text:
Why can't humans use dietary citric or acetic acid as a primary source of energy?
As the Krebs cycle is involved with the conversion of food in to citric acid, why can't eating citric acid be used as a temporary primary source of energy - in place of fat/carbohydrate/protein?? It seems like a waste of energy to convert food into citric acid if there is freely available citric acid in your diet why wouldn't that preferentially be used for energy - as it would skip a lot of steps and therefore be more efficient. And what about drinking acetic acid for similar benefits, as "it is changed to citric acid by combining with oxaloacetic acid with the help of CoEnzyme A and ATP".

how do you get citric acid in nature?

I order it online via amazon. Citric acid. ;-)
Or I can find it in lemons too.

I might be wrong, but it seems that you would need 100kg of citric acid a day for 2400 kcal diet http://www.myfitnesspal.com/food/calories/495309621

I think you mean 1kg. a day of citric acid, there are 2.5 calories per gram of citric acid. But the thing is I think that comparing equally to food calories is misleading, because if it were to be used for energy - it would be processed more efficiently than actual food which requires a lot of cellular energy to assimilate.

Please read what you have written: "If the krebs cycle is largely about converting food in to citric acid which then enters the krebs cycle." This is a conditional clause, rather than a sentence, but is obvious nonsense even if there were a main clause. How can a cycle do something to something if it is not already in the cycle in the first place? Please rewrite so it makes sense and in doing so spell Krebs with a capital K — it is the surname of Hans A Krebs who received the Nobel Prize for discovering the tricarboxylic acid cycle that bears his name.

Will do, David. There are various tiers to the Krebs and I should have been more specific.

If, as a non-scientist, you wish to post here about the Krebs Cycle you need first to learn about its place in energy metabolism. The "main" purpose of the Krebs cycle is not to produce citrate, but to oxidase acetate (from sugars or fats) to CO2, ultimately generating ATP. It is a cycle of reactions between metabolites, one of which is citrate, with entry from acetylCoA and oxaloacetate. No energy is used ("wasted") if a dietary metabolite has first to be converted to acetylCoA — quite the reverse. And your concept of efficiency bears no relation to scientific reality. I have voted to close.

Seems like a completely legitimate question to me. (there is no requirement to be knowledgeable in backgroun info for your question; just that you've done prior research, which is indicated sufficiently in the OP's post). I vote to keep open.

Why can't eating citric acid be used as a temporary primary source of energy - in place of fat/carbohydrate/protein?

No reason it can't. Citric Acid technically contains 2.5kcal/g -- which is almost half of protein/carbohydrates, almost a third of alcohol, and a fourth of fat.
So if someone needed 2500kcal/day, they'd need 1kg of straight Citric Acid. There's about 47g/L of Citric Acid in citrus fruit juice. So if you wanted it all from "natural" sources you'd need to drink 21.3L of your favorite citrus juice, though that's a bit comical.
In terms of being more efficient since Citric Acid bypasses the first two enzymatic reactions,the part where Citric Acid is processed into alpha-ketoglutarate via Isocitrate Dehydrogenase is the rate limiting step of the entire cycle. You wouldn't be saving any time by flooding your system just before the bottleneck.
Interesting question, though!

Thank you MCM! So this raises the question, how is it possible to raise the rate of the citric acid in to alpha-ketoglutarate via isocitrate dehydrogenase step?

In vivo? No idea. That would require either a lot more enzymes floating around waiting for substrate (not sure how you'd do that or maintain it), or a much more efficient enzyme -- something that could be theoretically done if you had a few hundred hours of world-class supercomputer access and the right research team, but also suffers from the "I don't know how to get it in you and keep it around" problem.
Chances are there's a better solution to whatever problem you're thinking this solves.

I'd like to try and research the idea more, I am not a scientist but would like to try form a better hypothesis and connect a few dots if possible, could you point me towards some easy to digest literature that could help a layman such as myself? Thanks!!

As far as getting citrate in to the blood stream, one idea would be a jello or an emulsion with lecithin, either with citric acid or sodium citrate, something that would slowly release it so as to optimize the transfer to the blood stream rather than the nullification by bicarbonate in the small intestine. I feel there must be a simple method to optimize the conversion of ingested acid in to cellular energy.

Another delivery idea would just be to slowly sip a citrate drink continuously throughout the day.

@ol_matty_man - I'm afraid I don't have some literature suggestions, as I don't fully understand what you wish to do. Basic metabolic processes are pretty well described via Wikipedia, and I'd suggest starting there if you're not familiar with the language. And, as I said, the problem is NOT the citrate -- it's the step going from citrate to alpha-ketoglutarate. That's the limiting step, and the bottleneck in the Krebs cycle.

Thank you. What I was trying to get at is, I think most of the citrate calories do not make it to the bloodstream, I think they are urinated out for the most part, so I was saying perhaps a way to deliver more citrate calories to the mitochondria would be to ingest citrate at a steady rate instead of all at once. I could be wrong though.

@ol_matty_man - About 95% of the citric acid we ingest goes through a metabolic process in our bodies. Unless you ingest an unusually high amount, the majority of what you eat/drink is used and not directly urinated out. That said, I still think you fail to see the problem: Getting citric acid into our bloodstream is easy. Getting more energy after doing so isn't. It is not the amount of citrate that's the problem, but the rate at which it is processed. Like a road with a stop light, the thing that determines traffic speed isn't the number of cars (the citrate), it's the stop light (enzyme).

thank you @MCM - I had read conflicting information about citric acid here: https://www.livestrong.com/article/327212-what-products-contain-citric-acid/ where it said most is urinated out.

one last thing. Is there a chance that on an extramitochondrial level that more citrate or acetate consumption can increase the output of acetyl-coa which then enters the cytoplasm, therefore providing more energy than eating equivalent calories without citric acid??

@ol_matty_man - No, in fact it's the opposite. Citrate is an inhibitor of one of the enzymes in glycolysis.

@MCM About 95% of the citric acid we ingest goes through a metabolic process in our bodies... And that's only if you don't "purposefully" ingest a high amount like the OP is suggesting! Think about it -- how would you even metabolize "excess dietary citrate" anyway? Cytosolic citrate lyase would split it into OAA and cytosolic acetyl-CoA, the latter of which is a substrate for fatty acid synthesis. So you would have to "synthesize" a bunch of fats just to burn them off later? A very impractical proposition!

Not only impractical, but those processes cannot even simultaneously occur in the same cell for that matter either -- https://en.wikipedia.org/wiki/Fatty_acid_synthesis#Animals_cannot_resynthesize_carbohydrates_from_fatty_acids . So, chances are, all that "excess" citrate (from the OP) is simply just going to be excreted out of your system -- with no "metabolism" to speak of! (Unless you're claiming the body can somehow "metabolize" cytosolic acetyl-CoA, or "somehow" run the citrate-malate shuttle in reverse!)...


text:
How do plants grow year after year even though they die?
How do plants grow, die, and then grow again? For instance, when my plants die during the winter, how do they grow again next year? Does it have something to do with the root system? Or do they even die?

There are these things called seeds.

@TwistedGenes There's no need to be condescending.

It depends on the type of plant, but basically not all of the plant dies.  Plants have evolved a number of strategies for winter* dormancy.  These are common ones, but probably not an exhaustive list.
Deciduous trees and bushes simply drop their leaves in the fall, and so may look "dead" to the unskilled eye - though with practice, it's usually easy to distinguish between dead and dormant.  Then when the weather warms in the spring, new leaves grow.
Other perennial plants may lose some or all of their top growth, even dying back to ground level, but the roots will be alive, and will start growing when the ground warms.
Still other plants have developed specialized underground structures like bulbs & rhizomes - think daffodils, tulips, irises, and similar.  The rest of the plant dies, only to grow again from the bulb when conditions are right.
It's worth noting that most, if not all, of these are used for propagation as well, often naturally, and frequently with a bit of human help.  Bulbs and rhizomes multiply: the daffodil bulb you planted a few years ago may now be a dozen bulbs, each of which can be moved to grow new ones.  Many perennials can be increased by dividing the root mass into pieces, each of which will become a new plant.  And cuttings from many trees & bushes can be induced to form new root systems, and become new plants.

Or summer, dry season, &c.  For simplicity, I'll just say "winter".

source: Stack Exchange

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

sort: votes


text:
When using a primer to replicate DNA in a plasmid, does it replicate the whole plasmid?
I've been learning about PCR and plasmids. I understand that the reason for having both a forward and a reverse primer is to extract and amplify the specific piece of DNA between these two primers.
What I'm struggling to understand is that why after the first replication, a fully circular DNA strand isn't formed and hence, why isn't a fully circular DNA strand formed for each replication.
For the following diagram , let the strands be labelled strand 1, strand 2, strand 3, strand 4 from top to bottom. (Diagram from Lehninger Principle of Biochemistry, 5th Ed).

For example, in the diagram here. When cloning a plasmid I assume strand 1 is fully circular, so strand 2 (which was transcribed from strand 1) should also be fully circular and in the diagrams it should show DNA to the left of the site of interest.
Does the transcription stop somewhere along the line, preventing it from copying the whole strand? Or does the strand never join up into a circle, so that the DNA that would appear to the left of strand 2 has been copied, but doesn't join up to the site of interest so wasn't included in the diagram.
Thanks for your help.

The diagram clearly implies that strand 2 and 3 are products from the first round of replication. You're therefore correct that it would be more accurate if the diagram showed the grey parts on the left and right side respectively, but then having a small gap between the end of the grey part and the start of the blue part (to indicate the linearity of the product). However, that would make the diagram less illustrative and necessitate more explanation, so I think this is an acceptable inaccuracy.

