text:
Does the Plasma Membrane have a hydrophilic interior/exterior/contain vesicles?
I am very new to the study of biology, and have been unable to find information in other sources which could tell me whether the plasma membrane has the following traits:

has a hydrophilic interior
has a hydrophobic exterior
contains vesicles

Thank you!

Where did you look for sources?

The plasma membrane is a lipid bilayer. Plasma membrane lipids have a hydrophilic head group and hydrophobic tail groups. Since cells are usually in an aqueous environment (and are filled with aqueous cytoplasm), the hydrophilic head groups is face both the exterior and interior of the cell. Between these head groups facing the interior and exterior, the hydrophobic tail groups of opposing lipids associate with each other to create a hydrophobic core within the membrane.
Vesicles are also made of lipid bilayers. Vesicles can exist within cells or be released by cells.

Please add some references to your answer.

The plasma membrane typically refers to the double lipid bilayer, which has a hydrophillic exterior and a hydrophobic interior.  In your case, the only thing I can think of is a layer/mixture of inverted micelles, which would fulfill your three criterion.

Image is from "Lecithin-based nanostructured gels for skin delivery: An update on state of art and recent applications"

Please add some references to your answer.


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Can Mother-to-Child Transmission Occur in Relation to Mycotoxins or Mycoestrogens?
There are 17 officially noted cases in which leukemia or melanoma cancer cells crossed the placenta from mother to child. Other crossings include metals (or metalloid elements), such as mercury or arsenic (just as an example). There are also crossings of bacteria, viruses, and general foodborne illnesses.
With all this in mind, my question is: "Can a mother who is hosting a mold, transfer that to her unborn child?"
(Please don't supply an answer about how the child is at risk during the birthing process or caesarean section. Other than that, even opinions are welcome. Thanks in advance.)

source: Stack Exchange

license: Creative Commons - Attribution Share-Alike - https://creativecommons.org/licenses/by-sa/3.0/

sort: votes


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How to annotate the SwitchGear gene models?
According to this page(http://switchgeargenomics.com/wp-content/uploads/2009/02/switchdb_technote1.pdf), the SwitchGear gene models can be annotated by the NCBI annotation associated with Refseq accession numbers, but I couldn't find such information in this page(https://www.ncbi.nlm.nih.gov/refseq/), which is indicated in the above pdf page...
How can I annotate the SwitchGear gene models?

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Do species ever go extinct by becoming too successful?
Are there examples of species that have driven themselves into extinction by being too good at what they are doing? Like a predator that evolves to hunt so efficiently that it kills all it's prey and then goes extinct itself.

Humans seem like they're on this course. You may be interested in predator-prey dynamics.

There is evidence that lemming populations approach this in ~4-year cycles of population proliferation and crashing. They've rebounded through these cycles, so it's not quite an extinction example, but it shows that catastrophic success definitely has precedent. Here's a brief article on the relationship between predator-prey trends: http://vetmed.illinois.edu/wildlifeencounters/grade9_12/lesson2/adapt_info/predator.html.

Seems like there's a need to define "success".  If a predator wipes out its own food source, is that really "success", or just a different kind of failure?  If a human becomes wealthy and uses all of that money to eat McDonalds until they die, then would you say that they died from "success"?

@Nat It is a success in the species's ability to gather resources and proliferate. The failure is in both its predators and prey. I suppose it could be argued that it has a failure to adapt to starvation conditions, but in the case of lemmings at least, they evidently are adapted well enough to have some survivors and rebound.

@HarrisWeinstein Seems like any species that drives itself to extinction's failed in the most basic of senses.  But, this question words it is in such a seemingly positive way - "becoming too successful".  Like a heroin addict who overdoses dies from being too successful at getting heroin.  Or like gunshot victims are die from being too successful at getting free bullets.  Positivity's great, but when examining how a species drove itself to extinction, it'd seem appropriate to characterize that suicidal behavior as something other than "success".

yes, infectious bacteria are a good example, a highly destructive infection may often kill its host before it can spread the disease.  https://www.ncbi.nlm.nih.gov/books/NBK27114/


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Does liver regenerate quicker if idle?
I recently heard a proposition that fasting (especially fruit-only diet) can improve liver function because it removes the load usually induced by toxins in common diets, thereby allowing the liver to regenerate itself quicker.
This is a common proposition in "detox diets" but I am not sure if it has any ground in science? Does consuming less toxic food allow liver to "recover" and regenerate quicker?

Welcome to Bio. Could you add your source to your claim? It may be a mythbuster-typed question and sourced are especially  relevant with those.

Thanks. It was a Facebook discussion from a closed group. Not sure how that fits with the rules here?

That'll do I guess. It's not the most reliable source, however. Was there a consensus in the whole group that this diet helps? How many folks were in the group? Sorry for the questions, just trying to get this clear. Personally I like the mythbusters, but they often hinge on the source of info.

Well it was a skewed crowd, the group is Bali based, and Bali is huge on veganism, detox, organic juices etc, so alternative propositions are usually threated like heresy. Not really a fact-based, paper-supported discussion, but I'd like to improve my own arsenal to participate in these discussions better.

This idea is prevalent in naturopathy and with popular health enthusiasts so I think it's a relevant question. Scientific consensus is a bit more elusive. Here's a link to one article: https://www.sciencedaily.com/releases/2016/05/160509085347.htm


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Preserving/disinfecting meat with alcohol?
I'm considering safer ways to handle raw meat and it occurred to me that alcohol might be useful.
I'm considering, say, sealing pieces of meat in a container with 40% alcohol or higher in fridge or possibly freezer.
My question is what effects will this have on potential bacteria/parasites in and on the surface of the meat, and what will happen over time.
Different results as per higher concentrations/volume of alcohol and various temperatures are a plus.

Since, then the solution is more concentrated than the eco , osmos will take place, resulting in dehydration of cells , ultimately cells collapse.

So it will actually dry it out in the center?


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What is Genome wide analysis and Locus specific analysis
I am reading some articles on genetic variations and I see there are two types of analysis one is genome wide genetic variation analysis and second one is locus specific genetic variation analysis. I don't understand what these two, genome wide and locus specific analysis mean and what is the difference between these two analysis or why do we need both type of analysis?

Welcome to Biology.SE!
A locus (plur. loci) is a region of arbitrary size on a chromosome. A locus can be a single nucleotide or it can much larger (like $10^7$ sites).
A genome-wide analysis is therefore an analysis using the whole genome at once while a locus-specific analysis is the same analysis performed at the level of individual loci.
To make an analogy, if a genome-wide analysis is like a country-wide analysis, then a locus specific analysis is like a city specific analysis.
Without more context, it will not be possible to say more than that!

So what I understand is that, Genome wide SNP analysis means detection of SNPs in whole Genome, this gives us the location of the SNP and then this Location specific analysis is done on different people to find out if that SNP is present in certain group of people(Europe/Asian for example)?

I would need to read the paper to know what they really did but the term "locus-specific" does not mean "individual-specific" or "subpopulation-specific", it means "locus-specific", where locus is an arbitrarily defined genomic regions.


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Differing number of "things" in mammals
I'm not a biology expert, but I have often wondered about the following facts of life:
All mammals have precisely 5 fingers on each of our 4 extremities. Granted, some may not be seen, but the bone structure of 5 fingers is there in all mammals, from whales to bats to humans. This, I guess, tells me that changing the number of finger bones is, genetically speaking, fairly difficult (as it never happened during the evolution of mammals.
On the other hand, pigs have 12 nipples, dogs have 6, and humans have 2. Pigs have 44 teeth, dogs have 42, and humans (the lucky ones) have 32. This, I guess, means that it is easy to change the number of teeth in a species, as this happened often during the evolution of mammals.
My question is this: What is the reason behind this discrepancy? Why is it that much easier to change one thing and not the other? And a subquestion: why do we still have 32 teeth when the 4 wisdom teeth cause nothing but trouble? Wouldn't having only 28 teeth be an evolutionary advantage?

The number of fingers is not really same for all mammals: See this picture. It shows limb bones of some even-toed ungulates. And whales have totally lost the hindlimb. So your presupposition is not correct.

The genes, and the complexity of the genetic networks, underlying each trait are not necessarily the same.


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New ORFs occurring in SARS-CoV-2 due to mutations
Are there examples of new ORFs in SARS-CoV-2 created by mutations?
The ORFs should not be present in the reference virus, but they should occur in a lineage occurring in the wild (at best, being part of the definition of the lineage). Of course those ORFs will somehow overlap with the well-known ORFs of the virus, potentially frame-shifted.
Bonus: Is there evidence that a protein is produced from the newly emerged ORF?

Not a new ORF but new or increased occurence of non-canonical subgenomic mRNA https://virological.org/t/genomic-gymnastics-in-the-nucleocapsid-gene-of-sars-cov-2-during-transmission-in-humans-transposition-of-acgaac-and-creation-of-the-novel-n2-gene/715 confirmed in raw sequencing data https://www.biorxiv.org/content/10.1101/2021.03.02.433156v2

There is surely better but

A few sequences have G881T which extends MKIFKKTGTLNIAVVLPVNSCVSLTEGHTLAMSITTSVALMATLLSALKTF
to  MKIFKKTGTLNIAVVLPVNSCVSLTEGHTLAMSITTSVALMATLLSALKTFYHVLVKLHALCPNNWTLLTLRGVYTAAVNMSMKLLGTRNVLKRAMNCRHLLKLNWQRNLTPSMGNVQILYFP in frame -1 at the beginning of ORF1a.

A few sequences sequences have A2182G which extends MKNSNPSLIGLKRSLRKV to MKNSNPSLIGLKRSLRKVWSFLETVGKLLNLSQPVLVKLSVDKLSPVQRKLRRVFRHSLSL in frame +1 in ORF1a

An so on, in fact most "stop codons" in alternative frames seem to be mutated in some sequences. Of course most of those "new ORF" are probably not detectably translated. Introduction of new TRS has more chance to produce new subgenomic mRNA whence translation of new proteins.

