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Are there known chains of beneficial mutations?
Are there known examples of chains of beneficial mutations?
What I mean by that is a mutation that leads to a series of mutations occurring after each other over a relatively short period of time and all of those being beneficial for the organism. And I mean also that there is some etiological impact of the prior mutations on the subsequent ones, that is any mutation in the chain will increase significantly the likelihood of occurrence of the next mutation in the chain. And if there are such chains then would those be considered as a mechanism for speeding up evolution?

The answer will strongly depend on how you define "relatively short" (minutes? months? millennia? generations? and if so how many?) — please clarify this in your question. ——— Note that in general this will be very difficult to know since you would need genomic sequences from many generations of organisms and I would guess from many individuals in each generation to have any hope of seeing this happening. The best candidate I know of for finding such evidence is an ongoing long-term evolution experiment in E. coli.

Adaptive radiation

In evolutionary biology, adaptive radiation is a process in which organisms diversify rapidly from an ancestral species into a multitude of new forms, particularly when a change in the environment makes new resources available, creates new challenges, or opens new environmental niches.

The key-innovation that can lead a species to go through rapid adaptive evolution might well be an initial beneficial mutation. You might want to rad about these key-innovations at Salzburger et al. (2005).
As an example, much of the diversification in ciclid fishes is thought to be driven by jaw morphology driven by a few key genes (a ligand; bmp4, a receptor; bmpr1b and an antagonist; nog2; Brawand et al., 2014). While I don't know the literature well on the topic, it sounds plausible to me that a key mutation may have allowed for the diversity of jaw morphology to diversify (which lead lineages to diversify).
Note, I am aware, I focused my answer on diversification and not on single lineage adaptation per se but I do not know better examples (or a better concept) of a single mutation that could lead to a "chain of beneficial mutations".


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Are the social-distancing measures implemented against SARS-CoV-2 also suppressing the spread of other viruses?
With social-distancing measures being implemented in many countries I would expect other viruses, like the ones that cause seasonal flus, to have also a hard time propagating in these circumstances. Are there any estimates or research (epidemiological models) I can check, about the possibility we are winning by accident a war against many other less alarming viruses?

relevant XKCD

@Dirigible full page (so you can read the hover text as well)

Of course there's an xkcd. How couldn't there be?

Anoter relevant XKCD

I think "killing" is the wrong therm here. Social-distancing is reducing the spread of viruses.

Not enough reputation for an answer, but this is the respiratory infection rate in Germany: https://grippeweb.rki.de/Diagrams/2019_2020/2020-22-01.png It’s at ~2% compared to the usual ~5% for this time of the year. I think this even includes COVID19.

Not enough rep to answer. Norovirus in Sweden  https://imgs.aftonbladet-cdn.se/v2/images/65de546d-9803-4977-9e51-ba8d44636c6d?fit=crop&h=720&q=50&w=960&s=2d38e1da546acb07b726e76334a900f34c5cbfab

It seems that at least for pneumonia in the US the lower numbers could be entirely caused by incomplete data. https://skeptics.stackexchange.com/questions/47265/has-the-number-of-pneumonia-deaths-in-the-us-dramatically-dropped-in-2020

Yes, this helps as well with other infectious diseases. A good example is the flu, which season was measurably shorter this year than in other years on record. See the figure from the reference 1 for comparision:

Reference 2 shows that this is also true for other respiratory diseases (figure 2):

This shows very well that the isolation measures and the social distancing work very well to control such transmissable diseases.
References:

How coronavirus lockdowns stopped flu in its tracks
Monitoring respiratory infections in covid-19 epidemics

The flatline of on that second chart is absolutely remarkable compared to previous years.  I wonder if these effects will last a significant period of time or if spread of common viruses will be back to normal next year.

Of course there are possible reasons for that flatline in addition to limiting the spread.  For instance, people who otherwise might have made a doctor visit for the flu may have decided to skip it this year.

@jamesqf That graphic is as a percentage of analysed specimens, so those people staying home are not part of the sample at all. Additionally, "there may be other contributing factors, such as people choosing not to go to a place where sick people often congregate" is really killing two birds with one stone in this specific case.

Looks like the flu season was off to an unfortunately strong start before social-distancing guidelines and lock-downs were put in-place, then presumably the safety procedures helped drive the curve down.  But for reference, is there some simple way to qualitatively describe when lock-down procedures kicked in?

The second chart makes it seem like there was a single case of covid-19 and then all diseases dropped.  Given it became a global pandemic, I'd expect at least one line to shoot up before the drop.

@DavidStarkey The chart does not include COVID-19, since it is not an influenza. As you said, once the pandemic was declared everywhere people started to apply precautions (whether imposed by the government or not) and thus all other deaseses started to drop pretty quickly.

@DavidStarkey, if you look into the reference, that chart only applies to Hong Kong. Given their proximity to mainland China, they started taking aggressive precautions before COVID showed up, as I recall.

In addition to Chris' answer above, the effect is even more pronounced in Southern Hemisphere countries where flu season started during the pandemic.  The New Zealand lockdown and health response dramatically lowered the prevalence of reported flu-like symptoms.

Reference:
  Flu Tracking reports - New Zealand – week ending 31-May-2020

NZ's winter is only just beginning, and their lockdown is over.

@curiousdannii flu season =/= winter, flu season lasts a lot longer

I don't have points to write my own answer, but this is a great account of Lab confirmed flu cases in Australia over the past few years and early 2020 (updated 15 June). https://www.immunisationcoalition.org.au/wp-content/uploads/2020/03/15Jun-Aust-Flu-Stats-2020.pdf

source: Stack Exchange

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

sort: votes


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Is there a way to determine corresponding differential equations from fitted Hill equation parameters
I am currently doing some work with GCaMP, a genetically encoded calcium indicator. According to the literature the Hill equation parameters for GCaMP6m is $K_d=167\pm3\, \text{nM}$ and $n=2.96\pm0.04$. Usually the "derivation" of the Hill equation assumes that a number of binding sites equal to the the Hill coefficient, but I understand that the Hill Coefficient should be interpreted more as an effective "interaction coefficient" rather than an actual indicator of how many calcium binding sites GCaMP6m has. This is certainly true here, since GCaMP is a fusion of GFP and Calmodulin, which has 4 calcium binding sites.
However, given that $K_d=167\pm3\, \text{nM}$ and $n=2.96\pm0.04$, is there a way we can formulate a set of differential equations describing the kinetics of calcium binding to GCaMP? Both "intuitive" ways I can think of don't seem to be valid. If we take the naive approach similar to the Hill equation "derivation" we would end up with equations like
$$\frac{\text dc}{\text dt}=-k_\text{on}c^n(g_T-g_c)+k_\text{off}g_c$$
$$\frac{\text dg_c}{\text dt}=k_\text{on}c^n(g_T-g_c)+k_\text{off}g_c$$
Now, $n=4$ is invalid because this would not produce the correct equilibrium behavior determined experimentally. However, $n=2.96$ would also appear to be invalid, as it doesn't correctly give the actual number of calcium ions taken up per GCaMP molecule.
Therefore, my question is how can we set up a correct (or reasonably correct) set of differential equations for a reaction given experimentally determined $K_d$ and $n$ that are more of "effective" parameters rather than literal ones?

@com.prehensible I am not asking a genetics question. Did I say something to make you think so?

I study digital signal processing, I'd have that in code for a graphical illustration. I can't figure out if the 6m version is very different from the GCaMP.

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


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Did the old world have relatives of plants which were brought after the discovery of Americas?
When the Americas were discovered many plants were brought back to Europe. For example: potato, tomato, strawberries, chilies etc. At the same time many animals were brought to the Americas including: horses, cattle, sheep, and camels. It seems from the records that there were relatives of these animals in the Americas — for example llamas are in the same family (Camelidae) as camels. I wonder if there were relatives of these vegetables from the Americas already present in Europe or anywhere else in the old world.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, note that asking about "related" leads to a trivial answer (Yes) since all known life on earth is related! ——— We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). E.g. the wikipedia article on strawberries has links to its genus, from which you can find "old world" species. Thanks!

Three of your examples: potato, tomato, and chilies, are from the genus Solanum. Along with the rest of the Solanaceae family, they are most diverse in the Americas but some species are found worldwide.
Species that would be found originally in the 'old world' from the Solanum genus and Solanaceae family include the black nightshade, bittersweet nightshade, and deadly nightshade. There is also at least one cultivated plant variously known as eggplant, aubergine, or brinjal (Solanum melongena) that is thought to have been domesticated in Asia.
The strawberry genus, Fragaria, also has species world-wide.
Of course, because all life on Earth is related, the answer to the general question "are there relatives of X found in some place" will always be "yes" as long as there is life there, it's only a matter of the extent of relation.

Thank you so much, could you give any resources I can refer?

@FrkEr I've linked to a variety of Wikipedia pages, all of which contain pretty substantial taxonomy. If you want to get more scientific references to dig deeper than basic phylogeny you're probably best off doing it at a species level rather than systematically. You could also ask more specific, detailed questions here at Biology.SE, but you'll have to make them specific.


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Genomic location-coordinate of RdRp of SARS-CoV2
I understand that nsp12 is the RdRp protein in the ORF1 of SARS-CoV2 genome. And nsp12 starts from the starting nucleotide base of orf1ab. Could you please tell me the exact genomic location coordinate of RdRp?
Is there and database from where the FASTA sequence (nucleotide and aa) of RdRp of SARS-CoV2 can be obtained?
Any answer to this question would be highly appreciated.

The following is a standard and quite straightforward way to obtain the information requested that is generally applicable and does not require any programming.

Go to the NCBI website or its Genbank page, select Genome from the pull-down menu and type your search term, ‘SARS-CoV2’ into the search field:

On clicking Search, you will be taken to a page with a brief summary of information about the genome. In the Reference genome summary box click on the RefSeq ID, NC_045512_2:

This takes you to the record for the nucleotide sequence of the virus genome. Scroll down (or do a Find in your web browser) to the gene of interest, nsp12. There you will find an entry with the genomic co-ordinates (13442–13468 and 13468–16236) and a cross-reference to the protein, [YP_009725307.1(https://www.ncbi.nlm.nih.gov/protein/1802476815).