PCR produces linear DNA, not circular. You can replicate whole plasmids using PCR, but the DNA will still be linear, as if you cut the plasmid with a blunt-end restriction enzyme.
So why doesn't the whole plasmid get copied when using PCR? Let's assume the primers are designed to bind 1000 bases apart from each other. The first round of PCR will probably produce longer pieces of DNA, because the oligos can only bind to the plasmid and the Polymerase can keep going. But the polymerase will fall off at some point, either randomly or when the temperature is pushed up for the next round of PCR. But in round 2, there should be equal numbers of circular plasmid and linear copy. The proportion of linear copy will increase every round. As the linear copies increase, the oligos are more and more likely to bind to linear copies than to circular plasmid.
Binding to linear copies is why the PCR product size is controlled. Let's assume that a linear copy is 1500 bases, because the polymerase ran an extra 500 bases past the other oligo site on the plasmid. But when the reverse oligo binds that site on the linear copy, the polymerase will run 1000 bases and fall off the end of the linear copy. This new copy will have the forward and reverse oligo sites at the ends, so it's the right size. Any copies produced from this strand will also be the right size. As the reaction proceeds, the proportion of correct-sized strands increases, and create more correct-sized strands.

This makes good sense. Thank you. Is there any way to know how long before the polymerase falls off?

@meldob Most polymerases used in PCR are pretty good at staying on. I used to PCR entire 10,000 base plasmids on a regular basis. When setting up the PCR you choose the extension time based on the length you want to copy and the speed of your polymerase. So if your enzyme runs at 1000 bases per minute and you need to copy 2000 bases, use 2 minutes. Going longer probably won't hurt anything, but it wastes time. Going shorter will cut off the reaction before you get the entire sequence copied.

We have different polymerases optimised for different purposes nowadays. Some focus on high fidelity (i.e. low error rate during copying) but sacrifice speed and range, others can copy 1kbp in less than 10s but make more errors and fail if the desired sequence is too long.

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


text:
How exactly is the wood fossil process?
I would like to know in deep how exactly is the wood fossilisation process. I am fascinated how after millions of years the fossil wood preserves its microscopic characteristics. Look at this cross section where you can see clearly differences in the cellular tissues as parenchyma, vessels, and rays.

I know that in the fossilisation process the wood was replaced by mineral particles, but I don't understand how the organic material went outside to stay only the minerals.

there are actually more than one process, but in the case of high detail wood fossils the process is the slow filling in of all the spaces in the wood (filled with water in life) with dissolved minerals from the groundwater. this is called permineralization. Of course this only works is the wood is buried so it cannot rot while this is happening. Since permineralization happens on the molecular level is can preserve great detail as the minerals form around the remaining hard tissue.
This video is a decent representation,


text:
Which data source gives the present status of research in extending human lifespan?
I have seen this book in Springer:
The Future Of Aging (Pathways to human life extension)
That book seems to be of 2010; I am not finding any such new books, giving data on the present status of the research.
Which data source (journal articles, books, etc) gives the present status of research in extending human lifespan (longevity)?
I read Wikipedia (Life Extension, Immortality), they don't seem rigorous.

Are you asking for a more recent review paper/book of the topic?

Thank you for the reply. Yeah, I asked for a recent paper/book, to know on what conformations/actions in nutrition or exercise are to be made for becoming compatible for getting those life extending processes. I found certain summaries of the present status, which seem to be saying on there being none, now, allowing the life extension beyond what is normally known or possible from nutrition/exercise Summary. I....

....have now shifted to other question: Which sources give fitness programs for living longer?


text:
What do you call clearly different sub-groups within a species?
If you look at species of bees and ants, you can clearly see there are drastically different specialized ants, like queen ants and workers. They're both part of the same species, yet are still obviously different. What is the proper name for that phenomena?

Just to clarify; you are asking specifically about non-taxonomic groupings right, e.g. functional or behavioural groups/phenotypes within species?

Right, specifically the physical/behavioral differences within one species.

also allotype

In eusocial insects, especially ants and bees, these groups are called "castes" (see e.g. Hölldobler & Wilson, 1990. This is the same term that is used for social stratifications in some human societies e.g. in India.
One definition of caste is:

...the physical or the behavioural/physiological phenotype of a eusocial individual, or both.

(from Hölldobler & Wilson, see also antwiki.org)
Some division of labour as well as collective rearing of young can occur in prosocial animals as well, but there the term caste is not used.

Is it really just as simple as alleles which accounts for castes like honeypot ants?

@JohnJoe In ants, the traditional view is that the worker-queen determination is largely due to nutrition/environment, but some studies also show a clear genetic component. Males/drones are determined by being haploid, so that is a separate issue.

@JohnJoe Just to clarify, there is infinitely many possible ways to define sub-groups within species. The term "castes" is not a general term, it is a term that applies to the specific subgroups you describe in eusocial insects. For other types of subgroups different words may exist such as subspecies, subpopulation, family. One could decide to make any kind of arbitrary grouping such as considering the set of all individuals that went to the woodstock festival for example. There is of course no general term to refer to any kind of subgroup, other than just subgroup.

The difference here is that these individual castes have the capacity to reproduce as part of the same species, whereas this can't happen between other generalized groups.

Or not. Typically there are only two castes which are fertile.

Which still result from the reproduction of castes within the same species.


text:
Is this a texas sage?
So for a project in one of my classes we must identify two monocots and two dicots growing at our school. We've managed to identify all but one:

So more information:

My school is in southern nevada
It's about one foot tall
It's growing with joshua trees and oak trees and some rosemary.

Update: I think it's a texas sage, but I'm not completely certain, verification would be nice.

The link doesn't work for me. Looks like that link is private, and I cannot access it.

@TwistedGenes Thanks for informing me, I've posted the image

That's a good guess, but I doubt it is Texas sage or Leucophyllum frutescens -- which is a common urban landscape shrub in the USA southwestern deserts.  L. frutescens is more upright and bushier, and in particular, much grayer than the plant in your picture.  Can you provide better/more pictures, from different angles, and especially pictures of any flowers that might be present?


text:
Are the transverse septum in sharks and the diaphragm in mammals homologous structures?
Are the transverse septum in sharks and the diaphragm in mammals homologous structures?
I have searched on Google Scholar and Web of Science, but haven't found substantial evidence to prove or falsify the claim.

What is your reasoning one way or the other? Let us know your reasoning. What are the two structures made of?

A beginning of answer here below, I hope. Please first consider that many structures are involved in the question here, the diaphragm (UBERON:0001103), the diaphragmaticus muscle (UBERON:0036071) and the septum transversum (UBERON:0004161). At Bgee (bgee.org) we aim annotating relations of similarity between anatomical structures, please have a look at our GitHub
https://github.com/BgeeDB/anatomical-similarity-annotations
We already annotated 'diaphragm' as a mammalian structure, not homologous in Amniota (please see https://raw.githubusercontent.com/BgeeDB/anatomical-similarity-annotations/master/release/similarity.tsv). In our next release, you will see the annotation for the 'diaphragmaticus muscle' which is an analog organ in Crocodylians (and Turtles) but not homologous to the mammalian diaphragm either. See here for more details about this new Uberon class:
https://github.com/obophenotype/uberon/issues/1229.
Based on the comments here above, I would say that currently we can argue that there is no evidence for a homologous relationship between the 'septum transversum' in sharks and the mammalian diaphragm. Please note that UBERON:0004161 septum transversum describes the (mammalian) embryonic structure that will give rise to the central tendon of the diaphragm, while here you are talking about a adult structure closer to a 'diaphragmaticus muscle'-like septum, as far as I understand.
But anyway thank you for your interesting question that points out a very exciting and rapidly evolving evo-devo field, as this recent paper also suggests
https://www.ncbi.nlm.nih.gov/pubmed/?term=27859325


text:
Why structures of many proteins are still unknown?

https://www.learner.org/courses/biology/textbook/proteo/proteo_3.html
Despite advances in techniques for determining protein structure, the structures of many proteins are still unknown...

My question is why? We have many researchers all over the world. We know what our 3 billion DNA is. The governments invest billions of money into medical research. We should have sufficient human resources and technology.
What's stopping us determining structure for all proteins? We need more money? We need more people? We need better technology?

How much you already know about determining protein structures?

Instead of standing on a soap box making speeches, how about making an effort to find the answer yourself? This is what is expected of people who post to SE Biology.

What's stopping us determining structure for all proteins? We need
  more money? We need more people? We need better technology?

Each unknown structure has a different story. Importantly, not all of the proteins have well-defined structures. But this hasn't historically been appreciated, so lots of effort has been spent structurally resolving regions that are not that ordered. But there are many other explanations for a protein's structure being unknown, most of which fit into two categories.
The putative function can be uninteresting. Most researchers only express and purify proteins that are potentially interesting. There is usually some genetic or pharmacological manipulation that implies a given protein is "interesting." Only the large scale structural genomics projects randomly solve structures, aiming for completion. Even then, these projects have to prioritize proteins that look feasible "on paper."
The protein can resist structure determination Lots of proteins are difficult to express and purify, for a multitude of reasons. For example, the table I just copied from the NorthEast Structural Genomic consortium summarizes their pipeline as follows:
Production stage
targets
cloned          25,924
Expression tested           24,479
Expressed (E > 0)           18,992
Expressed-Soluble (S > 0)           13,946
Expressed-Soluble (ES >= 9)             11,054
Fermented           9,440
Purification attempted          8,691
Purified (>= 0.5 mg yield)          6,493
HSQC spectra recorded           2,853
"Good" HSQC spectra             1,476
HTP crystal screening           2,845
Crystal hit             1,480   1,672
X-Ray structures            608
NMR structures          496
Total structures            1,061

So using a combination of X-ray crystallography and solution-state NMR spectroscopy, they solved 1061 structures of 25924 clones, almost all of which were tested for expression. (http://nesg.org/statistics.html)
Crystallography is as automated as it can get right now. Protein NMR and cryoEM have their own niches, and will continue to fill out the gaps. But the science is difficult, and of the well-defined structures, there are still many that haven't been well-described.
(If we could really solve the protein folding problem, we wouldn't need to solve structures at all...)

Also consider that very often the structure of an individual polypeptide (i.e. single coding gene's product) is meaningless because it only functions as part of a complex, in which its structure is different.

