causal relationship from the hereditary material to its fitness, is towards increasing its fitness"; while the opposite is for negative direction.
Now for every hereditary material $g$ the population of all individuals in environment $E$ that harbour $g$, is to be called the "$g$ population in $E$".

There is an environment $E$ that has two anisofit$_E$ fitness related hereditary material populations living in $E$.

If we have 1 and 2 and 3, then we can have Natural selection!
The reason is because Natural selection is the differential (i.e., non-equal) size of populations of anisofit fitness related hereditary material, living under a common environment, that is caused by the differential causal relationship those hereditary materials have on survival and reproduction of individuals in their populations under that common environment.
The above serve as a definition of natural selection, albeit a long one, but I think it captures the intended meaning given to that term by evolutionary biologists.
Now from the above definition we get to infer two properties that natural selection has:

Natural selection is always not neutral. Note "non-equal" part in the definition. The reason is because we have two anisofit fitness related hereditary material populations living under a common environment, and the difference in their size is attributable to the effect of those hereditary materials on their fitness in that environment, so since those are aniso-fit, then clearly the size of populations of them would be different.
For the same reason outlined in 1, we expect natural selection to be "co-directional", i.e. the difference in sizes of the populations of those anisofit hereditary materials, must parallel the difference in the effect of those hereditary materials on their fitness in that common environment, so the population with the hereditary material causing "higher" fitness would have the "bigger" size! In other words natural selection increase the size of the population of the hereditary material that causes higher fitness on the expense of the size of the population of the hereditary material that causes lower fitness.

On the other hand suppose we have some environment in which there are two anisofit fitness related hereditary material populations. Now if some environmental, or recombinative genetic change inflicts those two populations, that works either in a neutral manner, i.e. causes equal population sizes of those anisofit fitness related hereditary material, or works in an opposite-directional manner, i.e. in a direction that is opposite of the expected direction mentioned above, better be termed as "contra-directional". In this situation even if the size of the populations of those hereditary materials is different (imparting the appearance of a selection) still that difference is not explained by the effect of those anisofit fitness related hereditary material on their fitness in that environment! So this would not be an example of natural selection! It would be an example of an environmental factor that caused a "genetic drift", or of a genetic recombination process that caused a "genetic drift" also.
So we in effect have a struggle between "natural selection" which works in the direction of increasing adaptation with the environment, on one hand, and "random selection" (or sometimes called neutral selection or non-selection) which doesn't necessarily work in the direction of increasing adaptation with the environment.
So in some sense "evolution" is determined by the struggle of those two kinds of mechanism of change.
If random change prevails, then evolution would not necessarily move in the direction of increasing adaptation of living organisms with their environment. While if "natural selection" prevails, then evolution would proceed in the direction of increasing adaptation to the environment.

This is far too long to be a focused SE question. Individuals who have genetic material that makes them more likely (not definitive, more likely) to survive and reproduce (===fitness) contribute on average more to the the next generation's genetic material.

@BryanKrause, I just wanted to know if there is a serious error with my understanding above. As regards your sentence, it appears to be more compact, but more compact is not always easily understandable.

You have a 12 line long sentence and a 8 line long sentence! This kind of impossibly long sentence make it hard to understand what you mean.

@Remi.b, thanks for drawing my attention to that, I've edited those sentences by breaking them into smaller ones. See again please.

one thing worth mentioning is a gene or phenotype is not unilaterally more or less fit, the fitness is dependant on the environment, a gene that increases fitness in one environment may decrease it in a different one. Even things like what percentage of the population a gene occurs in can affect its fitness, some genes are only adaptive while in the minority. Fitness is highly conditional.

@John, this is a good point! so fitness needs to be defined in a conditional manner, i.e. like saying finitness in environment "E", and not just fitness like that unleashed. However notice that in point 3 I've required common environment!

I see that but this is dependent on how you define environment, an environment is not static, the environment also includes all the other genes in an organism, the other individuals in a population, ect. selection also indirectly changes the environment. So each E is instantaneous, maybe an E prime to designate this.

