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Atelectasis due to decreased surfactant in lungs
Surfactant is a protein lipid mixture produced by alveolar pneumocytes composed of Dipalmitoyl Phosphatidyl Choline lipid, apoproteins and calcium ions.
This surface lines the alveolar epithelium thereby reducing surface tension preventing lungs from collapse.
Atelectasis is collapse of lung mainly due to lack of surfactant.
Moreover it may also be due to obstruction of the airway tract.
My question is why is this surfactant found to be lowered in patients who have undergone cardiac surgery under pump oxygentor? Why does long term exposure to 100% Oxygen affect the surfactant.
Is it due to its chemical composition or is it something to do with pulmonary circulation?
This Wikipedia article states alveolar collapse due to Oxygen Toxicity
http://en.m.wikipedia.org/wiki/Oxygen_toxicity

Long-term exposure to excessive oxygen will lead to damage in pulmonary tissue. This damage resembles the same damage which is seen in patients with Acute Respiratory Distress Syndrome (ARDS). In these patients surfactant specific proteins are damaged by proteolysis. This proteolysis is caused by the neutrophil elastase enzyme, after a massive influx of activated neutrophils.
The damage done by exposure to excessive oxygen is thought to be done by Reactive Oxygen Species (ROS).

Reactive oxygen species (ROS) are chemically reactive molecules containing oxygen. Examples include oxygen ions and peroxides. ROS are formed as a natural byproduct of the normal metabolism of oxygen...

These ROS can cause oxidative damage to DNA, RNA and proteins. They can form covalent bonds between molecules in the surfactant, thus inactivating them. Damaging of molecules can lead to cellular damage, causing ROS-mediated necrosis or apoptosis. Therefore there will be less surfactant production possible.
Also interestingly:

An important feature of pulmonary oxygen toxicity is that it is almost impossible to distinguish from damage caused by other lung injury processes. Consequently, it is unclear whether deterioration of lung function during high concentration oxygen therapy is due to worsening of the primary disease process or to oxygen-free radical-induced damage; the administration of high concentration oxygen may be perpetuating lung injury in some patients.

So in patients who undergo long-term 100% oxygen exposure, for example due to lung problems, the problems could be perpetuated or even worsened due to oxygen therapy and the oxidative stress caused by it.


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DNA length and annealing kinetics
I have a mixture plasmids and undesired short linear fragments that share the same sequences. During denaturation and annealing, I would like the plasmids to 'find each other' before annealing to the shorter linear fragments. Assuming the concentration of shorter fragments is significant, is there a temperature profile to bias towards re-annealing of longer DNA?
More specifically, this is for a variation of the Surveyor Mutation detection assay, where re-annealed DNA with mismatches are digested, leaving non-mutant DNA intact. I would like to keep non-mutant plasmids for E. coli transformation. However, some linear fragments  ~10-50% of the length of the plasmid have escaped exonuclease treatment and would compete with the plasmids during annealing.

it is unclear what you ask. And why not transform e. coli with your mixture, only circular plasmids will propagate and linear pieces will be degraded/purified-out

If the linear fragments anneal to the circular plasmids instead of the complement, the resulting DNA would only be partially double-stranded, which I assume would render it unusable by bacteria. This would lower the transformation efficiency.

did you think of just using DNAse that targets ssDNAs? For example, Mung bean nuclease. There should be another enzymes with similar activity, e.g. S1

I'm using PlasmidSafe which is a cocktail of exonucleases that do that. It's just not 100% efficient and I wanted to leave no room for error.

Short answer is that higher temperature favors annealing of longer sequences. There are number of ways to calculate melting temperature, but all of them produce similar results: longer polymers require more thermal energy to melt. Hence, quick cooling from higher (say, from 95C thermocycler can cool in 10-12 sec) to RT/4C will favor re-annealing of circular strands. Slower cooling should allow more ssDNAs to bind.
But again, if end goal is to select for circular dsDNA, simple transformation should take care of that.

Thanks for the answer! How about slow annealing down to slightly below the melting temperature of the plasmid and then snap cooling on ice from there?

Also, unlike oligonucleotides, longer DNA is flexible and contains local regions of higher and lower melting temperatures. Would the the overall melting temperature be accurate in this case in describing that half of the ssDNA molecules have completely annealed? In other words, would it be common to have two ssDNA molecules incompletely annealed to the same template, where one of the molecules is partially blocking the other one?

I don't know, what is really possible. What is true, is that at any temperature interaction that includes more bases is more favorable. Think about it as a dynamic equilibrium: at each moment ssDNAs will bind/try to bind and unbind. However, it takes only dozens of bases to unbind whole oligo, whereas circular DNA is on order of KBs. So oligo will unbind and go into solution much easier than second strand of circular dsDNA

source: Stack Exchange

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What are iPSC cells, and what are their applications?
I also searched it on internet, and just basically know it's related to the Stem Cells, but there are too many resources, can anyone help me find out more about them, like their applications? They really interest me.

have you seen this page? http://stemcells.nih.gov/info/basics/pages/basics10.aspx

From this article: iPSC's or induced pluripotent stem cells are somatic cells that have been driven to acquire an induced pluripotent cell state.  Somatic cells can be any cell of the body except sperm cells, egg cells and undifferentiated stem cells. Investigators can induce these cells to 'return' to a stem cell like state by forcing the expression of key transcription factors, and by genome-wide remodeling of epigenetic marks.
There is an entire spectrum of different iPSC's that can be generated, but much is not yet known. Future applications include using them for regenerative medicine, drug discovery, etc.
Recently there were several articles published in nature:

Stem cells: A designer's guide to pluripotency
Genome-wide characterization of the routes to pluripotency

amongst others. Also you can check out http://www.stemformatics.org/ for more information on stem cells and research being done.

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Why does polyploidy give an evolutionary advantage?
I would like to know what advantages polyploidy holds. I have come across a few examples during my research of polyploidy, for example human adults' hearts contain 27% diploid, 71% tetraploid and 2% octaploid nuclei, Deinococcus radiodurans can have up to 10 copies of genome, and most of the plants consumed by humans have more than 2 copies.
I have no source of any sort for these, but I think they could be advantages:

One of the most obvious one would be resistance to more physical effects.
In the case of plants it might be the increased need for protein construction during the development of the seed.

What I would like to ask is whether the ones I wrote are correct, and if there are any other possible advantage.

I have read similar questions but could not find what I was looking for.

New relevant paper: Selmecki et al. 2015. Polyploidy can drive rapid adaptation in yeast. Nature 519

First of all I am not sure if your examples are per se correct. But they might also be an additional bonus. Secondly, I would like to refer to two articles: "Polyploidy" and "The advantages and disadvantages of being polyploid".
One of the main benefits could be allowing organisms long-term evolutionary flexibility. Often adapted polyploids can undergo a proces that is called diploidization, during which genomic redundancy is removed. This means extra copies of genes will undergo less negative selection. Meaning alleles containing deleterious mutations at functionally important nucleotides are selected against. This allows more mutational freedom, leading to what is called subfunctionalization and neofunctionalization: new genes are created with slightly different or new functions. Other redundant genes are lost or become inactivated (pseudogenes).
Another example of benefits from polyploidy, this time not in an evolutionary, but in a more individual context, is the fenomenon called hybrid vigor or heterosis. Heterosis is a phenomenon in which a polyploid offspring of two diploid parents is more healthy and vigorous than its progenitors. One of the factors explaining this could be due to a protection against recessive characters, as being homozygous as a polyploid is even more 'uncommon'.

I really like the argument in the last paragraph. Reminds me a bit about genetic depression due to inbreeding.


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Grapefruits and CYP3A4
Grapefruit juice contains furanocoumarins, which irreversibly inhibit CYP3A4.  For this reason, when one is taking certain medications it is necessary to not eat grapefruits because the inhibition of CYP3A4 can reduce how much of the drug is metabolized before it can get used, resulting in an overdose.   It apparently takes 24 hours after eating a grapefruit before the enzyme level is 50% and up to 72 hours for it to be completely normal.  So, it seems that eating one grapefruit a day would substantially impair one's CYP3A4 levels indefinitely.
Wikipedia says, the purpose of CYP3A4 is "to oxidize small foreign organic molecules (xenobiotics), such as toxins or drugs, so that they can be removed from the body."   It seems like inhibiting CYP3A4, from a biological standpoint, would reduce one's immune system or at least the ability to tolerate and eliminate certain toxins.   Are there other enzymes that take up the slack, or is there something in grapefruit itself which does the job instead, or is a daily grapefruit just a bad idea?  What are the effects of extended inhibition of CYP3A4?  Will the body perhaps build up a tolerance or immunity, or (perhaps with negative effects) pump out more CYP3A4 to try to compensate?

Keep in mind that CYP3A4 is one of MANY cytochrome P450s. Many substrates are capable of bind to more than one of these and being metabolized. Grapefruits would probably only be an issue for compounds that are only metabolized by the same CYP450 that gets deactivated by the grapefruit.

CYP3A4 is the most abundant cytochrome in the liver - and the most important for the metaboization of drugs.

Non scientific resources claim that 10% of the liver capacity is enough to do the daily routine detoxification. I guess grapefruit cannot inhibit the liver enzymes that degree. Afaik. nobody talks about grapefruit as a poisonous fruit...

http://en.wikipedia.org/wiki/CYP3A4#cite_note-Flockhart-29 According to wikipedia grapefruit is only a moderate inhibitor of CYP3A4.

Though a moderate inhibitor, high concentrations of grapefruits/grapefruit juice will irreversibly inhibit CYP3A4 - a grapefruit every day is not recommended.

@Michael - don't confuse "foreign organic molecules" with the "immune system" - I don't know of any deficiency or immune-related problems that could result from inhibition of CYP3A4.

