text:
Are there any oxygen loving bacteria?
It seems we only found bacteria that hate oxygen. Are there any bacteria that love oxygen and would thrive in high oxygen environment?
If it slowed down or stop multiplying in low (as in normal earth atmosphere) oxygen content it would be the best.

Acetic acid bacteria need oxygen to turn alcohol into vinegar.

There are anaerobic bacteria and aerobic bacteria. Aerobic bacteria include: Mycobacterium tuberculosis (Tuberculosis), E. Coli (common model organism), and Staphylococcus auerus (that new superbug)

It's not true that all bacteria hate oxygen. Actually, there are some obligately aerobic bacteria that need oxygen to carry out cellular respiration. A notorious example of this type of bacteria is Mycobacterium tuberculosis, a pathogenic species that infects lungs and cause tuberculosis. Because it's obligately aerobic, in the classic case of tuberculosis, Mycobacterium tuberculosis growths are always found in the well-aerated upper lobes of the lungs where the oxygen requirement is satisfied.
Reference:
1. Levinson, W. (2010). Review of Medical Microbiology and Immunology (11th ed.). McGraw-Hill. pp. 150–157. ISBN 978-0-07-174268-9.

To improve the answer quality I suggest to add references to your claims

@havefun thanks for your opinion, will add it soon.

I am thinking along the lines of "rapidly duplicating itself in high oxygen environment like those bugs in 'The day the earth stopped'."

Are there any bacteria that love oxygen and would thrive in high oxygen environment?

Yes, the obligate aerobes.
Regarding the influence of oxygen on growth, we classify bacteria in 5 main groups (Tortora, Funke and Case, 2015):

Obligate Aerobes
Facultative Anaerobes
Obligate Anaerobes
Aerotolerant Anaerobes
Microaerophiles

This image (also from ) gives us a good summary:

As its text says:

Obligate aerobes: Growth occurs only where high concentrations of oxygen have diffused into the medium.

Regarding your second question ("If it slowed down or stop multiplying in low -
 as in normal earth atmosphere - oxygen content it would be the best"), I'm afraid that there is no such organism. If I understand the question correctly, you're trying to make a comparison with hyperthermophiles, for instance: a bacterium that survives in extremely high O2 concentrations but that dies (or don't grow adequately) in normal O2 concentration. The problem is that, except for very specific and small microenvironments, like a leaf's aerenchyma, there is no place with those higher O2 concentrations in which such bacteria could evolve.

Source: Tortora, G., Funke, B. and Case, C. (2015). Microbiology. Harlow, United Kingdom: Pearson Education Limited.

Species that require oxygen to survive can be classified into 3 groups(in bold). Their distinctions are also explained:

Microbes that use oxygen for energy-yielding purposes are called
  aerobes, if they require oxygen for their metabolism they are called
  obligate aerobes. Obligate aerobes are at a disadvantage because
  oxygen is poorly soluble in water and much of the environment is
  lacking in this necessary element. Often, aerobic bacteria have
  retained the ability to grow without oxygen; these are called
  facultative anaerobes. Those bacteria that are unable to use oxygen
  and in fact may be harmed by it are known as obligate anaerobes.
  Further groups include: the microaerophiles which are aerobic microbes
  that tolerate only a narrow band of oxygen concentrations usually
  lower than that of the atmosphere and are therefore often difficult to
  cultivate in the laboratory, and aerotolerant bacteria that grow in
  the presence of oxygen but do not require it. (Here)

Examples

Obligate aerobes:Mycobacterium tuberculosis and Nocardia asteroides
Microaerophiles:Campylobacter species and Helicobacter pylori
Aerotolerant anaerobe(anaerobe because they grow in the lack of oxygen)
: Streptococcus mutans


text:
Non-Ethical Issues with Eugenics
Notwithstanding the obvious ethical issues with the idea of eugenics, I have read in many sources that eugenics has practical issues or otherwise "would not work", but I haven't been able to find an enumeration of the reasons more complex than "genetics doesn't work like that".
From a biological or genetic standpoint, what are the main problems with eugenics, in its broadest sense as "organised, goal-directed human breeding"?

Eugenism is a set of believes on how to improve the "genetic quality" of the human population. There are no set of clearly defined practices that we could discuss here. If you want to question the practicality of a particular practice, can you please clearly defined this practice?

In its broadest sense, the most obvious biological concerns about selective breeding in humans are really sociological in nature. One of the potential issue is related to increase homozygosity and inbreeding depression . But it will really depenss upon the details of the eugenics program suggested.

Well, there can be multiple reasons about why eugenics won't work.
The first problem is related to pleiotropy of human genes. That is, one gene can control multiple traits, although the influence of a single such gene on a particular feature may be small. So eugenic practices will very likely pick out some characters caused by pleiotropic genes and amplify desired alleles in the gene pool, but there may be other anomalous traits linked with the very same gene. Thus eugenics introduces new problems in this scenario.
(Some afterthoughts: These antagonistically pleiotropic genes are not uncommon, and they could be rationalized from an evolutionary perspective. Some traits encoded by such genes may be beneficial to the organism in its early life but not later. Such benefits, if they come before sexual reproduction, confer greater fitness to that organism. An classic example is the sickle cell anemia. Heterozygotes have resistance to malaria while homozygotes suffered from reduced life expectancy.)
Then, it's easily understood that eugenic programs shall proceed slowly in comparison to Morgan's fruit fly experiment, for example, as a result of the extended period between birth and sexual maturity for our species. Therefore, we have to wait for decades to have some real accumulation of beneficial phenotypes.
Finally, critics of eugenics widely believe that it will sacrifice genetic variety. This argument makes sense because those desired phenotypes are chosen by us, not by nature, so they are not necessarily those best assist our survival. Though we live in comfortable environment nowadays, there may be plagues, droughts, and other large-scale natural disasters in far future that select against our chosen traits. If our species is too homogenized then by eugenics, we will probably face a grave situation...
Reference:
1.Carter, Ashley JR; Nguyen, Andrew Q. (2011-01-01). "Antagonistic pleiotropy as a widespread mechanism for the maintenance of polymorphic disease alleles". BMC Medical Genetics. 12: 160. doi:10.1186/1471-2350-12-160. ISSN 1471-2350. PMC 3254080  Freely accessible. PMID 22151998
2.Richard Lynn, The Science of Human Diversity: A History of the Pioneer Fund (University Press of America, 2001 ISBN 978-0761820406).
(Since this topic is really controversial, extreme care is needed to choose evidences to support the answer. For those who may disagree, please put a comment below about your opinion instead of immediately casting a down vote, thanks!)

source: Stack Exchange

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

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text:
What did the ancestors of textile moths eat?
These days I had to wrestle a lot with textile moths. From the Internet I got the impression that these moths don’t feed on naturally available furs in the wild, but have specialised on man made textiles(?). From the Wikipedia entry on textiles I gather humans started wearing textiles (not furs) about 6500 years ago.
Did the ancestors of textile moths (from the time of textile adoption) feed on furs and such, or were they akin to today’s kitchen moths, which eat food stuffs?
In the latter case, is not 8500 years a very small time for such a fundamental change in animal biology? Or must I take into account the short lifespan of insects, equating each human year to a dozen generations and each human generation to about 300 moth generations, so that the change moths can undergo in 6500 years is more akin to that humans can undergo in 250.000 years (which perhaps has to be increased even further due to moth simplicity and large population making non lethal mutation more common) ? For comparison, it appears Homo  Sapiens emerged some 200.000 years ago.

Modern textile moths actually eat a wide variety of material, including fur, feathers, shed exoskeletons, bran, and grain. humans just pay more attention to them when they eat textiles. They prefer human handled material because we tend to create larger concentrations than occur in nature.
if you are interested in changes in biology in response to humans you may want to look at starch digestion in dogs, nylon eating bacteria, and body lice.

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


text:
Selection of recombinant host by color selection method
In recombinant DNA tech,
To select a recombinant host from non-recombinants, we have different types of techniques available.
The one I'm talking about is the color selection method with the use of 2 markers(one antibiotic resistant gene for eg. Ampicillin, and the other Z-gene).
We use Z-gene as the reporter gene.
We use vectorless E. Coli as the host cell here.
Now, when we add add Ampicillin to the petri dish containing all of the variants (transformants and non-transformants), - the non-transformants will die.
The transformants survive.
Now, we add X- gal to the replica of this petri dish, and we see some of the colonies turning blue due to the action of the enzyme β- galactosidase, which in turn is produced by the intact Z-gene in the plasmid.  That means our blue colonies are the non-recombinant ones.
My question is-
The medium taken in the petri dish should contain glucose too , shouldn't it? Otherwise the recombinants would too give the colour reaction (X-gal is a homolog of lactose) due to the Z-gene present in their chromosomal DNA (operon concept).
The question maybe silly since it's kind of obvious we have to supply basic necessities for the growth of bacteria(which obioviously is glucose).
Just wanted to confirm in case we don't have glucose available ! =p

The Z gene you are talking about should be lacZ that encodes the $\beta-$galactosidase, which is made from $\alpha$ and $\omega$ peptides. Neither peptide is functional by itself.
$\beta-$galactosidase will cleave the glycosidic bond in X-gal and form galactose and 5-bromo-4-chloro-3-hydroxyindole. The latter product then dimerizes and oxidizes to 5,5'-dibromo-4,4'-dichloro-indigo, an intense blue product that is easy to identify and quantify.
Next, you should check out the genotype of your bacterial strain because they typically have only the $\omega$-peptide encoded in its genome. Thus, the enzymatic activity of the $\beta-$galactosidase is only recovered when the $\alpha$-peptide is in the environment, and the process is called $\alpha$-complementation.
Two commonly used strains for cloning and expression in E. coli are Dh5$\alpha$ and TOP10.
The genotype for Dh5a is like this:

F– Φ80lacZΔM15 Δ(lacZYA-argF) U169 recA1 endA1 hsdR17 (rK–, mK+) phoA
  supE44 λ– thi-1 gyrA96 relA1