@John, I think for the purposes of giving a general definition, its sufficient to state "common environment" as such, the specification of which and which environments is a particularization matter, it speaks about particular natural selections, but for the general purpose of a general definition of natural selection , all what is needed is to mention "common environment".

You may want to add the "computational-model" tag, it will draw in more poele who will understand the mathematical structure of your question. Changing your title to include some mention of modeling would help, right now the title is going to draw people with little experince in such an approach.

I've mostly skimmed the formalism you introduced, but getting to the 2nd half of your post, the answer is yes, you understood correctly the distinction between natural selection (aka adaptive evolution) and drift (aka neutral evolution), as well as the fact that it's not a given that natural selection would be the predominant effect in arbitrary circumstances. Small population sizes, high rates of mutation, weak genetic repair mechanisms, etc. can all lead to chance being the predominant effect.
The conditions needed for natural selection to be predominant have been investigated in lots and lots of publications. A quick overview and brief list of such publications is found in

Duret, L. (2008) Neutral theory: The null hypothesis of molecular evolution. Nature Education

One final point I'll make here is that we need to be careful to define what we're talking about being selected. In general, for phenotypes there's not much debate that adaptive (rather neutral) evolution dominates in nature. The research and debates mostly concerned what happens to genotypes. This is somewhat obvious since there are numerous mechanisms that mediate the translation from genotype to phenotype.
A departing teaser, there's still a lot debate concerning how the mechanisms that enable low-error genetic transmission (the surpassing the famous error threshold) came about in the primordial soup. One interesting adaptation we can observe today is that bacteria can alter their rate of mutation in response to environmental changes; they function a bit like the Hulk superhero does: if you stress them, bacteria mutate faster (aka stress-induced mutagenesis).

And to save you from rediscovering a certain wheel (and posting it here), in the biologically-inspired (but not biologically faithful) realm of "genetic algorithms", there's "fundamental theorem"  (of Holland) that states under what conditions (in that simplified world) [natural] selection is likely to be the source of high-fitness schemata (an equivalent of well-adapted genotypes). But the theorem doesn't exclude that such schemata can simply appear by mere chance mutation.
More generally, there's the Price equation; it partitions total evolutionary change in that due to natural selection and that due to other causes (including transmission changes, like mutation). However, without additional assumptions, this is as good as it gets. To quote from SA Frank:

No general conclusion about total evolutionary change is possible, because the complete range of forces that can perturb populations remains unpredictable. However, we can express an elegant equilibrium condition. At equilibrium, the gain in information by [natural] selection must be exactly balanced by
  the decay in information caused by other evolutionary forces.

In the simplified world of genetic algorithms, such additional assumptions are made (e.g. there's a specific transmission model) a point that is missed (IMHO) by people who diss Holland's theorem as merely restating the Price equation.
And I should at least name-drop the Wright–Fisher model which seems to be the most studied by those interested in a closer approximation of biology (as opposed to solving optimization problems, which is the goal of genetic algorithms). The Wright–Fisher model also makes specific assumptions about transmission; it seems a lot variants of it have been investigated. On this model and a lot more, see chapters 1, 6 & 7 in Durrett's book Probability Models for
DNA Sequence Evolution.
Anyway, my main point in this second half of my answer is direct you to well-known formal treatments of evolution by natural selection.

Thanks, I think there is a typo, you said at the 16th line.........natural (rather than natural)....I think you meant (rather than neutral)

Quote: "In general, for phenotypes there's not much debate that natural (rather than natural) selection dominates in nature".

@Fizz AFAI, "Neutral selection" is not a concept.

@Remi.b: fair enough, it's an abuse of language, so I've replaced it with "neutral evolution", which is more widely used, although... https://arxiv.org/abs/1211.3609

@Remi.b: Or... https://scholar.google.com/scholar?hl=en&as_sdt=0%2C5&q=%22neutral+selection%22&btnG=


text:
what is the name of this fish?
]2
fishes are of length 2 to 3 inches.

Welcome to SE Biology. Tank fish are pets so I suggest you search the Pets SE for an identification. There's little biological interest in pet identifications, if you want to leave this question here adding geographical information may avoid some downvotes.