If you only consider the consensus sequence of each pango lineage then you'll probably won't find much convincing event of this kind, except for the introduction of TRS in N which did happen in B.1.1, P.1, B.1.1.7,
as well as a deletion causing the merging of ORF7b and ORF8 in B.1.1.318

The answer to this is both yes and no.
The reason I say yes and no is that SARS-CoV-2 exists as what is known as a quasispecies. Quasispecies are the population of virions that exist in an infection, with each separate virion containing a genome with its own mutations as a result of natural error rate of the RNA dependent RNA polymerase. When we sequence a virus and call the result its genome, what we are actually looking at is a consensus sequence, not the individual sequence of each virion that went into the sample from which the genome was derived.
Now, the problem with a quasispecies is that not all the virions produced in an infection are actually viable and can go on to produce more virions. In some cases there will be defective genomes, some more will have defective capsids or defective packaging of the genome and so on. These together make up a series of defective particles with a range of different terms depending on how they behave in an infectious process.
In many cases there are defective interfering particles, which miss parts of the genome or have genomes that are otherwise defective but are capable of infecting cells, but not capable of producing infectious particles themselves, and can compete with functional particles for infection (hence the interfering part).
In some of these described particles and within the sphere of the quasispecies will be virions that contain new ORFs. How those ORFs behave in an infection is very difficult to say as they are very hard to study. In most cases these new ORFs will cause a failure of some other (already) critical function and produce non-viable virions, but without examining any potential new ORF functionally in a lab we can't be certain that a potential new ORF does anything or indeed what the product might do.
For an estimate of the coding capacity of SARS-CoV-2, you can look at this study (1), published in Nature, which revealed that there probably are unknown ORFs within the virus. However, I suspect that these were there already and are not newly evolved as such, just newly identified.

Finkel et al., Nature  589, pages 125–130 (2021)

I don't really see how it is related to the question. Please take a look at the ORF8 deletions in SARS, in particular the 29nt deletion present in the main epidemic strain but not in some earlier strains, causing a much shorter ORF8 protein, named ORF8a, and a new ORF8b ORF overlapping the end of ORF8a in a different frame. In the early strain https://www.ncbi.nlm.nih.gov/nuccore/AY390556.1 the long ORF8 is called ORF10-11 and in the epidemic strain https://www.ncbi.nlm.nih.gov/nuccore/NC_004718.3?report=genbank there is ORF8a and ORF8b

@reuns - Why don't you post that as an answer yourself. The reason I posted this is because they genuinely do produce new putative ORFs all the time because of the quasispecies thing. However, a new ORF does not necessarily produce a functional protein or may alter the function (e.g. decrease expression) of a functional ORF, so you end up with non-functional or less functional particles that don't lead to anywhere in evolution terms.

@reuns ORF8a/b was identified in SARS-CoV (the original one) so I don't think this is a new thing at all for CoV-2, which is what the question was about.

I appreciate this answer although I hadn't really asked for it, because it broadens my view on the virus genome of SARS-CoV-2. I am still interested in more answers, describing situations for SARS-CoV-2 like the one exemplified by @reuns' comment for the original SARS virus.

Right now, there is a new preprint by Harriet Mears et al. on biorXiv with interesting new ORFs in SARS-CoV2 opened by some mutations.

The mutation N:R203K N:G204R found in pango lineage B.1.1 creates a transcription regulatory sequence (TRS-B) that triggers the expression of a proteine starting with N:M210 to the end of N. This proteine acts as an interferon antagonist. This ORF is named N:iORF3 by the authors.

Other mutations create new ORFs in nsp16 (coded by ORF1ab) and in the Spike gene.

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Why is there extreme itching when we touch a hairy caterpillar? What are ways to stop itching?
I mean there are lot of caterpillars or hairy caterpillars to be more precise when we touch those hairs we get extreme itching on that area i want to know why we got that itching? Ok i know that it must be some chemicals but which? And if one has got itching how to remove it?

Google search caterpillar sting, the hairs themselves cause itching. http://www.wikihow.com/Treat-a-Caterpillar-Sting

how to remove it? makes your question more of either a medical question (should be asked on health.SE) or a life hacks question (should be asked on lifeHacks.SE).


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Why does our hair turn white before we get old?
White hairs are considered a sign of old age, but they often occur in young boys. I want to ask why my hair is turning white? And why black hair turns white?

Human hair color depends mostly on two pigments: eumelanin and pheomelanin. Eumelanin has brown and black variants, whereas pheomelanin is reddish/orange. Cells at the base of hair follicles produce those pigments and white hair is simply lack of those pigments. There may be many reasons why your hair is turning white at a young age:

melanocyte stem cell damage at the base of the follicles
vitamin B12 deficiency
problems with the thyroid
deficiency of catalase as in vitiligo (hydrogen peroxide would then accumulate and impair pigment production)

But most of the cases are purely genetic and you should not be worried if you are certain your B12 levels and thyroid are OK. Here's an article on that topic: https://www.ncbi.nlm.nih.gov/pubmed/23974581
There's also quite a bit of information on white hair on Wikipedia: https://en.wikipedia.org/wiki/Human_hair_color#cite_note-18
(sections Grey and white hair and Aging and achromotrichia)
Cheers!


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Can someone help me with this Pedigree Analysis?
$\text{So... here is the given pedigree chart:}$

My question is ... whether this is an autosomal or a X-linked recessive trait.

The book I was following gave me this info:

My Attempt:
Looking at the chart ... it all comes down to either X-linked recessive or Autosomal recessive.
According to Rule 1. under these conditions:

If it appears with equal frequency in both Males and Females -- Autosomal
Otherwise , if more male than female -- X-linked

But my teacher said ... "its not always so"

So.... I tried with both once (brute force method ... going through all possibilities) and I could not understand which one...
It seems both are correct (which obviously is not possible)
So can anyone please help me with this problem!?
Thanks!

Are squares males and circle females?

It is both possible that the trait is x-linked recessive and autosomal recessive. If autosomal recessive, that would require individual 12 to be heterozygous though.

@Remi.b Yes ... and the darkened ones are the affected ones

The rule is you have to see 1st if the pedigree obeys Y-liked inheritance, if not then whether dominant/recessive. Once you figure out that (say it turned out to be recessive) see if it obeys X-linked or not. If it does the pedigree shows X-lined(recessive) trait. If it doesn't then it is autosomal and applying the genotypes you'll see there's no conflict and it obeys Autosomal inheritance for sure. The list of characters they are not always true for all pedigree charts, you'll find some matching while others may not.

I would suggest you to consult your teacher because it is next to impossible to explain in a written Q&A format. Besides there are a number of ways this is taught, learning from more than one source will actually confuse you.

Looking through the table you provided, X-linked recessive trait seems the most plausible, since almost all of the conditions are precisely fulfilled. The only one that seems to challenge this conclusion is number 4: "is never passed from father to son". This is tricky because of the relationship between no. 4 and no. 7. However, this doesn't necessarily rules out X-linked recessive, since it is possible that no. 7's mother (no. 3) is a carrier and no. 7 got a defective X chromosome from her. We don't have her history, but this is possible and makes X-linked recessive a plausible option.

With the currently given information both autosomal and X-linked recessive is possible:
(WARNING extremely sloppy Paint editing ahead)
This is a possible scenario for an autosomal recessive trait:

And this is one for a X-linked trait:

Ideally you would extend the chart until you encounter a scenario where an affected female has healthy male offspring (which indicates an autosomal trait).

For both autosomal and X-linked recessive, we must make the assumption that 3 is heterozygous. The genotype of 1 shouldn't matter in either case, and is most likely homozygous.

Oops you are absolutely right

Thanks for your comment on my answer. You're absolutely right and, actually, the entire answer is now wrong.

@canadianer I suppose X-linked might still be slightly more likely as autosomal assumes subject 12 to be a heterozygous outsider.


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Does ingestion of alcohol with methylphenidate make it act more like dexmethylphenidate?
Methylphenidate (MPH) is a dopamine and norepinephrine reuptake inhibitor. It is the racemic mixture of d-MPH and l-MPH. According to the binding profile info on Wikipedia, based on studies, it is at least 6 times more potent at inhibiting the dopamine transporter (DAT) than the norepinephrine transporter (NET).
The dextrorotatory enantiomer, d-MPH, is said to be the main responsible for the therapeutic response of methylphenidate, and to be "much more bioavailable than levomethylphenidate when administered orally" (this paper from 1999 is given as reference). I read it "can be anticipated to be twice the strenght of the racemic product". One distinct property of d-MPH is that it is much less selective for DAT inhibition as opposed to dl-MPH - in fact, it is a bit more potent at inhibiting the NET (at a ratio of about 1.2 - 1.3) compared to the DAT).
The way I see it, this may have clinical significance since dopamine reuptake in the prefrontal cortex is mainly carried by the NET, since DAT expression is significantly lower in this region of the brain [1] [2].
The Wikipedia article also states that "Coingestion of alcohol (ethanol) also increases the blood plasma levels of d-methylphenidate by up to 40%". It references this study from 2011.
What I want to know is: Does that all mean that the ingestion of alcohol, when taking (racemic) methylphenidate can actually make it more potent, at least at lower doses?
Of course, alcohol has an increased activity effect on GABA receptors, which complicates things.
Thanks

Does the ingestion of alcohol, when taking (racemic) methylphenidate can actually make it more potent?
It is the 2011 study you've mentioned that answers most of the question.
In the study, ethanol co-ingestion with racemic MPH elevated maximal plasma levels of d-MPH by up to 40%. The participants reported greater stimulant effect after alcohol + MPH than after MPH alone (Table 2).
Now, the completely different question is if such combination of alco + MPH is also beneficial and safe.
Also:

MPH–ethanol coabuse has been widely reported in both annual Drug Abuse
  Warning Network data and the clinical literature.

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What are the chemicals present in body of paddle worm which makes it show biolumniscence
Paddle worm is the light emitting species i want to know that
1. What are the chemicals which produce this light?
2. For what purpose it needs this light?