Here, lacZΔM15 indicates that the M15 segment is lost from lacZ, and the mutant protein will only have the $\omega$-peptide.
The genotype for TOP10 is like this:

F– mcrA Δ(mrr-hsdRMS-mcrBC) Φ80lacZΔM15 ΔlacX74 recA1 araD139 Δ(ara leu) 7697 galU galK rpsL (StrR) endA1 nupG

Again, you will notice lacZΔM15, which is still a non-functional peptide segment after all.
Finally, to your question. Even if the there is no glucose as primary energy source in the medium and only X-gal is present, the operon of your host bacteria(I suppose it's E. coli) cannot produce the functional $\beta-$galactosidase on its own. Moreover, the recombinants, with the vector sequence encoding the $\alpha$-peptide disrupted, will not exhibit $\alpha$-complementation. No color reaction then! :D
Reference:
1.Genotypes of Invitrogen™ competent cells - TOP10, retrieved from: https://www.thermofisher.com/cn/zh/home/life-science/cloning/competent-cells-for-transformation/chemically-competent/top10f-genotypes.html.
2.Genotypes of Invitrogen™ competent cells - DH5a, retrieved from: https://www.thermofisher.com/us/en/home/life-science/cloning/competent-cells-for-transformation/chemically-competent/dh5alpha-genotypes.html.
3. Langley, K. E.; Villarejo, M. R.; Fowler, A. V.; Zamenhof, P. J.; Zabin, I. (1975). "Molecular basis of beta-galactosidase alpha-complementation". Proceedings of the National Academy of Sciences of the United States of America. 72 (4): 1254–1257. doi:10.1073/pnas.72.4.1254. PMC 432510 Freely accessible. PMID 1093175.
4.

So basically, we use different kind of bacterial strains here {the ones those have either of the 2 genes(the peptide coding ones) present in the chromosomal DNA, not both of them simultaneously}? Are they mutated versions (made in lab) of normal E.coli or were they present naturally?

In your case I believe they are mutated since you are doing recombinant DNA experiments. Wild type E. coli carry functional LacZ, while lab strains are deliberately mutated so we can apply the blue-white test at ease. But if you are still not so sure, I suggest you to check the precise genotype of the strains online, if you can get them.

I'll take your words for this. I'm not actually experimenting nor do I have the qualifications or the facilities to perform this experiment. Plus, i don't know how to check the genotypes of strains online. Anyways, thanks for clearing that up! =)

@anamikaSingh For commercial strains, you just look them up on its provider's website. Usually you will find details. Hope this can help you!

Yes! I looked it up. It was really helpful.  Thanks!  =)

@anamikaSingh No problem. :)


text:
Can proteins from different viruses be gathered in one virus?
There is a biology project I must do with some of my classmates and we're facing a problem.
We would like to choose proteins from different viruses that seem interesting to us (for example one protein from a negative-strand ARN virus and the other one from a DNA virus) and gather them (theory) together through this process called "directed mutagenesis". Is it possible ? If no, isn't there another mechanism that allows the gathering ?
Thank you !
(PS: Sorry for the english)

Please clarify. Explain what you mean by ‘gather’. What level class are you talking about — high school or university? Is this project practical or theoretical?

If I understand your question, you're asking if you can take a protein from Virus A, and make Virus B produce that protein. The answer is yes, you certainly can do that, although depending on the proteins and viruses there may be some constraints. There are many examples of this being done, and even more examples of making a virus produce proteins from humans or other species.
The actual process of inserting a new gene can be pretty trivial; you can pick up handy kits of viruses specifically designed to have new genes inserted into them.  If you're putting the gene into a virus of your interest, the design process can be a little trickier; you need to be sure that the inserted protein doesn't disrupt something essential for the recipient, isn't too large for its genome, and so on.
But in principle, it's pretty simple.


text:
What is the difference between nucleotide polymorphism (θ) and nucleotide diversity (π)?
In my population genetics book (see reference at bottom) they define them as:

Nucleotide polymorphism (θ): proportion of nucleotide sites that are expected to be polymorphic in any sample of size 5 from this region. Of the genome. $\hat{θ}$ equals the proportion of nucleotide polymorphism observes in the sample (S) divided by $a_1 = \sum_{i=1}^{n-1} \frac{1}{I}$. If n= 5, $a_1 = \frac{1}{1}+ \frac{1}{2}+ \frac{1}{3}+ \frac{1}{4}+ \frac{1}{5}=2.083$
Nucleotide diversity is the average proportion of nucleotide differences between all possible pairs of sequences in the sample. In R, I came up with that code which is in accordance with what is in the book.
   data # Only polymorphisms
   total.snp # This is the total number of sites that were looked (e.g. 16 might be polymorphic over the 500 sites that we've looked at. So 484 sites are monomorphic)

   n = nrow(data) # Number of samples
   pwcomp = n*(n-1)/2 # Number of pairwise comparisons
   for(i in 1:n.col){ # Compute the number of differences in the samples that are polymorphic
     t.v = as.vector(table(data[,i]))
     z = outer(t.v,t.v,'*')
     temp= c(temp,sum(z[lower.tri(z)]))
   }

   pi.hat = sum(temp)/(pwcomp*total.snp) # Nb of different pairwise comparison/(nb all pairwise comparison * total nb of loci (polymorphic or not))

In the book, they say

On the other hand, there is a theoretical relation between θ and π that is expected under simplifying assumption that the alleles are invisible to natural selection.

In summary θ = π with this assumption and large sample sizes.

So what is the difference in the
Why are we calculating both
(what could they tell us)?

Hartl, D. L., & Clark, A. G. (1997). Principles of Population Genetics (3rd ed.). Sinauer Associates Incorporated.

You are also confusing definition of these terms with their expected values (typically computed from coalescent theory). Let's look at an example.
Consider a haploid population of 6 individuals. We will represent these individuals with 5 sites that can take values 0 or 1.
00000
00001
00000
00010
00010
00000

Polymorphism
In this population there are $S=2$ polymorphic sites. In other words, there are two sites for which different individuals take different values in the population. Over these 5 sites, the fraction of polymorphic sites is $\frac{2}{5}$. You use $\theta$ for this quantity but to me, $\theta$ is typically used as a short hand for $2 N \mu$ (or $4 N \mu$ for diploid populations).
Under an infinite allele model, in a single panmictic haploid population (without selection and other assumptions), $E[S] = 2 N \mu a$, where $a = \sum_{i=1}^{k-1} \frac{1}{i}$, where $k$ is the sample size.
Genetic diversity
Genetic diversity is also known as expected heterozygosity. While it is most often called $\pi$, I will call it $H$ to avoid confusion. Imagine, you randomly sample two individuals in the population, what is the probability that there have different alleles at a given locus?

At locus 1, $H = 0$
At locus 2, $H = 0$
At locus 3, $H = 0$
At locus 4, $H = 2 \frac{2}{5} \frac{3}{5} = \frac{12}{25}$
At locus 5, $H = 2 \frac{1}{5} \frac{4}{5} = \frac{8}{25}$

You can average over all loci if you want.
The expected heterozygosity in panmictic population (without selection and other assumptions), $E[H] = \frac{4 N \mu}{1 + 4 N \mu}$. You should notice a relationship between $H$ and $F_{ST}$ here!
Nucleotide diversity
The nucleotide diversity is the equivalent of $D$ from Nei and Li (1979) and is highly related to $D_{XY}$ (Nei, 1987). Once you've managed to demonstrate that the expected coalesence time is $N$ (I won't do the demonstration here), then under an infinite site model, the number of mismatch between two individuals is logically $E[D] = 2 N \mu$ (it is the number of mutations that has happened in both lineages since the the coalescence event). For diploid population, multiply everything by 2.
Relatedness between $D$ and $S$
Under a neutral model $\frac{S}{a} = D$. Actually the standardize difference between $\frac{S}{a}$ and $D$ is what is used in Tajima's $D$ tests.
Source of information
Hartl and Clarck is good IMO but I would also like to recommend reading Population Genetics: A Concise Guide by Gillespie who explain all of that wonderfully.

Thanks! Actually, $S = nb.polymorphic.sites / total.nb.loci $. In my example θ = $S/a_1$. This is what you say is $S/a =D$. So in this case, it's not exactly $4Nμ$. And I guess here $μ$ is the mutation rate. Thanks for the book! I'm going to read this carefully.


text:
Would salt cause a pistachio nut not to be able to germinate?
If I buy a bag of pistachio nuts that have been hand picked off the tree when ripe, then salted in a (light) saltwater solution, then vacuum-sealed, and stored in a refrigerator, then will they germinate if I take them out and soak them in a moistened towel laying out in the sun?

Aren't commercial pistachios roasted?

These aren't commercial. They've been hand picked as described.

This article https://wikifarmer.com/how-to-grow-pistachio-tree-from-nut/
says unsalted.  Lots more on that site about growing them.


text:
is this a soft coral on sand?

Was diving a few days ago at Jervis Bay (Australian East Coast - temperate). Water temp 20 degrees C, depth 5m. Spotted this creature in the sand. About 150mm high. It isn't sea-pen (Cnidarian) as it doesn't retract if touched and is wrong shape. Has polyps 20mm long all over stalk. Its soft. I've never seen one before. Took a few snaps as I was sure everyone else would say they knew what it is. No-one does. Is it a soft coral? If so, what's it doing growing on sand in temperate water. It looked quite healthy but we've never seen any others there.
I wish I'd taken better photos now :)

looks like a sea anemone to me.

But given that there are multiple polyps it could only be some sort of communal sea anemone.....and I can’t find any reference to anything that looks like that across half a dozen marine ID text books

Ok - found it. It IS a type of soft coral...and in fact is a type of Sea-pan that doesnt look like a pen and doesnt retract! From the family Veretillidae possibly Cavernolaria obesa (at least Ive found a photo of that organism that is remarkably similar).

@ScubaAl you can add that as answer and accept it.


text:
Help identify the insects I keep finding at my house (Auburn, WA)
Could anyone tell me what is this living being is called? I keep finding his relatives flying/crawling in my house once in a while since late Summer this year. We live in Auburn, WA, in case it helps narrowing down the list of who it can be...