The gold standard for determining protein structures is x-ray crystallography. However, in order to perform x-ray crystallography you have to obtain your protein in crystalline form. Many proteins are not soluble in water, so crystallization is difficult or impossible. See this answer for information about the difficulty of crystallizing trans-membrane proteins.

The answer is most likely priorities. Yes, the process is easier, but it still requires at least some effort and time, which is better spent on other things. As such, grants are unlikely to be given for such trivial work - and this is researchers' job, so if they're not going to be paid for it, they probably won't do it.


text:
Why do living things go belly up as they die?
I have seen birds, lizards, frogs, fish, etc in various places on their back dead. May be insecticides cause them to flip over but I do not believe every upside down creature died by poison as stated in this question's answer: Why do cockroaches flip over when they die? and the roach question only covers roaches and insecticides. My question covers all animals not affected by poison that are belly up.
Other than poisoning is there any other reasons like DNA programming on behavior or muscle spasms that cause this?

Related: https://biology.stackexchange.com/questions/64333/if-an-insect-becomes-upside-down-do-they-have-mechanisms-to-turn-themselves-rig

@Muze This is just speculaion but it could also be partly due to confirmation bias. I've seen a lot of dead ladybirds on their front - even if organisms have a 50/50 chance of facing up or down, you might notice the upside down ones more, since its what you're looking out for. A lot of insects might simply be blown over onto their backs when dead. But also, some organisms could be flipped over by a predator, if the predator finds it easier to eat the organism from its underside (e.g. if there is a thinner shell around the organism's belly).

Possible duplicate of Why do cockroaches flip over when they die?

@Muze I did, and I still think the questions are the same. Others are free to disagree with me. That's how it works.

@kmm you are correct.

Can you back up the claim that "living things go belly up as they die"? I've been dead animals in other positions as well... Otherwise, this is just an unfounded/anecdotal claim.

@fileunderwater that is why I'm asking, but if you want I can find pictures online of animals dead on there back.

limbs are light weight compared to bodies, if you knock an animal around (and it has no active correction AKA is not alive) it will tend to end up on its back just due to where its center of gravity is.


text:
How is a very small quantity of poison able to kill a large organism?
Take cyanide for example: it prevents mitochondria from producing energy in form of ATP but, in the process, it binds with it and hence it's spent.
It's theorized that half a gram of cyanide can kill an average adult human. How is this possible? There surely is more than half a gram of mitochondria in an adult human. So, if cyanide molecules bind and hence get spent so fast, how are they able to kill so many cells so fast and continuously?
Is it something to do with the amount of molecules in half a gram of cyanide being several times higher than the amount of cells in one gram of human tissue?

I'm pretty sure cyanide deaths are due to high levels of oxygen in the blood vessels, rather than loss of energy to the individual cells.

@TwistedGenes Based on what?

"Cyanide" doesn't refer to just one compound, but given the lethal dose you mention of "half a gram" you are probably referring to potassium cyanide, with a molecular weight of about 65g/mol, so 0.5 gram is about $10^{22}$ molecules. Potassium cyanide becomes hydrogen cyanide in the stomach, and hydrogen cyanide is the gas (at body temperature) that causes toxic effects.
The toxicity of cyanide containing compounds is because they bind with high affinity to cytochrome c oxidase, an enzyme that is part of the mitochondrial electron transport chain. The result is that electrons cannot be efficiently transferred to oxygen molecules. The effect is roughly the same as if oxygen was not present in the inspired air.
$10^{22}$ is a huge number. That's about 250 million molecules per human cell in an adult (taking # of human cells from Bianconi et al). Even so, it isn't likely that cyanide molecules be perfectly bound at every molecule of cytochrome c oxidase, just that there is enough to cause massive brain damage or stop the heart.
By comparison, cyanide is not even close to the most toxic substance. Toxins that target neurotransmission can be much more potent. For example, the IV LD50 for botulinum toxin is about 2 ng/kg, so something like 125 ng for an average adult, equaling only $5\times10^{11}$ molecules.


text:
Genetic disease elimination: Possible?
This is a question having to do with my generation ship story but more specifically, genetics, and even more specifically, genetic disease.
Here are the conditions as far as people with or without genetic disease go:
People with disease: sterilization + alternative ways to have children and absolutely no sex before sterilization
Carriers: warn that their children might need sterilizing
Not carriers: Absolutely nothing
Now I know these types of genetic diseases would be eliminated in 1 generation:

Y linked(Azoospermia for example)
X linked dominant(Such as Vitamin D resistant rickets)
Autosomal dominant(For example Huntington's disease)

A truly codominant genetic disease is impossible because you can't both have and not have the disease simultaneously. Instead it would be better to say it is incomplete dominant.
But with these conditions, is it possible for genetic disease to be totally eliminated after hundreds of generations(say 500 generations)? In other words is it possible for these types of disease to be eliminated:

Incomplete dominant(Alpha-1 antitrypsin deficiency as an example(but I found out this also falls under multiple alleles))
Autosomal recessive(sickle cell anemia for example)
X linked recessive(such as Hemophilia A)
Multiple alleles(Again A1AT deficiency is an example of this)

I found out that human population growth globally averages around 1.1% per year. And a reasonable number to have on a generation ship is 44,000 people. About 9% of them would be 65+, 65% between 15 and 64 with 20% of that being women of reproductive age, 50% being men of reproductive age, 15% post-menopausal women, and a small 5% being those that are still not in puberty, with the other 26% of the population being from 8 to 14, of which 75% are not in puberty yet and 25% are. Sex ratio is 1:1. This would mean a minimum of 815 babies born per year to compensate for 343 deaths per year. Or about 2.3 times as many babies born as deaths.
So given this and the genotype ratios for the possible punnet squares which I already wrote down, how would I figure out the probability that all genetic disease is eliminated after x generations?

It seems you are excluding spontaneous mutations which could lead to genetic diseases. Is that on purpose?

To all the down voters, please leave a comment on how to improve the question. And please don't mix up the biological question "Is it possible?" with the ethical question "Should it be done?". Thank you.

Please rephrase the question (title) to include the detail of being on a starship colony; or generally the fictional setting. The current question suggests you're asking about human genetic engineering. Clicking on that and not reading your question might be the reason for some of the unexplained downvotes.

Or with slightly advanced technology you can simply edit the offsprings genome.

Given your severe selection pressure against disease allele you have implemented, you can have the disease allele eliminated within 1 generation for dominant allele and 2 generations for recessive allele.
You could eliminate all those disease alleles while you were selecting the crew, prior to boarding your generational starship.
Your primary problem is spontaneous mutations. However if you are doing genetic test and this is a starship, you should have access to IVF technology. This will allow you to screen every embryo prior to implantation for genetic defects.

Phenotype-level selection doesn't eradicate recessives
As long as you restrict yourself to purely phenotypic selection, you're extremely unlikely to eradicate recessive genetic diseases at your population size. That's the nature of recessive alleles - they persist in carriers that don't develop the phenotype. To eradicate this, you basically need the luck that in one generation, not a single child gets passed down a mutant allele from a heterozygous parent. The same goes for "incomplete dominant" (the appropriate term to use would be incompletely penetrant). X-linked recessive are more likely to be eradicated because you will never have male parents passing these on (males have only one X which means all recessive X-linked traits manifest in male phenotypes).
Predicted number of generations till eradication
As for the population statistics regarding your recessive eradication, it's not possible to predict after how many generations this will succeed. Depending on the initial prevalence, you will have an exponential decay due to your selection. At some point you will reach a near-zero level at which you won't be able to predict when that lucky moment will happen that no child receives a mutation. A small number of heterozygous individuals could produce a larger number of heterozygotes and infinitely cause low-level recurrence of the disease. At this point it's a computational rather than mathematical problem.
Practical genetics
A simple practical example is my experience with selecting the y allele out of a Drosophila population. y recessively causes yellow rather than brown body colour (basically a form of albinism). I've made a few attempts at selecting it out by discarding yellow-bodied flies, but there were always a few yellow-bodied individuals in the next generation. The only way I've succeeded in eradicating this is by doing crosses with a low parent number (~5 individuals) so that there is a reasonably high chance of picking parents without any mutant y allele.
Possibilities for eradicating alleles
The simplest solution to your problem is genetic screening at the embryonic level, which would allow theoretically to eliminate all pre-existing heritable genetic diseases in one generation. You would need continuous genetic screening to also keep de novo heritable mutations out. As for somatic genetic diseases (e.g. paroxysmal nocturnal haemoglobinuria), you will never eradicate those without targeted genetic engineering to make the problematic hotspots in the genome more damage-resistant.
Side note regarding multiple alleles: Multiple alleles don't require special consideration for your thinking because each allele can either be recessive or dominant to wildtype alleles in its phenotype. Also consider that "healthy" isn't an absolute standard. Genetically speaking, there is no "normal". Most (all?) genes have a range of alleles that persist in nature and cause nothing we would consider a disease or defect phenotype.


text:
What insect is this? I saw it in my house in Kolkata on 2 April 2018, at 8:00 p.m

I saw this insect in my house in Kolkata (India) on 2 April, 2018 after a storm at around 8:00 p.m.  I would like to know what insect it is.  Thanks in advance.

Is Kolkata the same as Calcutta, India? Also, that looks like some sort of fly to me, but I can't tell you exactly what kind of fly.

I highly suspect it to be Austrosciapus proximus

Yes, Kolkata is the new name for Calcutta, India.

Is Austrosciapus proximus found in India?

@Joyoti I'm not so sure about that, not so much information about them. However I also found out the species of the Condylostylus genus are found in India. They seem to be very similar to the one in the picture, but I'm yet to confirm: http://nathistoc.bio.uci.edu/diptera/Condylostylus2.JPG

It is a species of fly, or of the insect order Diptera, insect family Dolichopodidae.  The exact genus and species is uncertain as there are many hundreds of species. See the link below.  You can also search Google images for these names where many similar fly photos can be seen.
https://en.wikipedia.org/wiki/Dolichopodidae

More specific identification will be helpful

I would concur with user22542 --> order Diptera: family Dolichopodidae
Supporting evidence outside of wikipedia is on an Australian website. http://www.bowerbird.org.au/observations/35021
I don't suggest them to be the same species, however potentially related as they seem to live in grassy places across the globe.