Thanks charles but Can you please elaborate


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Hardy Weinberg Explanation
I am able to calculate frequencies for allele and genotype, but I don't understand how to tell if the population is at equilibrium. Or how to determine how many generations of random mating would be needed to reach HW equilibrium. I thought the proportions didn't change from generation to generation?
number of individuals: TT-200, Tc-200, cc-600
observed frequencies : TT-0.2, Tc-0.2, cc-0.6
HW frequencies       : TT-0.05, Tc-0.35, cc-0.60
p=.33, q=.77

The answer is logical if you understand the reasoning behind Hardy-Weinberg. I recommend that you to have a look at the post Solving Hardy Weinberg problems and try to answer the question yourself. Once you've done that, you can hover over the yellow zone below for the answer to compare against what you've understood.
The answer:

 If the assumptions of Hardy-Weinberg are respected (see Assumptions of Hardy-Weinberg rule), incl. random mating, then a population is back to Hardy-Weinberg equilibrium at the beginning of any single generation. H-W equilibrium is directly caused by the random sampling of gametes. This random sampling is happening at every single generation and therefore a single generation is enough to get back to H-W equilibrium.


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How not to kill a spider while moving out of my flat?
About two weeks ago, when it started getting cold, a house spider (tegenaria domestica I believe) has chosen my flat for spending the winter. I like those spiders so it's not a problem for me. Only problem is, two weeks from now, I'm moving out. I don't know anyone around here who would want to take the spider in.
Would the spider die if I move it back outside now ? In the morning it's around 10°C / 50°F
Since I got a liking to the little guy, is it reasonable to try to take it with me ? There's going to be 5 days between moving out and moving in the new flat, if I go down this road how should I take care of it during those few days ?
What should I do to have the least chances to accidentally kill it ?
Thank you very much

It looks like the standard tegenaria domestica, I'll try to catch a pic this evening but it runs fast.


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How to tell the difference between mould and condensed milk and sugar
I have had sweetened condensed milk in the refrigerator for some weeks (or months perhaps?). The can was covered with aluminium foil.
I noticed some disk-like artefacts on its surface, which are harder then the rest of the product:

Full-sized photo
How can I know if this is mould or simply further condensed milk with sugar? Is this safe to eat?
If it is relevant: the content of sugar is 56 g per 100 g, while this product has 8 % of fat content.

You could try picking up a piece and putting on top of a slice of bread or some other nutrient in a sealable bag  and leave it on a counter overnight and see if it grows?

@Cell, that's a good idea, thanks!


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Why are large amounts of DNA required for analysis?
I know PCR is used to create large amounts of copies of genes and that it's a scientific breakthrough but want to understand why. Why do we need large amounts of DNA to be able to analyse it, to utilise it. Isn't a single DNA molecule enough?

Firstly, A DNA sample obtained from a cell or whatever is never going to contain just the DNA sequence you want but will instead contain the entire genomic DNA, plasmids, RNA sequences and whatnot. By using PCR you can selectively multiply the amount of desired DNA sequence while the undesired sequences do not get copied. Keep the PCR going long enough and the amount of undesirable DNA versus the desired DNA sequence is going to become negligible. At that point you can do whatever experiment you want with your DNA sample and be reasonably sure that whatever result you get is caused entirely by your DNA sequence of interest.
Secondly, even if you could isolate a single DNA molecule what would you do with it? You couldn't determine its length by gel electrophoresis as a single DNA molecule wouldn't make a visible band and building it into a plasmid will most likely fail as you only get 1 chance. You probably wouldn't even be able to tell you had a DNA molecule as machines in your everyday lab aren't sensitive enough to detect a single DNA molecule.
Thirdly, having a large quantity of DNA allows you to perform different experiments from the same sample. Most DNA analysis methods I know of are destructive in that the DNA used cannot be reused for another experiment, so a large enough quantity of DNA to perform all planned experiments without having to obtain a new sample (and introduce all kinds of potential problems) is useful.
So, in summary, PCR allows us to filter the desired DNA sequence from a sample, perform meaningful analysis on this sequence and lets us use one sample for multiple experiments. There might be even more advantages to PCR that I have missed but these the ones that sprung to mind.

Many of the methods used to visualize the presence of DNA, such as gel electrophoresis, rely on visual analysis whether by human eye or machine. A significant amount of DNA beyond what might be extracted directly from a particular source is required for this. This need is exercerbated by the fact that the DNA is typically broken down into fragments for analysis.
Scroll near the bottom of this link to see an example of a gel.
https://en.wikipedia.org/wiki/Gel_electrophoresis


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Can translocation occur within a gene?
I know genes can be translocated between chromosomes but can nucleotide sequences be moved around within an individual gene?
Could the following gene:
MEN SAW OLD HEN
Become:
MSA WOL DHE NEN
By moving the EN at the beginning to the end?


text:
How do tapeworms aid weightloss?
The 5 second answer people come up with is, "well they consume calories you otherwise would have". This logic works great if we're discussing the impact of my brother consuming part of my meal but it does not however in this case. The speaker seems to have forgotten that the tapeworm resides inside of you. Any calories which aren't incorporated into your tissues are instead incorporated into the tapeworms tissues. Since the tapeworm is inside of you, your weight measured externally (i.e. including the tapeworms weight) still increases.
Analogizing again to my brother: there would be no difference in my final weight gain if a) I ate dinner and then my brother or b) my brother ate my dinner and then I ate my brother : ).
So, what is the explanation for why tapeworms lead to weight decrease?

Your question presupposes that they do help with weight loss (as opposed to being a folk-tail or quackery with no evidentiary backing). They are know, among other things, to increase appetite and weight-gain in many sufferers. Can you link to any study which supports your underlying assumption?

Tapeworms are parasites that live in the gut and absorb food. They lead to weight decrease because they reduce the amount of food that can be absorbed by the body. Tapeworms also cause malabsorption, which is when nutrients from food are not properly absorbed by the body. This can lead to deficiencies in essential vitamins and minerals, which can also cause weight loss.


text:
Where can I find these frequencies for several species?
Where can I find frequencies of nucleotides in the DNA for several species?

You mean the specific AT/GC content?

Assuming you mean AT/GC content, then this page wikipedia offers a table and links.

Since most of the genomes consist of double helix DNA, the only meaningful ratio is GC-content. A comprehensive list of the known genomes that includes GC-content data is available at NCBI (note that default Overview tab doesn't contain the GC-content numbers, you need to select another tab, e.g. Prokaryotes). They also provide an FTP access to the raw data, if you need to process the numbers with software.
If you're interested in particular genomes that are not present in this list, you can calculate all frequencies from the sequence. There are a number of programs to do this. For sequences in FASTA format you even don't need a special software, the analysis can be performed with standard tools, e.g. grep (should be installed in Linux/BSD/MacOSX, obtainable for other systems):
grep -v '^>' sequence.fasta | grep -o '[ATGCatgc]' > tmp
# number of AT pairs
grep -c '[ATat]' tmp
# number of GC pairs
grep -c '[GCgc]' tmp


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Do we understand how (some) proteins work?
Are there proteins whose operation we can describe from first principles using chemistry or physics?
I've had introductory college courses in biology, and some classes in neuroscience, so I know that the behavior or purpose of many proteins is well characterized. But the descriptions of how proteins work—at least in what I've read—are always sort of similar and vague, “X binds to Y and the shape of the protein changes, which does Z”. At the level of the material I'm reading, I wouldn't necessarily expect much more, but I am curious whether researchers actually have a more detailed understanding of how proteins work. Can we describe the way that (some) proteins work in the same way that an engineer can describe how an internal combustion engine works?

That depends strongly on the resolution scale you want to look at. How ribosomes work (a classical example for a molecular machinery) is pretty well understood, though surely not the binding partners for each and every amino acid in these huge complexes is known.

Ribosomes aren't really proteins, but yes we do understand how some individual proteins work, the problem is that the interactions of charge , shape,and bonding on each amino acid interact with each other so the larger the proteins the more difficult it is to understand all of the layered interactions. that's why de novo protein design is so difficult and why even simple design needs computers. If you want to learn more "Protein structure prediction"  or "Bioinformatics" are good search terms. Or you can get started here, https://www.expasy.org/proteomics

Yes. Hemoglobin is a very well studied example.

Yes. For a number of proteins, including certain classes of enzymes, we have a very good biochemical idea of how the reaction catalysis works - the metal catalyst ion binds to these amino acids here, the substrate binds to these other residues like so, and in doing so induces a conformational change bringing the catalytic ion and a water molecule in close proximity to the substrate, where X chemical reaction takes place, then the substrate is released and the reaction center is recharged likewise.


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Does a virus that spreads more rapidly have less chance to evolve?
Now that the COVID-19 pandemic has been going on for a while, there are reports of many new variants, which have presumably arisen in the past year through mutation and spread through natural selection.
I'll assume that the outcomes of COVID-19 infection are either death or a successful immuse , others would have developed antibodies. Suppose for the purposes of discussion that those are the two end consequences (or correct my answer in your thinking.)
If eighteen months ago, everyone in the planet had been infected with COVID-19 in one very bad day, then many people would die, and the others would end up with antibodies. That might stop the spread of the disease, which would stop its evolution. (Feel free to address Typhoid Mary-like scenarios in the answer; or of course any misconceptions in this paragraph.)
Is there a perspective from which—or set of circumstances under which—drawing out a pandemic can actually worsen the effect of a disease by giving it more chance to evolve?
(I've put the question in terms of COVID-19, but I think it's really a generally question, no less applicable to COVID-20 and above. :-) Please feel free to answer in general terms. I am not looking for a discussion about what public health measures may or not be appropriate to the current pandemic.)

Just guessing: if it has 10 generations of reproduction in your cells rather than 100, i.e. it gestates longer before transmittal, that's a factor... however it could reproduce 100 times in 2 days or 10 times in 3 days. As the other answers state, the virus also has an independent mutation rate per division, so that's 2 only half related factors, plus theres lots of others.