Knowing the name will help me figuring out:

whether it's dangerous for my wife, or our infant;
how to get rid of it (I start suspecting they either breed inside the house, or somewhere very close because I only find these insects when it's getting warmer outside).

Sorry for the low quality of the photo. By the way, this animal is about 15mm or 5/8" long (not measuring the legs).

It is a Halyomorpha halys, commonly known as a stink bug.  Your photo shows a brown marmorated stink bug.  More information can be found on this Wikipedia page.

As far as your two questions:

Stink bugs do not normally bite people and are not poisonous.
A good way of controlling them in your home is by sealing any
openings that they are entering through.

Source: http://stinkbugsguide.net/facts.htm

Wow! That was fast! Could you tell me how did you do that? Some kind of a book helped you, or you just 'happened to know'?

We see them all the time at our house-most commonly in autumn. I think it was my oldest child that knew what they are - I think he learned about them in school.  My children like to catch them and let them go outside.

I wish I knew a permanent solution to this problem. These buddies freak my wife out, and I'm not very comfortable with catching them... Still, many thanks, Kurt!


text:
Can one conduct “novel” research without an advanced laboratory? Has it been done by school pupils?
I want to conduct an experiment but as a secondary school pupil I will be using my school’s laboratory and to make novel or interesting discoveries, wouldn’t one need advanced equipment, a prospect which is not feasible for one of my station in life? I want to know if anybody has done a simple experiment and discovered anything new? Thanks.

Do you mean a groundbreaking discovery? That would be hard. But smaller ones that built upon others works are really feasible.

I'm voting to close this question as off-topic because it has nothing to do with biology specifically, and can be applied to most fields of scientific research.

@Charles It is about science but since I wanted to experiment in Biology I posted it here.

I would advise to conduct a field experiment. Field work typically requires many eyes (school pupils) and not necessarily a lab.

I can point to two published papers in which students performed useful experiments.

The present study (on the vision of bumble-bees) goes even further, since it was not only performed outside my laboratory (in a Norman church in the southwest of England), but the ‘games’ were themselves devised in collaboration with 25 8- to 10-year-old children. ... They also drew the figures (in coloured pencil) and wrote the paper.
Principal finding ‘We discovered that bumble-bees can use a combination of colour and spatial relationships in deciding which colour of flower to forage from. We also discovered that science is cool and fun because you get to do stuff that no one has ever done before. (Children from Blackawton)’.

--Blackawton bees

As part of a high school class project, influenza sequences with possible errors were identified in the public databases based on the size of the gene being longer than expected, with the hypothesis that these sequences would have an error. Students contacted sequence submitters alerting them of the possible sequence issue(s) and requested they the suspect sequence(s) be correct as appropriate.

--Sequencing artifacts in the type A influenza databases and attempts to correct them
You'll notice that both of these projects were guided by "professional" scientists. The biggest problem with doing your own experiments is that you're very likely to simply repeat something that's already done, or else do something that's not useful or is trivial. It's very difficult even for professional scientists to have a reasonable grasp of even a very focused field of science, and for someone outside the field to try to understand what has and hasn't been done, and what is and isn't considered interesting, is nearly impossible.

Thanks. I am not sure I will be allowed to do a data-based project for the science fair though.

All kinds of interesting stuff you can do.  How novel it is depends largely on your approach.
While it didn't lead to a paper, I heard the following story from a microbiologist an New Mexico State. I think it was second hand then.
School loses it's science teacher.   It's a small college town, and it was only a part time position. One section of biology is for "kids who are good with their hands" a euphemism for ones not on the college track, the dummies.  They take a lot of shop, industrial arts etc.
They hire a grad student from the local college to fill in.  The principle tells him that if can just keep the dummies quiet that's sufficient.
Grad student goes away and thinks about this.
Comes in first day of class with a mouse trap.  Doesn't say a word.  Sets the trap, then with a pencil nuzzles the trigger until SNAP.  Makes choking sound.  "Dead Pencil"
"As you can see, this is a trap for getting rid of mice.  But it makes the mouse hard to reuse.  I want a live trap.  I want a trap that will catch a mouse without hurting it. How do we do that?"
The rest of that class was spent brainstorming ideas.  At the end of the period he gave each kid a trap.  "Make a live trap."
Most of them came with traps the next day.
They went into the rough country behind the school and set the traps.
Next day some of the traps were gone.  Trap and all.  Coyotes thought they were box lunches.  The ones that were alive  were anesthetized, banded, sexed, weighed, and released.
The quality of the traps got better.  Fewer mice died.  Less bait used with no mouse to show.  Some of the kids had a half dozen traps.
He made them pool their data and make a map of every trap, and the distances to other things.  Trees, grassy areas, bushes.
After a couple weeks he taught them how to determine their age.
As they accumulated data they started catching some mice that had already been banded.
By asking questions he got the idea of sampling to them.  Based on the number of banded ones to unbanded ones, they could figure out how many mice there were out there.
He had them plot where the 2 and 3 time mice were caught.  From this they figured out how big a world a mouse lives in -- what was their territory.
They kept a few in the lab, and the kids watched them.  Watched them mate, and later deliver litters of pups.   They weighed pups.  Weighed mom.  Measured the food they ate.  Figured out how much food it would take in the wild.
Some of htem asked if wild mice would behave the same, eat the same.  "Good Question.  How would you find out?"
Often when they caught a mouse, it had been in there long enough to crap.  He taught them how to analyze the crap for parasite eggs.  He showed them lice, and fleas.
By mid winter they were doing all kinds of stats.  Since they were 'good with their hands' their math was chequebook and carpenter math.  He had them calculating variance, and correlations.
This is solid science.  Papers?  Probably not.  You'd have to find something different from the literature.  But as a teaching or learning exercise it's first rate.
There are lots of critters out there that we don't know a lot about.
Google "Citizen Science" for more ideas.  Locally we have a prof that crowd sources climate change indicators over western Canada.  She has a web site where you report when wild flowers bloom, when you hear the first boreal or chorus frog, when the first flight of geese with more than 12 birds goes overhead.  First tiger swallowtail.
Turns out that some of them don't correlate well with temperature.  Some do.  Then someone realized that this same dataset can be used to measure biodiversity, and see if the ranges are changing.  People near a sighting of X last year were asked to watch for it this year.  People were given a protocol for walking a known strip of land, and counting this and that.  If they couldn't id it they took a pciture with their phone, and said "30 of these thingies"  Prof had a grad student to turn 'thingy' into blazing meadow star.  Grad student asks people to stop in the middle of the strip and take 4 shots with their phone with the bottom edge of the image about 10 feet away.  From this and looking at grass seed head shapes, he gets an idea of what the relative population of different classes of grass are.
Citizen science.

The class of dummies doesn't have a happy ending.  Two weeks before the end of the year, the school inspector comes in, and sits in on the class.  The class is excited.  A lot of their mice got through the winter and they are seeing small mice -- mouse teenagers -- appearing in their traps.  The grad student is talking about reproductive success and population dynamics.
The superintendent goes to the principal.  "He's not teaching the state bio
curriculum."  Principal explains that no one has ever had this kind of success with the dummies.  "Doesn't matter.  He's not teaching the curriculum.  Fire him."


text:
Black insect with antennas and large abdomen
I found this insect crawling outside near my house, and I have never seen anything quite like it!

It was found in the summer in Denmark.
Length is approx 4 cm (1.5 inc) with the antennae.
What species is this insect from and what is the insect called? Is it rare? What caused it to have such a large abdomen?

What species is this insect from and what is the insect called?

This is a Meloe proscarabaeus, most commonly known as a black oil beetle. Looking at the antenna of the insect in your provided image, it's clearly a female.
M. proscarabaeus

Males have a "kink" in their antennas, females don't.

What caused it to have such a large abdomen?

The primary reason/cause for the large abdomen is eating. Initially, the abdomen is much smaller, but after eating it will rapidly swell. Another cause for such an abdomen is pregnancy.

@Bert If one of the answers helped you, consider clicking the "accept" button next to it. :-)

Meloidae  is a family of insects belonging to the order Coleoptera. In the world, this family has about 2,500 species divided into 120 genera. Adults use flowers and feed on pollen.
Scientific name: Meloidae
The females of the meloes have their abdomens filled with so many eggs that this organ acquires a considerable size, but the male's is small.

Please be sure to ALWAYS provide evidence/citations for answers on this site, especially for species ID questions. I advise that you update this answer with some sources. You should preferably only refer to reputable sources given the amount of misidentification and misinformation floating around the internet. The point here is for other people to learn to teach themselves, and showing them the sources/process is really a good start. Thanks!


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Looking to study botany, some general advice
I've been doing some hydroponics lately and I've noticed I don't have much insight about how plants really work under the hood, I would like to have the full picture and understand more about it.
My primary interest is to apply botany knowledge on my hydroponics projects, not to get a job/degree. But, I do understand that studying among my peers is a rich experience, reason why I'm considering this kind of training instead of just grabbing a book.
However, I'm not sure how extensive is the study of botany, if I need a degree in X before starting it, etc.
Also a good book is welcome.
Thanks.

Soil science, pedology is good for hydroponics knowledge because you learn agriculture history and chemistry, biological and industrial, which sais which chemicals the plants need, what pH does to chemical availability, root physics, micro and macro nutrients... And aquaculture, i.e. keeping fish books teach you about nitrogen cycles, pH, algal and fungal and other blooms, oxygenaton, stagnation, volumes of filters and throughputs, aquarium botanics, I did a pedology course in Uni and i kept fish for a while, and I know a bit of chemistry, although broad based books on hydroponics are cool.

Have you checked out Botany classes at nearby community colleges?  You may have trouble finding an evening class, but I'm sure you'll find daytime classes opening up in the January.
If you need to study independently, can I suggest checking out the Tree Care Industry Association's store. www.tcia.org  They have various learning material to read and watch, leading towards a professional arborist certification.
Good luck in your endeavor.