If you click on that ID you will be taken to the Genbank entry for the protein encoded by nsp12, with the sequence in FASTA format.

You can download a file containing the sequence from the Send to pull-down shown. There is also a link to the graphical interface for viewing the protein in the context of the genome (available from the nucleotide sequence page as well).

This is more informative.

Tks I didn't notice the hidden entries 1 and 2

A useful database and exploratory tool is the UCSC Genome Browser wuhCor1 assembly browser instance.
A synonym for nsp12 is Pol. Its position range in the wuhCor1 assembly is NC_045512v2:13,442-16,236.
There are several ways to extract sequence, but one programmatic way is to get the FASTA from UCSC Goldenpath for the assembly, and extract the characters of interest from the position range for the gene of interest using standard Unix tools:
$ wget -qO- ftp://hgdownload.soe.ucsc.edu/goldenPath/wuhCor1/chromosomes/NC_045512v2.fa.gz | gunzip -c | tail -n+2 | tr -d '\n' | cut -c 13442-16236 | awk '{print ">nsp12"; print $0}' > nsp12.fa
$ cat nsp12.fa
>nsp12
TCAGCTGATGCACAATCGTTTTTAAACGGGTTTGCGGTGTAAGTGCAGCCCGTCTTACACCGTGCGGCACAGGCACTAGTACTGATGTCGTATACAGGGCTTTTGACATCTACAATGATAAAGTAGCTGGTTTTGCTAAATTCCTAAAAACTAATTGTTGTCGCTTCCAAGAAAAGGACGAAGATGACAATTTAATTGATTCTTACTTTGTAGTTAAGAGACACACTTTCTCTAACTACCAACATGAAGAAACAATTTATAATTTACTTAAGGATTGTCCAGCTGTTGCTAAACATGACTTCTTTAAGTTTAGAATAGACGGTGACATGGTACCACATATATCACGTCAACGTCTTACTAAATACACAATGGCAGACCTCGTCTATGCTTTAAGGCATTTTGATGAAGGTAATTGTGACACATTAAAAGAAATACTTGTCACATACAATTGTTGTGATGATGATTATTTCAATAAAAAGGACTGGTATGATTTTGTAGAAAACCCAGATATATTACGCGTATACGCCAACTTAGGTGAACGTGTACGCCAAGCTTTGTTAAAAACAGTACAATTCTGTGATGCCATGCGAAATGCTGGTATTGTTGGTGTACTGACATTAGATAATCAAGATCTCAATGGTAACTGGTATGATTTCGGTGATTTCATACAAACCACGCCAGGTAGTGGAGTTCCTGTTGTAGATTCTTATTATTCATTGTTAATGCCTATATTAACCTTGACCAGGGCTTTAACTGCAGAGTCACATGTTGACACTGACTTAACAAAGCCTTACATTAAGTGGGATTTGTTAAAATATGACTTCACGGAAGAGAGGTTAAAACTCTTTGACCGTTATTTTAAATATTGGGATCAGACATACCACCCAAATTGTGTTAACTGTTTGGATGACAGATGCATTCTGCATTGTGCAAACTTTAATGTTTTATTCTCTACAGTGTTCCCACCTACAAGTTTTGGACCACTAGTGAGAAAAATATTTGTTGATGGTGTTCCATTTGTAGTTTCAACTGGATACCACTTCAGAGAGCTAGGTGTTGTACATAATCAGGATGTAAACTTACATAGCTCTAGACTTAGTTTTAAGGAATTACTTGTGTATGCTGCTGACCCTGCTATGCACGCTGCTTCTGGTAATCTATTACTAGATAAACGCACTACGTGCTTTTCAGTAGCTGCACTTACTAACAATGTTGCTTTTCAAACTGTCAAACCCGGTAATTTTAACAAAGACTTCTATGACTTTGCTGTGTCTAAGGGTTTCTTTAAGGAAGGAAGTTCTGTTGAATTAAAACACTTCTTCTTTGCTCAGGATGGTAATGCTGCTATCAGCGATTATGACTACTATCGTTATAATCTACCAACAATGTGTGATATCAGACAACTACTATTTGTAGTTGAAGTTGTTGATAAGTACTTTGATTGTTACGATGGTGGCTGTATTAATGCTAACCAAGTCATCGTCAACAACCTAGACAAATCAGCTGGTTTTCCATTTAATAAATGGGGTAAGGCTAGACTTTATTATGATTCAATGAGTTATGAGGATCAAGATGCACTTTTCGCATATACAAAACGTAATGTCATCCCTACTATAACTCAAATGAATCTTAAGTATGCCATTAGTGCAAAGAATAGAGCTCGCACCGTAGCTGGTGTCTCTATCTGTAGTACTATGACCAATAGACAGTTTCATCAAAAATTATTGAAATCAATAGCCGCCACTAGAGGAGCTACTGTAGTAATTGGAACAAGCAAATTCTATGGTGGTTGGCACAACATGTTAAAAACTGTTTATAGTGATGTAGAAAACCCTCACCTTATGGGTTGGGATTATCCTAAATGTGATAGAGCCATGCCTAACATGCTTAGAATTATGGCCTCACTTGTTCTTGCTCGCAAACATACAACGTGTTGTAGCTTGTCACACCGTTTCTATAGATTAGCTAATGAGTGTGCTCAAGTATTGAGTGAAATGGTCATGTGTGGCGGTTCACTATATGTTAAACCAGGTGGAACCTCATCAGGAGATGCCACAACTGCTTATGCTAATAGTGTTTTTAACATTTGTCAAGCTGTCACGGCCAATGTTAATGCACTTTTATCTACTGATGGTAACAAAATTGCCGATAAGTATGTCCGCAATTTACAACACAGACTTTATGAGTGTCTCTATAGAAATAGAGATGTTGACACAGACTTTGTGAATGAGTTTTACGCATATTTGCGTAAACATTTCTCAATGATGATACTCTCTGACGATGCTGTTGTGTGTTTCAATAGCACTTATGCATCTCAAGGTCTAGTGGCTAGCATAAAGAACTTTAAGTCAGTTCTTTATTATCAAAACAATGTTTTTATGTCTGAAGCAAAATGTTGGACTGAGACTGACCTTACTAAAGGACCTCATGAATTTTGCTCTCAACATACAATGCTAGTTAAACAGGGTGATGATTATGTGTACCTTCCTTACCCAGATCCATCAAGAATCCTAGGGGCCGGCTGTTTTGTAGATGATATCGTAAAAACAGATGGTACACTTATGATTGAACGGTTCGTGTCTTTAGCTATAGATGCTTACCCACTTACTAAACATCCTAATCAGGAGTATGCTGATGTCTTTCATTTGTACTTACAATACATAAGAAAGCTACATGATGAGTTAACAGGACACATGTTAGACATGTATTCTGTTATGCTTACTAATGATAACACTTCAAGGTATTGGGAACCTGAGTTTTATGAGGCTATGTACACACCGCATACAGTCTTACAG

Another option is to visit the Pol link again and look for the "View DNA for this feature (wuhCor1/SARS-CoV-2)" link, click on it, and click on "get DNA" to get a similar FASTA file. But if you're going to do bioinformatics, knowing how to string together Unix tools is a valuable skill.
To get the amino acid sequence, visit the Pol link, look for the Swiss-Prot record information, and do a search through UniProt for the record P0DTD1.
Via the "RNA-directed RNA polymerase" entry for P0DTD1, you can click on the "RNA-directed RNA polymerase" post-translation product to get to a record with the amino acid sequence: https://www.uniprot.org/blast/?about=P0DTD1[4393-5324]&key=Chain&id=PRO_0000449629


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How to model social structure in SIR models
I refer to J.H. Jones' Notes on R0.
More details in this question at Mathematics SE: How does the reproduction number depend on characteristics of the physical contact graph of a population?

The basic SIR model - as described in Jones' Notes - considers three factors that make up the reproduction number:

$\tau$ = the transmissibility (i.e., probability of infection given contact between a susceptible and infected individual)
$\overline{c}$ = the average rate of contact between susceptible and infected individuals
$d$ = the duration of infectiousness

The (basic) reproduction number then is
$$R_0 = \tau \cdot \overline{c} \cdot d$$
I wonder how to model social structure in a SIR model, which might influence both transmissibilty $\tau$ and average rate of contact $\overline{c}$ and thus the reproduction number $R_0$, resp. the infection rate $\beta = \tau \cdot \overline{c} = R_0 / d$.
Specifically I wonder which "control parameters" appropriately describe the social structure of a population and may influence transmissibilty $\tau$ and average rate of contact $\overline{c}$ in a specific and comprehensible way.
Among these parameters may be:

typical (mean) numbers of household members and acquainted persons
typical ratio of shared acquaintances
typical numbers of strangers one meets (e.g. per month)
typical times of contact to household members, acquainted persons, and strangers
the amount of persons with outstanding many social contacts, better: the standard deviation of the contact rate
the accepted physical distance to family members, acquainted persons and strangers
(source)

I am looking for approaches that let go such parameters into the infection rate $\beta = \tau \cdot \overline{c}$ in a quantitative way.


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How do fish transport egg to, and out of, coelom?
How do gametes get into coelom, and, later out of it? Excretion can be under quite heavy pressure, see https://www.youtube.com/watch?v=1OsRbuEINXI

As question has not received answer, will answer to best of my ability. Eggs are plopped off from ovary, into coelom. Duct out of coelom is the oviduct that opens into it. The fish must apply pressure to the whole of the coelom, I guess, to push it out. That part is a bit of a mystery to me, an expert answer would be better.


text:
How quicky does dental pH change after eating?
I would like to know how quickly after eating I can expect the pH do change in my mouth, and how quickly this will cause dental damage.
Obviously any answer to this will have plenty of caveats (diet, composition of oral bacteria, etc) but I would like some numbers for some scenarios please.