Any evolutionary process has two components to it:

generation of genetic diversity in a population, and
shifts in the distribution of genetic variants under selective pressure.

For a virus like SARS-CoV-2, every infection results in a vast amount of replication, some of which will be variants generated through imperfect replication. Thus, the more rapidly a virus is spreading, the more opportunity it has to generate genetic diversity. Conversely, if there's not many infections going on, then there won't be much evolution because there won't be much diversity generation.
With regards to selection, the more actions that we take against the virus (e.g., mask wearing, social distancing, vaccination), the more selective pressure that it is under, since these actions differentiate between strains that are more or less effective in evading them. If the pressure goes too high, however, this breaks down. With highly effective countermeasures (e.g., rapid vaccine distribution while not letting our guard down), then there won't be much evolution because most variants won't have an opportunity to infect any new host: each new generation of infections will be driven more by countermeasure failures unrelated to viral efficacy, and thus there will actually be little effective selection.
The highest opportunity for evolutionary change, then, is with poorly coordinated countermeasures. This produces an intermediate rate of spreading, with both much viral replication and many opportunities for selective pressure on infections.  It's really much the same as the problem with stopping a course of antibiotics prematurely, only on a societal rather than individual scale.
Bottom line: countermeasures are still a good idea, even when potential evolution of variants is included. People and governments that don't take the problem seriously, however, are threats to all the rest of us.

So a virus that spreads more rapidly has higher population and therefore higher chance of mutations, and also more variable habitats. also perhaps less gestation mutations.

RNA viruses, like SARS-CoV-2, influenza, HIV, etc all have high mutation rates caused by an error-prone RNA replicating protein (known as an RNA dependent RNA polymerase or RdRP) that they use to reproduce their RNA genetic component. The error rates are high enough in these viruses that you can say that the virus exists not as a single species, but as something known as a quasi-species, which you can visualize as a cloud of individual virions, each with genetic variants from the "original" genome, some of which will be more "fit" than others in terms of evolution. These more fit ones are the variants that you see being talked about in the news.  Note that the error rate of the RdRP is in terms of base changes per 1000 bases per 1 replication cycle, and the number is usually around 3-4.
The fitness of a virus is not necessarily related to any one variant, often a number of seemingly unrelated mutations in several proteins are required to make it fitter in any of the following characteristics:

Evading immune response
transmission
Invasion of the host/infectivity
viral titre (how many viral particles are produced)
replication rate
host-range (what species it can infect)
Tissues it can infect

Often, being better at one of these features means that it does poorly in others. A fine example of this is the H5N1 influenza that raged across the world a few years ago - it was great at killing people and even better at killing birds (it is an avian virus), but it was terrible at actually infecting people, it just couldn't sustain transmission in humans and even those exposed on a regular basis (i.e. working with chickens in endemic virus areas) didn't often get infected, even if they seroconverted.
SARS-CoV-2 has hit a pretty sweet-spot, it can transmit really well, it is highly infectious, has a fairly broad host-range, and has a long lag-time (~2 weeks) before people know they are infected, and some never do show symptoms. On the other hand, in some people it isn't at all great at evading the immune system, it actually seems to potentiate it, causing something known as a cytokine storm, where the immune system goes into hyperdrive and causes serious inflammation. This is what actually kills people - the swelling of their airways in response to the infection limits oxygen transport and slowly suffocates them.
Now, you talked about antibodies: Antibodies are not the be-all and end-all like they are often considered. An antibody response to an infection does not necessarily mean that you can not get an infection from it again, it simply means that the infection is minimized to some extent. The extent of the protection is highly dependent on the individual (i.e. your response will be different to mine), and on the organism with which you are infected. If you had say Smallpox and survived, you (and I too, if infected) would likely have a life-long immunity to smallpox. However, have an infection with a different pox virus, such as Orf virus, and you might only be protected for 6 months.
You, yourself (assuming you are >10 years old) and everyone around you is likely to have antibodies against at least 1 of the influenza viruses, but this won't stop you from getting sick from them again, it might however limit your infection so that you don't feel so bad for as long (and can then spread it more effectively...). So you have antibodies, but they don't eliminate the flu, and as a consequence we have a vaccine against influenza. Now the vaccine also doesn't cause complete protection, but that's beside the point. The reason you need to get an influenza vaccine each year is because the viruses have mutated over that year so that they are no longer the same as the previous year's flu viruses, so your body doesn't fully protect against the new viruses.
In the case of the SARS-CoV-2 vaccines being distributed currently world-wide. If you have been following the data, even in a fairly superficial manner, you will have seen something like "the Pfizer vaccine has a 95% protection rate" this means that it protects against 95% of illness from SARS-CoV-2 (i.e. symptomatic infection and actual infection in 95% of people). However, you might have also heard about people being concerned that there is less protection against the "South African" variant. This is an example of evolution causing an escape mutant. Evolutionary pressure has been applied to the virus, and it has produced a means to get around that pressure, to some extent. This will be an on-going process in terms of SARS-CoV-2; we will need new vaccines regularly to cope with the new variants as they arise.
TLDR: the virus will evolve anyway, the evolution happens in as little as a single cycle of virus replication.

Notes that influenza is actually much more complicated case that is not just based on mutation, due to its segmented genome.

@jakebeal yes, assuming genetic drift not shift. Genetic drift is the major component to needing a new vaccine... source: me who used to work at a WHO collaborating center for influenza research...

Are there models which could indicate the increase in variance due to systemic pressure (vaccines being applied to the population at a certain rate without a 100% coverage over time)? Or, could the hypothesis hold that given the slow rate of vaccination in densely populated areas, the evolutionary pressure in selection increases fitness rate and overall rate of variations in the virus? Any references besides adjusted SIR models with time-varying I and R0 rates, or modifications to  Fisher's fundamental theorem of natural selection?

@Moreaki - no idea. I would guess, not being an evolutionary biologist, that the standard models will apply.


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If excess sodium is bad for humans, why don't our bodies just remove it?
This is one of those questions where I realized two everyday facts don't connect for me. Excessive sodium in the diet is supposed to be bad for us. But surely our bodies have mechanisms for getting rid of excess sodium. (I don't know the details, but I know enough about neurons to know that our cells can move sodium when they need to.) Why don't our bodies just keep our sodium levels at a healthy level?

Are you talking about the long or short term effects of excess sodium?

I was thinking about blood pressure and stuff like that, but if the answer would be different for different conditions, that would be interesting too.

Because evolution doesn't care about what's good or bad, just about what lets organisms pass on their genes.  The bad effects of things like high blood pressure usually don't show up until long after most people have done their gene-passing.


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Is there any (practical) way to control a rodent population without predators?
It seems that New York has tried a number of ways to reduce their rat population, recently with fall traps. Unless they can kill all of the rats at once, it seems that this will just free up resources for the surviving rats to use. A feral cat population (which would increase in response to its food resource, i.e., the rats) seems to be the best way to control this. From an ecological perspective, are there alternatives to controlling a population of rodents, apart from using predators?

While your question is interesting, it is asking for opinions. Moreover, answer to this question would not be straightforward and require a lot of details and explanations and thus making it unsuitable for the stackexchange Q&A format. Perhaps you can search for some reviews on this topic.

There has been talk of controlling mosquito populations with CRISPR and gene drives. You can read about it from Nature (https://www.nature.com/articles/d41586-019-02087-5). In the future this may be possible for rodents.


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API for gene names by location
Is there any API where I can input chromosome location and it will provide us gene names, for example input chr: 1 location 154714693:154754070 and it will return a list of gene names or ID within this region?

Do you just want the gene names?  BioPython will allow you to subset a Genbank sequence, complete with all the features if you specify a start and end coordinate, but this is only useful if you want more than the name.

The NCBI as an API called 'E-utilities' (see short intro) that allows access to almost all their databases. It's a bit tricky to get used to it (and sometimes it wants stupid - even discontinued - identifiers as input), but has a lot of power, there are libraries for this in biopython & bioperl (I think), R might have one too. It's possible to exactly the kind of search you want with the 'efetch' method and rettype 'feature table' (or maybe the full xml record) as well as seq start and stop (you need to have the accession of the chromsome one sequence as a qurey ID).
Another thing I have used are genome annotation tables from NCBI. They are on the FTP server (where the structure is apparently in constant flux, so it's again hard to find), but they list all annotations of a given genome assembly and are sorted by position, so you can easily search them with a script - if you are looking for multiple positions this may well be faster then going through an online API (This folder seems to have multiple files, if you want to take a look at it).

You can use the Ensembl REST API. This is how to do overlap queries:
https://rest.ensembl.org/documentation/info/overlap_region
Your example query:
https://rest.ensembl.org/overlap/region/human/1:154714693:154754070?feature=gene;content-type=application/json


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What happens in lasik operation?
First of all,I am very bad at biology. So please bear if it sounds elementary.
I heard about lasik operation for reshaping cornea.
Assume the patient is suffering from myopia implying lens is thicker than expected.So if i think logically ,to correct the lens thickness ,lens must be reduced.
In lasik, do they cut the lens's tissue.If yes what happens to the part that is cut and if no then how exactly lens thickness is reduced?

There are two possible ways to perform refractive operation: first,  to perform the procedure on the cornea, the second - to exchange the crystalline lens with the artificial one.
The second approach is extremely rare, because the lens (1) is inside the eye and (2) it allows us to accommodate (=change the focus of vision). Thus, this method is relevant only to extremely high myops and people who have some degree of cataract (the clouding of the lens).
In "classic" myopia the eye is larger than "normal" one, and the lens thickness is less relevant in the terms of treatment.
Back to LASIK - the operation is performed on the cornea: for myopic eye the corneal thickness should be reduced, for hyperopic eye there are other protocols (special thickness reduction).


