text:
Difference in callus formation during healing of bones of different origin
My study material from pathology states that during fracture healing after hemorrhage and coagulum formation the mesenchymal progenital cells from periostium that are closer to the fracture differentiate into chondrocytes and form hyaline cartilage, while the ones that are farther differentiate into osteoblast.
Result is production of hyaline cartilage in which enchondrial ossification and subsequent remodeling into lamelar bone occurs.
My question is: Does this enchondrial ossification also occur in bones in which Intramembranous ossification normally occur during development? (e.g. clavicle and some skull bones.)
NOTE:
in this stackexchange post and Wikipedia article on this topic, only chondrocytes are noted.


text:
Gemini usage of --sample-filter
I am using gemini to query databases made from vcf files, which contain data from multiple samples. However, I need to query data only from one sample, (for which I currently use grep to filter the results and > it into a txt file).
I tried experimenting with the --sample-filter option in gemini, the documentation I found however says only:

gemini query --sample-filter "phenotype=2" -q "YOUR_QUERY"

db_info says the table samples contains name, but when I try doing

gemini query --sample-filter "name='S2'" -q "YOUR_QUERY"

I'll get error, that I have an syntax error in my query. I tried putting there "sample_name=='S2'" even tried other criteria, like sample_id, but couldn't get this work.
So please, do you know how should I get this work, or have any other advice?
Thank you very much.

I've found a possible workaround to my problem, I filter the vcf input file before loading it into the db by vcfkeepsamples from vcflib.
But I still don't know if the --sample-filter in gemini works, so if you have any ideas, it would be helpful.

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text:
What is biological intuition?
Whenever I read or learn about prediction tools or aligners or motif detectors, I also hear that they are lacking in something called biological intuition. But I haven't been able to find a solid definition of what that is. Can someone please explain?

This is how I understand it: Bioinformatics tools are amazing at answering questions. The more specific the question each individual module of a tool can answer, the better their quality.
However, what they cannot do is ask the right question. You can find motifs with scores attached to the hit, but you cannot predict the relevance of that find. Is it a motif for a transcription factor binding site that inhibits a promoter for a downstream gene thereby suppressing activity, or does it bind a different factor enhancing a gene further downstream?
These questions need knowledge of the domain and of the genomic context, and this knowledge base is constantly evolving. Tools are getting intelligent, but they cannot have this intuition because they are still designed my human beings and we are always ahead thanks to experience.

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text:
Background (null) distribution for higher observed frequency of an allele
I am testing the hypothesis that being heterozygote at a certain gene locus, say X, increases the chances of having the good allele of X compared to being homozygote. I have data of more than 6000 individuals with their zygosity for gene X. What could be the background distribution of allele frequency for testing the hypothesis if the observed frequency of good allele is more in heterozygotes compared to one expected by chance.
Thank you so much.

I'm voting to close this question as off-topic because it is not about biology but about statistics (see stats.SE). (Note: see comments under my answer for clarification about the nature of the question).

I don't really understand your hypothesis you want to test. Here are two things that may help you.
Test if allele frequency is the one expected from the genetic and demographic properties
The expected allele frequency is not that easy to calculate as you need much information. You need to know the mutation rate, the population size, the migration rate, assume random mating and most importantly know the selection coefficient associated with this allele. Once you've got all that, you'll find the equation in the old paper Wright 1937.
How to test?
Maximum likelihood ratio test is probably the way to go.
Test if heterozygosity is the one expected from the allele frequency
Now if you want to test if heterozygosity is not the one expected, it is much easier. The expected genotype frequencies are given by Hardy-Weinberg rule (see here for explanation on Hardy-Weinberg's rule and see here for the assumptions of this rule).
In short, for a bi-allelic loci with allele frequencies $p$ and $1-p$ the three genotype frequencies are $p^2$, $2p(1-p)$ and $(1-p)^2$, where $2p(1-p)$ is the frequency of heterozygote.
How to test?
You can simply do a chi-square test or a binomial test.

I ask if being heterozygote increases the odds of carrying a certain allele compared to being homozygote. So can I just compare the allele frequency in two populations (hetero- and homozygotes) using fisher exact t

Oh ok. If I understand you correctly, you have two loci. One for which heterozygosity is the variable of interest, while for the other locus, the variable of interest is the presence / absence of a certain allele is that right?
Sounds like your question is a pure question of statistics, not biology. Stats.SE is the place to go to but I will still try to address your question now that I started.
You can do a simple chi-square test you have the following 2 by 2 chi square table with the count of individuals in each cell
$$\begin{array}{c|c|c|}
 & \text{Homozygote} & \text{Heterozygote} \\ \hline
\text{Allele 1} & w & x \\ \hline
\text{Allele 2} & y & z \\ \hline
\end{array}$$
Now, that works well if you consider only a single, randomly picked allele per individual but that would reduce your sample size. If you pick both haplotype per individual, then I am not sure of whether you might suffer from pseudo-replication. In such case, you could do a logistic regression with a nominal random effect that is the individual ID. They will be better than me at giving you such advice on stats.SE though.

Dear Remi, thank you for the insights. I think my hypothesis is relatively simple but i could not phrase it well at first place. I ask if being heterozygote increases the odds of carrying a certain allele compared to being homozygote. So can I just compare the allele frequency in two populations (hetero- and homozygotes) using fisher exact test?


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Are there antibiotics for all bacteria somewhere in the earth?
When I read about Penicillin, I found that it came from a green mold to protect itself.
If all bacteria and/or molds in competition to survive,
can we believe that there is an antibiotic for each bacterium somewhere in the earth?
In other words, just like bad bacteria change themselves to resist against the existing antibiotics, could good bacteria/molds produce antibiotics against the bad bacteria?
If so, can we use them like Penicillin, or should we still develop most of them?

Life is a constant arms race between organisms and their pathogens, each pushing the other to adapt ways to survive. Humans with competent immune systems are able to make their own bactericides, the only issue is the time it takes to mount this response, days to weeks, versus the replicative power of the bacteria and the virulence of their exotoxins. Vaccines against the most potent of toxins provide steady levels of antibodies to neutralize proteins that make snake venoms seem wimpy. Many antibiotics just keep bacterial populations in check until the host immune system can respond.

One other point is that you would have to do extensive testing to see what the toxicity of a bactericidal compound is on mammals. Penicillin goes after bacterial ability to produce a Lipopolysaccharide cell wall, something we don't have. Others take advantage of blocking ribosomal subunits that are different than ours, so we can use them without blocking our own ability to produce proteins. If the compounds we discover have specificity for a receptor that we make as well, then we can't use it.

The number of antibiotics that remain undiscovered is huge, but is estimated to be tens of thousands of compounds.
The number of bacteria that remain undiscovered is also huge, but is estimated to be perhaps millions of species.
Resistance to antibiotics is developed by bacteria in response to other bacteria and human antibiotic use, but in theory all antibiotics should work on previously unexposed bacteria. In practice there are resistance mechanisms that operate on whole classes of antibiotics at once(drug exporters, for instance). So there might be a bacterium that happens to be actively or passively resistant to every antibiotic on the planet, but it's a question of statistics. I think it's pretty unlikely but there are a lot of bacteria, so it's theoretically possible. (It wouldn't be a dangerous pathogen, that amount of drug-resistance genes would 'weigh down' the genome and make it slow to divide, and all those transporters would be great immune system targets. The human immune system would eat it for breakfast.)
What is true is for every bacteria, there are at least some antibiotics it's already resistant to. Furthermore, some antibiotics aren't useful because they aren't selective enough and they are simply poisons. (We use them for chemotherapy agents sometimes, but they're not useful antibiotics).
Some fun examples: Vancomycin-resistant S. aureus is completely immune to nearly every antibiotic, including the last line of defense(methicillin) and the toxic really really last line of defense (vancomycin). It's susceptible to trimethoprim-sulfamethoxazole, one of the oldest antibiotics out there(~80 years old). On the other hand, the organism that causes tularemia is naturally immune to trimethoprim-sulfamethoxazole and always has been. It, in turn, is susceptible to nearly all other antibiotics.


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Can general soap kill bacteria?
I have read that general soap can kill bacteria by opening holes in the bacterial membrane.
http://questions.sci-toys.com/node/90
However, I found some articles as well saying that it cannot.
http://goaskalice.columbia.edu/answered-questions/does-soap-kill-germs
There seems split answers among experts,
so I would like to know which one is correct.
Could anyone advise me?
Thanks.

If you look all the way down at to bottom of that ask Alice post, you will see that it was originally posted in 2001. Many major health organizations have done efficacy studies since then and have weighed heavily in favor of the use of regular soap over antibacterial. However if the choice is antibacterial or not washing your hands, then go with the antibacterial.

Soap kills nearly all the bacteria it comes into contact with by dissolving the bacterial membrane.  Some viruses with protein coats can resist soap, but many viruses have similar membranous coats (like HIV) and are usually disrupted by soap.  I'm sure it washes some away too, but to say they don't kill bacteria is misleading. In the end, though, they are gone.
Antibacterial soap with triclosan does not kill bacteria on contact and are no more effective than if they had no triclosan at all.  That's actually a good thing since really using an antibiotic would probably accelerate antibiotic resistant bacteria which is a serious - probably catastrophic public health failure. A recent study showed that killing bacteria by soaking with triclosan took 9 hours to start showing an effect.
To achieve full sterility, surgeons bathe their gloves in iodine (see details in the comments below) and their instruments will be sterilized by heating them beyond the boiling point in an autoclave under pressure.   That's useful when you are breaching the skin in surgery, but the skin needs some bacteria to be healthy long term and works well to fend off bacterial infections.
Your confusion seems to come from finding a page full of errors. Alice didn't really do her homework.

In a surgical setting, isn't the iodine use in the form of Betadine (povidone-iodine)? Also, Chlorhexidine is use a lot as a patient preoperative prep and also a wound cleanser.

@AMR  you clearly know more than I - happy to accept these amendments!

"Soap kills nearly all the bacteria ... by dissolving the bacterial membrane."
I thought soap only worked to dissolve lipids. Aren't bacterial cell walls are made of peptidoglycan (non-lipids)?