In general, xenobiotic biotransformation (i.e. processing the xenobiotics aka drugs - detoxing the body) is accomplished by a limited number of enzymes with broad substrate speciﬁcities. In humans, for example, two cytochrome P450 enzymes— namely,CYP2D6 and CYP3A4 — metabolise over half the orally administered drugs currently used. (Gonzalez and Tukey,2006).
The various different CYP enzymes can act on various different foreign organic compounds with varying levels of efficiency. The CYP enzymes oxidise these organic molecules adding on -OH groups to make them more solube and thus more easily excreted.
Grapefruit contains compounds known as furanocoumarins that block the CYP3A4 enzymes. These compounds do this by irreversibly binding to the CYP3A4 enzymes, putting them out of commission. Like the wikipedia article says it takes about 24 hours for the CYP3A4 enzymes to return to normal levels after the average glass of grapefruit juice is consumed. During this time your body’s ability to process drugs for elimination is decreased because CYP3A4 is the main CYP enzyme for processing many drugs and toxins.
You might think that this could be used to reduce the dose for a drug, but the amount of furanocoumarin in your blood would vary widely (grapefruit isn't uniform in it's concentrations) and CYP3A4 levels vary between individuals.
 If you tried using grapefruit juice or another source of furanocoumarins to do this you'd be reduced to guessing how much of your prescribed drug is safe to take. Blood levels of the drug may rise, resulting in the risk for new or worsened side effects. it can essentially cause the normal, dose of a therapeutic drug to act like an overdose by increasing the bioavailabilty of the drug in your body. Better not to risk it.
Sources:

Gonzalez FJ, Tukey RH: Drug metabolism, in Goodman LS, Gilman A, Brunton LL, Lazo JS, Parker KL (eds.): Goodman & Gilman’s the Pharmacological Basis of Therapeutics. New York: McGraw-Hill, 2006, pp. 71–91. [I'm afraid I unable link you directly to it]

Textbook - Toxicology - the basic science of poisons, Cassarett & Doull (A PDF version of the textbook can be found here: https://ilmufarmasis.files.wordpress.com/2011/07/casarett-and-doulls-toxicology-the-basic-science-of-poisons7th-ed.pdf)
Half-remembered undergraduate lectures.


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Why doesn't yearly screening for lung cancer decrease mortality rates?
In a large trial, screening yearly for lung cancer hasn't reduced mortality rates. Why is this? Isn't cancer best treatable when caught early? Is this because lung cancer is hard to treat anyway, because yearly is not frequent enough, or why?

Not necessarily the root of what you are asking, but Diagnostic follow-up of positive screening results was determined by participants and their health care practitioners -- essentially, this leaves what to actually do with the positive result to the patient and/or the doctor.  Some patients may refuse care and some doctors may not be equipped to deal with the problem or hesitate to farm out to specialists.

Is lung cancer effectively treatable? The common theme with cancer is that although lots of “treatments” exist, not all of them do actually prolonge life expectancy after diagnosis …

This question is a bit vague. Rather than asking why screening doesn't prevent mortality, maybe you should ask yourself why screening would prevent mortality.

Shep I answered this on the topic. It should prevent mortality by giving a patient a chance to start a treatment earlier, which is said to increase dramastically the odds of recovery.

You'll get better answers if you make it clear what you're asking. I assume it's not whether cancer is easier to treat if it's caught early, or if lung cancer is hard to treat anyway, I think we both know those things are true. Do you want to know why we don't screen more? Why lung cancer is hard to treat even when we've found it? Why we typically don't catch lung cancer earlier? These are all questions that can be answered. Overall it's a good question, though.

There are a number of reasons, generally, why a screening test may fail to decrease cancer mortality rates:

The screening test may not be very good. I know this seems like an obvious one, but its something of a problem - a screening test will only reduce mortality if it catches cases that are both treatable and wouldn't be detected in time to treat using other methods. For example, it may be that even if caught slightly later by other methods, lung cancer is equally treatable (or equally difficult to treat).
Mortality from false positive tests and subsequent procedures in non-cases offsets any gain in survival among cases.
Diagnosis is only one step toward treating a disease. Even if detected, if a disease is not treatable or isn't treated, knowing you have the disease doesn't change your mortality risk.

In this case it appears that a chest radiograph isn't good enough at detecting lung cancer to manifestly improve mortality outcomes. The author's of the paper don't really specify why this is - though since they're just looking at lung cancer mortality, it's likely not #2.


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Is the eukaryotic nucleus composed of a single or double membrane?
I know that it is usually considered a double membrane like those surrounding mitochondria and chloroplasts, but I read a review that stated "according to topological details it is actually a single lipid bilayer; this distinction is important"1.
Could anyone please explain how this is true and why the distinction is important? And why this topological analysis wouldn't apply to other membranous structures in the cell?

The nucleus is topologically single membrane but functionally, and as visualized, double membrane.  Naturally, this is a bit confusing.
First consider the mitochondria and plastids.  One of these organelles has two entirely separate lipid bilayers, one of which is nested inside the other.  If you start inside the organelle and draw a line to an external point, the line will pass through two lipid bilayers (assume there are no membrane folds to be encountered), first through the nested one and then through the entirely separate outer bilayer.
The nucleus at a gross level appears to be structured similarly.  A line from the interior to the exterior will usually pass through two lipid bilayers, one that is the inner wall of the nucleus, then through the outer wall.  This may seem like the inner wall is separate from, and nested inside, the outer wall, but it is not.  As nicely illustrated in your reference (Martin 2005), the two walls are continuous with each other and not nested.  Because of this, a line from nuclear interior to exterior may in fact not pass through any lipid bilayers; it may pass though a nuclear pore.  Topologically (mathematically) speaking, the two walls are one surface, and the "inside" of the nucleus is on the same side of the surface as the outside.  (The topological interior is perinuclear space and the interior of the endoplasmic reticulum.)  Functionally though, the structure acts as a double membrane since it physically constrains its contents.
The distinction is not very important for most biological contexts, but for a few purposes needs to be considered.  The main reason to pay attention to the distinction is that it probably is related to the evolutionary history of the nucleus: it is likely to have evolved from a single bilayer somehow.  In contrast, the mitochondria and plastids, with nested bilayers, evolved from two bilayers, one from a separate cell and one from an enveloping piece of a host cell.  This is why the distinction is important in the cited paper, which concerns the evolution of the nucleus.


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Do all kind of unicellular asexual reproductions let mutations happen, resulting in evolution?
I know about fission, an unicellular asexual reproduction method, where the mother cell splits into two daughter cells. Does this kind of asexual reproductions let mutations happen, leading to much needed evolutionary process? Is it same for all unicellular asexual reproductions?

It is not essentially asexual reproduction that causes mutations. Mutations can be caused because of errors in DNA replication which can happen during both mitosis and meiosis.
Mutations can also be caused because of error-prone DNA repair mechanism.
Other than these intrinsic factors there are physical and chemical mutagens that alter the DNA or accelerate the intrinsic mutagenesis mechanisms.
These mechanisms are universally common for all living organisms (that we know of :P ), however, their tolerance to mutagens and rates of intrinsic mutagenesis may vary.
Have a look at this post too.

I don't know whether my choice of word "facilitate" was right. Can mutation happen in fission?

Mutations occur during the process of DNA replication (as well as at other times). Of course, DNA replication is necessary for fission.

@Gulshan Cellular fission (or cytokinesis) is preceded by DNA replication. Even during the formation of gametes (sperm and ova) DNA replication happens which is followed by some steps that are not present in the asexual cell division or mitosis. Click on the links in the above answers; you'll find all the relevant background information.

I can think of two kinds of asexual reproduction- i) each item of the mother cell is copied to daughter cell. ii) only DNA is copied from the mother cell and rest of the items are constructed from new DNA. I think, mutations can happen in both cases. But only in the second case, the mutation will result to a physical change of the new cell, thus making it subject to evolution. Is my idea alright?

@Gulshan DNA replication is a prerequisite for cell division. Any mutation in the DNA will be inherited and expressed in the progenies. There can be asymmetric distribution of cellular components but DNA is always replicated and each cell receives a copy. Read about cell division; your doubts will be clear.

Replication will always be there. But would the translation from genes to actual physical attributes happen in all the cases? As, all other components are directly being copied from mother cell.

@Gulshan Other components are dependent on the DNA; there is a constant turnover and the stock inherited from the maternal cytoplasm will not last long. Please go through the basics before arguing on a hypothesis. Not all mutations are translated to phenotypic effects. It would take much more than a comment to explain why.

Actually I do not know these things. I just wanted to be sure about my assumption.


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Is it possible for humans to digest and live on food that isn't based on DNA or RNA?
Our bodies digest food using enzymes that have evolved to convert food here on Earth. Could we even possibly get nutrients from something we haven't evolved alongside? - Is it possible for humans to digest and live on food that isn't based on DNA or RNA?

Welcome to biology.SE! I vote for not closing this question. Yes it is going to be speculative and probably breaks half of the "how to ask" rules (that you can find here) but an answer along the lines of non-carbon based life (e.g. sulfur-based organisms) might be interesting.

@cagliari2005 How do you want to answer this in a scientific way?

@Chris. Was reading the question as "Is there digestive enzymes for non-carbon based nutrients?". Someone might know something about that.

I was thinking of both carbon and non carbon based life - could we even possibly get nutrients from something we haven't evolved 'with'.

Then you should edit your question and add these information.

I've tried to make it less opinion based

Our food is not based on DNA or RNA. It is based on carbohydrates, fats etc. All of these can be made artificially if you want.

@Chris Thank you! - In that case, this is a rubbish question. If I edit it again to ask more about carbohydrates etc, I agree it'd be extremely opinion based.

this is still broad (after the edit)

This might be flagged for being somewhat of a subjective question, but to survey human diet:
Mnemonic SPONCH can be used to sum up the necessary building blocks of life, in the elements Sulfur, Phosphorus, Oxygen, Nitrogen, Carbon, Hydrogen. There are others, trace elements, which are necessary and come from diet (selenium, for example). These elements are used in building our biological macromolecules: Carbohydrates, lipids, nucleic acids, and proteins. The molecular interactions between these macromolecules, their cofactors, etc. are essential for life. Some of these compounds, however, can't be made in the human body from scratch; hence essential amino acids, and the necessity to consume foods which provide metals, carbohydrates, fats/triglycerides, etc.
So, at this point our body is optimized to incorporate terrestrial foods. Sometimes, though, we can see that the body will sometimes accept analogs to normal compounds, although this is often to disastrous effect (like chemotherapy in cancer). The real question, then, would be: does said extraterrestrial food compose of necessary biological elements or analogs in a way our body can actually use this food for sustenance? That, however, is 100% speculation as we have no reference in even a single case to base our assumptions.