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Endothermy in different species
Birds and mammals are both endothermic, meaning they metabolically generate the heat they need to keep their body within a certain temperature ranger.
But birds are closer relatives to reptiles than they are to mammals, and reptiles are not endothermic. Thus birds and mammals developed endothermy independently; and here is the question:
How does thermal regulation differ in birds and mammals?

This question is not too broad and deserves no close votes for that reason in my opinion.

This is in between a comment and an answer...
Notes

reptiles can have several definitions. Some of them causing birds to be a reptile.
You probably meant "evolved" instead of "developed".
Thermoregulation is performed by a set of different mechanisms and it is plausible that your question would be considered as too broad. Note however that I am NOT a physiologist and might overestimate the scope of the question.

Similitudes between birds and mammals
From wikipedia (here)

In cold environments, birds and mammals employ the following adaptations and strategies to minimize heat loss:

Using small smooth muscles (arrector pili in mammals), which are attached to feather or hair shafts; this distorts the surface of the skin making feather/hair shaft stand erect (called goose bumps or pimples) which slows the movement of air across the skin and minimizes heat loss.
Increasing body size to more easily maintain core body temperature (warm-blooded animals in cold climates tend to be larger than similar species in warmer climates (see Bergmann's Rule))
Having the ability to store energy as fat for metabolism
Have shortened extremities
Have countercurrent blood flow in extremities - this is where the warm arterial blood travelling to the limb passes the cooler venous blood from the limb and heat is exchanged warming the venous blood and cooling the arterial (e.g., Arctic wolf[3] or penguins[4][5])

In warm environments, birds and mammals employ the following adaptations and strategies to maximize heat loss:
Behavioural adaptations like living in burrows during the day and being nocturnal

Evaporative cooling by perspiration and panting
Storing fat reserves in one place (e.g., camel's hump) to avoid its insulating effect
Elongated, often vascularized extremities to conduct body heat to the air


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Fire Ant Behavior
I've noticed for the past few weeks that near a small fire ant nest near my house there will be a new concentrated "large" pile of dead fire ants every few days. I went and checked out the pile and noticed that one ant in the pile was very slowly moving so I moved it in front of a nearby ant to see if it would take it back to the pile. The ant immediately picked up the slowly moving ant and took it back to the nest, passing right through the dead pile I might add. I'm curious what would invoke this type of behavior among the ants. I'm also curious if fire ants dispose of all of their dead this way.

This might be a duplicate of Do insects respond to the detection of dead insects?

Although similar, this question asks about returning the live ant back to the nest rather than back to the "dead pile." The behavior might still be related to necromones.

I'm sure there is a more detailed answer out there, but ants identify the dead ones by smell.

@fileunderwater The question does help and I find the answers quite interesting but it still doesn't quite explain the the second part of the question. Thank you though.

They do! It's called necrophoresis, and it's a way of keeping infections from spreading. A paper published in 2009 suggest that ants constantly produce "I'm alive" chemicals while they're alive; once they die, the chemical is no longer produced and the ants are carted off.


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Within and Between Allelic Class Diversity
I am reading Charlesworth et al. 1997. They talk about diversity within and between allelic classes.

Nucleotide diversities ($π$) at each neutral site were estimated from the mean of $2 \sum z_t (1-z_t)$, over replicated introductions at the site of single variants, where zt is the frequency of the neutral variant at time t, and summation is over all times until either fixation or loss occurs.
The total genetic diversity at the neutral sites ($π_T$) was also decomposed into that within and between allelic classes at the polymorphic locus. Diversity within allelic classes, which will be written here as $π_A$, was estimated from the mean of $2 \sum \left( x_t(1-x_t)+y_t)(1-y_t) \right)$ where $x_t$ and $y_t$ are the frequencies of the neutral variant within the first and second allelic classes, respectively. Diversity between allelic classes with respect to the polymorphic locus was calculated as the difference between the total diversity values and $π_A$

Note that the parentheses don't match up but this this is what is written in the paper!
Why am I confused about this text?
I am confused about the term allelic class. I first think there is anything fancy in here and I think we can simply replace the term "allelic class" by "allele". but then when I saw the equation for $\pi_A$ I realize that the frequency of the two allelic classes does not necessarily adds to 1 (even though we consider only two allelic classes).
I also got also a little confused about the difference between $\pi$ and $\pi_T$ but I think that they just used two notations for the same think ($\pi = \pi_T$)
In population genetics's jargon, diversity just mean expected heterozygosity. $\pi_T$ makes sense to me. It is just the average heterozygosity $\left(2 z(1-z)\right)$ calculated over all time steps. Maybe a more intuitive to put it would to integrate rather than summing over time rather than time steps.
Question
I can read the equation for $\pi_A$ but I fail to get any intuition behind what it means. For example, I have no idea why it should be called within-allelic class diversity. Where does $2(x(1-x)+y)(1-y)$ come from? My whole issue might boil down to the definition of allelic class.
EDIT
The term allelic class is defined in Innan and Tajima (1997)

Suppose that there are two nucleotides, say A and T, in a particular site. Then, we can divide DNA sequences into two classes: one class includes sequences with A and the other includes sequences with T in this site. We call such a class an allelic class

(Slatkin 1996 might help as well).
I am still not quite sure what the within allelic class variance. Maybe it is: Take the most common sequence in the considered allelic class. For each, sequence, calculate the number of pairwise differences to the most common sequence and square this value. Sum over all sequence and divide by the number of sequences. In math form it would be: $\frac{1}{2N}\sum_i^{2N} (D_i)^2$, where $N$ is the population size and $D_i$ is the number of pairwise difference between the sequence $i$ and the most common sequence in the considered allelic class. Does it sound right to you?

@AMR I deleted my long list of comments...

From the way I have read what you have written z(1-z) translated into a sentence would be the frequency of the neutral variant (z) times the frequency of all other possible variants (1 - z) at the particular time t.
Nucleotide diversity is then the average of 2 times the sum of all of the frequencies of neutral variants (z) times the the frequency of all other possible variants (1-z) for all of the time periods until either there is no longer a change in the sequence or the allele is lost (which can happen over evolutionary time, especially if the allelic class is a deleterious variant, or the heterozygous allele provides enough expression to mask).
To me, this sounds like the result will be the probability of the neutral variant existing over time, which should be a number between 0 and 1. If z was 1, that would imply that the neutral variant is always the case, so the frequency of other variants is 0 making 2* 1(1-1) = 0 which makes sense to me as that would mean there is no nucleotide diversity. That sequence is always that sequence and so there is no sequence diversity.
As this looks like it is dealing with frequency distributions I think that total genetic diversity is implying the probability of all of the different allelic classes that make up an allele. So if you have class one which has the frequency  of x and a class two with a frequency of y it sounds like the overall diversity would be the probability of the neutral variant of x and the probability of the neutral variant y.
Generally, when you are looking at the probability of multiple events, you would multiply the probability of one event times the probability of the other event. As a result, I am inclined to say that the Nucleotide diversity within classes πA is 2 times the average of the sum of the frequency of x times the frequency of y, or 2∑ x(1-x)(1-y) + y(1-y) or factored 2∑ (x(1-x) + y)(1-y) or in words the Within Class Diversity (πA) is 2 times the average of the frequency of x as the neutral variant times the frequency of all other variants when x is the neutral variant times the frequency of all other variants when y is the neutral variant plus the frequency of y as the neutral variant times the frequency of all other variants when y is the neutral variant.
I think that the reason that this might be done is that, for reasons of selective pressure, x might be favored, so those times that the variant is y, some of those variants (possibly all of them) will be x, so by multiplying the within class diversity of x by the frequency of all of the variants when the class is y implies that there will be less diversity within class than if you just added the frequency probabilities together.
One thing I would do is to do a search to see if there was a correction published to this article, as there was a mistake in the formula. That might help to clarify. Also note, I could be wrong in my assessment as I do not have access to the actual paper you have referenced.
Best of luck in working this out.

when you are looking at the probability of multiple events, you would multiply the probability of one event times the probability of the other event. This is true if the events are independent, so P(X,Y)=P(X)P(Y). Otherwise, P(X,Y)=P(X|Y)P(Y)=P(Y|X)P(X).

@ddiez So which formula makes sense? Stats are not my strong suit and I was trying to work through the equation with Remi.b as it seems that there may have been a typo from the original article. Their formula did not have properly paired parentheses and is was difficult to determine whether it should be x(1-x) + y(1-y) or (x(1-x) + y)(1-y)? Thanks.

My comment is meant just as an extension to your statement, to note that the general formula is the later one (it is true in all situations) whereas the first one is only true under the assumption of independence. But that might be perfectly fine in this context (I haven't read the paper). Lets see the OP opinion on this.

The term allelic class is defined in Innan and Tajima (1997)

Suppose that there are two nucleotides, say A and T, in a particular site.Then, we can divideDNA sequences into two classes: one class includes sequences with A and the other includes sequences with T in this site. We call such a class an allelic class

Two elements that were misleading (for me at least) in the article

Implicitly, in the paper of interest (Charlesworth et al. 1997), they define allelic classes for a site that is known to be under selection (and that can only be bi-allelic). The concept of allelic class is not for a polymorphic neutral site they look at but always for the same site (the one under selection).
The formula has an extra parenthesis. The real formula should be $2 \sum x_t(1-x_t) + y_t(1-y_t)$.

What is $x$ and $y$?
Consider a polymorphic (bi-allelic) locus (that is not under selection) and calculate the frequency of one allele in the first allelic class (defined for the site under selection) (this is $x$) and calculate the frequency of the same allele in the other allelic class this is $y$. In other words, consider the selected has two alleles $A$ and $B$ and the neutral locus has two alleles $a$ and $b$. $x$ is the frequency of sequences containing $A$ that also contain $a$ and $y$ is the frequency of sequences containing $B$ that also contains $a$.
Meaning of the formula
The formula is just the sum of the expected heterozygosity within each allelic class. $$2x(1-x) + 2y(1-y) = 2 (x(1-x)+y(1-y))$$. Then, we just have to sum over all time step during which the neutral locus is polymorphic and we get $$\pi_A = \sum_{i=1}^T 2 (x_t(1-x_t) + y_t(1-y_t)) = 2 \sum x_t(1-x_t) + y_t(1-y_t)$$, where $x$ and $y$ are now function of the instant (time) considered and $T$ is the total number of time steps.
What values can $\pi_A$ take?
This measure takes values between 0 and $T$ as all $x_t$ and $y_t$ take values between $0$ and $1$ (and therefore $x(1-x)$ and $y(1-y)$ take values between 0 and 0.5). Dividing the whole thing by $T$ will result in a measure that is bound between 0 and 1.