Looks like Jewel Fish, a cichlid that has been kept for a long time. Hemichromus bimaculatus , native to west Africa a bit different from "African Cichlids" which are from east Africa. Source : Exotic Aquarium Fishes by W. T. Innes ( the guy neon tetras are named after), 1937 ; But I don't think you can find it online .


text:
Barr body in mitosis
In early embryonic development, some female cells pass through a process called lionization and one of the X chromosomes get condensed and began to be called Barr body.
What I don't understand is how the Barr body behaves during mitosis. Specifically, if a cell had condensed a paternal X chromosome, all of its children will have a paternal Barr body. But aren't  the barrbodies supposed to decondense to be able to be copied during mitosis? If so, when they recondense, why isn't the choice of which chromosome will condense random?
Thank you!

X inactivation is mediated by several epigenetic marks on DNA that cause condensation into heterochromatin. These include DNA methylation and histone modifications:
https://en.wikipedia.org/wiki/X-inactivation#Silencing
As you suggested, a newly copied DNA strand would be free of the epigenetic marks that mediate heterochromatin condensation. Yet epigenetic modifications are inherited, along with DNA molecules, by the daughter cells during cell division. That is, cells have ways of copying these modifications from the old DNA strands to the new ones. These mechanisms are not all known, and are the subject of much research.
In this fashion, each cell division produces two cells that inherit the X-inactivation status (i.e. heterochromatic state) of the parental cell.
This cycle of epigenetic inheritance only ends when the chromosomes are reactivated in primordial germ cells before meiosis and the production of eggs or sperm. The embryo of the animal's offspring can then make that initial, random X chromosome inactivation that is inherited by all of the cells in its body.


text:
Is there a relationship between HDL-C and LDL-C?
For a gentle introduction to cholesterol and its functions, see a great answer on SE Biology
Whenever I read about how to deal with cholesterol level, the rule is to keep a low LDL fraction, ad a high HDL one.
How to achieve this usually falls into the categories of a healthy body (sport), a healthy diet and possibly medicamentation.
Since generally the advice is more or less the same for both goals (lowering one fraction and increasing the other one), I was wondering if there is a strong relationship between these fractions. In other words - is moving one in the right directions automatically drags the other one (also in the right direction)?
Anecdotally (and this is what triggered my question), I saw my LDL crash almost by 250% (not by chance but through a good diet, etc. - over a few months) and, surprisingly, the HDL go down by 30% as well.


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What is a Archival Tumor Tissue ? For What Purpose is it collected?
Over the course of Conducting trials various tissue and tumor samples are collected  from the patients.
One such sample is the Archival Tumor Tissue.
Could someone kindly clarify what is the meaning of the term archival tumor?, and what data is gleaned from it.

Welcome to Bio.SE! What attempts to answer this question have you already taken? A Google search pulls up many hits. We ask that all question posters here attempt to search for an answer to their own question & explicitly indicate research they've already done, what they learned, and what is still confusing or unknown to them. 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 :). Please take a moment to edit your post with this additional detail, & it will likely be received more positively by our community. Thanks!

When a tumor is removed from a patient, it is usually send to the pathology the make sure that it has been excised completely to make sure there are no residues. Often this tumor is also used to analyze the mutation status of the tumor to determine, which further treatment is possible. For example, this is routinely done for melanoma where the mutation status excludes some drugs for further treatment.
Afterwards these tumors are important material for the scientific tumor research to isolate fresh cell lines or analyze them further. Parts of it are usually stored either frozen or as formalin fixed tissue to build tissue banks. These can be used for later research on this type of tumor and have a high value.
These tissues can then be cut and stained with antibodies or used for nucleic acid extraction (either DNA or RNA) or to test new ideas or methods which where not available to the time when the samples was archived.
Another famous case (although not from tumors) are tissues samples which have been archived from people deceased from the spanish flu in 1918, where parts of the virus was reconstructed using these samples decades later.


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What is this white, winged insect?
I saw this insect crawling on a wall in the UK (Birmingham) today (March 28th). It's about 5mm long. I assumed it was a white fly, but having looked at other images of white files on google, I don't think it is! I assume the fact it has jet black eyes means it's normally nocturnal?