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


text:
Which books give data on how humans grow physically from birth till death?
I am searching books on how humans grow physically from the birth till death. I am not a biology student, and don't know any technical terms. I searched amazon but didn't find any such books. I need book to be precise. Even if the book is a textbook, it would be helpful.
If it is not possible to get all the data in one book, is there any other alternative reading to be made via multiple source reading.

The 'Illustrated textbook of paediatrics' by Lissauer et al. (ISBN 9780723438717) contains a section about the average growth of children from birth up until puberty. After puberty humans don't grow anymore unless there is a medical condition. However it is important to understand that growth is influenced by many factor including ethnicity, sex, socioeconomic status and health and therefore precise numbers are hard to find.
For the most accurate information you should look for scientific publications for you specific population.

Thank you for the reply. I seem to have been not precise in question, I intended to ask on how humans grow from the beginning and age till death. I am searching book(s) having these data, for knowing on what is to be made for living longer.....

... These books might allow knowing on what chemicals (food) is to be had for increasing time of aging or to decrease the rate of growth, and to check on whether the ready-made exercise or food program are allowing to live longer or not. I have till now found Embryology (Developmental Biology) books, I still need to search adolescent developmental biology and might need to find books on how humans age physically. I will try reading journal articles, if I don't find books.


text:
What kinds of animals does insular dwarfism affect and how large does an island need to be to escape it?
3
down vote
favorite
1
I've been wondering about insular dwarfism, and would like to know if it only affects certain animals (Since some animals grow larger upon colonizing an island, often due to the absence of predators.) Do only big animals get smaller, and if so, how big is "big"? Are there any taxonomic groups that are more or less prone to insular dwarfism?
The second thing that I'd like to know is the minimum size of an island without insular dwarfism could be. Also, I'm not sure if resources, biodiversity or climate affects it too (Considering Bergman's rule, the increased competition in jungles, etc.) This may sound like a lot of questions, but the main components of an answer I'd like are shown in the title - who and where.

There are no general rules. We have just observed repetitively that organisms living on small pieces of lands tend to be particularly large (insular gigantism) or particularly small (insular dwarfism) compared to the main land counterparts.
There are several possible reasons for these changes and those reasons vary among species. Dwarfism is most definitely not always a consequence and there is no hard coded minimal island size for such change to happen or not happen.


text:
Can Wasps smell fear?
There are two conflicting things I have heard. One more anecdotal:

Wasps can smell when you are afraid of them

The other from reading popular science magacines:

Humans don't produce any pheromones

As far as I know, a pheromone is a smell produced to communicate with members of your own, but also other species. From my understanding these two statements are mutually exclusive.
So: Can wasps smell if a human is afraid?
Any answer with sources is appreciated.

If anyone with enough reputation would be so kind to create a [pheromones] tag, that would be great ;)


text:
Number of different clones of B lymphocytes
My professor told us that there are about a million different B cells based on their surface receptor.
I have read that we have about 30000 genes in all. Since receptors are proteins how do these 30000 genes make such a large number of receptors?
I read about something called alternative splicing. Is this the mechanism behind this?

You're looking for VDJ recombination: https://en.wikipedia.org/wiki/V(D)J_recombination

Alternate spicing of mRNA is a real phenomenon, but it's not the source of immune cell receptor diversity.  The DNA of immune cells is rearranged in a slightly random manner, to make a receptor with a random sequence in the variable portion of the receptor.  As Armatus already said, the process is VDJ recombination.  Here is a link to a textbook on NCBI
https://www.ncbi.nlm.nih.gov/books/NBK27113/

Yes - in short, splicing enables one gene to be 'read' in multiple different ways. Imagine you have a set of letters; you can make one long word out of them, or cut some words out to make a shorter, different word. The same logic applies to gene expression, in that one gene could be made to code for a variety of different proteins (in this example, surface receptors).


text:
Measurement equation of Tree-Step pathway model
I am not specialist in biology but I want to test a parameters estimation method (based on Kalman filter) on the Tree-Step pathway model, but I cannot find a document that gives the measurement equation of the Three-Step Pathway model (Moles et all 2003, Parameter Estimation in Biochemical Pathways: A Comparison of Global Optimization Methods"), can someone give me some references?


text:
The threshold of Ki
Is there any threshold (Ki) between strong and week small molecule inhibitors?
When I see the (Ki) values in any published work, how can I decide if this good or bad inhibitor?

K$_i$ values represent the binding affinity of an inhibitor and are typically in the picomolar to micromolar (10$^{-12}$ to 10$^{-6}$ mol/L) range (ref: (a), (b)), but have also been seen as low as femtomolar values, albeit rarely (10$^{-15}$ mol/L) (ref: (c)). A small K$_i$ value (e.g. femtomolar) represents an enzyme with a high affinity, i.e. a "strong" inhibitor. But your decision of whether an inhibitor is "good or bad" or "strong" will depend on context, and how well the inhibitor fits its purpose and compares to other inhibitors. There is no standardized "threshold".
Furthermore, other factors apart from the K$_i$ value could affect how "strong" the inhibitor is. The K$_i$ value just tells you how well the inhibitor can bind to the enzyme, but other factors that affect how well the inhibitor is able to inhibit the enzyme:

What type of mechanism does the inhibitor display? Competitive? Noncompetitive? Other types? Different mechanisms of binding could change qualities of the inhibitor, such as whether it is surmountable or not. Also, if the inhibition can involve binding to the enzyme-substrate complex, does this binding have a different affinity constant to K$_i$?
Does the inhibitor interact with the substrate? Two inhibitors could have equal K$_i$ values but a different strength due to interactions with the substrate.

Lastly, the IC$_{50}$ is practical measure of the potency (i.e. the strength) of the inhibitor. It describes the concentration needed to inhibit enzyme activity by 50%. However, the IC$_{50}$ is dependent on the experimental conditions, such as enzyme and substrate concentrations. For some competitive inhibitors, the IC$_{50}$ may relate to the K$_i$, [S] (substrate concentration) and K$_M$ (Michaelis constant of the enzyme) with the Cheng-Prussoff equation:
$$K_i=\frac{\text{IC}_{50}}{1+\frac{[S]}{K_M}}$$
Reference K$_i$ values:
(a): Flurbiprofen at PGHS1 or PGHS2: K$_i$ = 0.5 uM to 0.6 uM
(b): Methotrexate at DHFR: K$_i$ = 7.3 pM to 2.3 nM
(c): Ribonuclease inhibitor protein at ribonuclease: K$_i$ = 1 fM.

Could use more explanation for context. Like, is mechanism is a type of context?

Not sure about point 2 (that the IC50 is a function of temperature).

@xusr Thanks for the (+1)! I added notes about the tight binding of femtomolar Ki inhibitors and that the IC50 is dependent on experimental conditions - I agree, it has its limitations, but it's nice to have practical models of the theory :)


text:
Can Anyone Identify This Insect?

I keep seeing these bugs on a wall in my house in Istanbul (Turkey) walking up and down generally during evening and night. They are about 1 mm long and have a brownish color. I see more of them through late hours. Does anyone know what they are called?

I don't recognize it, but it might be possible to identify this insect using an automated species identification program.

Related: Bug Identification: Tiny Bugs in Fairport NY, What are these tiny, swarming, jumping bugs?, Help identifying tiny jumping bug, Taxonomy: Categorising Collembola, What kind of small insect is this?, Unknown aquatic larvae

Those are collembolans. Common name, springtails. Do you have a potted plant nearby? They are completely harmless.
Here is an example:

(picture from bugguide.net

Could you please add, why  you think these are collembolans?

SIze and shape. See https://biology.stackexchange.com/questions/54878/taxonomy-categorising-collembola

Agreed. The picture is poor but it looks very much like a typical springtail


text:
What is the purpose of co-transport?
My current understanding of co-transport is that, first, a substance is actively transported across a membrane, establishing a concentration gradient across said membrane. This same substance then diffuses down the established concentration gradient, effectively travelling back to where it began, but this time travelling via a transmembrane protein that transports another substance also, regardless of its concentration gradient. Thus, this second substance is transported to wherever it is necessary.
Would it not then make more sense for the latter substance to simply be actively transported to its destination, as opposed to involving another substance which has no net movement at the end of the process? What is the advantage of co-transport?

This is a useful question and I have upvoted it, but there is no reason to talk about evolution. Keep it simple and just talk about the rationale of a process, or its advantage over some alternative, or why it is used in some situations and another process is used in other situations. Leave talking about evolution for situations where you are considering this — comparing the biochemistry of different organisms, for example.

@Jam is correct — if a little long-winded — in pointing out that one of the benefits of co-transport (no need to involve evolution) is that the concentration gradient of one co-transported molecule can provide the thermodynamic energy for the transport of the other molecule against a concentration gradient. This is dealt with in a quantitative manner in Section 13.1.2 of Berg et al. and in a qualitative manner in Section 13.4.
However, there is another factor to consider. This is the maintenance of electrical neutrality.  Typically it is charged ions that are transported (anions in the examples shown below, taken from Ch. 18 of Berg et al.) so that co-transport of a counter ion is needed to maintain electrical neutrality.

The diagram above also highlights another important point. You need to look at the biochemistry of the co-transporting systems, rather than just considering them in abstract. One of the sites of many co-transporters is the mitochondrial membrane, where transport is part of a co-ordinated process.
Consider for example ATP, ADP and phosphate. ATP is synthesized in the mitochondrion from ADP and phosphate, and then much of it must be transported into the cytoplasm. At the same time ADP and phosphate must enter the mitochondrion as substrates for the generation of more ATP. Active transport is clearly a non-starter here (it would use the ATP that is to be transported!) and co-transport ensures that the influx of ADP is balanced by the efflux of  ATP.  Phosphate influx (which is balanced by hydroxide efflux, to preserve neutrality) must be coupled to this process, although I am not aware of how this achieved (contributions welcome here).
Analogous considerations apply to NAD+ and NADH, but it is the electrons that are transported, rather than these compounds themselves, using surrogate oxidized or reduced compounds. Shuttle systems of this sort integrate the biochemical functions of the mitochondrion with those in the cytoplasm, and need to be studied individually to understand the choice of co-transporters. Section 18.5 of Berg et al. is a convenient starting point.