Soap is a detergent. It actively emulsifies the bacterial membrane, thus killing them by breaking this membrane. So yes, soap kills bacteria. Some bacteria are more or less resistant to this depending on the constituents of their lipid-bilayer membrane.
The reason why soap doesn't hurt your own cells is that for the most part, your outer skin layer is comprised of dead cells that have numerous cross-linked keratin filaments mixed with oils from your sebaceous glands that provide a nice nearly airtight, watertight barrier.
Excessive hand-washing or washing hands with stronger detergents can actually get rid of this protection and break down the barrier mentioned in the prior paragraph, leading to dry and cracked skin.

How does the soap get passed the bacteria capsule and cell wall to the bacteria's cell membrane to emulsify the membrane? The capsule and wall are not made of lipids.

Are you confusing a viral capsid coating made of proteins with bacterial cell membranes?  Some bacteria, under stressful environmental conditions can also encapsulate, but most of the bacterial we pick up from the environment and food are not encapsulated.

I'm looking at the gram-positive bacterial cell here. https://en.wikipedia.org/wiki/Bacteria#Cellular_structure It seems like at least that bacteria has a capsule and also a cell wall, then a cell membrane. Ah, but maybe where I'm confused is that not all bacteria are structured like that?

No, you aren't confused. Gram negative bacterial have two "lipid bylayer membranes (inner and outer)", but also a peptidoglycan layer between.  That layer between is much harder to disrupt with detergents, and thus they present more of a problem!

Generally, the goal for using non-antimicrobial soap is simply to pick up and remove organisms and dirt from our skin. This is achieved first by the soap chemically bonding to certain molecules (i.e. oil or lipids). Second, friction from rubbing mechanically and rinsing with water pick up and removes the soap and chemically bonded particles. Thus, the more soap and the longer the hands are rubbed together, the less oil and microbes left on your hands.
For a more scientific answer:
Soap is a detergent, meaning one side of the molecule is hydrophilic (likes water), and the other is hydrophobic (likes oil). Cellular membranes are also made out of a dual sided hydrophobic and hydrophilic molecule called a lipid. The soap solvates the hydrophobic parts of the lipid cell membrane, and you're left with a mixture of lipids & oils suspended in the soap. These are washed away when you rinse with water (imagine how cooking oil floats on top of water).
For another (longer) response to this question see here.

Comments on website credibility:
I'll also comment that at any point that you do an online search, you REALLY need to pay attention to the source of the information you're looking at. The internet is crawling with misinformation and inaccuracies -- often represented as fact or even presented by a so-called 'expert'! Typically, .edu websites (from academic institutions) are MUCH MUCH more trustworthy than .com, .org, etc. because they typically originate from some kind of peer-review or life-long study of a topic.
Be cautious, however, that you don't end up on a .edu page that contains a student's (or other non expert's) thoughts/opinions/or (possibly wrong) response to a question. Further, unfortunately it's not always this simple, as .org or .com info isn't necessarily wrong.
If you want to increase your odds of finding the most accurate information,  go straight to the peer-reviewed literature (start a search here). If this is too daunting a task or if you can't find what you're looking for, then I'd suggest focusing on .edu websites for info. You can use the "site:" operator in a Google search to specify a domain -- specifically, if you’re looking for high-quality references, you could use site:.edu to only pull up results from .edu domains.
That being said, I think it's clear that your first link is not nearly as trustworthy as your second, and in this case can be dismissed as internet misinformation.
Hope this helps!

Great comments on the credibility of that website.  It was horrid.

Please upvote the response then, so that more people are drawn to it. Thanks!

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text:
What is the process of aging exactly?
Getting old
Hello community, I have been thinking about age, and I thought that aging is the reverse of how a biological system is able to fix itself over time. Actually, some species actually are able to reverse it completely, such as the jellyfish and lobsters for up to 400 years in the Greenland sharks. Moreover, by evolution principle, those species must've exchanged this ability over others, which is noticeable considering they're really adapted to their habitats.
What does research tell us on aging so far?

According to Britannica, aging affects many dimensions for all humans.

So, when scientists are talking about "a cure to aging", I cannot comprehend whether they're proving that those are symptoms of some biological factor (such as producing a certain gene, etc.) or whether all of them share the likelihood to appear more often over a certain age?

How can studying those species help science advance in research?

this is an awfully broad question. Can you start with https://en.wikipedia.org/wiki/Ageing#Biological_basis and narrow down your question?

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Microarray gene expression matrix format
After scanning the microarray chip we get RAW data with different formats depending on the type of microarray used. However, these RAW data files can be normalized and processed to generate gene expression data matrix.
I've been trying to figure out what exactly is the result of the processed data and what is the format of that data. As I've seen so far, there's no specific format for processed data. Of course most of them agree that columns represent experiments and rows represent genes, but the additional information at the top, they're usually different but I'm not sure based on what. Can anyone suggest me with the most common used formats? Is there any additional information to that processed data file in case I wanted to apply classification on it?

Just to be clear, it sounds like you're asking how microarray data is typically displayed, as in a publication. This would be different from the actual content of the processed data. In the simplest case, processed microarray data consists of a numerical value for each point on the chip, i.e. each gene you are testing. For each point on the chip (i.e. for each gene), the data is the ratio of mRNA abundance from one experimental condition vs another. You can imagine a lot of ways this data might be presented, e.g. a heat map of relative abundance of mRNA for each gene.

@A.Kennard Do you mean it depends on the type of microarray used? Affymetrix has different Array design than illumnia for example

I think I might not be understanding your question. What do you mean by "the additional information at the top"? Could you provide an example of processed microarray data you are having trouble understanding?

The RAW signal values from each microarray are transformed and processed to give you normalized signal values for each microarray. The transformation and processing steps are standard but different for each manufacture. Each manufacture uses a different method/technology to obtain signal values. Thus, signal values are not directly comparable between different microarray technologies.
Experiments using different technologies might get similar RANK of results but the normalized signal values will be different. You can have a look at GEO for a list of datasets and commonly used technologies. I have no clue what you mean by applying classification (are you looking to cluster the results from different microarray technologies run on the same experiment? I'm pretty sure a comparison of microarray technologies has been done before/already)


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Are fish roe unicellular?
Are roe (fish eggs, caviar, etc.) single cells?
I have tried looking this up on google (sadly, to no avail), and I am guessing they might be multicellular (like bird eggs) or consist of one cell plus corona cells, or indeed unicellular.

I was under the impression that bird eggs (unfertilized or immediately after fertilization) were unicellular.

I always assumed, that the yolk sack consisted of lots of other cells which are responsible for repositing all the nutrients. Otherwise all of that would just have to be secreted by cells outside of the egg somehow? But now that I actually looked it up, I was unable to find any reliable info on that either :-/

Be careful not to confuse "egg" (the macroscopic structure) with "ovum" (the haploid cell). The vast majority of a bird's egg--even the yolk--is external to the ovum. (The wikipedia entry on yolk gets this wrong, by the way, based on a citation to a 65 year old embryology text).

@Corvus Do you have an actual citation? A similar question on Reddit had the opposite answer, backed by a link to a dev bio textbook. I would not personally upvote the Quora answer were it posted here.

@TheChymera Related question from here at BioSE on egg anatomy: Why are hard boiled eggs so homogeneous?

@Corvus Are you sure? From my understanding, yolk granules are stored in the oocyte cytoplasm, and is therefore part of the actual egg. See also the answer to the question I linked above.

@fileunderwater My comment was based on what we were told in an embryology lecture I had as an undergraduate many decades ago, so I acknowledge that I could easily be wrong. My impression was that the yolk was external to the ovum in the germinal disc.

Yes; the first division starts at around 45min post fertilization in zebrafish. This picture is stuck in every zebrafish lab.

If the fish eggs are unfertilised, then they are single celled (but in the haploid state - a state with half of a full set of DNA for an organism). However, if it is fertilised it will only remain in the single celled stage for approximately 45 minutes (depending on species (in this case I'm using the zebra fish). After that 45 minute period the cell begins to divide.
What actually makes caviar so expensive is that (according to most websites I've found) it actually is an unfertilised egg collected from a Sturgeon. There seem to be a few different ways that caviar is extracted. Extracting the ovaries after stunning the fish (which is explained on Science: How Stuff Works - and gives more information on caviar), more or less giving the fish a Caesarian section, and the final way that I noticed was called "stripping" which is a non-sergical way using an ultrasound.
The News Article on the ultrasound procedure of collecting the roe suggested that it wasn't yielding good results.
So, caviar is actually a single haploid cell.

Do you have a source for your claim? Also, did you mean "Caesarian section"?


text:
EMBOSS matcher and supermatcher - incongruent results?
I am trying to align a sequence to the mouse genome. I know a priori that part of my sequence should align to chromosome 9, but not all of it.
I gathered that EMBOSS' matcher and supermatcher would be adequate tools to do this locally on my machine - with supermatcher being (a lot!) faster and matcher being (allegedly) more accurate. Strangely enough, the two functions give me very similar fits (quality-wise) which are however at non-identical but very close positions.

How can I explain this?
What are the odds that an ~800-bp sequence has multiple equally good fits right next to each other (how can I test if I hit a repeat-heavy area?)?
Why do match and supermatch not give me both fits then?