Thanks for your reply! I've altered the question to try to make it less opinion based. Any extra thoughts based on the change?

@jenga So, here's my thoughts, in part: We can only extract energy from sources we can break apart, absorb, and transport efficiently. We have specific proteins that get this job done. If we have an enzyme to do the job, the job gets done, and if we don't.. well, vice versa. How can we make sources of nutrients we wouldn't otherwise be able to process usable? Perhaps a system of ingesting exogenous enzyme.. but it's again mostly speculation.


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Does freezing microorganisms such as probiotics kill them?
Does freezing microorganisms such as probiotics kill them?  If not, what is the process that allows them to "come back to life" after the temperatures are increased?
As an example, lets say you freeze a yogurt (whether it be Greek, Australian, Turkish, Indian, Russian, European, or Western) and eat it while frozen.  Would the probiotics in the yogurt "come back to life" and be beneficial?
Specifically, I am referring to freezing refrigerated yogurts, and not products that are sold as "frozen yogurts".
What's the biological basis for this?

I can't say anything about the bacteria in yogurts (usually Lactobacillus) but labs routinely freeze E. coli to -80 degrees C without killing them.

@MarchHo Are those glycerol stocks? If so, the glycerol probably acts as a cryoprotectant. I don't know if anything in the yogurt would have similar enough properties to protect the cells.

This question inspired me to freeze some vanilla yogurt with added chunks of chocolate. No word on the bacterial content, but 100% of survey respondents agree that the results are delicious

@Luigi Yep!  For an even better culinary experience, stick a popsicle stick through the seal or lid before freezing it!  In a few hours, you'll have a delicious frozen treat on a stick!

I work for a probiotic manufacturer. We use a cryoprotectant in the process. We are able to freeze and thaw bacteria many times with little to no loss in cell count. Odds are most of the bacteria in your yogurt are still alive after you freeze it. If there is loss it is probably not much. Don't have any exact numbers, but know from experience.

Yes, they do. For a look at survival of Lactobacillus and other bacterial species after multiple freeze/thaw cycles, check out Harrison 1955 (below).
The awesome hand-drawn graphs show that many bacteria survive after being frozen for 11 weeks. There's also a figure on the following page showing that many bacteria also survive after multiple freeze-thaw cycles, but I won't include that page here for brevity.
Prof. Don Schaffner of Rutgers also supports this conclusion:

So it's possible, even likely, that frozen and thawed yogurt will contain
  living lactic acid bacteria, although it may only be 10% or 1% of the
  total number of bacteria that were there before the yogurt was frozen.

I couldn't find a great deal of official resources on the topic, hence the paper from 1955 and random quote from a food science professor. However, in a lab setting, scientists regularly freeze bacteria and even eukaryotic human cell lines. Usually scientists use a cryoprotectant like glycerol, but many foods (like yogurt and ice cream) may contain an FDA-approved cryoprotectant (Wikipedia):

One recent, successful business endeavor has been the introduction of [anti-freeze proteins] AFPs into ice cream and yogurt products. This ingredient, labelled ice-structuring protein, has been approved by the Food and Drug Administration.

So, yes, at least some of the bacteria in your frozen yogurt are still alive, and will have whatever beneficial/harmful/lack of effect when you ingest them.

Judging from figures 1-3 above, bacterial survival depends on how long and how many times you freeze the bacteria. My rough estimates of the graph above say 40%-10% after a single freeze, and after multiple freeze-thaws getting into the 1% range. Also, it doesn't matter whether you thaw it first or eat it frozen as far as bacterial content is concerned, the bacteria will be unfrozen either way when they reach your digestive tract.

Thank you for your answer.  After reading your answer, I realized that my question needed clarification.  After you contributed your answer, I updated my question to clarify that I am speaking about freezing standard yogurts, and not products sold as "frozen yogurts".  It's a little unclear if your answer needs to be updated accordingly.  I'm sorry that my original question needed to be clarified.

Thanks!  Now the big question: how much survives?

Judging from figures 1-3 above, it depends on how long and how many times you freeze the bacteria. My rough estimates of the graph above say 40%-10% after a single freeze, and after multiple freeze-thaws getting into the 1% range.

Note that even 1% of bacteria left is still a lot of bacteria

When thawed, wouldn't the remaining (live) Lactobacillus grow and populate in the yogurt?

usually the growth of bacteria is slowed down as they are in freezing temperature and they almost carry out no metabolic reaction at this stage.but another problem occurs that is ice crystals formation which disrupts or pierce the bacterial cell wall causing the death of bacterial cells,this problem can be solved by adding  glycerol or any other cryoprotectant into it which will make the concentration equal,inside and out side the bacteria,thus bacteria will not be harmed.
in case of lactobacillus,they are psychrophile and also facultatively anaerobic so yes,they can survive in freezing condition
http://www.ncbi.nlm.nih.gov/pubmed/10843056

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Why wrap a dolphin in wet towels?
In this video, a dolphin jumps into a vessel.  Even though the guides know they will be quickly helping the dolphin back into the water, they first make sure they wrap the mammal with wet towels.
Why did they rush so quickly to wrap the dolphin with wet towels?  Is there something about the biology of dolphins that made that action essential?

I don't have any scientific sources for this, which is why this is a comment instead of an answer, but it's my understanding that their skin can dry out very quickly, killing the skin cells and reducing its flexibility. Dolphins don't have sebaceous glands or other forms of lubricating and moisturizing their skin, so drying could potentially be rather harmful, not to mention painful.

@MattDMo Thanks.  Before posting, I asked a friend, and she said something very similar.  She said "it hurts them to go dry", but she didn't know why.


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Why does the SARS-CoV2 virus not remain infectious forever? Or does it?
Given that the majority of biologists do not currently consider viruses to be alive, a virus can never die.  It can, however, get destroyed by long exposures to soapy water, alcohol, and apparently certain frequencies of UV light.
Why is an individual SARS-CoV2 virion not infectious forever?  Or is it?

Would it help to think a little differently? Rubber bands (for example) aren’t alive either, but there are several ways they can be destroyed, including physically pulling them apart or just by having them exposed to air enough. Viruses are the same, conceptually.

@Laurel Yes, that does help!  So is it simply that being exposed to air very slowly destroys SARS-CoV2 (so slow, in fact, that it takes many days)?

@RockPaperLizard Probably best to think of it more like something like radioactive decay... Individual viruses may be destroyed immediately, or only after a long time. You're waiting for some sort of chemical reaction to occur that is sufficient to make each individual virion no longer capable of infecting. When people talk about the virus staying on some surface for 72 hours, they have given some % reduction in the concentration that they are waiting for. Almost all of the virions are inactivated well before the 72 hour marker, just not enough to consider them effectively gone.

@BryanKrause Thanks Bryan.  Your comment helps as well.  When you write "may be destroyed immediately", are you referring to environmental reactions, similar to the ones that take longer to destroy an individual virion?

Think of it like "x% of viruses inactivated each minute", starting from a very large number. Depending on what "x" is, it may take a long time to reach something like 0.0000001% of the initial virus concentration where you might say "it's basically all inactive".

@BryanKrause Thanks.  And now all we need to know is how many virions it takes to get someone sick (which will obviously vary quite a bit from person to person).

Very little is known connecting "# culturable viruses on a surface" and "chance to be infected". The associated experiments aren't really ethically supported for the most important viruses - we're left with just best practices (wash hands, clean surfaces that can be cleaned, distance from people) and general safety margins. Additionally, it's going to be probabilistic so any estimate is going to come with error bars that make it not that useful. Best just stick to the general guidelines, this isn't a problem with a closed form solution.

Would it help to think a little differently? Rubber bands (for example) aren’t alive either, but there are several ways they can be destroyed, including physically pulling them apart or just by having them exposed to air enough. Viruses are the same, conceptually.
Soap works in part by dissolving the layer of fat that keeps the virus together. It also ends up surrounding dirt so that it doesn’t stick to your skin and can be washed away with water. (These mechanisms take some time to work so that’s why people are recommended to wash their hands for 20+ seconds.)
As for when a virus is just on a surface, logically we know that how long a virus remains viable depends on both the air and the surface because the science reports different numbers depending on what the humidity is and what the surface is like. One helpful source notes:

Similar molecules appear to interact more strongly with each other than dissimilar ones. Wood, fabric and skin interact fairly strongly with viruses.
Contrast this with steel, porcelain and at least some plastics, such as Teflon. The surface structure also matters. The flatter the surface, the less the virus will “stick” to the surface. Rougher surfaces can actually pull the virus apart.
The surface of fibers or wood, for instance, can form a lot of hydrogen bonds with the virus.
In contrast, steel, porcelain or Teflon do not form much of a hydrogen bond with the virus. So the virus is not strongly bound to those surfaces and is quite stable.

Thanks Laurel.  So if wood, for example, forms a hydrogen bond with the virion, it has the potential to destroy it in the process?  And conversely steel has no such potential since it does not bond with the virion?

Viruses are made of nucleic acid (DNA or RNA), a few proteins and often lipids (like Corona viruses). they are not alive as they cannot reproduce without host cells but they are delicate and when they lose the ability to reproduce with exposure to the host, the virus is just completely dead...
Its possible to maintain viruses possibly forever by preserving them and freezing them. Just like reproducing - they can't live for prolonged time without help... in this case a human lab tech.

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Are small peppers inside others twins?
This happens frequently enough that we've probably all seen it at some point - you buy a pepper, and when you cut it open you find another small pepper inside it. There's plenty of pictures out there if you don't know what I mean.
The other pepper obviously didn't grow from a seed; a sprouting seed would generate a plant and not a fruit.
My first guess is that it's a twin. But seeds should be the equivalent of a fertilised animal zygote, so "monzygotic twins" would be split-seeds, not fruit-inside-fruits.
The only reliable-sounding information I was able to find online is this 8 year old blog post: https://www.csmonitor.com/The-Culture/Gardening/diggin-it/2010/0401/Have-you-ever-found-a-pepper-inside-a-pepper which concludes that it's unknown what these mini-peppers are.
Is that still accurate or has anyone figured out what exactly peppers inside peppers are?