At first I was thinking Trichoptera, but the antenna were not long enough and I noticed your size is quite small (~5mm).
The small size and body stance made me think of the order Neuroptera (the net-winged insects).
Specifically, this specimen reminds me of the family Coniopterygidae (or the dustywings).

A distinguishing feature is that like many other Neuroptera, dustywings carry their wings nearly side-by-side when at rest, whereas whiteflies carry them almost flat across the back  [the last part being related to the OP's original thought that their specimen was a whitefly]

Interestingly, unlike many other net-winged insects, the dustywings do not actually have "net-winged" venation -- just like the OP's specimen.
If this is in fact a dustywing, according to Wikipedia:

These tiny insects can usually be determined to genus with a hand lens according to their wing venation, but to distinguish species, examination of the genitals by microscope is usually necessary.

Just as a reference, according to here and here, a similar looking species called Conwentzia pineticola lives in the UK. You can see a picture of this species below:

 Source: NatureSpot
Comments on appearance and characteristics:
From Catherine A. Tauber et al. (2009) in Encyclopedia of Insects (Second Edition):

The Coniopterygidae is generally a very homogeneous family characterized by very small adults (forewing length 2–5 mm) with bodies covered by white waxy (“dusty”) secretions.

The family name means "dusty wing" [source] due to the usually conspicuous whitish dust of waxy scales on the wings of these insects. I can't tell if this "dusty" nature is apparent in your picture or whether your picture is simply blurry.
Regarding the antenna, Tauber et al mention:

Adults have chewing mouthparts, large compound eyes located laterally on the head, and multiarticulate antennae that are usually filiform (thread-like) or moniliform (with bead-like segments).

You can see a similar looking (and similar sized) specimen from the U.S. here and one from Spain here. Additional images on bugguide.net seem to suggest that your specimen is in the subfamily Coniopteryginae.


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What is this plant's scientific name?
This is the picture of a tree in my college's botanical garden.
First I thought it to be a banana tree for its leaves but then seeing its lower part, I don't think it is a banana tree. So what is it's scientific name? I am just curious. Is it any hybrid or something like that plant?
Edit: This tree is from Bangladesh in South Asia. This tree is approximately 9-10 feet (I think, I cannot go near the tree). This picture is from Spring season.

Please [edit] your post to provide your location and the approximate size of the plant. See here for guidelines for writing well-received [tag:species-identification] questions. Thanks

The name of this plant is:
Ravenala madagascariensis
Check: wikipedia

It is not a banana . I have seen them but don't know the name.

@blacksmith37 edited my answer

@Muath It's plant not planet


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How to detect specific mRNA dsRNA by Northern analysis?

I silenced a gene by RNAi method, for that i chose the gene and the size of the gene is 1.5kb and my insert size is 500nts. i did the transfection and i want to confirm the silencing by northern analysis. when i did i got the ribosomal RNA instead of my specific mRNA reduction and dsRNA accumulation.
Total RNA was prepared with TRIzol reagent (Sigma), and 20 μg/lane was fractionated on a 1.2% agarose, 2.2 M formaldehyde gel. The RNA was visualized with ethidium bromide. The RNA was transferred to a nylon membrane (Hybond; Amersham Biosciences) for 14 hrs and probed with [α-32P] UTP-labeled used SSC for transfer and Prehybridization at 55 for 2hrs incubation, in the probe for 10hrs and Washing at 60 for 2X SSC 20 mins two times.

In this image you can the samples TET induced and uninduced RNA. but the result was confusing and am getting such a strong ribosomal RNA (2.2 Kb) contamination.

Did you try a dot blot or northern with your pure dsRNA to check if the probe is even working? You can use IVT to produce it. You can even use your plasmid as a proxy for dsRNA for dot blot. How big is the probe?

Not really a constructive comment but nowadays hardly anyone uses northern blot. qRTPCR is commonly used for quantification of RNA: it is fast, clean and sensitive.