My current alignments:
#=======================================
#
# Aligned_sequences: 2
# 1:
# 2: CM001002.2
# Matrix: EDNAFULL
# Gap_penalty: 16.0
# Extend_penalty: 4.0
#
# Length: 357
# Identity:     322/357 (90.2%)
# Similarity:   322/357 (90.2%)
# Gaps:           2/357 ( 0.6%)
# Score: 1458.0
#
#
#=======================================

                   1 AAAAACGTGAAAAATGAGAAATGCACACTGTAGGACCTGAAATATGGCAA     50
                     ||||.|..|.||||||||||||.||||||.||||||.|||||.|||||.|
CM001002.2    35305253 AAAATCACGGAAAATGAGAAATACACACTTTAGGACGTGAAAAATGGCGA 35305302

                  51 GGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCACTATAGGACGTGG    100
                     ||||||||||||||||||||||||||||||||||||.||.||||||.|||
CM001002.2    35305303 GGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCTCTGTAGGACATGG 35305352

                 101 AATATGGCAAGAAAAATGAAAATCATTGAAAATGAGAAACATACAGTTGA    150
                     |||||||||||||||.||||||||||.|||||||||||||||.||.||||
CM001002.2    35305353 AATATGGCAAGAAAACTGAAAATCATGGAAAATGAGAAACATCCACTTGA 35305402

                 151 CGACTTGAAAAATGATGAAATCACTGAAAAACGTGAAAAATGAGAAATGC    200
                     .||||||||||||||.|||||||.|.||||||||||||||||||||||||
CM001002.2    35305403 TGACTTGAAAAATGACGAAATCATTAAAAAACGTGAAAAATGAGAAATGC 35305452

                 201 ACCCTGTAAGACCTGGAATATGTCGAGAAAACTGAAAATCACGGAAAATG    250
                     .|.|||.|.|||||||||||||..||||||||||||||||||||||||||
CM001002.2    35305453 CCACTGAAGGACCTGGAATATGGGGAGAAAACTGAAAATCACGGAAAATG 35305502

                 251 AGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAACTGAAAAAGG    300
                     ||||||||||||||||||||||||||||||||||||||||||||||||||
CM001002.2    35305503 AGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAACTGAAAAAGG 35305552

                 301 TGGAAAATTTAGAAATGTCCACTGTAGGACATGGAATAT--GGCAAGAAA    348
                     |||||.||||||||||||||||||||||||.||||||||  |.|.|||||
CM001002.2    35305553 TGGAATATTTAGAAATGTCCACTGTAGGACGTGGAATATAAGTCCAGAAA 35305602

                 349 ACTGAAA    355
                     .||.|.|
CM001002.2    35305603 CCTAAGA 35305609

and:
#=======================================
#
# Aligned_sequences: 2
# 1:
# 2: CM001002.2
# Matrix: EDNAFULL
# Gap_penalty: 16
# Extend_penalty: 4
#
# Length: 417
# Identity:     377/417 (90.4%)
# Similarity:   377/417 (90.4%)
# Gaps:           2/417 ( 0.5%)
# Score: 1713
#
#
#=======================================

          180       190       200       210       220
       TGAAAAACGTGAAAAATGAGAAATGCACCCTGTAAGACCTGGAATATGTC
       ::  : ::   : :: :  ::  ::::: ::: : ::::::::::    :
CM0010 TGTCACACACTATAATTTTGAGGTGCACACTGAAGGACCTGGAATTATGC
       35305200  35305210  35305220  35305230  35305240

          230       240       250       260       270
       GAGAAAACTGAAAATCACGGAAAATGAGAAATACACACTTTAGGACGTGA
       ::::::::::::::::::::::::::::::::::::::::::::::::::
CM0010 GAGAAAACTGAAAATCACGGAAAATGAGAAATACACACTTTAGGACGTGA
       35305250  35305260  35305270  35305280  35305290

          280       290       300       310       320
       AATATGGCGAGGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCACTG
       :: ::::::::::::::::::::::::::::::::::::::::::: :::
CM0010 AAAATGGCGAGGAAAACTGAAAAAGGTGGAAAATTTAGAAATGTCCTCTG
       35305300  35305310  35305320  35305330  35305340

          330       340       350       360       370
       TAGGACATGGAATATGGCAAGAAAACTGAAAATCATGGAAAATGAGAAAC
       ::::::::::::::::::::::::::::::::::::::::::::::::::
CM0010 TAGGACATGGAATATGGCAAGAAAACTGAAAATCATGGAAAATGAGAAAC
       35305350  35305360  35305370  35305380  35305390

          380       390       400       410       420
       ATCCACTTGACGACGTGAAAAATGACGAAATCACTGAAAAACGTGAAAAA
       :::::::::: ::: :::::::::::::::::: : ::::::::::::::
CM0010 ATCCACTTGATGACTTGAAAAATGACGAAATCATTAAAAAACGTGAAAAA
       35305400  35305410  35305420  35305430  35305440

          430       440       450       460       470
       TGAGAAATGCACACTGTAGGACCTGGAATATGTCGAGAAAACTGAAAATC
       :::::::::: ::::: :::::::::::::::  ::::::::::::::::
CM0010 TGAGAAATGCCCACTGAAGGACCTGGAATATGGGGAGAAAACTGAAAATC
       35305450  35305460  35305470  35305480  35305490

          480       490       500       510       520
       ACGGAAAATGAGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAA
       ::::::::::::::::::::::::::::::::::::::::::::::::::
CM0010 ACGGAAAATGAGAAATACACACTTTAGGACGTGAAATATGGCGAGGAAAA
       35305500  35305510  35305520  35305530  35305540

          530       540       550       560       570
       CTGAAAAAGTTGGAAAATTTAGAAATGTCCATTGTAGGACATGGAATAT-
       ::::::::: ::::: ::::::::::::::: :::::::: ::::::::
CM0010 CTGAAAAAGGTGGAATATTTAGAAATGTCCACTGTAGGACGTGGAATATA
       35305550  35305560  35305570  35305580  35305590

            580
       -GGCAAGAAAACTGAAA
        : : ::::: :: : :
CM0010 AGTCCAGAAACCTAAGA
       35305600


text:
0.9% Saline or Ringer's Solution for in vivo work
A few of the labs where I currently work routinely use 0.9% saline for in vivo work (washing out debris during surgery, diluting substances for IP/IV/SC injections, etc.)
A few years ago I worked in a lab where the standard was to use Ringer's Solution. Obviously, in both labs the choice was based on an organizatorical/historical reasons. But I was wondering: Does either of these solutions perform any "better" (i.e. causes less physiological disturbances) than the other?
My guess would be Ringer's is better, since it is also suitable for keeping cells alive in vitro - and there is also this paper that calls 0.9% Saline into question altogether. But I could not really find any good comparison tests.

saline versus lactated Ringer's is still a matter of preference - but I agree with you that Ringer's is better - pH and electrolyte composition are more closer to physiologic values, while saline is pH of 5.5 and slightly hyperosmolar compared to plasma.


text:
Modern Classification of Introspective Psychopharmacological Drug Profiles?
In the effort to better relate neuronal mechanisms to states of mind, it makes sense to have - in addition to pharmacological classifications of drugs and imaging/physiology classifications of their effects - classifications of the states of mind they evoke, according to introspective reports.
I have been unable to find such a data-driven classification in the literature (I would imagine a cluster analysis of reported terms, or a factor analysis of ratings on statements could be appropriate). Instead, "subjective effects" classification seems to be restricted to single-substance profiling, and elsewise is remarkably top-down - based on ad hoc models by the same authoritative people or entities which commonly make psychoactive substances available to consumers (introducing confirmation bais). I'm wondering if there's anything else out there?

A couple things...1) This might be better suited for psychology.SE, and 2) I think you might be having too high a view of the state of neuroscience. Very few psychoactive drugs are truly understood from an imaging/physiological/pharmacological nature; they are pretty much all classified by their effects. Consider anesthetics, for example. Drugs like propofol, isoflurane, etomidate, etc have diverse chemical and pharmacological profiles - we group them because they cause anesthesia.

What you suggest could be done but I ponder on its usefulness. Say we relate mood swings with 60% serotonin and 40% GABA. Does that mean that if we have mood swings we adjust our serotonin and GABA levels accordingly? I think modern neuroscience is aiming at a more in-depth understanding. I suggest instead that we'd need to know which circuits it up- or down-regulates.


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the evolution of the human brain size
I was thinking, as I know, sometimes the process of producing DNA did not work well(correct me if I'm wrong), so it gives us some changes in the object we gonna have(for example: increasing or decreasing a part, enabling  or disabling  a part), could human brain grow more that it is now?

Short answer: yes.

This question basically asks if there is a possibility that human brain can evolve to be bigger or more complex. This is an open ended question and cannot be addressed based on facts.

I assume, you mean by "producing DNA" Neanderthals had larger brains than us. Basically, this is possible and generally, brain size correlates with body size. What you may ask here is: Can our brain size to body size ratio increase? Probably yes... I can't think of a reason, why not?
But please please be aware of that intelligence, does not have to correlate with brain size. e.g. elephants and humans. There may be some limits of the smallest possible brain size for certain mental tasks and skills. But wiring and plasticity is probably more important than the bulk size.

Referenced material would be useful. Right now it's just your opinion and I see no attempt to answer the question beyond a purely opinion based "yes"


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How do I interpret this graph regarding introduced genes and virus-infected cells?

This graph appeared in a practice test for the MCAT. I am trying to interpret it, but it confuses me a bit. On the x-axis we have some introduced genes, and on the y-axis we have % of cells infected. What I don't get is what the top part represents. How do the "Culture cell genotypes" relate to the rest of the graph. I would also like to know what -/- and +/+ mean. By the way, information in the passage lists CatB and CatL as mammalian proteases, and their inhibitors reduce the infectivity of viruses with the EGP glycoprotein (found in Ebola virus).
Here are some questions based on the graph:
Based on the passage, does optimal VSV-EGP infection in vitro require CatB, CatL, or both?
Based on the passage, is CatL expression sufficient for VSV-EGP infection of the mouse cell lines presented in Figure 1?

For -/- and +/+ see this recent answer: http://biology.stackexchange.com/questions/20593/what-is-an-ihh-mouse/20594#20594

Plus and minus describe what is happening in a specific locus in the genome. When a + sign is shown, the locus contains the natural, fully working gene (wild type). When a - is shown, it means that by natural mutation or lab manipulation, cells lack that natural gene, or make a negligible amount of it, or make a broken variant etc.
These cells are diplod, meaning they have two homologous chromosomes. If +/+ is shown, both chromosomes carry, in that locus, a working gene. If -/- is shown, both copies are not working. If a cell is CatL -/-, both its natural copies of CatL are missing or defective, and the cell is unable to make the corresponding protein. The manipulation through which a naturally occurring +/+ is turned into a defective -/- is called a knock out.
The top part of your chart shows what is happening in the nucleus, on the chromosomes, at the actual places where normal cells store their CatL genes. You don't give much detail, but the bottom of the chart appears to show some manipulation away from the normal locus. There are ways to introduce more copies, to stick them into the nucleus, or even in chromosomes etc, but the main point about introducing DNA is that often it will not work as well as the natural thing.
Optimal infection means something close to the first column, about 25%. By skimming through the chart we are definitely seeing good infection in column 3. Also by comparison with the low levels, we could call acceptable the infection in column 8. The other columns are all clear failures to infect.
The second column is the simplest to interpret: knock out CatB alone, and the infection is gone. Thus, CatB is required for infection. The third column reinforces the same point: restore CatB and infection is back to normal.
The sixth column shows cells where CatL and CatB were knocked out, but then CatB was reintroduced. We know from column 3 that knocking out and restoring CatB should keep infectivity, but in column 6 infection is gone. The only difference between columns 3 and 6 is the knockout of CatL, and its consequence is lack of infection. Thus, CatL is also required for infection. You may say both CatL and CatB are required.
The other columns are control conditions which show that the experiment was well designed and yielded expected results, rather than gibberish. For example, column 5 show that if you knock out both, infection is gone. It would have been very concerning if it weren't gone. Etc.
Your second question is really one of logic: is CatL sufficient? We established that CatB is required, and so there is little CatL could do to supplant its absence. Therefore, logically, CatL should not be sufficient.
But we have a better proof, from the experiments. In column 4, those cells have their natural (endogenous) CatL, topped by some more CatL. But they are still not infected, beause they lack CatB. So CatL, even in larger-than-life amounts, cannot compensate the absence of CatB. CatL is not sufficient.