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Are any arthropods poisonous to the touch?
I'm particularly interested in whether any insects are poisonous to the touch.  Note that toxic-bristled caterpillars are actually venomous, since in all species I'm familiar with, the bristles puncture the skin.  If there are any arthropods poisonous to the touch, I'm also curious as to what the most dangerous one is, but that may be beyond the bounds of this site.

The blister beetle genus Meloe, also known as oil beetles, secrete an oily substance containing a poison called cantharadin which causes blistering and swelling of the skin.

Source: http://statebystategardening.com/state.php/articles/do_not_touch_these_backyard_bugs

I agree with Kurt, but there is a great deal of variance in the concentration of cantharadin among blister beetle species. Some millipedes (Myriopoda: Diplopoda) also ooze toxic secretions from glands along their sides. http://www.sciencedirect.com/science/article/pii/S0305197815001167


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Simulating Migration in SimBit Software Program
How is migration incorporated into the SimBit program of Remi Matthey-Doret and Michael Whitlock?
Is an island model or stepping stone model assumed?

In SimBit, no specific model is assumed as the user can very much chose for himself/herself what migration scenario to be simulated. The migration scenario can be set with the option --m (or equivalently with --DispMat).
There are four ways (what is called "Mode" in the manual) to indicate migration.
 A, LSS, OnePatch, Island and LinearNormal.

A

This mode stands for "All". This mode allows the user to enter a matrix with the migration rate between any two patches. Any migration scenario including the ones achieved with the below modes can be achieved with A. The interest of the other modes is to simplify the user's life esp. when dealing with many patches. I rather recommend using the other modes when these apply.

LSS

This mode stands for "Linear Stepping Stones". It allows the user to set linear stepping stones with any number of stones and potential asymmetry.

OnePatch

This is the default. It means no migration scenario apply as there is only one patch (or one deme if you prefer)

Island

This is a classical island model. The user must input the probability of not migrating.

LinearNormal

This is just like a linear stepping stone model except that the dispersal kernel follows a normal distribution.

Note also that the migration scenario (as well as the number of patches) is a time specific argument and therefore it can vary through time at will. You can have a look at the manual for more information.
Note that I have been working quite a lot on new versions that I have not put online yet, mainly because I was too lazy to rewrite the manual! The last version online is 3.69 but I am currently working on version 3.139! I will upload a more recent version in the coming week(s). Most notable improvement with the new version include:

Easier user interface; no need for all these quotation marks. Migration scenario will be given by the user as forward migration while it currently is backward migration which is a little less intuitive for the user.
More freedom on demography.
Possibility to simulate several species interaction with ecological relationships. One can simulate a whole ecosystem!

Thanks Remi for such a detailed response! Is there any justification for a user to have to input the probability of not migrating in the island model?

Would you prefer inputting the probability of migrating? It was just to avoid the possibility where the sum of the probability to migrate over all patches is greater than 1 (which would have thrown an error message). It felt more intuitive to me to go this way but it might not be for others. It was also quite intuitive to me to input backward migration rate but I already got a few people telling me forward migration rates are more intuitve so, I've changed it in more recent (not online yet) versions.

I'm actually interested in how SimBit accounts for migration "under the hood". While there are many simulation tools already existing, I find that for my particular question, a new tool is needed.

At every generation, SimBit loops through each patch, ask how many individuals this patch will contain (this number can be affected by a fair number of different options) and then for each offspring look for where the father come from and where the mother come from. Select the mother and the father and then make them reproduce to get the offspring. I am not sure that really answered your question. If you have more specific questions about how SimBit works under the hood, I'll be happy to answer.

Note that it is not so unusual to not have a simulation platform that does exactly everything we want for a particular project. But many of the things you might want to implement might be done quickly by the author and they / I may accept to help. If it is a big change, then the author of the simulation platform may expect authorship on the paper resulting from the project. Note that for the moment, you have not specifically indicated anything that either SimBit, Nemo or Slim could not do.


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Are natural daylight lamps for Seasonal Affective Disorder just about the color temperature?
I've seen many expensive lamps made for people who have Seasonal Affective Disorder (SAD) and/or who live in regions where there isn't much daylight during the winter. I'm wondering if the benefit of these lamps is simply the color temperature (typically advertised at 6000K or more), or if there are other aspects of these lights that are meant to be theraputic? Some of these lights are also advertised as "ion therapy lamps".


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Trick fruit trees into flowering later in the spring
There is a common problem with fruit trees in temperate climates where the trees flower before the last frost. Generally speaking, if the tree has flowered, and the temperature drops below freezing, the flowers die and do not produce fruit.
This is certainly not a new problem. It's my understanding that the problem affects almost the entire fruit farming industry in temperate climates.
I've heard that fruit farmers have large-scale commercial techniques that they use to mitigate the issue, such as:

Covering
Fog or smoke
Wind Machines
Sprinkling
Heating

While these methods might be practical for commercial farmers, not all of them are practical for small-scale urban farmers like me.
Instead of actively protecting the open flowers, would it be possible to trick fruit trees into not flowering as early?
I'm dealing specifically with plants in the prunus genus:
Examples:

Prunus tomentosa
Prunus besseyi x prunus salicina hybrids
Prunus avium x prunus salicina hybrids

Note: I have a related question here: What triggers plants in the prunus genus to flower?

Unfortunately, your assumption ("I'm making an assumption that trees don't flower when the ground is frozen") is incorrect, which makes both the question and the current answer a little bit meaningless. Plants don't rely on temperature (ground or air) to set the time to flower. They measure the length of the night, which varies according to the seasons. Also, it's worth mentioning (unfortunately, again) that on SE sites you cannot receive your bounty back. As this question has no answer (because it's based on a wrong assumption), you lost your points for nothing.

@GerardoFurtado : So, does this mean that a plant would flower on the exact same day, every single year? No other factors influence bloom time?

Not the same day, but very close. Other factors do have influence, I'm just saying that the main factor is the photoperiod, not temperature.

@GerardoFurtad: no, temperature on root is the main factor on common fruit plants (e.g. in many Rosaceae, where flowers appears before leaves). E.g. Prunus armeniaca (apricot) should be planted on colder places, to make them flower later (such plants hate cold weather during flowering). I live in a mountaneous region, and I can tell you that leaves (or flowers) on wild tree are phased out according altitude (same latitude, so same light period). Just few perennial plants in botanical gardens use the light period.

Ok then, if you say that temperature is the main factor then temperature is the main factor, forget all I said.

@GiacomoCatenazzi I have a related question here: What triggers plants in the prunus genus to flower?

@Wilson Good. That's a specific question, better than this one to discuss that subject, so you can get proper answers explaining photoperiodism and the effect of vernalization on the floral evocation.

The Principles of Fruit-Growing By Liberty Bailey 1898 (from page 92):

Thanks for this answer.  Definitely contradicts my answer.  More research needed.

You are on the right track, but snow is the wrong way.  When the snow is around it insulates the ground.  Soil surface temps stabilize at close to freezing.
Instead, do the reverse.  Remove, or firmly pack the snow.  Do so about 1.5 times the dripline radius.  (If the dripline is 10 feet from the trunk, pack out to 15.)
This allows the ground to freeze deeper.  However see other answers.  I'm not nearly as confident about this now.
Now once melt starts in earnest, cover the ground with a couple of layers of the insulated tarps used by contractors to pour concrete in freezing conditions.  This will keep the ground cold, both by reflection (most tarps of white) and by insulation, and by wind reduction.  This should slowdown bud break by at least a week, and more likely two weeks.

For a single tree, you may be able to do protection with an oscillating sprinkler (for a big tree) or a impact rotary.  Key thing with these is to start them before the temperature gets down to freezing.  The initial few minutes while it's working with dry air you can get supercooled droplets that kill your buds instantly.   Start the sprinkler when the temps are about +6

A third way that may help is to graft onto a different root stock.  The russians work with pear on cotoneaster.  This dwarfs the pear strongly, but also forces it into dormancy earlier.  I haven't read what it does to bud break, but given that pears also tend to be early bloomers, it must help.  These interspecies grafts are working in Siberia in zone 2.
Look at using prunus that tend to go into dormancy early in the fall.

Another way to experiment with would be to keep them a bit thirsty in the fall.  If the roots are slightly dehydrated, then the first moisture they get in spring will be used to rehydrate.  This may delay bud break by a day or two.

Some trees do their budding on reserves in the bud and twig itself.  I see this some years when a winter has killed roots.  The leaves break bud, inflate about to about 1/4 size, then wither.  For these guys it's a matter of enough degree days or the day length on the bud itself.
If it's degree days, you may be able to stretch things out by making the tree lighter coloured.  Many people spray dormant oil in late winter anyway.  By adding some cheap latex paint to the dormant oil mix, you lighten the colour of the twig, and so reduce sun warming.

I have a related question here: What triggers plants in the prunus genus to flower?


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Can C. elegans be raised on Lactobacillus as the only food source?
I'm interested in running some C. elegans experiments for educational purposes, but would like to avoid having to grow or handle E. coli.  I was wondering if C. elegans need E. coli specifically, or if they would grow well on most (non-pathogenic) kinds of bacteria.
In particular, I'm curious about whether C. elegans would grow on (either live or pasteurized) yoghurt, including strains such as Lactobacillus acidophilus and L. delbrueckii.
I did a quick literature search and found a few articles (like this) which talk about screening probiotics in C. elegans by adding them as part of their diet, but I haven't been able to find any reference to using them as the only food source.


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How can individual strands of coat hair have only a single color when considering codominance?
I understand how codominance works. We have two (or more) alleles for one gene, neither having dominance over the other. They are both expressed independently, which means that different phenotypes are visible simultaneously. However, I'm not sure how it really works when we take, say, coat color. If both alleles are active, assuming each one produces a different pigment for each color, that means there are both pigments in a cell. What I see explained is that, if you look closely, each hair has a different color, and when you see it from far away, it gives the impression that the coat is made of one single color. But how can one hair have the same color all throughout? How can the different pigments be aggregated like this? As in, how is it that they do aggregate like this?

