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Would a transparent iris serve its purpose?
The function of the iris is to regulate the aperture of the pupil. How does the iris obstruct light? Is it due to the pigment present in it? Or is it just due to the sheer presence of it?
I am doing a project where I need to maintain a constant light intensity for albino rats. I was suggested to administer a mydriatic topically but when their iris is transparent, does dilating their pupil make sense?
How is it in human albinos? Does pupil dilation and constriction make a difference in them?

Human albino Iris is not transparent. Translucent maybe. Administering mydriatics might be at least slightly better than relying on their transparency.

What did you do in the end? Feel free to self-answer, if you have one?


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Microinjection intestinal organoids
I am attempting to microinject small intestinal organoids, using the Eppendorf FemtoJet 4i microinjector and Femtotip capillaries, and have come across several issues. This is a new set up in our lab, and I am first to attempt it so I apologise for the basic questions.
When attempting to fill the Femtotip capillaries using a needle or Western blot tip the liquid backs up and does not fill the capillary, leaving a large air bubble. Is this a common issue with the Femtotip capillaries? Are there other methods for filling (that do not require specialised microloader)?
When I attempted to use a tip where I had let the liquid be pulled to bottom by gravity, I had issues with leakage out of the tip bottom. Just to be absolutely clear, is it necessary for the entire tip to be filled with liquid prior to injection (no air bubbles)?
Finally I would be grateful for any advice on injection pressure and time used for organoids.
Thank you

Hi, initially I too had the same problem. Then I figured out that just gently tapping the injection needle would remove the air bubbles from the needle. Give a try

@MosquitoMan delighted to see this answered so quickly, less delighted to see it as a comment. Can you possibly post it as an answer? :)

I found that using the Femtotip loaders gives a continuous block of liquid, which can then be moved to the end of the tip by injecting several times. It is fine to have a air above the liquid at the tip.

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Consistency of consciouness
So I was wondering if consciousness is continous and I found out it might not be the case. But in that case it begs a question, what if in every frame of consciousness my old me dies and new is reborn or rather there is nothing as consciousness but its just a reaction?
What I mean is if I clone a person, the clone would think its the original and we would be unable to determinate it either (if by clone i mean literall copy on the atomic level and with exclusion of any effect of quantum mechanics). If we would annihilate original and put clone into its place noone would be able to tell and to him it would look like everything is continous and nothing happened.
So can it be just illusion in our minds that we are continous sentient beings because we have access to our memory which tells us its like that, same as a clone but as the perception lost focus we die - frame stops to exists?
Can someone clarify this to me or point me to some interesting literature/article on this topic?

This is really not a question biology can answer.  You may find people willing to discuss the definitions of consciousness in a philosophy forum.

I was wondering if there is some sort of scientific view/consensus on this topic. If you suggest that this thing is still rather philosophical question without any viable explanation or evidence then I am OK with it being unanswered but I feel it might be OK to leave it hanging here for times to come when biology will be able to answer it. Anyways thanks for info.

The basic problem is that, so far, there is not a definition of consciousness that provides a way to test by experiment whether a system is conscious or not.  If it can't be tested by experiment, then it belongs to the philosophers (or sometimes to those mathematicians for whom logical consistency is the basic constraint, and to whom physical meaning is irrelevant).

I am not sure it is completely valid to say what you've said in the first sentence. We are not able to determine that something has no consciousness but we are able to state if it does. Well at least that was told to me when I was attending high school (there are some tests to qualify if living organism is indeed conscious). But I understand what you mean. More I think about it, it might be a thing which will be out of our grasp forever.

@S.McGrew "there is not a definition of consciousness that provides a way to test by experiment whether a system is conscious or not" - this is certainly not true. It's true that there isn't agreement but there have certainly been attempts at definitions. I do agree with you, though, that this question as it is framed is not a question for biology.

OK, I need to agree with you: it's certainly possible to make a definition for consciousness that is testable; but there is no consensus that any such definition is useful or correct.

I'm voting to close this question as off-topic because it belongs on psychology.SE.

It is a more psychology than biology I realise that now but I do not think it is completely off and also if in biology manages to get a proof then it is relevant.

You trespass upon a question as old as antiquity: what properties constitute consciousness? The best means to respond to the question concerns a metaphysical answer and an answer in modern biology
We can perhaps divide consciousness into two categories: contiguous thought from past experience and identity and secondly, self-awareness.
The reputed example of the Sorites problem of Theseus' Ship describes how the physical entity of Theseus' ship, during his various battles and broils, loses certain components of his ship: his braces or mast, in example. They are replaced with exact replicates until the time that every component of the ship has been supplanted by a replaced component. Is it the same ship? It is dependent on your definition of identity.
Leibniz's Law of Identity whether in humans, ships or spaghetti monsters, states that objects x and y hold the same identity if and only if they share all the same predicates - qualities or attributes. If this be of functionality, the ship completes the same function and comprises the same components, albeit of different origin - thus, the ship has the same identity. This is important regarding your question whether your 'old [you] dies'. Over time, your cells undergo mitosis and eventually apoptosis. Hence, although your parts are in constant flux, the predicates between your old self and latter self are constant. Ideologically however, there is no set identity!
If you read David Hume's literature, you will observe the notion that one is only the composition of impressions (sensory reception) and thus there exists no identity.
Your question regarding clones is a challenge for biology. Behaviourism is an approach in biology concerning the interpretation of behaviour as a response to a stimulus. Furthermore, humans express complex instinctive behaviours in response to various stimuli. If there exists no 'mental substance' distinct from the body, then it seems plausible to consider human consciousness merely an extension of an advanced instinctive epiphenomenon: self-awareness is a by-product to these advanced behavioural patterns. To support this position, simply recall what factors allow one to discriminate individuals whom one meets, behavioural patterns and appearance.
Finally, one could attempt to assess consciousness in regard to self-awareness by conducting the mirror assessment. If one is capable of identifying himself/herself, then it is indicative of an ability to discern one's personal existence from general matter.
This is by no means a comprehensive answer to this question yet I bid you well in your continued explorations of human consciousness.

Wow thanks, this certainly broadened the way I look at it.

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DNA described somewhere?
This is not purely biological question but how do the companies making DNA analysis know what your DNA means? Is there some database describing human DNA?
I watched some documents about DNA, gene editing... and people in the documents were often working with some infographical like documents which described some chromosome or desease (I don't know what exactly that was, I am an amateur trying to make sense of it) but I was not able to find anything as they had on the internet.

They don't know what your "DNA means", but there's data about the function of particular genes and the effect of some mutations in these genes. "Describing human DNA" is hard to interpret, I think; the full sequence of human genome has been sequenced since 2003, but the "meaning", the full implications of the sequences is still a matter of research. The Human Proteome Project is one initiative headed in this direction of study.

It might be useful to look at how 23andme works, to see how this analysis product is generated, in general:

The 23andMe genotyping platform detects single nucleotide polymorphisms (SNPs). A SNP is a DNA location, or "marker," in the genome that has been shown to vary among people in terms of the DNA base or bases. There are four DNA bases: adenine (A), thymine (T), guanine (G), and cytosine (C). So, for example, at the same genomic location, you might have a C and someone else might have a T. These DNA base differences are known as "variants."

These SNPs can differ by population types. Some subsets of a population type might suffer a disease and appear to have SNPs that others do not. So-called GWAS studies (discussed below) work at associating SNP distributions with diseases or other phenotypic traits.
You send some spit to 23andme, they tell you who you are likely related to and what diseases or other physical attributes you may have, based on patterns of these SNPs.
23andme uses Illumina chips for figuring out what genotypic variants you have in the spit sample you send to them. Illumina is a company that manufactures "chips" that react to the presence or absence of markers in the DNA sample you send to 23andme. Each chip in this platform calls different sets of markers.
These markers often have identifiers associated with them, each called an rsID.

The rsID number is a unique label ("rs" followed by a number) used by researchers and databases to identify a specific SNP (Single Nucleotide Polymorphism). It stands for Reference SNP cluster ID and is the naming convention used for most SNPs.

They also map variants that do not use rsIDs, and instead use some other internal identifier.
Whatever the identifier, GWAS — Genome-Wide Association Studies — are research projects that analyze populations of people in different ethnicities or other cohorts, looking for over- or under-presence of various markers, compared with the larger human population.
For instance, here is such a GWAS study that is used by 23andme to indicate risk factors for Parkinson's disease, in sample donors who have these variants. There are other such studies for schizophrenia, for autoimmune diseases, and so on.
The power of these studies to make a positive, correct association depends on various factors, but the product 23andme sells is ultimately a packaged summary of a lot of work by researchers around the world.

Great read and links, thank you. :)

This question is both easy and hard to answer: DNA and its (known) functions have been described in scientific literature, textbooks and databases for the last few decades, but because this is a enormous amount of data there is no single source or collection that could comprehensively catalog all this information.
Information on genomes and genes has been collected into (somewhat) standardised databases hosted by NCBI or ENSEMBL, however those will probably not be helpful to anyone without established background knowledge. Indepth information about specific genes, procedures or diseases is usually just linked in these databases and comes from actual research papers.
If you want to understand more about DNA genetics and so on the best approach is to start with the basics and take a look at a textbook or online course, if you then have specific questions you can still come back here and ask those.