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Effect of pH on life? Use buffer or HCl? How about lactic acid?
I'm trying to find the effect of pH on living things like E. coli and such. At first I thought of using a buffer solution which maintains its level of pH, but it's possible that the inactive ions of each buffer have their own effect on living things that I can't account for. On the other hand, I could use hydrochloric acid and sodium hydroxide at different concentrations by diluting it. This will be a little bit more effort (I'll be diluting the acid and base myself), but much cheaper than the buffers, and I'll know that the only other ions present beside H+ and OH- are just Na+ and Cl-, the ingredients of table salt. According to this paper, the effect of pH on the population also depended on the acid (HCl vs lactic acid).
I would like a second opinion on this:
If I'm investigating the effect of pH on growth of living things, do I use specially made buffers or just properly diluted HCl and NaOH?

What makes you think that Na+ and Cl- can be ignored? Just because they're what makes up table salt does not mean they are harmless. I am not saying they can't be ignored for the purposes of this experiment either, just pointing out that you may be jumping to conclusions.

@terdon  Not saying they are to be ignored, but if anything, these are controls. I KNOW that they're there. OTOH, I have no idea what went into those buffers.

That is a variable that you have the pleasure defining yourself. Just know that using a buffer will introduce other atoms that could affect the "living things". Conversely, if you don't use a buffer, it is likely that the pH of your "living things" will be easily altered by the metabolism of your living things (IMHO, this is worse).
I don't know the details of your project, but recommend:
-use a buffer like.. Tris, phosphate...
-use 10 mM Tris-Cl without any extra electrolyte (aside of the HCl or NaOH that you use to modulate the pH of your buffer to different pH's that you want to test)
-e.g. Tris-Cl pH 7, 8, 9.. or Phosphate pH 2,3,4,5,6,7,8,9..


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Melatonin production - requires nighttime, or just full darkness?
Is melatonin properly produced in daytime sleep in full darkness? Or does it require only nighttime sleep?
Additionally, what other biological implications are there, if any, to daytime sleeping? Melatonin production is the only biological implication I could find so far.

I think this question is answered by the answer I gave to another question. http://biology.stackexchange.com/questions/7667/what-causes-humans-to-be-sleepy.

Thank you, but the main part of my question remains unanswered - is night required for melatonin production, or does it only require full darkness (such as in a dark room, blindfold, etc)?

"It is released by the pineal gland and production starts when the light fades, as it's production is inhibited by light stimulation of the retina, the onset of the production is called dim-light melatonin onset."

The immediate thought came to my mind was relation between Melatonin and Serotonin. Because both hormones have sleep related function. I read that both are light sensitive. Melatonin is produced by pineal gland in brain whereas Serotonin is at gut and CNS.
Light dependence(Wikipedia) of Melatonin is explained here where they say blue light produces more Melatonin and wavelength of light <530nm will have effect on Melatonin production. If the light intensity is more then Melatonin will not be produced. So what they say is if there is darkness(artificial) or dim light environment then this hormone will be produced and induces sleep. Almost everywhere they explain Melatonin whose production is sensitive to light.
(But even in the afternoon when there is bright light some of us feel sleepy which is mainly due to Serotonin released after heavy meal which is produced from tryptophan. This will again effect the sleep. It is obvious that without food we can not sleep at night. So Serotonin and Melatonin are interrelated as explained here Link1 and Link2).

Thank you for the detailed answer. However one part relevant to my question is still unanswered: is Melatonin also dependent on time, hour, day\night? If I am to stay in darkness during daytime, will Melatonin be produced as well as in the same darkness at night?

@UriP: This one might be interesting for you as it explains melatonin production with respect to light: http://biology.stackexchange.com/questions/5503/what-light-intensity-starts-melatonin-release-in-humans?rq=1

It certainly does not require full darkness.  I've often slept quite restfully with the reading lamp left on all night, and children who are afraid of the dark do this habitually.  However, full darkness may PROMOTE melatonin release.

I see, thank you for your clarification. However, the main focus of my question is: Can melatonin also be released in daytime (in partial\full darkness), or only at night?


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pI and pH relationship in context of ion exchange protein purification
I am confused about relationship between isoelectric point and pH in context of ion exchange protein purification. Why we cannot use this method for protein with pI below 7? Thank you very much for any tips.

The pI (iso-electric point) is the pH at which the protein (or other molecule), overall has a net zero charge.
As @Chris points out, the buffer you are using will change the pH the protein finds itself in.  This will change the charge of the protein.
In ion exchange chromatography, there are charged chemical groups on the resin and these can cause a protein to be retained on the resin if the protein is complementary (opposite charged)  to the resin.
So if you have a protein with a pI of 5 say, it would neutral with the presence of excess H+.  This implies that the protein has an overall negative charge.  A cationic resin would tend to retain this protein in a pH 7 buffer.
I hope that makes sense.
In most cases, ion exchange chromatography is used when most of the protein is separated out and there are a few proteins (maybe a couple of hundred) mixed together.  It can get tricky if you see that the protein is mixed in with something that is also negatively charged.  In that case you might change the pH of the buffer so that other negatively charged proteins are closer to their isoelectric point and come through the column faster than the one you desire to purify.

Have a look at this table, it really depends on the buffers you use:

The table is from this website, which is definitely worth reading when you are interested (or work) with ion exchange chromatography.


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The antibiotic 'kanamycin' in the growing of culture E. coli
I'm a first year student and I'm not sure if I understand correctly the role played by the antibiotic 'kanamycin' in the growing of culture E. coli (Rosetta).
Can anybody explain me why we use 'kanamycin' antibiotic and kanamycin resistance gene during that process?

Absolutely, Positive Selection
You are looking for the bacteria which have the gene (probably a plasmid) you (or someone else for you) put into the bacteria.  That gene lets them live in the presence of kanamycin, and any bacteria that don't have it, or that try to get rid of it, will die.  Thus you can select for the bacteria you want by killing everything else off (hopefully your sample is not contaminated with other bacteria also resistant to kanamycin).
I totally thought there would be a good wiki article on positive selection but there isn't.  The reason it's positive selection is that you are selecting for bacteria that have something; instead of negative selection where you would be killing them for having something.
You can find plenty more if you search "positive selection" or more generally "artificial selection."

According to this data sheet, the genotype of the strain RosettaTM(DE3)pLysS is F- ompT hsdS (r- m-) gal dcm (DE3) pLysSRARE (CamR).
This strain carries certain tRNA genes on the same plasmid as the LysS gene, and these tRNAs boost expression from genes containing rare (in E. coli) codons. The plasmid encodes chloramphenicol resistance (CamR).
If you have a protocol that suggests growing your strain under kanamycin selection then presumably you have an additional plasmid present which carries your gene of interest. Then, as the accepted answer says, you are selecting positively for the correct strain.
I don't know how stable the pLysSRARE plasmid is, but I would have expected that you should also maintain selection for chloramphenicol resistance.


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Question about the DNA glycosylase enzyme assay/formamide gel loading buffer
Often for the DNA glycosylase enzyme assay we can see that the DNA glycosylase is incubated with oligonucleotide in 37C and then reaction is stopped by addition of formamide gel loading buffer (80% formamide/1 mM EDTA, pH 8.0y0.1% bromophenol blue/0.1% xylene cyanol). How the reaction is stopped by this buffer?

Do you have a reference for that?

Cloning and Characterization of a Functional Human Homolog of Escherichia coli Endonuclease III
Aspinwall, Richard ; Rothwell, Dominic G. ; Roldan-Arjona, Teresa ; Anselmino, Catherine ; Ward, Christopher J. ; Cheadle, Jeremy P. ; Sampson, Julian R. ; Lindahl, Tomas ; Harris, Peter C. ; Hickson, Ian D.
Proceedings of the National Academy of Sciences of the United States of America, 1997, Vol.94(1), pp.109-114 [Peer Reviewed Journal]

Formamide is a common loading buffer for denaturing gel electrophoresis of nucleic acids. I'd assume that it also denatures most enzymes and stops the reaction that way.

Escherichia coli endonuclease III (which I will now refer to as Nth), and the human homolog hNTH1, has both glycosylase and AP lyase activity. The section of the article you're referring is describing an assay of lyase activity. The assay tested both Nth and hNTH1 as well as HAP1, a human AP hydrolase that cleaves 5' to the AP site. Nth and hNTH1 were found by this assay to cleave 3' to the AP site. HAP1 is dependent on $Mg^{2+}$ for catalytic activity. hNTH1 (and likely Nth, given the high conservation) are dependent on $Mg^{2+}$ for substrate specificity (Eide et al., 2001). hNTH1 and Nth contain an $Fe-S$ cluster that is involved in DNA binding (Thayer et al., 1995).
Originally I thought that the reaction is stopped with EDTA. EDTA is a chelating agent; it binds and sequesters metal ions and prevents their use by enzymes. EDTA would prevent catalysis by HAP1 and DNA binding by Nth/hTNH1.
However, Chris pointed out that the loading buffer contains 1 mM EDTA while the reaction buffer contains 5 mM $MgCl_2$. While the paper doesn't give the volumes of reaction and loading buffer mixed together, it is perhaps unlikely that EDTA chelation of $Mg^{2+}$ is the sole mechanism for stopping the reaction. The high concentration of formamide (80%) in the loading buffer could then be responsible. Formamide is commonly used to denature nucleic acids and, at high concentrations, would likely have an effect on enzyme function.
References

Eide L, Luna L, Gustad EC, Henderson PT, Essigmann JM, Demple B, Seeberg E. 2001. Human Endonuclease III Acts Preferentially on DNA Damage Opposite Guanine Residues in DNA. Biochemistry-US. 40(22):6653–6659
Thayer MM, Ahern H, Xing D, Cunningham RP, Tainer JA. 1995. Novel DNA binding motifs in the DNA repair enzyme endonuclease III crystal structure. EMBO J. 14(16):4108–4120.