Why do some cells produce hair, and others fingernails, or insulin?  FTM, why do some animals have spots or stripes?

This paper may help get you started, how spots and stripes form . https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380182/, how simple rules/interactions can create complex patterns is quite interesting.

@jamesqf, why does a strand of hair have one color only if every one of the cells it's made of produces both pigments? That's what I mean. I was looking for something in broad terms, but it seems to be impossible to generalize.

The point I was trying to make is that (AFAIK - I'm not a biologist) each cell does not produce both pigments.  Indeed, hairs are not produced by single cells, but by rather complex organs called follicles.  At some point in their development, they've differentiated to produce different colors and types of hair.  So you get coat patterns in animals, differences between head & body hair in humans, &c.

Right! That's closer to what I was looking for. So there's a kind of centralization and differentiation at work here. I'm only in 12th grade and was curious about the details of how this works. The book we use doesn't go into any length about this, and I'm pretty sure asking my teacher would be pointless.

@ixjf: I'd start by just doing a Google search on "hair follicle development" - that's what I did, to reinforce what I thought I remembered from past reading.

The terms dominance/recessivity, additivity, co-dominance, incomplete dominance, etc... express a relationship between genotypes and phenotypes but the mechanism behind this relationship is not being defined by these terms.
There might be a large number of mechanisms associating genotypes at a given locus with phenotypes. There is, in general, no reason to expect a mechanism of relationship of dominance at a given locus to be similar to that at another locus. In other words, there is no general mechanism leading to dominance/recessivity, additivity, co-dominance, incomplete dominance, etc...
On top of that, the actual mechanism in specific cases leading to particular genotypes - phenotype association are often unknown and I don't think we have good knowledge about what mechanisms could be more common or even how to categorize such mechanisms.
You might want to have a look at the posts

Why are some genes dominant over others? What is the mechanism behind it?
Evolution of dominance

or some papers such as

Llaurens et al. (2009)

In general, it appears suggested that one needs to know the specifics of the biological pathway to be able to predict dominance relationships and gene interaction network (see Llaurens et al. (2009)).

I do realize there isn't a general mechanism for this. That's why I asked the question specifically for coat hair (need not even be generalized, just a light), hoping that would narrow it down. The question still intrigues me. I was hoping something that I would think is a given would have been understood by now!

You will need to be even more specific than coat color. For example, in female cats, X inactivation (dosage compensation) has an important role in determining coat colour. In human, 378 markers affecting skin color have been identified! You might want to narrow the question to a very specific study system.

I would recommend cherry picking your system of interest so that you have best chance that an answer exists. Consider the Mc1r gene in mice (Hoekstra et al. 2006) for example. Also, as the current post has already received an answer, I would recommend asking this new (narrowed down) question on a new post.

The gene isn't specified here, but the general idea expressed is variegation.  There are individual hairs (it could be larger regions) that are controlled by one of the two genes, but there is some randomization of which one.
An easy system to picture this in would be the X chromosome.  One X chromosome is inactivated in the female, and the other is not.  If the gene is on the X chromosome, each allele controls specific hairs.
Position effect variegation is well known to affect coat color.  If one allele is dominant but silenced randomly in some cells, an effect akin to codominance could be seen, though it seems dubious to say it really is codominance.

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


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Breeding mosquitoes at lower temperature
It is well known fact that, to slow down the growth of drosophila, they are grown at 18-19 degree Celsius. It helps in maintaining stocks for longer time without frequent change of food. Is it applicable to mosquitoes? especially Aedes aegypti?  can we slow down its growth by growing them at lower temperature?

I think there are 2 questions : temp for breeding and, temp for growing larva. I see larva dormant at about 45 F, then at 60+ F they are active.  again.

@blacksmith37 Possibly even three, as written - temp for maintaining larvae, and temp for maintaining adults. I'd suggest editing out "breeding" from the title, unless you really want to know about this, but I think effects on larvae and adults can be answered as two parts of the same question.

Check "breeding temperature" and similar obscure phrases for the search.
There's a study on physical aspect of mosquitos bred in cold, they perhaps didn't note any significant metabolism change, you can read the articles, they mostly cover wing length scales and follicles.
There's a study on lave development speed which passes over breeding temps, it may however cover "egg temperature".

Maybe:  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3992806/ is a NIH paper that gives a quick overview on maintaining an A. aegypti colony.  From the description they are somewhat fussy, but some of the lines imply temperature sensitivity at least at certain stages.
try google 'protocol for maintaining mosquito colony'

Dear Sherwood, I hope u did not understand my question properly. I know the standard protocol for rearing mosquitoes. My question is whether rearing them will slow down their metabolism and thereby their growth? if so will rearing at lower temperature harm them in any way other than their growth? (like their survival, lifespan, mating behavior,egg laying behavior etc.,)

Also just wanted to comment that Aedes aegypti is widely accepted to be the least fussy mosquito species to care for. We have far more trouble with Culex and Anopheles than any of our Aedes.


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Chromonema and Chromonemata
A chromonemata is composed of two chromonema. Which are again composed of chromatin fibre. Thus my question is chromonemata is composed of how many chromatin fibre ?

It's the opposite: singular -> chromonema, plural -> chromonemata.

To my understanding, a chromonema is the filament of DNA constituting a chromosome during interphase; its equivalent during DNA replication is chromatid. The plural of chromonema is chromonemata.
The chromatin is the form in which DNA is found within the nucleus of a eukaryotic cell, that is in complex with proteins such as histones.


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law of laplace and pressure developed in arteries
in arterioles the pressure depends on
the impedance of the vessel(elasticity and youngs modulus)
cardiac output
pre arteriolar resistance
what i want to ask is will the pressure also depend on law of laplace
for eg.
if a there is peripheral vasodilation( the muscles of the artery wall are relaxed) so the tension is less
the radius is high
and hence using the equation( pressure=2*tension/r)
the pressure in the arteriole is low
is this arguememt valid??


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Live birth versus eggs
Would it be right to say that animals or birds that have ears visible outside, including say holes in the head, give birth, and those that have ears concealed inside the head, lay eggs? The point is not to go to minute biological terminology, and if we can resist that urge of vengeance, would the above be an OK statement?
Thank you

Welcome to Biology.SE. I am afraid the terminology might matter more than you'd hope. Maybe you could give specific examples that pushed you to think that such correlation would exist. I don't know much about hearing (and I am not a very good naturalist) but when I think of lizards and birds, I think of many species that 1) lay eggs and 2) have holes in the head for hearing.

You might want to read a little bit about phylogenetic signal to avoid the misinterpretation of such correlation as being the result of selection. You might typically want to have a look at the post Why don't mammals have more than 4 limbs?.

Thank you  nothing pushed me  simply, please tell me  three species that have holes in the head for hearing which are visible from outside, and also lay eggs?

You said "holes in the head", not "visible from the outside" in your question. By saying "visible from the outside", I don't really know how visible they need to be but these details probably won't matter much. Consider any owls (pics) or many lizards such as for example this alligator lizard.

you might want to accept LinuxBlanker answer just so that the question is marked as answer.

No.
Animals without noticeable outer ear that give birth: cetaceans (dolphins, whales and such), lots of pinnipeds (sea lions, seals and such).
Animals with noticeable outer ear that lay eggs (as suggested in @Remi.b's comment): owls, lizards.

No
Vivipary and ovovivipary have evolved multiple times in multiple lineages, laying eggs is the ancestral/basal condition for tetrapods but it has been lost multiple times.


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How to make GABA pass the blood brain barrier?
I thought of methylating GABA at the gamma amino group in order to make it pass the blood brain barrier, but would it work?
The goal is to make a sedative. Like GHB or benzodiazepines (I know that benzos have a totally different structure)
Any ideas on how to make GABA  pass the blood brain barrier?

Short answer
Chemical reversible shielding of the aminogroup in GABA seems to be sufficient to get it into the brain as a Trojan horse.
Background
Given that you ask

...how to make GABA pass the blood brain barrier?

I assume that

You wish to elevate GABA by exogenously administering a compound;
That compound has to cross the blood-brain barrier (BBB) and physically turn into GABA;
A drug indirectly elevating GABA through unknown (e.g., GHB) or known mechanisms (Gabapentin) does not suffice your needs.
If you are happy with indirect actions, the links above will help you out. Now on to the real stuff :-)

GABA (Fig. 1) has 3 hydrophylic groups that may prevent it to cross the blood-brain barrier (BBB), namely a hydroxyl-, a keto- and an amine-group. The BBB generally only permits passive entry of small hydrophobic molecules. The amino-group in turn is also prone to de-amination by mono-amino oxidase inhibitors.
An often-used method to get drugs into the brain is shielding of pesky hydrophilic and/or fragile chemical groups by certain molecules that are irreversibly bound to them. A well-known example of shielding a fragile amino-group is the B-methylation of phenetylamine compounds into their amphetamine analogues. Alpha-amination to a methamphetamine further stabilizes the essential amino-group. Amphetamines and methamphetamines are way more stable in the brain than their phenetylamine precursors and likely enter the BBB also more swiftly because they are more hydrophobic by shielding the amino group (Shulgin, 1990).
However, those methyl groups are irreversibly bound, so it's not an option here, as apparently you wish to increase GABA, and not an active derivative of it.
Now, another way is using a Trojan horse method (Pardridge, 2006); by reversibly shielding the essential amine group the drug can enter the brain, where it is converted back to its original compound. Picamilon does the job here. Smarter Nootropics say;

First developed in the early 1970s in the Soviet Union, picamilon (alongside phenibut) is an “enhanced” form of GABA that is capable of crossing the blood brain barrier when taken as a supplement.Inside the brain, picamilon is rapidly hydrolyzed into its constituent parts; niacin and GABA. Niacin helps to enhance brain blood flow through its vasodilatory properties [].

Fig. 1. GABA and Picamilon. source: Smarter Nootropics
Reference
- Pardridge, Discov Med (2006); 6(34):139-43
- Shulgin, PIHKAL, Transform Press, U.S. (1990)

By the way, if I methylated GABA just before the amine group (like phenethylamine to amphetamine), would it be a GABA receptor agonist or at least a PAM? (positive allosteric modulator)

@ostal123 I guess yes, but it's an interesting question for sure!