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How to differentiate coyote vs wolf tracks
I spotted these canine paw prints in the snow on crown (public) land in Eastern Ontario, Canada. They're not dog prints; the location is too remote for that.
I figure the only options are coyote or wolf. How can I differentiate between the two?

The most noteworthy way to differentiate is by size. Wolves are bigger:

 Image source: WDFW
Regarding the size of young wolves (from here):

Young wolves’ feet grow large very quickly, and by the time they are about three months old (around July) even young wolves’ tracks are larger than most coyote tracks

Some additional characteristics from the Washington Department of Fish and Wildlife :

Wolf tracks are about 5 inches long by 4 inches wide, with four symmetrical toes and evident claws, and a single lobe on the front of the foot pad. Coyote tracks are similar, but about half that size, and even the largest domestic dog breeds usually have smaller tracks. The paths of wolves usually show a direct, energy efficient or purposeful route, whereas those of dogs often meander.

It'd be pretty hard to tell in soft snow like in the question, but there are some pretty obvious differences in the print that I can see in the image you supplied - front toes aimed together for the coyote and the pad has a central bump as opposed to the arch seen on the wolf.

Great answer, and one I'll remember next time I'm alone in a snowy forest far from civilization. @bob1 - How do you know so much stuff???

Regarding young wolves/etc - would the ratio of paw size to stride length also give evidence for/against?

What's the verdict on the picture's tracks, then?

Coywolf seems like another option to consider, especially given OP's location.

@anongoodnurse Fair bit of an autodidact, academic access to libraries and moderately good at use of search terms to find what I want to know...

The answer by theforestecologist covers the basics of differentiating the tracks, so I won’t repeat that in detail here.
As for the actual tracks pictured, they are too large for a coyote, which suggests either a wolf or a dog, but they’re a bit on the small side for a wolf, which would suggest either a young wolf or a large dog. The stride length isn’t a huge help in differentiating, as there are plenty of dog breeds that have that short of a stride relative to the size of their paws.
Beyond that it would require seeing both the overall path taken, and the area in general. For example, if the path the tracks take is meandering significantly it’s probably a dog (wolves generally don’t wander aimlessly or get constantly distracted like many dogs do), while a lack of accompanying human tracks nearby would make it all but certain that these are wolf tracks (if it were a dog in such a remote area, it would almost certainly be accompanied by a human).


text:
Why do morning people have shorter biological clocks?
First of all, we all have a circadian clock than is run endogenously by differential gene expression and controls our change in awakeness, temperature, hormone levels, etc.. Circadian clocks are not exactly 24 h and they vary among people: some people have shorter clocks and other have longer ones. Apparently, people who have shorter circadian rhythms are morning people, and those that have longer one, are night owls.
How is this possible? In the following article "https://www.futurity.org/biological-clocks-sleep-disorders-protein-mutations-2289312-2/" it says that a 20-hour biological clock will make a person fall asleep earlier because they will get tired earlier and they will get awake also earlier. But for me, that would only be possible the first period or two if both cycles start at the same point time. Afterward, the cycles will get out of phase and that will not be true any longer.

Circadian rhythms are entrained by light via the suprachiasmatic nucleus, a part of the brain that receives signals from special retinal ganglion cells that are directly sensitive to (mainly blue) light.
However, light is not strictly necessary: the internal circadian clock is the result of shifting gene expression that proceeds without outside stimulus. Light is only used to entrain (or "reset") the clock each day.
When people talk about the duration of an individual's circadian rhythm, they are referring to what happens in the absence of a light cycle (that is, without entrainment).
https://en.wikipedia.org/wiki/Circadian_rhythm
https://en.wikipedia.org/wiki/Suprachiasmatic_nucleus
https://en.wikipedia.org/wiki/Circadian_rhythm_sleep_disorder

So the clock is reset each day, meaning that both periods will start at the same point every day, and since a morning person has a 20-h cycle then indeed, it will wake up earlier and go to sleep earlier than a longer biological clock, I am saying all that right?

@Laura That's the general idea, yes. However the circadian clock isn't everything and isn't the only factor in people being "morning people" or not. It's an influence rather than deterministic, like most biopsychology.

The Circadian Rhythms of humans is reset by light exposure cycles, but for a cycle to be reset it has to exist first.
Without light there are cycles created by protein production and gene inhibition.
In the relevant 24 cycle there is a is a gene complex that produces a set of proteins that react and decay into a product shuts down the gene's expression (protein production) as long as it is present. that stops the initial proteins production thus creating a cycle based on the proteins reaction and decay rate. So the gene is active and the protein is produced, over a roughly se amount of time the protein reacts and decays into a protein that shuts down the gene expression (inhibitor), Will say this takes time A, of course the gene was till produce the protein until the inhibitor stopped it so the reaction and decay continues for time A again until all the inhibitor is used up and the gene starts producing the proteins again. So you get a cycle of expression and inhibitor that resets once every times Ax2.
But as you can guess genes and proteins a small change in the protein can change can change how long it takes to react and decay. This is how you get some people with slightly longer cycles and others with slightly shorter cycles.
https://pubs.niaaa.nih.gov/publications/arh25-2/85-93.htm


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Why is the ordinary cardiac muscle’s target value of the action potential 0mV?
Why do some excitable cells have a target of 0mV for the action potential, even with a slight overshoot?
Excitable cells such as muscles and nerves have the ability to rapidly change their membrane potential through depolarization. This mechanism is often explained by the influence of the equilibrium potential, as expressed in Nernst's equation, as illustrated in Figure 1,below. In other words, it is commonly stated that the mechanism behind the depolarization of nerve cells is as follows:

Originally, potassium ion channels are open, and the equilibrium potential for potassium is the resting membrane potential.
However, when sodium ion channels open, the influx of sodium ions brings the membrane potential closer to the equilibrium potential of sodium ions.

However, in the case of ordinary cardiac muscle, it appears that even with a momentary slight overshoot, the height of the action potential approaches around 0V. This seems to be the case in specialized cardiac muscle as well.
My question is as follows:

In the case of ordinary cardiac muscle and specialized cardiac muscle, why does the height of the action potential tend to reach around 0V, even with a momentary slight overshoot, despite being different from the equilibrium potential of any ion?"

Fig.1
https://openbooks.lib.msu.edu/neuroscience/back-matter/images-of-animations/

Fig.2
https://www.youtube.com/watch?app=desktop&v=JaL8lYPMscc

Fig.3 https://www.backoftheboxtalks.com/resources/ventricular-action-potential

Fig.4 https://www.youtube.com/watch?v=m-pzyhVmRJM

Fig. 5 Quoted from this book, written in Japanese;https://www.amazon.co.jp/dp/4784931813/
We apologize that some of the annotations in Fig. 5 are in Japanese, but we could not find a clearer figure.　Here, English translation of the Japanese annotations in the upper panel of Fig. 5;

膜電位:Membrane potential
脱分極：Depolarization
オーバーシュート:Overshooting (Overpolarization)
再分極：Repolarization

And, here　is for the Japanese annotations in the upper panel of Fig. 5;

電流量： Intensity of the current, it means the strength of Ion each current; For example"ナトリウム電流"（Blue curve) represents the Intensity of the current due to sodium ions.
↑外向き：Outward. That means the direction from the inside of the cell toward the outside,
↓内向き：Inward. Direction from outside to inside of cell.

This Fig. 5 is essentially equivalent to Fig. 3, but　Fig.5 gives the impression that "the Ca ion current seems insufficient to balance the K ion current　at Phase 2" in the two phases.

Membrane potentials are determined by the combination of all the membrane-permeable charges, not single ions.
You can use the Goldman Equation to calculate the reversal potential for any combination of ion permeabilities and concentrations.
Sodium and calcium will be the primary contributors to the action potential height, but the kinetics of all the involved voltage gated channels are relevant, too: the Goldman Equation gives you a steady state/equilibrium voltage. The actual membrane potential will move towards this voltage, at a rate depending on the membrane capacitance, but need not reach a given equilibrium potential before permeabilities change which then changes the equilibrium.
I would recommend looking at a plot of the permeabilities to different ions over time and think about these relative to the Goldman Equation. Here's an example plot:

from Sigg et al., 2009 via http://www.vhlab.umn.edu/atlas/conduction-system-tutorial/cardiac-action-potentials.shtml

♦ Thanks for your answer. I also initially attributed it to the contribution of multiple ions. But if so, I think there must be an opposing ion current antagonistic to the K ions in Phase 2. the Ca2+ ion current would be strong enough for that in phase 1, but not strong enough in phase 2 (See lower panel of Fig. 5).

@BlueVarious The site really doesn't work well if you abuse answers and comments to ask your actual question.

I don't think of it as abuse. I added this because, to put it mildly, I may not have explained the intent of my question well enough. The fact that multiple ions would actually be involved is also mentioned in Figure 3, which was quoted from the beginning and gives a bit more detail. So I am sorry that I should have emphasized that I understand such a vague level of detail.

My question is, with the information shown in Figure 3 in mind, why would phase 2 have a value of 0mV? If you are saying that it is 0mV by chance when you substitute the actual condition into the Goldman equation, then that could be the answer you seek if it is true. But at least my question is not about what tug of war membrane potentials are generally determined by. Your answer answers that question perfectly, but does not provide any reason for 0mV at all. My question is specific to 0mV, as has been clearly stated from the beginning.

@BlueVarious Yes, it's 0 mV when you calculate a weighted sum of all the permeable ions using the Goldman Equation. Biology can't break physics. Nothing is special about zero in that equation. You'll note in the plot that the actual membrane potential is only briefly exactly zero, which it must be for any continuous function that goes from positive to negative.

Ok. That is answer, I needed !! Thank you.

At the risk of being called abuse again, there is a reason I did not mention the Goldman equation at first. I also looked at the Wikipedia page you referred me to and the equation presented there does not address divalent ions.

However, the transparency data you gave me is very useful. Once I have that data, I can understand it by assigning it to a form written in the form "Em=gA VA + gBVB" (which is also not written in Wikipedia).

Just for a Comment;
I know the Goldman equation (https://en.wikipedia.org/wiki/Goldman%E2%80%93Hodgkin%E2%80%93Katz_flux_equation), and I asked this question because I thought maybe this does not explain "0mV" at all or more specified explanations are required;
In fact, the Goldman-Hodgkin-Katz flux equation cannot be adapted to the divalent ion Ca2+, at least in the following formula. And the contribution of Ca2+ appears to not be negligible in this discussion.