How much magnesium is present in the buffer? The EDTA in the buffer is only 1mM, so only 1mM of magnesium is complexed. I doubt that this is enough. Additionally, this buffer is not only TE but contains 80% Formamide.

@Chris: Thanks, that's a good point. The reaction buffer contains 5 mM &Mg^{2+}$. However, they don't give the volumes of reaction and loading buffer that are added to each other and electrophoresed. Do you think that formamide is the major factor stopping the reaction? I assumed it was there to denature the DNA. Does it also denature enzymes? Or perhaps the enzymes don't function on ssDNA.

I think so. I haven't checked if formamide reacts with proteins. That would be one possibily.

I've edited my answer, though I don't feel it answers the question anymore. I wish I could find some literature about it.

Thank you very much for your help. As you mentioned in your response, AP andonucleases may  incise 3’ and 5’ to the AP site. I read more about it and I am confused at some point. I have found:
There are four possible incision sites for AP endonucleases, and the enzymes have been classified according to their sites of incision:
class I and class II AP endonucleases incise 3’ and 5’, respectively, to the AP site, both leaving 3’-OH and 5’-P termini.
If for class II AP endonucleases incision is at 5' to the AP site, how it is that there is generated 3'-OH and 5'P?

Gary M. Myles and Aziz Sancar (1989). "DNA Repair". Chemical Research in Toxicology 2 (4): 197–226

@Piesel Perhaps you should ask that in a new question. Basically the phosphate will be on the 5'C of the AP ribose.


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A question on ImageQuantTL
I am confused about using the ImageQuantTL application as a tool to analyse the Urea Gel. My problem is that I am not sure if the 'shape' for calculation should be the same for all samples (like on picture A) or as close to the band as possible (like on picture B)? And what about the background subtraction? The `Image Rectangle/Ellipse' option says:

Uses the average pixel intensity in a defined rectangular or elliptical area of the image. To define the area for background calculation, select the background shape in the navigator and then drag with the mouse. Background areas are identified by a broken colored border, and are numbered in the sequence in which they are created. If you have defined several background areas, select the area to use in the Parameters tab.

Does it mean that the shape for the background subtraction not necessarily has to be exactly the same size as the shape for the band? (See Figure C.) I attach some pictures for your convenience.
Thank you very much for any help.

I would definitely go for option A. If you are assuming that the staining in band 6 is all due to whatever you are measuring, there is no reason to think that the signal at the top of lane 1 is not meaningful.
That said, this type of measures is only semi-quantitative, so being too "picky" in how you choose your region probably won't really increase the precision of your result. If you want to get a quantitative measure I am afraid you will have to turn to some other technique.
Finally note that the area obviously means a lot if you are looking at total intensity of the bands, rather than average intensity.

I can only agree to tihs answer. Be careful with too "exact" measurements here.


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Were there any flying dinosaurs?
I've seen some articles which came in contradiction with each other.
The first article was talking about flying dinosaurs, dinosaurs with feathers and so on.
A couple of other articles are talking about misconceptions about dinosaurs one of them being that there are no flying dinosaurs but just flying reptiles (from scholastic.com and livescience.com).
So, which one is right?
Also if possible please provide a source for argument.
I cannot find the first article again.

Beside the question of "Could the Pterodactyle fly?", there is the second "What is a dinosaur?". This question is related to the second one. But anyway, @kmm already provided a very good answer that you could accept.

The title of the question is a little bit scary u know. I was under the impression that there is currently no flying dinosaurs :D

Related: If dinosaurs could have feathers, would they still be reptiles?

Birds are both flying dinosaurs and flying reptiles. Yes, that's potentially confusing.
To understand the apparent contradiction, you have to understand how modern classification of organisms works (phylogenetic systematics). Under the old (Linnean) classification system, Reptilia (reptiles) was an order and Aves (birds) was a separate order. Phylogenetic systematics, which has completely replaced the Linnean system, views all organisms as interrelated in a nested set of monophyletic groups (clades). It's like a set of venn diagrams, where all organisms fall into a giant circle and then successively smaller circles classify more and more specific groups.
The clade Reptilia includes snakes, lizards, crocodiles, and lots of extinct groups, including dinosaurs. So all dinosaurs are reptiles. The clade Dinosauria includes all the extinct dinosaurs (Stegosaurus, Triceratops, sauropods, etc.), including theropod dinosaurs, which include well known dinosaurs like Tyrannosaurus and Allosaurus. Based on a mountain on anatomical evidence, including lots of transitional fossils, living birds are a sub-group of theropod dinosaurs.
So all birds (Aves) are theropod dinosaurs (Dinosauria: Theropoda). All dinosaurs are reptiles. Therefore, birds are dinosaurs and reptiles. They are just more closely related to dinosaurs than to other reptiles.
The tricky part is that most people have an intuitive idea of what "reptiles" and "dinosaurs" are. To a systematist, whose job it is to classify organisms, these terms don't mean the same thing as they do to most people. Systematists think about groups like Reptilia and Dinosauria and how those groups are related to one another. So they have no problem saying that birds are dinosaurs and reptiles, because birds are nested within both of those groups.
A few words about pterosaurs
Along with birds and bats, pterosaurs are the other clade of vertebrates capable of powered, flapping flight. Pterosaurs fall within Reptilia (and Diapsida and Archosauria) along with Dinosauria, which includes birds. There are a lot of other extinct lineages in the tree that are not shown, e.g., ornithodirans that are not dinosaurs and not pterosaurs. Pterosaurs and birds share anatomical features that all reptiles, diapsids, archosaurs, and ornithodirans have, which is how we know that they are more closely related to each other than to other groups, like crocodiles. But their flight structures evolved independently and are anatomically distinct fro one another. So pterosaurs are flying reptiles but not flying dinosaurs.
These images might help you understand the above explanation.

Nice answer, but having said that, there's no reason why dinosaurs can't be a paraphyletic group. (I don't know if they are, but it's potentially a taxonomic leap to equate monophyly with calling them the same name.)

"Flying reptile" is often used not to mean "a reptile which flies" but instead as a synonym for Pterosaur.

This is a good comprehensive answer - but I think the OP needs to also understand that pterosaurs are not dinosaurs, and that this is a separate question from whether birds are flying dinosuars. You might want to edit your answer to include this information, since it's also a matter of systematics.

The most important take-away being that ostriches (Struthio camelus) are the largest remaining dinosaurs :-) And sure @Sparhawk, dinosaurs can be a paraphyletic group in the sense that you can define a jargon term any way you like. But cladists will refuse to utter the word with such meaning.

@SteveJessop I'm an evolutionary biologist (amongst other things), primarily in protists, a polyphyletic group. There are certainly other poly/paraphyletic groups that are defined as such (e.g. fish), although I agree that most of them are not useful from a classification perspective. I am unfamiliar with dinosaur taxonomy, but I was just making the point that birds being nested in the dinosaur clade doesn't necessarily imply that they are dinosaurs. I think the answer has to explicitly mention the claim that dinosaurs are monophyletic.

@Sparhawk: sure, I think statements like "views all organisms as interrelated in a nested set of monophyletic groups (clades)", are intended to make the more general claim that clades are the only groups used in formal classification and hence dinosaurs necessarily must be a clade if it's a classification at all. This is what cladists want us to believe, that there's no taxon to describe what you study and you should come out and call it "radishes, emus and spanners" or whatever ;-)

@SteveJessop Oops. I totally missed that quote. Good point.

A 2017 study suggests that Theropoda are not under Saurischia. Not that this detracts from your answer at all, but it is interesting :)

@M.M A lot of people disagree with that study.

to further blow your mind, flight likely evolved at least twice in dinosauria, with sort of bat like wings in the Yi lineage and feathered wings in the bird lineage.

In addition to kmm's excellent answer, I'd like to present the xkcd point of view.

By any reasonable definition, T. Rex is more closely related to sparrows than to Stegosaurus.

Separation by time
Phylogenetic distance
Physical similarity

Birds aren't descended from dinosaurs, they are dinosaurs.
Which means the fastest animal alive today is a small carnivorous dinosaur, Falco Peregrinus.
It preys mainly on other dinosaurs, which it strikes and kills in midair with its claws.
This is a good world.

I'm not an expert, but I think that you have to be specific about the flying animals to which you are referring. Pterosaurs are not classed as dinosaurs, whereas modern birds are descended from theropod dinosaurs which is where feathers appeared.

I don’t rightly know what to make of it, but there seems to be some evidence for feather-like structures on non-theropod dinosaurs.