I would have not been able to understand without the help of @AMR. Thank you


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Forward versus backward numerical simulations in population genetics
My question is closely related to this post.
There are a number of existing platforms to perform numerical individual-based simulation in populations genetics. An almost exhaustive list of such platforms can be found here.
Some program (like NEMO or SFS_CODE for example) perform forward simulations while some others (like SIMCOAL2 for example) perform backward (coalescence) simulations.
I am asking for a general comparison between those two methods.

Is one faster than the other? Why? (Intuitively I'd expect backward simulations to be faster).
Does backward simulation allow for simulating selection, recombination, gender-specific mutation rate, complex demography, etc..
Why/when would one use a backward/forward simulation model rather than the other type of model?

Your intuitions all seem correct. Coalescent simulation should be faster, because you don't track the entire population history over all t generations as you do in the forward simulation. Rather, as you work backwards in time you are tracking a smaller and small population. And with coalescent simulations it is probably very hard to incorporate the full range of evolutionary processes whereas doing so is more or less trivial with forward simulations.
A 2008 paper by Carvajal-Rodriguez reviews some of the issues in more detail that I have here.


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Are chromosomal and plasmid DNA in the nucleoid?
I know plasmid DNA is not part of the chromosome, according to my textbook, but can you still class it as being part of the nucleoid?
Also is chromosomal DNA in the nucleoid?

Please consider researching your question before making it into a post on Bio Stack Exchange for elementary concepts are considered off-topic until they are supported with prior research. See help


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Raw food diet digestion
I haven't really paid attention to the raw food diet and the claims of its supporters until now. A passage from this website says:

The basic premise behind preparing raw food is not to cook food above 118ºF. Cooking food denatures both the protein and the fats. So instead of your body using the food it simply stores it.”
  When food is cooked above 118ºF, 85% of the food's natural enzymes are destroyed. This forces your body to generate the enzymes necessary to digest the food. This results in partially digested foods that can clog the body's intestinal tract and arteries.

It's possible this passage, which is from a chef describing the main benefit of raw food diets, misquotes the chef or wasn't phrased properly. I am assuming that the chef is talking about plant-based foods, like vegetables and legumes, when she says food. But given what's here, I read this as:
'-When cooked food (food prepared above 118ºF) is eaten, denatured proteins and fats are not 'useful', other than fat (storage).
-Food has natural enzymes (and the speaker may be equating proteins and fats with enzymes?); they get destroyed by cooking.
-Digestion that occurs via the enzymes an eater creates are ... bad? Not as efficient as the enzymes that are 'naturally' in the food?
-Digestion via the enzymes that an eater produces lead to partial digestion.'
My shoddy recollection of biology class is that we produce saliva and related enzymes to break down food items we ingest, like a tomato cut from the vine. Those items will not produce enzymes within themselves that will aid digestion inside other animals that consume said tomato. Why would it?
My question is: do I have the wrong understanding of digestion? Should humans rely on the "natural enzymes" that are in uncooked plant food for digestion and good nutritional benefits?


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Is ivy (genus Hedera) a shrub or an herb?
It seems like the difference between a bush (shurb) and an herb is that a bush has a woody stem.
What does that make ivy (genus Hedera)? I know that ivy can get a pretty hard stem, does that count as woody? Is there something between a bush and an herb?

Woody plants are usually either trees, shrubs, or lianas. Ivies are lianas, they can have 40 years of woody growth rings and bark. The categories are flexible. It's an arbitrary division for convenience, it isn't that clear cut. Bamboos for example, are a woody grass.
https://weedwise.conservationdistrict.org/weeds/english-ivy#foobox-1/7/Untitled-4-copy.jpg
Does that count as a woody plant? yes it's a woody liana.

Wow, that is one impressive ivy stem. - Thanks for the info, it does seem like liana would be the category to place ivy in.

Cheers, villager. It's happened often that I chop through an ivy and that it takes a few minutes with a saw and I think "I can't believe how tough these darned ivies are!!!" they are so tough. it's so woody it's surprising, you'd think it was another vascular flesh than a tree... ivy is like a real tree inside.


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Lack of skin in a certain area of the body --- hypo[what]?
Lack of skin in a certain area of the body. How shell I name this?

Hypocutaneousis?
Hypo[somethingElse]?

What is the correct term?

Exactly what are you referring to? A permanent lack of skin in an area sounds like a permanantly open wound to me.

I mean to a partial lack of skin, like when someone has too little skin after bad surgery or after an accident (I'm not aware of diseases that will reduce the amount of three-layers skin).

First, this is not an area where I have any education or experience. However, out of curiosity I consulted google and found two genetic castle diseases that should be relevant to your question:

Epitheliogenesis imperfecta (vetbook.org)
Ectodermal dysplasia

Both diseases are very serious, and Epitheliogenesis imperfecta is fatal (due to infections).
I chose not to include any pictures of the diseases in this answer since they often look quite horrible, and some people might find them unsettling. If you click the links there are pictures of the conditions though.
A "similar" condition in humans might be  Epidermolysis bullosa, which is caused by decreased anchoring between dermis and epidermis, which cause a very fragile skin:

Epidermolysis bullosa (EB) is a group of mainly inherited connective tissue diseases that cause blisters in the skin and mucosal membranes, with an incidence of 20 per million newborns in the United States.[1] It is a result of a defect in anchoring between the epidermis and dermis, resulting in friction and skin fragility. Its severity ranges from mild to lethal.

(Wikipedia)

You can say skin atrophy or just thinning where dermal thickness is reduced.
https://m.iliveok.com/health/skin-atrophy_77524i15941.html

Thinness does not seem to be the same thing as the OP's question about lack of skin.

@kmm what can I say but the question is unclear but being a specialist physician for 40 years my answer is likely correct for most instances.


text:
What is the opposite of a mutation (the regular state)?
What is the term, if there is one, to describe the natural state of a gene? The one single word to describe it, just like mutation is the one single word do describe a deviation from that state.

If you brought this up and mentioned clearly that the two are not synonymous, what is it for Mutant? I'm asking for general knowledge.


text:
Identification of Unknown Insects found in landfill (tiny, full of hair on body)
Could someone help me to identify the following insect with full hair on body? They are very small, so I use macro lens to capture them. I have tried to capture them as clearly as possible.

They were collected from a closed section of Tseung Kwan O Landfill and Clear Water Bay Country Park of Hong Kong. This area is revegetated so the ecology is much like a country park just nearby the landfill.

They were found in natural setting, the site that is similar to forest with tree planted. While there are decaying matters deep down in the soil as the site was used as landfill previously, because the gas analysis shows that there is no gas leaking from decayed matter (methane, CO, H2S etc.) I am not sure if the environment flavour the growth of Dermestidae.

I agree with @prefectionist , they look like carpet beetle larve


text:
What's the technical difference between fainting (and being unconscious) and falling asleep (and sleeping)?
This is actually a popular question along google results but the answers usually sound like:

sleep is voluntary (oh is it?) and healthy
fainting is result of accident and is not normal

I read those answers and I'm like: "You don't say?". So yeah, I know that falling a sleep is a result of some preparation to planned unconscious state, whereas fainting is some defensive reaction trying to protect you from moving (or maybe thinking) when you shouldn't.
But I fainted once and when I woke up it was pretty much like waking up from sleep - including the fact I don't remember the moment I fainted. This gave me an idea that maybe, if you faint in your bed, you'll just fall asleep and wake up in the morning, which would be actually pretty sweet.
Therefore my question is, what's specifically going on when you faint and when you fall asleep. Is there any part when these two situations merge and the final state is the same - you're asleep?
And to my original idea: If you hold your breath to the point where you faint in your bed, what will the result be?

I'm afraid this wont be easy to answer, because, as far is I know, the process of falling asleep is not fully understood by now. But there must be a difference between those two states, because you can actually become conscious while sleeping (this is referred to a lucid dreaming state) And you can even stay conscious while falling asleep, when using a methode called "wake induced lucid dreaming (WILD)". However, fainting is defined as a unconscious state.

Perhaps read the Wiki article on sleep and on your kind of fainting. Falling asleep is typically less fast, in the order of one or a few minutes. Sleep is based on the circadian rhythm and body warmth, so people that faint wake up rather fast, as the brain is not primed to rest at that time. There are three broad categories of causes: heart or blood vessel related, reflex also known as neurally mediated, and orthostatic hypotension.

For this answer I assume that we are talking about sleep in healthy individuals as well as fainting as an isolated event without underlying disease or injury.
The most common form of what we call "fainting" is vasovagal syncope. It is caused by a drop in blood flow to the brain (cerebral hypoperfusion) e.g. by (false) activation of the parasympathetic nervous system and inhibition of the sympathetic system, resulting in low blood pressure or drop in heart rate (reviews 1,2,3). This can be triggered by the Bezold-Janisch reflex. Syncope can also be a symptom of underlying diseases or a side effect of drugs.
The reduced blood flow results in a transient loss of consciousness, a 'shut down' of the brain, which we don't really understand. It is sometimes accompanied by a flattening of an EEG signal, even though the data doesn't seem to be very consistent. Consciousness is defined by two factors, arousal and awareness. The fainted person cannot be 'woken up' and is not aware of the situation (as you said, you don't remember the moment of fainting). But this state normally only lasts for a few seconds or 1-2 minutes.
Sleep, on the other hand, is a mechanism highly regulated by the brain, circadian rhythms and hormones. The brain is thought to switch between the states of sleep and wakefulness by an interplay of different sleep-promoting and wake-promoting areas, including the hypothalamus.
You can argue that sleep is not a state of unconsciousness, since dreaming or even lucid dreaming are connected to a conscious experience. While sleeping lasts longer than the unconsciousness during syncope, it can be reversed by an external stimulus. The sleeping person can be woken up, even though the arousal threshold is increased (loud noises from the alarm are needed). The brain, in fact, is highly active during sleeping (as can be seen in characteristic EEG signals), with energy use close to the state of wakefulness in REM sleep and about 85% during non-REM sleep.
Since these are two different mechanisms, you should not be able to switch between them. After fainting you should regain consciousness very fast. Activation of sleep mechanisms is unlikely in a healthy individual, where sleep regulation is normal and syncope is a rare event.