Thanks, I glanced over NCBI before and as you say, I was quite lost. ENSEMBL looks more useful to me. I wish some compilation of all those research data will eventually be created, it would be incredible to have possibility as an ordinary person to see what part of DNA (at least from the known parts) is responsible for which manifestation of human body. Anyway definitely gonna dive deep on this one. :D

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Using different polysaccharides for coagulation
Would a particular type of polysaccharide be better at coagulation than another? For example, would the presence of cellulose in a bio-coagulant be more effective at coagulation than the presence of starch or glycogen? I would like to know as I am doing an experiment about it and since nobody has done this before, I don't know whether having a higher concentration or ratio of a certain polysaccharide in a bio-coagulant compared to other polysaccharides will have an effect on coagulation efficiency?


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How does gold chloride stain neuromuscular junctions?
Gold chloride is used in muscle biopsies to stain the NMJ. What is the substrate that it binds to?


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Ratio of oxygen produced / consumed by plants
Related questions:
How long can a plant generate oxygen from its own carbon dioxide, produced during nighttime?
Are plants actual oxygen factories?
But the actual question I'm interested in is:
What is the ratio of oxygen produced during the day vs. consumed at night.
Even ballpark numbers are sufficient, as this came up in a conversation about a Mars colony game where a tree produced 2 units of oxygen during the day and consumed 1 at night (with the game-night being half the length of a game-day because...reasons). Colonists would then need about 1 to 1.5 oxygen per full day/night cycle.
My friend and I were like "this ratio does not sound right" and haven't been able to find any any decent numbers to back up our opinion...or refute it.
Obviously the chemical reactions involved are mirrors of each other, and the output depends on the amount of light, and so forth...But wouldn't trees just be...less active at night in order to conserve energy, while more active during the day?

define plant, the answer is vastly different for cacti, trees, grass, or algae.

@John Given the context of what my friend and I were discussing: Trees. If you want more specific than that, I don't honestly care, pick one.

well it depends on what your colony is using, algae is the best at producing oxygen, about 1.9grams per cubic meter of algae , https://www.sciencedirect.com/science/article/pii/0043135488901054

@John 1.92g is a net value. For all I know it could produce 1g per hour of daylight and consume 0.84g per hour of nighttime for a ratio of 1.2:1. Or it might be that it produces 0.2g per hour of sunlight and consumes 0.04g per hour of night for a ratio of 5:1, that's the number I'm interested in.

This quoestion may help you , https://biology.stackexchange.com/questions/58238/how-much-oxygen-does-a-plant-use-up-at-night

@John Hmm. So that does make it seem like half (2:1) is the right number. The paper linked in the answer is about something else, but that statement is part of the conclusion.


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Trying to identify this insect
Can anyone help me identify what kind of beetle this is?
It's ~1/4" in size and was found on some air-dried hardwood lumber in the Pacific Northwest.

This looks more like a hemipteran than a beetle: You can see that the rear part of the wings is membranous. There also seems to be a rostrum starting from the front of the head. https://australianmuseum.net.au/what-are-the-differences-between-bugs-and-beetles

thanks for helping! I think you're right;  it looks like it might be some sort of chinch bug.

I am reasonably certain we have a member of superfamily Lygaeoidea here, but which of the many families that group now contains (aside from Berytidae; the stiltlike legs of that group are clearly not present here) is represented cannot be ascertained from the evidence we have available.


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What are the good and bad cholesterol ?
I have question about cholesterol, as I know we can get cholesterol using vegetables and meat, so what is good and what is bad ?

Whats wrong with question ?

@xusr the comment as written makes a fine answer - it's referenced and all.

Possible duplicate of What is/are the molecular differences between HDL and LDL cholesterol?

Original Answer (posted originally as a Comment)
It is now accepted that high cholesterol causes atherosclerosis. Cholesterol a major component of the plaques that block arteries. 'Good' and 'bad' cholesterol refer to the way cholesterol is transported in the bloodstream.
'Bad' cholesterol is cholesterol in the form of low density lipoproteins or LDL, and 'good' cholesterol is in the form of high-density lipoproteins or HDL.
Or at least that is how it used to be. It is still accepted that high concentrations of LDL in blood promote atherosclerosis, that is high levels of LDL may still be considered 'bad', but drugs that specifically raise the levels of HDL have had serious adverse effects.
Check out this great article: Cholesterol and Controversy: Past, present and Future by  Jeanne Garbarino, especially the section on "Deconstructing Cholesterol: “Bad” is still bad, but is “good” still good?". It is hard to know what the current position is. And check out the work of Brown and Goldstein.
Edit
Goldstein, in his Nobel lecture, famously said (see here)

Cholesterol is a Janus-faced molecule. The very property that makes it useful in cell membranes, namely its absolute insolubility in water, also makes it lethal. For when cholesterol accumulates in the wrong place, for example within the wall of an artery, it cannot be readily mobilized, and its presence eventually leads to the development of an atherosclerotic plaque.

Cholesterol may be synthesized in the body, or obtained from the diet.  The site of biosynthesis is mainly the liver. Cholesterol and fats (triacylglycerols) are transported in the bloodstream as lipoprotein particles, which may be roughly described as a lipid core surrounded by a protein coat, and may be viewed as a mechanism for transporting insoluble fat molecules (by 'coating' them with a soluble protein exterior).
There are five main classes of lipoprotein particles (see, for example, Berg): chylomicrons, very low density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and high-density lipoproteins (HDL)
Cholesterol (and fats) are transported from the liver to other tissues in the form of low-density lipoproteins (LDL).  High-density lipoproteins, on the other hand, pick up cholesterol and fats in the blood and from specialized cells and transport them to the liver. Hence the names 'bad' and 'good' cholesterol.  (In reality, of course, things are more complex than this simple scenario: for a very readable account, see Berg).
The ratio of 'bad' to 'good' cholesterol, ie the ratio of LDL to HDL may be used diagnostically, and a healthy LDL/HDL ratio is about 3.5 (see Berg), but in view of the studies cited by Garbarino a low ratio due to high concentrations of HDL (rather than low LDL) might not be so great either. In fact, if LDL is in check, there may be no benefit to raising HDL (Garbarino article).  But I suppose the physicians will always find a way to waffle (and to charge for the privilege).
It is a common misconception that plants do not contain cholesterol. (My original answer to this question attempted to promulgate this nonsense). In particular, plant membranes do contain cholesterol. However, the amount of cholesterol in plants is low compared to that found in animals (Behrman & Gopalan, 2005).  But it is certainly not zero. The nucleus of maize shoots contain significant amounts of cholesterol, for example (Kemp & Mercer, 1968).
This great reference, Cholesterol in Plants, by Behrman & Gopalan (2005) suggests that the following paragraph should be inserted into biochemistry texts.

More than 250 steroids have been described in plants.
  Of these,  perhaps  sitosterol,  which  differs  from  cholesterol by an ethyl substituent at position 24, is the most
  common.  But  plants  also  contain  cholesterol  both  free
  and esterified. Cholesterol occurs as a component of plant
  membranes  and  as  part  of  the  surface  lipids  of  leaves
  where it is sometimes the major sterol. The quantity of
  cholesterol is generally small when expressed as percent
  of  total  lipid.  While  cholesterol  averages  perhaps  50
  mg/kg total lipid in plants, it can be as high as 5g/kg
  (or more) in animals.

A great generalization is the following (Behrman & Gopalan, 2005)

Prokaryotes do not contain cholesterol

These authors also suggest that one of the reasons for the common misconception that plants do not contain cholesterol is "legalities of food labeling that allow small quantities of cholesterol in foods to be called zero".
I suppose we should not be too surprised that plants can make cholesterol. They can of course, make steroids, the Mexican yam being the original source of a precursor of a particularly important one.
A key enzyme in the biosynthesis of cholesterol is HMG-CoA reductase, which is the target for statins, and these drugs  may be used to lower serum cholesterol levels (but there may be side-effects).
One interesting thing about the biosynthesis of cholesterol is that the final cyclization step requires oxygen which has lead to much philosophical and evolutionary debate (see, for example, here).
Finally, another quote from Goldstein

Cholesterol is the most highly decorated small molecule in biology. Thirteen
  Nobel Prizes have been awarded to scientists who devoted major parts of their
  careers to cholesterol. Ever since it was first isolated from gallstones in
  1784, almost exactly 200 years ago, cholesterol has exerted a hypnotic fascination for scientists from the most diverse domains of science and medicine

You cite: "While cholesterol averages perhaps 50 mg/kg total lipid in plants, it can be as high as 5g/kg (or more) in animals." That is a factor of 100. How can this make you consider your first answer "promulgating nonsense"? Quantities do not count?

The question as stated is unclear as to what is being asked.
If the question is whether ingested cholesterol from whatever source is good or bad, then the answer is that dietary cholesterol is superfluous to human nutrition since it can be synthesized by the liver, and the latest guidelines suggest to keep intake as low as possible.

While adequate evidence is not available for a quantitative limit for dietary cholesterol in the 2015-2020 Dietary Guidelines, cholesterol is still important to consider when building a healthy eating style. In fact, the Dietary Guidelines states that people should eat as little dietary cholesterol as possible. 1

The main source of dietary cholesterol is overwhelmingly from animal sources. A meta-analysis published in August 2017 of vegetarian diets found that

Of the 8385 studies identified, 30 observational studies and 19 clinical trials met the inclusion criteria (N = 1484; mean age, 48.6 years). Consumption of vegetarian diets was associated with lower mean concentrations of total cholesterol (−29.2 and −12.5 mg/dL, P < 0.001), low-density lipoprotein cholesterol (−22.9 and −12.2 mg/dL, P < 0.001), and high-density lipoprotein cholesterol (−3.6 and −3.4 mg/dL, P < 0.001), compared with consumption of omnivorous diets in observational studies and clinical trials, respectively. Triglyceride differences were −6.5 (P = 0.092) in observational studies and 5.8 mg/dL (P = 0.090) in intervention trials. 2

concluding that plant based diets reduced total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol ( as the latter is used in reverse cholesterol transport so with less circulating cholesterol there is naturally less to transport ) but triglycerides were unaffected.
So, if you eliminate animal based foods (and therefore the main source of dietary cholesterol) then the studies suggest you are likely to improve your lipid profile which is presumably one reason for the guidelines.

https://www.choosemyplate.gov/2015-2020-dietary-guidelines-answers-your-questions
Association between plant-based diets and plasma lipids: a systematic review and meta-analysis https://academic.oup.com/nutritionreviews/article/75/9/683/4062197

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what is the classification of this stream insect?