At first, I did not quote the Fig.5,belowt  because it was written in Japanese, but I additionally quoted this figure as Fig5. Fig.5 shows the changes of each ion current over time, together with the action potentials of the myocardium and the timescale. If you read carefully, you should be able to read the same story from Fig. 3, but Fig.5 should be easier to understand.
We apologize that some of the annotations in Fig. 5 are in Japanese, but we could not find a clearer figure.　Here, English translation of the Japanese annotations in the upper panel of Fig. 5;

膜電位:Membrane potential
脱分極：Depolarization
オーバーシュート:Overshooting (Overpolarization)
再分極：Repolarization

And, here　is for the Japanese annotations in the upper panel of Fig. 5;

電流量： Intensity of the current, it means the strength of Ion each current; For example"ナトリウム電流"（Blue curve) represents the Intensity of the current due to sodium ions.
↑外向き：Outward. That means the direction from the inside of the cell toward the outside,
↓内向き：Inward. Direction from outside to inside of cell.

Fig.5. Quoted from the book, written in Japanese;https://www.amazon.co.jp/dp/4784931813/
(1) In the Fig. 5, a spike-like inward Na current occurs during phase 0 and phase 1. In other words, the Na current suddenly becomes strong and stops immediately. It should be clear that this is the true nature of the depolarization.
The reason why the Na current stops long before it reaches its own equilibrium potential is probably because the Na ion channel closes when the membrane potential reaches about 30 mV. Am I right?
(2) Then, the Ca current is generated just after the Na ions start up, and

since the equilibrium potential of the Ca ions is in the negative direction, and
since the period when the Ca current is flowing roughly coincides with the phase 1 period,

we can also see that the Ca current is probably the main cause which compensates  "phase 0 -induced overshoot" to 0 mV during the phase 1.
(3) The reason why the Ca current stops at a membrane potential near 0 mV is probably due to the property of the Ca ion channel to close at a membrane potential near that level. Perhaps. Am I right?
(4) And the biggest question is why the membrane potential is kept at 0V in phase 2, even though the K current is flowing and no current is depicted in the figure that is antagonistic to the K current, at least in phase 2? but I really don't understand this.

Perhaps there is another current, such as Cl ions, if so, it may explained from the Goldman–Hodgkin–Katz flux equation(https://en.wikipedia.org/wiki/Goldman%E2%80%93Hodgkin%E2%80%93Katz_flux_equation)
or perhaps the K current in the other direction is flowing from a different ion channel.

This Fig. 5 is essentially equivalent to Fig. 3, but Fig.5 gives us the impression that "the Ca ion current seems insufficient to balance the K ion current　at Phase 2.

https://cvphysiology.com/arrhythmias/a006


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What species of bird is this?
We found this fledgling (location: Stellenbosch, Western Cape, South Africa) under a tree next to the road (the tree's branches are high up, so we could not put it back into the tree). We are trying to find out what species it is, what to feed it and how often it should be fed.
It seems quite healthy as it is chirping and flying around in the house.
Little bird found:

Welcome Amanda. I'm no expert so this is not an answer, just a suggestion in a comment, but it seems to resemble the red-billed buffalo weaver, a juvenile. If you scroll down the page on this bird ID site, you'll see the youngster that resembles your new companion. +Wikipedia article. Hopefully someone will come along who can give you something more definitive. It's thought inadvisable to offer dairy products as birds on the whole are not adapted to it, but insects/seeds should work. Mash first

This is an immature Cape Canary. It is really difficult to find reliable evidence of the fact, so a good answer will be hard to put together. Try googling "Cape Canary chick identification"


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Are spores seeds?
It seems to me that the spores produced by bread mould are actually its seeds but my textbook says that they are not.
My rationale is that spores are seeds of bread mould because both spores and seeds perform similar functions: both of them develop into a new organism under favourable environmental conditions.
So, are spores seeds, or is there a flaw in my reasoning?

Don't forget that fungi are phylogenetically closer to animals than they are to plants.

It really is about language, and science uses precise terms. So although spores seem similar to seeds, "seed" is a specific term for a fertilized ovule that is restricted to conifers and seed plants, or gymnosperms and angiosperms. Moss and ferns, which are deeper on the phylogeny of plants, don't make seeds either, but reproduce with spores.

Spores are actually haploid structures created from the sporophylls of lower plants and thallophytes (Some pteridophytes, Bryophytes, Algae, Fungi and bacteria). However, seeds are the structures formed by higher plants like gymnosperms and angiosperms and are diploid. Spores are a result of meiosis of spore mother cells or zygote(thallophytes) and are usually a characteristic of a predominantly haplontic life cycle or haplo-diplontic life cycles.
Fungi form spores by meiosis of the nucleus formed after plasmogamy and karyogamy.

No as as a seed is a specific multicellular structure formed from a fertilised ovule found only in most spermatophytes
Furthermore a spore is at one stage produced within the ovule however it grows into a gametophyte without being dispersed

It mostly depends on what you define spores and seeds as, but according to the "official" definition, the answer is no. And just because two things do the same thing, doesn't mean they're the same. Pens and pencils do the same thing. They're different. See the Internet or something for the "official" definition.

What is the"official" definition? You don't even cite a source! What would you consider the official source in this case? Please provide a source, or your post will be deleted


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Current Trend in Evolution of Human Intelligence
Up front, I am specifically not interested in philosophical or ethical considerations re Eugenics and related concepts. In an effort to receive a concise answer I'll post a narrowly defined question following this preamble to set the stage.
Preamble:
In the movie Idiocracy there is a montage at the beginning "explaining" how the human population degrades, vis-à-vis intelligence, to an alarming (and absurd?) extent due to unplanned differential breeding resulting from several generations of the intellectually "more capable" people limiting their number of progeny, through active and passive family planning, while the bulk of humanity leaves caution to the wind. This exponential social differentiation eventually makes for a global imbalance that degrades our species' overall intellectual fitness to a debilitation level.
Question:
Is the premise of this movie merely a gag or is our species already doing something very much like this?
If yes or no, how might one measure the impact of differential procreation of this sort? Since testing results are always relative to the population as a whole and computers along with the Internet of Things would tend to obfuscate the initial degradation of mental capacity.
EDIT:
Based on the brief discussion in the comments - a summary of fecundity and IQ would potentially answer my question but only if it accounted for the current selection process we see going on in modern technophile societies. That is, it must account for the effect of our most educated couples generally choosing not to procreate and here I'm assuming there is in fact an effect (cf. Idiocracy for the (absurd?) degree to which the present-day trend may work itself out).

Welcome to Biology.SE! You might want to read about the Flynn effect

@Remi.b - Thanks. I was aware of this phenomenon. Thus my last sentence in the question that says, in part, "Since testing results are always relative to the population as a whole". This covers both the Flynn Effect and testing bias resulting from test design in a given culture. - --- - There are many ways of measuring welfare spending against population data but, all politics aside, it seems to me that the 50-year trend (which no one disputes) may be a proxy for an answer to the question I ask above.

Here is a Ted talk by Jim Flynn

@Chris (or Matt) --- I understand the Flynn Effect. I am not asking a question about it. --- What I want to know is if there are any published studies that are looking for the Idiocracy Effect. --- It's a well known phenomenon that kennel breeding in dogs (e.g.), if poorly managed, can engender many genetic diseases and otherwise increase susceptibility to health problems in general. --- Won't the same thing happen with humans? How is this controversial? --- I understand that such a question can engender poor quality answers but that's why I posted on a moderated forum.

Sorry, I was unclear. I really didn't mean that the links I posted would answer your question. I just hope it could eventually help. I know nothing on the subject. From wikipedia I read that it doesn't seem to have any correlation between fertility and IQ.

@Remi.b - Actually the comments attached to the Ted Talk helped the most but still leaves me hanging. I was hoping for something about "regression to the mean" ameliorating bad breeding choices over the long run and how that might apply to human culture generally under our current experimental regime. Something like that. --- I read the SE rules on how to ask questions and, reviewing them again just now, am still at a loss as to how this is a bad question... other than it has gotten zero answers but that could be because it's on hold. ?? O_o

It is not clear to me either why it has been closed. Would be good to give comments when voting for closing. Would a summary about the research on the correlation between fecundity and IQ answer your question? Eventually a discussion about statistical issues in these studies (I am assuming this is what you mean when talking about the effect of regression to the mean)?

@Remi.b - voted to re-open too. Without some constructive comments to improve it it deserves to be active

There appears to be some - note that this, of course, is highly controversial - evidence pointing at the direction that intelligence declined in the US and UK during the last century. There is a relatively new review by Michael Lynch (2016) in which he suggests that modern humans are accumulating slightly deleterious mutations with increasing rate due to relaxed purifying selection (a consequence of technology, medicine, ...), resulting in a 'future genetic load'. Let me just sum up some of the major points he makes that are relevant to assess current evolution of human intelligence:

Heritable mutations that lead to a reduction in fitness of 1% take about 100 generations to be eliminated by selection. Many of these mutations have a direct or indirect effect on the mutation rate (mostly increasing) and relaxed purifying selection on them might cause a positive feedback loop that causes even more mutations. Additionally, parental age increases the number of mutations passed on to the offspring. Most mutations will be slightly deleterious (keep in mind that the majority of new mutations is neutral, the majority of the remainder is deleterious and only very few mutations are beneficial. Therefore the really deleterious ones will still be selected against, but the slightly deleterious ones will not be removed by purifying selection). Accordingly, relaxed purifying selection increases the amount of slightly deleterious selection and decreases the efficiency of getting rid of them.
Lynch argues that the brain might be particularly sensitive to mutations as brain function depends on the finely tuned expression of thousands of genes which for him leads to the proposition that the effect of germline mutation rate on psychological disorders could be higher than expected by chance. In support, he cites Iossifov et al. (2015) who have suggested that autism spectrum disorders might be caused by de novo mutations in at least 30% of the cases and also looked at mutations interfering with IQ measurements.
Finally, he cites two papers that are of interest here as they deal with the change of intellectual abilities of humans over time (Crabtree (2013) and Woodley (2015)). The latter is a meta-analytic study based in the US and UK and Lynch already points out that there there are the usual issues with entangling genetic and environmental factors. However, in that study a slow decline of general intelligence of about 0.39 points per decade due to selection and about 0.84 points per decade due to mutational load is suggested. Interestingly, Woodley points out that there are two major hypothesis for this decline: (i) Since the industrial revolution people with lower general intelligence have higher average number of offspring (that might be the 'differential procreation' you have been hinting at). (ii) Mutation accumulation due to relaxed purifying selection against deleterious variants. Woodley concludes that the decline is a combination of both.