Would it not then make more sense for the latter substance to simply be actively transported to its destination, as opposed to involving another substance which has no net movement at the end of the process?

But where would the energy for the transport come from! Thermodynamics tells us that the universe tends to increase the amount of disorder (Entropy). If we have active transport of a solute, then by definition, this is going against a concentration gradient. So we could end up with a substance being entirely on one side of a plasma membrane, which wouldn't be disordered at all - clearly thermodynamics wouldn't let this happen by itself since we would be reducing entropy.
This is why energy is needed for active transport. We need to put in the leg-work by using some energy to locally reduce entropy, and ultimately move something to one side of the plasma membrane. Think of the concentration gradient like the pent up energy of a spring. We can release this energy when we want, in order to make it thermodynamically feasible to move a solute against its concentration gradient.

What is the evolutionary advantage of co-transport?

We've established that we need an energy source to drive active transport. But indeed, why would we use a concentration gradient? Couldn't we equivalently use a different energy source? Well yes, we could use ATP (for instance in Na$^+$/K$^+$-ATPase). But a concentration gradient might already be established over a plasma membrane, so its already there as an existing source of energy. Perhaps this is why co-transport evolved with this mechanism.

I follow your answer completely, and had considered your suggestion. However, in companion cells of the xylem for example, a concentration gradient (of H+ ions, I believe) is actively and deliberately established in order to transport sucrose via co-transport. What purpose would you suggest this, then, has?

@ElizabethT It's been many years since I've done any plant biology :) but aren't companion cells in the phloem? I know that phloem companion cells partake in active transport of sucrose from sap (which they can then use to feed themselves). Most cells have some sorts of uptake mechanisms because there are things like amino acids that they want inside, but things like ammonia that they want outside. So cells can use concentration gradients (and co-transport) to control this.

You are completely right. Rookie mistake - I do know some plant biology, I promise! That's an interesting point, thank you :)

@ElizabethT No problem! And I didn't mean to be condescending with that remark about plant biology, I just meant that you should take my answer with a grain of salt :)

That's honestly not the way it came across, you did put forward new ideas that I hadn't considered before. Consider my mind broadened!


text:
difference between neurotransmitters and hormones
I have been reading a lot about neurotransmitters and hormones but what's the difference between them both or are they the same? It's been confusing for a while now. Also, why do some neurotransmitters act as hormones?

At heart, the distinction between neurotransmitters and hormones is how they are transmitted - not necessarily a difference in the chemicals themselves.
Neurotransmitters are sent over synapses, between neurons. They may be small molecules (e.g. dopamine) or larger molecules such as proteins (e.g. substance P). Conversely, hormones are sent through the circulatory system but could also be small molecules (e.g. adrenaline) or large molecules (e.g. growth hormone).
Looking at the structures of these chemicals, we can see that both neurotransmitters and hormones have an enormous variability in the chemicals they involve. Furthermore, dopamine looks much closer to adrenaline than it does to substance P. But dopamine is primarily a neurotransmitter and adrenaline is typically thought of as a hormone!
There may also be overlap between roles of chemicals as neurotransmitters or hormones. In fact, adrenaline may act as both a neurotransmitter and a hormone. So, to answer your question of "why do some neurotransmitters act as hormones?" - the distinction is in the context of how the chemical is sent through the body. There's variability in which chemicals are used for either purpose, and no rule saying a chemical can't be sent via multiple mechanisms.
Furthermore, neurotransmission also involves spillover of neurotransmitter, which in theory could find its way into the circulatory system. So there could be overlap between neurotransmission and hormone signaling. And lastly, as @Remi.b points out, the particular mechanisms of neurotransmission and hormone signaling have implications on the dynamics of the signaling.

Wikipedia > Neurotransmeter

Neurotransmitters, also known as chemical messengers, are endogenous chemicals that enable neurotransmission.

Wikipedia > Hormone

A hormone [..] is any member of a class of signaling molecules produced by glands in multicellular organisms that are transported by the circulatory system to target distant organs to regulate physiology and behaviour

There is even a section called Comparison with neurotransmitters in the wikipedia > hormone page

There are various clear distinctions between hormones and neurotransmitters:

A hormone can perform functions over a larger spatial and temporal scale than can a neurotransmitter.
Hormonal signals can travel virtually anywhere in the circulatory system, whereas neural signals are restricted to pre-existing nerve tracts
Assuming the travel distance is equivalent, neural signals can be transmitted much more quickly (in the range of milliseconds) than can hormonal signals (in the range of seconds, minutes, or hours). Neural signals can be sent at speeds up to 100 meters per second.
Neural signalling is an all-or-nothing (digital) action, whereas hormonal signalling is an action that can be continuously variable as dependent upon hormone concentration.


text:
Deuteranopia confusion lines
For people with protanopia (absence of "red" cones), confusion lines look like this (which is quite intuitive for me)

Analogous picture for tritanopia (absence of "blue" cones)

But picture for deuteranopia is quite different. Confusion lines are
  intersecting at one point. But this is not a point nearby green color,
  it is opposite. Why?

I have a conjecture.
Let me remind you about RGB. There is a three-dimensional space (coordinates are RGB coordinates). There is a cone in this space which corresponds to all colors which we can possibly see. Then we consider a section of this cone by a plane. And this is your RGB diagram.
I think that people have chosen a random plane. There is a line for excitation of green cones only. And this the plane intersected negative part of the line. If we chose this plane more carefully, this the picture for green confusion lines would be similar to red and blue.
A friend of mine says that that choice of this plane is not random. It is a plane of constant brightness.
He even conjectured that "green" cone cells are activated not when they absorb green light, but when there is no green color at all.

Is this plane indeed random?

For more details look up here

Is this plane indeed random?

Answer : I don't think so.
HUMAN CONE RESPONSE
Let's take a look back at human cone response curve.
This is cone response curve for normal people :

But picture for deuteranopia is quite different. Confusion lines are intersecting at one point. But this is not a point nearby green color, it is opposite. Why?

In case for Deuteranopes, let's take a look at their cone response :

As you can see Deuteranopes have their green cone sensitivity shifted very close towards red.
This also why Protanopia and Deuteranopia is what we know as Red-Green color blindness, where they have difficulty in distinguishing shades of red from shades of green since its cones sensitivity is very close to each other (almost similar).
So for deuteranopia, why the intersecting point is it not green ? Well, despite the actual missing cone is green, its sensitivity is shifted towards red. Also, this "intersecting point" is called copunctal point.
CONFUSION LINE :
Now about confusion line, indeed each cones in our eyes is sensitive to each RGB primary (even though it's a little bit misleading). And yes, RGB color space is in 3-dimensional. But confusion line is mapped based on chromaticty diagram from CIE 1931, not RGB. Some specific transformation and normalization method need to be performed to convert 3-dimensional RGB into 2-dimensional chromaticity diagram.
As we know before, Protans and Deutans have their cone sensitivity close to each other, thus their copunctal point (point where the fundamental color is missing, point where all the lines converge) is also close to each other.
Here's the copunctal points (1) for all dichromats :
COPUNCTAL POINT     x         y
Protan             0.747     0.253
Deutan             1.080    -0.800
Tritan             0.171     0.000

CIE is quite tricky, they can have negative value as well (RGB can't have negative value). This copunctal point is very important since it's the fundamental information of the missing wavelength from colorblind, and this missing wavelength is converted into CIE colorspace and then mapped into the diagram. So, even though the deuteranopes confusion lines looks a bit confusing, it is the correct mapping from actual missing point in wavelength.
(1) Wyszecki & Stiles, Color Science (2nd ed.), 1982, Table 1 (5.14.2) p. 464


text:
Confusion about mitochondrial electron transport chain Complex I Wikipedia article title
The Wikipedia article title for Complex I (the NADH dehydrogenase enzyme complex) is "NADH dehydrogenase (ubiquinone)". This is confusing to me because this title sounds like ubiquinone is another name for NADH dehydrogenase, but ubiquinone is in fact the Coenzym Q, which is reduced by the hydrogen transferred from NADH through Complex I. What is the reason behind this title? I mean, what is the point of having "ubiquinone" in parentheses in the title?

I've changed the title of the article. The reason for the title was just poor writing (I agree that it seems to imply that the enzyme is ubiquinone) but also the fact that someone had previously tried to change the title to the accepted name tht @xusr has mentioned but they did so incorrectly.


text:
What would cause a single white eyelash?
I couldn't find a paper who could give me the explanation. Unfortunately, according to my search, it seems there are not many reported case, particularly for the younger population (<30). Would stress cause this?

Hair ( and eyelashes ?) comes in a spectrum of colors  ( at least for Caucasians ). In our lab we were testing a new microtome ( really good knife) ; A pinch of hair ( about 30) was pulled out of my head and sliced . The magnified image of the  dozens of round cross sections showed white, black, red , and 10+ shades of "brown" from light yellow to dark brown. Back when I had hair , the overall appearance  was light brown.

What Causes Hair to Have Colour and How is Colour Lost?

The colour of hair is due to the presence of melanin, which may be found as eumelanin or pheomelanin. Melanin is produced by melanocytes and is transported to keratinocytes. The hair then grows out from a root at the bottom of the hair follicle. A hair without melanin is a grey hair. The exact specifics of how hairs go grey is quite complex and poorly understood.
The growth and pigmentation of hair grows are both regulated by many factors, including genes such as MC1R and DLX3. This provides some explanation why people of particular ethnicities or families can go grey at different times - their genetic makeup changes how quickly they go grey.
Another factor affecting hair pigmentation is reactive oxygen species (ROS). The generation of ROS (oxidative stress) has been shown to have a role in the greying of hair.. Moreover, ROS are generated by smoking, which could lead to premature greying.
Other factors that have been found to be associated with premature hair greying include UV light, vitamin B12, iron, copper, ferritin, calcium and vitamin D3 (source).