This insect I found from Southers region of Bangladesh. Its limbs are larger than its body.and the picture shows its dorsal part.

This is a Water Strider (Order Hemiptera, Family Gerridae); the end of the abdomen is not in focus, so it's impossible to say if you have an apterous adult (of a subfamily other than Gerrinae) or a nymph; if the latter is the case a species-level identification will likely not be possible.

Most probably it is Trepobates sp.


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Are we "more evolved" than present-day bacteria?
The common ancestor of humans and modern bacteria was most likely a prehistoric bacterium. Does this mean that humans are "more evolved" than today's bacteria?

To be precise, the last common unified ancestor was likely closer related to archaea than to bacteria: https://doi.org/10.1038%2FNMICROBIOL.2016.116

@NoOne that's an impressive misunderstanding of pretty much everything in biology you've got there.

"More evolved" doesn't mean anything in biology.

This is a standard question. The whole problem boils down to what you mean by "more evolved"? Below I am answering the question considering a number of possible definitions. If you have other ("clearly defined") definitions in mind, let us know.

Are [humans] "more evolved" than present-day bacteria?

If "more evolved" == "more evolution time"
Then, both bacteria and humans are exactly as evolved!
As all life on earth shares a common ancestor, all currently living creature has evolved for exactly the same amount of time (about 3.8 billion years).
If "more evolved" == "more generations"
Then, bacteria are more evolved.
Bacteria typically have a much shorter generation time than humans do, so with this metric, bacteria would be more evolved.
If "more evolved" == "more fixed mutations since the MRCA"
Then, it is a little more complicated and may depend upon which bacteria lineage you are considering.
If the genome-wide mutation rate is $\mu$ and the haploid population size is $N$, then there are $N\mu$ new mutations every generation. Given that each one of these mutations has a probability of fixing (fixing = reaching a frequency of 1 in the population) is $\frac{1}{N}$, the rate at which mutations fix is $\mu N \frac{1}{N} = \mu$ at each generation. If a species has $g$ generations per year, then over $t$ years, $\mu g t$ mutations would have accumulated.
The genome of bacteria is typically much smaller than the one of humans, but their mutation rate per nucleotide is much higher. Overall, the genome-wide mutation rate is rather higher in humans but that might well differ from species to species. However, again, bacteria have had more generations per year than humans and therefore bacteria species likely have fixed more mutations than humans have. So from this metric, bacteria are rather more evolved than humans.
If "more evolved" == "able to resist higher acceleration"
Then, bacteria are more evolved although that might among bacteria lineages
Some bacteria have been grown under 400,000 g (National Geographic), while a typical human can only tolerate about 5 g and for only a short period of time!
If "more evolved == more impact on the environment"
The term impact is a little hard to define but I think it is of interest to highlight that, even here, bacteria would probably win because cyanobacteria caused the great oxygenation event which is probably the largest planet-wide environmental change caused by biological organisms.
(thanks @Thawn for this definition he gave in the comments)
If "more evolved" == "having more lungs"
Then, humans are more evolved.
Bacteria have no lungs, humans have two.
If "more evolved" == "bigger genomes"
Then, humans are more evolved. Note also that corn would be more evolved than humans with this metric!
If "more evolved" == "higher fraction of the genome that is encoding for proteins"
Then, bacteria are more evolved.
If "more evolved" == "more protein coding sequences"
Then, humans are more evolved.
If "more evolved" == "more phenotypically different from the MRCA"
You would have to list specific phenotypes of interest. So, here the term "more evolved" still remained a little undefined.
Also, we do not have much information about the MRCA of these two highly distantly related lineages. The question could be more easily answered for more closely related lineages. For example, in mammals, if you consider the following traits and always ask what species is (likely) most different from the MRCA of all mammals

body mass -> blue whale
brain mass -> sperm whale (yes, sperm whales have a very big brain)
lips shape -> platypus (they have a beak)
time taken to type Hello\nWorld on a computer keyboard -> humans

Related posts

What is meant in biology by the term “evolved”?
Why have humans evolved much more quickly than other animals?

+1, wouldn't you reckon this question to be a duplicate, as you state in your answer?

@AliceD Good point. I posted two related posts. The post 'What is meant in biology by the term “evolved”?' kinda make a similar point than the one I am making here. By listing potential definitions, I am hoping to make the naive reader realize that it is not that easy to come up with a good definition that would give us a good intuition about what more evolved mean.

I think the phrase more evolved implies the notion of more valuable information, more sophistication and less genetic junk being encoded inside the genetic material of the organism. If there was ever anything worth of being called genetic junk to begin with, that is... It might be good to add this to the list of interpretations, since that's the most obvious one.

Your definition is unclear though. What do you mean by valuable information, sophistication and genetic junk? All of these terms are very undefined. Try to think of a way to measure these things. If you can come up to way to measure these concepts, then I'll happily add it to the list and try to answer who is more evolved if I can. I added If "more evolved" == "bigger genomes" and If "more evolved" == "higher fraction of the genome that is encoding for a protein" though in reaction to your comment. Thanks

@Remi.b Valuable information and genetic junk are related to what portion of the genome is required to be preserved in order for the organism not to loose any functionality or features. Sophistication is indeed a vague concept, but it is clearly distinguishable between e.g. mammals and prokaryotes. I guess you can say that it is a measure of the complexity of the non-junk genetic material of the organism - if we ever manage to fully understand its functions.

non-junk genetic material does not mean much. You are maybe trying to refer to the concept of junk DNA. I already have "the fraction of junk DNA" as possible definition.

Re "genetic junk", please try to understand that there's a difference between "we don't understand what this DNA does" and "we don't understand what this DNA does, therefore it must be junk".

junk DNA was actually first defined as a synonym of noncoding DNA, so it does not even imply that we don't know what it does. It might be a well known regulatory sequence that is being called junk DNA. But the term "junk" became very popular, took a number of weird definitions and is today onlny very rarely used in the scientific literature.

more evolved == more impact on the environment even here bacteria win because cyanobacteria likely caused the great oxygenation event which is the largest planetwide environmental change caused by biological organisms

I think it's pretty obvious to every thinking person that the objectively correct definition of "more evolved" is "able to resist higher acceleration". (More seriously, this is a fantastic answer, thank you.)

While I believe that all the definitions given by Remi.b are very valuable and have merit, I would like to add one definition which I think is closest to what is commonly understood under the term "more evolved":
"more evolved" == "more genetically complex" (Edit: more specific definition as suggested by Bryan and Remi)
To be more precise I define "more genetically complex" as:

more different protein-coding genes (different being important here because some plants have extremely large genomes due to polyploidy. But this is not adding complexity because polyploidy means that they have many copies of the same genes)
more expressed gene variants
more posttranslational modifications
more genetic control mechanisms

Under this definition, humans are clearly more evolved than bacteria:

Humans have close to 20.000 protein coding genes, while bacteria have somewhere between 1500 and 7500
Humans have RNA splicing, enabling the expression of several different protein variants from the same gene. Bacteria do not have RNA splicing.
Humans use a wide variety of post-translational modifications of proteins to tune protein activity and for signalling cascades. This point is not as clear as the points above because the entire biological domain of bacteria has developed many post-translational modifications, and the exact number of modifications used in the entire bacterial domain is much less well understood than the post-translational modifications in humans. However, it is safe to say that each individual species of bacteria uses much fewer post-translational modifications than the human species (and comparing a single species to an entire domain would be quite unfair).
Humans use a wide variety of very complex interlinked genetic control mechanisms which span from expression control by cell signaling via expression control and gene silencing during embryonic development to heritable epigenetics (Lamarck was not that wrong after all). Like the post-translational modifications this is a very active field of research and more and more expression control mechanisms are being discovered both for bacteria and humans all the time. But again, there is no argument that humans have a more wide variety of genetic control mechanisms than any individual bacterial species.

I think it's quite a stretch to say "more evolved" == "more complex". I mean, certainly you an assert this just due to flexibility of language, but there's zero reason to throw the word "evolved" in there: If you mean more complex, just say more complex (and then get ready to defend your definition of complexity...). Although over time evolution will produce some more complex organisms than started, evolution need not result in higher complexity in all cases.

I think it is a good add +1. I would just note that definition "evolved" based on "complex" and then defining complex is a little of a work around that may lead a naive reader to just retain that "human are more complex" without understanding what this means. I would rather have 4 categories and drop the term complex. I am not sure my criticism is the same as @Bryan's

@BryanKrause; @Remi.b I changed the definition to "more genetically complex". This is more specific and hopefully more clear. What do you think?


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Construct picture of person's face from DNA
Would it be possible to construct a picture of a person's face from his/her DNA?

Apparently so:
http://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1004224
Did you not try a google search before asking?