Of course, these points are strongly debatable. One of the major conceptual criticisms on Lynch's view is that slightly deleterious mutations (that Lynch claim to be accumulated as a consequence of relaxed purifying selection) are not slightly deleterious but totally neutral if they do not have a fitness effect. In terms of evolution it does not make a difference if an allele is neutral or negative selection is not acting on it because of technological interference. Another objection - more relevant to your question - is that measuring intelligence in general, or the IQ in particular, is a controversial thing to do and not at all easy to standardize which causes great difficulty in obtaining comparable data. Moreover, tracking down underlying genetics, estimating heritability of intelligence (a trait we even have difficulties to properly define and that is known to be strongly influenced by the environment), and consequently putting together a comprehensive assessment of the evolution of intelligence in humans is really tricky, set aside the ethical problems that may arise which we have not even touched yet.

A last note: In your edit you write:

[...] a summary of fecundity and IQ would potentially answer my question but only if it accounted for the current selection process we see going on in modern technophile societies.

This is problematic as to date it is really difficult, if not impossible, to detect recent selection. This is mainly due to the fact that most methods depend on detecting changes in allele frequencies over time and this needs a considerable number of generations to integrate over.
There have been some efforts to develop more accurate methods, but looking at selection in the last 100 years (which you would need to be able to when looking at the technologically modern populations) is not possible so far. The best attempt I am aware of so far is Field et al. (2016, preprint) who looked, based on genome-wide association study data, at recent selection in the last 2000 years. However, they do not mention intelligence.
Update: This paper was a pre-print. It is now published in Science: Field et al. (2016).

"One of the major conceptual criticisms on Lynch's view is that slightly deleterious mutations are not slightly deleterious but totally neutral if they do not have a fitness effect." -- This criticism of Lynch is not valid. In the absence of human culture the criticism would be true (a truism) but the non-natural selection imposed by human culture is precisely what I think would be interesting to measure.  -- And yes, the whole concept is "loaded", a politically correct bombshell. I hesitated asking the question for just that reason. You'll note the paucity of answers my Q has garnered!

@user23715: I see your point, but selection does not differ depending on the source of selective pressures. It is totally unimportant if we as humans classify it as 'artificial' or 'natural' selection. It is the same thing. This would only not be true if human culture would disappear instantly as this would take away the neutral status of some of the mutations Lynch considers as slightly deleterious. This is actually what Lynch is hinting at: Intelligence levels might drop so strongly that modern medicine cannot be maintained, exposing all these mutations. For me this is a bit far-fetched ...

Human selection, especially modern human selection, is more Lamarckian than Darwinian. -- It's possible genetic medical science will exceed our ability to harm ourselves through non-selective breeding. Maybe the next generation (or three) AI after IBM's Watson will get us what we need to keep from running off the cliff. -- I would think the rate of bad mutations would increase geometrically at some point so the cliff could seem far away and then... too late! -- Thanks for the answer. I'll let it sit for a week or ten but it will likely become the accepted answer.

@user23715: As you might have seen in my answer, I also still have to let it sit as it is a very difficult topic both scientifically (intelligence is the on of the 'worst' trait one can work with) and ethically. Interesting to think about though.

You're right that the Field et al paper is the best broad attempt at an answer. -- I found How fragile is our intellect? Estimating losses in general intelligence due to both selection and mutation accumulation to be useful too as a primer on the topic with an excellent short list of citations going back to the heyday of eugenics. -- As Woodley points out, this topic is critical to human flourishing; too bad the "well was poisoned" with politics in the 1920's/30's. -- Germline repair will be a worthwhile investment.

@user23715 My guess is that the advances in genetic research regarding intelligence will make it possible in a couple of decades to screen/select for intelligence. At that point someone will start providing services for future parents, perhaps in China and in Russia. The undeniable success will very quickly change the mind in the West because competitiveness is at stake. The hope is then that everyone has access to this technology so as to select/engineer their embryo/child, not just the rich.

@user23715 There is already evidence that average IQ is going down, despite the Flynn effect (the effect has come to an end, as the Flynn effect was most likely due to poor nutrition that afflicted the lower strata of the population). Rindermann has collected some data about this. As sad as it is, the modern welfare state we all treasure seems to have adverse effects. If you really want some bad news from the verboten corners of the internet, check out Nathan Cofnas, for some good news about progress in the science check out Steven Hsu.

@user23715 You might also want to visit Gregory Cochrane's blog. I think he discusses the paper you linked to and criticises it. Somewhere in his twitter feed there is a discussion of this paper with people disagreeing as to whether Woodley is too pessimistic or optimistic. One thing is for sure, the Flynn effect has not much to do with genetics. If it would, the constant rise in IQ that was observable for most of the last century would have lead to a significant increase in geniuses, and we failed to see that.

@AlexDeLarge You wrote "measuring intelligence in general, or the IQ in particular, is a controversial thing to do and not at all easy to standardize". Could you elaborate? It might be controversial in some circles but IQ research is some of the most robust research there is in psychology. And intelligence is actually quite easy to measure. For a good defense of psychometric testing see Russell T. Warne's "In the Know".


text:
Whole Genome Sequencing and B Chromosomes
Do whole genome sequencing techniques detect B chromosomes if such chromosomes are present?
My understanding is as follows:
How the DNA material in a B Chromosome is mapped depends on the reference map and not on how the material is packaged into chromosomes for the sample being sequenced.
Is this correct?

You can use differences in coverage (number of reads mapping to certain regions in reference) to infer if there is a B chromosome.

The analysis of NGS reads coverage rate can give information on B chromosome genomic content. Have a look at the article mentioned below:

 Valente GT et al. (2014). Origin and evolution of B chromosomes in the cichlid fish Astatotilapia latifasciata based on integrated genomic analyses. Mol Biol Evol. 2014 Aug;31(8):2061-72

Can you add a little explanation on how coverage can be used to infer B chromosome genomic content. An illustrative figure from the mention reference would also do. We would greatly appreciate some explanation in addition to providing a link to the reference.

The attached figure shows the Illumina reads coverage for two 0B, two 1B and one 2B samples. Note that the figure shows a specific genomic regions with a higher reads coverage for the 1B and 2B samples compared to the 0B ones.

Welcome to Bio. Could you provide sources to your data and answer? References are encouraged here.


text:
How Does Green Tea Increase Metabolic Rate?
According to the article "Green Tea Supplementation Affects Body Weight, Lipids, and Lipid Peroxidation in Obese Subjects with Metabolic Syndrome", Green tea increases metabolism and fat loss:

Green tea beverage consumption (4 cups/d) or extract supplementation
  (2 capsules/d) for 8 weeks significantly decreased body weight and
  BMI. Green tea beverage further lowered lipid peroxidation versus age-
  and gender-matched controls, suggesting the role of green tea
  flavonoids in improving features of metabolic syndrome in obese
  patients.

Is there any information available concerning the mechanism of that metabolic increase?

Caffeine maybe?

@Armatus, Caffeine was used as the negative control.

@Dale Your link is broken.

I updated the link, but the full article is behind a paywall.

Interesting question! Green tea increases metabolic rate of body because it contains antioxidants known as catechins1. Catechins are actually polyphenol flavonoids, and have been shown by Wang et al and team to affect body composition and decrease body fat in intra-abdominal area. Also, as per Khalesi et al, catechins improve blood pressure, especially when systolic pressure exceeds 130 mmHg, while some studies, such as Ellinger et al, have indicated that catechins may have effect on endothelium-dependent vasodilation which might lead to normal blood flow regulation. Another study, by Weinreb et al, shows that catechins can also reduce the risk of Parkinson's and Alzheimer's. However, their exact mode of action is unknown because of their extensive metabolism during digestion6.
Green tea also contains a little amount of caffeine. Now, as we all know, caffeine is known for its stimulating effects on the body. Caffeine, as stated by Nehlig et al, blocks the formation of adenosine in brain, thus increasing concentration of dopamine and norepinephrine in the brain which, in turn, allow quicker firing of neurons. Along with caffeine, another compound with similar effects is L-theanine, which increases the activity of GABA and leads to anti-anxiety effects, as reported by Nathan et al. Caffeine and L-theanine can together have synergistic effects on the brain and give much more pronounced effects together than individually.
A yet another, and probably less spoken of, effect of green tea, as concluded by Lee et al, is that it can even kill some bacteria and viruses (obviously, killing means preventing growth here) and thus reduces chances of bacterial and viral infections.
Obviously, there might be even more benefits of green tea than I've put here. To the precise point you were asking, we don't yet know how green tea helps in burning calories and fat oxidation. The proposed mechanisms of action are10:

catechins act on catechol-o-methyltransferase (COMT), an enzyme which degrades norepinephrine. Norepinephrine is known for regulating thermogenesis and fat oxidation. Thus inhibition of COMT by catechins may lead to prolonged effects of norepinephrine on fat metabolism.
caffeine can also affect thermogenesis, but by inhibiting phosphodiesterases & thus prolonging effects of cAMP in the cell. As a result, cAMP stimulates hormone - sensitive lipase and promote lipolysis.
catechins and caffeine can also work together and increase thermogenesis in body by 35-43% by increasing fat oxidation.