What Would Make an Individual Eyelash go Grey?

As far as I know, the regulation of eyelash growth and pigmentation is very similar to that of hair on the scalp.
Given that the regulation of hair pigmentation is controlled by genetic factors, it could be that there is a change in the function of the genes at that particular hair follicle. This could possibly involve mutations which change signaling pathways, melanin generation, etc. such that melanin is no longer transported into the hair.
There could also be an extrinsic (outside of the body) factor which has locally stopped melanin production. Perhaps at some point, there was an elevated level of ROS or UV light at that particular hair follicle. This could have introduced mutations in the genes, or could have changed how the hair was pigmented.
Alternatively, there could be death of melanocytes in that specific area, which could stop the generation of melanin. There could also be a local change in the levels of the factors associated with greying (e.g. a local vitamin B12 deficiency).

Does Stress Cause Premature Greying?

Surprisingly, despite common knowledge telling us that hair makes us go grey, there is conflicting evidence about this. Stress has been shown to make us go bald earlier but whether it also makes us go grey is not conclusively known. But given that stress has a clear negative impact on health, it's probably best not to be too stressed regardless.

Regarding the reasons for this pigmentation change; would it be plausible to think that the eyelash can regain its original color following the improvements on the mentioned factors?

@matlabcrz I'm not certain but I think that's unlikely. If the melanocytes are dead, it seems unlikely that they'd come back to life. I'm not sure what would happen if the genes are altered. But hey, it's just an eyelash - it's going to fall out anyway at some point and it's not like anyone would notice that it's white! Plus, I know plenty of people with white patches of hair, and it's really not noticeable :)


text:
How would one go about isolating a specific mRNA out of a pool of others?
I'm writing an essay about DNA recombinant techniques where the question asks to outline all the steps to arrive at having a colony of bacteria expressing a  gene of interest.The question makes you start with a pool of mRNAs, which I assume is for making cDNA. However, how do you go from having thousands of different mRNAs to just one kind?

Your cDNA approach is correct - you use poly-A primers to make cDNA for all mRNAs in the mix, resulting in a mix of cDNAs. Now how do you isolate the one you want from the mix?

Would you use Southern Blotting on the cDNA? would Northern blotting on the mRNAs bring you to the same end point?

Try reading this product insert (downloads a PDF) from Miltenyi GmbH. Half the battle is knowing what techniques or products exist, and when/how to use them. Granted there are other things you could do.

First of all you need to figure out what your goal is: an expression vector (i.e. plasmid) which will drive expression of a gene in bacteria (let's say E.coli), and your gene's coding sequence needs to be downstream of the promoter in that construct.
Your task is asking for a pretty routine lab task known as cloning (https://en.wikipedia.org/wiki/Molecular_cloning). Your mRNA pool might be the result of an RNA extraction from a tissue sample and your goal is to get bacteria that produce lots of the desired protein.
As this is homework, I will only give a broad overview and leave you to figure out the details.
Indeed one way you could approach this is actually some method to specifically extract the desired mRNA, then generating cDNA from it and pasting that into the vector. This is unlikely to give you good success rates, and in practice nobody purifies a specific mRNA unless they are interested in other molecules naturally bound to that mRNA.
Since this is a procedure with a very practical purpose without a scientific question behind it, there's a much more efficient way to achieve it.

Generate cDNA for all mRNAs in the mix ("first-strand cDNA synthesis").
Instead of removing unwanted RNAs, simply amplify the desired one using specific primers you designed and PCR. This gives you what is called the "insert".
Most likely if you ordered the expression vector online, you actually receive bacteria containing it, so you first have to culture those and extract DNA from the culture ("miniprep").
Next step is to paste the DNA into the expression vector. For this you need to digest both the vector and your insert using the same restriction enzymes ("restriction digest"). (Your insert will not have restriction sites on it, so you will need to introduce them by designing the primers for the PCR in step 2 appropriately.)
Run the restriction digest mixes on a gel (electrophoresis), identify the bands corresponding to the insert in one lane and the vector in the other, and extract them (gel extraction).
Ligate the insert and vector
Transform the finished product into competent E.coli


text:
Did the construction of the Panama Canal lead to a huge change in the local marine ecology?
Before the Panama Canal opened in 1914, its two ends were only 77 km apart over land, but the closest sea route was 32,000 km long (around the entirety of South America) and passed through much colder waters near Cape Horn. Therefore, I suspect that the Atlantic and Pacific marine ecosystems were more or less completely isolated from each other and contained very different species before the Canal opened. It also seems plausible that once the canal opened and a 77-km marine route opened up, these two ecosystems very quickly came into contact and may have reached a new, drastically different equilibrium. Is this correct? I could imagine the ecological effects being equivalent to the sudden creation of a 77-km bridge connecting the ecosystems of, say, the United States and Kenya.

This book answers your question pretty well. I was going to put together an answer based on it and other papers I found, but suddenly lost the will to.

Many organisms are transported across the channel by ships, as hull fouling or in ballast tanks (which bypasses the salinity barrier of Lake Gatun). The book mentions that oil tankers routinely dump tens of thousands of tons of ballast water from the Caribbean into ports in Alaska.

Water treatment is performed in onshore facilities by US and some other countries. But the open ocean and many other countries have no requirements.

The panama canal is not just a long contiguous connection between the two oceans as you might think. It operates under a system of locks of varying height because the surrounding region is actually fairly mountainous, so a ship has to enter a lock, let it fill until equilibration with the next lock whilst the boat rises, the barriers open, the boat moves into the next section and the process repeats. It is fairly unlikely much wildlife would be able to pass through this system thus not causing the vast ecological effects you might imagine. https://www.youtube.com/watch?v=hoQ7RHyG-EA this link visualises it for you :)

It doesn't seem unreasonable, to me, that at least some marine life could pass through the locks with ships.

Also, IIRC the canal and locks are fresh water, so it doesn't seem likely that most marine organisms could survive a passage.

I agree with @canadianer. It often takes surprisingly few members of an invasive species to completely change an ecosystem, since none of the original organisms have evolved to resist it from taking over. And if there have been 10 million lock cycles, then quite a few organisms could have passed through even if most cycles don't transfer any organisms.


text:
Can insects or mosquitoes be astonished(shocked)?
Can insects like mosquitoes get astonished by sudden happenings?
Background
I missed hitting a mosquito on a wall with great force. However even though I missed hitting it, it was dead.
So I wonder if insects can reach death or at least astonished by sudden happening, or lead to something like cardiac arrest.
Hope it isn't a noob question :)

+1 for the title. By the way, astonished is maybe too strong a word, but I guess that you could have its monocle fall out of surprise and maybe spill a drop or two of tea on the armchair. :-)

Have you considered alternative explanations? Seems like simpler explanations include: you hit the mosquito but didn't realize it (because it was not trapped between the wall and your hand), or that you caused a sufficient air pressure wave to damage the wings of the mosquito. They are relatively delicate, after all.

@BryanKrause Thanks, that could be. However I am curious about this question (Insects' abilities to get shocked)

I originally thought there was no way anyone had studied this - it felt like one of those questions we get here a lot where people seem to assume "scientists know (almost) everything" - but I decided to give a check anyways.
Short answer
There is in fact evidence that some insects could be scared to death. However, the process is a bit less dramatic than the one you suggest.
I didn't see much on mosquitoes specifically, but your question seems to allow extrapolation from other insects.
Longer answer
I found at least one paper, McCauley, et al. 2011, that studied whether the mere presence of a predator could cause fatal reactions, in this case in dragonflies. There are several others that show more generic stress-induced responses.
McCauley, et al. exposed dragonfly larvae to predators (either fish or a larger dragonfly) who were unable to actually eat the larvae because the larvae were contained within a 'cage' within a larger aquarium.
The larvae exposed to either predator type had substantially more mortality, and only about 30% as many survived to adulthood. This is not precisely insects being startled to death, but rather they propose that the chronic stress of predator exposure caused their growth to be impaired. An alternative explanation is that the larvae exposed to predators simply spent too little time eating to obtain enough nutrition, but they argue in their discussion that this is not likely to be the only cause in the case of the dragonfly predators, because unlike the fish those predators did not reduce their foraging behavior.
There are many other papers that talk about "non-consumptive mortality" more generally but these often include causes of death such as succumbing to injury from failed/incomplete predation, energetic expenditures, etc (Siepielski et al., 2014; Veselý et al., 2017) - few others actually use a highly controlled environment to prevent physical contact between predator and prey like in McCauley. Other studies do show that exposure to increased stress levels causes changes in gene expression and impacts on the immune system in insects (De Block & Stoks, 2008; Slos & Stoks, 2008).
On the point of mosquitoes, I did find one paper that showed reduced lifespan duration in adult mosquitoes exposed to increased predation as larvae (Bellamy & Alto, 2018) - again not exactly what you were looking for in terms of an acute event, but still somewhat related.
In summary
I think an important takeaway is that insects, like vertebrates, can be susceptible to stress.

References
Bellamy, S. K., & Alto, B. W. (2018). Mosquito responses to trait-and density-mediated interactions of predation. Oecologia, 1-11.
De Block, M., & Stoks, R. (2008). Compensatory growth and oxidative stress in a damselfly. Proceedings of the Royal Society of London B: Biological Sciences, 275(1636), 781-785.
McCauley, S. J., Rowe, L., & Fortin, M. J. (2011). The deadly effects of “nonlethal” predators. Ecology, 92(11), 2043-2048.
Siepielski, A. M., Wang, J., & Prince, G. (2014). NONCONSUMPTIVE PREDATOR‐DRIVEN MORTALITY CAUSES NATURAL SELECTION ON PREY. Evolution, 68(3), 696-704.
Slos, S., & Stoks, R. (2008). Predation risk induces stress proteins and reduces antioxidant defense. Functional Ecology, 22(4), 637-642.
Veselý, L., Boukal, D. S., Buřič, M., Kozák, P., Kouba, A., & Sentis, A. (2017). Effects of prey density, temperature and predator diversity on nonconsumptive predator-driven mortality in a freshwater food web. Scientific reports, 7(1), 18075.