There's a TED talk from a top researcher on that subject, his answer is YES the science of that is advancing alot. https://www.ted.com/talks/riccardo_sabatini_how_to_read_the_genome_and_build_a_human_being


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Why don't vegetables taste good despite being healthful?
This is more a question about the evolution of taste than about the chemical composition of vegetables. Why don't vegetables taste good despite being healthful?

Probably because vegetables are usually the parts of plants that plants don't want to be eaten by others.

This question might in fact be a question about the inferior quality of vegetables that are grown in greenhouses or other industrial facilities.

Who says vegetables don't taste good?  Depends on the vegetable, of course, but IMHO peas picked fresh from the vine are in the top 10 or so of yummy things.  Carrots, cucumbers, peppers (or are they a fruit?) and more are all quite good.

@jamesqf Everyone agrees they don't taste as good as fruits.

@Thomas: Everyone does NOT agree.  Of course it depends on the particular vegetable and fruit, and on the individual.  But there are a great many vegetable that IMHO taste better than say an uncooked quince, cornelian cherry, or even some of the modern store varities of apples.

@Cell What is the basis for saying that?

We are evolved to survive starvation, and live to be perhaps 35. So fatty foods with lots of calories taste good to us. Our genes (and preferences) lag thousands of years behind our present environment.

I'm not sure about your statement that humans evolved to live 35 years. Prior to modern medicine, that was the mean, but it was skewed left by very high infant mortality. If they survived infancy, neandertals would live 60-70 years.

I have not heard that @kmm. What is your source. Mine is admittedly a TV show, and I am an entomologist. But as far as I understood, Neanderthals lived to be 30 or 35. Even if they lived longer, it does not matter, because evolution only acts on child bearers.

Because your primary school cafeteria used to serve canned vegetables, you've hated vegetables ever since, and you haven't tasted them cooked properly yet.
To make vegetables taste good, one thing you can do is going to your local farmers market, buying whatever looks appealing to you and asking the farmer for suggestions on how to cook it.


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Pangenesis and Lamarck's theory of inheritance of acquired characteristics
I've read that Darwin had split ways with Lamarck's evolutionary ideas. Yet his theory of pangenesis seems to support Lamarck's theory of inheritance of acquired characteristics. What am I missing?

Pangenesis and Darwin's Gemmules theory suggests a mechanism so that the body's information can travel to and be transmitted by the gametes. Today we know that the information is present in every cell.
Stephen Gould estimates that Lamarck was the first to develop a truly coherent evolutionary theory.
Lamarck's biological and metaphysical theories comprised entirely correct premonitions, 70 years before Darwin. His book was "Philosophie Zoologique" and Lamarck was not illustrious in his lifetime. His lack of evidence made him an impious, profane author, of the pre-enlightenment style of Voltaire, Rousseau, and prior to Emile Zola and Jules Verne.
Scientists have recently attacked Lamarck with great energy, in favor of Darwin:
http://www.textbookleague.org/54marck.htm
Basically Darwin emulated Lamarck's skeletal theory, perhaps independently, and fleshed it out in a modern writing style. He also discovered the foundations of an entire scientific field of his own which tied into Lamarck's, and he fought the church and the science institutions with it.
The evidence of Darwin was copious and meticulous, completing the work of Lamarck (with lesser or greater brilliance, for you to judge).
Lamarck's speciation theories were correct, and his trait-inheritance theory was metaphysical.
First law
Life by it's own force, tends to increase the volume of all organs which possess the force of life, and the force of life extends the dimensions of those parts up to a extent that those parts bring to themselves;
Second law
The production of a new organ in an animal body, results from a new requirement arising. and which continutes to make itself felt, and a new movement which that requirement gives birth to, and it's upkeep/maintenance;
Third Law
The development of the organs, and their ability, are constantly a result of the use of those organs.
Fourth Law
All that has been acquired, traced, or changed, in the physiology of individuals, during their life, is conserved through the genesis, reproduction, and transmitted to new individuals who are related to those who have undergone those changes.
Darwin convinced many scientists and wrote about it continuously from his 30's till his 70's non-stop, sent letters to everyone, and used evidence to define a scientific and mechanical reality to the theory of adaptive radiation. Darwin also coined catchy phrases:
The English and French view of Lamarckism differ.
The English view slights his status, due to lack of evidence and some alchemical bases for the selection process, even though Lamarck is the father of adaptive radiation theory, in the age of the printed book.
The French view gives him more influence, firstly because he may have inspired Darwin as an eloquent writer on the topic of adaptive radiation, the father of the adaptive radiation theory, and secondly because a glimmer of Lamarckism can be found in the new discoveries of Epigenetics, non genetic inheritence.


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Inheritance of partly genetic conditions
Suppose Anne has a condition like OCD, that has a significant genetic component. Neither of Anne's parents have OCD, though. Does this mean that each of Anne's OCD genes were carried by at least one of her parents?

You should read the post Why is a heritability coefficient not an index of how “genetic” something is?

Many things are possible theoretically. Consider the following hypothetical example for illustration. Imagine, if you had two genetic variants A and B affecting a trait with the following probabilities
AA: 5% chance of having OCD
AB: 10% chance of having OCD
BB: 20% chance of having OCD
In this case, clearly having OCD has a genetic component, and yet no matter which genes a person has (and its parents had), it is possible for that person to get OCD. Probabilistically, however, they have increased risk if they inherit certain genetic variants over others.
In practice, most common psychatric disorders tend to be highly polygenic. I have answered a similar question (Q: Bipolar disorder genetics) of yours which may be relevant again.

This is a correct answer and could be improved with a reference. I realize this is basic textbook level information, but that makes the reference easy. I'd suggest wherever you learned about this, or possibly Thompson & Thompson Genetics, Ch. 8. There is a discussion about this here. Feel free to contribute!


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Height prediction based on genetics
My height, as predicted by my genetics, is 156 cm whereas my actual height is 172 cm. What could be the reasons for this substantial discrepancy? Does it just mean I had very good nutrition as a child?

Is the difference substantial? Is 156cm the average height for your gender in your family, or within your genetic background? The percent difference between 156cm and 172cm is only 9.8%. Think about that for a moment!

Sources of phenotypic variance
There is phenotypic variance in height in the human population. This phenotypic variance is in part explained by genetic variation, but there are also non-genetic variations, incl environmental variation (what you eat, your physical activity among many other things). See this post for more information.
Sampling error
On top of that, those measures of "genetic height" are based upon a limited number of SNPs and a limited number of individuals sampled. There is therefore a bit of room for a little bit of sampling error here. Note sampling error is not a mistake. It is just the fact that parameters estimated from a sample don't necessarily match perfectly the population parameters.
Training data set
Finally, the estimate is based upon correlation made from previous people. There might have a generational gap in height, typically present in countries that have recently largely changed their diets, such as many Asian countries.
For all of the above reasons, there might have a gap between your actual height and what has been predicted by some genetic testing. In short, yes your nutrition might part of the reason for this gap.


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Is evolution always unidirectional?
Is it possible, at least in theory, for a species to evolve into another species and then evolve back into the first species?

It's possible, but very unlikely.  Usually it takes a substantial number of genetic differences to qualify two organisms as different species.  One might think that reversing the direction of selection pressure could reverse a genetic change, but genetic change begins with random mutations which are not determined by selection pressure.  It's very unlikely for one random process to undo another random process (imagine mixing black and white sand in a jar by shaking it, then trying to unmix by unshaking!).

While it doesn't go nearly to the extent of speciation, the classic example is the British peppered moth: https://en.wikipedia.org/wiki/Peppered_moth_evolution  Originally it was mostly white with black spots, which made a good camoflage on tree trunks &c.  During the industrial revolution, the "dark satanic mills" put out a lot of soot, turning the tree trunks dark.  The whiter moths were easy to spot, and got eaten before reproducing, so within a few decades most of the moths in industrial areas were black.
Later on, emissions control laws drastically reduced the amount of soot, the tree trunks became light again, and the moths evolved back to white.


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Bipolar disorder genetics
My understanding is that bipolar disorder is polygenic.
1) Does one need to have all the genes for bipolar disorder in order to have the disease?
2) Is it possible for a person to have all the genes for bipolar disorder and still not have the disease?

Does one need to have all the genes for bipolar disorder in order to have the disease?

No. In genome-wide association studies (GWAS) of psychiatric conditions, it is a constant finding that the associated variants each influence the probability/risk. The effects of all known variants can then be summed up to a polygenic score (PGS). A person with higher PGS is more likely than someone with a low PGS. But some people with low PGS (i.e. people who don't have "all the genes") still get the condition, it is just not as frequent as people with high PGS.
Another reason why we can say 'no' to this question is through findings of quantitative genetics studies. These estimate the heritability of certain traits. For the answer to be 'yes', the heritability would have to be one ($h^2 = 1$). However, as far as I know, there are no known psychiatric conditions that have heritabilities of one. Some high (e.g. $h^2\approx 0.8$), yes, but not one.
It's also worth mentioning that there is probably no sharp line between having bipolar disorder and not having it. It's a medical diagnosis that is useful but rough. Most likely, all of us have a little "bipolar" in us. I think it's probably most useful to view it as a spectrum.

Is it possible for a person to have all the genes for bipolar disorder and still not have the disease?

This is not known and it may not even be a well-defined question. We don't know all the variants that affect the risk of bipolar disorder (or most other polygenic disorders). So we cannot say for sure.
Some 'omnigenetic' hypotheses propose that all genetic variants have some effect on all traits. Some effects are just smaller and some larger. In this case, the expression 'all the genes for X' may be technically meaningless.