However, these are just the proposed mechanisms and more detailed studies are required to reach a conclusion.
References:
 1. Beneficial Effects of Green Tea—A Review; Carmen Cabrera, Reyes Artacho, and Rafael Giménez; Journal Of The American College Of Nutrition Vol. 25 , Iss. 2,2006
 2. Wang, H., Wen, Y., Du, Y., Yan, X., Guo, H., Rycroft, J. A., Boon, N., Kovacs, E. M.R. and Mela, D. J. (2010), Effects of Catechin Enriched Green Tea on Body Composition. Obesity, 18: 773–779. doi:10.1038/oby.2009.256
 3. Khalesi, S., Sun, J., Buys, N. et al. Eur J Nutr (2014) Green tea catechins and blood pressure: a systematic review and meta-analysis of randomised controlled trials, 53: 1299. doi:10.1007/s00394-014-0720-1
 4. Epicatechin ingested via cocoa products reduces blood pressure in humans: a nonlinear regression model with a Bayesian approach; Sabine Ellinger, Andreas Reusch, Peter Stehle, and Hans-Peter Helfrich
 5. Neurological mechanisms of green tea polyphenols in Alzheimer's and Parkinson's diseases; Orly Weinreb, Silvia Mandel, Tamar Amit, Moussa B.H. Youdim
 6. "Flavonoids". Linus Pauling Institute Micronutrient Information Center, Oregon State University
 7. Caffeine and the central nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects.; Nehlig A, Daval JL, Debry G.
 8. Nathan PJ, Lu K, Gray M, Oliver C.. The neuropharmacology of L-theanine (N-ethyl-L-glutamine) a possible neuroprotective and cognitive enhancing agent. J Herb Pharmacother (2006) 6(2):21–30.10.1080/J157v06n02_02
 9. Lee H.J., Lee Y.N., Youn H.N., Lee D.H., Kwak J.H., Seong B.L., Lee J.B., Park S.Y., Choi I.S., Song C.S. Anti-influenza virus activity of green tea by-products in vitro and efficacy against influenza virus infection in chickens. Poult. Sci. 2012;91:66–73. doi: 10.3382/ps.2011-01645.
 10. Jówko E. Green Tea Catechins and Sport Performance. In: Lamprecht M, editor. Antioxidants in Sport Nutrition. Boca Raton (FL): CRC Press/Taylor & Francis; 2015. Chapter 8. Available from: https://www.ncbi.nlm.nih.gov/books/NBK299060/

May be because it contains xanthines that boosts Cyclic AMP and Subsequent Stimulation Of Oxidative Pathways .

References for both statements would be great =)

Green tea contains caffeine and catechin polyphenols. There are various proposed mechanism of these compounds
(1) These compounds have an effect on sympathetic nervous system (SNS). SNS is involved in flight and fight situations and controls thermogenesis and fat oxidation. In put in simpler words, the bioactives in green tea stimulate the part of nervous system which is involved in preparing body for emergency response by increasing the metabolism [1].
The catechins, inhibits Catechol-O-methyl transferase (COMT) that degrades norepinephrine resulting in prolonged shell life of norepinephrine in the synaptic cleft,
Caffeine inhibits phosphodiesterases which increases the life of cAMP, result in an increased effect of norepinephrine on thermogenesis.
(2) Catechins found in teas have shown potential to inhibit carbohydrate absorption in the intestines.
A very detailed review of literature can be found here [2]

[1] http://ajcn.nutrition.org/content/70/6/1040.long/-
[2]https://macsphere.mcmaster.ca/bitstream/11375/20419/2/Martin_Brian_J_Finalsubmission2016September_PhD.pdf


text:
What are calories and how to burn them?
What exactly is a calorie? When burning calories, do we always lose fat?
I have tried many apps to measure calories, do they give exact amounts? How many calories should be taken a day?

I'm voting to close this question as off-topic because  the latter part of the question is off topic (try sports or health SE) and the first questions show no research effort, and calorie is chemistry, - read on calories and ask about what you are unsure of.

A calorie is a measure of energy. In nutrition, we usually mean the kilocalorie (kcal), which is the same as about 4.2 kJ (kilojoule). A average person needs about 2,000--2,500 kcal per day, but this of course varies quite a bit between people, depending on size (muscle mass, particularly) and level of physical activity (physical work, exercise).
Nutrition guidelines found on the labels of food products give a pretty good summary of the amount of energy they contain. I'm not sure what applications you have been using, but they most likely rely on the same basic data, so the values should be similar. You can use these values to figure out roughly what your calorie intake is, and to spot very calorie-rich foods. But counting calories exactly is actually quite difficult --- you need to carefully weigh everything you eat and keep track of lots of numbers, and it's easy to make mistakes.
Burning calories does not always mean burning fat. Fat is a long-term energy storage form in the body. When exercising, the body tends to burn stored carbohydrates (glycogen) first, and turns to burning fat when carbohydrates are exhausted. Therefore, prolonged, low-intensity exercise like long walks are usually better for burning fat than short "sprint" type of exercise. The body also burns fat during normal daily activity if your energy intake is lower than the daily need (when dieting). But it is also possible that some muscle mass is degraded (to amino acids) and used for energy as well.
See also Wikipedia articles on food energy and exercise. Please note that "how to burn calories" is a heavily debated issue, there is an entire industry of weight loss methods, and various claims about "easy" methods or products to lose weight quickly are generally not true. The only reliable method to lose weight is to reduce food intake and increase exercise, for a long period of time.


text:
Why is aneuploidy usually lethal?
So, I was reading about aneuploidy and how a zygote with one extra or less chromosome usually would not survive to full term. I suppose this happens because aneuploidy leads to some kind of protein imbalance. So, in case of monosomy we would have a shortage of proteins, and in case of trisomy we would have an excess of proteins.
On the other hand, a conventional argument for having two copies of each gene is that, if one gene gets corrupted because of some kind of mutation, we still have another copy that produces the correct protein. So, in case of a recessive genetic disorder, the zygote can survive even with half the amount of protein.
My question is then, why can't monosomic aneuploidy be looked at the same way? Moreover, I read that monosomic aneuploidy is almost always fatal, while trisomic aneuploidy is sometimes tolarated.

What causes zygotic termination in aneuploidy often isn't an issue with proteins or other gene products i.e. being "too sick" to live. It's that the zygote is basically "self error checking" and if it encounters a serious genetic error (e.g. aneuploidy) it self-terminates, as it would likely not survive anyway. Sometimes this self-termination fails, and the zygote develops. Depending on the specific aneuploidy, it may not make it to term, or perhaps it will, and you will have a child born, albeit the child will usually have a decreased quality of life/life-span.
A similar mechanism works in your somatic (non-reproductive) cells everyday when they replicate and divide - if they detect and error in their DNA that cannot be repaired, the cells SHOULD kill themselves. Sometimes this fails, and can give rise to cancer.

Thanks for your reply, can you add something more about the "self error checking" mechanism, maybe a link?.

Just one doubt, but people with aneuploidy have problems because their aneuploidy translates into some sort of protein imbalance,  and that brings me back to my question

This sounds self-contradictory: you're saying that extra chromosomes are not harmful in themselves, but the cell detects them and self-terminates because extra chromosomes would be ... harmful? I'm no expert on this topic, but I would guess the main underlying problem is that aneuploidy causes problems in cell cycle/mitosis, which is lethal. Also, it probably would result in even more scrambled cells in the next generation (after meiosis), and so would endanger the whole genetic material.

@Roland Forgive me, my response was written past midnight. I meant to say that rather than progressing to the stage of dying from protein imbalance, the cell terminates before this point, usually.


text:
Relationship between immunologic response to specific gluten epitopes and clinical antibody testing
Celiac disease is understood to be an immune response to certain proteins which occur in a group of cereals; most commonly they are glutens (wheat), secalins (rye) and hordeins (barley). A clinical test for celiac examines serum levels of two specific antibodies: Deamidated Gliadin peptide Ab IgG and Tissue Transglutaminase Ab IgA.
Is it possible to test positive for the above antibodies while being sensitive (raise an immune response) only to hordeins?
There are two components to this question:

Can a person be sensitive to hordeins while being unaffected by either wheat gluten or rye (secalins)?
Would the above test produce a positive result given only hordein-specific antibodies? In other words, is the test specific to wheat gluten antibodies or will antibodies to any gluten epitope produce a positive result?

The reason behind this question in a short case history:

Mature adult subject experienced mild/intermittent IBS symptoms, onset vaguely extending back several years. Diet notably included regular/daily consumption of wheat/rye products as well as intermittent (2-3/week) beer (barley).
Recent clinical screening for celiac (serum levels of Deamidated Gliadin peptide Ab IgG and Tissue Transglutaminase Ab IgA) performed to investigate cause of suspected osteoporosis; both antibody levels assessed as positive.
Symptoms apparently abated within about one week following an initial dietary change successfully removing only barley gluten (beer), while regular consumption of wheat/rye continued.

Observations suggest a specific response only to barley, and raises the question about specificity of the clinical antibody test.

You might find this answer to a related question to be of interest — it doesn't address celiac directly, but it does answer the first part of your question.

@tyersome it does help with general understanding. Still hoping for an on-point answer to reconcile some specific facts and observations.

I would recommend editing your question to focus on the IBS specific portions — since you already learned the answer to 1. and 2. I recommend rewriting your post to include that information and delete extraneous material. (The website keeps track of edits so you don't need to have an 'Edit' section.) This will show people that you have done your research and allow people to focus on what you still don't know, rather than getting distracted by questions for which you already know the answers. ——— Specifically, I would delete anything not relevant to understanding your final paragraph.

@tyersome Thanks for the suggestion; hope my latest edit does the job

You're welcome — this is much better! (+1) It's great that you've put in so much effort to improve your question. The only other suggestion I can make at this point is to include references for the background statements you make. In particular, references that describe the basis for the clinical tests might allow someone with the correct background to rapidly come up with an answer for you. This also provides a resource for other users and documents all the work you've put into your question! ——— I hope you get a good answer soon.

1) Can a person be sensitive to barley hordeins, while being unaffected by wheat gluten or rye secalins?
Possibly, but I haven't found a documented case.
According to What is gluten? (Journal of Gastroenterology and Hepatology, 2017):

A variety of sequences from α, γ, and ω gliadins, as well as from the
  glutenins, have been identified to activate coeliac disease. However,
  several hundred gluten peptides are predicted to be immunogenic and
  trigger the T-cell mediated response.6 The most immunodominant T-cell
  epitope is from α gliadin, although T-cell cross-reactivity against
  gluten-derived, secalin-derived, and hordein-derived peptides have
  been confirmed. Additionally, within each grain, there exists a
  distinct hierarchy of immunostimulatory gluten peptides.6 Of all the
  peptides known to stimulate the T-cell response in coeliac disease, a
  given patient may react to only a few.