Dental damage is mainly caused by the demineralization of the tooth enamel. Demineralization can happen due to a low pH caused either by acidic food/drinks like fruits or carbonated beverages or by bacteria producing acid while breaking down sugars.
Measurements (1, 2) have shown that food intake changes the pH (increasing or decreasing, depending on the food source), returning back to baseline after 15-30 min due to the buffering capacity of the saliva via bicarbonate and phosphate.
The drop in pH happens immediately after food intake. If teeth are not cleaned, the acid producing bacteria can have a longer-lasting effect on the pH for more than an hour. In these studies, participants are asked not to clean their teeth, so bacteria will populate the mouth. Removing bacteria or their food source as well helping the remineralization with fluoride toothpaste can counter the effects.


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Exact definition of homoplasy?
I am a poor mathematician looking into the Sars-Cov-2 genome. Is there a proper definition of the word homoplasy? Is it just mutations that happened independently or does there have to be indications that the mutations give an improvement in fitness?

Homoplasy just refers to the fact that the mutation happened independently. While several sources only discuss homoplasy as a phenotypic characteristic, and in contrast to homology (and thus suggest an adaptive implication), in general,  there is no assumption that the mutation gave increase in fitness (see this paper).

According to Wikipedia (obviously not the final authority on scientific questions, but often reliable), homoplasy occurs

when a trait has been gained or lost independently in separate lineages over the course of evolution

There's nothing in this definition about the fitness implications of the trait (beneficial, deleterious or neutral).
"Trait" is a more problematic/nebulously defined term, because you have to carefully define what the trait means in different lineages, but in this case it's probably relative to aligned sequences, e.g. "a G at position 575 of the aligned sequence", or "a deletion from positions 575-580".


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Removing DNA from a cell
Stupid question perhaps but what does happen if one completely removes DNA from a single cell organism? As far as I know DNA is only needed for propagating information to descendants doing it's removed from a grown up cell and put some artificial source of protein there will it just lose ability to mate or will it die immediately?

Welcome to SE Biology! It is helpful when asking questions to do a minimal level of research first to help you focus your question. For instance, there is a huge amount of information if you google "role of DNA in a cell".

@MaximilianPress well, I did actually. I knew from school and from research that DNA is essential for producing proteins and thus life. I should have specified the question perhaps.

@SPr thanks for your answer.

@SPr would suggest putting your comment into an answer.

@s0nicYouth I mean... I think with a quick due-diligence search you would have easily found what @S Pr commented. But maybe I am overestimating the usefulness of science information on the internet.

That depends on the status and activity of the cell. Red blood cells purge their nuclei and DNA contents and continue to perform their function quite well, though they lose their ability to split and form new cells (i.e. are terminally differentiated). Most cells, however, require the genome to transcribe and translate genetic information into protein to maintain their metabolic and functional activities. As you say, DNA would also be required to divide and build new cells, so that would be one major downside of removing all DNA. Adding exogenous proteins or amino acids will not help with ensuring correct protein production and maintenance, because proteins are coded for by mRNA which act as mobile transcripts of DNA. They are dependent on DNA transcription, without which they cannot exist. Proteins do not spontaneously form. Long story short, DNA is almost always absolutely essential, and it is the case that if you removed the nucleus from most cells, they would die very shortly thereafter.

(migrated comment to answer by request)


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fibrous skeleton of the heart
is it true to say that "fibrous skeleton is between all of the myocardium and most of the cardiac muscle attach to that"? cause I can't get this that how can it be between all the muscles.

Where is this quote from? The phrase "myocardium muscle" is strange usage (muscle is redundant with myocardium).

edited it. I wrote it wrong sorry


text:
Identity little brown lady bugs taking shelter in my home
Can someone please identify this little creature for me. They are appearing more frequently in my room. What are they doing here? Could it be those basic needs and requirements?
The size is about 2 x 1 millimetre. My location is the Netherlands. I am on the 20th floor of a flat. The season is now heading towards end of spring.

Could you please edit your question to include the size of the insect as well as your location and season?

Thanks for the tip, description updated. Getting all biological now hehe


text:
Do some birds really clean themselves using wet leaves?
While researching native shrubs to put in my garden for bird habitat, I read that some birds will take advantage of bushes to clean themselves by rubbing themselves against a wet leaf after rainfall (emphasis below is mine).

Water: Birds that sip nectar from the flowers on shrubs will enjoy the liquid refreshment, and larger shrub leaves will collect small amounts of water that different birds may sip. Birds may even rub against damp leaves for a quick bath.
  --The Spruce, "Shrubs for Birds"

I've been unable to find any reference to this from further search on the internet, though - the only cleaning strategies I've found written about are puddle bathing, dust bathing, and anting. Is this strategy of cleaning with wet leaves something that actually happens in nature, or just a product of a gardening website's imagination? Is there another process that could be misinterpreted by an observer here?
If this is real, I would love to read more about it, or even find a picture or video of the behavior.

Yes, birds do clean themselves using wet leaves. It is called leaf bathing. Mainly small birds do it but this behavior can be observed in big birds too.

Leaf bathing is the term used when birds make use of the water droplets accumulated on large leaves to bathe. The water in this case came from the rain but it may well come from dew, condensed fog or even from the garden sprinkler or water hose.
Leaf bathing was first reported by L.F. Baptista. In 1971 he observed a Rufous-crowned Sparrow (Aimophila ruficeps) bathing on leaves of an eucalyptus in Berkeley, California.
https://besgroup.org/2007/03/05/leaf-bathing/

Here is a video of an olive-backed sunbird having a leaf bath:
https://www.youtube.com/watch?v=23M6nsLNCFs
I've created a short animated gif from the video also:

Further sources:

Mass leaf bathing of sunbirds
https://besgroup.org/2008/02/25/mass-leaf-bathing-of-sunbirds/
Tomás, X., Senar, J. C., 2021. Leaf bathing in ring-necked parakeets Psittacula krameri. Arxius de Miscel·lània Zoològica, 19: 131-133, DOI: https://doi.org/10.32800/amz.2021.19.0131
Beat about the Bush: Birds
by Trevor Carnaby - Google Books

My god that's adorable.


text:
Why do humans have flat faces, as compared to chimps?
Apparently adult, particularly older human faces resemble infantile chimps more tham they resemble any other adult hominid.
And adult humans even have as many body hair follicles as infantile chimps.
Is there a possibility that humans evolved those facial features in order to look younger?
Eg: An adult hominid skull structure barely resembles that of a human but younger ones are more similar to us.
This kind of face makes our jaws weaker and possibly not good at anchoring strong canines, and that is probably why humans have very small canines when compared to any other hominid- and even the vegetarian ones.
So my thought is that chewing power and intimidation was sacrificed for more sexual selection as in looking younger.
But I guess I might be wrong, what is the real reason for the flat face?

(By humans I also mean H.neanderthal and Denisovans as apparently they were so similar to H.sapiens they bred and therefore I prefer to consider them the same species since the definition of species is animals which can't breed.)

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular note that questions should be clear — in this case are you asking about possible selective advantages or are you interested in developmental mechanisms? ——— We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

I have found that when learning about a new area starting with a relatively accessible and reliable source like Khan Academy is very helpful. Wikipedia is also generally a good starting point and you can then check their references. Online platforms called MOOCs offer free (or very low cost) courses on a wide variety of subjects — two I am familiar with are Coursera and edX. Finally, textbooks with a good level of detail are also freely available online e.g. from NCBI.

You are right in saying that older human faces resemble infantile chimps more than the adult ones, but then you say:

And adult humans even have as many body hair follicles as infantile chimps.

Well, humans have the same number of follicles as that of adult chimpanzees, and some other close relatives.(1)

Is there a possibility that humans evolved those facial features in order to look younger?

'Younger' in what sense? Your idea of 'sexual selection' does not make sense- because both sexes of the species evolved simultaneously. For being 'sexually selected', only one of the sexes should have the feature.
These features rather were a product of evolution- for example, you mention the lack of a protruding jaw. In modern humans, the area beneath the nose and around the upper jaw – known as the maxilla – is rich in cells that absorb bone. But in Neanderthals, H. heidelbergensis and other early hominids like Australopithecus, this area had lots of cells that deposit bone, causing the face to protrude forwards. Modern humans show widespread areas of resorption all over the maxilla. It is this resorption that helps maintain the human face where it is under the cranium, rather than protruding far forward. Similar patterns of bone resorption can be seen around the canine fossa in modern humans, whereas Neanderthal skulls show widespread bone deposition.(2)

So my though is that chewing power and intimidation was sacrificed for more sexual selection as in looking younger.

That is clearly incorrect. Our branch of the primate family (the genus Homo) evolved to have smaller and smaller canines, even as humans became increasingly more carnivore. It is believed that this evolutionary path is linked to our usage of tools and fire, which reduced considerably the need of long and sharp teeth to hunt and eat.
1- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6289065/
2-http://www.bbc.com/earth/story/20170214-your-face-is-probably-more-primitive-than-a-neanderthals

I just provided you factual explanations for your assumptions (which we do here), most of which were incorrect. I apologise, if anything I conveyed, affects your potential to continue asking and learning biology. Since you are new here, I want to add, the downvotes you got for your question should not demotivate you from thinking and having a wild imagination! :)

Why does only one of tge sexes need to have that feature in order to be selected?

Read this: https://www.britannica.com/science/sexual-selection


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Population Dynamics problem concerning Allee Effect
I am reading Nonlinear Dynamics and Chaos with Applications to Physics, Biology, Chemistry, and Engineering, 2nd Ed. (Strogatz 2015).  I came across a problem involving the Allee Effect which I have not been able to solve.
Problem:
I tried comparing terms with the Allee effect as stated on Wikipedia,  but it is still not clear to me how to solve this.  Can someone please help?
Since my last post, I have tried plotting several values for the parameters, and I solved for the zeros of this equation.  My guess, is that I am supposed to qualitatively analyze this plot and see that it is maximized for intermediate values of N.  I am including a picture from Mathematica of my work.  Please let me know if I am on the wrong track.