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Is it possible to deduce facts about a person's parents just by studying his/her genome?
As an example, suppose Anne had abusive parents. Is it theoretically possible to deduce this from her genome even if she didn't inherit this quality (of being an abusive parent)?

Is there any evidence at all that being an abusive parent has a genetic component?

@jamesqf It's likely to have some genetic component, as do most things in life, I guess.

It might seem pernickety but you often can't deduce from a genome; you can only infer from it. For many characteristics about a person, there are only rough, probabilistic associations between genotype and phenotype. Not one-to-one relationships.
You can take an educated guess that someone with a certain genotype could be a social person of European ethnicity with a low risk of psychosis, which might suggest things about their parents. But there are likely many genes that influence those characteristics and still more non-genetic factors. So you couldn't be certain.
For a factor like whether the persons parents had abusive personalities, I think the genetic differences would be so subtle (if existent) and there would be so many other factors (such as the habits and choices of the parents) that you would be very unlikely to be able to draw any conclusive associations. Articles and studies about linking human genetics with a person's characteristics are listed below. If any of the genes in question are linked with those characteristics then the parents of someone with the gene could possibly have those genes and characteristics too.

Personality types including belligerence, charisma, cynicism, housekeeping, lack of personality, obsessive-compulsive behaviour and gullibility.
Psychosis and Schizophrenia risks.
Ethnicity and European ethnicity, which in turn correlate with geographical location, language and certain phenotypes.
Height.

If anyone would like to suggest additions to that list, I'll happily add them.

Not the kind of complex phenotype that you describe (because nobody knows for example if/how "being abusive" is written in the genome), but yes, some things can be determined.
The easiest is through sex chromosomes.
For example: if you look at the X chromosome of a man, you can tell for sure that it comes from his mother (because the Y can only come from the father, quite logically) so any allele that you see there is also part of the mother's genome - but since she has a second copy, maybe it does not translate into a phenotype.
Sometimes you can even guess the phenotype of one of the parents: if you study a woman's X chromosomes and see that both have alleles that cause color-blindness (encoded on this chromosome) it means that the only X chromosome of the father has this allele, so the father is probably color-blind.
See: https://ghr.nlm.nih.gov/condition/color-vision-deficiency


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Intelligence as measured by DNA tests
Suppose a person has an IQ of 130, as measured by a standard IQ test, when he is 18 years old. He then goes on to develop severe mental illness, which reduces his IQ to 100. After this, he takes a DNA-intelligence test, like the one offered by GenePlaza, which claims to measure his intelligence from his DNA. Will this test show an IQ closer to 130 or 100?
Note that mental illness is governed by a combination of genetic and environmental factors.

Note that the "IQ test" on GenePlaza is not meant to be taken seriously: 'The results come with disclaimers saying the results don’t mean much yet, because they predict only about 5 points of IQ. “I hope people are not getting it thinking that this is a true measure of their intelligence,” says Alain Coletta, a bioinformatics scientist and the founder of GenePlaza.'

What are the causes of this severe mental illness in your scenario?

@Remi.b As I said, my understanding is that mental illnesses like schizophrenia are governed by a combination of genetic and environmental factors.

I'm voting to close this question as off-topic because this is a question about intelligence tests, not about biology.

@ David I'm basically asking if a person's true IQ can be accurately predicted from his DNA. How is that not a biology question?

The answer will depend on the data that genetic model was developed from. I would suspect that most research on genetic factors of IQ has been performed in healthy, normal adults, so the model will predict IQ from DNA as if the subject were a healthy, normal adult (whether they are or not). It's unlikely that the DNA-IQ model was developed using a large cohort of mentally ill people, so the model may produce inaccurate results when applied to those people. I would expect the test to produce a score closer to 130 (if it is indeed an accurate model, which I will not discuss here).
Even if there are genetic predictors of the mental illness, it's likely not a 1:1 correspondence between DNA features and the illness, so this effect would be diluted when correlating against a third variable like IQ.


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As electrons are moving through the ETC, how is ATP produced for the active transport to even happen?
A lot of websites aren't being specific and they are just saying that when electrons move from a high to low energy state during the ETC, "energy" is being released and that energy is used to pump (active transport) H+ ions through the membrane. I want to know more. Isn't ATP formed by adding a phosphate to ADP? If so, where do electrons moving through the ETC get that phosphate from? BTW, I'm not talking about ATP synthase, because you need H+ ions for ATP synthase and I'm not understanding how those H+ ions are being actively transported through the membrane in the first place.

On SE we expect you to do more research before posting, as you will find if you read the help on asking good questions. It's not sufficient to say "a lot of websites aren't being specific" — you need to find sources that treat the subject at a more advanced level. And the best sources are books, not websites. If you have the money, buy as many as you can afford. If not, try NCBI Bookshelf. For Biochemistry use Berg et al. — Try Chapter 18.

If you are referring to the active electron transport by complexes I-IV (which I guess you mean, by saying you're not referring to ATP synthase), then the most likely answer is 'we don't really know'. For ATP synthase the mechanism is quite well known, but for the ETC complexes I think I've only ever seen some structural/mechanical theory for one of the complexes.

ATP formation is done using the Complex V called as ATPsynthase (also called as F0/F1 particle) and the theory explaining this process is called as the Chemiosmotic Theory2.
During cellular respirationKreb’s cycle (in the mitochondria) and Light dependent Photophosphorylation photosynthesis (in the chloroplast thylakoids) a set of reactions establish a proton gradient across the inter-membrane space ( hereby referred to as IMS) of the mitochondria/chloroplast( if you remember mitochondria/chloroplast are double membrane bound organelles).
Just as in a battery/cell we have EMF(electron motive force) we have, in the IMS of the mitochondrion/chloroplasts, a proton motive force.
Since substances always flow from higher potential to lower potential, the IMS of mitochondrion/chloroplast having a high amount of protons is a region of high potential and lumen of mitochondrion/chloroplast is a region of low potential since there are less number of protons.
The only way protons can move from the IMS  of the mitochondrion/chloroplast to the lumen of the mitochondrion/chloroplast is via the complex V (also known as ATPsynthase).
The ATPsynthase is a lollipop shaped protein structure that is freely rotatable and it brings ADP & phosphate molecules close together so that a covalent bond can be formed in between them.
How does it exactly do this you ask?
So let’s summarise what all we have here:

ATPsynthase that can rotate about its rotor.
Proton gradient across the IMS ( high potential) and the lumen ( low potential).
The only way out for the protons is via the ATPsynthase.

Now we can see a link here.
So what happens is, there’s the F0 subunit of the ATPsynthase through which the protons are able to move across the membrane and during that movement the rotate the F1 subunit.
During this rotation shown in animation here  the ADP & the phosphate group which are present in the active site of the F1 subunit are brought near each other and due to atomic interactions a bond is formed.
The mechanical energy ( movement of protons across the membrane) is converted into chemical energy ( covalent bond) between the two molecules.
This is the process via which the currency of the cell, ATP, is produced.
Hope that answers the question.

I don't think you should answer questions in which the poster has not done his homework properly, but it you do, please read them first. What he writes is "I'm not talking about ATP synthase, because you need H+ ions for ATP synthase and I'm not understanding how those H+ ions are being actively transported through the membrane in the first place." You have described the ATP synthase — he wants to know how the proton gradient is established in the electron transport chain. I have told him where he can read about it for himself.

Oh, I see. Thank you for pointing it out. I thought he needed the mechanism of it. I think he needs to learn the cycles to completely understanding how H+ ions are being transported. I’ll be more careful next time.


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What determines the reversibility of cell of G0 phase in cell cycle?
From Weinberg's The Biology of Cancer: A cell that has been recently formed by mitosis must decide whether it will once again initiate a new round of active growth and division or retreat into non-growing state G0. This decision is strongly influenced by mitogenic growth factors in the cell's surroundings. Their absence or presence of anti-mitogenic growth factors will trigger the default decision to proceed from mitosis into the G0 quiescent state.
Withdrawal from the cell cycle into G0 is often reversible (cell can re-enter into active growth and division), however some cells irreversibly leave the cell cycle (such as neurons).
Here comes my question : What determines in the cell whether the cell will go to reversible (quiescent) or irreversible (senescent) state of G0? I have found that it has something to do with the amount of RNA (low RNA content in reversible), but I do not understand why low RNA content means that the cell should proliferate again. And are there any other criteria that determine whether the cell will go to quiescent or irreversible state? (I am looking for exact molecules and mechanisms, the more into detail the better !)

The answer is quite complicated. One of the major issues in understanding what factors drive senescence vs quiescence has been the absence of a clear, uniform molecular definition of senescence. That said, multiple tumour suppressors, including p16 (and the other genes that occupy the INK/ARF locus) , as well as TP53, can modulate the expression of senescence associated transcriptional programmes.
Additionally, epigenetic remodelling, including heterochromatinisation at E2F target genes (which are a major driver of cell cycle progression through the S phas) , is also known to be a feature of senescence.
A very good starting point to survey the literature surrounding the topic is https://www.nature.com/articles/nrc3960?message-global=remove


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Why is DNA polymerase added at the end of PCR reaction?
PCR reaction is used to amplify DNA fragment. Each reaction requires a DNA template, buffer, dNTP mix and a unique pair of primers, one ''forward'' primer and one ''reverse'' primer. The DNA polymerase should be added last to the reaction, just before starting the PCR programme.
My question is, why is DNA polymerase added right before the PCR starts? Is it because it can begin to amplify DNA before adding the reaction to the thermocycler? How could it amplify the DNA when the DNA is not denaturated until added to the thermocycler?