Yes, i did IVT to synthesis my probe, its 500nts, in our lab we don't to qRTpcr, we believe in basic biology, i put my insert in tetracycline inducible plasmid..when i induce the cells with TET the dsRNA synthesis and it blocks mRNA production. my question is there any way to reduce the rRNA...if i reduce my rRNA i can get my mRNA specific band, any suggestion?

Since your probe is 500nt long, you can increase the hybridization temperature. You can increase the washes too. You can also check if your probe has any complementarity with rRNAs. If so, you may design a better probe. By dot blot, I meant doing a blot with pure RNA samples instead of total RNA. BTW, you may like and prefer to do northerns for whatever reason but don't justify by saying that it is "basic biology" as if qPCR is something that belongs somewhere else.

Thank you for your suggestion i will do that. sorry for that, I mean to say the qPCR enzymes are too costly as compare to alpha-UTP..

Hi, it does not have any complimentary to rRNA because when i designed the construct i did cross check with the whole genome of my organism of interest to check whether they have any off-target. It is fine. i do prehybridization on 55 degree now i am going to increase to 60 degrees. once i get the result i can update.


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What is "beto carotene" and how can it turn lakes pink?
The BBC News article Pink lake in Australia attracts and delights tourists describes an artificial salt lake in Westgate Park, Melbourne, Australia that tuns pink around February and then in "late Autumn, until cooler temperatures restore it back to blue."
I am not sure about the autumn part as it's in the southern hemisphere, but my question is about the color change.

Could they mean beta carotene rather than beto carotene?
And if so, does the pigment stay inside the algae or is it released into the water to produce this color change?
And why pink, rather than the orange color we associate with carrots?

In those conditions, the lake's algae produces a red pigment called beto carotene

The lake's pink colour typically lasts through to late Autumn, until cooler temperatures restore it back to blue.

It's definitely a typo and should be beta.

Carrots actually come in a variety of colors, orange carrots is just a fluke of political history and has little to due with beta-carotene.

Note there are other ways to get pink lakes halobacteria dominated lakes (hypersaline) are often pink becasue they don't use chlorophyll but bacterioruberin. Salt itself tends to be pink which can contribute. Lake hiller in Australia is one such lake. https://en.wikipedia.org/wiki/Lake_Hillier

@John see my comment below questioning if "Salt itself tends to be pink".

The "beto" is a typing mistake. Beta is an organic chemistry label referring to a beta-ring of 6 carbons that exists at either end of a carotenoid polymer C40-Hx.
It is localized in the chloroplast. The plants don't really have a mechanism to release pigments, they can re-metabolize chlorophyll. The volvocalean algea Dunaliella salina is used to harvest beta-carotene in Karratha, Western Australia, from salt lakes. The can have 12% beta-carotene as dry-matter content, the highest of any known source.  The squares are probably salt.

the algea afterwards:

There are over 1,100 known carotenoids of which at least 700 have been identified in plants. They include carotene and xanthophylls, and carotene include beta-carotene. The plants and algea use it to protect themselves from intense sunlight and UV's. It is an anti-oxidant.

Pink doesn't actually exist as a color. It is imagined when green and blue light is sensed by the eye, while red is at a maximum. In the lakes, we know there is 80% red and 20% green pigment in the algea. All that is required would be 20% blue to percieve pink. I don't know where the blue color comes from, the sky/water.
Orange is complex for the eye, and so is pink, because we can only see red green and blue.

Oh, this is a thoroughly wonderful and wonderfully thorough answer, thank you!

Hey thanks!  People should be warned that the BBC takes 150 dollars per year in taxes from the 51st state and is keener on hiding state secrets than journalism, it's the same as RT in higher secrecy.

oh-kay.... I've been duly warned ;-)

worth noting that yellow and cyan are actually parts of the spectrum magenta is not. you can have pure yellow wavelengths, not so for magenta.