You're not interpreting that Wikipedia page correctly. That equation provides an example of the Allee effect, but is not exclusive.
The Allee effect occurs when the non-zero steady state of a system is not globally attractive, so that such populations may be stable at non-zero population levels for a long time, but are unable to recover once the population density drops below a certain threshold.
In terms of your problem, the tricky bit (conditions for global attraction) is done for you as it instructs you to find parameters so that $\frac{\dot{N}}{N}$ is maximum for intermediate (positive) $N$.
So when does $f(N) = r - a(N-b)^2$ have a maximum admitted at some positive $N$? This is a quadratic, so simple mathematics is enough.

$a>0$ is needed to ensure the parabola admits a maximum
$b>0$ is needed for the maximum is attained at positive $N$.
$r>0$ is also needed to ensure the maximum is positive. This is not clear from the information in the question, but the non-trivial steady states involve $\sqrt{\frac{r}{a}}$ and so $r > 0$ for these steady states to even exist.

So overall quite boring conditions and not a very satisfying question.

In general, a population $x$ with reproductive rate $b(x)$ and death rate $d(x)$ with dynamics $$\frac{dx}{dt} = x(b(x) - d(x))$$ displays the Allee effect if $b(0) < d(0)$. This is easy to prove with a basic grasp of ODE stability.

Thank you!  It is quite clear, now!


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Do chilli peppers change in composition after they change color?
I grow some chilli peppers and was wondering when the time is right to harvest them. Of course gardening-focused sources say that they are ripe when they change color. This usually happens very quickly (1-2 days) after a long period when they remain green (1-2 months), which would suggest that the gardening advice might be right.
However, I would like to know the full story, so I tried to find some relevant research. Here's what I found so far (mostly paywalled, sadly, so I cannot read the details)
Development of pepper (Capsicum annuum) seed quality
Quite unrelated, but suggests that the end of the ripening process is not simply the end of it all
Variations in germination and longevity of pepper (Capsicum annuum L.) seeds harvested at different stages of maturation
Similar to the above, seeds still continue to change while the pepper changes color
Changes in Carotenoid Esterification during the Fruit Ripening of Capsicum annuum Cv. Bola
New carotenoids are produced during ripening
Formation and transformation of pigments during the fruit ripening of Capsicum annuum Cv. Bola and Agridulce
More information on the above
Carotenoid Biosynthesis Changes in Five Red Pepper (Capsicum annuum L.) Cultivars during Ripening. Cultivar Selection for Breeding
Carotenoid Composition in the Fruits of Capsicum annuum Cv. Szentesi Kosszarvú during Ripening
Researchers were apparently really interested in carotenoids in the 90s...
Variation in phenolic compounds, ascorbic acid and antioxidant activity of five coloured bell pepper (Capsicum annum) fruits at two different harvest times
This one suggests that there are still some changes happening after ripening: With advanced maturation, total antioxidant activity increased, however some antioxidant components such as ascorbic acid, total phenols decreased.
The influence of fruit ripening on the phytochemical content and biological activity of Capsicum chinense Jacq. cv Habanero
This one, while apparently full of interesting data, only deals with two stages of ripening(immature and mature).
Ripening of pepper (Capsicum annuum) fruit is characterized by an enhancement of protein tyrosine nitration
Very promising, but once again, research ends at the color change.
Evolution of total and individual capsaicinoids in peppers during ripening of the Cayenne pepper plant (Capsicum annuum L.)
The only article which actually deals with peppers which were left to ripen a bit more. Capsaicin content decreases as the pepper ripens, followed by an increase when it's over-ripe. Weird, but at least I was able to legally obtain this article. Unfortunately it deals with capsaicinoids only.
Is there more information about what happens to the chillies after they are ripe? I'm not really interested in heat, but rather in other chemicals which affect flavor and nutritional properties of chilli peppers.
Edit: Based on what I observe at home, the peppers do indeed seem to be changing for at least a week or so after the change in color. I left some red chillies on the tree and their color is now noticeably darker than those which have just ripened a few days ago.

I welcome answers here, but this might be a case where it's best to do your own research a bit: you have an experiment already in place, so harvest at different points and see what you think.

@BryanKrause Of course I'm trying in the absence of reliable outside information, but my sample size is very small and this could take a long time, so I'd rather trust a scientific source than my own crappy research. The chillies I keep on the plant seem to not change very much anymore. I also read that keeping them on slows down the development of other fruit, which would support the hypothesis that there are still some resources being used by the ripe fruit.

When ripe the seeds become viable too.


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How effective is rinsing in removing microbes from surfaces
Microbes including viruses stay alive on surfaces depending upon the type of the surface like steel, wood, plastic, glass, marble etc. How effective is rinsing these surfaces with tap water in removing the existing microbes. I couldn't find this information on internet. Please provide source for your answer.

I guess this is too broad: there are many types of surfaces, some with pores (marble, wood), and also a huge variety of microbes. The method by which they attach often has nothing to do with biology (exception: biofilms). If you're curious to do some experimenting yourself, you can apply soot to a sample surface and try removing it by rinsing.,

I am not asking answer for every microbe and every surface. Whatever research and information is available on the subject is valuable and can be used to theorize.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and then [edit] or delete your question accordingly. In particular, avoid "questions with too many possible answers or that would require an extremely long answer".  ——— We also expect you to do some research on your own and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Rinsing the surface will make the micro organism growth static on the surface i.e it removes the micro organisms from the surface,but it is only for time being.But it is not effective in killing the micro organism.Mostly in labs,70% Alchohol is used to disinfect the surface.It is more effective in killing the organism.

As you are a new contributor, can I make the friendly suggestion that you would benefit from reviewing the Help on Answering questions. One key point is that stating an opinion is not sufficient. Evidence should be cited in support of your answer, generally in the form of references to papers or websites, preferably with links. Otherwise nobody can judge. Otherwise, how can the poster or readers judge whether your answer is correct or not? And it's worthwhile reading the section on only answering well-asked questions.


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Interpreting the reciprocal of $R_0$
$R_0$ is the average number of secondary cases arising from a single infectious individual in a fully susceptible population.
In many of the compartmental models for epidemiology, the parameter $\frac{1}{R_0}$ appears frequently.
In particular, in an SIS model, the non-trivial steady state is $(S^*, I^*) = \left(\frac{1}{R_0}, 1 - \frac{1}{R_0} \right)$.

Is there any intuitive interpretation one can give to the reproductive ratio's reciprocal?

I'm thinking some sort of average rate of secondary cases, but this doesn't feel right since $S^*$ is a number.

It's funny: $R_0$ doesn't actually follow as nicely as $1/R_0$ when focusing on the infected class.
In a SIS model:
$$\frac{\mathrm{d}S}{\mathrm{d}t} = -\beta SI + \alpha I \\ \frac{\mathrm{d}I}{\mathrm{d}t} = \beta SI - \alpha I$$
take finding the steady state of $I$. Whether a disease is able to invade is dependent on whether or not the steady state is greater than 0, which means that $I(S\beta - \alpha)$ must be positive. That is, $S\beta$ must be greater than $\alpha$, and $I$ isn't important as to whether or not the infected class changes (unless infecteds are extinct at 0). This means that $S$ must be greater than $\alpha / \beta$ for the disease to invade. Since disease prevalence is $I/(S+I)$ and there is usually a negligible-sized initial prevalence (i.e., $S(0) \approx 1$), we often care about $\alpha / \beta$, which is known as the relative removal rate. This is intuitive because $\alpha / \beta$ is the ratio of the rate of loss to the rate of gain of the infected class. If the rate of loss is greater than the the rate of gain, $\alpha / \beta$ will be greater than 1 and the disease will go extinct.
The reciprocal of the relative removal rate, $\alpha / \beta$, is $\beta / \alpha$, which is known as $R_0$.

1/R0 is the threshold fraction. If fraction of population vulnerable to particular infection is  more than 1/R0, only then infection can spread further. And if it is less than 1/R0 then infection can not progress and eventually goes away
And, 1-1/R0 is the fraction of population which requires vaccination so that we can have herd immunity.
(Reference
http://home.iitk.ac.in/~peeyush/mth426/Epidemiology.pdf
https://www.slideshare.net/singh_br1762/r0-value-herd-immunity)

Thanks for the response - however everything you have said is an immediate corollary of the fact that it is the steady state, so I was aware of this already. I was hoping for a more intuitive explanation for how one could "see" that $\frac{1}{R_0}$ is an obvious threshold from its definition? For example, the reciprocal of the rate of recovery is the average period of infection obviously, but I'm not so sure what abut the definition of $R_0$ means that $\frac{1}{R_0}$ is so important or lending to be a threshold?


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What species is this marine invertebrate sighted 2m below the surface near Halifax, NS?
This image was taken at ~2m depth, with a small ROV in Halifax, NS in May. We're in the Northwest Atlantic Ocean and as far as I know, don't have gooseneck barnacles.
Considering that it may be a polychaete worm as several other species were sighted during same dive (Tomopteris ?, Chaetopterus) and the fan appears to have more than 10 appendages. Possibly a sabellid or goblin worm?
Sizing is difficult to estimate but ~5cm in length.

Adjusted, enlarged version:


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Why all negative ssRNA viruses have helical capsids?
You can always say it's a coincidence, but is there particular need to have a helical capsid? Do they need their RNA to be more protected than +ssRNA? Is it better for RdRp attachment?
This paper suggests it is mostly for RNA synthesis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993539/:

For negative-strand RNA viruses (NSVs), eight families have been recognized by the International Committee on Taxonomy of Viruses (ICTV). The unique feature that distinguishes NSVs from the rest of the virosphere is that the nucleocapsid, instead of the naked genome, is used as the template for viral nucleotide synthesis. It is indubitable that the assembly of the NSV nucleocapsid is related to the unique mechanism of its viral RNA synthesis.

Also this one: https://www.sciencedirect.com/science/article/pii/S0042682215001543. But I don't know if anyone has tested inserting naked -ssRNA with RdRp and see if it does something.

Can you provide sources that support your assertion that all such viruses have helical capsids?