True, the template is double stranded, but the primers could begin amplifying themselves, and any other stray DNA. You don't want any nonspecific amplification in the early stages that could compete with the target fragment. Also, even though Taq polymerase is a very hardy enzyme, it is standard practice to treat enzymes with special care, on ice so they don't degrade (although I have forgotten them on the bench overnight, and they survived that).


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Is it fine to state every learned behavior has an innate component ? ie. Behavior X is largely/ mostly laerned with an innate component
For example human acquisition of language, can we say it is learned, but has an innate component -- because there is a particular structure of the tongue, and perhaps also a specific cognitive ability which is requisite to speaking/ learning a language.
The aforementioned requisites are ones which are reliant on genetics, thus can we say there are innate components to it, even though it is largely, based on experience, as stated in the assertion below.
"The behavior of language acquisition is based on experience, and subject to continual refinement and therefore can be classified as largely learned, however, due to the requisites it also has an innate component to it"

Think of a cake. Is a cake determined by its ingredients or by its preparation (mixing, baking, etc)? It's a meaningless question. The cake is determined by both.
Now think of two cakes. In principal, we can now begin to talk about the causes of their differences. For example, if they had identical ingredients but were prepared differently, then we could say that the differences in the resulting cakes were due to different preparation.
Humans are baked cakes. Quantitative genetics is a field which tries to estimate to which extend differences between organisms are due to genetic factors. Learned behaviors are consistently found to be heritable in quantitative genetics studies. For example, adult vocabulary size is substantially heritable. It is not that the words are literally transmitted to the offspring, but rather genes that influence the cognitive abilities, interests and personality of the individual. That vocabulary size is "heritable" means that a substantial portion of the differences between individuals' vocabulary sizes are due to genetic differences (although by no means only due to genetic differences).
In short, what I'm trying to get at, is that you can only talk about the relative contributions of genes and environment if you're talking about it in the context of differences between individuals. In that case, yes, learned behaviors have an innate component.

Re: vocabulary size being heritable, In the child psychiatry literature, shared environment accounts for the largest component of the variability in vocabulary size, followed by unique environment, then genetic factors. This is seen in English and Chinese.  Where do you see data that "vocabulary size is substantially heritable"?

@DanHall Nope. Shared environment accounts for nearly nothing in vocabulary size. (Once the person is entering adulthood.)

can you share your data?

@DanHall For example, vocabulary tests are well known to load fairly highly on g, and it's well known that g has little shared environmental influence. But there are also studies that directly estimate heritability in vocabulary, see for example (van der Berg, Posthuma, Boomsma: A Longitudinal Genetic Study of Vocabulary Knowledge in Adults).

Are there in fact any (practically reachable) limits on vocabulary size?  Personally, I have a good vocabulary in English (including Shakespearean and a good bit of Middle English), the technical jargon of several disciplines, and a reasonable bit of several other languages, yet previously-learned vocabulary doesn't seem to disappear when I add new.  So where is the heritability?

@jamesqf Can you clarify more precisely what you want answered? Perhaps you have some misunderstanding of what heritability means. More likely, I simply don't understand what exactly you're asking.

@Eff: What I'm asking is how it's possible for vocabulary size to be inherited, when 1) So much of one's vocabulary depends on environment - learning another language or the jargon of a profession demands a large increase in vocabulary; and 2) The practical limit on the size of vocabulary seems to be the amount of time one has to learn.  Within that constrant it seems to be limitless.

@jamesqf As for your (2), you can simply control for age if you wish. Whether vocabulary is limitless, perhaps it will help to think in percentiles. For example, a person may have a vocabulary in the 85th percentile (of a particular population in question). Yes, it is possible for a person to suddenly gain a huge boost in vocabulary for whatever reason. However, when you look at population level, there will almost certainly be fairly high stability in a statistical sense. Rank order people, then test them later again. The rank orders will correlate substantially (not perfectly, obviously).

@jamesqf For your first point that so much of vocabulary being environmental. Well, that has to be tested before you know that. The main goal of the entire field of quantitative genetics is to estimate to which extend differences within a population are due to genetic differences of any sort or environmental differences of any sort. For example, the study I referenced in a previous comment estimated that >50% of variance is explained by genetic differences. This means that genetics matter, but since it is not 100%, the environment clearly matters as well.

@jamesqf How can vocabulary size be (partly) heritable? The reason is, that while external factors may have an influence on vocabulary, so does individual factors. How good is the person's memory? How much does the person read? How interested is the person in learning new things, and how easily does the individual learn? Etc. All of these things are influenced by the individual's psychology and brain. And genes are important for the creation of the brain.

@ Eff: The problem is that all of those are so strongly affected by environment and personal choice that teasing out any heritable effect seems impossible.  A heritable factor would have to affect the POTENTIAL vocabulary size, not actual (since that is so strongly a product of environment), and again, the potential size seems effectively unlimited.

@jamesqf "A heritable factor would have to affect the POTENTIAL vocabulary size, not actual..." No. I strongly advise you to look up what heritability actually means in the field quantitative genetics. What I am saying is completely mainstream science. However, here is a fact that you may find interesting. Identical twins who are separated at birth have more similar verbal abilities in adulthood than non-related adoptives who were reared together in the exact same family and went to the same school and had same teachers. Just because you think it is impossible, that doesn't mean it is.


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Are fluoroquinolone antibiotics (Cipro, Levaquin, etc) chemotherapy drugs?
I read a claim (I can't find the source) that fluoroquinolone antibiotics are actually chemotherapy drugs, or maybe to be more specific, are "chemotherapeutic." Is this claim true? Additionally, if true, does this claim apply to all antibiotics, or only fluoroquinolones?

Chemotherapy of what? Chemotherapy literally means using of chemicals to treat a disease/condition. All drugs are chemotherapeutics, technically.

Short answer: Yes, fluoroquinolones are chemotherapy drugs
In layman's terms, fluoroquinolone antibiotics kill human cells as they divide. Fluoroquinolones are a class of drug called "topoisomerase interrupters." Every drug in this class is directly labeled as a chemotherapy drug except fluoroquinolones.
This is not well known by the medical community and is in part why irreversible damage from fluoroquinolone antibiotics is not well understood.
Long answer: Fluoroquinolones are definitely chemotherapy drugs, and they're dangerous
A refresher on how fluoroquinolones work, in case you slept through molecular pharmacology :
If you want you can skip this first section and instead watch YouTube: Fluoroquinolones: Mechanisms of Action and Resistance
How topoisomerase works
Bacterial cells have double helix DNA, meaning two strands twisted around each other. When bacterial cells divide, the two DNA strands are separated (untwisted), and eventually each side is turned back into a full double helix, making two copies.
If you think of a tightly twisted rope (representing double helix DNA) and start to pull the two ends apart, the rope will twist tighter and tighter and eventually you can't untwist it further. Nature's fairly primitive solution is an enzyme called topoisomerase.

topo-: dealing with topology, as in the structure of the DNA
-isomerase: a class of enzymes (enzymes are usually bundles of proteins)

The job of topoisomerase is to cut the the double helix DNA strand, untwist it, and then glue it back together.
There are several types of topoisomerase, which we'll come back to.
How fluoroquinolones kill bacteria
Fluoroquinolones bind to the glueing action of topoisomerase. So, as part of normal cell division, topoisomerase cuts a DNA strand, untwists it, then tries to glue it back together. However, fluoroquinolones block the gluing action ("plug the glue bottle"), so the cell literally cuts up its own DNA. Insidious, isn't it?
Don't human cells have topoisomerase?
Yes, since humans have two sets of DNA, let's focus on one at a time.
How fluoroquinolones kill human mitochondria
Human mitochondria are bacteria, and they do contain double helix DNA and topoisomerase. So why don't fluoroquinolones kill mitochondria? Trick question: they do, and it's worse than that.
Human mitochondria keep around backup copies of their mtDNA (we often call mitochondrial DNA "mtDNA" to distinguish it) to use when there are replication errors in DNA synthesis. Fluoroquinolones "deplete" mtDNA, meaning irreversibly destroy backup copies. The organelle desperately tries to pull in backup copies as it cuts up its own mtDNA during replication, and may die, or may become permanently damaged.
Insidious, isn't it?
Many other studies have proven that fluoroquinolones kill human mitochondria as they divide. Interrupting topoisomerase isn't the only way they kill mitochondria, but it's an important one.
How fluoroquinolones kill human eukaryotic cells
Human "eukaryotic" cells (cells with a nucleus, such as tissue cells) also have topoisomerase. So why don't fluoroquinolones kill eukaryotic cells? Trick question, they do:

Compared to an [actual DNA poison], ciprofloxacin produced comparable dose-dependent SCE frequency increases

(an SCE, "sister chromatid exchange" is a marker for how genetically damaged a cell is)
and

topoisomerase type II and DNA gyrase are physiological targets for [ciprofloxacin]

Insidious, isn't it?
Like mitochondria, topo binding is a small part of the kaleidoscope of how fluoroquinolones cause permanent cellular damage, but it's an important one.
As you can imagine, fluoroquinolones killing a cell's main source of energy (mitochondria), while also causing the cell to irreversibly destroy its own DNA lead to human cells dying as they try to divide divide
Even clearer: Compared to other chemo drugs
There are several oral chemotherapy drugs on the market, one of which is Topotecan (notice the topo-?). Here's how they work:

Topoisomerase I inhibitors:  Ironotecan, topotecan
Topoisomerase II inhibitors:  Amsacrine, etoposide, etoposide phosphate, teniposide

And, as linked in the earlier study, fluoroquinolones are topoisomerase II inhibitors. (They probably bind to other forms of topo, but we don't know for sure).
Even clearer: Fluoroquinolones are used for chemotherapy
There are a few
"novel" studies using fluoroquinolones as chemotherapy drugs. In this study, ciprofloxacin is used to target leukemia cells.
Why are chemotherapy drugs used as antibiotics?
When (non-fluorinated) quinolone antibiotics were first invented in the 60s-70s, we didn't know about mitochondrial DNA, and certainly not how fluoroquinolones affect mitochondria.
Don't fluoroquinolones have a good safety profile?
No.
Fluoroquinolones were released in the 70s, but the FDA warning for permanent nerve damage wasn't added until 2013. Because the symptoms of permanent fluoroquinolone damage are so outrageous (permanent nerve damage, tendons spontaneously rupturing, organ failure, psychosis, and dozens more). Doctors simply didn't know (and still don't know) to look for the symptoms, so they aren't documented.
There have been other fluoroquinolones that had "good" safety profiles, passed all medical standards, and then were promptly removed from the market after they started killing patients outright. One such drug, temifloxacin, was removed because it caused so many cells to die that the kidneys became clogged, killing patients.
The fluoroquinolones on the market are all able to, and have, killed patients through multiple mechanisms, but it's more rare, and the permanent damage symptoms are not connected by doctors.
All fluoroquinolones have the same core method of action, and all have a fluorine moiety allowing them to penetrate anywhere in the human body ("hard to reach" infections), so even though the current ones haven't been removed from the market, it doesn't follow that they are safe.
Why continue to prescribe them?
I sincerely believe that if doctors understood how fluoroquinolones worked, they would stop prescribing them, and use them only in life or death situations. The FDA has already advised never to use fluoroquinolones for "uncomplicated" infections, but this advice is not known nor heeded.
If only doctors read studies from over 10 years ago:

In view of the present genotoxicity, ciprofloxacin should be administered with caution.

Holy moley... what an answer! I will take some time to digest it

I can't upvote answers (yet?) but thanks a lot! could you also answer about other antibiotics?

"The FDA has already advised never to use fluoroquinolones for "uncomplicated" infections, but this advice is not known nor heeded." How do you know? How many doctors have you asked about this?

23 so far by my count?

So, 23 doctors you've asked admitter that they used fluoroquinolones for "uncomplicated" infections? Or admitted they used fluoroquinolones? There's a difference.

Most antibiotics can affect mitochondria (macrolides, aminoglycosides, tetracyclines etc). This is a statement from wikipedia article on quinolones: The overall rate of adverse events in patients treated with fluoroquinolones is roughly similar to that seen in patients treated with other antibiotic classes.[23][24][25][26]

Plus, if some drug affects prokaryotic topoisomerase/gyrase then it doesn't mean that it will affect eukaryotic topoisomerases. Your answer is misleading (statements like "mitochondria is bacteria") and uses flawed logic. Your "short answer" is basically wrong if you are talking in context of cancer chemotherapy.

@WYSIWYG to clarify, I've talked to more than 23 doctors about FQs, those are just the ones that talk about treating uncomplicated infections with them. And there's more than that, some of them are in hospitals that have guidelines on what to prescribe, and all follow the same rules.

@WYSIWYG the study I linked to shows the dose dependent action on eukaryotic topoisomerase. Number needed to harm for FQs is misleading if you research the history of symptoms.

Yes they are chemotherapeutic drugs. They enter the cells and destroy the mitochondria of the cell and it can no longer produce energy. Problem is these antibiotics target all cells whether they are healthy or not so they are systemically poisoning your whole body. Hence the wide variety of problems reported by patients who have taken them. They are commonly given along with a steroid such as Prednisone. Unfortunately, those patients often suffer more acute damage.

Your reasoning is not entirely correct. Please cite reliable references. If you don't improve your answer, it will be deleted.


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Is the xylem like a tissue paper?
I am a 5th grader learning about the plant transport mechanics and I learnt that the xylem is made up of dead cells.So if water travels up the xylem and water travels only 1 way, is it like how water travel up a tissue paper?

I'm in year 5 too; and (with a bit of help of my dad) I have some bits of answers (my challenge of the day).
A paper tissue is principally made of cellulose. And cellulose is a polar molecule. And so is water. So, the paper will easily absorb water.
See these short clips [1] for water polarity and here for cellulose [2].
In plants, xylem vessels are also made of cellulose and that helps the small molecules of water to stick to the vessels walls.
Think of it as a lot of tiny drinking straws made of wood.
There are at least two reasons why water manages to 'climb up' from the roots to the leaves through the xylem.
During the day, when the sunlight is available, water will be consumed by the leaves during photosynthesis [3]. For each molecule of glucose, 6 molecules of water are needed.
So the water already present from the xylem in the leaves needs to be replenished by water (sap) from the twigs, which is replenished by the water from the xylem in the branches,... And so on, till the water is pulled from the roots.[4]
Remember little molecules of water cling to each other because they are polar.  This is why they tend to pull each other up, as they are consumed in the leaves [1'].
And this is why it is important that both the water molecule and the cellulose molecule are polar.  If H2O would be like CO2, there would be no vascular plants as we know them.
But there is no sun, so no photosynthesis, during the night.
Then the stomata, which are holes used by vascular plants to "breath" (
transpiration), are usually closed.
There is also another reason why water moves up the xylem. Here it is.
Roots not only 'pump' water, their role is also to capture nutrients.
These nutrients are like salts, not table salt, more like ions (potassium, phosphorus, zinc, mangnese, etc) which are needed by the plant cells.
So the water is a bit more 'salty' inside the roots.  Water outside the roots tends to try to diffuse into the roots in order to compensate the relative saltiness [5].
This in turn pushes the water from the root below the ground towards the branches.[4]
What is remarkable is that the whole cycle of water is passive, the plant does not spend energy to move the water 'upwards' to the leaves.
Here are a few sources which I can recommend and from which I learned most of these things. Crash course biology.
They talk fast but it's quite funny.
[1] water polarity: 'Water - Liquid Awesome: Crash Course Biology #2'
https://youtu.be/HVT3Y3_gHGg?list=PL3EED4C1D684D3ADF&t=171
[1'] To picture molecules of water pulling one another up the xylem... well:
https://youtu.be/IlmgFYmbAUg?t=154 (Monkey chain in Madagascar 3)
[2] cellulose: ' Plant Cells: Crash Course Biology #6'
https://youtu.be/9UvlqAVCoqY?list=PL3EED4C1D684D3ADF&t=255
[3] Photosynthesis ' Photosynthesis: Crash Course Biology #8'
https://youtu.be/sQK3Yr4Sc_k?list=PL3EED4C1D684D3ADF&t=75
[4] For a simple presentation of xylem, I use Simple English in
https://simple.wikipedia.org/wiki/Xylem_vessel
and 'Vascular Plants = Winning! - Crash Course Biology #37'
https://youtu.be/h9oDTMXM7M8?t=373
[5] Osmosis (water compensating solutes) "In Da Club - Membranes & Transport: Crash Course Biology #5"
https://youtu.be/dPKvHrD1eS4?list=PL3EED4C1D684D3ADF&t=148
Ian (and dad <= all errors and approximations are his :) ).

Ah, and yes, this is me in the avatar. When I was one.

Thanks for your highly informative answer. But at night, if the temperature is still higher than 0° so won't some water evaporate through the stomata?

@Joshua, under normal circumstances, stomata are closed during the night.
https://youtu.be/IlmgFYmbAUg?t=154 but you are also right to add that photosynthesis is not the main reason why leaves consume water. Water evaporation is also the way plants regulate their temperature in warmer conditions.

Yes, the analogy is quite correct with respect to the mechanisms involved. In xylem as well as in tissue paper there are there are tiny pores throught out them through which water rises up. This mechanism is called cappilary action of water which you shall study in high school physics course. In fact tissue paper is made up of the same substance that xylem is made up of, i.e Cellulose.When you dip tissue paper in a bucket it spreads in all directions but imagine looping it to form a pencil like shape. Now thats like a real xylem.
Hope it helps.....


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Why didn't these scientists restore electrical activity in this pig's brain?
This experiment was published in Nature Magazine: Pig brains kept alive outside body for hours after death. The researchers used a system called BrainEx to revive certain metabolic and physiological functions to a disembodied pig's brain, but they never attempted to restart electrical activity.
Why did they stop short of restarting electrical activity in this pig's brain?

Read the paper, and presumably they will say. This site is about biological problems, not about mind reading.

I'm not asking for anyone to read the researchers' minds. I was simply hoping that someone could provide a science-backed reason why restarting electrical activity in this brain would be inadvisable. I was expecting that some aspect of the brain's physiology made it too challenging and that someone with the appropriate expertise could explain this physiology to me.

Restarting electrical activity would mean that at least parts of the brain become active again and possibly restoration of almost all cognitive functions. While this would be a tremendous scientific and medical break-through, it would also mean that effectively locked-in syndrome would have been induced for these pig brains. Therefore just attempting to restore electric activity in isolated brains has huge ethical problems and was for this reason probably not allowed (or ever attempted).
Whether or not it should be allowed to test this in pig brains (in order to learn how to adapt the procedure to humans) is a different question (and not one for this SE) - the best way to go about would probably be to restore electric activity not in isolated brains, but with the brains still in animals.

Is this your hypothesis or are there any references in the field that say that's why it's not done?