There are several combined reasons.
first salt itself in such lakes is often pink, so part of the color comes from the salt crust itself. this is more noticeable in more extreme salt lakes where the deposits can be quite thick. It can be due to iron impurities but can also be further dyed by trapped carotenoids in the salt as it is deposited.
Part is also coming from salt loving halo-bacteria which use are not algae but are photosynthetic. They use bacterioruberin and salinixanthin for photosynthesis but not chlorophyll. these are carotenoids and pink, and responsible for many pink salt lakes like lake Hiller. (there is an interesting link between these bacteria and why chlorophyll is so inefficient that is worth reading)
the last is indeed beta-carotene, produced by salt tolerant algae.
In the case of that particular lake algae appears to be the major factor. However there are many pink lakes each caused by a different mix of carotenoids produced by salt loving organisms which depends on just how salty it is.
As for why it looks pink instead of orange, the answer is carrots have other pigments that shift the color further towards orange, particularly yellow pigments. Also water is transparent so mix a pigment into it and you get a lot of subsurface scattering which can shift color towards blue, this is part of the reason water is blue. Purple and pink are artifacts of how the human eye sees color and not "real" colors so when you combine reds and blues you get pinks and purples.

Thanks for your answer! "...salt itself in such lakes is pink..." is surprising to me, I've never heard of pink salt. Your comment also mentions that the salt can be pink but I've never heard of at least an inorganic salt solution that has such a color. Can you support this with a source? I don't see it stated explicitly in the Wikipedia article linked in your comment that it's the salt itself that produces the color.

In solution? Can you find a source supporting that iron makes salt solutions pink? The optical properties of crystals are often affected by dopants (e.g. the variety of colors of diamonds and sapphires) but those effects are related to the crystal structure. Once dissolved, they crystal structure is destroyed and thse effects are no longer relevant.

trace minerals (mostly iron) turn sea salt pink. Not all sea salt is pink but many are.  this is especially noticeable in thick layers of salt. Interestingly you can get darker pink and even red salt  due to a build up of carotenoids in the deposited salt when it is deposited in isolated basins (allowing hyper-saline conditions to persist and the micro-organims to thrive).

Not the solution, the solid salt deposited on the bottom of the basin/lake.

The water in the image is quite opaque, we can't see the duck's legs much less the bottom of the lake. If the lake is saturated such that there are crystals of otherwise soluble salts at the bottom 1) the duck would not be drinking the water (it's incredibly painful to mucous membranes) and 2) they'd be visible near the shore as well where the lake is thin enough to become transparent.

I was referring to pink lakes in general, I stated that the lake in question algae was the major factor.

Okay, maybe it's good to add to the answer that the salt effect does not apply to the question specifically? Are there algae that can live in lakes that are saturated solutions such that there are also crystals of salt at the bottom? I think that saturated solutions are sterile, aren't they? In other words aren't pink salt crystals and pink organisms mutually exclusive?

please read my answer, I already mentioned that these organisms prefer hypersaline conditions. hypersaline solutions are not abiotic, there are plenty of organism that like hypersaline conditions. hypersaline lakes lack FISH which is a very different thing.

Yes going off-site and reading Wikipedia I see that ...extreme halophiles or haloarchaea (often known as halobacteria), a group of archaea, which require at least a 2 M salt concentration and are usually found in saturated solutions (about 36% w/v salts) There will be no ducks drinking that water but I see that it can happen. But I'm not sure that such a saturated lake would look pink because of both iron-doped pink salt crystals at the bottom and simultaneously because it's full of pink organisms. Anyway thanks for the helpful discussion!

read the one about the algae which is a different orgaimsims, that survives in less salty lakes, said lakes are sill MUCH saltier than normal sea water. also look at salt farming in which halo bacteria often take over super saturated brine pools turning them pin, often getting pinker as they become more salty. you will rarely get all there at the same time but it is very possible to have two of them at the same time.

Not sure which kind of microorganism they talk about, but beta-carotene is a red-orange~ish pigment (as you pointed out, also produced by carrots). The pink coloration I would assume is the product of the color mixture of the pigment with green-blue from the water (not the water itself but the blue reflection from the sky + any other algae in the water). If they release it (the beta-carotene) to the water, again not sure which organism they talk about but it's probably not like it, since beta-carotene is a photosynthetic compound. Therefore is pretty likely they may want to keep it inside.

Do you have any sources?