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What is the function of epiglottis?
The last time I came across this question was when I was in high school. And the explanation I was given is that epiglottis works like a valve, it prevents foods from getting into the windpipe. Still, if I google the majority of the top results agree with this answer.
Recently I got interested in rabbit anatomy after I bought a pair as pets. I learned they are "obligate nose breathers due to their epiglottis positioned rostrally to the soft palate". Then I tried to revise my understanding of epiglottis and that let to some sources that claim that epiglottis is not essential for swallowing. For example:

It was at one time thought that the epiglottis acted as " the lid of
  the larynx"; it was supposed that during deglutition it fell back like
  a flap over the laryngeal aperture in order to prevent ingress of food
  or water. This erroneous view as dispelled by Stuart, who proved that
  during swallowing the epiglottis actually moved forwards, to be
  squeezed between the base of the tongue and the rest of the larynx.
  This view cannot be disputed by anyone capable of judging, and the
  truth of it is borne out when observing a patient whose epiglottis has
  been almost entirely destroyed by lupus, but whose powers of
  swallowing remains unaffected.

Negus, VE (1927). "The Function of the Epiglottis". Journal of Anatomy.

Controversy has continued for well over 100 years regarding the role
  of the epiglottis in deglutition. We describe the effect of isolated
  epiglottectomy on swallowing success in a case series of 3 adult human
  subjects with isolated epiglottectomy due to trauma, surgery, or
  cancerous erosion. The patients were 42, 51, and 70 years of age, and
  swallowing was analyzed objectively with videofluoroscopy. All
  subjects exhibited successful swallowing with all food types: thin
  liquid, puree, and solid food. Specifically, the patient with
  traumatic epiglottectomy exhibited rapid swallowing success, the
  patient with surgical epiglottectomy exhibited a short period of
  dysphagia due to postoperative edema, followed by swallowing success,
  and the patient with epiglottectomy due to cancerous erosion of the
  entire epiglottis exhibited long-term adaptation, with successful
  swallowing maintained. We conclude that the epiglottis is not
  essential for successful swallowing in humans, because individuals
  can readily adapt to isolated epiglottectomy and avoid tracheal
  aspiration.

Leder, Steven B et al. “Epiglottis is not essential for successful swallowing in humans.” The Annals of otology, rhinology, and laryngology vol. 119,12 (2010): 795-8.
Judging from google searches and Wikipedia entry on the topic it seems the dominant view is: epiglottis prevents food from getting into the trachea. But many research like the ones  I have mentioned above says that people can swallow without epiglottis. How to make sense of these apparently contradictory claims?
Edit: My question is not the same as the question suggested. The suggested question seeks the function of "hyoepiglottic ligament" which is a ligament that connects epiglottis "to the upper border of the body of the hyoid bone". My question is related to the function of epiglottis itself in the background of contradictory claims found in the literature.

@tyersome No it doesn't. I have added the reason in the OP.

@tyersome As the user who asked the question you proposed as dupe, I can say that this post is clearly asking a different question and should not be closed. (this is akin to comparing the function of the knee and the funciton of the MCL ligament or to comparing the function of the lungs vs the function of the trachea)

AhmedAbdullah and @theforestecologist — Ok, close vote withdrawn.

You are right, The main function of the epiglottis is to seal off the windpipe during eating, so that food is not accidentally inhaled.(quote from here).
It's a flat shield of cartilage, which is obviously an efficient valve, It's a valve between the trachea and the esophagus.
It lets lions to eat a pound of meat without choking on their prey. It lets humans drink tea without coughing on their buddies.
Information stating that it's "possible" to eat without an epiglottis doesn't imply that it's "efficient and safe", and contradicts medical interventions where they use a piece of ear cartilage to build a new epiglottis.
Survival didn't encourage the "possibility to eat"... it has made animals very robust and efficient at it. Herbivores can spend most of their day eating, and are often attacked while they are eating and drinking. Carnivores also have reasons for efficient swallowing, big carnivores can eat many pounds of meat very fast while fending off competition from hyenas and other predators.
Sleep apnea patients have their epiglottis modified to give room to breathe at night, and they risk choking and aspiration for a while, although they can adapt because they keep some of the cartilage, so they still have a valve.
Different animals have different breathing habits, with some being obligate nose breathers, including human babies of under 6 months and up to 6 years. That's because the epiglottis either contacts the trachea or it leaves space there.

I would strongly advise refraining from using healthline.com as a source of "reputable" information (read here). Healthline.com competes with equally non-reputable WebMD and is associated with additional non-reputable medical websites such as Yahoo! Health and DoctorOz.com.  --------- More reputable sources could include the CDC, medlineplus.gov, mayoclinic.org, or actually reporting from primary literature  (try searching PubMed).

You also make a number of claims throughout your post that are not supported (e.g., ear cartilage procedures, feeding efficiency of animals, sleep apnea patients and adaptation to treatments, and breathing habits). Please update your post with support for these claims. Thanks!


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Why are diseases generally specific to a particular species
"Zoonosis" is the process of transmitting a disease from an infected animal to a human. This suggests that animal-to-human transmission is not common. HIV is believed to have first spread to humans zoonotically, but has since mutated to a human-only strain.
This all raises the question: Why do diseases mostly just target a particular species? Aren't most metabolic processes very similar across species, especially within the same order and class? Dogs and cats can't catch the common cold, but they have similar diseases of their own.
There are obviously enough similarities that mice can be used in preliminary tests of human drugs, but the results are very tentative until human trials are done.

The pathogens which are responsible for certain diseases have adapted to their hosts. Viruses need to attach to structures on their cells they invade to replicate. These structures usually consist of proteins and are unique for the respective species (e.g. the ACE2 receptor in the case of Covid-19). During an infection, there will be billions of viruses released and some carry mutations, which are just mishaps in the replication process. In most cases, these errors are leading to a virus that is not viable or cannot infect, i.e. the mutated virus can't replicate and the mutation gets lost, but sometimes it can infect the host better and thus will have a higher chance to propagate.
If this happens with a zoonotic pathogen after it has spread to a human, a new disease has emerged.


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Bats, bees and nectar
I have been thinking about this for a long time and your thoughts would really help. Since it's known that bats spread Covid 19, I studied more about places that they may have contacted. The first place that I came across was how they feed. Bats usually feed on nectar, now say that the bat is tested positive for covid 19. This may lead in others animals like bees getting their nectar contaminated. Now when these bees use the nectar to produce honey, and then the beekeepers collect the honey.
This may cause us humans getting positive for covid 19 when we eat honey. So why haven't we already tested positive for covid a long time back? It would be great if you can help me out over here.
Pardon my English, for it's my second language.

There are a number of incorrect assumptions here, including the basic premise of your question: bats absolutely do not spread COVID-19. This is a misunderstanding that has unfortunately gained a lot of traction amid the pandemic hysteria, and one that only serves to deepen the public's mistrust of bats and encourage people to harm or kill wildlife that pose no threat to anyone.
It's true that SARS-CoV-2 is similar to other bat coronaviruses, and it's not implausible that it could have originated there, but that's literally all we know at this point - we haven't even definitively established the true origin of the virus, much less unraveled the mystery of how it spread to humans.
What is clear, though, is that it's not being spread by bats. If nothing else, the rampant speculation about possible intermediate hosts suggests that it didn't come about merely as a result of direct contact between humans and bats, but through a much more circuitous pathway involving a specific combination of hosts and conditions that favored the jump to humans. Going beyond that, the idea that nectar-feeding bats could somehow "contaminate" the flowers, and that this in turn could somehow lead to live viruses showing up in honey produced by bees that visited those flowers, is mistaken on several levels.
You might be interested in this article, which gives an overview of what we currently know about the virus' origins: https://www.nature.com/articles/d41586-020-01449-8.
In short, there are a lot of things to be concerned about when it comes to the spread of the pandemic, but one thing you definitely don't need to worry about is the possibility of contracting SARS-CoV-2 from bat-pollinated flowers.


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Is this a black carpet beetle and how do I keep it alive?

About 3mm in length, location Hong Kong. Is it possible to keep it as a pet? I currently have it in a clear plastic case (kinda cubic, 6.5cm per side) with a piece of moist paper. It rarely flies.


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How much energy is used to construct a pound of fat tissue?
A widely cited figure is a pound of fat contains 3500 calories of energy in fatty acids.
However, a pound of fat also contains adipose cells, arranged in adipose tissue, connective tissue etc.
When a human breaks down fat to use as energy, from what I understand it doesn't break down the fat cells, just liberates the triglycerides stored inside those cells.
Those fat cells, and connective tissue took energy to assemble as well.
How much energy is used to create a pound of fat tissue?
Let's assume that all the cells and the triglyceride stored inside them are created from scratch.

A rough answer to a rough question
According to a study conducted in the 1960s, human adipose tissue, on average, contained (per 100g wet weight) 87g fat, 2g protein, 2g sodium and potassium and 10g water. (Nothing else was measured.) This suggests that approx. 3% of adipose tissue is solids other than triglyceride.
The figure quoted is presumably the energy yield for the complete oxidation of triglyceride. The energy yield for the complete oxidation of the non-triglyceride solids in adipose tissue  — the appropriate, if hypothetical, comparison would be less than that for triglyceride, which is much more chemically reduced, so the yield for the oxidation of non-triglyceride might be approx. 1–2% that of triglyceride.
The energy needed to bio-synthesize any organic compound (triglyceride, carboyhdrate or protein) is more than is obtained from it by oxidation because a negative free energy change is needed to drive reactions. Hence, as regards the relatively constant (slowly turning-over) portion of the adipose tissue, the cost would be higher — perhaps 2–3% of that quoted produced by oxidizing the triglyceride.
The problem with this question
Some people say that there is no such thing as a stupid question. Nevertheless, there are questions that are formulated as if their answer will establish solve some problem, when in fact it will not because the premise on which it is based is false.
In this case a comparison is made between the triglyceride and non-triglyceride content of adipose tissue with the implication being that the latter should be assessed in the creation of the former:

“Those fat cells, and connective tissue took energy to assemble as
  well. How much energy is used to create a pound of fat tissue?”