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Organism and plants reduce radioactivity?
I would like to ask if there are organisms or plants that could help in reducing any one of types radioactive contamination?

What do you mean by "reducing"?

Your magic search word is 'phyto-remediation'
There a bunch of plants used for this.
None of them remove radioactive material as such.  With the possible exception of deuterium, the chemistry of isotopes aren't distinguishable by biological organisms.
So to remove strontium 90, you need something that picks up strontium.  It will pick up both the radioactive and non-radioactive forms.
In some cases the metal will combine forming compounds.  This may make the radio-isotope inaccessible to a given plant.  If, for example, strontium was in the form of SrO and SrSO4 you might need two different plants, or add a reagent to the soil to convert it to an accessible form.
Once the plant tissue has picked up the radio isotope, the usual process is to drive off the plant tissue by burning or destructive distillation, then processing the material to either make it insoluble for disposal, or convert it for use.  For material with a fairly short half life and low solubility, it may be sufficient just to bury it.

I recall reading that sunflowers were planted after the Chernobyl nuclear disaster, and I just now read that fields of sunflowers were also used in and around Fukushima.
Apparently sunflowers have an affinity to absorbing toxic heavy metals from the soil.  The radioactive isotopes are stored in their stems and leaves. The plants have to be cut down and disposed of as radioactive waste.  However, that cost is considerably less than digging up and disposal of topsoil.
Doing a brief google search, I learned other plants such as certain mustard plant species and other herbs can be used for lead and mercury environmental damage.  To learn more, I encourage you to spend a little time using your favorite search engine.  Undoubtedly you'll learn more than what little I have shared now.


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Can skin acclimatize to a the humidity level?
When the outdoor temperature is low, the absolute humidity is low because cold air holds less water. When the heat is turned up indoors the relative humidity decreases and during days with cold weather it can fall below 10%. This can lead to cracked skin or lips because, I assume, dry air draws more water from the skin. So my question is, can skin acclimatize? Around here in New York, some people get cracked knuckles every winter or use moisturizer to prevent them (I use nasal saline for nosebleed prevention). If those people lived in dry climates would they have this all year around? Or does the skin (and nose) eventually acclimatize?
If I install a large humidifier in my home could that actually have adverse effects by preventing me from acclimatizing (that is, making my nose less naturally lubricated), thereby possibly causing problems when I enter other houses or buildings?

Some lifestyle things cause symptoms like high blood pressure, and thin or inflexible capillaries. for oily skin, My scalp sebaceous glands produce more or less oil depending on how often my skin is devitalized. If i shampoo every day, my scalp skin eventually makes at least 7-8 times more protective oil after one month. probably the same for the rest of the body. I didn't know you can use saline for nose. dunno if the sinuses have a lot of sebaceous glands and I don't figure you can snort almond oil. Cracked skin is protected by daily moisturizer. I had that in India doing manual laundry

@com.prehensible According to this article, the claim that scalps  produce more or less oil based on how often you shower isn't true: http://www.oprah.com/style/biggest-hair-myths-do-frequent-trims-make-hair-grow-faster/all

That's not a study, that's a self styled doctor's opinion. Doctors always disagree until they have measured the study. I'd believe that if I had an explanation of why my hair goes greasy faster when I shampoo more often... If I use soap my scalp very seldom, it becomes annoyingly oily after about 7 days. I can do that for a year. If I shampoo every day to stop it becoming greasy, my hair becomes annoyingly greasy faster and faster and eventually after about 20 hours it becomes oily versus 7 days. I've observed the effect first hand so I'd have trouble agreeing with someone who has 2nd hand.


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Is there any antibody-forming immune system without immunological memory?
Is it possible for an immune system to exist that makes antibodies but does not possess any kind of immunological memory? If so, what examples are there?

have you tried googling this?

@aaaaaa yes, but I couldn't find the answer of my question.

Disagree with the close votes. This may not be a particularly sophisticated question but it's certainly within the scope of biology.

There is no system that makes antibodies but that doesn't have memory.
The title of this question is was originally very different from the body. The title asks if there's "any immune system without immunological memory", while the body asks if there's "any immune system that makes antibodies but has not immunological memory". That suggests you may think that antibodies are an essential part of an immune system, or that immune systems comprise only antibodies. Neither is true. The vast majority of animals have immune systems that do not have antibodies and that do not have immunological memory; for example, arthropods, the various kinds of worms, etc.
Immunological memory is a relatively recent addition to the immune system, having arisen approximately 400 million years ago, in the lineage that originated with shark-like fish.  The species that evolved from sharks -- fish, amphibians, reptiles, birds, mammals -- all have immunological memory, and all have antibodies. Those species that didn't arise from that lineage do not have antibodies, and with two exceptions do not have immunological memory.

The origins of vertebrate adaptive immunity

The exceptions are lampreys and hagfish, which have a common ancestor with sharks but which ended up forming an immune system that is related to, but often quite different from, that of sharks (and us). Lampreys and hagfish have molecules that are not antibodies but that function in a similar way, including having a form of immunological memory, though it's quite different from ours. So if you're looking for an example of something that kind of has antibodies but that kind of doesn't have immunological memory, that's as close as you're going to get.

Lamprey Immunity Poised to Evolve
Harnessing 450 Million Years of Evolution: Lamprey Antibodies for Modern Biomarker Technology

Note that virtually all species, including mammals, have branches of the immune system that don't have immunological memory. Those branches don't have antibodies, though.

Innate Immunity
The innate and adaptive immune systems

I’m not sure I agree with your characterisation of immunological memory as recent. I couldn’t find its evolutionary age with a cursory search but for all I know CRISPR (an immunological memory) could well be ancient. Similar for other cell-based immune mechanisms that rely on integration of foreign genetic material.

I don't really accept that CRISPR is "immunological memory" other than in semantics.

Huh. How is it not?

Any argument that it is relies on semantics and definitions. I don't find that an interesting game to play. Bacteria may have "immunity", but they don't have "immune systems". I'm not saying you can't call it "immunological memory" if you want, I'm just saying that I don't call it that and I don't find attempts to shoehorn it into the same category to be at all interesting.

I’m not playing semantics games. But we do seem to have different definitions. There are different kinds of immune systems, and I wasn’t aware that there was a consensus(?) that bacteria’s immunity wouldn’t count as an immune system. In fact, I know researchers (apart from me) that would call it an immune system (and it’s trivial to find publications supporting this). So what about RNAi then? Is that also not an immune system? Because, once again, I know that others call it an immune system. I don’t think your definition has special status.

I’m not playing semantics games. But we do seem to have different definitions. That's what semantics means. Really, I don't want to make a big deal of this. What I'm saying is that bacterial "immunity" is so utterly different from animal immunity that there's virtually no biological insights to be gained from grouping them together. The dictionary certainly lets you do that, but there's no biological utility to it. It's like asking if a virus is alive. It tells you about the word "alive" but nothing about viruses. It's not (biologically) interesting.

Well “games” suggests that I’m baiting you but I’m not — rather, I simply don’t understand you. Your last comment clarified that somewhat although now I could complain about eukaryotic chauvinism (but I shan’t!).

thank you for your very specific answer. actually I already knew the broad-brush concept of the innate,acquired immunity, I'm sorry for confusing you. it's very interesting that there are such unusual  type of immune system(Lampreys,Hagfish) that you mentioned.

actually I was just wondering and thinking what if there wasn't immunological memory, then how would the immune system evolve, would it just increase its diversity of antibodies or would it decrease its delay time to activate and prepare acquired immunity system, are they two trade-off relationship etc... so these are the reason why I asked the question. anyway, thank you!

@Mr.Konrad Rudolph Thank you for proofread My informal and silly english grammar!

There seems to be some evidence of immunological memory in insects. See this article, for example.

I wrote about that article, and others, on my blog in 2007: Invertebrate memory, or wishful thinking?; also here, here, and here. TL;DR, very unlikely to be real immunological memory.


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Could we detect GMO foods if there were no samples to compare with?
In my understanding, there’s nothing “special” in how a GMO product is composed inside compared to a “natural” product. I mean, still, same principles apply to both: some DNA that controls protein building, and so on.
Now, having read about all existing methods of GMO detection, I still can’t understand how it works: e.g., given two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?
Once you change someone’s DNA, does it contain any signs that it was changed? Or do we need a database of “natural” products’ DNA to compare with in order to be able to detect DNA ones? Or do we need a database of GMO products to compare with?

It seems like you'd have to have some way to distinguish between organisms genetically modified by human action and those genetically modified through natural processes. Plausible, maybe, but not trivial.

This isn't an answer, but there is off-the-wall practical solution:  Grow both foods, and if one of them is bigger, juicer, or (insert other economical improvement here), then that's the GMO one.

@NathanMerrill Is it? How do you know there aren't naturally occurring (if rare) instances of the traits?

@jpmc26 Fair enough: I am assuming that the GMO DNA was mutated from the other one you are given.

@jpmc26 - You're right, that's not a valid test. First, either one could have a gene replaced by either mutation, natural replacement, or human replacement, and second, there's no assurance that the replaced gene makes the plant better in the particular way you're looking at. It might mutate to be less good, or it might mutate to have better disease resistance at the sacrifice of quality root structure.

Check the DNA for a copyright statement.

If two people are floating in outer space, and can only see each other and nothing else...

[G]iven two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?

No, you can't distinguish them without knowing a priori the DNA sequence of the wildtype and of the GMO. There is no other mark left within a GMO in the general sense.
Of course, one particular GMO is created with one particular goal in mind. One particular phenotypic effect. If you detect the phenotype of a GMO, then you can recognize it. For example, if you make a GMO tomato that produces a new type of pigment, you can, of course, recognize it by the presence of this pigment! However, there is no general attribute of being GMO that you can recognize. You need to look for something specific that you know about a specific GMO (or specific wildtype).
There are also phenotypic traits that you find (quasi) exclusively in GMO such as Cytoplasmic Male Sterility (CMS) for example. If you find CMS in a plant, then you can be pretty sure it is a GMO. But if you can't find CMS though, you can't be sure it is not a GMO.

given two potatoes, one GMO and one natural, would you be able to detect which is which without having any samples or knowledge about what parts of DNA to consider engineered by humans?