Asides from flight-capable modern birds and their early ancestors1, there are several other therapod dinosaurs which palaeontologists suspect were capable of flight, "but in a manner substantially different from that of modern birds":
Dromaeosaurids

Image
Dinosaur
Source

Microraptor
Scapular orientation in theropods and basal birds, and the origin of flapping flight, Acta Palaeontol

Changyuraptor
A new raptorial dinosaur with exceptionally long feathering provides insights into dromaeosaurid flight performance, Nature Communications

Sinornithosaurus
Feathered coelurosaurs from China: new light on the arboreal origin of avian flight, Feathered dragons

Deinonychus (juveniles)
Morphological Variations within the Ontogeny of Deinonychus antirrhopus (Theropoda, Dromaeosauridae), PLoS ONE

Rahonavis
Glorified Dinosaurs: The Origin and Early Evolution of Birds, Sydney  Gravity-defying Behaviors: Identifying Models for Protoaves, American Zoologist  Avian ancestors. A review of the phylogenetic relationships of the theropods Unenlagiidae, Microraptoria, Anchiornis and Scansoriopterygidae, SpringerBriefs in Earth System Sciences  The Theropod Ancestry of Birds: New Evidence from the Late Cretaceous of Madagascar, Science

Zhenyuanlong
A large, short-armed, winged dromaeosaurid (Dinosauria: Theropoda) from the Early Cretaceous of China and its implications for feather evolution, Scientific Reports

Troodontids

Image
Dinosaur
Source

Jianianhualong (not guaranteed)
"Barb geometry of asymmetrical feathers reveals a transitional morphology in the evolution of avian flight", Proceedings of the Royal Society of London B: Biological Sciences

Paraves (basal)

Image
Dinosaur
Source

Anchiornis (possibly juveniles)
*The wings before the bird: an evaluation of flapping-based locomotory hypotheses in bird antecedents, PeerJ

Scansoriopterygidae
And interestingly, not using feathered wings but membranous ones similar to bats or pterosaurs:

Image
Dinosaur
Source

Yi qi
A bizarre Jurassic maniraptoran theropod with preserved evidence of membranous wings, Nature

Ambopteryx longibrachium
A new Jurassic scansoriopterygid and the loss of membranous wings in therapod dinosaurs, Nature (2019)

Sources:
 • 1. A Jurassic avialan dinosaur from China resolves the early phylogenetic history of birds, Nature
 • Wing bone geometry reveals active flight in Archaeopteryx, Nature Communications
 • The wings before the bird: an evaluation of flapping-based locomotory hypotheses in bird antecedents., PeerJ
  Note: flight in Anchiornis only suspected of being possible in juveniles


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Why do fishes have both a gustatory and an olfactory system?
I would like to know if there is a reason why fishes (and many aquatic species) have both an olfactory and a gustatory system. As far as I know, in all fish species the chemoreceptors, organs and neuronal pathways are different for taste and olfaction, but why is it an asset to have two distinct sensory systems for chemical compounds in an aqueous medium ?
For terrestrial animals it makes sense to separate information stemming from remote sources mediated by volatile molecules and from the oral cavity, where the molecules are everything one can find in food. But in aqueous medium this distinction is far less obvious, especially when one considers that in some species there are taste receptors located on the body surface (lips, barbels).
I've read a few articles and this thread describing the physiological and neurological aspects of this separation, but it's not answering my question (and it actually aroused my curiosity even more).

In addition to olfactory and gustatory, fishes have two more chemoreceptor systems, solitary chemoreceptor cells and free nerve endings (Finger TE 1997). Asking why do they have all these chemorecepor systems is 'little bit' difficult in the light of evolution. But we can definitely look at this question by using some comparative studies. Hence, this answer will not give you answer to 'why' but will give you enough information to understand roles of these systems.
Reference provided by you explains much of the mechanism of olfactory and gustatory system. I will highlight the important difference between these mechanisms.

In olfactory system, signal is directly detected and transmitted to Central Nervous System (CNS) by neurons of cranial nerve I (Liu and Zhang 2019)
In gustatory system, signal is first detected by specialized gustatory cells and then transmitted to CNS via cranial nerve VII (Purves D et al 2001)

As both of them have similar function, it has been difficult to assign specific function to specific system due to lack of robust behavioral assays (Hara TJ 1994)*
Nonetheless, there are following functions in different kinds of fishes are preferred by one system over another,

Hara TJ 1994 comment that spatial feeding behavior is supported by olfactory system in contrast to gustatory system which helps in consummatory feeding like turning, biting, snapping and mastication**
Morais s 2016 suggests, olfactory system is involved in kin-nonkin recognition, prey–predator interactions, and territory or homing recognition because it is less plastic while gustatory system only plays a role in feeding behavior.
Discrimination of Pheromones is done by olfactory system (Lastein et al 2014)

From reading all these papers, I can 'guess' answer lies in the physiology of these sensory systems. Following conclusion is mine and I am no expert to tell whether this is correct. So just take it with pinch of salt :)
Fish has to survive in the water which is filled with tons of different chemical signals. So it has to distinguish these signals from each other. Many functions might not need very careful separation of signal (e.g. searching for resources) while other might need (e.g. which resources to eat). Some functions might need quick response (e.g. presence of predator) while other can be delayed for short time (e.g. migration). If you give responsibility to one system to perform all these functions simultaneously, it might get confused when multiple important signals arrive. From this I can speculate that this would have put some selection pressure during evolution so that there are multiple chemosensory systems.
From the literature cited above it looks like, Olfactory is less plastic and less sensitive than gustatory and hence involved in functions where you need little sensitivity to distinguish between multiple signal. While gustatory is involved where you need more specific selection of chemical signal.
*I could not get any recent paper directly comparing these two systems in fish. My hope is now we will be in more favorable place to perform some complex behavior experiments. **I did not understand difference between these behaviors conceptually, but you can look it up if you are interested.

Nice, well referenced answer, +1. One comment I have is that I doubt "Olfactory is less plastic and less sensitive" -Though I have little knowledge about fish, there are fairly obvious ecological reasons for olfaction to be very very sensitive. I wonder if you really meant a different word here. Maybe less specific, in that the olfactory system is responding to a broader range of odorants versus just a few in the gustatory sense? Additionally the review you cite does say that about plasticity but also later says "showing low plasticity" about taste; I think the earlier statement is a typo.

@BryanKrause, yes. I also wondered first. But I thought maybe it is like this for aquatic animals. The review I cited did not go into those details.

Imagine what happens inside a fishes mouth after it has eaten an insect or another fish, It's the same if I eat a sardine... the sardine stays stuck in my mouth for a while afterwards. Then if i used my mouth to smell, I would just smell sardines everywhere, literally for an hour.
If the fish only used it's mouth to sense the water, it's sense of smell would be impaired for a while after it has crunched a meal. So it hunts a lot better if it has the ability to check healthy and moldy food through taste, and also sense pristine water for other meals.
The scientific research states that the precise function of the olfactory system is not totally known, it seems to aid behavioral functions not related to eating, for mating and prey detection.
This research is very well written and it's recommended reading.
https://www.tandfonline.com/doi/full/10.1080/23308249.2016.1249279
Ultimately, a different olfactory receptor repertoire confers specialization towards different tasks. Take a shark's ability to detect blood, it makes sense to have a receptors to detect chemicals that are abundant at close range, it's specialized sensing abilities which are geared towards different peak detections and that guide responses in different zones of the brain.
Fish don't have as many receptor genes as mammals, so the evolution pressure is apparently less strong in water, i.e. mice and frogs have 1500 receptor genes versus 50-100 for fish.
catshark: 65 genes
elephant shark: 54 genes
zebra fish: 176
lamprey: 56
frog: 1500
elephant: 1900
stickleback: 159
platy: 98 ( https://academic.oup.com/gbe/article/doi/10.1093/gbe/evp003/597551 )
mammals: 1000 ( https://www.a.u-tokyo.ac.jp/english/topics/2014/20140812-1.jpg )
https://www.google.com/search?ei=Hz89XaK2JuCGjLsP4rGJoAk&q=receptor+repertoire+size+fish+gustatory


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Giardia lamblia cases of infections
I am wondering if anyone has seen a data of Giardiasis (Giardia Lamblia) cases  in different countries on the world? I have found for different diseases and also for 'diarrhoea diseases' in general, but I need especially for Giardia Lamblia.
Any suggestion where I can try to look for this data will be useful.
Thank you very much!

If you have or can get access to it, you might try looking in the Incidence and Prevalence database: http://thomsonreuters.com/incidence-and-prevalence-database/
Another possibility is the GIDEON database: http://www.gideononline.com/. It is possible to sign up for a 15-day trial.
For Europe, statistics are available from the WHO CISID at http://data.euro.who.int/cisid/ (select "all infectious diseases", then "Giardiasis").
The WHO does not have any global statistics available on their website, so otherwise you might have to piece together data from individual publications. Some examples:
Thailand, 2005: http://www.ncbi.nlm.nih.gov/pubmed/16438174
Germany, 2006: http://www.ncbi.nlm.nih.gov/pubmed?term=19404678
United States, 2006-2008: http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5906a2.htm
Portugal, 2002-2008: http://www.parasitesandvectors.com/content/5/1/22
Quatar, 2008: http://www.parasitesandvectors.com/content/4/1/211
Tajikistan, 2009: http://www.parasitesandvectors.com/content/4/1/195
Ivory Coast, 2009: http://www.parasitesandvectors.com/content/4/1/96
Tanzania, 2011: http://www.parasitesandvectors.com/content/6/1/3
Ghana, 2006-2009: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3170632/?report=classic
Canada, 1999/2002: http://www.biomedcentral.com/1471-2334/5/72
Canada, 1990-1998: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC194172/
China, 2012-2013: http://www.biomedcentral.com/1471-2334/14/25
Ethiopia, 2009: http://www.biomedcentral.com/1471-2334/13/419
Kenya, 2010-2011: http://www.biomedcentral.com/1471-2334/13/243


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What exactly are "floaters"?
i was reading this artical after hearing about it on the news, while reading i saw the term "floaters" which made me remember of a recent Family Guy Episode in which there is a joke about them in Peter's vision.
I am wondering, what exactly are they? what is their technical term? and is it possible to remove them permanently (apart from the obvious gouging out your eyes).

Every question regarding floaters that you have asked is answered on the wikipedia page: http://en.wikipedia.org/wiki/Floater


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Is COVID-19 more deadly than swine flu?
I have a question about the novel coronavirus and swine flu.

How do the death rates compare between the two diseases?
How do the transmissions and rate of transmission compare?
Was a vaccine developed quicker for swine flu?

I ask because I don't recall this level of global disruption during the swine flu outbreak.

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

“Swine flu” is an obsolete name.  The official name for the virus that was briefly called “swine flu” is “H1N1pdm09”.
H1N1pdm09 has a mortality rate of around 0.01-0.1%. That’s roughly 10- to 20-fold lower than COVID-19. Its R0 was estimated at between 1 and 2, which is roughly half the estimates for SARS-CoV-2 (the virus responsible for COVID-19].
A vaccine for H1N1pdm09 was available in the fall of 2010.  It was possible to make it that quickly because it’s just another influenza strain, and the normal techniques for for vaccines against influenza strains worked fine.
Most importantly, H1N1pdm09 never went away.  It is still one of the main influenza strains circulating today, and if you were vaccinated for influenza since 2010 you received a vaccine against it.