As already mentioned, it is invalid to make a numerical comparison between the energy required to synthesize one compound with that released by the oxidation of another compound, as it costs more to synthesize a compound than is released by its oxidation.
However, quantitatively more fundamentally wrong is the implication that the one-time synthesis of the structural components of the cell should be costed into the repeated oxidation of triglyceride in that cell. How many grams of triglyceride are synthesised per gram of cell structural material during the lifetime of a cell? Very many, I should imagine if the cells turn over much more slowly than the lipid they contain.
It would be more pertinent (assuming that you are interested in such things) to ask what the cost is in terms of the energy used by whatever muscles are used by the lungs to breath in the oxygen needed to oxidize the fat, and the energy used by the heart muscle to pump the blood containing the oxygen to the fat cells so that it can be oxidized.
Finally, it is naïve to think of the energy cost of maintaining a fat cell in terms of the synthesis of its structural components. Other metabolic processes are continually occurring that require energy even in fat cells.
No doubt it would be possible to perform a calculation that took all these things into account (although what would you start with “from scratch” — ingested carbohydrate or carbon dioxide and water?). Personally, I am happy to accept that the system makes a profit and interest myself with the details of how it operates and adjusts to different circumstances.

Maybe more to the point regarding the second half of this answer: all of the maintenance of fat cells themselves (as well as all the activity of the lungs, heart, etc) is wrapped up in the concept of "basal metabolism", so it's sufficient to consider the calories stored in a given mass of fat when approaching the issue from a 'calorie economy' perspective.

@BryanKrause — You’re right, the basic metabolic rate stuff would take all that into account. It’s the kind of thing physiologists do, and no doubt they have figures for different tissues. Perhaps one of them could enlighten the poster.

Great answer thank you!


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Floats of Algae, a house-made conjecture
Background
In North of Scotland there are many seaweed types. One is a green algae (chlorophyta).
They are full of 'bubbles'. According to web searches one of those bubbles (there are two types you can notice by sight) are spores; the other ones are called floaters.
According to searches, Kelp (or brown algae) floaters are full of gases. But we find most of the Chlorophyta full of water, some of them contain bubbles but tiny ones.
Conjecture
The water inside could be of a lower density than the sea water, instead of air bubbles.
Question
Any information on this respect?

One consideration is the energetic costs to the organism. It's going to be energetically more favorable for an organism to be in osmotic balanced (isotonic) with its environment than to constantly work to maintain lower internal osmolarity through active transport of water or solutes. Second thing to consider is cell size and density differentials. Air at sealevel is several hundred times less dense than water, so even tiny gas bubbles would create significant buoyancy for a cell. On the other hand, pure water is only about 2.5% less dense than sea water, which means a much (much) larger volume would be needed to generate equivalent buoyancy.
All that said, there seems to be some plausibility to your conjecture, as there are some large marine phytoplankton that use active water transport to maintain vacuoules at lower density than that of seawater (Source).
This paper discusses some other competing mechanisms as well, but as the author of the article states:

"... most of the cases of positive buoyancy in phytoplankton not
  generated by gas vesicles concern diatoms..."

That's not an incontrovertable refutation of your conjecture, but it seems to me that gas vesicles are a much more efficient means of generating buoyancy, and would probably be energetically favored over other biological means of generating buoyancy.

I really appreciate your knowledge, thanks. (I can't yet upvote answers.) Where do you take the energetic considerations from?

My reasoning is this. For the water in a cell compartment to be less dense, it would need to have a lower solute concentration than the surrounding seawater. Maintaining that disequilibrium between the cell and its environment requires constant energy expenditure to overcome the constant osmotic diffusion of water across the cell membrane.
Full disclosure, I'm a microbiologist, so there may be some aspect of algae cell physiology I'm overlooking. I tend to think of every problem from a bacterial POV.


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Area under the curve in a drug concentration curve
I am not from a background on pharamacokinetics and trying to learn some concepts.
I noticed that the definition for AUC involve the first 24 hours. For example in here AUC is defined as "the area under the concentration–time curve over 24 h
divided by the MIC."

Is there any reason why this 24 hours is selected?
Say I test 2 treatment strategies. Strategy 1: 500 mg tablets given 3 times a day (500m g×3, 8 hours apart) and Strategy 2: 500 mg tablets given 3 times a day for 2 days (500 mg×6, 8 hours apart).
In this case if I simulate the change in the drug concentration over time assuming exponential decay, then the two concentration curves would have the same values for the first 24 hours. Therefore the AUC obtained in the first 24 hours for these two strategies are the same. But strategy 2 performs better than strategy 1. So, in this case isn't the total area under the curve above MIC a better index than consdiering AUC in the first 24 hours?
Is it wrong to inform why a particular dosing strategy is effective than the other one using 'Total area under the curve (rather than of the first 24 hours)'?

The link in the question body isn't working, could you please correct it? Thanks.

This definition of AUC is non-standard.
The usual definition does not involve the MIC or 24h: it is the area (~ integral) of the plasma concentration curve as a function of time, from first administration time $t_0$ time to infinity. (You will sometimes see it subscripted as $\mathrm{AUC}_{0 \to \infty}$)
In the case of so-called time dependant antimicrobials (beta-lactams, macrolides, vancomycin), the bacteria are inhibited from replicating as long as the concentration stays above the MIC (minimal inhibitory concentration). Often a second threshold, the MBC (minimal bactericidal concentration) is defined corresponding to the required concentration to kill rather than just inhibit replication.
As you stated, the second strategy has indeed a longer duration above MIC. It is more effective from a purely kinetic standpoint. Whether than translate to clinically relevant effects depends on the antibiotics, the bacteria and the tissue under consideration.
A second point is whether a higher AUC is beneficial if the time spent above MIC or MBC is the same (nb: not the case here). However this also depends on factors beyond just pharmacokinetics.
As an aside, some antimicrobials like the aminoglycosides display a "concentration dependant" effect where the peak drug concentration determines the effect, dictating different dosing schedules.


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Why are antibodies Y-shaped?
I generally know how antibodies work by binding to antigens, but what is the specific purpose to being Y-shaped, as opposed to any other shape? Does this aid their function? Thank you.

In a comment on this question, asking the poster what research had been performed before posting, I drew his attention to illustrations of antibody–antigen interaction in general articles about antibodies. In order to be inclusive to users of this site with visual impairments (who are perfectly able to use the web but may rely on screen readers) I added a rider. The fact that this comment was removed suggests the rider was interpreted as an insult to the poster of the sort "anyone who is not blind…". This was categorically not the case.

Having two antigen-binding sites allows agglomeration or clumping of antigens, which stimulates further immune response (phagocytosis).

Antibodies also known as immunoglobulins consists of two heavy chains and two light chains linked via disulfide bonds to form Y-shaped structure (as shown in figure below).
This Y-shaped structure bestows antibodies with two properties. Firstly, antigen-binding through the antigen binding fragment(Fab); and secondly, interaction with immune cells and proteins through fragment crystallizable region (Fc) to stimulate and regulate host immune defense mechanisms.
Fc and Fab portions of the antibody molecule are joined by flexible hinge region which enables antibodies to interact with the antibody-binding proteins and thus help in mediating immune effector mechanisms. So, this Y-shaped structure provide proper flexibility for binding to antigens and proteins/immune cells of immune system.

Reference
https://www.ncbi.nlm.nih.gov/books/NBK27144/
https://immense-immunology-insight.blogspot.com/2013/10/antibody-structure-simplified.html

Your answer is dominated by a graphic that is predominantly text. While graphics are often important to describing concepts in biology, in this case the parts of the graphic text that are necessary could (and should) have easily been written as text, making them accessible to users with visual difficulties. This might also have helped you focus on what was important in your answer.

Thanks for your advice, will keep it in mind from now onward.

IMHO, this does not explain the Y structure. Single chain Fragments (ScFv) also have an Fab and an Fc, and, due to their smaller size, can even better diffuse into tissue.


text:
Are there any proteins assembled from non-adjacent parts of the genome?
Many proteins are assembled from multiple exons with the introns between adjacent exons being spliced out. But are there any proteins that have unrelated to them exons in the middle of their sequence?
I think the equivalent question would be: are there any protein-coding genes (in any species) that are broken in two or more parts by another protein-coding gene(s)?

Not directly related to the question as you have asked it, but do consider https://en.wikipedia.org/wiki/Protein_quaternary_structure as well.

I think that you are talking about trans-splicing. This does indeed happen. It is fairly common in protist organisms, though in humans it is quite rare. For more information about how this process works, including mechanisms in vertebrate organisms, see this paper.
Here is one model from that last paper for how it works:

Yes, this is what I was thinking about. Thank you!


text:
Available Protein sequence alignment dataset and HMM model
I am new to biology and I find my algorithm may be used in the Protein sequence alignment, since it is a henced HMM model. I find that people use HMM to generate noisy copies of the consensus sequence of different lengths. There is a figure show the process:

It seems Professor Richard Durbin may release some dataset. But how can I find available datasets? I lost in the bio-vocabulary and fail to find datasets. Also I am wondering whether or not this topic is very minor in this community?
Update:
Since I may abuse the vocabulary, it may be better to post the original word I read.

It may be helpful to post this on bioinformatics.stackexchange.com, which is specifically focused towards bioinformatics questions such as this. Additionally, when you say "dataset", what do you mean? Are you talking about sequence alignments, HMM parameterizations, profile HMMs, or consensus sequences? I would guess sequence alignments, but those are extremely common and fairly trivial to generate so it seems unlikely.

@MaximilianPress Thanks for your comment. Maybe it is a good place to post it. I add more details. When it comes to the dataset, I mean we need some data to train the HMM model and learn the model parameter. I guess the dataset is some real sequence instead of generated artificially.