Possibly, assuming they're the same variety, you might get lucky by simply diffing the sequence data. This also assumes the natural variety doesn't change significantly between generations, such that even if the chromosomes have crossed-over (homologous recombination) you could still do pattern matching to realize correlation. Genes/sequences with no correlation at all would then be suspect as novel/introduced.

No.  Furthermore, the line "once you change someone's DNA" contains a wealth of misconceptions.
Once you have your potato/tomato/whatever, the DNA does not change during the life of that individual specimen.  The genetic modifications change the seed before the individual specimen grows, and do not change the individual specimen during its life.
As far as genetic modifications go anyway, each seed inherently has different DNA from its parents.  "Normal" breeding has given us a diversity of plants and animals which are so massively different from the originals as to be virtually unrecognisable as the same species in many cases.  (If you didn't know better, would you think a dachshund and a husky were the same species?)  And whilst we might think of it as "normal" today, when the techniques around selective breeding were first developed, they in turn were seen as highly unnatural, particularly the practise of breeding an individual with a parent or sibling.
This still relies on normal rates of DNA mutation within the same species.  More interestingly though, DNA can also be picked up from other sources.  This is identical to how scientists insert or replace genetic material for GMO - indeed, GM techniques to carry this out were founded on understanding how this takes place in nature.
This is where objection to GMO falls down.  Sure, the result may or may not be healthy.  However you are already using/eating/breathing pollen from individual specimens which have carried out gene transfers with other species.  The difference between the natural version and what happens in the lab is only the same as the difference between natural breeding and selective breeding - it's simply that someone is deliberately choosing which attributes to pass on to the next generation, using tools which already exist within the organism's DNA.

It would depend on whether you knew the markers they used to identify the transformed organisms.
When I (briefly) did Genetic Engineering back in the mid eighties we would add antibiotic resistance genes as well as the gene we wanted to insert.  The combination would then be incubated with the vector (e.g. bacteria) and the transformed bacteria could be filtered out by growing them on antibiotic laced plates.  Then you'd grow up a transformed bacteria and insert it into the target organism.
So, the presence of bacterial antibiotic resistance genes in your hypothetical potato could be an indication but not a guarantee of human modification.

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


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What is the replacement period of gastrolithes in doves?
Gastrolithes are common in doves and pigeons. Do they keep ingested stones for ever? If not, how often are they to be replaced?


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Value of r (intrinsic rate of natural increase)
What is the current value of 'r' (instrinsic rate of natural increase) in India? How do we calculate it?
My book says that In 1981, the r value for human population in India was 0.0205. But this link (https://www.google.co.in/amp/knoema.com/atlas/India/topics/Demographics/Population/Rate-of-natural-increase%3fmode=amp) says it was around 22.50 in the year 1981. Such big discrepancies are a query.

Perhaps you should check the census report. You should add details to your question and be clear about what you are asking. [Edit] the question to add all necessary details. Comments should be used for asking clarification.

About the value of 22.5 (in your question); that is referring to a growth of 22.5 persons per one thousand population. So a growth of 2,3% (22.5/1000= 0.0225).

From the UN database (this info is also reported on wikipedia), the growth rate in India in 2016 was $r=1.019$.
It is computed as $r = \frac{N_{2017}}{N_{2016}}$, where $N_{y}$ is the population size at year $y$. This estimate is based on the total number of residents (regardless of their legal status).
More explanations
$r$ is simply defined as $r = \frac{N_{2017}}{N_{2016}}$. Often, you will read statistics in the sense of percentage of increase. Let's call this value $x$. $x$ is then defined as $1+x = r$.
It is just like when you put money in a bank account. If your interest rate is $x = 2\% = 0.02$, then if you had $N_{2010} = 1000$ dollars in 2010, in 2011, you'll have $$N_{2011} = 1000 + 1000 * 0.02 = (1+0.02) * 1000$$. Note that $1+0.02 = 1 + x = r$. Over $k$ years, you'll have $$N_{2010+k} = N_{2010} (1+0.02)^k$$.

My book says that r is calculated as birth rate minus death rate, and calculating it through the values mentioned on the internet, it shows big discrepancies!

https://en.m.wikipedia.org/wiki/Demographics_of_India Considering Wikipedia, the birth rate minus death rates comes out to be 11.

Per 1000 individuals, yes. Divide 11 by 1000 and you get $0.011$, which means $N_{2016} = N_{2017} + N_{2017} * 0.011$, which can be rewritten $N_{2016} = (1 + 0.011) \cdot  N_{2017}$, hence $r = 1.011$, which is pretty close to $r=1.019$. Does it make sense to you?

Do we always take the original population size as 1 for a year, while calculating this rate?

I don't really understand this follow-up question. But please see edit.

You calculation is of lambda ($\lambda$), not $r$ (instrinsic rate of increase), where $r$ is $ln(\lambda)$.

NCERT shows per capita value is divided by 1000, not hundred (%). So the data you see is 22.50 per thousand! So, the per capita rate is 22.50/1000 = 0.02250 that is almost equal to 0.0205 given in book!
To make you understand better, remember that GDP and per capita GDP is different, the same way birth rate or death rate is calculated per 1000 but when we ask per capita we have to actually divide it by 1000.
Now in 2016 , it is 0.01019 i.e. 0.0102
I hope you understand!!

It the most basic form, the intrinsic rate of increase, $r$, is defined as:
$\frac{dN}{dt} = rN = (a-b)N$
where $a$ is the birth rate per unit time and $b$ is the death rate per unit time. So $r$ is the birth rate minus the death rate. The modell can naturally also be extended to e.g. include carrying capacity or to make $r$ (or underlying parameters) functions of time or environmental variables.
However, from census data (taken at fixed points in time), you can calculate lambda ($\lambda$), the discrete-time per capita growth rate (also called the finite rate of increase), as:
$\frac{N_{t+1}}{N_t} = \lambda$
This shows the growth across a fixed, discrete time intervall. $\lambda$ can  be converted to an instantaneous instrinsic rate of increase as $r = log(\lambda)$. Using the values in Remi.b's answer (from https://esa.un.org/unpd/wpp/DVD/), this yields and $r$ of 0.0188 (i.e. log(1.019)). For a bit more background see https://en.wikipedia.org/wiki/Population_dynamics and http://www.zo.utexas.edu/courses/thoc/PopGrowth.html (or any textbook on population dynamics).

Population growth curved à when responses are not limitting the growth , plot is exponential , b when response are limitting the growth , plot is logistic , k carrying capacity

Please provide additional details in your answer. As it's currently written, it's hard to understand your solution.

this doesn't answer the OP's questions, which is specifically about the value of r for a particular population (humans in India)

Welcome to Biology.SE. If you can address the problems noted in the above comments, please also provide a citation/source for the image you are using — images should be credited to their creators just like quotes are to their authors. This is generally considered good practice in scientific communication and will help other users by providing context. ——— If you are unwilling or unable to fix these issues, please delete your post. Please take the [tour] and then consult the [help] pages for more advice on [Answer] effectively on this site.


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What does 'per capita births and deaths' mean?
My book says,

If in a pond there are 20 lotus plants last year and through reproduction 8 new plants are added, taking the current population to 28, we calculate the birth rate as 8/20 = 0.4 offspring per lotus per year.

..

If 4 individuals in a laboratory population of 40 fruitflies died during a specified time interval, say a week, the death rate in the population during that period is 4/40 = 0.1 individuals per fruitfly per week.

What does per lotus per year, and, per fruitfly per week imply?

Please rewrite the quote. Images are not searcheable and can pose problems to visually impaired people

0.4 offspring per lotus per year means that each lotus produces on average 0.4 offspring every year.

@Remi.b All should be good now. :)

Thanks! +1 You might want to comment on my answer if something is still unclear to you.

I'm not the OP. =P

1 per 1000 capita is 0.001 per capita.

I will use an ever so slightly more specific scenario than what your book offers.

At the beginning of 2017, there were twenty lotus plants in a pond. By the first day of 2018, eight of those twenty lotus plants reproduced. Using this information, we now want to describe the birth rate of lotus plant population.
To do this, we need the number of plants that produced offspring, and, the population size at the beginning of 2017.
$$\frac{no. \ of \ parent \ lotus \ plants}{initial \ population \ size} = \frac{8}{20} = .4$$
This means that, when considering the twenty lotus plants that first existed at the beginning of 2017, each of those twenty plants contributed an average of 4/10s of a lotus plant offspring for that year.
To generalize this, we say, "a birth rate of .4 offspring per lotus plant per year."
The same method and persective can also be applied to the fruitflies, however, they're considering death rate.

Hey Thanks, this was comprehensible. Could you please explain the meaning of 'per capita' also please?

@ShreyaVarshney Per capita is just another way of saying Per lotus plant. :)

@Charles , the numerator should be the "number of offspring." Per capita birth rate is the average number of offspring at the next time step produced by mothers at a particular time. Your equation is the proportion of number mothers to total population at a particular time.


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Is it possible to lose weight doing brain exercise?
According to this article human brain consume a comparable amount of energy with skeletal muscle. So is it possible to do some brain exercise (calculate something in mind etc.) instead of physical exercise to lose weight?
More specific questions:

Is it theoretically possible?
Is there any real-life example?
What kind of brain activity require more energy?
Pros and cons (brain exercise vs. physical exercise)

There have been several studies that show that even physical exercise itself isn't that good at causing weight loss unless you work out at athlete levels; dietary intake is much more important. Health.SE would be a more appropriate place to address that, however. As far as the brain, most of the energy the brain uses goes to just maintaining brain activity, metabolism doesn't change much during waking hours. Having seizures might cause a bit more energy use but I wouldn't suggest that for health.

only way to use serious calories is by upping heart rate to 100 - 140.