CDC info here: 2009 H1N1 Pandemic (H1N1pdm09 virus)
WHO info here: Evolution of a pandemic:
A(H1N1) 2009, April 2009 – August 2010, 2nd edition


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Do non-human primates have mental disorders like humans?
I was at the zoo today and watched a gorilla pick at a scab on its finger, compulsively, until it started bleeding. Is this OCD or is it just a nervous thing that non-human primates do at the zoo? Do gorillas share any of the same mental disorders that humans have?

Hi and welcome. What attempts have you made to answer this question? We ask that all question posters show an attempt to search for an answer to their own question, show what they learned, and why iit s still confusing/unknown to them. (Studies exist on this subject.) Our goal is not to just be an answer site, but rather a site that promotes self-learning with some expert help along the way :). Please take a moment to edit your post with this additional detail and it will likely be received more positively by out community. Thanks!


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Spider identification (Caribbean)
I live in the Caribbean (Puerto Rico) and found this spider in my garage. Is it venomous?
It measures about 8 inches as a whole.

Please provide a more specific location. Country is necessary, but even more specifics (town/city, local habitat that your garage is surrounded by, etc.) are helpful. Thanks.

It appears to be a Banana Spider:

... a male Heteropoda venatoria, also called a Banana Spider. The female is a more robust spider with shorter legs. This is the spider that is responsible for the rumors that tarantulas come into the U.S. with bananas because they are often spotted emerging frrom a bunch of bananas in a fruit store in the North. This Giant Crab Spider is usually the culprit. The species is found in all tropical regions, its range extending clear around the world. It is very abundant in all tropical seaport towns, being transported in trading vessels. Its chief food is cockroaches. The female carries her eggs beneath her body. According to this site it is also called the Huntsman Spider.

https://www.whatsthatbug.com/2003/11/11/banana-spider-from-peurto-rico/


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Where can I find SARS-CoV-2 genome sequences for the UK?
I have downloaded and analysed the sequences of 832 complete samples from the European Nucleotide Archive but I cannot find a single one that was from the UK. I have also tried Genbank and they do not seem to have any UK ones either. I'm still waiting for my logon for Gisaid - looks like they may have some. Is there anywhere else I can try?

European Nucleotide Archive has only the genbank sequences but they have a link to download them all.
Gisaid refuses to make the sequences at disposal. On https://bigd.big.ac.cn/ncov/variation/analysis https://bigd.big.ac.cn/gbrowse/2019-nCoV/?gbgff=1;s=0;f=save+gff3;format=gff3;l=hCoV-19/France/B2337/2020 you can find all the high quality sequences in a diff form, except they didn't take the N in account.

@reuns i think this is a reasonable answer that you could add, probably more helpful than mine.

Thanks for the bigd link. Over 10,000 sequences but unfortunately most of them are stored on Gisaid and they don't let you download these. I thought this information would be in the public domain.

GISAID certainly does allow downloads. You need to register and follow their guidelines for acknowledgement if you publish, but it’s completely false to say they don’t allow downloads.

Just to clarify, if you go to the bigd link you cannot download any of the sequences held on Gisaid. I'm still waiting to see if my registration for Gisaid gets approved - it's been over a week since I filled in the form. I don't understand why this information is not in the public domain. The irony is that Chine (and most other countries) has been open and shared its genome information with the world, but the UK has not.

I deleted my answer as there are now better answers posted here.

https://twitter.com/arambaut/status/1254809662257606656

Oxford University's Bugbank project is designed to collect SARS-CoV-2 samples (and other microbial cultures) from UK Biobank participants for sequencing. Once completed this data will be available to researchers through the UK Biobank:

We originally developed this system as a pilot study to determine the feasibility of prospective microbiological culture collection from UKB participants to create a microbiological biobank (‘bugbank’) for joint studies of epidemiological, human genetic and pathogen genomic risk factors for infection. In light of the COVID-19 pandemic, we have repurposed the system to provide near-to-real-time data on SARS-CoV-2 positive and negative test results for UKB participants.

Dynamic linkage of COVID-19 test results between Public Health England’s Second Generation Surveillance System and UK Biobank (2020) *

* Disclaimer: I have worked on this project.

Thanks for this. Unfortunately I don't meet the admission criteria - I'm not a researcher, just a curious member of the public.


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Why would a 2019-nCoV protein sequence in the NCBI database match a protein submitted in 2018?
There seems to be a bit of a conspiracy theory brewing over some data in the NCBI database, and I don't have the necessary knowledge to make sense of it.
It basically goes like this:

Go to NCBI BLAST
Click on the big Protein BLAST button
Enter AVP78033 in the main search box and click BLAST
Click on the first result that shows a 100% match and click "See 5 more title(s)" in the first entry

This shows that the search is a complete match for a Bat SARS-like coronavirus protein from a 2018 research paper, for Wuhan seafood market pneumonia virus (which the NCIS site indicates is an alias for 2019-nCoV), and for Bat coronavirus from 29 Jan 2020.
My question is - why would a protein from Bat SARS-like coronavirus and 2019-nCoV be showing up as a perfect match for one another? Does this mean that 2019-nCoV might actually be a previously-discovered coronavirus that very recently started infecting humans? Or could it be that a recently collected sample from Wuhan was mis-identified as 2019-nCoV when it is actually the same coronavirus from the 2018 submission?
Clicking around the links on that site seem to bring up dozens of similar but different pages that I don't have the knowledge to distinguish, but the Accession column from the search results described above contains a link to this page, which says that it is a provisional refseq and acknowledges that it is identical to the bat coronavirus:

PROVISIONAL REFSEQ: This record has not yet been subject to final
              NCBI review. The reference sequence is identical to QHD43418.
              Annotation was added using homology to SARSr-CoV NC_004718.3.

Can somebody who actually understands these things please make sense of this?

How does a previously-discovered virus being identical to the coronavirus, indicate any sort of conspiracy in any way shape or form?

@IanKemp It's not identical to a previously-discovered virus. Only the envelope protein is identical. The claim is that someone took an existing virus and gene-swapped part of it to weaponize it while leaving other large parts intact. This is built on a false premise, but I think most laypeople (including my self prior to asking this question) would not know this.

Can you post screenshots of what we should click on? I'm not able to find it with your instructions. There was no result with "5 more titles", only 2, 4, 14, etc. Maybe a link to the final result would help as well.

2019-nCoV is a virus that originated from the bat (at least this is the current hypothesis). It shows 96% squence similarity to the BatCoV RaTG13 sequence (see reference 1), showing its origin.
It still is 87,99% identical to the "Bat SARS-like coronavirus", which explains the hit you found and is not unexpected, as these viruses are very closely related (see reference 2).
These viruses are closely related, so I wouldn't expect too many differences at all. Then envelope proteins can be critical for function/structure of the virus, so mutations there might occur less frequent. And if they occur, I would only expect few changes over time, so with this little time gone, probably no mutation is seen yet. Additionally, due to the redundancy caused by the codon degeneracy, not every mutation in the genomic material translates into changes in the protein.
References:

Full-genome evolutionary analysis of the novel corona virus
(2019-nCoV) rejects the hypothesis of emergence as a result of a
recent recombination event
Genomic characterisation and epidemiology of 2019 novel coronavirus:
implications for virus origins and receptor binding

Thank you for your answer. What is the meaning of the apparent 100% match between the respective envelope proteins? Is it common for distinct viruses to have identical envelope proteins?

@JLRishe It is not common for viruses from different virus families to have identical envelope proteins, except probably when they emerged from each other through evolution. But the case here is to compare the genome of chimp and man and then find identical proteins. Only that these viruses are much closer together from an evolutionary point of view.

What I'm trying to ask is - I'm surprised that two viruses with ~88% sequence identity would have identical envelope proteins. Is there a reason for this? Do envelope proteins evolve a lot more slowly than other parts of a virus?

@JLRishe These viruses are closely related, so I wouldn't expect too many differences at all. then envelope proteins can be critical for function/structure of the virus, so mutations there might occur less frequent. And if they occur, I would only expect few changes over time, so with this little time gone, probably no mutation is seen yet. I adapted the answer, is this clearer now?

Thank you again! I just found this paragraph in Wikipedia that seems to address the different rates of evolution between DNA and proteins: https://en.wikipedia.org/wiki/Molecular_evolution#Relation_to_nucleic_acid_evolution

Nitpick: coronaviruses do not have DNA. They're RNA viruses. The virion, IIRC, includes an RNA-to-RNA transcription enzyme.

@CarlF You are absolutely right, thanks for reminding :-)


text:
How long the homologous arms of the "repair" sequence must be to do homologous recombination?
I am trying to figure out the details of the homolougous recombination in order to be able to insert a certain piece of DNA in the host genome after double strand break.. Does anybody know how long the homology arms of the repair template must be ? Can the left arm be longer than the right one? I have read several papers which have different sizes 90 bp vs kb..
In my case, i am not so much preoccupied by off target but the insertion should occur also on the desired site possibly at high frequency and as fast as possible.
Thank you,
Paola

As little as 14bp of homology can work. See this reference.
I would recommend at least a length of 90bp but 1kb is probably overkilled. Yes both arms can have different length (staying in the same order of magnitude).


text:
Is chocolate poisonous?
I have heard that chilli peppers and coffee evolved to contain toxic chemicals which help to protect them from predators.  And recently I learned that star anise, liquorice and aniseed are not actually related plants, but each independently developed the ability to produce anethole, which can also deter predators.
However humans have evolved resistance so they can ingest all these substances, and tend to enjoy their extreme flavours.  Some more examples are onions, garlic, peppercorns and tea (for its stimulative effect rather than for its flavour).
It made me wonder:
Did the active ingredient in chocolate also evolve to deter predators?
And I am also curious, are there any other foods which I haven't mentioned that humans also enjoy due to their toxic or deterrent components?  (I'm thinking more about flavour than psychoactive effects here, as I know there are many examples of the latter.)

Are you sure people enjoy those flavors because they come from toxins? Even though it sounds very interesting, I can't think of any evolutionary reason we would like to consume them because of their toxicity.

Caffeine is also present in chocolate and toxic to many carnivoras.