@Cell The authors of the original paper refer to ethical concerns directly as the motivation for their limited approach.

@Cell This article explains the ethical implications more extensively: https://www.nature.com/articles/d41586-019-01168-9


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How are epiphytes symbiotic?
I understand epiphytes are not parasitic. But how exactly are they helping the tree on which they grow?

It's important to note that not all symbiotic relationships must be expressed in terms of a positive-negative (parasitism) or a positive-positive (mutualism) framework. I would guess that most tree epiphytes exist in a commensal framework with their host trees. That is, the epiphyte has a positive interaction (it gets somewhere to grow), and the host species has neither positive nor negative effects.

I didn't realise symbiotic relationship is superset of mutualism and parasitism!

@yathish the terminology in the ecological literature gets pretty malleable, but the Greek root basically means "living together" so can describe a range of relationships.


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What are these flower like cells in the photo attached?

I am a student of BSc. Zoology... I was doing a TC of RBC of my blood when I encountered these strange flower like cells. Are they lysed RBCs ? If so, why are they so geometric in shape ?


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Major effects on cells grown with 5% FBS supplemented media instead of 10% FBS?
I maintain a few cell lines in the laboratory (industrial R&D) that I use regularly for experiments. I realized today that the media i prepared for the week on monday was only supplemented with 50 mL of FBS into 1 L of DMEM, instead of the usual 100 mL that i usually do. I was in a hurry and absentmindedly didn't add the second 50 mL autopipettor's worth.
My cells are fine morphologically but I think they're growing a bit slower than usual, my guess is due to the 1/2 concentration of all the FBS growth factors, etc. Are there any other effects that would be pronounced in these?
I understand that it will be apples to oranges to do compare results with these cells to, say, an experiment done with a batch of cells grown in complete (10% FBS supplemented) media.

If you were to run a flow-based viability assay (annexin V, live/dead fixable dyes, 7-AAD) or dual-fluorescence count (like acridine orange/propidium iodide, popular method as of late), you might find that more cells are undergoing apoptosis, or an increase in dead cells. I say this because trypan blue often overestimates viability. Your most pronounced effect should simply be a reduction in viable cells or a slower growth curve if you take those data points. Otherwise you'd need to run some test (fair example).
The problem being, these observations vary wildly based on what cell line you're using, lot-to-lot variability of the serum, and reagent handling. For example, the serum was heat-inactivated improperly, medium was degraded, bad lot of serum, and so forth. So take this as a generalization and a good reason to validate your serum lots.


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Measurement equation of Tree-Step pathway model
I am not specialist in biology but I want to test a parameters estimation method (based on Kalman filter) on the Tree-Step pathway model, but I cannot find a document that gives the measurement equation of the Three-Step Pathway model (Moles et all 2003, Parameter Estimation in Biochemical Pathways: A Comparison of Global Optimization Methods"), can someone give me some references?


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What does "optimal balance of biological control" mean in nematodes?
I have been reading several articles on nematode life-history for my insects class. Several articles say that Entomopathogenic nematodes(EPNs) are the only nematodes possessing an "optimal balance of biological control attributes". What does this mean?

It is a long-winded way of saying that these are the only nematode genera that are useful for biological control. In particular the article is referring to Steinernema and Heterorhabditis, both of which genera are used for control of some pest insects.


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Vasoconstriction and blood flow
The resistance in a blood vessel is equal to the pressure difference divided by the blood flow. Let us now say that a sympathomimetic causes vasoconstriction which increases the resistance. Does this primarily increase the pressure in the blood vessel? Does it primarily reduce the blood flow in the blood vessel?
In context, the filtration fraction of the kidneys is the GFR divided by the plasma blood flow through the afferent arteriole. The sympathomimetic would in general increase the filtration fraction by reducing blood flow. However, the GFR is also dependent on hydrostatic pressure which may increase if there is a rise in resistance. Therefore, shouldn't the filtration fraction change minimally due to the rise in GFR counteracting the fall in blood flow?


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Do antimuscarinic drugs increase cAMP or cGMP
Activation of muscarinic receptors M2 and M4 inhibits adenylate cyclase which reduces cAMP levels. It would be expected that antimuscarinics such as ipratropium would increase cAMP levels. However, the pharmacological action of ipratropium is said to be mediated through increased cGMP levels [1]. Why is this the case?
[1] https://www.ncbi.nlm.nih.gov/pubmed/138578

M2 and M4 receptors are Gi-coupled receptors. M3 which is relevant for the effects of ipratropium is Gq coupled. Similar receptors have different effectors and therefore different effects on cAMP/cGMP.


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Cardiac cycle and atrial contraction

During atrial contraction ("a" in the figure), why does the ventricular pressure match the atrial pressure? The ventricular pressure generally stays the same throughout passive filling until it reaches the point where atrial contraction occurs. Why is there a sudden change in the ventricle pressure during atrial contraction? I can understand the atrial pressure would increase when the atria contract, but the ventricles have not contracted yet so the ventricle pressure shouldn't increase. The ventricle pressure can increase greatly when the volume exceeds a certain value and the elastic tissue of the heart cannot stretch anymore. However, the volume here is only about 110ml, so it has not reached that point. I can only think of one explanation:

The pressure is equilibrated between two sides of an open valve.

However, this doesn't explain why the atrial pressure is slightly greater than ventricle pressure during filling; it also doesn't explain why the aortic pressure is slightly greater than the ventricle pressure near the end of ejection.

Two things to think about: 1) Does the pressure in a balloon increase only when it is full and cannot stretch anymore, or does it increase while it is stretching? 2) If A and B are connected, under what conditions will there be flow from A to B? Pressure_A == Pressure_B? Pressure_A>Pressure_B? Pressure_A<Pressure_B?

Well I've mentioned that ventricular pressure generally stays the same throughout passive filling. So stretching, based on your question, still doesn't explain why there is a sudden change during atrial contraction. Are you saying stretching of the ventricles only occurs during atrial contraction? However, your final point does rule out my hypothesis or attempt at explaining it.

Maybe one more thing to think about: 3) While there is flow from A to B, is there any circumstance where B could have greater pressure than A?

Well if we are talking about systole, the ventricles relax (A) near the end, as blood flows into the output blood vessels (B). As they relax, the pressure of A decreases and becomes less than B. Also, if we are talking about the atria (A) and ventricles (B), the same situation would occur. I'm not sure how your question explains my main query though. If you would like to clarify?

Mostly just wanted to make sure you were putting some thought into answering the question yourself because I think that's the best way to learn about these things. I think you've done sufficient thought that I can provide an answer explaining things - let me know if anything remains unclear.

While blood is flowing into the ventricle, it can never be at a higher pressure than where blood is flowing from: if it was, the flow would be going in the other direction. Flow is always from higher to lower pressure, if there is no pressure difference there is no flow.
Before atrial contraction, the ventricle can have no more pressure than the uncontracted atrium, which in turn can have no more pressure than the veins (vena cava or pulmonary depending on which side of the heart we are talking about). When the atrium contracts, it increases the pressure in the atrium, which causes a flow of blood into the ventricle. Whenever a fluid flows, there is a pressure drop that depends on the resistance (very much like voltage in an electrical circuit). However, the AV valve is fairly big and open, so there is little pressure drop from the atrium to ventricle.

The pressure is equilibrated between two sides of an open valve.

...is mostly true if the valve is large enough. There is still some pressure drop, though: if there wasn't, there wouldn't be flow.
There is no need for the ventricle to be at maximum capacity for pressure to increase. Imagine if you squeeze one side of a balloon: the pressure in the balloon increases, which you can tell because the balloon stretches and expands in the areas you are not squeezing; it need not be at the maximum capacity of the balloon for this to happen. Same for the heart.
As far as the higher pressure in the aorta, I this diagram is slightly exaggerating where the pressure difference starts, but as the ventricle relaxes there is a brief time where you get a small backward flow because the relaxing ventricle ends up having less pressure than the proximal aorta. This pressure drop is what closes the aortic valve (or the pulmonary valve, same process).

Thanks for you answer. I agree with most of what you have said but there are a few points that I am not entirely convinced with. Firstly, the figure was from the Guyton and Hall textbook and corroborated by others (e.g. https://www.aafp.org/afp/2004/0601/p2609.html). I do agree that flow is from higher to lower pressure but I don't agree that "if there is no pressure difference there is no flow". For one, the figure shows that ventricle volume continues to fall even when aortic P is higher than ventricular P, likely do to kinetic energy propelling it forward.

"if there is no pressure difference there is no flow" is physics (or at least no net/bulk flow...you will still have diffusion equally in both directions) and there is no controversy. The figure is a cartoon for demonstration. There could be some inertial effect but you wouldn't expect it to be a major contributor for the overall flow.

Secondly, I didn't mean that the ventricle had to be at a maximum capacity. What I wanted to understand is why there is a "sudden" increase in pressure when there was only a slight increase during passive filling. The main idea I was putting forward was that once the heart reaches a certain volume there is "sudden" rise in pressure for given volume b/c elastic tissue can't stretch as well after this point. I now realise that I may have underestimated what that pivot point is for the "sudden", also I didn't account that the ventricles are still contracting for some time.

https://physics.stackexchange.com/questions/157038/do-particles-always-flow-from-high-to-low-pressure and Bernoulli's equation

There isn't enough velocity or constriction for it to matter on the filling side. On the outflow side you might get a little effect of velocity but not much. I'd suggest starting with understanding how fluid moves without momentum before thinking about the exceptions, that's the level I based my answer on.