Great Answer, but sad.. At which taxanomical level should we stop messing with being's lives?


text:
How can diving with 100% oxygen not destroy your lungs?
It is possible this should be moved to physics, depending on the nature of the answer (i.e. if the reason is physical). But I suspect the explanation is biological, so I posted it here.
Sometimes technical divers dive with 100% oxygen. I don't understand how can this not burn, oxidize or at least damage their lungs. To begin with, even if someone would breath 100% oxygen in atmospheric pressure, I'd suppose he'd damage his lungs, because the 79% of the volume that would normally be filled with inert nitrogen is now filled with oxidizing oxygen.
If, however, someone dives to, say, 30 meters, with pure oxygen, he'd have to fill his lungs with oxygen at 4 atmospheres to equalize the pressures. That means the pure oxygen filling his lungs is even more concentrated. How can this be? A friend of mine who dived with pure oxygen even says the breathing feels just normal. How is this possible? How are the lungs not damaged?

I think you might be misinformed about the gases that divers use. https://chemistry.stackexchange.com/questions/61406/why-would-breathing-pure-oxygen-be-a-bad-idea No one is really breathing 100% oxygen at depth, they are at most using a 100% oxygen supply. And yeah, the answers here aren't really based on biology. Maybe physics/chemistry, but you are probably going to get a better answer at a more specialized source for that particular niche of diving.

From what I recall, nitrox is at max 40% oxygen. Do people really dive with 100% oxygen? Can you please give a link that support this claim? Do they breath from it directly or do they use these tanks in a rebreather system?

@Remi.b It's a rebreather. They are recycling the nitrogen/other gases, scrubbing the CO2, and replacing the metabolic O2 from a 100% O2 tank to reduce mass.

I am VTC because I think the question is based upon OP's misunderstanding of diving equipment. Outdoor.SE might be of help to you to improve your understanding of diving equipment.


text:
Does IQOS/HEETS emits CO?
I am researching the safety of IQOS (THS2.2) for heat-not-burn cigarettes (HEETS).
I am particularly interested in appraising the impact of IQOS/HEETS on CO emission and inhalation.
Is there evidence of this?


text:
Why do some reflex actions involve interneurons, but some don't?
According to what I know, the reflex arc of knee jerk reflex doesn't involve interneuron, but other reflex action (e.g. removing your hand when touching hot things) do involve interneurons. Why is that the case?

I believe the knee jerk reflex does involve interneurons.

@John my biology textbook specifically say knee jerk reflex doesn't involve interneurones and the teacher also kept telling us to remember that knee jerk reflex is the only reflex in the exam syllabus that doesn't involve interneurone

The "knee jerk" reflex is a stretch reflex, as @John's answer indicates. It is unfortunately named the "knee jerk" for the response observed in the corner case where rapid, short extension of the leg at the knee is elicited by tapping the patellar tendon with a percussion hammer during a physical exam. Despite being named for this specific phenomenon, this reflex contributes to setting resting muscle tone, controlling the response to a load, and coordinating synergist and antagonist actions. You can read about this in some detail in Kandel's Principles of Neural Science, Chapter 36.
The sensory portion of this reflex involves a proprioceptive sensory organ called a muscle spindle that detects the stretch of a skeletal muscle.  All human (and most mammalian) skeletal muscles have these sensory organs, so this is not specific to the quadriceps at the knee. Several are tested in a similar way to the quadriceps as part of a neurological exam (see Brust, Practice of Neural Science, Chapter 6), but, as is the case with most reflexes, they are more complex than is taught in introductory biology. This sensory organ is continuously active, sending information to the cortex, the cerebellum, synergist and antagonist muscles, as well as back to the muscle in which the organ itself is found (again, see Kandel).
Answers about "why" a physiologic system is set up in a particular way are generally speculative, but stretch reflexes in muscle are definitely different from other reflexes. Unlike, for example, the withdrawal reflex, the sensory organ (the muscle spindle) is actually part of the effector (the muscle), and provides continuous feedback to the effector, controlling its primary function (contraction/production of tension). Additionally, the processing and sensitization/desensitization that an interneuron might provide in a different reflex arc are provided by innervation and control of the spindle itself by $\gamma$-motonuerones, among others.

$\gamma$-motoneurone function is essential for controlling the sensitivity of muscle spindle afferents as length detectors

There are additional reflex arcs with the same sensory part that involve processing and inhibition/excitation by interneurons. But in these cases the outflow is to a separate effector (antagonist muscles). See the figure below from Brust, Chapter 6.

I did not realize it but the knee jerk reflex is a stretch reflex and thus only involves two neurons (monosynaptic). Many many more reflexes use 3 or more neurons (polysynaptic) so include interneurons.
monosynaptic are common for muscle stretch limiting reflexes, that is why I knew them by their more common name stretch reflexes and did not make the connection. They don't involve interneurons becasue they would offer little benefit, they are self regulating most of the time and only involve a single source and a single destination and will not see much benefit from modification of the signal.
This slideshare on reflexes can provide some detailed information and a place to keep researching from.

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


text:
Log2 vs Quantile normalization
I am learning normalizations, I wonder when log2 and quantile normalization is used in each situation, may I ask if there is any material that compare these two types especially in microarray expression matrix for differentially expressed gene analysis? Thank you!

Welcome to Biology.SE. I'm voting to close this question as off-topic because it is not about Biology but about statistics.

Note that the tag 'human-biology' that you chose does not apply


text:
How likely is it that we will discover a new species of big cat?
So, I've been reading some articles about these "scandals" where everybody thought that there was a new species of feline discovered, from some weird skull or carcass or whatever. And always, by the end of the article, they would have concluded that it was just a jaguar or an ocelot or not even a feline. But, it got me thinking, and I was wondering - Is it possible (As in, are there more than minuscule chances) that we will discover a new species of big cat, or Panthera species?

Welcome to BiologySE! Please cite the source from where you heard that. Also, do take a moment to check out the [tour] of our site.

Extant (alive) extremely small. There just is no place left to hide so to speak. If we do it will most likely be what we thought as one species being split into two along some currently unknown factor, similar to how chimps and bonobos were thought to be the same until fairly recently.
Extinct extremely high, we have discovered such a small fraction of a percentage of the number of species that have ever existed that any group is a candidate for future discovery.

Actually the last big cat discovered was only 2011 so it's remotely possible that another can be discovered.

Comparisons between the clouded leopards of mainland Asia and the Sunda Islands of Southeast Asia, which include Borneo, Java, Sumatra and Bali, revealed the Sunda clouded leopard was genetically distinct, making it the newest species of big cat known to science.
(Despite their name, clouded leopards are not actually a kind of leopard, but are completely separate from the genus that includes lions, tigers, leopards and jaguars.)

https://m.csmonitor.com/Science/2011/0125/That-new-species-of-big-cat-Turns-out-it-s-actually-two-new-species

Yeah, that was one of the things that got me thinking for this question.


text:
Why do men have a greater chance of suffering from hair loss?
If we look around we'll find that men are more likely to suffer from hair loss when compared to women. Is there is any specific reason for this?

some hair loss is related to testosterone, as to why eununchs tend to preserve hair better. https://en.wikipedia.org/wiki/Pattern_hair_loss      (article about eununchs)        http://www.bbc.com/future/story/20131127-will-we-ever-banish-baldness

@RoSiv Please make an answer rather than posting an answer in the comments.

@BryanKrause      I wasnt really confidant with my answer but ok.

As per my comment above, some types of hair loss is androgenic, and therefore related to testosterone levels. This is why eunuchs can be resistant to some forms of hair loss.


text:
Can predator-prey relationship be an example of negative feedback?
Predators eat their prey, prey population decreases. This results in the predator population to decrease, so less prey are consumed which causes the prey population to increase.
Therefore, if the reduction in prey population results in its increase then can this be described as negative feedback?

Somewhat related: What prevents predator overpopulation?

From my experience, "negative feedback" is more often used in the context of processes in the body which attenuate themselves or in the context of stimuli and sensors. However predator-prey dynamics could fit the general definition of the term. In general, negative feedback is just when a process or output of a system leads back into the system to attenuate itself.

Negative Feedback:
"A feedback in which the system responds in an opposite direction to the perturbation. "
Source: biology-online.org, access date: 2018-04-06.

In a general case of a closed-loop (feedback) control system, you've got a stimulus that gets sensed by a sensor, which sends a signal to a controller. The signal is then passed on to an effector, which can change the original stimulus. In the case of negative feedback, the stimulus is attenuated. In positive feedback, it is potentiated.
$$\begin{array}{ccc}
\fbox{Stimulus}&\rightarrow&\fbox{Sensor}
\\
\uparrow&&\downarrow
\\
\fbox{Effector}&\leftarrow&\fbox{Controller}
\end{array}$$
A common example of this would be high body temperature being detected by neurons, which send a signal to the brain to cause the body to sweat more. In this case, the sweat glands are the effectors and can lower the body temperature.
$$\begin{array}{ccc}
\fbox{Change in body temp.}&\rightarrow&\fbox{Neurons}
\\
\uparrow&&\downarrow
\\
\fbox{Sweat Glands}&\leftarrow&\fbox{Brain}
\end{array}$$
In your case, I think you could describe it with an increase of prey population being the stimulus, which is detected by the predators as they see more prey. The predators would then choose to eat the prey (I suppose this could be the controller) and then act as the effector by eating the prey (and thus, reducing the prey population). Though I'm a little iffy on this since you'd have the predator acting as both the sensor, controller and the effector. Conversely, if the prey population were lowered, the opposite would be true.
$$\begin{array}{ccc}
\fbox{Change in prey pop.}&\rightarrow&\fbox{Predators sense prey}
\\
\uparrow&&\downarrow
\\
\fbox{Predators eat prey}&\leftarrow&\fbox{Predators choose to eat prey}
\end{array}$$

Yes, in the fields population dynamics/ecology, the standard predator-prey system is routinely described in terms of a negative feedback loop. See e.g. Lewontin & Levins, 2007 for an online exemple (the term is commonly found in articles and textbooks though).


text:
is it possible that there is no gene at a locus?
"the location of a certain gene on a chromosome " is the definition I know for locus. ı just read that a gene is not necessarily present on a locus. how would that be possible?