Most of this is good. I would note, that you don't have to restrict this to vasovagal syncope. The final common pathway of syncope is reduced blood flow to the brain, and the EEG shows a characteristic series of changes (if you manage to record during the loss of consciousness).

Two other suggestions for improvement. There is no need to preface this with a "we don't understand the brain" statement. We understand it well enough to answer this question unequivocally :)

Finally, your last paragraph is a little speculative, though probably partially true. I would consider cutting it. The key (which you've described) is that sleep and fainting are very different brain states, with characteristic patterns on EEG, and behavioral differences (e.g., you can wake someone from sleep). I don't think you need to add a statement about whether it is ever possible to transition from syncope to sleep or sleep to syncope . This is different from the side question of "is fainting a good way to fall asleep?"

This is a nice answer. Fainting is involuntary loss of consciousness. During sleep, there is very little difference in the brain between awake and asleep states in that the brain is quite active.

@anongoodnurse I agree in general, though fainting is a little more specific: transient, involuntary loss of consciousness due to hypoperfusion. Concussion, seizure, anesthesia, other medication or chemical intoxication, hypoglycemia, these all involve involuntary loss of consciousness, but are not fainting. But yes, Frieke has hit the important points here.

@DeNovo I have edited some parts for more information or less speculation. I added the last paragraph since it was part of the question to use fainting as a way to fall asleep. I think that any reported connection between sleep and syncope does refer to 'healthy individuals', which I tried to focus on here. There are a lot of reports about e.g. epilepsy, syncope and sleep, but this is beyond the scope of the question.


text:
Do skin mites reproduce on human face during night?
I've seen this circulating on social networks:

I was wondering to what extent is it true. Do skin mites really get on the skin surface to reproduce? Why is it so?

Yes, it is true that these mites exist on healthy human skin, on >98% of people, no matter the country or hygiene.
However, I'm sorry to say that this photograph is not the follicle mite Demodex folliculorum. This image has been widely circulated around the internet as Demodex, but it is actually the head of a silkworm, Bombyx mori. The above version has been modified slightly from the original, but you can see the original here: https://www.sciencephoto.com/media/720736/view/silkworm-head-sem
And here is a zoomed out version of a silkworm: https://macrocritters.wordpress.com/2012/11/26/photographing-down-the-food-web-silkworms-bombyx-mori/
You can find a real close-up of Demodex here: https://www.sciencesource.com/archive/Demodex-folliculorum-(SEM)-SS2367855.html

Is there a reference on the Demodex population spread? Also the last link is behind paywall.

Doesn't answer the main question about mite reproduction, but it does address the "is it true?" portion of the OP's post. Good on you for catching it. +1


text:
How exactly do mosquitoes navigate directly on target?
There is a question on mosquito orientation in darkness, however the answer does not address it very specifically and I'm more interested in mosquito ability to lock on target than general navigation.
I know that they use their antennae to detect CO2 and lactic acid. However smell alone doesn't seem good enough for precise landing.
They do have eyes, however they can operate in complete darkness which means the eyes are redundant system for the attack.
They can sense heat, but they do not seem to attack non-fire based heat sources.
So how exactly does a mosquito succeed to land on piece of uncovered skin? Does this tell us anything about interfering with their navigation system?

In my experience, they don't navigate directly to their target: they fly around for a long time making an annoying high-pitched whine that's worse than the actual bite, at least if you're trying to sleep.

Mosquitoes do not rely on a single cue to find its host. It is the combination of CO2, temperature and odor cues, that makes mosquito an efficient blood feeder.
 These two papers might help you in understanding how mosquitoes target their hosts.
Genetic analysis of mosquito detection of humans
Multimodal Integration of Carbon Dioxide and Other Sensory
Cues Drives Mosquito Attraction to Humans

+1 for an answer from Mosquito man about mosquitos


text:
Can I identify this black ant queen?
I have an ant queen in a jar. This is what she looks like:

Because I'm planning to start an artificial ant nest, I'd like to learn something about that specific species of ant. This particular queen is very common in the Czech Republic, central Europe. It's also very common in cities.

Could you tell what kind of queen is that?
Is there any image reference that would help me find out? Ideally with some location search possibility.

I am not an expert of ants, but it looks very much like the common black garden ant. http://en.wikipedia.org/wiki/Black_garden_ant

For a moment, I hoped she will be some special badass ant queen. But I love her anyway.

This is not a common black garden ant "Lasius niger" because these ants do not have alternate mat and shiny bands on the gaster.

This cannot be a Lasius queen, it is a Formica queen. Although one of the main characteristic is the shape of the first segment of the funicula which cannot be seen on this picture, the general aspect of this queen (elongated, with red legs, does not have a bulky aspect) indicates this queen is from the genus Formica. It is similar in shape and coloration to many queens in the subgenus Serviformica, for example Formica cunicularia, Formica cinerea.

As @skymnige said it is definitely Black garden ant (Lasius niger)

This is wrong, the pronotum is not elevated enough, the tergites that are half mat and half shiny don't match with Lasius, same for the general aspect of the ant (more elongated than Lasius), the legs are dark red which is common in the genus Formica whereas they are more often black or yellow in Lasius.

@Nakx: I believe you are right. https://www.antsrus.com/store/p80/Formica_%28Serviformica%29_cunicularia_Queen_with_1-5_workers_%28Starter_pack%29.html

Thank you @Devashish_Das, I am an ant taxonomist and most ant identifications on stack biology are wrong.


text:
Do ants feel acceleration?
The organ we have to provide us with current acceleration information is quite complicated. Because an ant queen didn't seem to notice when I picked up the bottle she was in, I have a suspicion that ants don't really care about acceleration and therefore can't tell where it's up and where it's down.
Am I right? If not, how do they sense acceleration?

can you explain what you mean by The organ we have to provide us with current acceleration information is quite complicated? its confusing sentence.

The organ is complicated. - talking about human organ that detects acceleration.

If you snorkel with weights on you find that the buoyant force of water nearly matches the pulls of gravity. It's easy to become disoriented even though we are quite sensitive to the acceleration of gravity. Ants may have a similar issue because their mass is very small and the acceleration of gravity is unlikely to cause them injury. But an insect which carries large loads and walks probably has an acute sense of gravitational acceleration, even if it's tuned in a different way.

Sorry, I misinterpreted your question. I have removed my answer, which is now available in two different question.  http://biology.stackexchange.com/a/19678/8186 and http://biology.stackexchange.com/q/19677/8186

According to Clinical Neurophysiology of the Vestibular System
 By Robert William Baloh, Vicente Honrubia, page 8, the vestibular system (animals' "accelerometer") is as old as 600 million years and is present in invertebrates.
I assume (without a precise source) that this is especially important for flying insects (after all, accelerometers were engineered for flying machines in the first place!) and that the ant didn't respond because the acceleration to which you submitted it was not deemed harmful.

I hope somebody will find a research which proves that. Thanks for your input.

You can find a lot of data searching for "flight control" for insects. Concerning the decision whether to react or not to an acceleration input, it is probably to be found in cognitive science publications. Maybe you should ask another question about it, as it is not linked with ''feeling'' acceleration but to cognitive decision-making.


text:
Why did plants evolve to use opioids?
I'm reading about medicine and specifically opioids. There seems to be a wide variety of forms of these chemicals, I'm curious as to what purpose these serve in these respective plants, and why they function the way they do in mammals.

Please tell us what you found in your reading. :)

Welcome to Bio and thank you for this interesting questions. I must say this question is too broad imo. A way to narrow it down, for a starters, is split this question up in two separate questions. One on plants, one on brains. Does that make any sense?


text:
How would extraterrestrial organisms be categorized?
Suppose we find bacteria on Mars, we sequence its genome, and find it is genetically similar to $E. Coli$. Would we categorize it in the $Escherichia$ genus? Or would we put it into a seperate system of classification?

This question is indirectly about classification systems of biology. The main points in this question seem to be answered if we ask 2 questions. What happens if we find "life" that is not from the original cells that form our tree of life? Can and do we still base some of our trees of life on aesthetics alone?

@James that's put much more eloquently


text:
What species is most prolific?
What species represents the largest biomass on earth, ie, how much does the entire population weigh? Also, what species has the most members?

have you googled?

This article covers your desires. Briefly, the single species that weights the most is the cow (520 million tonnes in 2011, now probably way more). About the most members, it looks like that the prize could go to the Antarctic krill (7.8 x 10^14 according to Wikipedia. [
This BBC article, instead, argues that collembola might be the most numerous group on Earth, being present in the number of 10000 per square meter (I leave the calculation to the reader). Collembola, however, are made up of ~6000 species. The same goes for ants and termites.
Regarding bacteria, the same article mentions
cyanobacteria, and more interestingly Wolbachia, an intracytoplasmic parasite that can bend the sex of the progeny of its host to spread more effectively.

The discovery of this giant Armillaria ostoyae in 1998 heralded a new record holder for the title of the world's largest known organism, believed by most to be the 110-foot- (33.5-meter-) long, 200-ton blue whale. Based on its current growth rate, the fungus is estimated to be 2,400 years old but could be as ancient as 8,650 years, which would earn it a place among the oldest living organisms as well.
And in 2003 Catherine Parks of the USFS in Oregon and her colleagues published their discovery of the current behemoth 2,384-acre Armillaria ostoyae

No weight is given.
https://www.scientificamerican.com/article/strange-but-true-largest-organism-is-fungus/

But this is about the size of an individual, not of the entire species.