DNA and protein sequences (both are reasonable to use in HMMs) are available at a variety of sources, such as EMBL, NCBI, and others.
To input them into a model such as an HMM which draws on comparisons between different sequences, you will most likely need to produce a sequence alignment, which is a data format in which the sequences are processed into a matrix (generally not delimited in any way but rather where each column is a single string character) where columns or positions of the matrix are considered to occupy the same position in the sequence. These positions can be "gaps", represented usually by "-". The diagram at the top of the Durbin figure is such an alignment.
There are many many many tools for aligning sequences, both protein and DNA (DNA is a "nucleotide"; RNA is also a "nucleotide" sequence, but DNA is much more common to align in most applications).
Some of the common tools for generating multiple sequence alignments are ClustalO and MAFFT. Notably, you are not as interested (I think) in tools such as BLAST which are mostly about searching single sequences against databases using local alignment, rather than for generating multiple sequence alignments for input to other programs.
I believe that with some searching you can find existing multiple sequence alignment databases. People do not usually save them and put them in databases or repositories because usually which data you use is very specific to the problem that you are interested in, and they are quite simple to generate. Most of the databases are likely to be quite old for this reason; I found one such old database (described here) with a bit of googling.


text:
Why are the products of Meiosis 2 different?
In Meiosis I, 46 chromosomes crossover. These mixed chromosomes then split off into new cells. In these new cells, Meiosis II occurs, where these mixed chromosomes have their chromatids ripped apart.
What I'm confused about is why does Meiosis II produce 2 different new cells if you're just separating 2 identical chromatids? Is it because when crossing over the genes makes the both chromatids different?

would someone care to explain why the downvote? I think this question meets community guidelines

Indeed, this is all due to the crossing over between different alleles. For example, put the case of one cell that contains 2 chromosomes, one from the mother and another from the father. Each chromosome contains two alleles: Ab (mother) and aB (father).
The first thing that they will do is divide into two chromatids each one getting to: Ab[1M] (one mother's chromatid) and Ab[2M] (second mother's chromatid) and the same for the father aB[1F] and aB[2F]. Notice that the chromatids still joined by the centromere.
Now, the crossing over comes: in this case, if the A[2M] from mother's chromosome gets exchange with a[1F] of the father's chromosome, we get: Ab[1M], ab[2M], AB[1F], aB[2F].
As you see, when they segregate you will get 4 different cells with two alleles: Ab, ab, AB and aB.
I hope this answers your question.


text:
How can prokaryotes repair double strand breaks by homologous recombination if they're haploids?
Title says it all, I must be going crazy.

Several answers to this question:

Much of the time what bacteria are doing to repair DSBs is actually non-homologous end-joining, which does not require strict homology. This is the more likely mechanism earlier in the cell cycle when copy number is more likely to be ~1.
If cells have completed DNA replication (later in the cell cycle), there are at minimum 2 copies of all DNAs present in the cell. These can be used for homologous recombination.
Bacterial chromosome copy number can be overreplicated in some situations, such that DNA replication is not synchronized to the cell cycle and is more than normal for a cell. In these situations copy number can be >2.


text:
Why the major gene model can be supported by finding de novo mutations in affected cases?
I found a sentence which I can't fully understand in a publication on the genetics of autism.

The unified major gene model is supported by the significant increase
  in damaging de novo mutations found in subjects with ASD as compared
  to their unaffected siblings.

Is it saying under the major gene model, the de novo mutations comprise the majority of genetic risk?

It helps to give context and a source citation in questions like this. With some research I identified the source of the quote as Torre-Ubieta, "Advancing the understanding of autism disease mechanisms through genetics".
The quote comes from a section of the paper discussing the main two different genetic models of ASD: (1) the polygenic (many genes contributing small influences) model, and (2) the major gene model, where a variation of a single gene is responsible. The first two sentences of the paragraph having the quote are:

The unified major gene model62,63 is supported by the significant increase in damaging de novo mutations found in subjects with ASD as compared to their unaffected siblings44,49. Further support for this model is seen in the phenomenon that there are more inherited SNVs that disrupt protein function in conserved genes transmitted from the mother to individuals with ASD than in unaffected siblings73.

The sentence in question (the first) is simply citing evidence supporting the second kind of model; it is not claiming that the majority of risk is due to de novo mutations.  As to how de novo mutations support the major gene model, it helps to consult the papers cited in the sentence.  Review of citations 44 and 49 show that those with ASD often have rare de novo mutations that look to be gene-disabling, whereas their unaffected siblings do not.  This suggests that disabling of a single gene can bring on ASD, and thus fits with the major gene model, but does nothing for the polygenic model since it supposes one gene difference has only small effect.
Let me add that the two models are not mutually exclusive: a polygenic model might explain the observed familial occurrence of ASD, while a de novo major gene model might explain why only a few in a family are affected.

Thanks a lot for your detailed answer! I'll do better in posting a complete question with context or reference next time. I was confused yesterday because I didn't figure out the reason why the evidence raised in the sentence I cited can't support the polygenic model. Now it's much clearer after your explanation.


text:
Factors of infection rate
I refer to J.H. Jones' Notes on R0.

Preliminaries
The standard SIR model consists of a system of three differential equations
$$ds/dt = -\beta  s  i$$
$$di/dt = \beta s  i - \nu i$$
$$dr/dt = \nu   i$$
for the fractions $s, i, r$ of susceptible, infected, and recovered (removed) individuals, $dt$ = 1 day.
$\beta$ is the infection rate, i.e. the number of individuals an infected indiviual infects per day, $\nu$ is the removal rate, being defined as the reciprocal of the duration of infectiousness $d_i$ (measured in days), i.e. $\nu = 1/d_i$. The reproduction number $R$ is the product of infection rate and duration of infectiousness, i.e.
$$R = \beta \cdot d_i$$
To reduce the growth of spreading of a disease, mitigation measures typically target at the infection rate, at least when a reduction of the duration of infectiousness is not at sight.
To estimate the impact of a mitigation measure on the infection rate, it is worth to consider it as the product of several factors, which may be influenced separately and more specifically.
One common approach is to consider the infection rate as the procuct of

transmissibility per contact $\tau_c$, i.e. the probability of getting infected when being in one contact with an infected person and

mean rate of contact $c$, i.e. the number of single contacts an average individual has per day, i.e.

$$\beta = \tau_c \cdot c$$
Let alone that it is not so easy to define what a contact is, other factorizations are conceivable when considering these candidates:

transmissibility per hour $\tau_h$, i.e. the probability of getting infected when being in contact with an infected person for one hour

mean duration of contact $h_c$ (measured in hours)

Let "being in contact" specifically mean "closer than 1.5 m in the average".
We then have
$$\beta = \tau_h \cdot h_c \cdot c$$
We can group factors:
$$\beta = \tau_c \cdot c$$
with $\tau_c = \tau_h \cdot h_c$, and
$$\beta = \tau_h \cdot h_d$$
with $h_d = h_c \cdot c$ the number of hours per day an individual is in contact with other persons.
Question
I am looking for references where such factorizations of the infection rate are considered, especially in the context of Covid 19.

I have not found texts relevant to your question and related to the spread of SARS-CoV-2.  However, here is a publication that discusses the utility of contact duration data when constructing infection models, in the general case --
Simulation of an SEIR infectious disease model on the dynamic contact network of conference attendees
Methods
At a conference, 405 attendees volunteered to wear RFID tags. Over two days, the time and duration of 28,540 face-to-face interactions between these individuals were recorded, with a temporal resolution of 20 seconds. Note the spatial limits of the RFID data:

RFID devices engage in bidirectional radio communication at multiple power levels, exchanging packets that contain a device-specific identifier. At low power level, packets can only be exchanged between tags within a radius of 1 to 2 meters.

From these data, three networks were constructed:

dynamic network (DYN) -- this network preserves the sequence and duration of contacts between individuals.  Using the language of graph theory, this is a directed network with weighted edges.
So, if individual A comes into contact with individuals B and C, and individual B is infectious, individual A must contact individual B before individual C in order to have a chance of A → C transmission.  Causality constrains the chain of transmission.
heterogenous network (HET) -- this network preserves the duration of contacts between individuals but disregards the sequence of contacts. The graph of this network is weighted but undirected. Adopting the previous example, B can infect C via A regardless of the relative order of the A ↔ B and A ↔ C interactions.  Causality is suspended, and the probability of transmission depends on the number and duration of contacts.
homogenous network (HOM) -- this network inherits the topology of HET, but ignores the duration of contacts.  The graph of this network is unweighted and undirected. Each contact event carries an equal probability of resulting in transmission, so the probability of transmission depends solely on the number of contacts.

To simulate the spread of an infectious disease over realistic time-scales, each network was longitudinally extended using three procedures:

repetition (REP) -- the recorded contacts are repeated with the same duration and order.
random shuffling (RAND-SH) -- the structure of the network is preserved, but the IDs associated with the nodes in the network are shuffled between iterations.
constrained shuffling (CONSTR-SH) -- same as RAND-SH, but the reordering of IDs is constrained to preserve individual social activity (i.e. IDs with many contacts are not assigned to a low-contact node in the network) and repeated contacts.  This procedure rectifies the oversimplifications of REP and RAND-SH by acknowledging that people tend to interact with the same people day-to-day, with occasional contacts with strangers.

The authors applied a SEIR epidemic model (Susceptible, Exposed, Infectious, or Recovered).  For each network-procedure pair, they considered two disease scenarios with different assumed values of mean latency period (σ -1), mean infectious period (ν -1), and transmission rate (β):

very short incubation and infectious periods

σ -1 = 1 day
ν -1 = 2 days
β = 3.10 -4/s

short incubation and infectious periods

σ -1 = 2 days
ν -1 = 4 days
β = 15.10 -5/s

A note from the authors on why these values were chosen:

These sets of parameter values were chosen to maintain the same value of β/ν, which is the biologic factor responsible for the rate of increase of cases during the epidemic outbreak, while changing the global timescales of incubation and infectious periods, and assessing the role played by the social factors embedded in the contact patterns.