I will add some info in my answer

@Probably I think with coffee, nicotine, alcohol, and perhaps also chocolate, we enjoy them less for their bitter flavour but rather for the association with the changes they cause in our brain chemistry. For things like spices, the strong flavour seems to be related to the toxicity. Presumably before our resistance had developed, those strong flavours were a warning signal, but now the residual effect is an exciting taste. (Chilli has the additional effect of causing a release of dopamine.)

Alkaloid synthesis is energy consuming for plants and have complex metabolic pathway.
If their evolutionary history is not known with certainty, they have numerous uses and are often toxic to potential plant or animal aggressor.

Chocolate contain many alkaloids including caffeine and theobromine. But apparently do it with a different pathway and is the result of convergent evolution.
It is safe to assume these alkaloid protects cocoa plant in the same manner it protects coffee and that the benefits of such poisons allowed poisonous cocoa plant to become predominant.
However, alkaloids of chocolate are solely responsible for its bitter taste. (Cf. Wikipedia page "Alkaloids" for more info).
If bitterness is part of its flavour, we prefer its fats the numerous volatile compound gained during fermentations of the beans. According to this article published on academy.org :

The distinctive chocolate flavor evolves throughout its production. Odorless, tasteless “precursors” form during fermentation, and these precursors react during roasting to form taste and aroma compounds.

Also many essential oils are poisonous to insects, fungi or bacteria. These properties are sometimes used by humans : for instance cinnamon oil is toxic to mosquito larvae


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Would "Pox Parties" of the young/healthy (while isolating the vulnerable) be an effective method of combating the COVID-19 outbreak?
It is commonly said that most people, especially the healthiest would only develop mild syndromes.
Therefore, shouldn’t we, instead of confining all the population as a whole proceed as follows :

isolate the most fragile people (older people or those with known health issues) in their home or in some other safe places.
invite healthy people to join some kind of "controlled contamination" campuses for 3 to 4 weeks. During this period, these people would get the virus inoculated on purpose, will get sick, will most of the time recover since they are healthy, and will become immune to the virus.

This way the general population will, step by step increase its immunity and as a result, the more fragile people would become less exposed to the virus.

This strategy is known as a "Pox Party".

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

Apart from the inherent wisdom or lack thereof of this course, it assumes that "smart people" are in charge.  Observation suggests otherwise :-(

This is a proposed/tentative answer only...
Statements from official public health sources could be summarized as: older people and those with certain pre-existing health conditions including compromised immune systems are more likely to be more severely affected.
"More severely affected" means requiring hospitalization, suffering permanent lung damage, or dying. "Requiring hospitalization" may be equivalent to a death sentence if the health care system is so overwhelmed that not all who need the necessary care can receive it.
"More likely" means that younger or otherwise healthy individuals are by no means certain to recover from an infection free of any long-term consequence... they are just more likely to.
There are already reports in the media of younger, otherwise healthy individuals dying as a direct result of COVID-19 infection. There doesn't yet seem to be enough known about this disease to make any reliable predictions about the effects of an infection on any given individual; it can at best be expressed as a probability.
Regardless of age or health status, deliberately allowing people to become infected knowing that as a direct result, some fraction of the population will suffer permanent lung damage or die is not ethically sound policy. There can be no guarantee that isolation measures will be good enough, or that there will be a high enough level of public compliance to protect the safety of the vulnerable, so it will place the vulnerable at risk anyway.
The whole point of immunization vaccines is to do the same thing as you suggest, but without suffering the effects or consequences of the disease. The problem is that it takes time to develop, mass produce, and distribute a safe, effective vaccine targeting a new virus. The whole point of social distancing is to slow the spread of a disease in order to minimize the harm it will do, and if a vaccine is ultimately coming, buy the time it takes for that be accomplished. The other possible outcome from social distancing is that the virus could eventually "burn out" - when all infected individuals recover and and become non-infectious before they have an opportunity to infect anyone else.


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Is the Basic Reproduction Number in epidemiology dependent on population size?
I am assuming that the basic reproduction number $R_0$ of a disease depends on the population size (or the number of susceptible individuals). When $R_0$ is reported it seems to be without such information. Is there a standard population size for reporting $R_0$?

I'd think there'd be a required sample size to get your data within the necessary margin of error, but agencies like WHO actually provide standard population data I believe. Someone let me know if i'm mistaken!

Actually, population density and structure is far more important than population size.

OK, so $R_0$ depends on the environment. For example, different countries experience different $R_0$ for the same pathogen. So the commonly reported values correspond with what environmental conditions?

From what I understand (as an ecologist/population modeller), $R_0$ in epidemiology is not dependent on host population size per se, at least not in its basic form. It is also not dependent on the number of susceptible individuals, since it is defined as the number of secondary infections in a fully susceptible population, see e.g. this section in Farrington et al (2001):

The basic reproduction number of an infectious agent in a given population is the average number of secondary infections which one typical infected individual would generate if the population were completely susceptible.

This is also consistent with the Wikipedia description ("...in an otherwise uninfected population"). $R_0$ is however dependent on the environment (dispersal routes, host-host interactions etc), which also why it is used to evaluate and compare the effect of control measures. Host-host interactions is also dependent on population density, so $R_0$ is indirectly influenced by host population density, and this is partially why estimated $R_0$ values for the same disease will differ between countries and populations.
Fundamentally and conceptually, $R_0$ is the same thing as the Net reproductive rate (often also labelled $R_0$) in demography and population modelling, and it was originally borrowed from demography to epidemiology. As such, the net reproductive rate is often used in for instance pest control to evaluate the potential impact of pest species on agricultural crops, in direct analog to the basic reproduction number in epidemiology (see Emiljanowicz et al, 2014 for a randomly picked, recent example). Most commonly, $R_0$ (both in population dynamics and epidemiology) is calculated from static demographic rates, but nothing prevents you from considering stochastic effects, density dependence or e.g. ways that demographic rates are functions of host density or population size. This could lead to formulations where $R_0$ is an explicit function of host population  density, but that is not the standard use of $R_0$.
To me, it seems like you are asking for the effective reproduction number ($R(t)$), which can be defined by:

...the average number of secondary cases that result from an infectious case in a particular population (Box 1). R depends on the level of susceptibility in the population, in contrast to the basic reproduction number (R0), which is the average number of secondary cases arising from one infectious case in a totally susceptible population."

This section is from a WHO paper on meases (Chiew et al, 2013). So basically, $R(t)$ is the average number of secondary cases per primary case at time $t$ (including the effects of immunity and/or control measures). As you can see, $R(t)$ is a function of time, and it can e.g. be used to describe the temporal dynamics of SIR-type models.

But a well established result in epidemiology models (e.g., the standard SIR model) is that a disease will die out before infecting all susceptible individuals in the population. Also an epidemic will not even take place if the population size is small. This is because $R_0$ itself is a dynamic quantity.

@quibble That diseases will die out is not a function of the $R_0$, but of the buildup of immunity described by the dynamics of SIR models. $R_0$ is not supposed to describe this, and bringing it into discussion is just confusing things.The dynamics in small populations is also another thing (related to e.g. low host density or stochasticity). Remember that $R_0$ is mainly a measure of maximum growth, similar to e.g. $r_max$ in population models, which is describing exponential growth under "ideal" conditions (e.g. a completely susceptible population).

@quibble What you seem to be after is the effective reproduction number ($R_t$), which can be described as "...the average number of secondary cases that result from an infectious case in a particular population (Box 1). R depends on the level of susceptibility in the population, in contrast to the basic reproduction number (R0), which is the average number of secondary cases arising from one infectious case in a totally susceptible population." (Chiew et al, 2013)


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Why are Aardvarks capable of burrowing given their size?
I was wondering if large animals could possibly dig extensive burrows for themselves to live in. The polar bear burrows, but snow is not dirt. The aardvark goes about 4' long, ~150 lbs: similar to a sheep. I think the aardvark might be the biggest dirt-burrowing animal, the only sheep-sized burrower.
I wonder why.
Is there anything special about the aardvark that at its size it burrows, while other burrowers are smaller?

Welcome to SE Biology! This question is quite broad and open-ended, making it difficult to answer. It's helpful to ask somewhat more targeted questions to get good answers. I'd recommend looking a little at the wikipedia page for aardvarks (if you haven't already) and see what it has to say on this topic: https://en.wikipedia.org/wiki/Aardvark. Perhaps you can find a way to sharpen the question to be more specific and easier to answer.

Thanks to ukemi for finding a good answer and thank you for the asking tips! I did read Wiki and a few other pages about the aardvark and burrowing before I asked. 'Fossorial' was a very useful search term to learn.

The following paper examines the link between burrowing ability and the stress and strain resistance provided by increased endosteal tissue formation (specifically compacted coarse cancellous bone (CCCB)) in aardvarks:

Physiological constraints associated with digging, however, are known to be strongly influenced by body size, and larger burrowers are likely to exhibit a histological profile more conspicuously influenced by fossorial activity. Here, we describe for the first time the limb bone histology of the aardvark (Orycteropus afer), the largest extant burrowing mammal...
We hypothesize that the unusual histological profile of the aardvark is likely the outcome of physiological constraints due to both extensive digging behavior and strong metabolic restrictions. Adaptations to fossoriality are thus the result of a physiological compromise between limited food availability, an environment with high temperature variability, and the need for biomechanical resistance during digging. These results highlight the difficulties of deciphering all factors potentially involved in bone formation in fossorial mammals. Even though the formation and maintaining of CCCB through ontogeny in the aardvark cannot be unambiguously linked with its fossorial habits, a high amount of CCCB has been observed in the limb bones of other large burrowing mammals.

Digging the compromise: investigating the link between limb bone histology and fossoriality in the aardvark (Orycteropus afer), PeerJ Life & Environment (2018)

Further reading:

Ecosystem engineering through aardvark (Orycteropus afer) burrowing: Mechanisms and effects

These articles discussed factors affecting burrowers, and linked to many more useful ones. They need strong limbs (probably short), a way to support their weight if they dig fast with all fours digging (e.g., tail), and not to overheat while digging hard. The first article seemed to take the body size for granted and discussed that eating ants limits further bone grown and higher metabolic rate. Other links in that paper make lower basal rate important for larger size. So I guess bigger burrowers would need that much more help working cool, and that much better diet, plus reason to burrow.

So that answers about bigger burrowers, though I still wonder why the aardvark itself is comparatively large :) Myself, I didn't figure that out from the article and the links I looked through there.