Humans are the obvious and boring answer. 7.5 billion at 50 kg each is a lot of species, and getting heavier all the time from fast foods

...But humans is not the answer. We could be the second heaviest species, but the first is the cow, as I mention in my answer.

I don't see how your comment addresses mine.


text:
What organism has the longest Hayflick Limit?
Assuming I am understanding the concept correctly, Hayflick Limits are reflective of a cells capacity for stable division. Additionally, the Hayflick Limits of various organisms differs.
My question is, what organism has the longest Hayflick Limit? I know humans have one ranging from 40-60, just to give a bit context.

The Hayflick limit is generally associated with telomere length. Human telomeres are a little on the long side as species go, but are not extraordinary. Many species of mice, and other rodents, have far longer telomeres than humans, for example, and obviously have much shorter lifespans. There's also such a thing as a "mega-telomere", found in a number of bird species, which can hundreds of times longer than human telomeres.
There's only a vague correlation between telomere length and a species' lifespan.  See Comparative biology of mammalian telomeres: hypotheses on ancestral states and the roles of telomeres in longevity determination for a starting point.  Telomeres are a part of the longevity story, but probably a fairly small part.
That said I don't see an explicit statement that those species with very long telomeres have a higher Hayflick limit. I assume this is because the Hayflick limit is an ultra-simplistic and not very useful description of a very specific set of conditions, but I don't know that for sure.

Testing the Hayflick limit is extremely tedious and expensive (hundreds of cell passages may mean  years of lab time, maybe thousands or tens of thousands of dollars worth of lab equipment) and has little biological interest today. It's unlikely there's going to be any kind of comparative study, so this is probably as good as you're going to get.

I don't understand the link between telomere and lifespan: why do longer telomeres give shorter lifespan? It should be the opposite, isn't it?


text:
Are there examples of cells with more than one nucleus?
I've always wondered why cells have only one nucleus, as having multiple would seemingly prevent mutation. Are there examples of organisms with multiple nucleuses? If not, is there a reason?

From a certain standpoint, your own cells have more than one nucleus, in the sense that they contain mitochondria.

Are there examples of cells with more than one nucleus?

Yes, they are called Multinucleate cells. There are two types of multinucleated cells

Syncytia
Coenocytes

I highly recommend having a look at this answer for the definitions.
Examples of Syncytia include

Osteoclasts
Skeletal muscle fibers (thanks @kmm)

Examples of Coenocytes include

Codium (Thanks @GerardoFurtado; see picture below)
Blastoderms early in the development of a fruit fly

Are there examples of organisms with multiple nucleuses?

Side note: The plural of nucleus is nuclei
In many fungi, during sexual reproduction, a fusion of cytoplasm happen early in the mycelium but a fusion of the nucleus happens only very late (just before sporulation). This is a type of Coenocytic mycelium. In these species, non-negligible fractions of their cells are multinucleated.
There are endosymbiotic and endoparasitic eukaryotes in other eukaryotes that would result in a cell containing several nuclei but that would not count I would guess as the nuclei belong to different species.

Picture of Codium. The entire algea is a single multinucleated cell.

There is a branch of life called the Diplomonads, most of which have two nuclei. They are single cell organisms and an early offshoot of the eukaryotic linage. A good example is Giardia lamblia.
https://en.wikipedia.org/wiki/Diplomonad
Giardia lamblia

According to this article The hairy beast with seven fuzzy sexes
Tetrahymena thermophila has two: a large macronucleus and a small micronucleus. The macronucleus controls the everyday functions of the cell, while the micronucleus deals with its complicated sex life. In fact this is true for all ciliates.

When a "slime mold" enters the "plasmodium" phase n cells merge together to form one cell with n nuclei.  This means plasmodiums can have thousands or tens of thousands of nuclei...

Skeletal muscles (striated) are multi-nucleated-have more than one nucleus per cell as they are formed as a result of the fusion of myoblasts.
Reference-   Skeletal Muscle: Form and Function (2006)
By Brian R. MacIntosh, Phillip F. Gardiner, Alan J. McComas


text:
How can a species switch from r to K - reproductive strategy in a single generation?
I ask because it seems as though humanity is in the midst of doing exactly this. Only a few decades ago, human population was growing exponentially, and it seemed destined to keep growing until hitting constraints of food supply, at which point we would devolve into resource wars and famine. But then it didn't happen -- over the last few decades, fertility rates in the developed and developing world have plummeted and the world population is expected to stabilize in the second half of this century around 10-11 billion people. Demographers list a number of reasons for this -- education and empowerment of women, urbanization, decreased child mortality and increased life expectancy, availability of safe and effective contraception, etc. The common thread is that these trends encourage people to invest more into fewer offspring. It's as though our entire species is spontaneously deciding to switch from an r-strategy of reproduction to a K-strategy.
My question is whether this is unprecedented or not. I had the impression that r or K strategy was typically a function of species, but here we have a case where humans seem to be switching between the two strategies in a single generation. Are there other species which can change their entire reproductive strategy when the population approaches its carrying capacity? If so, what kinds of environmental cues or epigenetic factors trigger the switch? How do they manifest themselves in the case of humanity's current switch?

The issue in your reasoning is to associate a $r$ or $K$ as being a property intrinsic of the species which, while not entirely wrong, is rather misleading.
The classical and simplistic model of population growth is the model of logistic growth
$$n(t+1) = n(t) + rn(t)\left(1-\frac{n(t)}{K}\right)$$
, where $n(t)$ is the population size (number of individuals in the population) at time $t$, $r$ is the growth rate and $K$ is the carrying capacity. Of course, there exist also continuous time equivalent of this discrete time recursion equation. Here is a quick and dirty R code to compute this recursion equation
r = 0.0004
K = 1e4
f = function(n) {return(n + r * n * (1-(n/K)))}

nbGenerations = 1e5
n = numeric(nbGenerations)
n[1] = 1
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

If you want to compute such function fast you can look for the general solution of the recursion equation (it is a good exercice if you are a little uneasy with recursion equations).
As you can see, the population grows exponentially until some point and then the growth is slower and slower until reaching the carrying capacity. If you look at this species at $t=2000$, then you will deduce that it is a r-strategy species because its growth is dictated by the parameter $r$ (the growth rate). If you look at the same species at generation $t=6000$, then you will deduce that it is a K-strategy species as the population dynamic is dictated by the parameter $K$. Yet, the species has not changed so much.
Being r or K strategic is not a intrinsic characteristic of the species as much as it is a characteristic of the species population size in a given environment.
Now, in my example I chose $r=0.0004$, just pick some greater $r$ value and you'll see that such change from being a r- to being a K- strategy species can change very quickly. Consider for example
r = 0.02 # growth rate
K = 1e10 # carrying capacity
f = function(n) {return(n + r * n * (1-(n/K)))} # recursion function

nbGenerations = 1e3    # number of generations to computer
n = numeric(nbGenerations)
n[1] = 1e7             # starting population size
for (t in 2:nbGenerations)
{
    n[t] = f(n[t-1])
}

plot(y=n,x=1:nbGenerations)

You can now look for realistic estimates of $r$ and $K$ for humans (data from after the industrial revolution), plug them in this equation and see what you get! You can also try to estimate $r$ and $K$ from data (from after the industrial revolution only) of population size over time.
If you play with high values of $r$, you can get overshooting and you can even get chaotic population dynamic.

Are there other species which can change their entire reproductive strategy when the population approaches its carrying capacity?

Of course, this change in a conscious. It is not a decision of the species. It is not either so much an evolutionary process. It is just a consequence of their environment. Yes, all species follow some kind of model of population growth. The famous example of logistic population growth comes from daphnia which growth dynamic has been highly studied. Daphnia can have quite a high $r$ value (depending on the environment) and they can typically show overshooting behaviour of the carrying capacity before settling down back to the carrying capacity.

If you enjoyed this simple models, you'll find another model of population growth with a predator in the post What prevents predator overpopulation?

I see your point -- a simple logistic growth model with constant $r$ and $K$ does seem to fit human population growth pretty well after all. So I think I misstated my question. The logistic growth model doesn't say anything about birth and death rates -- just an overall growth rate. The simplest interpretation of the logistic model is that the birth rate remains constant but the death rate increases as the population approaches the carrying capacity. My question is why that doesn't seem to be the case currently with humans -- for some reason, the birth rates are changing drastically.

$r$ is simply $r = b - d$, where $b$is birth rate and $d$ is death rate as measured at the carrying capacity at which the population growth is maximal (the steepest part of the graph). The realized growth rate at any time is of course simply $b - d$ at that time.

In humans, the death rate dropped like crazy since the industrial revolution. The birth rate is slowly going down to match the death rate. In other words, for humans at the left side of the graph both $b$ and $d$ where large, then $d$ dropped suddenly, population grew like crazy and slowly $b$ is also reducing causing the approaching plateau.

Right, I guess what I'd really like to know is what the actual biological mechanism is which modulates the birth rate in response to the death rate and carrying capacity. As you say, it's not simply a matter of each individual organism consciously estimating the death rate and carrying capacity, and consciously choosing to create the appropriate number of progeny in response. It has to be something more subtle.

Typically, individuals just fail to get enough ressource to produce or feed more youngs. That logic does not really hold for humans though. Many people have asked the question why rich humans tend to produce fewer children than poor humans. I am not sure of what the consensus is if any consensus has been reached.

Okay, maybe that's a better way to frame the paradox I outlined in the first paragraph of my question: it seems that human population dynamics are essentially following a very simple logistic pattern, but not via the simple mechanism motivating the logistic model. As I pointed out, some things are known about the sociology leading to the flattening of the growth rate. But from a biological perspective, it seems very odd that humans and dahlias do the same thing for very different reasons...