Results
Epidemic outbreaks in the three networks across the three data-extension procedures were compared by computing the mean R0, defined by the authors as the mean, over all iterations, of the number of secondary cases from the single initial randomly chosen infectious individual.
Considering the simplified REP procedure, higher values of R0 were observed in the HOM network compared to the HET and DYN networks, for all scenarios.  The authors explain this observation by noting that the probability of rapid extinction of the pathogen was smallest for the HOM network; indeed, this held true independent of procedure.
In terms of the final number of cases (R∞) and the rate of spread, the HET and DYN networks were similar for both disease scenarios.  The peak of the epidemic was reached first in the HOM network, on average, consistent with the reduced probability of extinction.
In the RAND-SH procedure, spread was slower but lasted longer, leading to a larger R∞ for all networks.  In general, greater shuffling of ID tags led to more efficient disease spread, such that R∞(RAND-SH) > R∞(CONSTR-SH) > R∞(REP) for all networks and scenarios.  The interaction of more efficient disease spread in the RAND-SH procedure with increased values of σ -1 and ν -1 in the "short" scenario seems to produce consistently higher R0 values across networks (see Figure 3), though high variance in R0 means the effect of this interaction is not significant.
Conclusions
By comparing the different network types across all procedures and scenarios, it was shown that ignoring the direction and duration of contacts overestimates both the rate at which a disease spreads and the total number of individuals infected.  Additionally, shuffling individual positions in contact networks while preserving network topology increases disease spread when compared to a static model, though this effect is buffered by the "realistic" inclusion of preserved sub-networks of repeated contacts.
While this publication does not directly integrate factors for the duration and rate of contacts into the SEIR model, as suggested by Hans-Peter Stricker, the authors are able to show that mapping such a model to networks in which the direction and duration of contacts are encoded as edge weights leads to different measured outcomes (R0, R∞, time to peak) when compared to topologically identical networks lacking these encodings.

Thanks for this great answer which will give me a lot of reading. It - and the study you point to - seems to be related to this question I asked at Mathematics SE: https://math.stackexchange.com/questions/3682077/how-does-the-reproduction-number-depend-on-characteristics-of-the-physical-conta

@Hans-PeterStricker, if you do really believe mine is a "great answer", I'd appreciate if you accepted it.  Given the bounty is now a week old and no other answers have popped up, I think it's appropriate.

I usually wait until the bounty would expire - which will be tomorrow - but thanks for the hint.


text:
Why does the gravity of Earth appear in this formula estimating speed?
I'm currently reading the wonderful book The Dinosaurs Rediscovered by Michael J. Benton. It contains the formula
$$v = 0.25 * g^{0.5} * SL^{1.67} * h^{-1.17}$$
where $v$ denotes velocity, $SL$ is stride length in $m$, $h$ is hip height in $m$ and $g$ is the gravity of earth. Not being a biologist (in fact not being really familiar with any natural science), I don't quite understand why gravity appears in this formula. I can't imagine this would hold in any meaningful way in circumstances where gravity where different from earth's, so why not simply express the term $0.25 * g^{0.5}$ as $0.78 m^{0.5}/s$, which I assume stems from some fitting of terms to observed speeds given stride length and hip height.

I know nothing about this, but this formula appears to be the work of one Robert Alexander. If you can find some of his papers, he likely explains how this formula was developed. Alternatively, this website seems to go into the derivation.

Reading a little bit about the derivation of the formula as well as the corresponding wikipedia article, I would assume the g stems from the origin of the equation in Froude's number.

This question is about physics or engineering, not biology. The fact that the formula can be applied to biological movement is irrelevant.

Units
G is going to be different depending on what units you use, the original formula was derived using FEET not meters. As it stands the formula works both with metric and imperial units. With your change this would not be true. Paleontology is often uses both units so a formula that is not unit dependent is preferable.

This is because a leg can be modeled as an inverted pendulum (like a metronome). A pendulum is a function of gravity. This creates a simple relationship between hip height, stride length and speed. There is more to it but you would need to ask the physics community for details.
You can in facts build a mechanical robot that walks downward slopes by itself with nothing else than 2 inverted pendulums.
McGeer, T. (1990). Passive dynamic walking. I. J. Robotic Res., 9(2), 62-82.

Thanks, that answer also clarifies some things for me. I have to say, I didn't even know about the origin of this formula in physics when I asked the question. I just love dinosaurs (and mathematics) and this formula appeared to me quite beautiful and surprisingly universal.

What McGeer work showed is that there is a speed at which walking is almost effortless because you just let your legs act as pendulums (which is function of g, SL and h). Alexander seems to have showed that there is indeed a fixed relationship between v, SL and h across animal species, as you would expect, and used it to predict the walking speed of dinosaurs. That's an interesting use of biomechanics.


text:
Is "Cloning" exact or almost similar to parent?
I was studying "Reproduction in Organism" as an interest of my own and there was a line

offspring produced through single parent are exact copies of their parent. Also, they are genetically identical.

So, in here, it says, "genetically identical" (I assume that identical here implies exactly same) but then the next line quite confused me.....

The term clone is used to describe such morphologically and genetically similar individuals.

Here, the term "genetically similar" is used.
So, clones (offspring produced through asexual reproduction- involvement of one parent) are "genetically exact" to their parents or genetically similar?
If "genetically exact", Then how is it possible since, there is 'No 100% efficient DNA Replication' that can be achieved?

Aren’t you splitting hairs rather?  I have no idea what book you are reading — you should always give a reference and preferably a link in questions — but the author of a book, like a lecturer in front of students is trying to communicate the essence of a concept, and if he hedged ever statement with disclaimers he’d never get his message across. Is it really important for what is being described and the distinction being made that there can be mistakes in DNA replication?

Biology is a lot messier than pure math, so if you insist on the same level of perfection and rigidity in definitions you are going to be very frustrated. You are correct that DNA replication is never 100% efficient, so "genetically similar" is probably a more literally accurate description of a clone.  However "genetically similar" is a very vague term, which we might apply (depending on context) to two cells from the same individual, clones and parents, two siblings, a child and a parent, two unrelated members of the same species, or even two members of the same biological kingdom. It is sometimes useful to distinguish different levels of similarity, even if we acknowledge that the boundaries of our definitions are fuzzy and arbitrary. Saying two individuals are "gentically identical" is really a short-hand for "in the context of the phenomena we're looking at, genetic differences are so small as to be irrelevant"
If you look at the level of DNA base pairs, it's estimated the average number of base pair differences between two humans is about 20 million or 0.6% of the 3.2 billion base pairs in the human reference genome. Clearly that 0.6% difference can generate a lot of variation in readily observable traits. During development some cells in an individual will undergo somatic mutations, so even two cells from the same individual may not be literally genetically identical. For the most part (excluding catastrophes like cancer), these differences will be in only a handful of bases out of the 3.2 billion, and won't cause any observable difference in the two cells. The difference between a parent and their clone will mostly be these somatic mutations, probably with some additional mutations caused by the cloning process.


text:
Is self-fertilization in hermaphrodite animals an asexual or sexual reproduction?
There are various Hermaphrodite animals, which can self fertilize.
So can this be called sexual reproduction because  there is fusion of gametes though from the same individual
? Or asexual because the involvement of a single parent(characteristics of asexual reproduction)?
There is a similar question-
Can Self-Fertilization in flowers be called asexual reproduction?
Can I extend the same logic mentioned in the  @Hawkeye's answer to the given question link on the animal case above and say that it is a case of sexual reproduction?

You can (and should) extend the logic in Hawkeye's answer. Self-pollination is sexual reproduction.


text:
Replicate DNA so its visable to the naked eye
So my question has a few sub sections after the main title question.
Firstly, is it possible to replicate a pure sample of an individuals DNA to an amount that is visible to the naked eye?
If possible, how long would this take?
What would be the estimated cost?
How could you preserve the sample once obtained? I.e. Under acrylic or some other medium.
Thank you for any help provided.

Welcome to Biology.SE! Please take the [tour] and then go through the help pages starting with [Ask] questions effectively on this site and [edit] your question accordingly. In particular, each question should be posted separately — this improves the chances that you will get answers for each question and makes the answers more accessible for future users and your last two questions are not biological and so are off-topic for this site. In addition, for the first two questions to be answerable would require more information: how much DNA are you starting with? Visible under what conditions? ⋯

I think you would greatly benefit from exploring some of the introductory material available online such as Khan Academy. That will help you avoid asking questions that seem to fit this sites criteria for "homework".  ——— Finally, we encourage you to always do some research on your own first and then, informed by what you have learned, ask any questions you still have (ideally with references to reliable sources). Thanks!

Are you only interested in human DNA? There are children's science kits for extracting DNA from onions, strawberries, or other fruit, and vegetables, which produce readily visible amounts of DNA. See for example https://www.amazon.com/ScienceWiz-7811AZ-DNA-Experiment-Kit/dp/B001DTD0H2 (I have no connection to the vendor, it's just provided as an example).

I downvoted this because it appears to be an inquiry about services which might provide a visible lump of DNA (supposedly many copies of a particular human's genome) preserved in the form of a knick-knack conversation piece for a gift.  That seems inappropriate for this biology site.

No need to replicate the DNA in a test tube by PCR, there are protocols out there galore to extract enough DNA from buccal swabs or from isolated white blood cells.

The general steps involve lysing the cells (breaking the cell membrane) in order to get a mix of nucleic acids (some of which you want), sugars, proteins, lipids, and other detritus (which you don't want). Then you separate out this mix with a series of steps of washing, spinning down with a centrifuge, and extraction.
A DNA extraction kit is involved. Here's one from Qiagen, for example. A kit usually contains a mix of salts and buffers specific to the source of DNA, to get as much pure sample back as you can.
You might not start with much DNA, so picking the right kit can help you get back a high enough yield of genetic material to do other experiments.
Kits are often based on ethanol or isopropanol, which precipitates out the DNA from the rest of the gunk. You add some buffer and run it through the centrifuge, removing and discarding what is on top (the "supernatant"). After repeated wash and spin steps, what's left is mostly purified DNA, in visible pellet form.
As a specific example, here is a paper that describes one approach to isolate DNA from human sperm, with a detailed protocol: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4486329/