A locus is not necessarily the position of a gene. It is a position in the genome, whether or not, there is a gene at this position. A locus often refers to the position of a SNP (which may well be outside a coding region) or any other type of genetic marker.
A gene is typically defined as a sequence that is coding for a protein. Most of a eukaryotic genome, such as the human genome is not made of sequences coding for proteins. It is rather made a various regulatory sequences, introns and especially repetitive DNA. So, if you randomly pick a sequence in the human genome, chance are it is not going to be a sequence that gets translated.

so would this mean that the definiton ı stated for locus is not exact?

Indeed. I edited the answer to clarify that.

Like you said in your question - "locus" means location.  A locus may be anywhere on a chromosome - an entire "gene" coding locus, a non-coding locus (junk DNA), a regulatory sequence locus (example - the promoter region of a gene), or just a single nucleotide locus (SNP) etc.  A "locus" is the location of interest on the chromosome.
Yes, it is also possible that any genetic "locus" may be absent if it has been lost by a "deletion".  A deletion is a type of mutation.  They might be a single nucleotide deletion or a very large deletion of thousands of nucleotides. Genetic deletions can happen in several natural ways (a DNA repair error for example), and by other mechanisms, but also through "man made" genetic manipulations.

Locus just means location, as (non-)specifically as in any other use of the word.
Remember the word originates from traditional genetic studies, which didn't know how genes work. Back then, scientists gave some name to "that region in the genome" and they determined the approximate position relative to other known loci through recombination studies. For many of these, we have in retrospect figured out that all of the findings by these older studies were related to a specific gene and now we refer to that gene by the name originally used for the locus. If you read older papers about the white gene in Drosophila, you'll see this usage.
In vertebrates, functionally related genes are often located close to each other (in a cluster) and it's useful to have a name for the whole group. For example, some transcription factor's function might depend on how the genes are arranged in the genomic region. One example is the human beta-globin locus.
Even when a locus contains something like a "gene", it might not be a traditional protein-coding gene but rather a miRNA (or others like tRNA, rRNA) locus. These again sometimes cluster.
The sequence at that location in the genome doesn't need to be functional in any way. For DNA fingerprinting, you could determine the number of VNTR repeats at each VNTR locus.
And finally, like Remi.b mentions, "locus" can very specifically refer to a single position within a gene's sequence.


text:
What are the interactions between mtDNA and nucelus' DNA?
In an exam situation I have been presented with the following question by the teacher:

What are the interactions between the mitochondrial DNA and the cell's nuclear DNA?

To my knowledge there is no such interaction. At the best you could say that the nuclear genome provides the mitochondria with some proteins and vice versa the mitochondria may participate in intrinsic apoptosis by releasing cytochrome C. Unfortunately this answer was not accepted by the teacher and I was not given an explanation. My question is wheter there is an actual interaction I've never heard of or if maybe the poorly worded question was alluding to something else.

IMO, the question is rather broad and a little vague. Knowing the subject of the course may help us. What was the subject of the course?

Hello. I am studying medicine in europe. The exam in question is just a first year Bio & Genetics course.

Sounds as if you have a good grasp of the biochemistry of mitochondria. Probably better than your instructor, who may be embarrassed at his poor question. Certainly there are no contemporary physical interactions, although if you are considering evolution then mitochondrial genes were lost to the nucleus. Move on.


text:
sweet receptor's affect on insulin release
So I understand the basics of how the body releases insulin to keep blood glucose levels in check and (loosely) that higher insulin levels can lead to more (or at a faster rate) glucose being stored as fat rather than being made readily available for energy. For this reason, I try hard to keep a good balance of carbs/protein/fat with each meal... operating on the principle that the protein and fat will slow the breakdown of carbs into glucose and eventual absorption into the bloodstream.
Recently, I have heard some chatter suggesting that in addition to the absorption of glucose into the blood stream, the mere activation of our sweet receptors can/does cause the release of insulin as well.
If this is the case, when I have a snack of say an orange and some cheese, while I think I'm avoiding the insulin spike (by adding the protein and fat of the cheese) that an orange ingested by itself may cause, it's actually still occurring due to, not the high glycemic index of the orange, but it's sweet taste.
Does anyone know if there is any truth to this? And if so, what does the data say... are the spikes elicited by activation of the sweet receptors of similar levels to those from actual high glucose levels in the blood?
In Googling cephalic phase insulin release, I've read abstracts for a few studies that seemed to be more focused on the effects of artificial sweeteners... which isn't really what I'm looking for. But one study seemed to indicate that solutions of sucrose tended to elicit higher insulin levels (than other solutions tested), but not being from the bio/physiology world, it quickly became over my head. I know some fruits (such as my aforementioned orange) are quite high in sucrose.
In practical terms, I'm trying to figure out what other foods, if any, may cause this response and if it is significant enough that one concerned with maintaining consistent, low insulin levels should stay away from such foods.
Can anyone help shed some light on this for a curious layperson? Thanks!


text:
At what minimum distance the direction at which eyes point becomes parallel?
This is very similar, but different than this question about focus, let me explain why it's not a duplicate at all.. That other question is about the distance of EACH individual eye FOCUS, this one is about VERGENCE, focus plays no role in this question, here what matters is the angle formed between the direction each eyes points. When objects are close to our noses, eyes get cross-eyed. As objects get further away, the eyes get more parallel, so called wall-eyed. There must a distance just become totally parallel, I deduce this by analogy to what happens to the focus, for which the distance is 6 m as this answer says. What is the corresponding distance for vergence?
I couldn't find the answer in the relevant wikipedia article on vergence.

Mathematically, the eyes are parallel when they fixate at, and only at, infinity. Now, because of noise, there is a distance after which it's not really going to make a difference (otherwise you would be able to tell the distance between stars at night). There are 2 parts for your question. First, at what distance it doesn't matter because the eyes won't stay still enough to accurately maintain this vergence angle. Second, at what distance it perceptually makes no difference because you can't tell if the object is closer or not. Concretely it means looking at the distance where each of these metrics is smaller than detection threshold (the value below which your performance on a detection task is lower than a specified value). Conveniently, Chopin et al. (2016) measured both values (these numbers can of course be found in older papers too).
For the first question, they measured vergence noise of 225 arcsec (or 225*pi/(60*60*180)=0.0011radians). The distance for which vergence becomes smaller than that is approximately 55 meters (vergence~=IPD/FD, with IPD interpupilary distance of approx 6cm). So farther than that you wouldn't be able top tell whether they fixate at infinity or not.
For the second question they measured relative disparity thresholds. Relative disparity is the difference in vergence angles between 2 points. So for relative disparity angles lower than threshold you cannot tell whether point A is closer or farther than point B. They unfortunately don't report the exact value but from the graph it looks like 300arcsec, corresponding to a distance of about 40 meters. In other words, after this distance you can't tell whether an object is farther than where you look at.
Finally, you could also ask: at what distance can't I tell whether an object is at infinity or not? The distance of a point in isolation is called absolute disparity, and is known to be much worse than relative disparity (i.e. it is much easier to compare the distance of 2 points than to report the distance of a single point in isolation). This distance turn out to be quite shorter. From the same paper the absolute disparity threshold is about 3000arsec (again, they unfortunately don't report the exact value). This gives a fixation distance after which you cannot tell whether you fixate at infinity or not of about 4 meters.
This is all very approximate and making lots of assumptions but I hope this more or less answer your question.
Chopin, A., Levi, D., Knill, D., & Bavelier, D. (2016). The absolute disparity anomaly and the mechanism of relative disparities. Journal of vision, 16(8), 2-2.


text:
DNA Sequencing - Sanger termination method: What effects will more ddNTPs in solution have on the resolution on agarose gel via electrophoresis?
Say instead of a small amount of ddNTPs, you add a significant percent of ddNTPs to dNTPs. I was thinking this would reduce the resolution for larger fragments due to more ddNTPs terminating elongation earlier on.
I am doing a project on Sanger Sequencing and was wondering this, thank you. (Any suggestions would be appreciated)

You are correct. The greater the ratio of ddNTPs to dNTPs, the more frequently ddNTPs will terminate the reaction, resulting in shorter mean fragment size. However, Sanger sequencing is not done with agarose gels. The result visualizing a Sanger reaction on agarose, using more ddNTPs would result in a smear closer to the bottom. For actually visualizing the sequences on acrylamide, or with capillaries, increasing the ddNTPs would reduce the resolution of longer fragments. It is a balance you need to optimize.


text:
Bird Identification: New Delhi, April 2018
I've looked in Birds of the Indian Subcontinent (BNHS version, not Inskipp) and two phone apps and still can't find this, although I am a newbie tourist so am probably making a basic mistake. Seen today, 2018-04-07, 9:00 local time, in a New Delhi urban garden.

Maybe 25cm long. Uniform grey above, mottled grey below, grey legs with slight orange tinge. Orange-yellow bill, very slim light eye ring. I wondered about a large grey babbler, but all the pictures I can find seem less grey.
Thanks!

It looks like you're on the right track.  Here's a photo of a Jungle Babbler (Turdoides striata).  They are found on the Indian subcontinent.

Source: https://en.wikipedia.org/wiki/Jungle_babbler

I'm no pro at species identification, but being in New Delhi (although I see them everywhere I go), I can pretty much confirm this. +1 for this ;)