However, according to Coeliac disease: immunogenicity studies of barley hordein and rye secalin‐derived peptides (International Journal of Experiemntal Pathology, 2016):

In conclusion, barley hordein and rye secalin appear to contain CD
  toxic epitopes that are found in wheat gluten, as demonstrated by the
  observed cross‐reactivity of CD‐derived gluten‐sensitive small
  intestinal T‐cell lines to wheat gliadin, barley hordein and rye
  secalin‐derived peptides.

2) Are the blood tests specific to wheat gluten antibodies?
I can't say for deamidated gliadin peptide Ab IgG test, but tissue transglutaminase antibodies IgA test (anti-tTG IgA) is not specific for wheat gluten; antibodies can be triggered by wheat gliadins, barley hordeins and rye secalins.
Gluten peptides (gliadins, hordeins, secalins) bind to tissue transglutaminase which deamidates them. Individuals with celiac disease have HLA DQ2/DQ8 dendritic cells, which present deamidated peptides to T cells, which stimulate B cells to produce antibodies against tissue transglutaminase:

In CD, deamidation of gluten by tissue transglutaminase (tTG) in the
  small-bowel lamina propria promotes presentation of gluten peptides
  (gliadin in wheat, secalin in rye and hordein in barley) by
  HLA-DQ2 or HLA-DQ8 dendritic cells to pathogenic local CD4+ T
  cells...The most widely used serological test is anti-tTG IgA
(Medscape)

3) Can barley affect the gut differently than wheat?
Possibly.
Nutrition and Celiac Disease (Nutrients, 2014):

There is very limited data looking at the effect of barley hordein or
  rye secalin on CD outcomes in the published literature (e.g.,
  [66,67]), but evidence exists that these prolamins induce effects
  different to wheat gluten, at least at an immunologic level.

4) Do positive DGP and TTG test confirm celiac disease?
The specificity of IgG deaminated gliadin peptide (DGP) is 98% and of IgA tissue transglutaminase (TTG) 95% (American Family Physician, 2014), so when both tests are positive, celiac disease is very likely. The final diagnosis is by histological examination of a tissue sample obtained by duodenal biopsy.
5) Is it possible that, in celiac disease, symptoms disappear after removing only beer, but not wheat and rye from the diet?
It could be possible to have celiac disease confirmed by blood tests without any symptoms despite consuming wheat, barley and rye. Beer could trigger symptoms by irritating the bowel, not by gluten, but by alcohol or other substances, like in people with irritable bowel syndrome (American Journal of Gastroenterology, 2013).

Thanks for the comprehensive answer. I was hoping for a more definitive answer, but this is very helpful and useful info.


text:
Assumptions of the models for haploid and diploid selection
For a bi-allelic locus, the model for haploid Natural Selection is:
$$\frac{dp}{dt} =  \frac{pW_A}{pW_A + (1-p)W_B}$$
, where $p$ is the frequency of the allele $A$, which relative fitness is $W_A$. $W_B$ is the fitness of the allele $B$, which frequency is $1-p$. $\frac{dp}{dt}$ is the change in allele frequency through time.
The same model for diploid selection is:
$$\frac{dp}{dt} = \frac{p^2W_{AA} + p(1-p)W_{AB}}{p^2W_{AA} + 2p(1-p)W_{AB} + (1-p)^2W_{BB}}$$
, where $W_{AB}$ is the fitness of the diploid genotype carrying the allele $X$ on one chromosome and the allele $Y$ on the other chromosome. We define $W_{AB} = W_{BA}$ and therefore we use only the symbol $W_{AB}$ in the above calculations. Note: This equation assumes Hardy-Weinberg equilibrium.
Those equations can be found in any introductory courses in population genetics. For example, here is a source where you can find this same equation for diploid selection. They just express $q$ instead of $1-p$.
My questions are:

Do these models assume constant population size? Why?
Do these models assume threshold selection? Why?

Thank you!

See my updated question!

Unless I am missing something the equations you have posted are incorrect. The second equation should be:
$$p' = \frac{p^2 W_{AA} + p(1-p)W_{AB}}{p^2W_{AA}+ 2p(1-p)W_{AB}+(1-p)W_{BB}} $$
$p'$ is not interpreted as $\frac{dp}{dt}.$
$p'$ is the frequency of allele A in the next generation. If zygotic frequencies via random mating are
$p^2(AA) + 2pq(Aa)+q^2(aa) = 1$
then all of AA individuals and 1/2 the Aa gametes bear the A allele. So we can find $p$ in the next generation as
$p^2+pq = p^2+p(1-p) = p^2+p-p^2 = p$ which shows that in a Hardy-Weinberg population the frequencies are stable.
The assumptions here are those underlying the HW model, which includes infinite population size (hence constant).

Yes indeed you'r right. I was curious about how changing in population size may change selection pressures and change allele frequencies, but the model I gave assumes infinite population size. And yes, dp/dt is not the same as p'. Thank you!


text:
How can oxygen production during photosynthesis be measured?
I'm curious how people measure quantitatively photosynthetic rate in labs.
I've seen many qualitative examples with direct observations of bubbles forming in water due to photosynthetic output of aquatic plants.
The ways I have come up with are:

to measure the CO2 intake.
to measure the O2 output.
to measure the amount of sugar produced.

The 3rd option seems most trivial, but I don't know how to measure the amount of CO2 present in a container. With a reaction? Or with a measuring machine of some sort? What about O2?

Similar post


text:
Why does some skin hold perfume longer than others
I was wondering my girlfriend and I used the same perfume for a while and we sprayed the same place. And after a day her skin still smells nice while mine smells normal.
Will different types of perfume hold longer on different skin types?


text:
Why glycoproteins are better than non-glycoproteins in fulfilling biological tasks?
I have just an intuition that the carbohydrate part of glycoproteins help them to fulfil those tasks like in plasma membranes.
You can also get many more receptors if you can use carbohydrates too.
For instance, glycoproteins are necessary in recognising white blood cells. Antibodies are examples of glycoproteins. So they play a crucial role in our innate and adaptive immunity: MHC interaction with T cells in adaptive immunity.
Other examples: necessary in platelet aggregation and adherence, components of zona pellucida and connective tissue. Some hormones are also glycoproteins so necessary in humoral adaptive immunity: FSH, LH, TSH and EPO.
But why glycoproteins are "better" than proteins without carbohydrates moiety in fulfilling biological tasks?
I still see that both are important, but why the one is better than the other one.
In other words: Are there any biological tasks that only non-glycoproteins can fulfil, not glycoproteins? Are non-glycoproteins necessary in some essential biological tasks?
I think the answer to the last two questions is "yes", so why would one say that glycoproteins are better in fulfilling biological tasks than non-glycoproteins.

Essentially all cytosolic, nuclear and mitochondrial proteins are non-glycoproteins, so I think that the premise of the question is flawed. In fact, it isn't really clear what you mean by "better".

@AlanBoyd I completely agree with you. The thing is that the teacher wants explanations why some thing is better than other. I however do not see any sense in it. It is like comparing bananas with apples.

@masi, there are good reasons why membrane bound glycoproteins are suited for certain tasks. You cannot generalise though, it depends on the task in question.


text:
Reliability of SARS-CoV-2 tests - false negatives
This is about the entire process from sample collection through transportation to lab processing and assessment. In Canada, we are seeing about one COVID-19 test in 10 produce a positive result. Can we be confident that the number of false negatives is negligible? There have been reports of issues potentially occurring at every step which could result in a false negative, from failed collection of the sample to degradation of the sample in transit, to perhaps process or reagent issues in the lab.
Also, is there any possibility of the virus mutating in such a way that what makes it COVID-19 from a public health point of view remains the same but its genetic identity changes enough to no longer be recognized by the existing tests?
Is the testing process from end to end reliable enough that we can trust the reported result be it positive or negative?

SE Biology is a question and answer site — not a discussion site or a site for floating ideas. It is concerned with the mechanisms of biological processes, not medical or social aspects of biology. For one of these reasons I think  that your question on the coronavirus outbreak is off-topic here. Question of a medical nature might be on-topic at SE Medical Sciences. Otherwise you are advised to consult more appropriate reputable sources for such information, some of which are listed here.

Also, is there any possibility of the virus mutating in such a way that what makes it COVID-19 from a public health point of view remains the same but its genetic identity changes enough to no longer be recognized by the existing tests?

That's unlikely. These assays look for several specific regions of the viral genome under high selection pressure (i.e., highly conserved) to make a clinical diagnosis (such as orf1ab, N, and S genes, ref. https://www.thermofisher.com/us/en/home/clinical/clinical-genomics/pathogen-detection-solutions/coronavirus-2019-ncov/genetic-analysis/taqpath-rt-pcr-covid-19-kit.html and https://www.fda.gov/media/136286/download for examples), with the aim to minimize test error from off-target effects (varieties of genomic mutations, ref. https://en.m.wikipedia.org/wiki/Off-target_genome_editing) and misidentification with other respiratory viruses.
I can't speak to the other questions in your question with numerical error rates of tests, except to say that controls, procedures, and better PCR primers can be used to increase sensitivity, to get a true positive (ref. https://en.m.wikipedia.org/wiki/Sensitivity_and_specificity). Sensitivity is a real issue for test kits in Russia, where one must have high viral counts (and likely be very ill) in order for a test to give a positive diagnosis (ref. https://abcnews.go.com/International/russia-reporting-covid-19-cases-cover/story?id=69717763)

According to PCR News, the Russian test is based on the same method used by other countries.
But the Russian test, PCR News wrote, only detects the virus when there are over 100,000 copies of it per milliliter in a sample. That is far more than in other countries’ tests. A test in use in the U.S., for example, will pick up the virus with just 6,250 copies.
“That would mean it’s about 10-16 times less sensitive than what’s available in the U.S.,” Carmen Wiley, president of the American Association of Clinical Chemistry, told ABC News by a phone. At such a level, she said there was a risk the Russians were missing cases, in particular where people were asymptomatic.

From a public health standpoint, I suspect diagnosis of sick people is less useful than diagnosis of asymptomatic carriers who feel fine but are shedding virus everywhere. You want a test to let you quickly tell positive people to self-quarantine, before spreading it around.