It was pure guess, but here you go

@N.P. the message "...requires additional references. Please edit to add citations to reliable sources..." should be interpreted literally. If you can edit your post to add your citation to your answer, along with a short description of how the reference supports your answer (usually a short block quote from it is sufficient) that would improve the quality of your answer. Thanks!


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Fuel from photosynthesis
I was reading how plants make use of sunlight, CO2 and some other stuff to make energy. So why can't we create artificially engineered bio solar panels which will take sunlight, C02, water and other things and give us energy (maybe electricity or heat etc). So basically instead of solar panels which are made of silicon or something we can have bio panels made of organic materials. Then we need to supply it with water and it will convert sunlight into electricity.
I googled this on the internet and I don't find anything relevant in this regard. So I am assuming there must be a very good reason we are not trying to do this. I want to know if there is any research going on in this regard and if not why this idea is not feasible.

Here is one group working on it. There are others, of course.

What you are suggesting is an organic photosynthesizer,but that's not necessary when you already have plants that have genetically adapted for millions of years just to be suitable for this very purpose.
 Of course,artifical photosynthesis already exists,essentially using the same process;photons,chloroplasts,calvin cycle,photosystems 1 & 2,etc.It utilizes the general concept with photoelectrochemistry,so basically just replacing the organic tools with artificial photoelectric cells,which also uses h20 and light.What you are asking is why we have not developed genetically engineered organic matter to produce higher efficiency.As a matter of fact,GMO plant's already exist with immunity,though I have not heard of GMO that catalyzes photosynthetic reactions,and best not,because genetic engineering is still at it's best a new field that is too complex,for example,the general GMO is to incorporate the bacterial enzyme cas9 to cleave away specified DNA to alter an organism's genome,such as inhibiting receptors to cannabinoids,or to fight pests with substances that are not harmful to humans,etc.But it has consequences,such as permanence of that edited genome,so if the organism/plant reproduces,the progeny would also exhibit the same GMO properties.
 Photosynthesis is a complicated series of reactions that uses complicated enzymes and such.For example,the enzyme rubisco that changes co2 to energy rich molecules such as glucose,from highly unstable phosphoglycerates.Artifical photosynthesis is quite new,but it also uses the same fuel;co2,h20,and light,not sure if it uses biological nutrients like soil,but the process also uses Nicotinamide adenine dinucleotide phosphate,or NADP+.It is used for anabolic reactions,so it builds up molecules,vice versa are catabolic reactions,which is when enyzmes break down lipids and molecules in metabolism.Albeit I do not know for sure if this molecule has the same purpose in artifical photosynthesis,but for general photosythesis,yes.NADP+ also absorbs electrons for independent and dependent reactions to generate ATP and NADPH,etc.
 I hope this simplifies some things.CONCLUSION:we do have artifical photosynthesis,but gmoed photosynthesis may be harmful to a plant's heredity if we damaged it's genome,causing potential harm.
  Artifical is quite similar to organic,so I guess you say they are biopanels,using h20,co2,and light.

Hi Hypothetical. Thanks for taking the time to write a post. Just some advice since you're a new contributor here...Generally, answers get better responses (& prove to be more helpful to others) if you avoid large paragraphs of unformatted text. Please consider breaking up your text, using proper capitalization for chemical compounds, and see here for how to format posts like a pro! More importantly than all that, though, is the need for you to provide support for your answer through links or citations. That way others know where you got your info. thx


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What are all the elements affecting human reaction time?
I'm helpless at biology/science-y stuff in general. But, as a writer, for the sake of story research, I often have to delve into it. I make use of the Worldbuilding Stack Exchange, but this question didn't seem like it would be a good fit for that site, because it's more about clarifying my understanding of certain scientific concepts than about anything specifically worldbuilding related.
I am looking to create a character with high-speed reflexes and reaction time. However, my question is not about how to accomplish this (scientifically dubious) feat, as this would belong on the worldbuilding forum, but rather whether I have properly identified the elements necessary to do so.
From the research I've done, it seems that the most basic steps regulating how quickly someone reacts to something are a) sensory neurons recognize a stimulus b) they send a signal to the brain/spinal cord and c) this signal is processed and another signal is sent to the muscles, resulting in whatever physical reaction observably occurs.
Hypothetically, then, no matter how fast any single element in this chain (if given a brain that could process signals 10x faster than normal or nerve signals that traveled 10x faster (bear with me)), the speed with which the final action was triggered and completed would still be limited by, say, the eyes' tracking speed and the speed with which the eye converted light into electrical signals on one end, or the speed the muscles were capable of contracting at the other end of the chain.
How am I doing so far?
So, by my estimation potential limiters of reaction speed are as follows:

the speed the eye moves (or would speeding up other things, such as muscles and nerve signals, also increase this?)
the speed the eye converts light into signals
the speed that signals can travel from sensory neurons to the brain/spinal column
the speed with which the brain can process these signals (and potentially its ability to handle multiple tasks/stimulus simultaneously)
similar to (3), the speed that signals from the brain (or spinal cord) can travel to the muscles
the speed with which muscles can contract

Am I confused about or missing anything? Thank you!


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What is this agglomeration of pink cells I found attached to a stone?
Photo taken in a garden in Singapore. The organism is attached to a stone, close to water. Many of these were there.
Size approx 3cm.
The shell of this eggs is very soft. When touched, a pink colored liquid drops out.

They are Apple snail's eggs; check the picture:
Check this.

This could very well be the eggs from an apple snail (family Ampullariidae).
According to Wikipedia

Several apple snail genera (Pomacea, Pila and Asolene/Pomella) deposit eggs above the waterline in calcareous clutches. This remarkable strategy of aquatic snails protects the eggs against predation by fish and other aquatic inhabitants.

If these are in fact the eggs from an apple snail, then the parent is likely in the genus Pila since this is the only major genus found in Asia [source].
You can see a timelapse video of a snail laying eggs here and a short gif below:

 Source: gfycat
See applesnail.net for more info.


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How does the nucleophilic attack in DNA replication occur?

Hi there,
I am confused about how the nucleophilic attack occurs in DNA replication.I watched this video from a biology professor (https://www.youtube.com/watch?v=y4hKibS2fAo)
I watched this video which stated that during DNA replication, the hydroxl group forms a covalent bond with the phosphate and the two phosphorus groups are a leaving group.
I understand the basics of these kinds of reactions, but this one just seems confusing. I can see that the oxygen which was part of the hydroxl group forms a covalent bond with phosphorus. But what happens to the hydrogen? And why does the the double bond and position of the HO change position from the first picture to the second picture?
There are also some pictures which show water being produced. But the video states that the hydroxl group is forming a bond with the phosphate group. How does that work?
Thanks a lot

See Chemistry of phosphodiester bond formation by DNA polymerase and What makes/breaks the hydrogen bonds between DNA and RNA during transcription? for very related questions.

Also related: Is water released when a phosphodiester bond is made between two nucleotides during DNA replication?.

Polymerases uses a two-metal ion mechanism to carry out the addition of a new NTP to a growing RNA strand. Two Mg2+ ions are used in this process; metal ion A is involved in the formation of the nucleophile (O-) for the SN2 reaction to occur and metal ion B is involved in the stabilization of the transition state in the reaction. For the addition of a NTP to a RNA strand to occur, an activated 3’ hydroxyl group (O-) acts a nucleophile and attacks the alpha phosphate of the incoming NTP. The reaction is initiated by a deprotonation event. Metal ion A aids with this deprotonation as it reduces the pKa of the hydroxyl (so it is more acidic), making it easier to deprotonate and form the nucleophile, the proton is accepted by a nearby aspartate residue (not water) - doi: 10.1021/ja403842j. After the hydroxyl attack, the mechanism proceeds through a pentacovalent transition state like in a standard Sn2 reaction and the pyrophosphate group (PPi) is kicked out. The image is not mine but comes from this paper: https://doi.org/10.1038/34542, which is quite good, as is this paper: doi: 10.1074/jbc.274.25.17395 and this one https://doi.org/10.1016/j.molcel.2006.03.013

Perhaps you could properly cite the references you are using in case the links become broken in future.

I have included the doi's instead, hopefully this is better