No The amount of calories the brain consumes is basically the same whether it is doing anything or no. Best case only about 3% increase in calories consumed by the brain or about 50 calories per day, which is miniscule and most studies do not even show that much.
Additionally buring calories is only important for weight loss once consumption is controlled. It is too easy to out eat any amount of exercise.
https://www.scientificamerican.com/article/thinking-hard-calories/


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Why is Sleep apnea only risk to males?
I was reading this article. In Risk Factors, it clearly mention "Being a male".
Why is Sleep apnea only risk to males?

you may want to learn what a risk factor means, it does not mean it is only a risk to males.

http://www.sleepreviewmag.com/2004/03/gender-differences-and-sleep-apnea/

Wikipedia actually means that being male is a risk factor for sleep apnea, which is a jargony way of saying that males have been observed to develop sleep apnea more often than females.
The article pointed out by com.prehensible suggests that this difference in the prevalence of sleep apnea between genders is due (in part) to a difference pharyngeal airway length (illustrated below), which is longer in men than in women even when corrected for (body) height.

Since the pharyngeal airway lacks any bones or cartilages for structural support, the theory goes that a longer pharyngeal airway is more likely to collapse during sleep, when breathing is reduced via mild to moderate hypoventilation (in everyone). Here's an illustration (3rd one in the set below) what that collapse looks like (source):

Another theory of this structural kind is that the pharyngeal cross-sectional area is smaller in women relative to men, but studies measuring this cross-section didn't all come to the same conclusion.
Finally, an experimentally observed difference between males and females during sleep is the so called "hypocapnic apneic threshold", which means that relative to men, women require a more substantial reduction in PETCO2 (a measurement of carbon dioxide partial pressure during expiration) before they show signs of apnea. A more prosaic way of saying this is that men's bodies are more prone to go into a state where a reduction CO2 in the expiration causes the brain to decide to stop breathing for a bit because it seems it has enough oxygen (based on the lack of CO2). This mechanism is substantially inhibited during wakefulness and least inhibited during NREM sleep (and in REM sleep it's somewhere in between).
Why there's a difference in this threshold between men and women is not known precisely, but another experiment established that giving testosterone to women increased their breathing instability during sleep. And conversely, blocking some of the effects of testosterone by administration of finasteride increased breathing stability in healthy men during sleep. Note that this is a pretty new (2013) study. Neither finasteride nor any other medication is currently FDA-approved for treating sleep apnea.
And one more thing to point out is that there are different types of sleep apnea, so the two mechanisms discussed above are not necessarily contradictory or competing; the first one (airway length and its collapse) is mostly relevant to obstructive sleep apnea, while the second one is more often discussed in the context of the so-called central sleep apnea.


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Intersex Genetalia
Hypothetically if someone who is born intersex has both sets of fully functioning genitalia (one male one female) could they potentially self fertilize? And if so would it be possible for any genetic variation to take place?

Coincidentally, I was just reading about this today on Wikipedia.

Given the lack of observation and evidence, I don't think this question can be sufficiently answered without including a great deal of unsupported speculation. VTC.

Someone born intersex does NOT have "both sets of functioning genitalia". It simply does not happen. That is a common misconception. Nearly every male organ has a female equivalent. The same embryonic tissue for each organ develops as male, female or gets stuck in between. Which parts do what depends on the specific condition. One cannot have a clitoris AND a penis for example because both  come from the same original structure. The only exception are the organs originating from the Mullerian Ducts (female) and Wolffian Ducts (male) but again it is nearly impossible for both of those to develop as fully functional in the same person.
Also, when both an ovary and a testicle develop it is because two embryos joined together forming a composite human with two different sets of DNA, one forming an ovary and the other a testicle. The genitalia would be rather jumbled making fertility as one sex difficult and as both sexes pretty much impossible.


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Neurological response to food cravings caused by bacteria
Our microbiome (Kurzgesagt video) is thought to send our brain information to chose certain foods to eat over others and it's our increase in a certain type of bacteria that will form a stronger craving for whatever that bacteria happens to appreciate the most. I'd like to know more about how the brain makes those choices in relation to the bacteria, than in relation to a general reward (The brain receives dopamine for things that are achieved, how does bacteria affect that?). Do the bacteria affect the amount of dopamine released- if so then how are the neurons that appreciate that bacteria award, broken or less interested when another type of bacteria now wants a different type of food?
NOTE Neurons are formed when the brain "achieves something" like when bacteria are given the food they thrive on I suppose, so when another type of bacteria receives more food and takes over in your gut, how is it that your neurons are broken and seemingly replaced? I understand this is a stretch but bare with me I just spoke to a neuroscientist about a month back who informed me about the basics of this process.


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Visual phototransduction, neurons depolarization when no light: why?
While reading into visual phototransduction I was surprised to learn that photoreceptor cells are actually depolarized when there is NO excitation (no light, i.e. when you see nothing, black) and hyperpolarized when there is light (I expected the opposite).
This got me thinking...
Let the collection of neurons located within the eye be referred-to as IEN (inside-eye neurons) and, similarly, the collection of neurons directly linked to the eye, yet external to it be referred-to as OEN (outside-eye neurons).
Let the collection of neurons directly getting input from the retina be referred-to as RN (retinal neurons). I'm assuming RN < IEN (subset of -
 correct me if I'm meaningfully-wrong).
And finally, let the collection of neurons that directly link to OENs but are part of IEN be referred-to as XN (eXporter-neurons, in the sense that they export visual information from the eye to the "listeners" outside of it).
So the path of visual stimulus would then be RN -> [...] -> XN -> OEN.
Now, if my eyes were to be completely popped-out I'm assuming that relative to OENs that would have the same effect as XNs not passing along any excitatory/inhibitory information at all. Also, since what I'd perceive would be pure black, that seems to imply that XNs also don't get activated at all when we actually see black (e.g. close our eyes in a very dark room).
So, when we perceive black => RNs get depolarized => they release glutamate continuously => XNs don't excite/inhibit OENs at all (seems to also imply that RNs don't intersect XNs). It is this inversion that intrigues me - why is it that for XNs to transmit NO information RNs have to continuously be excited? By that sense, this makes me think of the eye as if it was a big NOT gate.

Short answer
The reason for the depolarized state of photoreceptors in the dark is unknown as far as I know. It probably has its roots deep in the evolution of the eye.
Background
Indeed, photoreceptors are continuously active in the dark. A steady current flows through open channels (mainly Na+ ions). This current is called the dark current and it partially depolarizes the photoreceptor cell. The depolarized photoreceptor releases neurotransmitter (glutamate) to secondary neurons. Upon illumination of the photoreceptors rhodopsin molecules are isomerized to the active form and the photoreceptor cascade (Fig. 1) is initiated. This ultimately closes the cation channels in the photoreceptor's membrane, stopping the dark current.  This leads to cell membrane hyperpolarization and inhibition of glutamate release to the second-order neuron (Fig. 1).
Admittedly, I do not know why phototransduction exactly is organized this way. There is a lot known about the evolutin of phototransduction (e.g., Lamb et al., 2016), but why the dark current exists is unknown as far as I know. I surmise it is probably an evolutionary relic. Evolution eventually has to work with pre-exisiting features to generate new structures, or alter them. Simple photosensitive spots evolved into the complex eyes observed in today's vertebrates. Evolution thereby used what was there and that happened to be an energetically unfavorable 'NOT' gate.

Fig. 1. Phototransduction in photoreceptors. source: Kolb, (2012)
Reference
- Kolb, Webvision. The Organization of the Retina and Visual System (2012)
- Lamb et al., Molec Biol Evol (2016); 33(8): 2064–87

Thank you very much for your detailed answer. As I was reading it, another possible explanation struck me that might make the NOT gate behaviour actually energetically favourable: with a NOT gate it's always one or the other (primary/secondary neurons) consuming energy - the alternative would make both consume energy at the same time when there's light. So maybe a NOT gate makes it possible overall to consume less energy.

And yet another idea: even if the overall energy consumption is slightly larger with the NOT gate behaviour, there might actually be another trick evolution has played - energy consumption is still smaller in the case when there is light - but unlike darkness, light also means substantial visual content to process. In short, it might matter more to consume less energy in light (to "redirect" the rest to the secondary neurons processing the visual content) than consuming none in darkness.


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Is my Y-chromosome the same at 78 as it was at 18?
How accurate is a Y-dna test at age 78?

For those who VTC -- I'm just wondering, how is this question seeking medical advice? The OP simply asks if the Y chromosome is vulnerable to aging, and, how accurate Y-DNA testing is.. Nothing about this question has to do with medicine, but instead, lies within general biology/genetics.

On the other hand, if you want to VTC due to lack of effort on the OPs part, to answer their own question, then I may agree with you..

Your Y-chromosome most likely isn't the exact same as it was 60 years ago, however, this isn't such a big deal since the Y-chromosome is some 60 million base pairs long. Generally speaking, the accuracy of a Y-DNA test is influenced by the type, and number, of markers used. That being said, age shouldn't diminish test result accuracy.

By and large, yes.  Some telomeres might be shorter, but the rest of the sequence will not change.  Certainly, any regions used for ancestry testing will be stable.


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Is this a common garden spider?
Spotted this outside my window today. Looks like an orb-weaver, but I can't tell whether it's a regular garden spider or not. What species could this be?
This picture was taken in Bangalore, Karnataka, India.

Looks like an orb-weaver ..

I agree! This spider definitely belongs to the genus Argiope, though, due to the angle of your provided image, it's difficult to be more specific than that (if I had to guess, A. anasuja).
The confidence in my genus suggestion comes from the stance the spider is displaying. Spiders within the Argiope genus carry a common nickname of "signature spiders", due to the fact that they'll intertwine additional webbing within their web, called stabilimentum, that, given the design of the support webbing and the spider's stance, will allow for the spider to appear much larger than it really is.

If you can provide an image that reveals the top of the abdomen, a more confident species suggestion may be possible.

Is this a common garden spider?

From the looks of it so far -- yes, this is a common garden spider.